Percutaneous cardiopulmonary bypass-supported coronary angioplasty in patients with unstable angina pectoris or myocardial infarction and a left ventricular ejection fraction ≤ 25%

The objective of this study was to determine the acute and long-term results of percutaneous cardiopulmonary bypass-supported angioplasty in treating high-risk patients with unstable presentations and severely depressed left ventricular (LV) function (ejection fraction [EF] ≤ 25%). One hundred seven consecutive patients with a mean LVEF of 19 ± 3% were studied. Seventyfour patients (69%) had unstable angina, 60 (56%) had New York Heart Association class III or IV symptoms, 74 (69%) had recent (< 15 days) documented acute myocardial infarction, 103 (96%) had 3-vessel disease, and 58 (54%) had only 1 remaining patent artery. A total of 50 patients (47%) were deemed unsuitable for bypass surgery. Of 196 severe narrowings attempted in 166 coronary arteries, 193 (98%) were successfully dilated in 105 patients (98%), and there was no procedure-related mortality, Q-wave myocardial infarction, or urgent requirement for coronary bypass surgery. There were 5 in-hospital deaths (4.7%) and the remaining 102 patients have been followed for 24.5 ± 1.3 (mean ± SE) months. Twenty-three patients (21%) died between 1 and 23 months after the procedure. Oneand 2-year survival free of cardiac death was 83% and 77%, respectively. Of the 79 surviving patients, 65 have survived event free of myocardial infarction and revascularization; event-free survival for 1 and 2 years was 76% and 69.5%, respectively. In the 64 patients in whom LV function was measured before and after the procedure, global EF increased from 20.6% to 29.3% (p < 0.001). Patients who remained event free had a greater improvement in LVEF than those who had a cardiac event during follow-up (p < 0.05). Thus, this study demonstrates the safety and efficacy of percutaneous cardiopulmonary bypass-supported angioplasty in the immediate treatment of high-risk unstable patients with multivessel coronary artery disease and severely depressed LV function.