Attenuation of Unfavorable Sympathetic Hyperactivity Induced by Long-Term Physical Training in Postinfarction Patients: Fact or Speculation?

Abstract

Recently, Giannuzzi et al 1 eloquently described the beneficial effect of long-term exercise training on left ventricular remodeling in postinfarction patients. An earlier report from Coats et al 2 demonstrated that training can improve autonomic function (mainly in terms of RR variability and norepinephrine spillover) in patients with chronic heart failure but failed to show significant changes in resting catecholamine levels after a short-term exercise program.In an attempt to explain their findings, Giannuzzi et al used a series of reports describing the reduction of catecholamine levels by exercise training in subjects with normal left ventricular function 3,4 and speculated that this effect exists in patients with left ventricular dysfunction as well. However, this phenomenon is no longer conjectural because it has been demonstrated clearly in postinfarction patients with severe left ventricular dysfunction after long-term exercise rehabilitation. 5 Moreover, that study 5 also showed a beneficial effect of the rehabilitation program on atrial natriuretic peptide. We hope that clarification of these points will provide additional support for the findings of Giannuzzi and his team. ResponseWe greatly appreciate the letter of Drs Tenenbaum and Shemesh, who give us the opportunity to provide additional comments concerning the role of exercise training in the remodeling process among postinfarction patients with left ventricular dysfunction and the long-term effect of physical training on the autonomic balance and neurohormonal activation.After the initial conflicting results, an increasing body of evidence has now demonstrated clearly that patients with poor left ventricular function after an uncomplicated myocardial infarction may benefit from regular exercise training without any additional deterioration of ventricular volumes and function.1,2 More importantly, we 2 recently documented in a large group of postinfarction patients with left ventricular dysfunction that long-term exercise training may attenuate the unfavorable remodeling process and even improve both regional and global function over time. We 3 also reported similar results in preliminary form in patients with chronic heart failure, in whom training actually lessened left ventricular dilatation and dysfunction.Exercise training has been shown to increase functional work capacity and at the same time to reduce catecholamine levels and vascular peripheral resistances and enhance heart rate variability and baroreflex gain, both in subjects with normal ventricular function as well as in patients with left ventricular dysfunction and heart failure. Shemesh et al 4 briefly reported significantly lower levels of resting norepinephrine and atrial natriuretic peptide in postinfarction patients with reduced ejection fraction who were undergoing longterm cardiac rehabilitation. This result and previous observations strongly indicate a lower sympathetic activity after training. The real point of speculation in our article was not the existence of this e...

Prevention of Ventricular Fibrillation, Acute Myocardial Infarction (Myocardial Necrosis), Heart Failure, and Mortality by Bretylium

“…This can also induce chronic and insidious neurohormonal dysfunction, which often occurs in situations of acute or sustained stress as elegantly described by Minc 37 and Rozanski et al 39 This is most certainly a pathway to both IsHD and CAD and its complications. 37-52, 55 The adrenergic nervous system as described by Mann and Cooper 72 is a 2-edged sword that is normally physiologically very useful for rapid cardiovascular metabolic adaptation (or even in anticipation of changing mechanical workload demand), but when dysfunctional (ie, triggered without need) this multifaceted and complex adaptive mechanism can cause serious cardiovascular disease 22,37,39,[41][42][43][44][45][46][47][48][49][50][51][52] and immune system dysfunction 96 and may be a possible factor in causing autoimmune diseases. The concept of being "scared to death" is not an "old wives tale" but actually occurs frequently in Las Vegas casinos (M. Weisfeld, personal communication) as a response to emotionally triggered adrenergic actions commonly causing SCD.…”