M Ranieri1, J Finsterer2, G Bedini3, E A Parati1, A Bersano4,5. 1. Cerebrovascular Disease Unit, IRCCS Foundation "C. Besta", Neurological Institute, Milan, Italy. 2. Krankenanstalt Rudolfstiftung, Vienna, Austria. 3. Laboratory of Cellular Neurobiology, IRCCS Foundation "C. Besta", Neurological Institute, Milan, Italy. 4. Cerebrovascular Disease Unit, IRCCS Foundation "C. Besta", Neurological Institute, Milan, Italy. anna.bersano@gmail.com. 5. Fondazione IRCCS Istituto Neurologico "Carlo Besta", Via Celoria 11, 20133, Milan, Italy. anna.bersano@gmail.com.
Abstract
PURPOSE OF REVIEW: This review paper aims to provide a complete and updated overview on the clinical and pathophysiological aspects of Takotsubo syndrome (TTS), including prognosis, therapy, and the association with cerebrovascular conditions. RECENT FINDINGS: TTS is an increasingly recognized non-ischemic cardiomyopathy characterized by sudden, temporary weakening of the myocardium, of which the pathogenesis is unknown. Although pathogenesis of TTS remains unclear, a complex interaction between catecholamine-mediated stimulation, myocardial stunning, and subsequent stress-related myocardial dysfunction seems to be the main pathophysiological mechanism. Stroke is linked to TTS by a dual relationship since it may induce TTS by catecholamine release even if TTS itself also may be complicated by left ventricular thrombi leading to stroke. Given its possible complications, including the association with neurological diseases, both cardiologist and neurologists should be aware about TTS in order to diagnose it promptly and to initiate appropriate therapeutic measures.
PURPOSE OF REVIEW: This review paper aims to provide a complete and updated overview on the clinical and pathophysiological aspects of Takotsubo syndrome (TTS), including prognosis, therapy, and the association with cerebrovascular conditions. RECENT FINDINGS: TTS is an increasingly recognized non-ischemic cardiomyopathy characterized by sudden, temporary weakening of the myocardium, of which the pathogenesis is unknown. Although pathogenesis of TTS remains unclear, a complex interaction between catecholamine-mediated stimulation, myocardial stunning, and subsequent stress-related myocardial dysfunction seems to be the main pathophysiological mechanism. Stroke is linked to TTS by a dual relationship since it may induce TTS by catecholamine release even if TTS itself also may be complicated by left ventricular thrombi leading to stroke. Given its possible complications, including the association with neurological diseases, both cardiologist and neurologists should be aware about TTS in order to diagnose it promptly and to initiate appropriate therapeutic measures.
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