"Crackers, breakers, stretchers, drillers, scrapers, shavers, burners, welders and melters"--the future treatment of atherosclerotic coronary artery disease? A clinical-morphologic assessment.

Although various public health preventive efforts and prescribed pharmacologic treatment methods will have long-term benefits in the reduction of coronary artery atherosclerosis and subsequent cardiac events, the immediate and short-term future in the treatment of coronary artery disease will focus on several interventional devices designed to remodel or remove causes of acute and chronic coronary artery obstruction. Certain clinical-morphologic aspects of these interventional devices or techniques that result in remodeling of the coronary lumen shape (balloon angioplasty, thermal probes, intravascular stents) or removal of obstructing material (lasers, atherectomy devices) are reviewed. Two new areas in the pathology of atherosclerotic plaque (plaque fissures, eccentric plaque) and their clinical relevance in coronary heart disease are described.

Intracoronary ethyl alcohol or phenol injection ablates aconitine-induced ventricular tachycardia in dogs.

The hypothesis whether localized ventricular tachycardia could be ablated by myocardial necrosis induced with chemical agents injected into a coronary artery was tested. In 59 anesthetized dogs, a diagonal branch of the left anterior descending coronary artery was cannulated either occlusively or nonocclusively. Localized ventricular tachycardia was induced by injecting approximately 0.01 ml of 30 micrograms/ml of aconitine solution into the left ventricular wall perfused by the cannulated diagonal branch in 54 dogs. In eight untreated control dogs, aconitine-induced ventricular tachycardia lasted 10.2 +/- 2.3 minutes or degenerated into ventricular fibrillation after 7.0 +/- 4.0 minutes. In the remaining 46 dogs, 1 ml of saline solution, 25, 50 or 100% ethyl alcohol or 0.94 ml (mean [range 0.4 to 2.0]) of 25% phenol at room temperature was injected into the occluded coronary artery and 1 ml of 100% ethyl alcohol at body temperature was injected into the nonoccluded coronary artery. Ventricular tachycardia was eliminated in 9 (82%) of 11 dogs receiving phenol, 7 (88%) of 8 dogs receiving 100% ethyl alcohol occlusively, 6 (75%) of 8 dogs receiving 100% ethyl alcohol nonocclusively and 6 (67%) of 9 dogs receiving 50% ethyl alcohol for an entire follow-up period of 10 to 60 minutes. However, saline solution and 25% ethyl alcohol suppressed ventricular tachycardia only transiently in 8 (53%) of 15 and 3 (60%) of 5 dogs, respectively. Left ventricular end-diastolic pressure rose from 8.0 to 11.2 mm Hg (p less than 0.05) immediately after injection of 100% ethyl alcohol in seven dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Morphologic evidence of accelerated left main coronary artery stenosis: a late complication of percutaneous transluminal balloon angioplasty of the proximal left anterior descending coronary artery.

Histologic evidence of restenosis after percutaneous transluminal coronary angioplasty has been confined to the site of previous dilation. In this study, attention is focused on the accelerated development of coronary stenosis proximal to the site of previous angioplasty in a necropsy patient who developed severe left main stenosis 4 months after successful dilation of the proximal left anterior descending coronary artery. The unique fibrocellular tissue proliferation at the site of previous angioplasty and involvement of the adjacent distal segment of the left main coronary artery make possible the histologic diagnosis of accelerated left main coronary artery narrowing. Mechanisms for development of coronary stenoses proximal to the angioplasty site include: intimal injury by guiding catheters, guide wires, dilating balloons or combinations; or retrograde extension of the fibrocellular response to an adjacent proximal coronary segment. Histologic analysis of left main coronary arteries from 11 patients who died within 72 hours of angioplasty of the left coronary system disclosed focal loss of luminal endothelium in 9. This finding suggests that intimal injury from catheters or balloons, or both, proximal to the angioplasty site probably initiates a fibrocellular reaction. The amount of underlying atherosclerotic plaque in the injured proximal coronary segment determines the clinical significance of a subsequent fibrocellular response.

Transverse aortic wall tears in infants after balloon angioplasty for aortic valve stenosis: relation of aortic wall damage to diameter of inflated angioplasty balloon and aortic lumen in seven necropsy cases.

