Sudden cardiac death secondary to demonstrated reperfusion ventricular fibrillation in a woman with Takotsubo cardiomyopathy

Pepe, Martino; Zanna, Del; Quagliara, Donato; Caiati, Carlo; Marzullo, Andrea; Palmiotto, Angela; Caruso, G.; Favale, Stefano

doi:10.1016/j.carpath.2010.06.006

Cited by 8 publications

(4 citation statements)

References 8 publications

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“…Excess catecholamines cause intramyocellular calcium overload, and this overload causes delayed after-potentials [11]. Delayed after-potentials appear to be responsible for the onset of the ventricular tachycardia.…”

Section: Discussionmentioning

confidence: 99%

An autopsy case of tako-tsubo cardiomyopathy presenting ventricular tachycardia after pacemaker implantation

Kinbara

Hayano

Otani

et al. 2013

Journal of Cardiology Cases

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We herein report a rare autopsy case of tako-tsubo cardiomyopathy (TTC) presenting ventricular tachycardia after pacemaker implantation. A 69-year-old male received a dual-chamber pacemaker implantation for complete atrioventricular block. He had no chest symptoms after the operation. Three days later, he developed severe chest pain, followed by syncope. Electrocardiogram showed sustained monomorphic ventricular tachycardia. Despite the use of amiodarone and frequent electrical defibrillation, ventricular tachycardia and ventricular fibrillation were repeated incessantly. He died 24 h after the syncope. The autopsy revealed no hemopericardial effusion, or perforation of leads. There were also no obstructive lesions in the coronary arteries. Myocardial necrosis was observed in the entire circumference and the all layers of the left ventricle. Microscopically, myocardial necrosis was plurifocal and contraction band necrosis. We speculate that catecholamine cardiotoxicity caused ventricular tachycardia in this case. Further studies are needed to clarify the heterogeneity of this disease.

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Section: Discussionmentioning

confidence: 99%

An autopsy case of tako-tsubo cardiomyopathy presenting ventricular tachycardia after pacemaker implantation

Kinbara

Hayano

Otani

et al. 2013

Journal of Cardiology Cases

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“…Reperfusion of the ischemic area is the first line therapy to decrease ischemic damage and prevent cell death; however, reperfusion itself can lead to a more severe damage, a phenomenon known as reperfusion injury [2–4]. Reperfusion is also associated with an increased risk of potentially fatal arrhythmias [5–7]. …”

Section: Introductionmentioning

confidence: 99%

Mitochondrial instability during regional ischemia–reperfusion underlies arrhythmias in monolayers of cardiomyocytes

Solhjoo

O’Rourke

2015

Journal of Molecular and Cellular Cardiology

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Regional depolarization of the mitochondrial network can alter cellular electrical excitability and increase the propensity for reentry, in part, through the opening of sarcolemmal KATP channels. Mitochondrial inner membrane potential (ΔΨm) instability or oscillation can be induced in myocytes by exposure to reactive oxygen species (ROS), laser excitation, or glutathione depletion, and is thought to be a major factor in arrhythmogenesis during ischemia-reperfusion. Nevertheless, the correlation between ΔΨm recovery kinetics and reperfusion-induced arrhythmias has been difficult to demonstrate experimentally. Here, we investigate the relationship between subcellular changes in ΔΨm, cellular glutathione redox potential, electrical excitability, and wave propagation during coverslip-induced ischemia-reperfusion (IR) in neonatal rat ventricular myocyte (NRVM) monolayers. Ischemia led to decreased action potential amplitude and duration followed by electrical inexcitability after ~ 15 min of ischemia. ΔΨm depolarization occurred in two phases during ischemia: in phase 1 (< 30 min ischemia), mitochondrial clusters within individual NRVMs depolarized, while phase 2 ΔΨm depolarization (30–60 min) was characterized by global functional collapse of the mitochondrial network across the whole ischemic region of the monolayer, typically involving a propagating metabolic wave. Oxidation of the glutathione (GSSG:GSH) redox potential occurred during ischemia, followed by recovery upon reperfusion (i.e., lifting the coverslip). ΔΨm recovered in the mitochondria of individual myocytes quite rapidly upon reperfusion (< 5 min), but was highly unstable, characterized by subcellular oscillations or flickering of clusters of mitochondria in NRVMs across the reperfused region. Electrical excitability also recovered in a heterogeneous manner, providing an arrhythmogenic substrate which led to formation of sustained reentry. Treatment with 4′-chlorodiazepam, a peripheral benzodiazepine receptor ligand, prevented ΔΨm oscillation, improved GSH recovery rate, and prevented reentry during reperfusion, indicating that stabilization of mitochondrial network dynamics is an important component of preventing post-ischemic arrhythmias.

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“…Reperfusion of the ischemic heart is crucial to limiting cell damage and initiating potential recovery, but it can also play a role in the injury process and trigger cardiac arrhythmias ( 1 , 2 , 3 , 4 , 5 ). Ischemia and reperfusion (IR) disturb ionic gradients, gap junctional conductivity, and many other factors in cardiomyocyte electrophysiology.…”

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confidence: 99%

Oxidative stress in the mitochondrial matrix underlies ischemia/reperfusion-induced mitochondrial instability

Solhjoo

Liu

Sidor

et al. 2023

Journal of Biological Chemistry

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Sudden cardiac death secondary to demonstrated reperfusion ventricular fibrillation in a woman with Takotsubo cardiomyopathy

Cited by 8 publications

References 8 publications

An autopsy case of tako-tsubo cardiomyopathy presenting ventricular tachycardia after pacemaker implantation

An autopsy case of tako-tsubo cardiomyopathy presenting ventricular tachycardia after pacemaker implantation

Mitochondrial instability during regional ischemia–reperfusion underlies arrhythmias in monolayers of cardiomyocytes

Oxidative stress in the mitochondrial matrix underlies ischemia/reperfusion-induced mitochondrial instability

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