Quantitative evaluation of blood row distribution to exercising and resting skeletal muscles in patients with cardiac dysfunction using whole‐body thallium‐201 scintigraphy

Abstract

SummaryBuckground and hypothesis: Decreased blood flow to working muscles makes an important contribution to exercise intolerance in patients with chronic heart failure. This study was undertaken to examine whether maldistribution of skeletal muscle blood flow is closely related to exercise intolerance in patients with cardiac dysfunction.Methods: Whole-body thallium scintigraphy was perfomed during one-leg exercise in 11 patients with left ventricular (LV) dysfunction (LV ejection fraction ~4 5 % ) .Blood flow distribution to the exercising and resting legs was quantified by expressing regional thallium counts as a percentage of the whole-body counts at rest, at the level of anaerobic threshold, and at peak exercise.Hesulrs: At anaerobic threshold, the thallium activity of exercising muscle increased from 4.2 * 0.7 to 14.0 * 2.5% (p< 0.0S)in thethighandfrom 1.7-t-0.3 to4.1+0.9%(p<O.O5)in the calf, compared with the resting value. Consequently, the ratio of thallium activity between exercising and resting legs increased to 2.7 * 0.7 (p<0.05) in the thigh and to 2.3 2 0.7 (p<O.OS) in the calf. When plotted as a function of anaerobic threshold, thallium activity of the exercising thigh (r = 0.78, ~~0 . 0 5 ) and the thallium ratio between exercising and resting thigh (r = 0.69, p<0.05) declined with the reduction of exercise tolerance. These correlations were not observed in calves. Conclusion:Whole-body thallium scintigraphy demonstrated a maldistribution of leg blood flow in patients with reduced aerobic exercise capacity, suggesting that this abnormality could play an important role in exercising intolerance in these patients.

Exercise and Heart Failure

“…Vascular resistance in the muscle fails to decrease normally during exercise in patients with HF, and flow to the nonexercising tissues may be preferentially maintained at the expense of hypoperfusion in the exercising muscle. 20,49 Ergoreflex Activation A new paradigm suggests the presence of a specific signal arising from the exercising muscle (possibly including respiratory muscle) that is abnormally enhanced in HF. 50,51 These signals contribute to the abnormal hemodynamic, autonomic, and ventilatory responses to exercise that characterize HF.…”

Exercise training in heart failure

“…Central factors Sullivan and Cobb [52] Cardiac Lower max HR and SV Stevenson et al [53] Vascular Elevated SVR Lung factors Guazzi [54] Diffusion impairment Alveolar-capillary membrane disruption Mancini et al [55] Respiratory muscle function Histologic changes Peripheral factors Zelis et al [56] Abnormalities in blood flow Lower vasodilatation Drexler and Lu [57] Endothelial function Lower NO release Floras [58] Autonomic changes Increased SNA, RAS Skeletal muscle Massie et al [59] Metabolism Early anaerobic Drexler et al [60], Sullivan et al [61] Composition Increased type IIB and lower I fibers Sullivan et al [62] Enzyme Lower oxidative Gielen et al [32], Vescovo et al [63] Inflammation Increased cytokines, apoptosis Wada et al [64] Distribution of cardiac output Lower muscle blood flow Ponikowski et al [8], Piepoli et …”

Effects of respiratory muscle unloading on leg muscle oxygenation and blood volume during high-intensity exercise in chronic heart failure

“…Indirect support to this hypothesis in humans has been given by O'Donnell and coworkers (39) who found that the improvement in exercise endurance with pressure support ventilation was associated with less exertional leg discomfort in patients with CHF. In addition, skeletal muscle perfusion has been shown to be selectively reduced as whole body exercise progresses in some patients with CHF (34,53); this effect, however, was not found with small muscle mass exercise where the ventilatory requirements are considerably lower (27). There is, therefore, a sound rationale underpinning the notion that respiratory and peripheral muscles could actively compete for the available cardiac output (Q T ), especially in pathological conditions where the ability to further increase O 2 delivery is impaired.…”