Coronary artery plaque morphology in stable angina and subsets of unstable angina: an in vivo intracoronary ultrasound study.

Little information is available regarding the in vivo composition of angina producing culprit atherosclerotic lesions in various anginal syndromes. In this study we used intracoronary ultrasound to determine the composition of culprit lesions in various subsets of anginal syndromes and correlated this composition with the patient's clinical presentation. One hundred and forty six patients referred for angioplasty or atherectomy were classified as having either chronic stable angina (angina which was clinically unchanged for > 2 months), crescendo angina (an accelerating pattern of frequent or prolonged anginal episodes), severe rest angina (abrupt onset of prolonged angina) or post-infarction angina (angina within 2 weeks of acute myocardial infarction). Intracoronary ultrasound imaging of the culprit lesion was performed before intervention. Lesions were classified as soft, mixed fibrous without calcium, mixed fibrous with calcium or calcified. Analysis of the ultrasound images revealed that the majority of culprit lesions were soft in severe rest (71%) and post-infarction angina (73%) whereas, the majority of culprit lesions were mixed fibrous or calcified in chronic stable (69%) and crescendo (53%) angina (X2 = 22.73, p = 0.007). In addition, the frequency of intralesional calcium in chronic stable or crescendo angina was significantly higher than that in severe rest or stable angina. We conclude that the composition of culprit lesions in various anginal subsets are different. The lesion morphology in crescendo angina frequently resembles that in chronic stable angina; while those in severe rest and post-infarction angina are frequently similar. These findings may have implications for medical or interventional treatment of patients with angina.

Intracoronary ultrasound-defined plaque composition: computer-aided plaque characterization and correlation with histologic samples obtained during directional coronary atherectomy.

The ability to classify lesion composition accurately may be important for selecting or guiding interventional therapy and for understanding the pathophysiologic basis of individual lesions. To assess the usefulness of ultrasound in classifying lesions, intracoronary ultrasound images were obtained from 44 atherosclerotic lesions in patients before directional atherectomy. Lesions were classified by visual analysis and by computer-assisted gray-level statistics. Atherectomy samples were evaluated histologically for elastosis and calcium and quantitatively by morphometric analysis for various tissue components. The computer-assisted quantitative classification agreed well with the findings on visual analysis. Visual and computer-assisted quantitative ultrasound images were found to have distinctive histologic features. Lesions with predominantly echogenic plaque had a larger fraction of dense fibrous, elastic, or calcified tissue. Lesions with predominantly echolucent soft plaque had a greater fraction of loose fibrous, smooth-muscle, thrombotic, or necrotic elements. Thus intracoronary ultrasound allows accurate classification of lesion composition in patients.

Correlation of intracoronary ultrasound plaque characteristics in atherosclerotic coronary artery disease patients with clinical variables.

It was examined whether intracoronary ultrasound-defined plaque morphology of symptom-producing, severely stenosed, atherosclerotic coronary artery lesions is related to patient-related clinical variables. Data regarding anginal pattern (stable vs unstable), age, sex, history of smoking, diabetes, hypertension, hypercholesterolemia and lesion location were recorded in 146 hemodynamically stable patients referred for clinically indicated balloon angioplasty or directional atherectomy. Intracoronary ultrasound images of the lesions were obtained before and after the intervention. Lesions were classified as soft (homogeneous echoes less dense than adventitia) or hard (bright echoes with or without acoustic shadowing). Eighty-three lesions (57%) were classified as soft and 63 (43%) as hard. Univariate analysis showed anginal pattern, age, vessel location and history of smoking to be significantly related to plaque morphology. Multivariate analysis revealed only anginal pattern, age and vessel location to be independent predictors of plaque morphology. The frequency of echogenic hard plaque was significantly higher in patients aged > 60 years (56 vs 30%; p = 0.001), those with stable angina (69 vs 35%; p = 0.002), and lesions located in the distal arterial segments (68 vs 31%; p < 0.001) than in younger ones, those with unstable angina, and lesions in proximal segments, respectively. Based on previous studies, echogenic hard plaques are likely to be predominantly fibrous or calcific, or both, whereas low-echogenicity soft plaques are likely to be fibrocellular, lipid rich or thrombotic, or a combination. This difference in plaque morphology is probably due to differences in the predominant mechanism of plaque formation (i.e., slow growth vs rupture/thrombosis).(ABSTRACT TRUNCATED AT 250 WORDS)

Local intramural drug delivery using an infusion balloon following angioplasty in normal and atherosclerotic vessels.

