Left Ventricular Apical Rupture Caused by Takotsubo Cardiomyopathy - Comprehensive Pathological Heart Investigation

Abstract

akotsubo cardiomyopathy is a novel heart syndrome characterized by a transient left ventricular (LV) dysfunction with chest pain, ECG changes and not a high increase in cardiac enzymes, mimicking an acute myocardial infarction. 1,2 Because of the specific abnormalities of the LV contraction (ie, preserved basal function with apical akinesis or dyskinesis) the disease is also called as 'transient left ventricular apical ballooning' or 'ampulla cardiomyopathy '. 2,3 The general prognosis is considered to be rather favorable, 2-6 although some investigators have reported cases with various complications including death. [7][8][9] We present a case of takotsubo cardiomyopathy in a female patient who suffered a fatal LV free wall rupture and the results of a comprehensive histopathologic investigation. Case ReportAn 81-year-old woman with hypertension started to feel chest pains after a quarrel with her son. Next day stomach pains and diarrhea appeared but the chest pain became intermittent, and the symptoms were accompanied by general fatigue. On the third day she was admitted to hospital because of chest discomfort at rest and ECG signs of ST-segment elevation myocardial infarction (MI) (Fig 1A). She had no history of prior angina or MI and no family history of heart disease and sudden death. On admission her heart rate was 104 beats/min, and blood pressure was 150/90 mmHg. Auscultation of the heart and lungs was normal, abdominal and neurological examination findings were negative, and there was no peripheral edema. Immediate coronary angiography did not reveal any significant coronary artery stenosis ( Figs 2A,B); the TIMI frame counts for the left anterior descending, circumflex and right coronary arteries were 29, 20 and 26 frames, respectively. However, ventriculography revealed a balloon-like LV motion abnormality with akinesis from the mid to apical portions and hyperkinesis of the base (Figs 2C,D). The LV end-systolic and end-diastolic pressureas were 150 mmHg and 15 mmHg, respectively, and there was no pressure gradient from the apex and midportion to the outflow tract; other hemodynamic data and the laboratory data on admission are shown in Table. After angiography the patient reported pain relief and was taken to the intensive care unit; however, the ECG recording showed no restoration of normal ST-segment (Fig 1B). The woman was stable during the first 40 h of admission, with no hemodynamic or arrhythmic problems, and she was given -blocker (metoprolol), angiotensin-converting enzyme inhibitor (ramipril) and aspirin; her blood pressure was within normal limits. She occasionally complained of chest discomfort; her creatine kinase-MB was maximal on admission and gradually diminished in further examinations, but the ST segment remained elevated ( Figs 1C,D). After 40 h of admission she reported a sudden pain in the epigastric region and the symptoms of acute abdomen soon appeared (C-reactive protein reached 267 mg/dl). After surgical consultation the woman was taken to the operation room for urgent surger...

Left ventricular function after takotsubo is not fully recovered in long-term follow-up: A speckle tracking echocardiography study

“…Cardiac rupture is the most severe and oftentimes fatal complication of TTC, which supports the transmyocardial damage [28,29]. Histopathological findings at the rupture site include myocardial necrosis with hemorrhaging, fused foci of coagulation necrosis and contraction band necrosis, as well as diffuse patchy infarction of myocardial in the surrounding tear area [30][31][32][33]. In myocardial biopsies, intestinal fibrosis, contraction band necrosis and mild cell infiltration have been described [13,32].…”

Pathology of Takotsubo (Ampulla) Cardiomyopathy

“…There have been many recent reports such as on a 77-year-old woman with myocardial infarction-like electrocardiographic pattern during the course of malabsorption syndrome 10 and on an 84-year-old woman who died from cardiac rupture 11 (four days after the onset, cardiac arrest occurred due to cardiac rupture). In the Circulation Journal, Sacha et al 12 stated the case of Ohara et al 13 in the same journal as the first autopsy case [of takotsubo cardiomyopathy] and their own case was the second one. However, this information is not accurate.…”

Fehldiagnose eines akuten Myokardinfarkts: die Takotsubo-Kardiomyopathie

“…Komplikationen werden in der Literatur in bis zu 17,7% aller Patienten beschrieben (kardiogener Schock, maligne ventrikuläre Arrhythmien, Obstruktion im linksventrikulären Ausflusstrakt, akute Mitralklappeninsuffizienz, Thromben im linken Ventrikel). In einem Fallbericht wird der Verlauf eines Patienten mit linksventrikulären Thromben und Mesenterialinfarkten beschrieben, bei dem es im Rahmen einer Takutsubo-Kardiomyopathie sogar zu einer Ventrikelperforation kam [2,7]. Allgemein wird die Kombination aus steigendem C-reaktivem Protein und einer über 3 Tage persistierenden ST-Strecken-Hebung im Sinne einer bleibenden Myozytenschädigung als prognostisch negativer Faktor diskutiert [7].…”

“…In einem Fallbericht wird der Verlauf eines Patienten mit linksventrikulären Thromben und Mesenterialinfarkten beschrieben, bei dem es im Rahmen einer Takutsubo-Kardiomyopathie sogar zu einer Ventrikelperforation kam [2,7]. Allgemein wird die Kombination aus steigendem C-reaktivem Protein und einer über 3 Tage persistierenden ST-Strecken-Hebung im Sinne einer bleibenden Myozytenschädigung als prognostisch negativer Faktor diskutiert [7]. Die Mortalität Pattberg SV, et al Takotsubo-Kardiomyopathie Med Klin 2008;103:441-4 (Nr.…”