Is 40% to 70% diameter narrowing at the site of previous stenting or directional coronary atherectomy clinically significant?

Traditional binary definitions of coronary restenosis based on 6-month continuous angiographic measurements (e.g., > 50% diameter stenosis) may give confusing results for lesions whose late percent stenosis falls near the arbitrary threshold. To determine the long-term clinical consequences of such lesions, the overall correlation between follow-up percent stenosis and the performance of subsequent ischemia-driven target vessel revascularization (triggered by significant angina or a positive exercise study result, or both) was examined in 443 consecutive lesions treated with directional coronary atherectomy or Palmaz-Schatz coronary stenting. Follow-up angiograms (available in 355 lesions, 82%) were stratified into 3 groups: severe late stenosis (> 70% stenosis, n = 59), moderate late stenosis (40% to 70% stenosis, n = 72), and minimal late stenosis (< 40% stenosis, n = 224). With an average clinical follow-up of 933 +/- 394 days, 92% of lesions in the "severe late stenosis" group were treated with ischemia-driven target vessel revascularization, compared with 0% of the lesions in the "minimal late stenosis" group. Ischemia-driven target vessel revascularization was performed in 38% of patients in the "moderate late stenosis" group. However, patients in this group who did not undergo revascularization (despite the fact that 43% of them had a late stenosis of > 50%) showed a similarly favorable long-term clinical outcome to patients with a minimal late stenosis. These results support a strategy of conservative management for the 20% of patients who have a moderate (40% to 70%) late stenosis after stenting or atherectomy, but do not have evidence of ischemia.

Effects of heparin and cardiac catheterization on serum lipoprotein and triglyceride levels.

This study determined whether heparin administration and procedures involving heparin significantly affect lipid measurement. Serum lipid and lipoprotein analyses (total cholesterol, triglycerides, high-density lipoprotein [HDL] cholesterol, low-density lipoprotein [LDL] cholesterol, apolipoprotein B, and apolipoprotein A-I) were performed at baseline and at several time points after (1) intravenous heparin or placebo in 6 healthy volunteers (group 1), (2) cardiac catheterization with heparin in 26 patients (group 2), and (3) peripheral angiography without heparin in 11 patients (group 3). In group 1, after heparinization, triglycerides decreased 50 +/- 12 mg/dl (-57%, p < 0.001 vs baseline and placebo) at 60 minutes. No changes were observed in other lipid or lipoprotein fractions. After cardiac catheterization (group 2), however, decreases were observed not only in triglycerides (58 +/- 26 mg/dl [-40%]), but also in total cholesterol (28 +/- 12 mg/dl [-14%]), LDL cholesterol (19 +/- 22 mg/dl [-15%]), apolipoprotein B (13 +/- 9 mg/dl [-14%]), and apolipoprotein A-I (21 +/- 14 mg/dl [-17%]) (p < 0.001 vs baseline for all), and HDL cholesterol (4 +/- 7 mg/dl [-3%], p = 0.07). With the exception of triglycerides, these values remained significantly decreased for > or = 24 hours. The change in HDL was variable: Whereas most patients had a decrease (n = 24), 2 patients had a dramatic increase (> 100%) after administration of heparin. Similar decreases in total cholesterol, LDL cholesterol, and apolipoproteins B and A-I were observed in group 3 undergoing peripheral angiography without heparin.(ABSTRACT TRUNCATED AT 250 WORDS)

Frequency and consequences of intimal hyperplasia in specimens retrieved by directional atherectomy of native primary coronary artery stenoses and subsequent restenoses.

Although intimal hyperplasia is a frequent occurrence after arterial interventional procedures, the overall frequency and significance of intimal hyperplasia in primary coronary lesions has not been previously addressed. The incidence of intimal hyperplasia was therefore examined using standard light microscopy in specimens obtained from native coronary arteries of patients undergoing directional coronary atherectomy. The associated clinical history, angiographic results and clinical outcomes were also tabulated. Intimal hyperplasia was identified in 51 of 55 patients (93%) treated with directional coronary atherectomy for restenosis after a prior intervention. These restenosis lesions had less acute gain in lumen diameter after directional coronary atherectomy, a smaller late lumen diameter, more severe late stenosis (p < 0.04), and tended to have more restenosis defined as late stenosis > or = 50% (restenosis rate 40% for prior restenosis vs 26% for primary lesions). Surprisingly, however, intimal hyperplasia was also identified in 45 of 102 (44%) primary stenoses. Primary lesions (n = 45) with intimal hyperplasia were more likely to occur in younger patients and in the left anterior descending artery than were either primary lesions without intimal hyperplasia (n = 57) or prior restenosis lesions. There were otherwise no differences in the baseline characteristics, angiographic findings or clinical outcome of primary lesions with or without intimal hyperplasia (restenosis rate 28 and 24%, respectively). The event-free survival (72% at 12 months) was similar in all 3 groups. Thus, even though intimal hyperplasia is an almost universal finding in restenosis lesions, intimal hyperplasia is not specific for restenosis since histologically identical hyperplasia may be found in nearly half of primary coronary artery stenoses.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical, echocardiographic, and electrocardiographic resolution of HIV-related cardiomyopathy.

Congestive cardiomyopathy has been described in 18% (25/141) of studied patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex, and myocarditis has been suspected as the etiology in 70% (14/20) of patients studied. In previous reports the cardiomyopathy has either been asymptomatic or has been progressive and directly caused significant patient mortality and morbidity. We report a patient with human immunodeficiency virus (HIV)-related cardiomyopathy due to a presumed myocarditis which caused life-threatening congestive heart failure and ventricular fibrillation. This patient's course was unique in that she had clinical, echocardiographic, and electrocardiographic resolution of her cardiomyopathy. This report adds new knowledge to the etiology and prognosis of patients with HIV-related cardiomyopathy.