Pathology of inverted Takotsubo cardiomyopathy

Maréchaux, Sylvestre; Fornès, Paul; Petit, S.; Poisson, Catherine; Thévenin, Didier; Tourneau, Thierry Le; Asseman, Philippe; Bruneval, Patrick; Ennezat, Pierre‐Vladimir

doi:10.1016/j.carpath.2007.08.002

Cited by 44 publications

(32 citation statements)

References 4 publications

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“…In our case, echocardiographic images showed akinesis of the basal anterior wall, and of the entire interventricular septum associated with hypokinesis of the basal segments of the inferior wall (Table 1) [14,[19][20][21][22][23][24][25][26][27][28][29][30][31][32][33]. Our case combined the anatomic abnormalities previously classified as type two, three and four.…”

Section: Discussionsupporting

confidence: 62%

An atypical case of inverted Tako-Tsubo syndrome: case report and review of the literature

et al. 2010

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A 69-yearold Caucasian woman was admitted to our emergency department (ED) for an acute and initial episode of substernal chest pain radiating to the left arm, which had lasted about 1 h, associated with dyspnea and diaphoresis. She had a past medical history of depression and first stage primary biliary cirrhosis. She was taking chronic low-dose sotalol therapy (80 mg PO bid) for a prior episode of supraventricular tachycardia. She had an otherwise normal heart, and was without cardiovascular risk factors.At admission, she denied any recent emotional or stressful event. The first EKG recorded 10 min after the ED admission showed mild ST-segment depression in the precordial leads V5 and V6 ( Fig. 1), without significant changes in the inferior, posterior and right precordial leads.The first blood sample analysis exhibited normal values of Troponin-I (cTn-I: 0.10 lg/L, normal range: 0-0.15 lg/L) and CK-MB (1.1 ng/ml, normal range: 0.5-3.6 ng/ml).The patient, fully asymptomatic, was admitted to our intensive observation unit.Based on our protocol, a second blood chemistry control was performed 6 h after the initial results. An elevated cTn-I value of 3.31 lg/L with normal CK-MB value (1.0 ng/ml) was observed. The EKG registered at the same time as the laboratory blood tests showed T-wave inversion in the precordial leads from V1 to V4 (Fig. 2), not present in the first tracing,and a small QT dispersion with a QT interval a bit longer than previous EKG. Trans-thoracic echocardiography showed normal left ventricular internal dimensions; the segmental wall motion analysis revealed akinesis of the basal anterior wall and the entire interventricular septum associated with hypokinesis of the inferior wall basal segments. Posterolateral basal segments and all mid-ventricular and apical segments appeared hyperkinetic. Preliminary diagnosisDr. Zanobetti, Dr. Conti, Dr. Pini: Based on the initial presentation, EKG abnormalities and a positive marker of myocardial necrosis, an acute coronary syndrome, myocarditis, or an atypical presentation of Tako-Tsubo syndrome were considered.None of the serial EKGs exhibited abnormalities characteristic of an acute coronary syndrome, and there was a mismatch between the limited extension of EKG abnormalities and the diffuse wall motion abnormalities in the echocardiographic examination. This mismatch can support the diagnosis of myocarditid, especially in the presence of limited abnormalities of myocardial specific enzymes. However, all indices of inflammation (C-Reactive Protein, leucocytes, erythrocyte sedimentation rate)

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Section: Discussionsupporting

confidence: 62%

An atypical case of inverted Tako-Tsubo syndrome: case report and review of the literature

et al. 2010

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“…These results are consistent with the analysis of myocytolysis by Luxol fast blue staining (Figure 4b). Marechaux et al 37 reported on the case of a woman presenting with takotsubo-like cardiomyopathy, subarachnoid hemorrhage and brain death. Histological analysis of the heart confirmed the absence of myocardial infarction and revealed only sparse foci of myocyte necrosis with contraction bands in the akinetic areas.…”

Section: Discussionmentioning

confidence: 99%

Effects of metoprolol on epinephrine-induced takotsubo-like left ventricular dysfunction in non-human primates

et al. 2009

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Takotsubo cardiomyopathy, alternatively known as stress cardiomyopathy, is an increasingly recognized clinical syndrome characterized by acute reversible apical ventricular dysfunction. To elucidate the mechanism, we tried to make a new model of takotsubo-like cardiomyopathy in non-human primates. Echocardiography revealed that repeated intravenous infusion of epinephrine overdose in cynomolgus monkeys induced takotsubo-like cardiomyopathy, which is characterized by progressive left ventricle and depressed systolic function with severe hypokinesis in apical regions and hyperkinesis in the basal region. Although this cardiac dysfunction almost normalized after a month even without any treatment, metoprolol, a b-blocker, improved the decreased ejection fraction earlier than in the control. Luxol fast blue staining, which is useful for estimating myocytolysis, showed that increased myocytolysis was observed in the apical ventricle of the epinephrine-infused heart. Metoprolol diminished epinephrine-induced cardiomyocytolysis. To explain the mechanism of takotsubo myopathy and the effect of metoprolol, gene expressions in apical or basal ventricle were compared. Heart failure-related genes, such as brain natriuretic peptide, connective tissue growth factor and osteopontin; calcium signaling-related genes, such as ryanodine receptor 2, sarcoendoplasmic reticulum Ca 2+ -ATPase 2A2 and adenylate cyclase 7; renin-angiotensin system-related genes, such as angiotensinogen, angiotensin II receptor, type 1 and type 2; and mitochondria-related genes, such as peroxisome proliferatoractivated receptor-c co-activator-1a, cytochrome c and transcription factor A mitochondrial, were significantly changed at the apical ventricle rather than at the basal ventricle. The changes of some genes improved with metoprolol treatment. These results indicate that this model is valuable in understanding the pathogenesis of takotsubo cardiomyopathy and the effectivity of b-blockers.

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“…More rarely, TTS has been reported in single patients with SAB [25,36,[38][39][40][41][42][43][44][45][46][47][48][49][50][51]. Some patients with SAB may develop the inverse Takotsubo pattern in which the basal parts of the myocardium become hypo-or akinetic, whereas the apical parts are hyperkinetic (hyperdynamic) ( Table 1) [25,39,41,42,48,49]. Since TTS may be the predominant manifestation, SAB may go undetected in some cases of SAB-induced TTS, and SAB should be excluded by a cerebral CT scan in all patients with TTS.…”

Section: Subarachnoid Bleeding (Sab)mentioning

confidence: 96%