Coronary circulation during heavy exercise in control subjects and patients with coronary heart disease.
Coronary circulation during heavy exercise in control subjects and patients with coronary heart disease.
复制标题
对照组和冠心病患者剧烈运动时的冠状动脉循环。
作者：
S. Holmberg;W. Serźysko;E. Varnauskas
抽象的。在 2-3 个增加运动负荷的时期内，测量了 10 名冠心病 (CHD) 患者和 11 名对照受试者的冠状动脉和体循环。最高工作负荷接近最大可耐受运动水平。在对照受试者中，剧烈运动期间的最大冠状动脉流量增加至静息值的 460%。随着工作负荷的增加，心肌 (a-v)O2 差异在个体间和个体内变化很大，但针对该组计算，这种 (a-v)O2 差异没有显着变化。因此，心肌需氧量的增加几乎完全通过冠状动脉流量的增加来满足。从休息到剧烈运动，心肌摄氧量增加了四倍，同时 BP8 × HR 乘积也增加了四倍，在整个值范围内呈线性关系，表明该乘积是心肌摄氧量的良好指标。冠心病患者对适度运动的冠脉血流反应与对照组相同。然而，在剧烈运动期间，与 BP8 × HR 乘积相关的冠脉流量增加低于对照组。冠状血管阻力没有降低到与对照组相同的水平。通过补偿性增加心肌 (a-v)O2 差异来满足增加摄氧量的需求，从而使必要的氧气输送成为可能。然而，在最剧烈的运动期间，与对照组相比，与 BP8 × HR 乘积相关的心肌耗氧量显着降低。这被解释为氧气供应不足，导致心肌收缩力下降。两名运动诱发心绞痛患者的心肌功能受损得到了最好的证明，他们的左心房压力迅速升高。
Abstract. Coronary and systemic circulation has been measured in 10 patients with coronary heart disease (CHD) and in 11 control subjects during 2–3 periods of increasing exercise loads. The highest work load was close to the maximal tolerable exercise level. In control subjects the maximal coronary flow during heavy exercise increased to 460% of the resting value. The myocardial (a-v)O2 difference varied considerably inter- and intraindividually with increasing work load, but calculated for the group this (a-v)O2 difference did not change significantly. The increase in myocardial oxygen demand was thus met almost exclusively by an increase in coronary flow. The myocardial oxygen uptake increased fourfold from rest to heavy exercise with a parallel fourfold increase in the BP8 × HR product, with a linear relationship over the whole range of values, suggesting that this product is a good index of myocardial oxygen uptake. In CHD patients the coronary flow response to moderate exercise was the same as in control subjects. During heavy exercise, however, the coronary flow increase was lower in relation to the BP8 × HR product than in the control subjects. Coronary vascular resistance did not decrease to the same level as in the controls. The demand for increase in oxygen uptake was met through a compensatory increase in myocardial (a-v)O2 difference, thus making the necessary oxygen delivery possible. During the heaviest exercise, however, a significantly lower myocardial oxygen consumption was recorded in relation to the BP8 × HR product than in the control subjects. This was interpreted as an inadequate oxygen supply, leading to decreased myocardial contractility. The impaired myocardial performance was best demonstrated in two patients with exercise-provoked angina pectoris who developed rapidly increasing left atrial pressure.