Lavine S J, Campbell C A, Kloner R A, Gunther S J
Division of Cardiology, Harper Hospital, Wayne State University, Detroit, Michigan.
J Am Coll Cardiol. 1988 Nov;12(5):1326-33. doi: 10.1016/0735-1097(88)92617-4.
Patients with congestive heart failure and elevated left ventricular filling pressures demonstrate an abnormal pattern of diastolic filling that is characterized by a redistribution of diastolic filling to early diastole with reduced reliance on late diastolic filling. The diastolic filling pattern superficially resembles that which is seen with constrictive pericarditis. To examine potential mechanisms for these clinical findings, a model of ischemic left ventricular dysfunction was produced in seven dogs by repeated coronary microsphere embolization, producing a dilated left ventricle with reduced systolic function. Measurements of left ventricular systolic and end-diastolic pressures, rate of rise of left ventricular pressure (dP/dt) and echocardiographic end-diastolic and end-systolic areas were obtained at baseline, during intermediate embolization (moderate left ventricular systolic dysfunction, dilation and mild increases in left ventricular end-diastolic pressure), postembolization (further embolization resulting in severe left ventricular systolic dysfunction, dilation and marked increases in left ventricular end-diastolic pressure), after thoracotomy and after pericardiectomy. The filling fraction at 1/3 and 1/2 of diastole and the time constant of left ventricular pressure decline were also determined. Repetitive coronary microembolization caused progressive left ventricular dilation and decreasing systolic function, which did not change after opening the chest or pericardium. The filling fraction at 1/3 and 1/2 of diastole declined with intermediate embolization (12.0 +/- 5.6% and 23.1 +/- 10.8%, respectively) as compared with baseline values (29.0 +/- 11.9%, 42.9 +/- 15.6%, p less than 0.05). After embolization, there was an increase in the 1/3 and the 1/2 filling fraction (47.5 +/- 8.9%, 72.0 +/- 6.0%, respectively, p less than 0.01) as compared with baseline values.(ABSTRACT TRUNCATED AT 250 WORDS)
充血性心力衰竭且左心室充盈压升高的患者表现出舒张期充盈异常模式，其特征是舒张期充盈重新分布至舒张早期，对舒张晚期充盈的依赖减少。这种舒张期充盈模式表面上类似于缩窄性心包炎所见的模式。为研究这些临床发现的潜在机制，通过反复冠状动脉微球栓塞在7只犬身上建立了缺血性左心室功能障碍模型，导致左心室扩张且收缩功能降低。在基线、中期栓塞期间（中度左心室收缩功能障碍、扩张及左心室舒张末期压力轻度升高）、栓塞后（进一步栓塞导致严重左心室收缩功能障碍、扩张及左心室舒张末期压力显著升高）、开胸后及心包切除术后，测量左心室收缩压和舒张末期压力、左心室压力上升速率（dP/dt）以及超声心动图舒张末期和收缩末期面积。还测定了舒张期1/3和1/2时的充盈分数以及左心室压力下降的时间常数。反复冠状动脉微栓塞导致左心室逐渐扩张且收缩功能降低，开胸或心包切除后未发生改变。与基线值相比，舒张期1/3和1/2时的充盈分数在中期栓塞时下降（分别为12.0±5.6%和23.1±10.8%）（基线值分别为29.0±11.9%、42.9±15.6%，p<0.05）。栓塞后，与基线值相比，1/3和1/2充盈分数增加（分别为47.5±8.9%、72.0±6.0%，p<0.01）。（摘要截断于250字）
