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Broken heart syndrome

Broken heart syndrome

Overview

Broken heart syndrome is a temporary heart condition that's often brought on by stressful situations, such as the death of a loved one. The condition can also be triggered by a serious physical illness or surgery. People with broken heart syndrome may have sudden chest pain or think they're having a heart attack.

In broken heart syndrome, there's a temporary disruption of your heart's normal pumping function in one area of the heart. The remainder of the heart functions normally or with even more forceful contractions. Broken heart syndrome may be caused by the heart's reaction to a surge of stress hormones.

The condition may also be called takotsubo cardiomyopathy, apical ballooning syndrome or stress cardiomyopathy by doctors. The symptoms of broken heart syndrome are treatable, and the condition usually reverses itself in days or weeks.

Symptoms

Broken heart syndrome symptoms can mimic a heart attack. Common symptoms include:

•          Chest pain

•          Shortness of breath

Any long-lasting or persistent chest pain could be a sign of a heart attack, so it's important to take it seriously and call 911 if you experience chest pain.

When to see a doctor

If you're having any chest pain, a very rapid or irregular heartbeat, or shortness of breath after a stressful event, call 911 or emergency medical assistance immediately.

Request an Appointment at Mayo Clinic

Causes

The exact cause of broken heart syndrome is unclear. It's thought that a surge of stress hormones, such as adrenaline, might temporarily damage the hearts of some people.

How these hormones might hurt the heart or whether something else is responsible isn't completely clear. A temporary constriction of the large or small arteries of the heart has been suspected to play a role.

Broken heart syndrome is often preceded by an intense physical or emotional event. Some potential triggers of broken heart syndrome are:

•          News of an unexpected death of a loved one

•          A frightening medical diagnosis

•          Domestic abuse

•          Losing — or even winning — a lot of money

•          Strong arguments

•          A surprise party

•          Having to perform publicly

•          Job loss

•          Divorce

•          Physical stressors, such as an asthma attack, a car accident or major surgery

It's also possible that some drugs, rarely, may cause broken heart syndrome by causing a surge of stress hormones. Drugs that may contribute to broken heart syndrome include:

•          Epinephrine (EpiPen, EpiPen Jr.), which is used to treat severe allergic reactions or a severe asthma attack

•          Duloxetine (Cymbalta), a medication given to treat nerve problems in people with diabetes, or as a treatment for depression

•          Venlafaxine (Effexor XR), which is a treatment for depression

•          Levothyroxine (Synthroid, Levoxyl), a drug given to people whose thyroid glands don't work properly

How is broken heart syndrome different from a heart attack?

Heart attacks are generally caused by a complete or near complete blockage of a heart artery. This blockage is due to a blood clot forming at the site of narrowing from fatty buildup (atherosclerosis) in the wall of the artery. In broken heart syndrome, the heart arteries are not blocked, although blood flow in the arteries of the heart may be reduced.

Risk factors

There are a number of known risk factors for broken heart syndrome, including:

•          Sex. The condition affects women far more often than men.

•          Age. It appears that most people who have broken heart syndrome are older than 50.

•          A history of a neurological condition. People who have neurological disorders, such as a head injury or a seizure disorder (epilepsy) have a greater risk of broken heart syndrome.

•          A previous or current psychiatric disorder. If you've had disorders, such as anxiety or depression, you probably have a higher risk of broken heart syndrome.

Complications

In rare cases, broken heart syndrome is fatal. However, most who experience broken heart syndrome quickly recover and don't have long-lasting effects.

Other complications of broken heart syndrome include:

•          Backup of fluid into your lungs (pulmonary edema)

•          Low blood pressure (hypotension)

•          Disruptions in your heartbeat

•          Heart failure

It's also possible that you may have broken heart syndrome again if you have another stressful event. However, the odds of this happening are low.

Prevention

There's a small chance that broken heart syndrome can happen again after a first episode. There's no proven therapy to prevent additional episodes.

Many doctors recommend long-term treatment with beta blockers or similar medications that block the potentially damaging effects of stress hormones on the heart. Recognizing and managing stress in your life may also be important in helping to prevent broken heart syndrome, though there's currently no evidence to prove this.

Link: https://www.mayoclinic.org/diseases-conditions/broken-heart-syndrome/symptoms-causes/syc-20354617

Takotsubo Cardiomyopathy

Takotsubo cardiomyopathy: Pathophysiology, diagnosis and treatment

Kazuo Komamura, Miho Fukui, Toshihiro Iwasaku, Shinichi Hirotani, and Tohru Masuyama

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This article has been cited by other articles in PMC.

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Abstract

In 1990, takotsubo cardiomyopathy (TCM) was first discovered and reported by a Japanese cardiovascular specialist. Since then, this heart disease has gained worldwide acceptance as an independent disease entity. TCM is an important entity that differs from acute myocardial infarction. It occurs more often in postmenopausal elderly women, is characterized by a transient hypokinesis of the left ventricular (LV) apex, and is associated with emotional or physical stress. Wall motion abnormality of the LV apex is generally transient and resolves within a few days to several weeks. Its prognosis is generally good. However, there are some reports of serious TCM complications, including hypotension, heart failure, ventricular rupture, thrombosis involving the LV apex, and torsade de pointes. It has been suggested that coronary spasm, coronary microvascular dysfunction, catecholamine toxicity and myocarditis might contribute to the pathogenesis of TCM. However, its pathophysiology is not clearly understood.

Keywords: Cardiomyopathy, Catecholamine, Heart failure, Myocardial Infarction, Stress

Core tip: Takotsubo cardiomyopathy (TCM) is an important disease entity that differs from acute myocardial infarction. It occurs more often in postmenopausal elderly women, is characterized by a transient hypokinesis of the left ventricular (LV) apex, and is associated with emotional or physical stress. Wall motion abnormality of the LV apex is generally transient and resolves within a few days to several weeks. The prognosis of TCM is generally good. It has been suggested that coronary spasm, coronary microvascular dysfunction, catecholamine toxicity and myocarditis might contribute to the pathogenesis of TCM. However, its pathophysiology is not clearly understood.

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INTRODUCTION

Takotsubo cardiomyopathy (TCM) is a transient wall motion abnormality of the left ventricular (LV) apex accompanied with emotional or physical stress that usually resolves completely. Takotsubo is a Japanese word meaning a pot with a narrow neck and a round bottom used to catch octopuses. Left ventriculography during systole of patients with TCM demonstrates such a shape. Although TCM is a novel concept, the number of cases reported is increasing rapidly. Other words have been used to refer this cardiomyopathy, including stress-related cardiomyopathy[1], transient LV apical ballooning syndrome[2,3], broken heart (heartbreak) syndrome, and ampulla cardiomyopathy[4]. In 2006, the American Heart Association incorporated this disease under the class of acquired cardiomyopathies[ HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B5"5]. This article aimed to review this newly recognized cardiomyopathy, paying particular attention to clinical characteristics, pathophysiology, diagnosis, and treatment.

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EPIDEMIOLOGY

TCM symptoms were considered extremely rare until the past 20 years. The increasing number of medical reports on these symptoms has highlighted the higher incidence of TCM than that previously reported. Currently, 1000 or more studies reporting cases of TCM have been published. According to a retrospective review, patients with TCM accounted for approximately 2% of all the patients with suspected acute coronary syndrome[6,7]. Further, 90% of these patients were postmenopausal women[8,9]. A few reports indicated that the average age of TCM patients was 68 years, although children or young adults may also be affected[10,11]. Another report indicated that most men with TCM were inpatients, which suggests that physical stresses might play a role for the progress of the disease[12]. In a recent study, demographic and clinical course data in patients with TCM were compared between the United States and Japan. Few Japanese patients with TCM had a history of overt coronary disease (CAD) and family history of early-onset CAD. However, there was no significant difference in long-term prognosis and the recurrence rate between the United States and Japanese patients with TCM[ HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B13"13].

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DIAGNOSIS

The diagnosis of TCM remains controversial. The diagnostic criteria most widely accepted were published by the Mayo Clinic[14] in 2004. In 2008, a new criterion was added to them: a normal epicardial coronary artery (Table ​(Table11)[15]. Kawai et al[16] classified this disease as a syndrome of unknown etiology that was characterized by acute balloon-like dilation in the LV apex (Table ​(Table2).2). As shown by these two diagnostic criteria, the patients with TCM have nonspecific or normal findings on physical examination; however, the clinical course resembles that of acute coronary syndrome or acute decompensated heart failure[14-16]. The most common presenting symptoms listed in the diagnostic criteria are chest pain and dyspnea. In rare cases, patients developed palpitations, nausea, vomiting, syncope, or cardiogenic shock[14- HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B16"16].

Table 1

Diagnostic criteria of the Mayo Clinic

AMI: Acute myocardial infarction; ECG: Electrocardiogram; LV: Left ventricular.

Table 2

Diagnostic criteria of Kawai et al[ HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B16"16]

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AMI: Acute myocardial infarction; ECG: Electrocardiogram; LV: Left ventricular; TCM: Takotsubo cardiomyopathy.

