Abstract
Stress-related cardiomyopathies can be observed in the four following situations: Takotsubo cardiomyopathy or apical ballooning syndrome; acute left ventricular dysfunction associated with subarachnoid hemorrhage; acute left ventricular dysfunction associated with pheochromocytoma and exogenous catecholamine administration; acute left ventricular dysfunction in the critically ill. Cardiac toxicity was mediated more by catecholamines released directly into the heart via neural connection than by those reaching the heart via the bloodstream. The mechanisms underlying the association between this generalized autonomic storm secondary to a life-threatening stress and myocardial toxicity are widely discussed. Takotsubo cardiomyopathy has been reported all over the world and has been acknowledged by the American Heart Association as a form of reversible cardiomyopathy. Four "Mayo Clinic" diagnostic criteria are required for the diagnosis of Takotsubo cardiomyopathy: 1) transient left ventricular wall motion abnormalities involving the apical and/or midventricular myocardial segments with wall motion abnormalities extending beyond a single epicardial coronary artery distribution; 2) absence of obstructive epicardial coronary artery disease that could be responsible for the observed wall motion abnormality; 3) ECG abnormalities, such as transient ST-segment elevation and/or diffuse T wave inversion associated with a slight troponin elevation; and 4) the lack of proven pheochromocytoma and myocarditis. ECG changes and LV dysfunction occur frequently following subarachnoid hemorrhage and ischemic stroke. This entity, referred as neurocardiogenic stunning, was called neurogenic stress-related cardiomyopathy. Stress-related cardiomyopathy has been reported in patients with pheochromocytoma and in patients receiving intravenous exogenous catecholamine administration. The role of a huge increase in endogenous and/or exogenous catecholamine level in critically ill patients (severe sepsis, post cardiac resuscitation, post tachycardia) to explain the onset of myocardial dysfunction was discussed. Further research is needed to understand this complex interaction between heart and brain and to identify risk factors and therapeutic and preventive strategies.
Highlights
Neurocardiology has many dimensions, namely divided in three categories: the heart’s effects on the brain; the brain’s effects on the heart; and neurocardiac syndromes, such as Friedreich disease [1]
By contrast the increase in plasma levels of metanephrine and normetanephrine, which are extra neuronal catecholamine metabolites, was within a similar range to that observed in Killip class III myocardial infarction patients [3]. This finding suggests that cardiac toxicity was mediated more by catecholamines released directly into the heart via neural connection than by those reaching the heart via the bloodstream
Bybee and Prasad suggested four “Mayo Clinic” diagnostic criteria for Takotsubo: 1) transient left ventricle (LV) wall motion abnormalities involving the apical and/or midventricular myocardial segments with wall motion abnormalities extending beyond a single epicardial coronary artery distribution; 2) absence of obstructive epicardial coronary artery disease that could be responsible for the observed wall motion abnormality; 3) ECG abnormalities, such as transient ST-segment elevation and/or diffuse T-wave inversion associated with a slight troponin elevation; and 4) the lack of proven pheochromocytoma and myocarditis [2]
Summary
Neurocardiology has many dimensions, namely divided in three categories: the heart’s effects on the brain (i.e., embolic stroke); the brain’s effects on the heart (i.e., neurogenic heart disease); and neurocardiac syndromes, such as Friedreich disease [1]. They have suggested that the myocardial depression was the consequence of the attenuation of the adrenergic response at the cardiomyocyte level due to down-regulation of the beta adrenergic receptors and depression of the postreceptor signaling pathways [42,43] This hibernation-like state of the cardiomyocytes during severe sepsis was probably enhanced by neuronal apoptosis in the cardiovascular autonomic centers and by inactivation of catecholamines secondary to the production of reactive oxygen species by oxidative stress [44]. Postcardiac arrest myocardial dysfunction Prengel et al reported that severe stress, such as that occurring with cardiac arrest and cardiopulmonary resuscitation, activates the sympathetic nervous system and causes a rise in plasma catecholamine concentrations, which could play a role in the onset of post cardiac arrest myocardial dysfunction [48] This postcardiac arrest myocardial dysfunction contributes with postcardiac arrest brain injury to the low survival rate after in- and out-of-hospital cardiac arrest [48,49]. Competing interests The author declares that they have no competing interests
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
