[Percutaneous transluminal coronary angioplasty after coronary artery bypass].

Anginal syndrome may recur early of several years after coronary artery bypass surgery (CABS), and may be due to narrowing of a bypass graft, progression of pre-existing coronary artery lesions, or the appearance of new lesions. Repeat CABS is associated with considerable morbidity and mortality. We therefore performed percutaneous transluminal angioplasty (PTCA) in saphenous or internal mammary bypass grafts or native coronary arteries in 23 patients after CABS. We successfully dilated 35 of 37 lesions (95%) present in 33 of 35 vessels (94%) of 21 of 23 patients (91%). The mean vessel narrowing decreased from 86 +/- 22% to 13 +/- 19% (p less than 0.001) and in all 21 patients with angiographic evidence of success functional capacity improved. Single vein grafts were successfully dilated in 9 patients. None developed acute myocardial infarction or needed emergency surgery, but 1 had a cerebral embolism. PTCA is effective therapy for recurrent angina after CABS, and in many patients is preferable to another operation.

[Annulo-aortic ectasia].

Aortic regurgitation due to annular aortic ectasia was diagnosed in a 29-year-old woman with heart failure. The primary pathology of this disease is cystic medial necrosis of the ascending aorta with aneurysm formation and dilation of the aortic valve annulus. In successful surgical correction, the ascending aorta was replaced by a dacron prosthesis, the aortic valve by a prosthetic disc valve and the coronary arteries were reimplanted into the aortic graft.

Synergistic effect of captopril and dobutamine on left ventricular pressure-volume and pressure-shortening relations in severe cardiac failure.

The acute effects of captopril and dobutamine, alone and in combination, on left ventricular contractility were assessed from left ventricular end-systolic pressure-volume and pressure-shortening relations in 6 patients with severe end-stage cardiac failure. Dobutamine was given by constant intravenous infusion on two occasions 48 hours apart, on one of these occasions the patient also received oral captopril in a dose of 37 +/- 12 mg 6-hourly. Pressures and cardiac index were measured, and left ventricular volumes and ejection fraction computed from simultaneously recorded radionuclide ventriculography. Dobutamine alone did not cause a statistically significant increase in stroke index, stroke work index, cardiac index and ejection fraction, although pulmonary capillary wedge pressure and right atrial pressure fell (P less than 0.05). There was no change in systemic or pulmonary vascular resistance nor in arterial blood pressure. Following administration of captopril, diastolic arterial pressure decreased (P less than 0.05), and the dobutamine challenge produced a greater and significant rise in stroke and stroke work index (P less than 0.05) and cardiac index (P less than 0.01). The left ventricular contractile state was unaltered by captopril but appeared to increase with dobutamine and more so during combined therapy with captopril and dobutamine, indicating a synergistic effect of the two drugs when given in combination.

Effect of captopril on left ventricular end-systolic pressure-volume and stress-shortening relations in severe cardiac failure.

The effects of captopril on cardiovascular dynamics and left ventricular (LV) contractility were studied in 11 patients with severe congestive heart failure and very poor global LV function. Pressures were measured using a flow-guided catheter, cardiac output by thermodilution, and LV contraction and ejection fraction by simultaneous radionuclide angiography. Ventricular loading conditions were altered by sublingual isosorbide dinitrate to facilitate construction of LV pressure-volume and stress-shortening curves. Captopril decreased mean arterial pressure (p less than 0.02) and systemic vascular resistance, while stroke and cardiac index increased in most patients. Left ventricular ejection fraction increased from 18 +/- 5 to 22 +/- 7% (p less than 0.05), but contractility, assessed from end-systolic pressure-volume and end-systolic pressure-shortening relations, was unchanged or decreased slightly. Heart rate and double product also tended to decrease. In contrast, arteriovenous oxygen difference widened and calculated total oxygen consumption increased during captopril therapy (p less than 0.05). The study showed that captopril improved forward blood flow, total oxygen extraction, and LV ejection fraction following the decrease impedance to LV emptying but not at the expense of an increase in ventricular contractility. This makes captopril an attractive drug for patients with end-stage cardiac failure and a severely damaged myocardium.