The following six symptoms are especially indicative of TCM: (1) acute onset and stressful inducement: One of the unique features of TCM is its relation with stressful emotional or physical events. This characteristic was described in nearly two-thirds of the patients who developed TCM[17]. Unlike acute coronary syndrome, with an onset peak early in the morning, TCM presents in the afternoon in most cases when stressful inducible events are likely to occur; (2) electrocardiographic characteristics: Although the initial electrocardiogram (ECG) of patients with TCM is nonspecific, an ST segment elevation can be found mainly in the precordial leads in 50% of patients at onset[18,19]. In addition, reciprocal ST-segment depression in the inferior wall leads is unlikely[20]. In comparison with patients with base deformity, inverted T waves are more frequently observed in patients with apex balloon-like dilation[21] and they resolve spontaneously within a few weeks to several months (Figure ​(Figure1).1). Furthermore, patients with TCM usually present abnormal Q waves in precordial leads. These Q waves are transient in most patients and generally resolve within a few days to several weeks[22]; (3) cardiac enzymes: In most patients with TCM, there is slight elevation in the cardiac enzyme level on admission[6,20]. The enzyme levels decrease rapidly and do not seem to have prognostic significance[22]; (4) absence of coronary lesion: It is characteristic that no specific coronary lesions are detected in TCM[23,24]. Generally, patients with TCM have chest pain, changes in ECG, elevation of cardiac enzyme levels, and wall motion abnormalities. Therefore, coronary angiography has to be conducted to rule out acute coronary syndrome; (5) balloon-like dilation of the ventricle: In contrast with acute myocardial infarction, LV wall motion abnormalities are found beyond a single coronary artery perfusion area in patients with TCM. Most patients with TCM show loss of motion or hypokinesia at the apex and an apical balloon-like dilation pattern associated with preservation of the base (Figure ​(Figure2).2). However, cases of a TCM subtype without abnormalities of the apex were reported recently[25,26]. TCM is essentially characterized by LV failure, although, approximately, one-third of patients also have abnormalities in the right ventricle[27]. Cardiac magnetic resonance imaging (MRI) is a suitable method to establish the diagnosis of TCM because this modality allows the accurate identification of reversible myocardium damage by visualization of wall motion abnormalities in each area, quantification of ventricular function, and assessment of inflammation and fibrosis. This modality brings new insight into the pathophysiology of TCM. It could enable early treatment of acute symptoms, raise awareness, and improve clinical outcomes. Cardiac MRI is appropriate to evaluate wall motion abnormalities and LV ejection fraction, and to confirm the absence of delayed gadolinium enhancement in patients with TCM. This allows differentiation of TCM from myocardial infarction and myocarditis, both pathologies associated with delayed gadolinium enhancement[ HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B17"17]. Although coronary computed tomography angiography is not applicable to the first diagnosis of patients with TCM, there are many reports on its use for clinical course evaluation after TCM onset; (6) recovery of cardiac function: One of the characteristics of TCM is that thorough recovery of cardiac function is achieved. In contrast to other serious wall motion abnormalities at onset, recovery of ventricular function is proven in follow-up evaluations. Most patients with TCM show significant improvement of systolic function within a week and achieve complete recovery by the end of third or fourth week after onset. Generally, another diagnosis should be considered in patients with suspected TCM whose systolic function is not normalized within 12 wk after onset.

Figure 1

Inverted T waves are found in the limb and precordial leads, which is a common characteristic of takotsubo cardiomyopathy with apex balloon-like dilation.

Figure 2

Systolic apex balloon-like dilation on left ventriculography (A) and normal diastolic dilation (B). A: Systole; B: Diastole.

The differential diagnosis of TCM includes the following: esophageal spasm, gastroesophageal reflux disease, myocardial infarction, myocardial ischemia, unstable angina, acute coronary syndrome, angina, aortic dissection, myocarditis, acute pericarditis, pneumothorax, cardiogenic pulmonary edema, pulmonary embolism, Boerhaave syndrome (spontaneous esophageal rupture), cardiac tamponade, cardiogenic shock, cocaine-induced cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, and coronary artery spasm.

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PATHOPHYSIOLOGY

The exact pathogenesis of TCM is unknown, but various hypotheses have been suggested and discussed, including coronary microvascular dysfunction, coronary artery spasm, catecholamine-induced myocardial stunning, reperfusion injury following acute coronary syndrome, myocardial microinfarction and abnormalities in cardiac fatty acid metabolism. Currently, catecholamine-induced cardiotoxicity and microvasculature dysfunction are the most supported theories.

Catecholamine theory (Figure ​(Figure33)

Figure 3

The catecholamine theory of takotsubo cardiomyopathy. LV: Left ventricular.

Wittstein et al[22] found that the serum catecholamine concentration was two to three times greater in patients with TCM than that in patients with myocardial infarction, and described that serious emotional stress is a precipitating factor. It has been reported that exogenously administered catecholamines and pheochromocytoma cause typical characteristics of TCM, which supports this theory further[28, HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B29"29].

Lyon et al[30] advocated a theory called “stimulus trafficking” that could explain the decline of myocyte contractile function in patients with TCM. Supraphysiological levels of catecholamines induce β2-coupling from Gs to Gi. Therefore, the decline of myocyte contractile function is evidenced by hypokinesia in ECG. Involvement of the apex can be attributed to higher adrenoceptor density in the apex than in the base[31]. The rationale of stimulus trafficking is that a switch to Gi occurs to protect the myocytes from the strong stimulation of Gs, which causes apoptosis. Slow increases in serum troponin level explain early minimal necrosis of the myocardial tissue. Nef et al[ HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B32"32] showed increased activity of the phosphatidyl inositol 3-kinase-protein kinase B (PI3K/AKT) signaling pathway, which has important anti-apoptosis functions and plays a role in the rapid recovery of myocytes. Thus, the transient LV dysfunction can be attributed to the PI3K/AKT pathway and inversely switching from Gi to Gs, associated with the homogeneous, prompt and clinically thorough recovery of systolic function observed in TCM.

Patients with TCM consistently present microvasculature dysfunction findings[33]. The characteristics of microvasculature dysfunction after acute psychological stress in patients with TCM include abnormality of endothelium-dependent vasodilation, excessive vasoconstriction, and impairment of myocardial perfusion[34]. Uchida et al[35] reported that extensive endothelial cell apoptosis was observed by myocardial biopsy. According to another report, increased susceptibility to ergonovine or acetylcholine followed by large vessel spasm, similar to vasospastic angina, may contribute to transient LV dysfunction[36]. However, because only 30% of patients showed the characteristics of vasospasm in a challenge test, this theory was ruled out[37,38]. Afonso et al[ HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B39"39] demonstrated that circulatory disturbance, indicating coronary microvascular dysfunction was found on a myocardial contrast echocardiography and the epicardial coronary arteries were normal.

Myocardial biopsy of patients with TCM showed regions with contraction band necrosis, inflammatory cell infiltration, and localized fibrosis[40]. These changes were caused by direct catecholamine toxicity on cardiac muscle cells[41]. Morel et al[42] found that C-reactive protein levels and white blood cell counts increased with the increase in norepinephrine levels in patients with TCM and inferred that catecholamines produced more systemic inflammation via the induction of proinflammatory cytokines such as tumor necrosis factor-α and interleukin-6. Several studies have pointed out that the remarkable myocardial edema, observed on cardiac MRI, occurs despite normal perfusion, which provides further evidence to support the inflammation theory[43,44]. Ueyama et al[ HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B45"45] examined restraint stress in rats with TCM and reported that heme oxygenase 1 (HO-1) levels, a marker of oxidative stress that has cardioprotective properties, was increased significantly. Macrophages play an important main role in oxidative stress induction and expression of β- and α-adrenergic receptors. As a result of pretreatment with β- and α-antagonists, HO-1 expression and its altering gene expression, decreased.

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RISK FACTORS

Lack of estrogen

More than 90% of patients with TCM are postmenopausal women. In fact, in a study to investigate if hormone replacement therapy had an effect on TCM, the authors concluded that none of the 31 patients with TCM received estrogen replacement therapy[46]. Moreover, Ueyama et al[47] demonstrated that the decrease in LV function was greater in ovariectomized rats subjected to restraint stress than in rats receiving estradiol supplementation. The myocytes are known to express estrogen receptor-α and estrogen receptor-β. According to Ueyama et al[47], estrogen enhanced transcription of cardioprotective factors such as heat shock protein and atrial natriuretic peptide, and in turn, protected against the toxic effects of catecholamines, calcium overload and reduced oxidative stress[ HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B48"48].

Emotional or physical stress inducers

A study reported on the prevalence of mood disorders and use of antidepressants in patients with TCM[28]. When patients with depressive disorders experienced a stressful event, vagus nerve tension was decreased and response to adrenal medullary hormone was increased, which may be relevant to the cause of the disease[49]. Further, some patients with depression showed very high noradrenaline extravasation[ HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B50"50].

Genetic factors

Certain polymorphisms of α- and β-adrenergic receptors are associated with neurogenic stunned myocardium that occurs as symptom of subarachnoid hemorrhage and has overlapping pathophysiology with TCM[51]. Although adrenoceptor polymorphisms have not yet been identified in patients with TCM, patients with this disease showed L41Q polymorphism of G protein coupled receptor kinase (GRK5) more frequently compared with the control group[ HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B52"52]. L41Q polymorphism of GRK5 responds to catecholamine stimulation and attenuates the response of β-adrenergic receptors. Under catecholamine stimulation, balloon dilation of the ventricle may occur either by negative inotropic effect by β-receptor decoupling or ischemia because of an imbalance between α1-adrenergic coronary artery vasoconstriction and β-adrenergic vasodilation. These reports suggest the very interesting possibility that the susceptibility to TCM in individuals may be partially related to genetic factors.

