Takotsubo Cardiomyopathy Topic Review
Takotsubo cardiomyopathy is also known as also known as stress-induced cardiomyopathy, broken-heart syndrome or apical-ballooning syndrome and occurs with a sudden increase in sympathetic nervous system activity.
Historically, this has been described with severe emotional upset. However, other causes of increased sympathetic activity including physical trauma, surgery or cocaine use can trigger Takotsubo cardiomyopathy as well.
Pathophysiology – Takotsubo Cardiomyopathy
The exact pathophysiology of Takotsubo cardiomyopathy remains unclear. Some theories suggest that coronary vasospasm or microvascular coronary dysfunction are contibutors.
Symptoms – Takotsubo Cardiomyopathy
The symptoms of Takotsubo cardiomyopathy are the same as those seen in myocardial ischemia and congestive heart failure. Chest pains typical of angina can also occur. Heart failure causes pulmonary edema and shortness of breath.
Diagnosis – Takotsubo Cardiomyopathy
Echocardiography is the best means to diagnosis the severe left ventricular systolic dysfunction and wall motion pattern present in a stress-induced cardiomyopathy. However, a coronary angiogram is usually required to be sure that an acute coronary syndrome is not present, as there is significant clinical overlap between the presentations of the two markedly different conditions.
The wall motion pattern is characteristic in Takotsubo cardiomyoathy and includes akinesis and “ballooning” of the cardiac apex, with hypercontractility of the segments at the base.
The ECG clip below is from a patient with a stress-induced cardiomyopathy:
Here is an LV angiogram from a patient with a stress-induced cardiomyopathy:
The ECG pattern during Takotsubo cardiomyopathy can vary from normal, to ST segment depression or elevation, to even a left bundle branch block.
Other atypical variants described include “reverse Takotsubo,” in which the basal segments of the heart become akinetic while the cardiac apex is hypercontractile.
Treatment – Takotsubo Cardiomyopathy
Universally, LV function returns to normal relatively quickly ― generally within one to four weeks. The mainstay of treatment is beta-blockers and, at least temporarily, angiotensin converting enzyme (ACE) inhibitors; however, there is no good clinical evidence to verify the reduction of cardiac endpoints, such as cardiac death or recurrence of the cardiomyopathy, with these therapies. Diuresis may be required if pulmonary congestion is present. Most clinicians will keep patients on beta-blockers for lifetime; but, again, there is no definite evidence to support this approach.
There are two potential causes when cardiogenic shock results from stress-induced cardiomyopathy, and it is very important to distinguish between them: Severe left ventricular systolic dysfunction and left ventricular outflow tract obstruction.
When the left ventricular systolic function is so severely reduced that hypotension and shock occur, inotropes such as dobutamine or milrinone are very helpful. These same drugs can actually worsen hypotension if the basal segments of the myocardium are so hypercontractile that they actually cause dynamic left ventricular outflow tract obstruction as can be seen in hypertrophic obstructive cardiomyopathy (HOCM).