Aortic wall tears resulting from rupture of dilating balloons in infants undergoing transluminal balloon angioplasty have not been previously recognized. A 2 day old infant had percutaneous transluminal balloon angioplasty to dilate a stenotic aortic valve, and after multiple balloon inflations the balloon burst. The infant died 2 days after undergoing transluminal balloon angioplasty and at necropsy a circumferential, transverse aortic wall tear was found. To test the hypothesis that rupture of appropriately sized balloons results in similar aortic wall tears, six unfixed, intact infant aortas were subjected to transluminal balloon angioplasty at necropsy: two infants had balloon rupture with inflated balloon diameter similar to that of the aorta, two had balloon rupture with an undersized balloon and two had dilation with an oversized balloon. Transverse wall tears occurred in aortas with similar aortic and balloon diameters; no aortic wall damage occurred with rupture of undersized balloons, and aortic rupture resulted from the use of oversized balloons. Thus, intimal-medial tears in the infant aorta may result from balloon bursting during angioplasty when aortic and inflated balloon diameters are similar.

Restenosis 1 to 24 months after clinically successful coronary balloon angioplasty: a necropsy study of 20 patients.

This report describes clinical, morphologic and histologic findings at necropsy late (range 1.6 to 24.1 months [average 8.2 months]) after clinically successful coronary balloon angioplasty in 20 patients with coronary angioplasty restenosis. Clinical evidence of restenosis occurred in 14 patients (70%), including 6 patients with sudden coronary death. Of the 20 patients, 14 (70%) had a cardiac cause of death and 6 (30%) had a noncardiac cause of death. Two major subgroups of histologic findings were observed: 1) intimal proliferation (60%), and 2) atherosclerotic plaque only (40%). Of the eight sites with atherosclerotic plaque only, six were eccentric lesions and two were concentric lesions. No morphologic evidence of previous angioplasty injury (cracks, breaks, tears) was observed in the eight patients with atherosclerotic plaque only. Proposed mechanisms for the development of intimal proliferation involve the reaction of smooth muscle cells and platelets, whereas elastic recoil of overstretched eccentric or concentric atherosclerotic lesions represents the most likely explanation for the findings in the latter subgroup. On the basis of these morphologic findings at angioplasty restenosis sites, specific treatment strategies for restenosis after coronary artery balloon angioplasty are proposed.

Research collaboration.

The complexity and cost of cardiovascular medical care dictate research to deliver high quality and cost-conscious cardiovascular care. This goal is aided by modeling medical decision making. To be useful, the modeling must be based on real data so that the results can serve as a guide to actual practice. It is suggested that a registry of randomized clinical trials and larger data bases in cardiovascular disease and health care delivery be established. The registry would be a resource for those desiring to model decision making. The registry would contain key words allowing retrieval by modelers accessing the registry and would contain contact information for consideration of possible collaborative work. The initiation of such a registry should contain plans for its evaluation to determine whether the registry itself is a cost-effective tool to encourage the needed research.

Status of the myocardium and infarct-related coronary artery in 19 necropsy patients with acute recanalization using pharmacologic (streptokinase, r-tissue plasminogen activator), mechanical (percutaneous transluminal coronary angioplasty) or combined types of reperfusion therapy.

In acute myocardial infarction, myocardial salvage is dependent on rapid restoration of blood flow. Pharmacologic (streptokinase, recombinant tissue-type plasminogen activator), mechanical (percutaneous transluminal coronary angioplasty, guide wire perforation) or combined forms of reperfusion therapy can accomplish this goal, but their effects on infarcted myocardium and vessel occlusion site have not been compared at necropsy. The heart of 19 necropsy patients who had received various forms of acute reperfusion therapy was studied: 14 had pharmacologic or combined forms of reperfusion therapy (13 streptokinase and 1 tissue-type plasminogen activator, including 4 with combined balloon angioplasty) and 5 had had purely mechanical (balloon angioplasty) reperfusion therapy. Reperfusion was initially clinically successful in all 19 patients with the average time from onset of symptoms to reperfusion being 3.7 hours. Necropsy observations separated the 19 patients into distinct subgroups based on changes in the myocardium and infarct-related coronary arteries. Of the 19 patients, 14 (74%) had hemorrhagic myocardial infarction and they all received pharmacologic or combined forms of reperfusion therapy. The remaining five patients (26%) had nonhemorrhagic (anemic) infarction and were treated with balloon angioplasty therapy alone. Increased luminal cross-sectional area was present in 8 of 9 patients with acute balloon angioplasty but severe coronary atherosclerotic plaque remained in 9 of 10 patients without acute balloon angioplasty. Severe hemorrhage surrounded angioplasty sites in all four patients who also received streptokinase or tissue-type plasminogen activator. Severe bleeding at the angioplasty site compromised the dilated coronary lumen in one patient. No patient with angioplasty alone had intraplaque bleeding. Thus, acute coronary balloon angioplasty reperfusion therapy alone appears to avoid the potentially adverse effects of myocardial and intraplaque hemorrhage while simultaneously increasing luminal cross-sectional area at the site of acute occlusion.

