Stress cardiomyopathy overview

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Stress Cardiomyopathy from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

MRI

Echocardiography

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Unstable angina/non ST elevation myocardial infarction in Stress (Takotsubo) Cardiomyopathy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2] Arzu Kalayci, M.D. [3]

Overview

Stress cardiomyopathy is a relatively new disease, with the first case documented in literature under the name of Takotsobu Cardiomyopathy in Japan in 1991. It is not very well understood, but the disease is thought to arise following intense emotional or physical stress. Stress cardiomyopathy mostly affects post-menopausal women. The clinical presentation, laboratory findings and imaging studies largely mimic that of anterior MI. However, the absence of significant coronary artery stenosis supports the diagnosis of stress cardiomyopathy. It is generally a self-limiting disease and the majority of patients have a restored cardiac function within a matter of weeks. Complications and death are relatively rare, but they are mostly related to the development of heart failure and pulmonary edema.

Historical Perspective

Stress cardiomyopathy is a relatively new disease, with the first case documented in literature in Japan in 1991. However, cases of death upon going through severe emotional or psychological stress have been described as early as the biblical times.[1][2]

Classification

Stress cardiomyopathy can be divided into several types, depending on the location of regional wall motion abnormality. The area of motion abnormality (whether hypokinesia, dyskinesia or akinesia) can be detected on echocardiography or left ventriculography. The most common type is the apical type, resulting in apical ballooning.[3][4][5][6]

Pathophysiology

The pathogenesis of stress cardiomyopathy is not completely understood. However, the most accepted theory behind it is thought to be due to catecholamine surge, which are thought to contribute to myocardial necrosis and stunning seen in stress cardiomyopathy.[2][7][8] On biopsy, findings include an inflammatory infiltrate, fibrosis and formation of contraction bands, which may or may not be associated with myocardial necrosis.[9][10] Stress cardiomyopathy is associated with various neurological and psychological conditions.

Causes

The cause of stress cardiomyopathy is largely unknown. However, it is usually triggered by emotional and/or physical stress and may be related to certain medical conditions.

Differentiating Stress Cardiomyopathy from Other Diseases

The clinical presentation, laboratory findings and imaging studies of stress cardiomyopathy resembles that of anterior MI and must be differentiated from it. Also, stress cardiomyopathy must be differentiated from other medical conditions, such as pheochromocytoma, dilated cardiomyopathy and hypertrophic cardiomyopathy.[11][12]

Epidemiology and Demographics

The true incidence and prevalence of stress cardiomyopathy is unknown. However, this disease most commonly affects post-menopausal women, with the mean age of diagnosis ranging between 58-75 years.[2][3][1][13][14]

Risk Factors

Stress cardiomyopathy seems to be triggered by intense emotional or physical stress, mostly the unexpected death of a loved one.[2]

Screening

There are no screening recommendations for stress cardiomyopathy.[15]

Natural History, Complications and Prognosis

The prognosis of stress cardiomyopathy is generally excellent, with most patients making a complete recovery within a matter of weeks. However, death from complications of heart failure and heart rupture may occur.[2][13][16]

Diagnostic Criteria

In 2004, researchers at the Mayo Clinic proposed a criteria for the diagnosis of stress cardiomyopathy. All 4 points of the criteria must be fulfilled, which include ruling out other medical conditions, such as obstructive coronary disease, myocarditis and pheochromocytoma.[13][2]

History and Symptoms

The most common presenting symptoms of stress cardiomyopathy are shortness of breath and chest pain.[2][10][13][14][3][17]

Physical Examination

Physical examination findings in patients with stress cardiomyopathy are non-specific and non-diagnostic. The diagnosis of stress cardiomyopathy is largely based on ECG, echocardiographic findings, as well as cardiac catheterization.[18]

Laboratory Findings

Elevated levels of catecholamines, cardiac enzymes and BNP may be seen in patients with stress cardiomyopathy. However, none of these laboratory findings are specific to stress cardiomyopathy.[2][10][14][17]

ECG

ECG findings in stress cardiomyopathy are similar to those seen in anterior MI. The most common findings include ST elevation in the precordial leads, T wave inversion and the formation of a Q wave.[19][2] Findings on ECG include:[2][10][13][16][14][3][17]

Chest X-Ray

 Typical findings on chest x-ray include apical ballooning and narrowing of the neck.