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TREATMENT

Treatment of TCM during the acute phase is mainly symptomatic treatment. Intra-aortic balloon pump equipment is required for hemodynamically unstable patients in addition to cardiopulmonary circulatory support and continuous veno-venous hemofiltration[53-55]. There is controversy on the use of cardiac stimulants because of increased circulating catecholamines[56]. However, cardiac stimulants are used in 20%-40% of patients with TCM[2,57]. Levosimendan may be beneficial because of its inotropic action and vasodilator effect[30, HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B58"58]. Usage of anticoagulants may be considered at least until systolic function is recovered.

For patients with severe LV outflow tract obstruction with hemodynamic compromise, treatment with a β-blocker or α-adrenoceptor agonist such as phenylephrine and volume expansion should be considered. Calcium channel blockers can be used to decrease LV outflow tract pressure gradient. It is of utmost importance to avoid treatment with nitrites or inotropic drugs in these cases[59-63]. For patients with suspected vasospasm, the use of calcium channel blockers such as verapamil or diltiazem is suggested[ HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B64"64].

Hemodynamically stable patients are often treated with diuretics, angiotensin-converting enzyme (ACE) inhibitors and β-blockers. To reduce the risk of thromboembolism, patients with loss of motion of the LV apex should be treated with anticoagulant therapy until the contractility of the apex is improved unless there is a definite contraindication.

There is no consensus regarding long-term management of TCM, although it is reasonable to treat patients with β-blockers and ACE inhibitors during the ventricular recovery period. However, no data support the continuous use of these drugs for the prevention of TCM recurrence or improvement of survival rate. After LV function normalizes, physicians may consider discontinuation of these drugs.

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PROGNOSIS AND RECURRENCE

Patients with TCM usually have a good prognosis, and almost perfect recovery is observed in 96% of the cases[65]. Mortality rate in hospital vary at one to two percent[18,66]. TCM was formerly thought to follow a relatively benign course. However, Sharkey et al[18] described that approximately 5% of TCM patients experienced cardiac arrest. While their long-term survival rate is the same as that in healthy subjects, patients with TCM have a greater risk of death at the time of initial onset[65]. Elesber et al[65] reported that the most frequent chief complaint was chest pain (30%) and that recurrence of the symptom occurred in 11% of patients with TCM after a 4-year follow-up. Some studies have been conducted to assess prognostic indicators such as ECG findings, signs of thrombolysis in myocardial infarction, grade of myocardial perfusion, and N-terminal pro-brain natriuretic peptide level. However, a definite outcome marker has not been established[66- HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/#B68"68].

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CONCLUSION

A lot of attention has been focused on TCM recently and this entity has been characterized as a transient LV dysfunction with rapid recovery generally induced by a stressful emotional or physical event. The number of TCM cases continues to increase. Because of close resemblance of its presentation and clinical course to acute myocardial infarction, we believe that TCM should be included in one of the differential diagnosis for acute myocardial infarction. Although the cause of this disease has not been completely understood to date, some promising hypotheses have been suggested. The occurrence of this disease is attributed to the large-scale production of catecholamines that causes myocardial hypokinesia viadirectcardiomyocyte toxicity and induction of coronary microvascular dysfunction. Further, the high prevalence of TCM in postmenopausal women suggests an important role of estrogen for myocardial protection. Another hypothesis includes oxidative/inflammatory stress-induced myocardial dysfunction. Although the treatment of TCM remains controversial, adrenergic blockade is suggested as a reasonable therapy based on the presumptive pathophysiology of TCM.

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Footnotes

P- Reviewer: Al-Biltagi M, Celikyurt YU S- Editor: Ji FF L- Editor: A E- Editor: Wu HL

Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110608/

Apical Ballooning Syndrome

Apical Ballooning Syndrome: The “Broken Heart” Syndrome

Kate E. Nyquist, MD, David W. Abramson, MD, and Jeff C. Huffman, MD

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Have you ever wondered about the “broken heart syndrome”? When a patient presents with cardiac symptoms in the context of acute stress, are you aware of the most important conditions in the differential diagnosis? Have you ever wanted to know more about how an acutely stressful situation can impact cardiac physiology? If so, this case and the resulting discussion may provide insight into the complex interplay of the heart and mind.

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CASE PRESENTATION

While riding the subway to work, Ms A, a 36-year-old woman, developed the acute onset of shortness of breath associated with dull, aching pain radiating down her left arm. Minutes later, she developed crushing substernal chest pain of 10/10 intensity; paramedics arrived and sublingual nitroglycerin led to prompt reduction of her pain to 4/10 intensity. In the emergency department, an electrocardiogram (ECG) revealed ST-segment elevations in the inferior leads, and a screening troponin value was positive. She was taken promptly for cardiac catheterization; angiography revealed patent coronary arteries, and an echocardiogram measured an ejection fraction of 35% with hypokinesis of the mid and apical segments of the left ventricle. Ms A was admitted for observation due to new-onset cardiomyopathy of unknown origin.

On evaluation in the hospital, Ms A was tearful, with her husband and daughter at her bedside. She reported never having similar symptoms in the past and was now free of chest pain; her physical examination was unremarkable. Further interview revealed a history of mild hypertension; her blood pressure had been well controlled with propranolol (40 mg twice daily), prescribed for “blood pressure and anxiety.” She was also prescribed paroxetine 10 mg daily for anxiety. Family history was significant for her father having hypertension and a stroke at age 39 years; there was no family history of cardiomyopathy or sudden death. Social history revealed no history of illicit drug use, and she specifically denied use of cocaine, stimulants, opiates, or intravenous drug, or abuse of alcohol. She was employed as a librarian and had been living with her 4-year-old daughter and husband of 10 years. However, when asked about stress, Ms A endorsed significant emotional distress and depressed mood since learning 4 days before that her husband had been unfaithful; on the day prior to admission, her husband had moved into a nearby hotel.

During the admission, she received treatment with β-blockers for blood pressure control. Her troponin T peaked at 2.45 ng/mL and subsequently trended down with no return of her chest pain. A subsequent transthoracic echocardiogram on hospital day 3 showed an improved ejection fraction of 60% without hypokinesis. Due to the spontaneous resolution of her symptoms, the classical apical ballooning pattern seen on the echocardiogram, and the significant emotional stressor preceding the onset of her symptoms, this event was consistent with apical ballooning syndrome (ABS), also known as Takotsubo's cardiomyopathy.

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HOW DO PSYCHIATRIC SYMPTOMS AFFECT CARDIAC HEALTH?

A variety of psychiatric symptoms and syndromes appear to have significant effects on cardiovascular outcomes. Among these, depressive disorders and anxiety have been the best studied. Depression has been established as a risk factor for negative cardiac outcomes across the spectrum of cardiac disease. Initially healthy adults who have depression are more likely to eventually develop heart disease, independent of standard cardiovascular risk factors.1 Furthermore, among those with known coronary artery disease, being depressed is associated with inferior cardiac health.2 Among patients hospitalized with an acute coronary syndrome or congestive heart failure, or those having coronary artery bypass graft surgery, depression is an independent risk factor for recurrent cardiac events and mortality. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib3"3,4

Anxiety has also been associated with the development of coronary artery disease, with 2 large recent studies finding a strong and independent association between anxiety and coronary artery disease.5 With respect to anxiety among patients with recent coronary events, several studies have found that anxiety after myocardial infarction (MI) is associated with elevated rates of in-hospital complications, independent of other medical factors.6,7 More specific anxiety states have been associated with cardiac events as well. Phobic anxiety, an agoraphobia-like condition, has been associated with cardiac disease, particularly sudden cardiac death.8 Panic disorder also appears to be more common in patients with coronary artery disease than in the general population9 and has been associated with the onset of MI.10 Finally, other serious mental illnesses, such as bipolar disorder and schizophrenia, have also been associated with elevated rates of mortality from cardiovascular disease. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib11"11,12

In sum, it appears that psychiatric symptoms and conditions appear to be consistently associated with the onset and progression of cardiovascular illness. The mechanism by which this link exists is likely a combination of the physiologic effects of these states (eg, inflammation) and the impact on health maintenance behaviors such as smoking, exercise, and medication adherence.

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WHAT IS APICAL BALLOONING SYNDROME?

Apical ballooning syndrome is a form of acute dilated cardiomyopathy. It was first described in the Japanese literature in 1991 by Dote and colleagues HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib13"13 and was originally named Takotsubo cardiomyopathy. Tako-tsubo is the Japanese word for octopus trap, and, in this disorder, the heart has this distinctive shape when viewed on end-diastolic ventriculogram, with a wide base and a long thin neck. In the literature, the terms apical ballooning syndrome and Takotsubo cardiomyopathy are used interchangeably, while broken heart syndrome is commonly used in the popular press. For the purposes of this article, ABS will be used to refer to the clinical syndrome.

Apical ballooning syndrome occurs most commonly in women, especially postmenopausal women. Patients with ABS classically present with anginal chest pain, often at rest and with associated dyspnea,14,15 following the experience of a stressful event (often within minutes or hours of the onset of symptoms). HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib16"16 However, one-third of patients ultimately diagnosed with ABS do not have an identified preceding emotional or physical stressor, and, therefore, the absence of a precipitating stressor is insufficient to rule out ABS when other findings suggest its presence.