Etiology of pure tricuspid regurgitation based on anular circumference and leaflet area: analysis of 45 necropsy patients with clinical and morphologic evidence of pure tricuspid regurgitation.

Despite recent renewed interest in the detection of tricuspid valve regurgitation by echocardiographic and Doppler techniques, little morphologic information is available on dysfunctioning tricuspid valves. This report describes 45 necropsy patients with clinical and morphologic evidence of pure (no element of stenosis) tricuspid regurgitation and provides morphometric observations (anular circumference, leaflet area) of the tricuspid valve useful in determining the etiology of pure tricuspid regurgitation. Of 45 patients, 24 (53%) had pure tricuspid regurgitation resulting from an anatomically abnormal valve (prolapse in 7, papillary muscle dysfunction in 6, rheumatic disease in 5, Ebstein's anomaly in 3, infective endocarditis in 2, carcinoid tumor in 1), and 21 (47%) had an anatomically normal valve with systolic pulmonary artery hypertension (cor pulmonale in 12, mitral stenosis in 9). Anular circumference was dilated (greater than 12 cm) in patients with various causes of pulmonary hypertension, floppy valve and Ebstein's tricuspid anomaly. Leaflet area was increased in floppy valve and Ebstein's anomaly. Of the 45 patients, 24 had pulmonary systolic artery pressure measurements available for correlation with tricuspid valve morphology. Pulmonary artery pressures accurately predicted morphologically normal from abnormal valves in 16 patients (89%). Morphologic overlap occurred in six patients with pulmonary pressures of 41 to 54 mm Hg. Of these six, the additional knowledge of normal or dilated anular circumference correctly separated valves with normal and abnormal leaflets.

Thermal compression and molding of atherosclerotic vascular tissue with use of radiofrequency energy: implications for radiofrequency balloon angioplasty.

The combined delivery of pressure and thermal energy may effectively remodel intraluminal atherosclerotic plaque and fuse intimal tears. To test these hypotheses with use of a non-laser thermal energy source, radiofrequency energy was delivered to postmortem human atherosclerotic vessels from a metal "hot-tip" catheter, block-mounted bipolar electrodes and from a prototype radiofrequency balloon catheter. Sixty-two radiofrequency doses delivered from a metal electrode tip produced dose-dependent ablation of atherosclerotic plaque, ranging from clean and shallow craters with histologic evidence of thermal compression at doses less than 40 J to tissue charring and vaporization at higher (greater than 80 J) doses. Lesion dimensions ranged between 3.14 and 3.79 mm in diameter and 0.20 and 0.47 mm in depth. Tissue perforation was not observed. To test the potential for radiofrequency fusion of intimal tears, 5 atm of pressure and 200 J radiofrequency energy were delivered from block-mounted bipolar electrodes to 48 segments of human atherosclerotic aorta, which had been manually separated into intima-media and media-adventitial layers. Significantly stronger tissue fusion resulted (28.5 +/- 3.3 g) with radiofrequency compared with that with pressure alone (4.8 +/- 0.26 g; p less than 0.0001). A prototype radiofrequency balloon catheter was used to deliver 3 atm of balloon pressure with or without 200 J radiofrequency energy to 20 postmortem human atherosclerotic arterial segments. In 10 of 10 radiofrequency-treated vessels, thermal "molding" of both normal and atherosclerotic vessel wall segments resulted with increased luminal diameter and histologic evidence of medial myocyte damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Right ventricular infarction with cardiac rupture in an infant with pulmonary valve atresia with intact ventricular septum.

This report describes an 8 day old infant with pulmonary valve atresia, hypoplastic and hypertensive right ventricle and myocardial sinusoid-left anterior descending coronary artery connections. A large right ventricular sinusoid complex developed that was associated with transmural right ventricular necrosis and cardiac rupture. This is the first report to document transmural myocardial infarction and rupture in pulmonary valve atresia with intact septum, and this condition should be added to the causes of myocardial infarction in infancy. A reduced number of caliber of sinusoid-coronary artery channels may be responsible for right ventricular damage in this condition.