CT Scan

A CT scan may be done in patients with stress cardiomyopathy to asses coronary anatomy, as well as detect the presence of regional wall motion abnormalities.[17]

MRI

Cardiac magnetic resonance (CMR) is a useful imaging modality in distinguishing between stress cardiomyopathy and myocarditis or MI. The most common findings on CMR in patients with stress cardiomyopathy include absence of gadolinium hyper-enhancement, as well as myocardial edema.[13][20][21][22][23][24][25][26][27][5][28]

Echocardiography

Echocardiography is done in patients with stress cardiomyopathy to document apical ballooning, dyskinesia/akinesia and reduced ejection fraction.[10][13][16][17]

Other Imaging Findings

In patients with stress cardiomyopathy, coronary angiography usually shows normal anatomy of the coronary arteries no evidence of coronary artery stenosis.[2][14][17]

Other Diagnostic Studies

Coronary angiography and cardiac catheterization are the diagnostic modalities of choice to distinguish between stress cardiomyopathy and acute anterior MI. Normal anatomy of the coronary arteries, along with a reduced ejection fraction supports the diagnosis of stress cardiomyopathy.[10][16][14]

Medical Therapy

Medical therapy in stress cardiomyopathy is indicated to treat the complications that may arise. The most common complications related to stress cardiomyopathy include heart failure and pulmonary edema. Diuretics and anti-heart failure medications are the treatment of choice in these conditions.[1][10]

Surgery

Treatment of stress cardiomyopathy is mostly supportive and medications are used to treat complications.[1][10] There is no role for surgery in the treatment of stress cardiomyopathy.

Primary Prevention

There are no means of prevention of stress cardiomyopathy.

Secondary Prevention

Stress cardiomyopathy is a self-limiting disease, which usually resolves within a few weeks. However, medical therapy may be necessary during the acute phase of the illness or when complications arise.[1][10]

References

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  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 Akashi YJ, Goldstein DS, Barbaro G, Ueyama T (2008). "Takotsubo cardiomyopathy: a new form of acute, reversible heart failure". Circulation. 118 (25): 2754–62. doi:10.1161/CIRCULATIONAHA.108.767012. PMC 4893309. PMID 19106400.
  3. 3.0 3.1 3.2 3.3 Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, Cammann VL, Sarcon A, Geyer V, Neumann CA, Seifert B, Hellermann J, Schwyzer M, Eisenhardt K, Jenewein J, Franke J, Katus HA, Burgdorf C, Schunkert H, Moeller C, Thiele H, Bauersachs J, Tschöpe C, Schultheiss HP, Laney CA, Rajan L, Michels G, Pfister R, Ukena C, Böhm M, Erbel R, Cuneo A, Kuck KH, Jacobshagen C, Hasenfuss G, Karakas M, Koenig W, Rottbauer W, Said SM, Braun-Dullaeus RC, Cuculi F, Banning A, Fischer TA, Vasankari T, Airaksinen KE, Fijalkowski M, Rynkiewicz A, Pawlak M, Opolski G, Dworakowski R, MacCarthy P, Kaiser C, Osswald S, Galiuto L, Crea F, Dichtl W, Franz WM, Empen K, Felix SB, Delmas C, Lairez O, Erne P, Bax JJ, Ford I, Ruschitzka F, Prasad A, Lüscher TF (2015). "Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy". N. Engl. J. Med. 373 (10): 929–38. doi:10.1056/NEJMoa1406761. PMID 26332547.
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  9. Akashi YJ, Goldstein DS, Barbaro G, Ueyama T (2008). "Takotsubo cardiomyopathy: a new form of acute, reversible heart failure". Circulation. 118 (25): 2754–62. doi:10.1161/CIRCULATIONAHA.108.767012. PMC 4893309. PMID 19106400.
  10. 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 Brenner ZR, Powers J (2008). "Takotsubo cardiomyopathy". Heart Lung. 37 (1): 1–7. doi:10.1016/j.hrtlng.2006.12.003. PMID 18206521.
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  15. U.S. Preventive Services Task Force https://www.uspreventiveservicestaskforce.org/BrowseRec/Search?s=stress+cardiomyopathy. Accessed on Jan 9, 2017.
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  21. Haghi D, Fluechter S, Suselbeck T, Kaden JJ, Borggrefe M, Papavassiliu T (2007). "Cardiovascular magnetic resonance findings in typical versus atypical forms of the acute apical ballooning syndrome (Takotsubo cardiomyopathy)". Int. J. Cardiol. 120 (2): 205–11. doi:10.1016/j.ijcard.2006.09.019. PMID 17175045.
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