Cardiogenic shock following hydrogen sulfide poisoning

Jiang, lianlian; Jiang, Jie; Chen, Xi

doi:10.22541/au.160509653.33194077/v1

Cited by 1 publication

(2 citation statements)

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“…Another recent case presented identical cardiac changes and clinical course, where the patient was free of ECG abnormalities on the first day of exposure, but showed extensive elevation of ST-segment and dramatic increase of myocardial enzyme index two days after exposure. The patient then developed VF on the next day (136). It can be easily observed from above cases that patients with H 2 S poisoning usually presented no clinical symptoms or ECG changes immediately after exposure, but could experience ST-segment elevation and develop lethal arrhythmias after 2∼4 days.…”

Section: Epidemiological and Clinical Reportsmentioning

confidence: 92%

“…Specifically, H 2 S was reported to inhibit cytochrome C oxidase (137), leading to the blockade of the electron transport in the respiratory chain and the utilization of molecular oxygen (135,138). The damaged respiratory chain could subsequently result in disrupted aerobic metabolism of cells and impaired ATP production, and ultimately leads to reduced oxygen use of cardiomyocytes and myocardial damage (136). Large dispersion in repolarization can be formed under myocardial injury conditions, e.g., in the border zone of the regionally ischemic heart or near the infarcted tissue area (139), and thereby increases the likelihood of induction of unidirectional block and arrhythmias.…”

Section: Potential Proarrhythmic Mechanismsmentioning

confidence: 99%

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Air Pollution and Cardiac Arrhythmias: From Epidemiological and Clinical Evidences to Cellular Electrophysiological Mechanisms

Zhang

Lü

Wei

et al. 2021

Front. Cardiovasc. Med.

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Cardiovascular disease is the leading cause of death worldwide and kills over 17 million people per year. In the recent decade, growing epidemiological evidence links air pollution and cardiac arrhythmias, suggesting a detrimental influence of air pollution on cardiac electrophysiological functionality. However, the proarrhythmic mechanisms underlying the air pollution-induced cardiac arrhythmias are not fully understood. The purpose of this work is to provide recent advances in air pollution-induced arrhythmias with a comprehensive review of the literature on the common air pollutants and arrhythmias. Six common air pollutants of widespread concern are discussed, namely particulate matter, carbon monoxide, hydrogen sulfide, sulfur dioxide, nitrogen dioxide, and ozone. The epidemiological and clinical reports in recent years are reviewed by pollutant type, and the recently identified mechanisms including both the general pathways and the direct influences of air pollutants on the cellular electrophysiology are summarized. Particularly, this review focuses on the impaired ion channel functionality underlying the air pollution-induced arrhythmias. Alterations of ionic currents directly by the air pollutants, as well as the alterations mediated by intracellular signaling or other more general pathways are reviewed in this work. Finally, areas for future research are suggested to address several remaining scientific questions.

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Section: Epidemiological and Clinical Reportsmentioning

confidence: 92%