Related Experiment Videos
Subarachnoid hemorrhage and myocardial damage clinical and experimental studies
1Department of Internal Medicine, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.
Insights
Sudden brain aneurysm rupture (subarachnoid hemorrhage) can cause heart problems due to a surge in stress hormones. This "panic myocardium" can lead to dangerous arrhythmias and heart failure.
Area of Science:
- Neurology
- Cardiology
- Pathophysiology
Background:
- Subarachnoid hemorrhage (SAH) frequently leads to cardiopulmonary complications.
- These complications, including sudden death, are linked to aneurysmal rupture.
- The exact mechanisms behind these cardiac issues require further investigation.
Purpose of the Study:
- To investigate the pathogenesis of cardiopulmonary complications in patients with SAH.
- To explore the relationship between catecholamine levels and myocardial damage.
- To clarify the link between sympathetic nervous activity and cardiac dysfunction post-SAH.
Main Methods:
- Clinical observation of 715 SAH cases.
- Measurement of plasma catecholamine, serum CK-MB, myosin light chain, and troponin T.
- Development of a novel animal model to study SAH effects on cardiac function.
Main Results:
- Transient left ventricular asynergy occurred in 9.4% of SAH patients, associated with elevated plasma catecholamines.
- Life-threatening arrhythmias correlated with higher catecholamine and cardiac biomarker levels.
- Animal models showed transient sympathetic hyperactivity followed by cardiac dysfunction and elevated CK-MB.
Conclusions:
- Elevated catecholamines contribute to myocardial derangement ("panic myocardium") in SAH.
- Myocardial damage, triggered by catecholamine surge, likely causes life-threatening arrhythmias in SAH.
- SAH-induced sympathetic overactivity can lead to significant myocardial damage.
Abstract:
Subarachnoid hemorrhage (SAH) due to aneurysmal rupture is frequently complicated by cardiopulmonary episodes, including sudden death. We investigated the pathogenesis of cardiopulmonary complications from clinical observation of 715 cases with SAH. There was transient left ventricular asynergy in 9.4% (67/715) of the cases, which consisted of mechanical heart failure and myocardial necrosis. Plasma catecholamine concentration was higher in these patients compared with those without left ventricular asynergy. Transient left ventricular asynergy was considered to result from myocardial derangement: "a panic myocardium," due to a sudden burst of catecholamine. Concerning arrhythmia in SAH, cases with life-threatening arrhythmia, such as ventricular tachycardia or ventricular fibrillation, had higher concentrations not only of plasma catecholamine but also of serum CK-MB, myosin light chain and troponin T, compared with patients who had no ventricular arrhythmia. This implies that life-threatening arrhythmia in SAH would result from myocardial damage due to catecholamine. We devised a novel animal model of SAH in order to clarify the relation between sympathetic nervous activity and myocardial damage immediately after the onset of SAH. The animal experiments showed that sympathetic nervous activity as well as cardiac contractility were transiently elevated, but cardiac function subsequently declined. Serum CK-MB was increased from the onset of SAH and a high value was maintained throughout the entire experimental period. In conclusion, extraordinary transient enhancement of sympathetic nervous activity induces myocardial damage resulting from what is characterized by "a panic myocardium."