In addition to chest pain, patients with ABS usually manifest ECG changes, especially ST-segment elevations in the anterior leads, with subsequent development of T-wave inversions; patients may have mildly elevated levels of cardiac enzymes (troponin I, troponin T, and CK-MB)3 and brain natriuretic peptide, a marker of congestive heart failure.14, HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib17"17 Finally, a hallmark of ABS is the presence of wall-motion abnormalities on echocardiograms, with abnormalities of the middle segments and apex of the left ventricle that extend beyond a single vascular distribution.

Although rare, more complications of ABS may occur; these include arrhythmia, hypotension, pulmonary edema, and cardiogenic shock.15,16 Wall-motion abnormalities may cause left ventricular outflow obstruction and mitral regurgitation, leading to hypertrophic obstructive cardiomyopathy. There are also rare reports of ventricular free wall rupture and ventricular septal defects, and thromboembolic events related to left ventricular hypokinesis or dyskinesis may also occur. Overall, in-hospital mortality rates from ABS are much lower than from other acute cardiac illnesses (approximately 1%–3%) HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib18"18; the most likely causes of mortality from ABS are cardiogenic shock and systemic embolization.19

In sum, ABS is an acute cardiomyopathy associated with anginal chest pain (often at rest), dyspnea, ST-segment elevations on the ECG, and characteristic wall-motion abnormalities on the echocardiogram. Such symptoms very often—but not invariably—occur in the context of an acute emotional stressor.

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HOW CAN APICAL BALLOONING SYNDROME BE DISTINGUISHED FROM OTHER CARDIAC CONDITIONS?

ABS is virtually indistinguishable from acute MI, on the basis of presenting symptoms and routine laboratory testing. Accordingly, per the 2007 guidelines from the American College of Cardiology and the American Heart Association, HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib2"2 ABS should be included in the differential for an acute coronary syndrome.

How can one differentiate ABS from an acute coronary syndrome? There are several factors that can help distinguish ABS from other acute cardiac conditions. First, ABS often presents following the occurrence of a stressful event. Common emotional stressors include unexpected death of a loved one, devastating financial loss, intense argument with friends or relatives, and receipt of a catastrophic medical diagnosis.16, HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib20"20 ABS may also be immediately preceded by physical stressors, such as intense pain, noncardiac surgery, and intense exercise.15

However, as noted, the presence or absence of a stressful event cannot be used reliably to diagnose ABS, as a substantial minority of patients with ABS cannot identify a physical or emotional stress preceding the symptoms. In addition, acute cardiac events, including MI, congestive heart failure, and arrhythmia, can all be preceded by a stressful event. Therefore, although emotional or physical stress is characteristic of ABS and can be a clue to the presence of this condition, recent stress is neither necessary nor sufficient to differentiate ABS from other cardiac pathology. Structural brain lesions, cerebrovascular accidents, subarachnoid hemorrhage, and other neurologic conditions can also lead to cardiac events, although it is not clear whether these events typically lead to apical ballooning.21

In contrast, the results of cardiac catheterization can much more convincingly distinguish ABS from MI or other syndromes associated with coronary artery disease. In general, patients with ABS have normal cardiac catheterizations, with minimal evidence of vessel narrowing or blockage, and most patients with MI have substantial abnormalities that require acute intervention. However, there are also caveats when using catheterization results to distinguish ABS from other syndromes. For example, symptoms of a coronary event could have been caused by the transient rupture of a plaque, which then spontaneously lysed prior to catheterization, giving the appearance that coronary artery disease was not the cause of symptoms. Conversely, some patients suffering from ABS may have baseline coronary disease (given the high base rate of this condition in the population), leaving the appearance that a lesion seen on catheterization caused the presenting symptoms. Despite these caveats, however, catheterization results are quite helpful in distinguishing ABS from other conditions when they are added to the remainder of the clinical picture.

Perhaps the most convincing finding that distinguishes ABS from MI is seen most clearly on the echocardiogram: the characteristic set of wall-motion abnormalities associated with ABS. Classically, one observes hypokinesis or akinesis of the mid and apical segments of the left ventricle. This is what gives the apical ballooning appearance: narrowing at the ventricular neck and ballooning at the apex, with the basal left ventricle often spared.15,18 Of note, up to 40% of patients with ABS may have only midventricle hypokinesis (the so-called “apical-sparing variant”).22 There is a corresponding reduction in left ventricular ejection fraction, generally ranging from 20%–49%. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib14"14 Even more suggestive of the ABS diagnosis is a normalization of the wall-motion abnormalities and ejection fraction several days later. The natural course of ABS is one of rapid restoration of cardiac function, and normalization of the echocardiogram (after characteristic abnormalities on echocardiogram acutely) strongly suggests ABS.

There are no universally accepted diagnostic criteria for ABS, in part, because the syndrome has only recently been described, and more information needs to be gathered. However, Prasad and colleagues HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib15"15have developed proposed criteria for the condition that focus on the objective findings of this condition that distinguish it from other cardiovascular syndromes. The proposed criteria include characteristic wall-motion abnormalities seen on the ECG; the absence of coronary disease or acute plaque rupture, ECG abnormalities, or elevated cardiac troponins; and the absence of acute head trauma, intracranial bleeding, pheochromocytoma, myocarditis, or hypertrophic cardiomyopathy.

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HOW CAN APICAL BALLOONING SYNDROME BE DISTINGUISHED FROM PSYCHIATRIC CONDITIONS THAT OCCUR IN THE CONTEXT OF ACUTE STRESS SUCH AS PANIC ATTACKS?

Just as it is important to differentiate ABS from other cardiac diseases, it is important to distinguish ABS from an acute presentation of psychiatric illness. As described earlier, there is evidence to support the interplay between chronic psychiatric disorders and the chronic course of medical illnesses. Conversely, acute symptoms of psychiatric disorders can mimic the presentation of other acute medical problems.

In this case, the most pertinent example is the similarity between a panic attack and acute coronary syndrome or ABS. As defined by the DSM-IV-TR,23 a panic attack is an intense fear or discomfort in which 4 (or more) symptoms develop abruptly and reach a peak within 10 minutes. Symptoms can include palpitations, pounding heart, or accelerated heart rate; sweating; trembling/shaking; sensation of shortness of breath or smothering; feeling of choking; chest pain or discomfort; nausea or abdominal distress; feeling unsteady, lightheaded, or faint; derealization or depersonalization; fear of losing control or going crazy; fear of dying; paresthesias; and chills or hot flushes. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib23"23(p432) Panic attacks frequently occur in the context of psychosocial stressors and can also at times occur in the setting of physical discomfort or exercise.

On the basis of diagnostic criteria, it is evident that a person presenting with symptoms of a panic attack might appear similar to someone experiencing ABS (or MI). The acuity of the patient's distress, the constellation of associated symptoms, and the association with stressful events make panic attacks and ABS quite similar with respect to their initial presentation. Indeed, for any patient presenting with such symptoms, it would be necessary to rule out all other relevant medical causes before making the diagnosis of a panic attack.

There are, however, some hallmark features (though not pathognomonic) that suggest a panic attack as opposed to MI or ABS. For instance, panic attacks are characterized by a rapid crescendo-decrescendo pattern of symptom onset. Furthermore, panic symptoms usually resolve completely within 1 hour, often sooner. Additionally, the experience of depersonalization and/or derealization may suggest a panic attack because both are less common in acute coronary syndrome. Panic attacks can occur at rest and are not necessarily precipitated by an acute stressor. Finally, panic attacks most often have an age at onset during the third decade of life. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib23"23 This is especially relevant to differentiating between ABS and a panic attack. The classic patient with ABS is a postmenopausal woman. If she has no past history of panic attacks, it would make the diagnosis less likely. Ultimately, although the clinical presentation of ABS and panic attacks is quite similar, the diagnosis is clarified by ECG, cardiac enzymes, and echocardiogram. Patients with ABS typically have characteristic abnormalities on these diagnostic evaluations, while such tests should be normal in a patient having a panic attack.

Finally, it is important to consider the potential for coexisting panic attacks and cardiac ischemia. Among patients with panic disorder who are predisposed to cardiac events, the catecholamine surge associated with a panic attack could lead to vasoconstriction, hypertension, and increased myocardial demand, and, thus, the panic attack may lead to the subsequent development of a true cardiac event. Such a connection could also go in the other direction—the organically driven shortness of breath, chest pain, and diaphoresis of a myocardial event could serve as a nidus for a superimposed panic attack.

In addition to panic attacks, there are other psychiatric illnesses worth noting because of their propensity to present with physical complaints. Major depressive disorder, generalized anxiety disorder, and the somatoform disorders are the most common psychiatric disorders to share overlapping physical symptoms. However, unlike panic attacks, the physical manifestations in these other disorders tend to be chronic, diffuse, and associated with symptoms of decreased energy and/or fatigue. Moreover, a diagnosis of a somatization disorder, by definition, requires the manifestation of somatic complaints involving multiple organ systems. As with panic disorder, the age at onset of symptoms or diagnosis usually occurs much earlier in life compared to the initial presentation of ABS. Table 1 outlines the ways in which these disorders are similar to, and distinct from, ABS.

Table 1

Psychiatric Disorders That May Mimic Apical Ballooning Syndrome (ABS)

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WHAT IS THE PATHOPHYSIOLOGY BEHIND APICAL BALLOONING SYNDROME?

