Percutaneous transluminal coronary angioplasty for the treatment of variant angina.

Among 268 patients undergoing percutaneous transluminal coronary angioplasty between February 1980 and January 1983, a total of 21 patients had variant angina, documented before angioplasty in 14 and after angioplasty in 7. Before angioplasty, all 21 patients had rest angina and 17 also had effort angina; single vessel coronary artery disease with 60 to 95% stenosis was present in all patients and the left anterior descending coronary artery was involved in all but 3 patients. Coronary angioplasty was successful in 19 patients (90%). Eight of the 19 patients remained symptom-free without coronary restenosis after successful angioplasty; in the other 11 patients, angina reappeared within 4 months, usually in association with restenosis. Of the nine patients with coronary restenosis, six had repeat angioplasty (five successful procedures and one failure), two received medical therapy and one underwent coronary bypass surgery. Patients in whom calcium channel antagonists were discontinued immediately after angioplasty had an exceedingly high coronary restenosis rate (8 [80%] of 10 successful attempts), but when calcium antagonists were continued for an average of 6 +/- 4 months after angioplasty, the restenosis rate was low (3 [21%] of 14 successful attempts). After a mean (+/- SD) follow-up period of 33 +/- 13 months, 1 patient had died and the 20 others (95%) were symptom-free; among these 20, 15 patients (75%) had been taking no antianginal drugs for more than 1 year, 2 still received calcium channel antagonists and 3 had had coronary bypass surgery. Repeat coronary arteriography performed 14 +/- 7 months after angioplasty in the 17 patients without angioplasty-related infarction or surgery showed 50% or less coronary stenosis in 13 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Failure of diltiazem to prevent restenosis after percutaneous transluminal coronary angioplasty.

This prospective randomized trial was carried out in 92 patients who underwent a successful percutaneous transluminal coronary angioplasty (PTCA) and had no evidence of coronary spasm before PTCA. All patients were premedicated with calcium antagonists and platelet inhibitors and received platelet inhibitors (aspirin and dipyridamole) for 6 months after PTCA. The diltiazem group (46 patients with 50 stenoses successfully dilated) received diltiazem, 90 mg three times a day by mouth for 3 months after PTCA; in the control group (46 patients, 53 stenoses), calcium antagonists were discontinued immediately after PTCA. All patients underwent a control angiogram 5 to 10 months after PTCA unless recurrence of angina dictated its need earlier. Baseline characteristics were similar in both groups, except for the number of diseased vessels greater than or equal to 70%, which was higher in the control group (1.2 +/- 0.55 vs 0.9 +/- 0.39 for the diltiazem group, p less than 0.05). In the diltiazem group, the degree of stenosis increased from 38 +/- 15% immediately after PTCA to 42 +/- 23% at repeat angiography 8.24 +/- 4.79 months after PTCA and there were seven restenoses. In the control group, the degree of stenosis increased from 37 +/- 12% to 44 +/- 23% at repeat angiography 8.26 +/- 4.91 months after PTCA and there were 10 restenoses (NS vs the diltiazem group). In conclusion, in patients without variant angina before PTCA, adjunction of diltiazem to platelet inhibitors does not decrease the incidence of restenosis. These data suggest that coronary spasm is not the major mechanism of restenosis.

Comparative diagnostic performance of the Telemed computer ECG program.

One thousand consecutive ECG's from an ambulatory population of patients with suspected or proven cardiac disease were evaluated using two versions of the Telemed computerized ECG system. Only minor differences were found between the two programs. In version 6 vs. version 5, 87% vs. 90% of 287 normal ECG's were correctly classified and 93% vs. 96% of abnormal ECG's were correctly classified; the percent of acceptable diagnostic agreement was 86.2% and 87.4% respectively (NS). The sensitivity for arrhythmia detection, transmural inferior infarction and ST-T wave abnormalities was slightly greater in version 6. The increased sensitivity was not accompanied by decreased specificity. The sensitivity for left ventricular hypertrophy decreased from 95.2% to 91.4% in version 6 with a slight increase in specificity (95.2% to 97.0%). In conclusion, criteria changes in the most recent version of the Telemed program have not resulted in a major change in diagnostic performance. Arrhythmia detection is slightly but not significantly improved.

Clinical and hemodynamic results with the Carpentier-Edwards porcine bioprosthesis.

Carpentier-Edwards bioprostheses were implanted in 605 patients, 509 of whom had a single valve replacement, and 96 of whom had a multiple valve replacement. There were 54 early deaths (8.9%) and 26 late deaths (4.3%). The five-year actuarial survival was 87% for aortic valve replacement, 83% for mitral valve replacement, and 81% for multiple valve replacement. Of the 525 survivors, all but 3 were followed for a total of 964 patient-years; 354 patients (68%) remained asymptomatic, and 95 patients (18%) were improved. The incidence of thromboembolism, endocarditis, and reoperation due to primary tissue failure of the bioprosthesis were 2.0, 1.3, and 0.1% per patient-year, respectively. The actuarial probability of being free of all valve-related complications was 93% after five years. Satisfactory hemodynamic performance of the bioprosthesis was demonstrated by postoperative studies done in 70 patients. Thus, the Carpentier-Edwards porcine valve provides good clinical improvement, with a low incidence of valve-related complications and tissue failure at five years postoperatively.