Morphologic observations after percutaneous transluminal balloon angioplasty of early and late aortocoronary saphenous vein bypass grafts.

Clinical and morphologic observations from two patients undergoing percutaneous transluminal angioplasty of stenotic aortocoronary saphenous vein bypass grafts early (3 months) and late (56 months) after graft insertion are described. Each patient had one or more clinically successful graft dilations resulting in an angiographic increase in luminal diameter and a decrease in mean trans-stenotic gradient, and each had restenosis of the graft at the site of previous angioplasty within 2 months of dilation. Both operatively excised grafts had diffuse but variable amounts of intimal fibrous thickening and severe narrowing at the previous angioplasty site. The early graft had no evidence of dilation injury, and the intimal thickening consisted solely of fibrocollagenous tissue free of calcific deposits. In contrast, the late graft had a healing intimal dissection at the angioplasty site, and the intimal thickening consisted of atherosclerotic plaque with calcific deposits. Angiographic and morphologic correlations suggest that the mechanism of saphenous vein angioplasty early (less than or equal to 1 year) after insertion is by graft "stretching," while late (greater than 1 year) after insertion it is by atherosclerotic plaque "fracture" similar to that observed in atherosclerotic coronary arteries subjected to angioplasty procedures.

Cardiac myxoma. A review.

Cardiac myxoma is a true intracardiac neoplasm, which is histologically benign but which on occasion may exhibit behavior suggestive of a true malignancy. It is the most common form of primary cardiac tumor, accounting for 50% of such neoplasms. Seventy-five percent of myxomas are found in the left atrium, typically arising from a stalk attached to the area of the foramen ovale. Cardiac myxomas typically present as a triad of obstructive, embolic, and constitutional symptoms and thus mimic many more common systemic illnesses. This report summarizes 9 cases of cardiac myxoma seen at this institution since a previous report in 1972. Four cases with unusual manifestations are high-lighted in the text to illustrate the protean manifestations of this potentially curable illness. Non-invasive cardiac imaging is essential to establish the diagnosis and differentiate myxoma from the other more common illnesses it imitates. Echocardiography is highly accurate for its diagnosis, has proved invaluable for the management of these patients, and is the imaging technique of choice for initial evaluation of patients in whom the diagnosis of cardiac myxoma is suspected.

Effect of chronic hypercalcemia on the heart. An analysis of 18 necropsy patients.

Certain clinical and morphologic cardiac observations are described in 18 necropsy patients, aged 33 to 58 years (mean 45 years) (14 women), with chronic hypercalcemia (11.6 to 34.4 mg/dl [19.4]) from one to nine years (mean five years). Primary hyperparathyroidism was present in nine patients and secondary hyperparathyroidism in the other nine (of renal origin in seven). Cardiac valve anular and coronary arterial calcific deposits were present in 10 patients (Group I) including four (mean age 51 years) with considerable narrowing of two or three of the four major epicardial coronary arteries. None of the other eight patients (Group II) had cardiac valve anular or cuspal calcific deposits; only two had coronary calcific deposits, small in each, and none had significant coronary luminal narrowing. Calcium was in the media ("medial calcinosis"), with or without intimal deposition, of the coronary arteries in five patients. Comparison of the patients in Group I to those in Group II disclosed similar mean ages, durations of hypercalcemia and serum calcium levels, but significantly (p less than 0.05) higher mean total serum cholesterol levels (216 versus 163 mg/dl) and heart weights (426 versus 320 g). This study demonstrates that chronic hypercalcemia is associated with accelerated deposition of calcium in the cardiac anuli and valvular cusps, in the media and intima of the coronary arteries and in individual myocardial fibers (dystrophic calcification), and that coronary intimal calcification may be associated with or produce luminal narrowing, especially in patients with serum total cholesterol levels over 200 mg/dl. Thus, chronic hypercalcemia may be viewed as a "risk factor" to accelerated coronary atherosclerosis.

Radiation heart disease. Analysis of 16 young (aged 15 to 33 years) necropsy patients who received over 3,500 rads to the heart.

