Sympathetic nerve activity in stress-induced cardiomyopathy

Abstract

PurposeTo evaluate directly recorded efferent sympathetic nerve traffic in patients with stress-induced cardiomyopathy (SIC).BackgroundSIC is a syndrome affecting mostly postmenopausal women following severe emotional stress. Though the precise pathophysiology is not well understood, a catecholamine overstimulation of the myocardium is thought to underlie the pathogenesis.MethodsDirect recordings of multiunit efferent postganglionic muscle sympathetic nerve activity (MSNA) were obtained from 12 female patients, 5 in the acute (24–48 h) and 7 in the recovery phase (1–6 months), with apical ballooning pattern and 12 healthy matched controls. MSNA was expressed as burst frequency (BF), burst incidence (BI) and relative median burst amplitude (RMBA %). One of the twelve patients in this study was on beta blockade treatment due to a different illness, at time of onset of SIC. All patients were investigated with ongoing medication.ResultsMSNA was lower in patients with SIC as compared to matched controls, but did not differ between the acute and recovery phase of SIC. RMBA %, blood pressure and heart rate did not differ between the groups.ConclusionMSNA is shown to be lower in patients with SIC compared to healthy controls, suggesting that sympathetic neuronal outflow is rapidly reduced following the initial phase of SIC. A distension of the ventricular myocardium, due to excessive catecholamine release over the heart in the acute phase, may increase the firing rate of unmyelinated cardiac c-fibre afferents resulting in widespread sympathetic inhibition. Such a mechanism may underlie the lower MSNA reported in our patients.

Epidemiology and pathophysiology of Takotsubo syndrome

“…This is usually measured hours after the initial stressful trigger and catecholamine surge, and so whether it is present immediately during the acute stress remains to be clarified. It is clear that there are abnormalities of peripheral sympathetic nerve function and arterial vasomotor regulation in the aftermath of the acute catecholamine storm 33, [80][81][82] . These vasodilating catecholamines may also activate myocardial β2ARs in addition to vascular β2ARs, and therefore this may reflect a mixed effect.…”

Maternal inflammation activated ROS-p38 MAPK predisposes offspring to heart damages caused by isoproterenol via augmenting ROS generation

“…As one major component of auto-regulatory response to stress, activation of sympathetic nervous system (SNS) is the key trigger of stress-induced cardiovascular disease 4 5 . For example, post-ganglionic muscle sympathetic nerve activity has been reported to contribute to stress-induced cardiomyopathy in post-menopausal women following severe emotional stress 6 . Therefore, activation of SNS could be considered as a potential second hit when combined with other risk factors such as prenatal detrimental exposure contributes to the development of heart disease.…”

The Sympathetic Nervous System in the Pathogenesis of Takotsubo Syndrome

“…All of the subjects in this study underwent microneurography within 72 hours of symptom onset. In contrast, Sverrisdottir and colleagues 54 found that patients with TC had a decrease in MSNA compared with healthy matched controls. This latter study provides less information regarding sympathetic tone during the acute phase of TS because more than half of the subjects were studied in the recovery phase at 1 to 6 months.…”