Serious takotsubo cardiomyopathy: an autopsy case presenting severe irreversible myocardial damage after frequent episodes of recurrence

Abstract

Background: Takotsubo cardiomyopathy is characterized by transient dysfunction of the medial to apical segment of the left ventricle. Recurrence within a few months or years has been reported and serious complications, including arrhythmia, acute cardiac shock and cardiac rupture, can arise; however, recurrence is rare and takotsubo cardiomyopathy is typically a reversible functional disorder. Case presentation: A 91-year-old Japanese woman with a past medical history of angina pectoris, hypertension and uterine carcinoma noted bilateral axillary pain and presented herself to an emergency room. Although the pain improved and she went home, there were several subsequent episodes of recurrent chest pain. At approximately 1 week after the onset, she was hospitalized as her symptom worsened. Electrocardiography showed low voltage in limb and chest leads, and ST-segment elevation in leads II, III, aVF and V3 to V6. Echocardiography revealed medial to apical dyskinesia and basal hypercontractility of the left ventricle, and cardiac tamponade. Pericardiocentesis improved the symptom, but not her cardiac dysfunction. At 3 days after her admission, cardiopulmonary resuscitation was performed due to ventricular fibrillation. She died on the 5th day of admission (2 weeks after the onset). At autopsy, the left ventricle was dilatated and the apical ventricular wall was thin. On microscopy, remarkable wavy change and thinning of myocardium were diffusely observed, especially at the apex and the anterior to lateral wall of the left ventricle, interventricular septum and right ventricle, intermingled with interstitial fibrosis, hemorrhage and neutrophil infiltration. Contraction band necrosis was mainly observed on the posterior to inferior wall of the left ventricle. Conclusion: Our case showed severe morphological myocardial change after several chest pain episodes that were considered to be takotsubo cardiomyopathy. This notable case suggests that the frequent recurrence of serious takotsubo cardiomyopathy is life threatening and can lead to irreversible serious myocardial degeneration.

Takotsubo Syndrome: Pathophysiology, Emerging Concepts, and Clinical Implications

“…77 Norepinephrine spillover can decrease myocyte viability, resulting in contraction band necrosis, which is one of the histological findings reported in takotsubo syndrome (Figure 2). 78,79 Contraction band necrosis is also found in patients with pheochromocytoma and subarachnoid hemorrhage, which have also been attributed to catecholamine excess. 78,79…”

“…hemorrhage, which have also been attributed to catecholamine excess. 78,79 Some authors have hypothesized that a surge in adrenoreceptor stimulation dysregulates myocardial calcium handling. Immunohistochemistry studies suggest that calcium-regulating proteins such as phospholamban, sarcoendoplasmic reticulum calcium-ATPase, and sarcolipin are altered, resulting in depressed left ventricular contraction during acute takotsubo syndrome.…”

“…78,79 Contraction band necrosis is also found in patients with pheochromocytoma and subarachnoid hemorrhage, which have also been attributed to catecholamine excess. 78,79…”

“…77 Norepinephrine spillover can decrease myocyte viability, resulting in contraction band necrosis, which is one of the histological findings reported in takotsubo syndrome (Figure 2). 78,79 Contraction band necrosis is also found in patients with pheochromocytoma and subarachnoid Cardiopulmonary exercise (treadmill) data from a patient with previous takotsubo syndrome 20 months earlier (A) and an age-and sexmatched healthy control subject (B). The maximal oxygen consumption (Vo 2, blue dots) achieved by the patient with takotsubo syndrome is markedly reduced, with an earlier anerobic threshold and a shorter duration of exercise than the healthy control subject.…”

Takotsubo Syndrome and Coronary Artery Disease: Which Came First—The Chicken or the Egg?

“…On the other hand, catecholamines that approach the heart through sympathetic nerves and are released directly into the myocardium may have greater cardiotoxic effects compared to those delivered by circulation [17]. Consequently, norepinephrine spillover can reduce myocyte viability, leading to contraction band necrosis-a histological characteristic associated with TTS [18].…”