Takotsubo Cardiomyopathy refers to a condition where the heart muscles are suddenly weakened due to sudden enlargement following acute stress occurrence but the heart muscle function reverts to the normal status in a few weeks. It is also known as apical ballooning syndrome or broken heart syndrome. It affects women of postmenopausal age and presents with features that mimic a heart attack i.e. chest pain, breathlessness and cardiopulmonary insufficiency. Unlike the ischemic disease takotsubo cardiomyopathy arises from stresses such as severe pain, domestic violence, serious illnesses, bad news, intense fear or financial strain. It is therefore the role of the doctor to differentiate takotsubo cardiomyopathy (TCM) from myocardial infarction as the treatment approach would be different.
The disease occurs following an acute stressful state that leads to the release of catecholamines and as a result there is stimulation of the β2 adrenoceptor pathway. This induces acute myocardial inflammation that is akin to myocardia infarction and the cardiac muscles shift to the glucose pathway as the source of energy as seen with ischemia leading to damage of the heart muscles. The inflammation causes reversible focal myocytosis and some necrosis of the ventricular muscles.
Relationship between Takotsubo Cardiomyopathy and Troponin
Diagnosis of Takotsubo cardiomyopathy and the Value of Troponin Levels in its Diagnosis
As seen with heart attack, diagnosis of takotsubo cardiomyopathy entails:
Electrocardiography (ECG): The electrical activity of the heart is monitored and since there are necrotic lesions waves of injury and/or death is evident. Therefore, one may see ST wave elevations, T wave inversions or Q waves. takotsubo cardiomyopathy features on ECG are more consistent with ST elevation myocardial infarction (STEMI).
Echocardiography: 2-Dimensional echocardiography identifies an abnormally shaped heart secondary to dilatation. There is a periapical area of hypokinesis or akinesia. These findings may also be seen in myocardial infarction and thus do not fully differentiate the two conditions.
Coronary Angiogram: Introduction of contrast to the coronary vessels to identify any obstructive lesions plots an angiogram with normal patency as the disease is stress induced and not ischemic. The angiogram however may show an altered shape and dilated heart chambers suggesting that Takotsubo cardiomyopathy is more likely. A major limitation of the test is that it is invasive and thus would not be preferred by many patients.
Troponin Levels and other Cardiac Markers: Blood work up for cardiac markers appears to be the most important test in diagnosis and follow-up of these patients. Troponin I and Troponin T are elevated in almost all patients with takotsubo cardiomyopathy. Inflammation and death causes release of these biomarkers into circulation hence their high levels.
Conclusion
Takotsubo cardiomyopathy is a disease with identical features to myocardial infarction with a sole differentiating factor that takotsubo cardiomyopathy is reversible and hence aggressive management is rarely required. On the other hand, timely intervention is needed for myocardial infarction to rescue ischemic areas and avoid further necrosis. A clinician should note that most tests carried out have identical findings to apart from angiography that is not a desired diagnostic test. Cardiac markers such as Brain natriuretic peptide (BNP), troponin I and troponin T are elevated in more than 90% of the cases of takotsubo cardiomyopathy.
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