The pathophysiology of ABS is not yet clearly understood. One proposed mechanism involves transient multivessel epicardial spasm causing the characteristic features of ABS; however, this has only been demonstrated in a small percentage of cases,18 and a study by Wittstein and colleagues24 of 19 patients with ABS failed to demonstrate epicardial spasm. A mechanism proposed by Ibanez and colleagues HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib25"25 is plaque rupture of the left anterior descending artery; however, this fails to explain the characteristic left ventricular apical ballooning pattern.

Another proposed mechanism implicates microvascular ischemia, and researchers have documented abnormal myocardial perfusion in the left ventricular areas in which wall-motion abnormalities are found.22, HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib26"26 However, imaging modalities have never been able to detect myocardial necrosis, despite the finding of troponin leaks in ABS, making it unlikely that this is the mechanism in all cases.

Perhaps the most likely of the proposed mechanisms involves abnormal levels of catecholamines.18Animal models have found that physical immobilization leads to ABS-like findings in the heart, and blockade of catecholamines prevents these events. Furthermore, myocardial biopsies in some ABS patients show findings consistent with catecholamine-associated cardiotoxicity. Finally, the study by Wittstein and colleagues HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib24"24 found that ABS patients had 2 to 3 times higher levels of catecholamines compared to matched controls with acute coronary syndrome, and the catecholamine hypothesis was further supported by findings of contraction band necrosis and mononuclear infiltrates in 4 of the 5 patients in the study who underwent endomyocardial biopsy. Still, for all of the proposed mechanisms, it has been difficult to determine whether these findings regarding catecholamines, spasm, plaque rupture, and ischemia are causative or epiphenomena, and further work is needed.

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HOW SHOULD PATIENTS WITH APICAL BALLOONING SYNDROME BE MANAGED?

Perhaps the most important aspect of educating patients with ABS is reassurance. By definition, ABS is a self-limited syndrome; unlike MI and other acute cardiac illnesses, the mortality from ABS is low. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib18"18 Since stress plays a role in triggering these episodes, it seems prudent to limit additional stress by assuring patients that cardiac contractility typically recovers quickly, with complete normalization of left ventricular function within 1–3 months, often sooner.

All patients suspected of having ABS should have an echocardiogram (or cardiac magnetic resonance imaging) acutely, as well as an echocardiogram before discharge to ensure that left ventricular dysfunction is improved. Monitoring via cardiac telemetry is indicated to observe for arrhythmias. If coronary artery disease is suspected as a cause of the presenting symptoms, cardiac catheterization is indicated to aid diagnosis and to allow intervention if needed.

On occasion, acute anticoagulation with heparin may be considered to prevent embolization if there is apical involvement and no contraindications to anticoagulation; for those patients with persistent depression of left ventricular function at discharge, transition to warfarin could be considered. Considering the stress/catecholamine hypothesis, β-blockers may provide protection from a recurrence; however, the rate of ABS recurrence is low, estimated at 2%–10%, and, therefore, the use of β-blockers is not standard.16, HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib27"27 Finally, follow-up echocardiograms performed 1 and 3 months postdischarge may be indicated for those patients without complete in-hospital restoration of ventricular function.

Given that symptoms of ABS frequently occur in the setting of emotional distress, it is often useful to assess such patients for treatable psychiatric conditions, such as panic disorder, generalized anxiety disorder, and major depressive disorder. Indeed, a recent study found that over one-half of 25 ABS patients had a prior history of anxiety or depression, far greater than a comparison group of MI patients. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/#bib28"28 If such anxiety or depressive syndromes exist, they should be treated. Furthermore, even if patients do not meet criteria for a formal psychiatric syndrome, the extent to which their body's physiology has responded to an emotional stressor suggests that they should be counseled about stress reduction and means of coping with distressing life events.

Drug names: nitroglycerin (Minitran, Nitro-Dur, and others), paroxetine (Paxil, Pexeva, and others), warfarin (Coumadin, Jantoven, and others).

Potential conflicts of interest: None reported.

Funding/support: None reported.

Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026006/

Stress Cardiomyopathy

Stress cardiomyopathy: aetiology and management

Radhakrishnan Ramaraj

Author information Article notes Copyright and License information Disclaimer

This article has been cited by other articles in PMC.

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Abstract

Stress cardiomyopathy is a condition caused by intense emotional or physical stress leading to rapid and severe reversible cardiac dysfunction. It mimics myocardial infarction with changes in the electrocardiogram and echocardiogram, but without any obstructive coronary artery disease. Due to the awareness created by the media and internet, every patient is aware that they should seek help immediately for chest pain. Therefore physicians should be aware of this new condition and how to diagnose and treat it, even though the causal mechanisms are not yet fully understood.

Stress cardiomyopathy is a condition in which intense emotional or physical stress can cause rapid and severe heart muscle weakness. The pattern of left ventricular dysfunction was first described in Japan and has been referred to as “tako‐tsubo cardiomyopathy,”1 named after the fishing pot with a narrow neck and wide base that is used to trap octopus. “Tako‐tsubo cardiomyopathy”, also known as “apical ballooning syndrome”, “ampulla cardiomyopathy”, “stress cardiomyopathy” or “broken‐heart syndrome” is now increasingly recognised in other countries as well.2,3 “Transient left ventricular apical ballooning” has also been used to describe similar cardiac contractile function in patients after physical or emotional stress (fig 1​1). HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref4"4,5

Figure 1 Ventriculographic assessment of cardiac function and magnetic resonance imaging (MRI) assessment of myocardial viability at admission in a patient with stress cardiomyopathy. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref6"6 Contrast‐enhanced ventriculography during diastole (panel A) and systole (panel B) demonstrates apical and mid‐ventricular akinesis, with relative sparing of the base of the heart (arrow). In panel C, MRI in the long‐axis view reveals that the akinetic regions seen on ventriculography are dark and hypoenhanced, consistent with the presence of viable myocardium. Panel D, which is presented for purposes of comparison, shows hyperenhancement (arrow), indicative of necrosis and decreased viability, after an acute anterior myocardial infarction. Reproduced with permission from Massachusetts Medical Society.

This condition can occur following a variety of emotional stressors such as grief, fear, extreme anger, and surprise. On the other hand numerous physical stressors such as stroke, seizure or acute asthma can also trigger the condition. Common presenting signs of this syndrome are chest pain, ST segment elevation in the precordial leads, mild elevation of cardiac enzyme and biomarker levels, and transient apical systolic left ventricular dysfunction in the absence of obstructive epicardial coronary disease. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref4"4,5

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CLINICAL FEATURES

Most of the patients with stress cardiomyopathy usually present with severe chest pain, dyspnoea, or both during emotional stress. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref6"6 The pain could be misleading as it resembles that of acute myocardial infarction in its nature (heavy, squeezing and crushing) and site (central portion of the chest and/or the epigastrium, occasionally radiating to the arms), causing anxiety. It can also simulate pain of acute pericarditis, pulmonary embolism, acute aortic dissection and costochondritis, as all these mimic acute myocardial infarction. Therefore all these conditions should be excluded through investigations including coronary angiogram to identify any significant blockages that would cause the left ventricular dysfunction.

Coronary vasospasm can lead to life‐threatening cardiac arrhythmias in patients without any haemodynamically significant coronary artery disease like stress cardiomyopathy.8 It can cause arrhythmias due to QT prolongation and is also reported to be associated with torsade de pointes.9,10 In the absence of critical coronary arterial disease, the diagnosis of stress cardiomyopathy should be considered when the history reveals that the cardiac symptoms were precipitated by intense emotional stress. Echocardiography reveals a unique pattern of left ventricular dysfunction characterised by apical and mid‐ventricular contractile abnormalities with sparing of the basal segments. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref6"6 Most of these patients have a complete recovery without any complications. There can be various electrocardiographic (ECG) and echocardiographic findings in stress cardiomyopathy (boxes 1 and 2).

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AETIOLOGY

Emotional stress can precipitate severe, reversible, left ventricular dysfunction in patients without coronary disease. Box 3 summarises various mechanisms postulated in relation to stress cardiomyopathy. Even though the mechanisms underlying stress cardiomyopathy are unclear, exaggerated sympathetic stimulation is probably central to its causation. Catecholamine excess has been implicated; nevertheless the association between the two is unknown. One possibility is ischaemia resulting from epicardial coronary arterial spasm. Increased sympathetic tone can lead to vasoconstriction in patients without coronary disease.11Multivessel epicardial coronary artery spasm has been reported, but microvascular spasm has also been suggested. Others have demonstrated reduced coronary flow reserve and regional defects on cardiac imaging in such patients, HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref12"12 suggesting the presence of sympathetically mediated microcirculatory dysfunction.

