Aroesty J M, McKay R G, Heller G V, Royal H D, Als A V, Grossman W
Circulation. 1985 May;71(5):889-900. doi: 10.1161/01.cir.71.5.889.
Both systolic and diastolic dysfunction have been described during pacing-induced ischemia, but the temporal sequence of systolic and diastolic impairment has not been established. Accordingly, 22 patients with coronary artery disease were paced at increasing heart rates and studied with simultaneous hemodynamic monitoring, electrocardiographic recording, and radionuclide ventriculography. In addition, with synchronized left ventricular pressure tracings and radionuclide volume curves, three sequential pressure-volume diagrams were constructed for each patient corresponding to baseline, intermediate, and maximum pacing levels. Eleven patients (group I) demonstrated a nonischemic response to pacing tachycardia without chest pain, significant electrocardiographic changes, or significant rise in left ventricular end-diastolic pressure (LVEDP) in the immediate postpacing period. These patients demonstrated a progressive decrease in LVEDP, end-diastolic volume, and end-systolic volume, no change in cardiac output or left ventricular ejection fraction, and a progressive increase in left ventricular diastolic peak filling rate and the end-systolic pressure-volume ratio. Pressure-volume diagrams shifted progressively leftward and slightly downward, suggesting both an increase in contractility and a mild increase in left ventricular distensibility. The remaining 11 patients (group II) exhibited an ischemic response to pacing tachycardia, with each patient experiencing angina pectoris, demonstrating greater than 1 mm ST segment depression on the electrocardiogram, and exhibiting greater than 5 mm Hg rise in LVEDP immediately after pacing. LVEDP, end-diastolic volume, and end-systolic volume in these patients initially decreased and then subsequently increased during angina, with no change in cardiac output but a decrease in ejection fraction. Left ventricular peak diastolic filling rate and the left ventricular end-systolic pressure-volume ratio both increased at the intermediate pacing rate but fell at maximum pacing. Pressure-volume diagrams for these patients shifted leftward initially, then back to the right, during intermediate and peak pacing levels, often with an upward shift in the diastolic pressure-volume relationship. LVEDP in group II was significantly higher than that in group I at the intermediate pacing level with no difference in end-diastolic or end-systolic volumes, suggesting decreased left ventricular distensibility in these patients before the onset of systolic dysfunction at the maximum pacing level.(ABSTRACT TRUNCATED AT 400 WORDS)
在起搏诱导的缺血过程中，已观察到收缩功能和舒张功能均出现障碍，但收缩功能和舒张功能损害的时间顺序尚未明确。因此，对22例冠心病患者进行递增心率起搏，并同步进行血流动力学监测、心电图记录和放射性核素心室造影研究。此外，利用同步的左心室压力曲线和放射性核素容积曲线，为每位患者构建了对应于基线、中等和最大起搏水平的三个连续压力-容积图。11例患者（I组）对起搏性心动过速表现为非缺血反应，无胸痛、明显心电图改变或起搏后即刻左心室舒张末压（LVEDP）显著升高。这些患者的LVEDP、舒张末期容积和收缩末期容积逐渐降低，心输出量或左心室射血分数无变化，左心室舒张期峰值充盈率和收缩末期压力-容积比逐渐升高。压力-容积图逐渐向左并略有向下移动，提示收缩性增加和左心室扩张性轻度增加。其余11例患者（II组）对起搏性心动过速表现为缺血反应，每位患者均出现心绞痛，心电图显示ST段压低超过1mm，并在起搏后即刻LVEDP升高超过5mmHg。这些患者的LVEDP、舒张末期容积和收缩末期容积在心绞痛期间最初降低，随后升高，心输出量无变化，但射血分数降低。左心室舒张期峰值充盈率和左心室收缩末期压力-容积比在中等起搏频率时均升高，但在最大起搏时下降。在中等起搏水平时，II组的LVEDP显著高于I组，舒张末期或收缩末期容积无差异，提示这些患者在最大起搏水平出现收缩功能障碍之前左心室扩张性降低。（摘要截短至400字）
