Acute myocardial and plasma catecholamine changes in experimental stroke.

Abstract

SUMMARY Focal cerebral ischemia hi humans increases the Incidence of cardiac arrhythmias, and serum cardiac enzyme and plasma norepinephrine levels. In addition, systemic administration of catecholamines causes myocardial damage. This suggests that cerebral ischemia may cause myocardial damage as a consequence of elevated plasma norepinephrine levels. Therefore, experiments were done hi 23 chloralosed, paralyzed and artificially ventilated cats to investigate the effects of occluding (n = 17) or sham-occluding (n = 6) the left middle cerebral artery on the myocardium and on circulating levels of plasma catecholamines. After occlusion of the middle cerebral artery for 12-22 hr, 41% (7/17) of the hearts had either acute myocardial necrosis (3/7), focal hemorrhage (3/7), or both (177). In anlmah with acute myocardial damage the levels of plasma norepinephrine and epinephrine were significantly increased compared to pre-middle cerebral artery occlusion values ( + 46 ± 18% and +142 ± 45%, respectively). As well, meats with acute myocardial damage, changes from initial levels of plasma norepinephrine and epinephrine were significantly Increased over those of experimental cats without acute myocardial damage. In animals which did not have acute myocardial damage (10/17) the circulating plasma levels of catecholamines were not significantly different from pre-occlusion values. Similarly, sham occlusion did not alter plasma catecholamine levels. These data demonstrate that a percentage of animals subjected to middle cerebral artery occlusion have myocardial damage and an increase hi plasma concentration of norepinephrine and epinephrine. This suggests that a rise hi plasma catecholamine levels, due to Increased sympathetic activity after middle cerebral artery occlusion, may cause myocardial damage. Stroke Vol 17, No 3, 1986 PATIENTS who begin to recover neurologically after a stroke may perish unexpectedly from cardiac complications or sudden death.1 Although some of these deaths could be attributed to concomitant heart disease, stroke patients have an excess of cardiac arrhythmias, increased cardiac serum enzymes and raised plasma catecholamines when compared to similarly managed controls matched for age, sex and the presence of heart disease. "5 Some patients dying from stroke show myocardial lesions, 6 similar to those observed in animals infused with catecholamines 718 and in animals with increased intracranial pressure, 9 or intracranial hemorrhage. "12 Taken together, these findings suggest that raised levels of catecholamines after cerebral ischemia, likely from increased sympathetic activity, contribute to myocardial damage. The present study was done to determine whether focal cerebral ischemia in the cat would produce cardiac lesions and whether changes in plasma levels of catecholamines were associated with the cardiac lesions. Methods Experiments were done in 23 adult cats of either sex weighing 2.0 to 3.5 kg. To isolate the middle cerebral artery (MCA) animals were anesthetized either with sodium pentoba...

Deterioration of baroreceptor reflex by transient global cerebral ischemia in dogs.

“…It is suggested that acute stroke may in crease sympathetic activity with resultant electrocardiographic abnormalities and myocardial cell necrosis (3,9). Therefore, one might speculate that the observed decrease in BRS might be due to the damage to the cardiac response to the vaga!…”

Elevated Plasma Brain Natriuretic Peptide Levels Independent of Heart Disease in Acute Ischemic Stroke: Correlation with Stroke Severity

“…Third, we cannot exclude the possibility that there are other important explanatory variables which may contribute to the plasma BNP level, since our three multivariate regression models explained only around 49% of the total variance. Finally, we cannot completely exclude acute myocardial damage due to increased sympathetic activity and catecholamines in the acute phase of ischemic stroke leading to elevation of the plasma BNP level (10,30), because we measured only creatine kinase and not catecholamines, creatine kinase-MB isoenzyme, or more specific biochemical markers of myocardial injury, cardiac troponin T or I. However, it is reported that these markers are elevated in only a small group if any of the acute ischemic stroke patients (7,31).…”

Regional Longitudinal Deformation Improves Prediction of Ventricular Tachyarrhythmias in Patients With Heart Failure With Reduced Ejection Fraction

“…9 Interestingly, in patients having a stroke, which is well known to cause an increased sympathetic tone 33 and impaired parasympathetic function 34 both of which are predisposing factors for sudden cardiac death, 35 impaired longitudinal function of the inferior wall has been demonstrated to be the strongest echocardiographic predictor of outcome. 29 Several studies have indicated that CRT treatment reduces the risk of VT/VF [36][37][38][39] ; however, other studies have shown a proarrhythmic effect of CRT.…”