Friday, March 2, 2012
Stress-induced cardiomyopathy, also called apical ballooning syndrome, broken heart syndrome, and takotsubo cardiomyopathy, is an increasingly reported syndrome generally characterized by transient systolic dysfunction of the apical and/or mid segments of the left ventricle that mimics myocardial infarction (MI), but in the absence of obstructive coronary artery disease. Stress cardiomyopathy is a more recently described form of reversible LV systolic dysfunction,
and the most common form of stress cardiomyopathy is transient apical ballooning. The Japanese have named this syndrome “takotsubo” because the shape of the ballooned apex in
systole is similar to the shape of an octopus trap. However, in acute stress-related cardiomyopathy, LV dysfunction is not always confined to the apex. Variations of this syndrome include wall motion abnormalities involving the basal, midportion, and lateral walls of the left ventricle. This is the reason why the term “acute, stress cardiomyopathy” or, more simply, “stress cardiomyopathy” may be preferable to transient apical ballooning.
The triggering event is commonly, but not exclusively, an emotionally traumatic one, but may also be an acute medical illness (eg, a severe asthmatic attack requiring intubation). In some cases, the trigger is unusually strenuous physical activity or a public performance.
The majority of patients exhibit chest symptoms (not necessarily chest pain) and electrocardiogram (ECG) changes consistent with acute myocardial ischemia. Experience with patients with stress cardiomyopathy suggests some features may differentiate it from LV dysfunction related to an acute LAD territory MI.
The onset of stress-induced cardiomyopathy is frequently but not always triggered by an acute medical illness or by intense emotional or physical stress (eg, death of relatives, particularly if unexpected, domestic abuse, arguments, catastrophic medical diagnoses, devastating financial or gambling losses, natural disasters). The pathogenesis of this disorder is not well understood. It is not known why this disorder affects postmenopausal women disproportionately or why the left ventricular mid-cavity and apex are predominantly affected. Although the clinical presentation simulates that of an acute MI, coronary arteriography typically shows no obstructive lesions, and only a minority of patients display coronary spasm with acetylcholine provocation. Postulated mechanisms include catecholamine excess, coronary artery spasm, and microvascular dysfunction. Alternatively, there may be dynamic mid-cavity or left ventricular outflow tract obstruction which may contribute to apical dysfunction. Analogous permanent (rather than transient) apical outpouchings develop in patients with hypertrophic cardiomyopathy and mid-ventricular obstruction. A potential role for plaque rupture and thrombosis with spontaneous thrombolysis has not been established and the results of intravascular ultrasound (IVUS) studies are mixed. Although one IVUS study found evidence of mid left anterior descending (LAD) coronary artery plaque rupture in 5 of 5 patients diagnosed with stress-induced cardiomyopathy, other IVUS series found no evidence of culprit lesions in the LAD.
Stress cardiomyopathy patients:
• usually do not develop Q-waves.
• have lower levels of biomarker release, especially total creatine kinase (CPK), usually not exceeding 400 IU.
• have wall motion abnormalities that appear to span a larger perfusion territory than one coronary artery.
• do not demonstrate delayed hyperenhancement by magnetic resonance imaging (MRI) with gadolinium.
• have wall motion abnormalities that improve on follow-up, some as early as 2 days following presentation.
• have extensive wall motion abnormalities and even severe hemodynamic compromise, but relatively low mortality, (in the range of 0%-8%).