Another possible mechanism of catecholamine‐mediated myocardial stunning is direct myocyte injury. Adrenoceptor density is higher in the apex, compared to other areas of the myocardium.6 Elevated catecholamine levels result in a concentration‐dependent decrease in myocyte viability, as demonstrated by a significant release of creatine kinase from cells and hence a decrease in the viability through cyclic AMP‐mediated calcium overload.13 Animal models have demonstrated that catecholamines are a potential source of free radicals, which by promoting lipid peroxidation may increase membrane permeability and myocyte injury leading to cardiomyopathy. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref14"14 Myocyte dysfunction can occur through increased transsarcolemmal calcium influx and cellular calcium overload due to the ability of the free radicals to interfere with sodium and calcium transporters.15

Abnormal coronary flow in the absence of obstructive disease has recently been reported in patients with stress‐related myocardial dysfunction. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref16"16123I‐MIBG (metaiodobenzyl guanidine) myocardial scintigraphy showed a unique pattern of ventricular asynergy suggesting the existence of cardiac sympathetic hyperactivity with maintained coronary blood flow. This implies that stress cardiomyopathy might have been caused by neurogenic myocardial stunning.17

Figure 2 Typical ECGs obtained 24–48 h after presentation in four patients with stress cardiomyopathy. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref6"6Pronounced prolongation of the QT interval and diffuse symmetric T wave inversion are present in all four ECGs. Loss of R wave progression in leads V1, V2, and V3 is also evident in panels C and D. Reproduced with permission from Massachusetts Medical society.

An angiographic study of patients with stress cardiomyopathy by Kurisu et al1 showed that 70% had coronary spasm in response to provocative manoeuvres, and electrocardiographic evidence of ST segment elevation was common at presentation (box 1). To the contrary, another study by Wittstein et al HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref6"6demonstrated no angiographic evidence of epicardial spasm, and ST segment elevation was seen rarely. According to the latter study, patients did initially have contractile abnormalities in multiple vascular territories, but multivessel epicardial spasm as an explanation for this finding seemed unlikely, given the relative absence of ST segment elevation and minimal enzymatic evidence of myocardial necrosis. The distribution of primary cardiac insult does not correspond to the perfusion territory of a single coronary artery, and there is myocardial stunning rather than infarction.

Patients usually have supra‐physiological levels of plasma catecholamines and stress‐related neuropeptides. Unlike polymorphonuclear inflammation seen with infarction, in stress cardiomyopathy there is contraction band necrosis, a unique form of myocyte injury characterised by hypercontracted sarcomeres, dense eosinophilic transverse bands, and an interstitial mononuclear inflammatory response. Endomyocardial biopsy demonstrated the presence of contraction band necrosis in patients with this syndrome.6 Contraction band necrosis is a type of cell death identified as early as 2 mins after cell injury has occurred and can cause release of cardiac enzymes.18 Focal myocarditis and contraction band necrosis has been found in states of excess circulating catecholamine‐like pheochromocytoma,19 subarachnoid haemorrhage,20,21eclampsia21 and in people who died of fatal asthma.22 It has also been documented in autopsies of patients with normal coronary vessels who suffered from coronary spasm due to various causes.21, HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref23"23 These suggest that catecholamines may be a link between emotional stress and cardiac injury.

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WHO ARE PRONE TO STRESS CARDIOMYOPATHY?

From the available medical literature so far, women—especially middle aged or elderly—are the most commonly affected. While it can also occur in young women and men, the vast majority of these patients are post‐menopausal women.24,25 Indeed, more than 90% of patients suffering from stress cardiomyopathy are females.26 The basis for this predisposition is unknown. Sex hormones exert important influences on the sympathetic neurohormonal axis27 as well as on coronary vasoreactivity,28 but sex‐related differences in catecholamine metabolism and responsiveness are complex and remain poorly understood. Reversible myocardial dysfunction can develop in critically ill patients without any primary heart disease. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref29"29 This syndrome is associated with systolic dysfunction, segmental contractile disturbance and electrocardiographic changes.

Methods to predict who will develop myocardial stunning would be very helpful. Serum catecholamine levels might be expected to reasonably coincide with the catecholamine surge and myocardial stunning; however, the available data have not borne this out.30 Cardiac troponins can be used as a screening test for predicting myocardial stunning.31 Although troponin is helpful, it does not answer several important questions: Why do some patients have an elevation in troponin and not others? What are the underlying mechanisms that lead to myocardial stunning? Genotyping was done for catecholamine receptor subtypes. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref32"32 Several genetic receptor subtypes were associated with both troponin release and depressed ejection fraction on echocardiography. This implicates the genetic code of receptor subtypes, and probably receptor function, in troponin release and myocardial stunning.

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MANAGEMENT

The management of stress cardiomyopathy mainly consists of supportive and symptomatic treatment.33 We should be able to exclude any significant coronary artery disease.34 Initially patients are managed as for myocardial infarction, including urgent coronary angiography with a view to primary coronary intervention. As is the case for patients with coronary artery disease, all patients should be started on aspirin, low molecular weight heparins, and angiotensin‐converting enzyme (ACE) inhibitors; β‐blockers and diuretics can be started if needed. Beyond the standard supportive care for congestive heart failure with diuretics and vasodilators, the treatment of stress cardiomyopathy largely remains empirical. With good initial medical support, patients with stress cardiomyopathy show good clinical and echocardiographic improvement (fig 3​3).). They also have an excellent prognosis.

Figure 3 Serial echocardiographic assessment of the ejection fraction in 19 patients with stress cardiomyopathy. HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref6"6 Echocardiography was performed on admission; on hospital day 3, 4, 5, 6, or 7 (median, day 4); and at outpatient follow‐up (a median of 21 days after the onset of symptoms). Gray lines illustrate values for individual patients. The black bar represents the median ejection fraction at each time; error bars show the interquartile range. p<0.001 for the comparison between admission and inpatient values, and p<0.001 for the comparisons between admission and outpatient values and between inpatient and outpatient values. Reproduced with permission from Massachusetts Medical Society.

Patients should be monitored for the development of arrhythmias, heart failure and mechanical complications. Patients can have acute haemodynamic compromise and require vasopressor agents and intra‐aortic balloon counterpulsation.7 Apical thrombus can form for which short‐term anticoagulation may be needed.26,35 Almost all patients who had left ventricular impairment return to normal within few weeks, and there are no reports concerning the proportion of patients left with significant long term left ventricular impairment.36,37 The evolution, although mainly uneventful, can be complicated, rarely, by left ventricular rupture, thus making stress cardiomyopathy a newly recognised cause of sudden death in up to 3% of patients.26, HYPERLINK "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/#ref33"33 Most of the patients will have normalised ejection fraction with restoration to previous functional cardiovascular status within 6±3 days. This syndrome may recur in up to 10% of patients, making it difficult to know how long to continue treatment.7

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CONCLUSIONS

With available studies, it could be concluded that “Stress cardiomyopathy is a reversible dysfunction of the myocardium due to significant physical or psychological stresses”. There are a lot of uncertainties about stress cardiomyopathy. Why is it more common in women? It was initially reported only in Japan but now it is widely described in other countries as well. A definitive mechanism of myocardial stunning is still unknown and therefore further research on this subject will be required for the complete understanding of the pathogenesis of this syndrome.

Key references

•        Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539–48.

•        Tsuchihashi K, Ueshima K, Uchida T, et al, Angina Pectoris‐Myocardial Infarction Investigations in Japan. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. J Am Coll Cardiol2001;38:11–18

•        Donohue D, Movahed MR. Clinical characteristics, demographics and prognosis of transient left ventricular apical ballooning syndrome. Heart Fail Rev 2005;10:311–6

•        Sadamatsu K, Tashiro H, Maehira N, et al. Coronary microvascular abnormality in the reversible systolic dysfunction observed after noncardiac disease. Jpn Circ J 2000;64:789–92.

•        Bybee KA, Prasad A, Barsness GW, et al. Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome. Am J Cardiol 2004;94:343–6.

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MULTIPLE CHOICE QUESTIONS (TRUE (T)/FALSE (F); ANSWERS AFTER THE REFERENCES)

Which of the following statements are true?

•        Most patients with stress cardiomyopathy present as acute myocardial infarction

•        Stress cardiomyopathy mainly affects males who are subject to stress

•        Adrenoceptor density is highest at the apex than in other areas of the myocardium

•        Vasoconstriction in patients without coronary artery disease can be caused by increased sympathetic tone

•        Even with good initial medical support, patients with stress cardiomyopathy do not show any clinical or echocardiographic improvement

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Abbreviations

ACE - angiotensin‐converting enzyme

AMI - acute myocardial infarction

ECG - electrocardiogram

MIBG - metaiodobenzyl guanidine

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ANSWERS

(A) T (B) F (C) T (D) T (E) F

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Footnotes

Funding: None

Conflict of interest: none

Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/

Panic Disorder

Panic attacks and panic disorder

Overview

A panic attack is a sudden episode of intense fear that triggers severe physical reactions when there is no real danger or apparent cause. Panic attacks can be very frightening. When panic attacks occur, you might think you're losing control, having a heart attack or even dying.

Many people have just one or two panic attacks in their lifetimes, and the problem goes away, perhaps when a stressful situation ends. But if you've had recurrent, unexpected panic attacks and spent long periods in constant fear of another attack, you may have a condition called panic disorder.

Although panic attacks themselves aren't life-threatening, they can be frightening and significantly affect your quality of life. But treatment can be very effective.

Symptoms

Panic attacks typically begin suddenly, without warning. They can strike at any time — when you're driving a car, at the mall, sound asleep or in the middle of a business meeting. You may have occasional panic attacks, or they may occur frequently.

Panic attacks have many variations, but symptoms usually peak within minutes. You may feel fatigued and worn out after a panic attack subsides.