Certain clinical and necropsy findings are described in 16 young (aged 15 to 33 years) patients who received greater than 3,500 rads to the heart five to 144 months before death. All 16 had some radiation-induced damage to the heart: 15 had thickened pericardia (five of whom had evidence of cardiac tamponade); eight had increased interstitial myocardial fibrosis, particularly in the right ventricle; 12 had fibrous thickening of the mural endocardium and 13 of the valvular endocardium. Except for valvular thickening, the changes were more frequent in the right side of the heart than in the left, presumably because of higher radiation doses to the anterior surface of the heart. In six of the 16 study patients and in one of 10 control subjects, one or more major epicardial coronary arteries were narrowed from 76 to 100 percent in cross-sectional area by atherosclerotic plaque; one patient had a healed myocardial infarct at necropsy and one died suddenly. In 10 patients and in the 10 control subjects, the four major epicardial coronary arteries were examined quantitatively: 6 percent of the 469 five millimeter segments of coronary artery from the patients were narrowed from 76 to 100 percent (controls = 0.2 percent, p = 0.06) and 22 percent were narrowed from 51 to 75 percent (controls = 12 percent). The proximal portion of the arteries in the patients had significantly more narrowing than the distal portions. The arterial plaques in the patients were largely composed of fibrous tissue; the media were frequently replaced by fibrous tissue, and the adventitia were often densely thickened by fibrous tissue. In five patients, there was focal thickening (with or without luminal narrowing) of the intramural coronary arteries. Thus, radiation to the heart may produce a wide spectrum of functional and anatomic changes but particularly damage to the pericardia and the underlying epicardial coronary arteries.

Status of the coronary arteries at necropsy in diabetes mellitus with onset after age 30 years. Analysis of 229 diabetic patients with and without clinical evidence of coronary heart disease and comparison to 183 control subjects.

Clinical and morphologic observations were made in 229 necropsy patients with diabetes mellitus (DM) with onset of diabetes mellitus after 30 years of age--65 without (DM-CHD) and 164 with (DM + CHD) clinical evidence of coronary heart disease (CHD). These observations were compared to those in 183 age-sex-matched nondiabetic control subjects who died from a fatal coronary event (CHD-DM). The average number of three major (right, left anterior descending, left circumflex) coronary arteries per patient narrowed > 75 percent in cross-sectional area by atherosclerotic plaques was identical in the 229 diabetic patients (DM-CHD and DM + CHD) and in the control subjects (CHD-DM), namely, 2.5/3.0. This similarity in the amount of coronary arterial narrowing was present irrespective of the age at onset (after 30 years) or duration of diabetes mellitus. The DM + CHD patients had more severe narrowing of the three major coronary arteries than did the DM-CHD patients (p < 0.01). The amount of severe narrowing in the proximal halves of each of these three arteries was similar to that in the distal halves. The amount of severe (> 75 percent in cross-sectional area) narrowing of the left main coronary artery was greater in the patients with diabetes mellitus than in the nondiabetic controls: 13 percent versus 6 percent (p < 0.01). The type of treatment received by the patients with diabetes mellitus or their adherence to the therapeutic program as measured by the level of random fasting blood sugar did not alter the amount of severe coronary narrowing observed at necropsy.

Osteogenic sarcoma metastatic to the heart.

Of 20 patients with fatal osteogenic sarcoma who underwent postmortem examination, four had metastases to the heart. One had recurrent ventricular tachycardia, and one had anatomic evidence of aortic regurgitation due to massive periaortic neoplastic infiltration that prevented coaptation of the aortic cusps during ventricular diastole, one had massive invasion of the peri-superior vena caval syndrome, and one had neoplastic obstruction of the inferior vena cava as it entered the thorax. Among patients with either primary or secondary neoplasms to the heart, osteogenic sarcoma is unique because the metastases contain bone and, therefore, may be radiographically visible; they are usually large and often intracavitary.

Amount of narrowing by atherosclerotic plaque in 44 nonbypassed and 52 bypassed major epicardial coronary arteries in 32 necropsy patients who died within 1 month of aortocoronary bypass grafting.

In 32 necropsy patients who died within 30 days of an aortocoronary bypass operation performed for relief of angina pectoris, the lumens in 42 (95 percent) of 44 nonbypassed and in 52 (100 percent) or 52 bypassed arteries were narrowed 76 to 100 percent in cross-sectional area by atherosclerotic plaque. Of 616 five mm segments of the 44 nonbypassed arteries examined histologically, 292 (47 percent) were narrowed 76 to 100 percent in cross-sectional area by atherosclerotic plaque; of 728 segments examined in the 52 bypassed arteries, 375 (52 percent) were similarly narrowed. Thirty-two (73 percent) of the 44 nonbypassed coronary arteries (in 23 patients) had been judged to be narrowed 50 percent or less in diameter on preoperative coronary angiography, but at necropsy 31 (97 percent) of these arteries were narrowed 76 to 100 percent in cross-sectional area and the other artery was narrowed 51 to 75 percent. Thus, significant amounts of atherosclerotic plaque tend to be present at necropsy in all three major coronary systems of patients with angina pectoris who die early after an aortocoronary bypass operation.

