Gonzalez A, Naqvi S E, Tak T, Choudhary R S, Rahimtoola S H, Chandraratna P A
Department of Medicine, LAC-USC Medical Center, University of Southern California School of Medicine 90033.
Am Heart J. 1991 Jan;121(1 Pt 1):118-25. doi: 10.1016/0002-8703(91)90964-j.
Twenty-three patients with angina who were undergoing diagnostic cardiac catheterization underwent cardiac pacing with simultaneous hemodynamic and Doppler echocardiographic evaluation to assess the effects of pacing-induced ischemic on mitral valve velocity. Seventeen patients had significant coronary artery disease, and six patients had normal coronary arteries. Doppler and hemodynamic measurements were performed at rest and immediately after pacing was discontinued to 91% +/- 7% of maximal predicted heart rate. Seven patients experienced new or significant increases in severity of mitral regurgitation after pacing as revealed by Doppler examination. This group had a significant increase (p = 0.007) in early but not in late peak filling velocities immediately after pacing was discontinued, with a resultant decrease in late to early ratios, which decreased from 1.01% +/- 0.12 to 0.70% +/- 0.19 (p = 0.006). Left ventricular end-diastolic pressure increased significantly from 16.7% +/- 6.8 mm Hg to 29.4% +/- 5.3 mm Hg after cardiac pacing (p less than 0.001). Patients with coronary disease who did not develop mitral regurgitation also had significant increases in left ventricular end-diastolic pressure from 18.7% +/- 5.8 mm Hg to 24.3% +/- 8.6 mm Hg (p less than 0.05). There were no changes in late or early wave amplitude, late to early ratio, or other Doppler measurements in any of the other groups. We conclude that mitral regurgitation caused by pacing-induced myocardial ischemia normalizes Doppler indices of mitral inflow, which in turn, may mask persistent or worsened left ventricular diastolic dysfunction.
23例正在接受诊断性心导管检查的心绞痛患者接受心脏起搏，同时进行血流动力学和多普勒超声心动图评估，以评估起搏诱导的缺血对二尖瓣流速的影响。17例患者患有严重冠状动脉疾病，6例患者冠状动脉正常。在静息状态下以及起搏停止后心率立即降至最大预测心率的91%±7%时进行多普勒和血流动力学测量。多普勒检查显示，7例患者在起搏后出现新的二尖瓣反流或反流严重程度显著增加。该组在起搏停止后早期峰值充盈速度显著增加（p = 0.007），但晚期峰值充盈速度未增加，导致晚期与早期比值降低，从1.01%±0.12降至0.70%±0.19（p = 0.006）。心脏起搏后左心室舒张末期压力从16.7%±6.8 mmHg显著增加至29.4%±5.3 mmHg（p < 0.001）。未发生二尖瓣反流的冠心病患者左心室舒张末期压力也从18.7%±5.8 mmHg显著增加至24.3%±8.6 mmHg（p < 0.05）。其他任何组的晚期或早期波幅、晚期与早期比值或其他多普勒测量均无变化。我们得出结论，起搏诱导的心肌缺血引起的二尖瓣反流使二尖瓣流入的多普勒指标正常化，这反过来可能掩盖持续或恶化的左心室舒张功能障碍。