Panic attacks typically include some of these signs or symptoms:

•          Sense of impending doom or danger

•          Fear of loss of control or death

•          Rapid, pounding heart rate

•          Sweating

•          Trembling or shaking

•          Shortness of breath or tightness in your throat

•          Chills

•          Hot flashes

•          Nausea

•          Abdominal cramping

•          Chest pain

•          Headache

•          Dizziness, lightheadedness or faintness

•          Numbness or tingling sensation

•          Feeling of unreality or detachment

One of the worst things about panic attacks is the intense fear that you'll have another one. You may fear having panic attacks so much that you avoid certain situations where they may occur.

When to see a doctor

If you have panic attack symptoms, seek medical help as soon as possible. Panic attacks, while intensely uncomfortable, are not dangerous. But panic attacks are hard to manage on your own, and they may get worse without treatment.

Panic attack symptoms can also resemble symptoms of other serious health problems, such as a heart attack, so it's important to get evaluated by your primary care provider if you aren't sure what's causing your symptoms.

Request an Appointment at Mayo Clinic

Causes

It's not known what causes panic attacks or panic disorder, but these factors may play a role:

•          Genetics

•          Major stress

•          Temperament that is more sensitive to stress or prone to negative emotions

•          Certain changes in the way parts of your brain function

Panic attacks may come on suddenly and without warning at first, but over time, they're usually triggered by certain situations.

Some research suggests that your body's natural fight-or-flight response to danger is involved in panic attacks. For example, if a grizzly bear came after you, your body would react instinctively. Your heart rate and breathing would speed up as your body prepared for a life-threatening situation. Many of the same reactions occur in a panic attack. But it's unknown why a panic attack occurs when there's no obvious danger present.

Risk factors

Symptoms of panic disorder often start in the late teens or early adulthood and affect more women than men.

Factors that may increase the risk of developing panic attacks or panic disorder include:

•          Family history of panic attacks or panic disorder

•          Major life stress, such as the death or serious illness of a loved one

•          A traumatic event, such as sexual assault or a serious accident

•          Major changes in your life, such as a divorce or the addition of a baby

•          Smoking or excessive caffeine intake

•          History of childhood physical or sexual abuse

Complications

Left untreated, panic attacks and panic disorder can affect almost every area of your life. You may be so afraid of having more panic attacks that you live in a constant state of fear, ruining your quality of life.

Complications that panic attacks may cause or be linked to include:

•          Development of specific phobias, such as fear of driving or leaving your home

•          Frequent medical care for health concerns and other medical conditions

•          Avoidance of social situations

•          Problems at work or school

•          Depression, anxiety disorders and other psychiatric disorders

•          Increased risk of suicide or suicidal thoughts

•          Alcohol or other substance misuse

•          Financial problems

For some people, panic disorder may include agoraphobia — avoiding places or situations that cause you anxiety because you fear being unable to escape or get help if you have a panic attack. Or you may become reliant on others to be with you in order to leave your home.

Prevention

There's no sure way to prevent panic attacks or panic disorder. However, these recommendations may help.

•          Get treatment for panic attacks as soon as possible to help stop them from getting worse or becoming more frequent.

•          Stick with your treatment plan to help prevent relapses or worsening of panic attack symptoms.

•          Get regular physical activity, which may play a role in protecting against anxiety

Link: https://www.mayoclinic.org/diseases-conditions/panic-attacks/symptoms-causes/syc-20376021

Yes, Fear Can Kill You

Yes, Fear Can Kill You

Posted Apr 07, 2010

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People who have suffered panic attacks - and I'm one - know that fear can be so intense that you feel like you're going to die. Your pulse races, your heart pounds, you find it hard to breathe. You might even pass out. But you can fear become so intense that it actually kills you?

This past Friday Danielle Goldberg, a 26-year-old Staten Island woman, was riding in her building's elevator up to her sixth floor apartment just before noon when her neighborhood suffered a blackout. For half an hour, she was trapped inside the small space, in the darkness, alone. In an effort to stifle a growing panic attack she used her cell phone to call her mother, but it was no use. By the time rescue workers freed her half an hour later, she was unconscious. She died in the hospital a short time later. At first glance, the cause of her death seems clear: pure fright.

But the truth is a bit more complicated.

Yes, being trapped inside an elevator triggered a panic attack that sent Goldberg's fight-or-flight response - the sympathetic nervous system - into full overdrive. Her heart beat so wildly that it was unable to handle the exertion, and she went into cardiac arrest.

The extenuating circumstance, however, is that Goldberg suffered from a congenital heart condition. She was unusually vulnerable, and any extreme exertion of her cardiovascular system might well have had the same effect. We can't truly say that she died of fear, any more that we can say of a jogger with a heart defect who drops dead while jogging "died of exercise" or that an elderly millionaire who dies in the saddle with a young admirer "died of sex."

This is not to entirely rule out the idea that you can die of fear, however. As I write in Extreme Fear, the full sympathetic nervous system response that we see in a panic attack isn't the body's only way of preparing itself for danger. Another is a state known as tonic immobility, or quiescence - in lay terms, "playing possum." When an animal is seized by an attacker, the caudal ventrolateral region of the PAG generates a response that from the outside looks like total collapse. In the teeth of a full-blown sympathetic response, the parasympathetic system now swings into overdrive.

The body, insensitive to pain, goes completely limp, often falling to the ground as awkwardly as rag doll, limbs splayed, neck thrown back. Eyes closed, it trembles, defecates, and lies still. It looks, in a word, dead.

This is the position of utter despair, a final last-ditch Hail Mary pass of a strategy. The one hope of quiescence is that the attacker, thinking its quarry has expired, will stop attacking. Indeed, many predators will not eat prey that looks dead. Hawks will starve to death if unable to attack moving prey.

The famed 19th-century missionary David Livingstone was a beneficiary of this effect when he was charged by a lion he'd shot at during a hunting trip in Africa. The animal grabbed him in its jaws and shook him like a rag doll. To his surprise, Livingstone found that he felt no pain, and that indeed it caused "a kind of dreaminess." Fortunately for him the immobility response worked as intended, and the lion dropped him to go after some other hunters who were moving nearby.

Quiescence is the most paradoxical form of terror. With both branches of the autonomic nervous system at full throttle, the organism is both utterly relaxed and completely alert and ready for action. Pupils are dilated, breathing and heart-rate rapid. Though paralyzed, incapable of voluntarily action, it can suddenly spring to life and flee if the opportunity arises. If quiescence goes on too long, however, heart rate and blood pressure can plunge dramatically, indeed to the point of death.

Walter Cannon proposed that this phenomenon might explain the demise of indigenous tribesmen who believe themselves cursed by witchcraft. In a 1942 paper entitled "‘Voodoo' Death," he relates several such incidents, including an account by adventurer Arthur Glyn Leonard of a trip to the Lower Niger: "I have seen Kru-men and others die in spite of every effort that was made to save them, simply because they had made up their minds, not (as we thought at the time) to die, but that being in the clutch of malignant demons they were bound to die." Cannon surmised that intense fear can cause such a catastrophic drop in blood pressure that the belief in one's death can became self-fulfilling.

Link: https://www.psychologytoday.com/us/blog/extreme-fear/201004/yes-fear-can-kill-you

You Really Can Be Scared to Death

•          By LIZ NEPORENT

Oct. 25, 2012

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WATCH'Scared To Death' May Not Just Be A Saying

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Here's something to keep in mind this Halloween: A good scare can kill you -- even if you're perfectly healthy.

If a shock to the system is sufficient enough it can trigger a massive surge of adrenaline, stunning your heart so severely it ceases to beat.

Consider the case of a 60-year-old woman who was given terrible news about her husband's health. As she and her hubby left the doctor's office, a tightness suddenly gripped her chest and she was unable to breathe. Lucky for her, she was standing right outside the office of cardiologist Dr. Holly Anderson when it happened.

"After I had whisked her off to the emergency room and hooked her up to an EKG, I was surprised to see her whole heart had stopped moving, yet she had perfect blood supply to the heart," recalled Anderson, who is also the director of education and outreach at the Perelman Heart Institute at New York-Presbyterian Hospital/Weill Cornell Medical Center in New York City. "She was so emotionally overwhelmed about her husband's condition it literally stopped her heart."

Women, particularly older women, are far more susceptible to dying of fright, also known as the "broken heart syndrome." They account for about 90 percent of reported cases, according to Dr. Martin Samuels, chairman of the neurology department at Brigham and Women's Hospital in Boston.

He said postmenopausal women are at risk mainly because they no longer enjoy the known cardio-protective benefits of estrogen, he said.

Experts estimate that about 1 percent of men and 7 percent of women with suspected heart attacks have stress cardiomyopathy instead.

And it is more common than thought. Samuels said the average sudden death in any major city is about one per day. Studies show this number goes up slightly for about a week after a catastrophic event such as an earthquake or a terrorist attack and may increase on days that have a negative cultural significance, such as Friday the 13th.

"I don't believe there are any studies showing that Halloween falls into this category," Samuels said.

This type of abrupt cardiac event goes by several names. Technically it's referred to by medical experts as stress cardiomyopathy because it usually occurs immediately following an intense emotional event. When the syndrome was first identified by Japanese scientists in 1990, they dubbed it "takotsubo syndrome," after the strange balloon shape resembling a Japanese octopus trap the heart takes on when it occurs. Here in the U.S. it's usually known as "broken heart syndrome" because it often strikes after the victim has received gut wrenching news, such as the death of a loved one.