Remnant saphenous veins after aortocoronary bypass grafting: analysis of 3,394 centimeters of unused vein from 402 patients.

To assess the status of a saphenous vein (SV) excised for coronary artery bypass grafting (CABG), 3,394 cm of remnant SV from 402 patients who underwent CABG were examined. The SV remnants were 0.5 to 52 cm long (mean 8.4). They were sectioned into 5-mm-long segments, and the resulting 6,788 five-millimeter segments were examined histologically: 5,896 (87%) were narrowed 0 to 25% in cross-sectional area by fibrous tissue; 853 (12%) were narrowed 26 to 50%; 23 (0.6%), 51 to 75%, and 16 (0.4%) segments were narrowed 76 to 100%. Of the 16 segments severely narrowed, 7 (44%) were nearly totally occluded by fibrous tissue. In 17 patients who died within 24 hours of CABG, similar degrees of luminal narrowing were observed in remnant segments and in utilized segments of SV. Thus, significant preexisting luminal narrowing of SV used for CABG is infrequent. The intimal fibrous thickening is variable within the same vein when each 5-mm-long segment is analyzed; it is variable from 1 vein to another in the same patient, and it varies among patients.

Frequency and significance of M-mode echocardiographic evidence of mitral valve prolapse in clinically isolated pure mitral regurgitation: analysis of 65 patients having mitral valve replacement.

To assess the reliability of M-mode echocardiographic patterns of mitral valve prolapse (MVP) (echo MVP) in detection of morphologic evidence of MVP (morphologic MVP), operatively excised mitral valves and corresponding M-mode echocardiograms from 65 patients with chronic, severe, isolated, pure mitral regurgitation (MR) were studied. Of the 65 patients, 45 (69%) had echo MVP (either holosystolic or mid-to-late systolic prolapse patterns on preoperative M-mode echograms) and 42 (93%) of them had morphologic MVP; of the 3 without morphologic MVP, 2 had ruptured chordae tendineae from infective endocarditis and 1 had papillary muscle dysfunction from atherosclerotic coronary heart disease. Of the 20 patients without echo MVP, 14 (70%) had no morphologic MVP (9 had papillary muscle dysfunction from coronary heart disease, 4 had infective endocarditis on previous normal valves and 1 had rheumatic heart disease). Of the 48 patients with morphologic MVP, 42 (88%) had echo MVP and most had considerably dilated mitral anulae; the other 6 had ruptured chordae tendineae with less degrees of anular dilatation. Of the 17 patients without morphologic MVP, 3 had echo MVP (coronary artery disease in 1 and infective endocarditis on a previous normal valve in 2); of the 14 with neither echo nor morphologic MVP, 9 had papillary muscle dysfunction from coronary artery disease, 4 had infective endocarditis on previously normal valves and 1 had rheumatic heart disease. The patients with very dilated mitral anuli and leaflet areas generally had holosystolic (hammocking) patterns on echo; the patients with small anuli and leaflet areas usually had mid-to-late systolic (buckling) prolapse patterns.

Early and late morphologic changes in major epicardial coronary arteries after percutaneous transluminal coronary angioplasty.

Certain clinical and morphologic observations are described in 4 men who had PTCA of the left anterior descending coronary artery early (4 hours) or late (80, 90 and 150 days) before sudden death. Histologically, each of the 4 patients had the site of PTCA narrowed 76 to 95% in cross-sectional area by atherosclerotic plaque. The early PTCA patient had coronary artery dissection at the site of PTCA. Each of the 3 late PTCA patients had a decrease in the mean transstenotic coronary gradient (17, 38 and 43 mm Hg) and an angiographic increase in the left anterior descending coronary artery luminal diameter (55, 60 and 65%) at the time of PTCA. At necropsy, 80, 90 and 150 days later, the LAD coronary artery in the area of the PTCA in each patient was narrowed 76 to 95% in cross-sectional area by plaques. No cracks in plaques or other lesions that may have resulted from PTCA were identified histologically in the left anterior descending coronary artery in any late PTCA patient.