Biomedical subjects
Publications and source records attributed to H S Cabin.
Percutaneous transluminal coronary angioplasty was first performed in a human coronary artery in 1977. In this article, we review the possible mechanisms of angioplasty, current indications for angioplasty, and complications of angioplasty including acute closure and restenosis.
The rule of anticoagulation therapy in the setting of an acute myocardial infarction has been debated for decades. The role of such therapy in reducing mortality, preventing deep venous thrombosis and pulmonary emboli, and in reducing the frequency of left ventricular thrombus formation and subsequent systemic embolization is discussed.
Precise targeting of laser energy to atherosclerotic plaque is crucial for the safe performance of laser angioplasty. The present study was designed to evaluate whether laser-induced fluorescence could distinguish atherosclerotic from normal aorta. Segments of human aorta obtained at necropsy were classified grossly and histologically as normal aorta (n = 7), thin yellow fatty plaque (n = 5), and thick white atheromatous plaque (n = 9), and analyzed by laser-induced fluorescence spectroscopy using a pulsed nitrogen laser. Fluorescence spectra were recorded over a wavelength range from 385 to 725 nm. Normal specimens had maximal fluorescence intensity at 514 nm. A prominent fluorescence peak at 448 nm was present in specimens characterized as white atheromatous plaque and at 538 nm in specimens characterized as yellow fatty plaque. The ratios of fluorescence intensity at 448 nm/514 nm and at 538 nm/514 nm correctly classified all specimens according to their gross and histologic type (p less than .001). Thus, a "smart" laser angioplasty catheter system might incorporate low-power laser radiation for arterial fluorescence spectroscopy to guide delivery of high-power laser radiation for plaque ablation.
Right ventricular myocardial infarction has been reported to occur exclusively in association with inferior left ventricular infarction. To determine the frequency of right ventricular myocardial infarction in association with anterior left ventricular myocardial infarction, all hearts with anterior myocardial infarction studied over a 3-year period were examined for evidence of right ventricular necrosis or scar. Of 97 hearts with anterior myocardial infarction, 13 (13%) had anterior right ventricular myocardial infarction. The right ventricular infarcts involved from 10% to 50% (mean 28%) of the circumference of the right ventricular free wall from base to apex. The associated left ventricular infarcts were all anteroseptal and large and involved from 36% to 67% (mean 50%) of the total area of the left ventricular free wall and septum. Nine of the 13 patients underwent equilibrium radionuclide angiography and six had demonstrable right ventricular regional and global dysfunction. Thus, right ventricular myocardial infarction does occur with anterior wall left ventricular infarction, and right ventricular dysfunction may be demonstrable by radionuclide angiography. Further investigation is needed to define the hemodynamic characteristics, clinical importance, and therapeutic implications of anterior right ventricular myocardial infarction.
Thirty patients with stable exertional angina undergoing percutaneous transluminal coronary angioplasty of an isolated obstructive lesion of the proximal left anterior descending artery were prospectively evaluated to investigate the relation between angina induced by balloon inflation and the quantity and severity of myocardial ischemia as determined by electrocardiographic (ECG) monitoring and by echocardiographic assessment of regional and global left ventricular wall motion. Anginal pain interviews, continuous two-dimensional echocardiographic recordings and 12 lead ECG recordings at 10 second intervals were obtained for the first two inflation sequences. Seventeen patients had angina with both inflations (symptomatic group), seven patients had no angina or related symptoms during either inflation (asymptomatic group) and six patients had both painful and painless inflations (mixed response group). Comparison of the three groups revealed that they did not differ in mean age, sex distribution, prior history of angina or the incidence of comorbid conditions. Echocardiographic measurements of global and regional left ventricular dysfunction during balloon inflation were comparable in the symptomatic and asymptomatic groups. Similarly, there were no significant differences in the time to onset or magnitude of ST segment changes. The results of the wall motion and ECG studies in the mixed response group paralleled the results in the symptomatic and asymptomatic groups, with no significant differences in any of the variables measured between the painful and painless inflations. These data demonstrate that silent myocardial ischemia occurs in an appreciable proportion of patients during coronary angioplasty and the absence of angina does not imply that a lesser amount of myocardium is jeopardized than with painful inflations.