Samuels has studied and treated stress cardiomyopathy syndrome. He said that it's likely set into motion by an excessive, uncontrolled activation of the sympathetic nervous system, the part of the brain responsible for the control of the body's "flight or fight" response including increasing heart-rate, respiration, perspiration.

"Sympathetic storming, as it's referred to, produces a rush of stress hormones. This can work to our benefit much of the time, but in the case of stress cardiomyopathy, the exaggerated response can damage the heart," he said.

For many years, cardiologists didn't understand stress cardiomyopathy. They thought it was some kind of weird heart attack.

"Shortness of breath, trouble breathing, sweating -– the symptoms are exactly the same," said Dr. Ilan Wittstein, a cardiologist at Johns Hopkins Hospital in Baltimore. "Even when we take an EKG or measure the levels of heart proteins that spill into the bloodstream, there is no difference."

It's only when doctors take 3-D pictures of the heart that they can see the telltale balloon shape of the heart and the clear blood vessels that would normally show clots or blockage during a typical heart attack. The large coronary artery that supplies the heart often appears unperturbed but Wittstein said that he suspects the tiny blood vessels that supply blood to the heart -- and which aren't normally scanned in cardiac patients -- may be affected.

Dying of Fright or Broken Heart Syndrome

The massive rush of adrenaline may also temporarily stun the cardiac heart muscle into inaction, Wittstein said. This may explain why the heart of someone who's had an episode of stress cardiomyopathy will return to normal in just a few days or weeks whereas with the damage from a standard heart attack usually remains for the rest of a person's life.

The triggering event doesn't necessarily have to be bad news. Samuels said he has treated cases of stress cardiomyopathy preceded by shooting a hole in one on the golf course, bowling a perfect game and a not guilty verdict in court.

"Any highly emotional event whether positive or negative can set it off," he said.

Reoccurrence is low. Studies show only about a 5 percent of patients have more than one attack, though Wittstein said it seems some individuals are highly susceptible to the syndrome. He has one patient who has had five episodes.

Fortunately it seems to take a real bombshell to stun the average heart into cardiomyopathy. Halloween in and of itself probably isn't enough of a fright to get the job done unless a patient is a true believer in ghosts and goblins, Samuels speculated.

Still, why take chances? Better to go with the treats and skip the tricks.

Link: https://abcnews.go.com/Health/die-fright/story?id=17554297

Can a person be scared to death?

A 79-year-old North Carolina woman dies after a heart attack brought on by terror

•          By Coco Ballantyne on January 30, 2009

Credit: Copyright iStockphoto.com/sculpies

A Charlotte, N.C., man was charged with first-degree murder of a 79-year-old woman whom police said he scared to death. In an attempt to elude cops after a botched bank robbery, the Associated Press reports that 20-year-old Larry Whitfield broke into and hid out in the home of Mary Parnell. Police say he didn't touch Parnell but that she died after suffering a heart attack that was triggered by terror. Can the fugitive be held responsible for the woman's death? Prosecutors said that he can under the state's so-called felony murder rule, which allows someone to be charged with murder if he or she causes another person's death while committing or fleeing from a felony crime such as robbery—even if it's unintentional.

But, medically speaking, can someone actually be frightened to death? We asked Martin A. Samuels, chairman of the neurology department at Brigham and Women's Hospital in Boston.

[An edited transcript of the interview follows. Thanks to AHCJ_Pia for the story suggestion.]

Is it possible to literally be scared to death?

Absolutely, no question about it.

Really? How does that happen?

The body has a natural protective mechanism called the fight-or-flight response, which was originally described by Walter Cannon [chairman of Harvard University's physiology department from 1906 to 1942]. If, in the wild, an animal is faced with a life-threatening situation, the autonomic (involuntary) nervous system responds by increasing heart rate, increasing blood flow to the muscles, dilating the pupils, and slowing digestion, among other things. All of this increases the chances of succeeding in a fight or running away from, say, an aggressive jaguar. This process certainly would be of help to primitive humans, but the problem, of course, is that in the modern world there is very limited advantage of the fight-or-flight response. There is a downside to revving up your nervous system like this.

How can the fight-or-flight response lead to death?

The autonomic nervous system uses the hormone adrenaline, a neurotransmitter, or chemical messenger, to send signals to various parts of the body to activate the fight-or-flight response. This chemical is toxic in large amounts; it damages the visceral (internal) organs such as the heart, lungs, liver and kidneys. It is believed that almost all sudden deaths are caused by damage to the heart. There is almost no other organ that would fail so fast as to cause sudden death. Kidney failure, liver failure, those things don't kill you suddenly.

What exactly happens in the heart when it's flooded with too much adrenaline?

Adrenaline from the nervous system lands on receptors of cardiac myocytes (heart-muscle cells), and this causes calcium channels in the membranes of those cells to open. Calcium ions rush into the heart cells and this causes the heart muscle to contract. If it's a massive overwhelming storm of adrenaline, calcium keeps pouring into the cells and the muscle just can't relax.

There is this specially adapted system of muscle and nerve tissue in the heart—the sinoatrial (SA) node, the atrioventricular node, and the Purkinje fibers—which sets the rhythm of the heart. If this system is overwhelmed with adrenaline, the heart can go into abnormal rhythms that are not compatible with life. If one of those is triggered, you will drop dead.

What is an example of one of these deadly heart rhythms?

In most cases, it's probably ventricular fibrillation that causes these sudden deaths from fear. Ventricular fibrillation basically causes the ventricles (lower chambers of the heart) to vibrate in a way that hampers their ability to deliver blood to the body.

What other emotional states besides fear could lead to these fatal heart rhythms?

Any strong positive or negative emotions such as happiness or sadness. There are people who have died in intercourse or in religious passion. There was a case of a golfer who hit a hole in one, turned to his partner and said, "I can die now"—and then he dropped dead. A study in Germanyfound an increase of sudden cardiac deaths on the days that the German soccer team was playing in the World Cup. For about seven days after the 9/11 terrorists attacks on the World Trade Center and Pentagon there was an increase of sudden cardiac death among New Yorkers.

Who is most likely to suffer from sudden death?

A predisposition to heart disease would probably increase your risk of sudden death, but it happens at all ages and can happen to otherwise healthy people.

Link: https://www.scientificamerican.com/article/scared-to-death-heart-attack/

Scared to Death: Can You Really Die of Fright?

Credit: Benoit Daoust | Shutterstock.com

'Tis the season of ghosts, goblins and other things that go bump in the night. And while most Halloween terrors are totally harmless (think jack-o'-lanterns and pointed hats), the frightful holiday might make you wonder: Is it really possible to be scared to death?

There's no question about it, the answer is yes, said Dr. Robert Glatter, an emergency physician at Lenox Hill Hospital in New York.

When people feel an overwhelming fear, their fight-or-flight response jumps into action. This response likely benefited early humans when they faced a menacing beast or aggressor, giving them the necessary adrenaline to either fight the attacker or flee the scene, Glatter said. [7 Weirdest Medical Conditions]

The rush of adrenaline is an involuntary response controlled by the autonomic nervous system. When faced with a fight-or-flight scenario, a person will experience rapid heart rate, dilated pupils and increased blood flow to the muscles, Glatter said.

Unfortunately, increased levels of adrenaline can damage the heart, Glatter told Live Science.

When adrenaline is released, it triggers calcium channels in the heart to open. "Calcium rushes into the heart cells, which causes the heart muscle to contract strongly," Glatter said. "Basically, in a massive response, the calcium keeps on pouring in, and the heart muscles can't relax."

If a person is scared and has a large amount of adrenaline reaching his or her heart, the individual can develop an arrhythmia called ventricular fibrillation — an uncoordinated contraction of the heart that makes it quiver, not beat regularly as it should, Glatter said.

"It ultimately leads to a drop in blood pressure, because without blood for the brain, you lose consciousness," Glatter said.

A terrifying event, be it a gun held to someone's head or a chilling Halloween trick, can trigger this disorganized heart movement, turning a scary situation into a deadly one, he said. [10 Ghost Stories That Will Haunt You for Life]

"It can happen even in normal [healthy] people," Glatter said. "It doesn't have to be a person with pre-existing heart disease, although those people would certainly be at higher risk."

Fear isn't the only trigger: Any type of extreme emotion can trigger the reaction. High levels of adrenaline can lead to death during sexual intercourse, religious fervor or sporting events, Glatter said. The fight-or-flight response can also be triggered by loud sounds, such as sonic booms, or horrible smells, including entering the house of a compulsive hoarder.

"We had a guy who came into the ER with chest pain after he opened his neighbor's door," Glatter said. "No one thought it was serious, but he was actually having a heart attack. And he was a young guy with no previous medical history."

What's more, "scaremongers" can be held legally accountable if they scare people to death. In May, an insurance company agreed to pay $300,000 to settle a lawsuit concerning an 85-year-old man who died after his vehicle hit a tractor-trailer in Detroit, according to the Associated Press. The man's family alleged that the tractor-trailer didn't have visible backlights, and that the man was literally "scared to death" when he suddenly saw the large vehicle during a rainstorm in 2008, the AP reported.

The man hit the tractor-trailer moments later, possibly because of his heart condition, the AP said.

"The next time you want to scare someone, be careful because you might be held responsible for it," Glatter said.

But there is good news. While the fight-or-flight response is involuntary, people can try to temper their reactions to scary events by practicing yoga, meditation or mindfulness, Glatter said.

Link: https://www.livescience.com/52573-can-you-die-of-fright.html

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