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.
Highlights
The maintenance of cardio- and cerebrovascular health is based on a complex relationship between the heart and the brain
Within the stress-induced cardiomyopathy (SIC) group, there was no difference in muscle sympathetic nerve activity (MSNA) burst frequency (BF), burst incidence (BI) or relative median burst amplitude between the acute and recovery phase (Table 2)
MSNA BF and BI did not differ between the control group and the SIC patients in the acute phase (41 vs. 40 b/min, p = 0.8 and 63 vs. 54 b/100 hb, p = 0.2, respectively), but was significantly lower in the SIC patients in the recovery phase as compared to the control group (41 vs. 26 b/min, p = 0.02 and 63 vs. 46 b/100 hb, p = 0.03, respectively), (Fig. 1)
Summary
The maintenance of cardio- and cerebrovascular health is based on a complex relationship between the heart and the brain. The Japanese observation from the early 1990s of a reversible stress-induced cardiomyopathy (SIC), the Takotsubo [2], a peculiar type of left ventricular (LV) dysfunction triggered by an acute strong emotional or physical stressor [3], supports this notion [4]. The syndrome, mostly affecting postmenopausal women, presents signs and symptoms of acute coronary syndrome without evidence of obstructive coronary artery disease. The cause for the evident female predisposition of SIC is unknown, Clin Auton Res (2012) 22:259–264 but may be related to gender differences in vulnerability to emotional stress [5] and myocardial sensitivity to catecholamine toxicity [6]. A lower level of estrogen in absence of testosterone in postmenopausal women was recently suggested to explain their greater vulnerability to SIC [7]
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