The relation of degree of regional wall motion abnormality by equilibrium radionuclide angiocardiography to the presence and mural extent of regional necrosis or scar at autopsy was evaluated in 23 autopsy patients who had a history of myocardial infarction and had equilibrium radionuclide angiocardiography within 40 days of death. Of the 228 regions evaluated by equilibrium radionuclide angiocardiography, 135 had abnormal regional wall motion and 102 (76%) of these 135 regions had evidence of myocardial infarction at autopsy. The overall sensitivity, specificity and predictive values of regional wall motion abnormality for regional necrosis or scar were 69, 59 and 76%, respectively. Of the 33 false positive regions, 20 (61%) had severe narrowing of the coronary artery supplying that region, 13 (39%) were adjacent to a region with a myocardial infarction and almost half (16 [48%]) were in the lateral wall. Eighty-three (36%) of the 228 regions were akinetic or dyskinetic, 52 (23%) were hypokinetic and 93 (41%) were normal. Sixty-three (76%) of the 83 akinetic/dyskinetic segments had transmural myocardial infarction at autopsy, 14 (17%) had nontransmural myocardial infarction and only 6 (7%) contained no necrosis or scar. In contrast, 14 (27%) of 52 hypokinetic segments had transmural myocardial infarction, 11 (21%) had nontransmural myocardial infarction and 27 (52%) were normal. Thus, the most severe regional wall motion abnormality (akinesia/dyskinesia) almost always indicates regional myocardial infarction which is usually transmural whereas less severe dysfunction (hypokinesia) is not necessarily associated with regional necrosis or scar. The severity of regional dysfunction must be considered if equilibrium radionuclide angiocardiography is used to evaluate the presence and mural extent of myocardial infarction within a region.
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We studied 142 consecutively autopsied patients prospectively to determine the frequency and clinical importance of right-sided endocardial lesions in patients who had undergone flow-directed pulmonary-artery catheterization within one month of death. Of the 55 catheterized patients, 29 (53 per cent) had one or more right-sided endocardial lesions: 12 (22 per cent) had subendocardial hemorrhage, 11 (20 per cent) sterile thrombus, 2 (4 per cent) hemorrhage and thrombus, and 4 (7 per cent) infective endocarditis. Of 41 lesions seen in the 29 patients, 23 (56 per cent) were located on the pulmonic valve, 6 (15 per cent) on the tricuspid valve, 6 (15 per cent) in the right atrium, 4 (10 per cent) in the right ventricle, and 2 (5 per cent) in the main pulmonary artery. All four patients with infective endocarditis had had positive antemortem blood cultures while the catheter was in place, but in only one had the diagnosis of endocarditis been suspected clinically. The unusual locations of the infected vegetations (on the pulmonic valve in three and in the right atrium in one) and the similar location of the uninfected lesions suggest that the infective endocarditis was a consequence of catheter-induced endocardial damage with concurrent or subsequent bacteremia. Among the 87 non-catheterized patients, there were two subendocardial hemorrhages and one resolving right atrial thrombus. We conclude that endocardial damage from flow-directed pulmonary-artery catheterization is common and that right-sided infective endocarditis should be suspected in bacteremic catheterized patients.
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The percent of left ventricular wall (including ventricular septum) replaced by scar was determined in 70 necropsy patients with a healed transmural myocardial infarct (MI). The MI involved from 1% to 55% (mean 13%) of the left ventricular wall. The ages at death of the patients ranged from 25 to 82 years (mean 62) and did not significantly correlate with MI size (r = -0.12). Of the 70 patients, 41 (59%) had unequivocal histories of an acute MI: the interval from the MI to death in them ranged from 2 to 276 months (mean 50) and correlated negatively with MI size (r = -0.32, p less than 0.05), and the age at the MI ranged from 26 to 79 years (mean 58) and did not correlate with MI size (r = -0.05). The four major epicardial coronary arteries were examined quantitatively in 56 patients; the number of coronary arteries with severe narrowing ranged from one to four (mean 2.9) and did not correlate with MI size (r = -0.24). The mean MI size in the 12 patients with and in the 44 without severe narrowing of the left main coronary artery was identical (each 13%). The entire lengths of the right, left anterior descending, and left circumflex coronary arteries in the 56 patients were divided into 5 mm long segments and the amounts of cross-sectional area narrowing in each of the resulting 2489 segments were determined by histologic examination. The percent of 5 mm segments with severe (cross-sectional area narrowing 76% to 100%) narrowing by atherosclerotic plaques in each patient ranged from 3% to 93% (mean 44% and did not correlate with MI size (r = -0.20). When the 28 patients with an MI involving greater than 10% of the left ventricular wall were compared to those with an MI involving less than or equal to 10%, a similar overall percentage of 5 mm segments of coronary artery was severely narrowed (43% vs 42%). In addition, a similar percentage of segments was narrowed severely in each of the three major epicardial coronary arteries. Thus in our necropsy patients with a healed transmural MI, the MI size correlated with length of survival after an acute MI (in patients with definite histories of an acute MI) but not with age at death or with the amount, location, or extent of coronary arterial narrowing by atherosclerotic plaques.
