Muscle, vessels, or nerves: which one of these plays a key role in the heart of patients with takotsubo syndrome?
- PDF / 154,352 Bytes
- 2 Pages / 595.276 x 790.866 pts Page_size
- 33 Downloads / 128 Views
Muscle, vessels, or nerves: which one of these plays a key role in the heart of patients with takotsubo syndrome? Vincenzo Marafioti 1
# Springer Science+Business Media, LLC, part of Springer Nature 2019
Keywords Takotsubo syndrome . MINOCA . Autonomic nervous system
I had the pleasure to read the review by Dr. Ali et al [ 1], focused on diagnosis, prognosis, and treatment of the takotsubo syndrome (TTS). I would appreciate a response of the authors on the following issues. The authors use the neologism “MINOCA” in order to consider the TTS part of acute myocardial infarction without obstructive coronary artery disease. This example shows how the word is used and render false equivalences. The term MINOCA coined with a great emphasis and not validated by the authority of a dictionary of scientific terminology is supposed to mean: “the presence of the universal acute myocardial infarction (AMI) criteria, absence of obstructive coronary artery disease (≥ 50% stenosis), and no overt cause for the clinical presentation at the time of angiography (e.g., classic features for takotsubo cardiomyopathy).” [2] Therefore, MINOCA should rule out the cardiomyopathies. Moreover, regarding the hypothesized mechanism for myocardial ischemia (coronary microvascular spasm and dysfunction) in TTS, several inconsistencies exist: 1. Endomyocardial biopsies in some TTS patients demonstrated structural changes associated with a particular histological pattern, in which the cell dies in a hypercontracted state with early myofibrillar damage and anomalous irregular cross-band formations. These cardiac lesions termed myocytolysis appear most likely to be associated with direct cardiomyocyte toxicity of endogenous catecholamines, released into the heart via nerve terminals and not resemble those seen in myocardial ischemia, in which the cell loses its * Vincenzo Marafioti [email protected] 1
Cardiovascular and Thoracic Department, University Hospital of Verona, P. Stefani 1, 37126 Verona, Italy
capacity to contract and dies in an atonic state with no myofibrillar damage. 2. These lesions do not appear adjacent to the coronary artery, but located around the end of the intracardiac nerves. 3. Wall motion abnormalities do not match with a coronary artery system, but are, however, congruent with cardiac nerve distribution mapped for the first time in 1794 by Antonio Scarpa, acclaimed anatomist and neurologist [3]. This review would provide a general overview of TTS and focuses on its pathogenesis, but no reference to the important role of the autonomic nervous system (ANS) is made. The heart is reciprocally regulated by the sympathetic and parasympathetic divisions of the ANS, directly under the influence of the central nervous system (CNS). The connection between the CNS and heart may allow a coherent explanation for most, if not all, of the mystery signa of TTS [4]: cerebrogenic QTc prolongation, myocytolysis lesions, evident emotional or physical triggers (71.5%), and a higher prevalence of neurologic or psychiatric disord
Data Loading...
