Coronavirus disease 2019 has been demonstrated to cause pneumonia and cardiovascular complications such as myocarditis, atrial fibrillation, heart failure, and arrhythmias. Recently, cardiologists have also witnessed an infamous cardiac complication known as ‘Takotsubo Cardiomyopathy’ (TC) or ‘Broken Heart Syndrome’ in Covid-19 patients.
The other easier-to-pronounce names of the condition are ‘apical ballooning syndrome’ or ‘stress cardiomyopathy’. The clinical presentation (electrocardiography (ECG) and cardiac biomarkers) and symptoms of TC i.e. shortness of breath, chest pain, nausea, and vomiting mimic heart attack. The major difference between the two is that there is no coronary artery blockade in TC, unlike heart attack. But due to startling similarity in symptoms and clinical presentation, TC often goes undiagnosed as it is easily mistaken for a heart attack. The year was 1990 when TC was first reported by a Japanese cardiologist Dr. Hikaru Sato.
The cause of TC is largely speculative to date but is believed to be triggered by intense physical or emotional stress. The release of stress hormones (adrenaline, noradrenaline) under stressful conditions such as bereavement, failures, devastation, or natural disasters alters autonomic nervous system activity resulting in a rise in blood pressure and impaired pumping activity of the heart. The abrupt malfunctioning of the left ventricle of the heart especially during the contraction phase (systole) renders it a characteristic shape- the apex of the heart dilates and the base contracts. This shape resembles the Japanese octopus trapping pot Tako (octopus) Tsubo (pot) with a round bottom and a narrow neck. And hence the name – Takotsubo Cardiomyopathy.
According to a recent study published in the Journal of the American Medical Association, the investigators have witnessed an increase in hospitalization with TC patients while comparing contemporary and pre-pandemic cardiac catheterization records. Even more surprising is that all of the TC patients were Covid-19 negative. The authors believe that the psychological and socio-economic stress of the pandemic in the form of job losses, deaths, and uncertainty in unprecedented times is equally traumatic and might be responsible for increased TC cases.
Cardiovascular complications were also documented in preceding epidemics (SARS and MERS) but not even a single case of TC was reported in either of them, leaving many researchers with a lingering question- what’s so peculiar about this (SARS-CoV-2) virus? Perhaps, one possibility could be that it might have gone undiagnosed back then.
We need thorough research before we come to any conclusion. But before that, we must apprehend what we know now. Viral infections are known to cause myocyte degeneration, inflammation, congestive heart failure, and idiopathic dilated cardiomyopathy. The SARS-CoV-2 spike protein binds to angiotensin-converting enzyme 2 (ACE2) which is highly expressed in the heart and utilizes it as an “entry gate”. After entering the heart, the virus can exert a direct toxic effect resulting in inflammation and death of myocytes (heart cells). SARS-CoV-2 also adversely affects blood vessels leading to endothelial dysfunction- blood vessels constrict (narrow) instead of dilating (opening). This, in addition to the fever which typically follows inflammation (as a sign of immune system activation), activates the sympathetic nervous system due to associated stress (stress-induced adrenergic discharge). Together, all these malfunctions could have resulted in transient left ventricular apical dysfunction (ballooning), a typical feature of lesser-known- Takotsubo Cardiomyopathy.
Needless to say, the anxiety and stigma associated with the Covid-19 infection can also manifest into a broken heart syndrome. Broken heart syndrome is a constant reminder of how stress can break our heart apart- not only emotionally by pathologically as well.