Local intramural delivery of various pharmacologic agents following angioplasty has been proposed as a means of reducing restenosis. This study tested whether local intramural delivery of aqueous solutions using an infusion balloon could be accomplished safely in normal vessels and whether such infusion was safe following standard angioplasty in diseased vessels. Infusion of aqueous agents into normal canine arteries had no adverse effect. Infusion of several aqueous agents (< or = 4 cc at 4 atm) into diseased swine iliac arteries following balloon angioplasty did not worsen existing or create new dissections. Histologically, infusion treated vessels did not differ in either model from vessels treated with angioplasty alone. We conclude that local intramural drug infusion does not create new, or worsen existing, dissections produced during standard balloon angioplasty in diseased vessels.

Application of intracoronary ultrasonography in the study of coronary artery pathophysiology.

Coronary endothelial function, arterial distensibility, and elastic recoil were assessed in various groups of patients using intracoronary ultrasonic (ICUS) imaging. We found evidence of endothelial dysfunction in patients with risk factors for coronary artery disease even before atherosclerosis could be detected angiographically or with sensitive ICUS imaging. There was marked reduction of arterial distensibility in atherosclerotic arterial segments even with minor disease. Distensibility was partially restored in lesions following coronary balloon angioplasty (PTCA) or directional atherectomy (DCA). We also noted significantly greater elastic recoil following PTCA in soft lesions compared with hard lesions. We conclude that the use of ICUS imaging in cardiac catheterization laboratory provides useful information regarding various physiologic parameters. This capability will add new dimensions to the evaluation and management of patients with coronary artery disease.

Mechanisms of angiographically successful directional coronary atherectomy: evaluation by intracoronary ultrasound and comparison with transluminal coronary angioplasty.

To assess the mechanisms of luminal improvement, 40 patients undergoing directional coronary atherectomy and a matched control group of 25 patients undergoing angioplasty were evaluated with intracoronary ultrasound imaging before and after intervention. Despite similar sized vessels, a similar angiographic severity of diameter stenosis (75 +/- 12% for the angioplasty group vs 69 +/- 15% for the atherectomy group, p = NS), and a similar plaque burden (percent plaque area) before intervention (84 +/- 5% in the angioplasty group vs 85 +/- 13% in the atherectomy group, p = NS), the residual plaque area after intervention was significantly smaller in the atherectomy group (54 +/- 14%) compared with the angioplasty group (65 +/- 13%, p = 0.002). Despite excellent angiographic results, significant residual plaque was noted after either successful intervention. Based on the absolute changes in lumen area, plaque area, and vessel area, improvement in the lumen area in the atherectomy group occurred as a result of plaque "compression" (48%), plaque removal (37%), and vessel expansion (15%). In the angioplasty group, plaque "compression" accounted for 94% of the improvement in lumen area, whereas vessel expansion contributed 6%. Thus "compression" of plaque remains the major mechanism of luminal improvement during atherectomy.

Use of heart rate spectral analysis to study the effects of calcium channel blockers on sympathetic activity after myocardial infarction.

We used spectral analysis of heart rate variability (HRV) to study the effects of the calcium channel blockers diltiazem and nifedipine and the beta-blocker metoprolol on the sympathetic nervous system in patients following myocardial infarction. Energy in the low-frequency range (0.04 to 0.12 Hz) in the standing (tilt) position was used as a quantitative index of sympathetic activity. Twenty-seven male patients, mean age 62 +/- 13 years, were studied 2 to 6 weeks after myocardial infarction. Eight patients received metoprolol, 100 mg twice daily; nine patients received diltiazem, 60 mg three times daily; and 10 patients received nifedipine, 10 mg three times daily. HRV and arterial blood pressure were recorded before and 5 to 7 days after initiation of therapy. None of the drugs had significant effects on the systolic blood pressure, and only nifedipine significantly reduced the diastolic blood pressure. Metoprolol and diltiazem reduced the low-frequency HRV in all patients studied, but nifedipine had no consistent effects. Our results suggest that diltiazem had a depressant effect on sympathetic activity similar to beta-adrenergic blockers. This effect was not observed with nifedipine. The reduction in sympathetic activity by diltiazem may contribute to its therapeutic effects in the post-infarction period.