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Clinical and necropsy observations are described in 61 patients with a healed transmural myocardial infarction, 33 with and 28 without a clinical history of acute myocardial infarction. There were no significant differences between the 2 groups of patients in mean age, sex, or frequency of angina pectoris, chronic congestive heart failure, systemic hypertension, sudden coronary death, or fatal acute myocardial infarction. Compared with the patients with clinically recognized acute myocardial infarction, the patients with clinically unrecognized (silent) infarction had a significantly (p less than 0.05) higher incidence of diabetes mellitus (43 versus 15%), death from noncardiac causes (39 versus 9%), posterior (inferior) wall infarcts (82 versus 55%), and smaller infarcts (mean size 7 versus 17% of left ventricular wall). The patients with and without clinically recognized infarction had similar numbers of the 4 major coronary arteries severely (76 to 100% in cross-sectional area) narrowed (mean 2.8 versus 2.9/4.0 per patient), insignificant differences in incidence of severe narrowing of the left main coronary artery (18 versus 29%), similar overall percents of 5 mm segments of the 4 major coronary arteries severely narrowed (43 versus 42%), and similar percents of severely narrowed 5 mm segments of the right (46 versus 55%), left anterior descending (39 versus 33%), and left circumflex (41 versus 41%) coronary arteries.
The amount of cross-sectional area narrowing by atherosclerotic plaques was determined histologically in each 5 mm segment of the entire lengths of the right, left main, left anterior descending, and left circumflex coronary arteries in 40 patients with fatal coronary heart disease and known fasting serum total cholesterol and triglyceride levels. The patients were divided into four groups based upon the serum total cholesterol and triglyceride levels: group I, total cholesterol of 250 mg/dl or less, triglyceride of 170 mg/dl or less; group II, total cholesterol of 250 or less, triglyceride of more than 170; group III, total cholesterol of more than 250, triglyceride of 170 or less; group IV, total cholesterol of more than 250, triglyceride of more than 170. The number of 5 mm segments of coronary artery narrowed severely (76 to 100 percent in cross-sectional area) by atherosclerotic plaques in each group was as follows: 172 of 505 (34 percent) 5 mm segments from group I; 242 of 353 (69 percent) segments from group II; 120 of 295 (41 percent) from group III and 425 of 884 (48 percent) segments from group IV. The mean percentage of 5 mm segments narrowed severely was significantly greater in group II than in group I (p less than 0.005) or group III (p less than 0.01). Additionally, the mean number of four coronary arteries per subject severely narrowed and the number of subjects with severe narrowing of the left main coronary artery were significantly greater in groups II and III than in group I. The percentages of 5 mm segments narrowed severely correlated significantly with the serum triglyceride level (p less than 0.03). Although it correlated with the number of severely narrowed coronary arteries per subject, the serum total cholesterol level did not correlate with the percentage of 5 mm segments of coronary artery with severe narrowing.
The amount of cross-sectional area narrowing by atherosclerotic plaque in each 5-mm-long segment from the entire lengths of the right, left main, left anterior descending and left circumflex coronary arteries and the size, predominant location and extent of myocardial scarring were determined in 59 necropsy patients with a healed transmural myocardial infarct (MI). The mean number of the four major epicardial coronary arteries narrowed severely (76-100% in cross-sectional area) was 3.0 in the 37 patients with posterior MI and 2.6 in the 22 patients with anterior MI (p less than .025). The mean percent of severely narrowed 5-mm segments from all four major coronary arteries was similar in the anterior and posterior MI groups, 38% vs 46%. The patients with anterior MI, however, had a higher percentage of severely narrowed 5-mm segments of the left anterior descending than of the left circumflex but not the right coronary artery, 46% vs 25% (p less than 0.001) and 40% (NS). The patients with posterior MI had a higher percentage of severely narrowed segments of the right and left circumflex coronary arteries than of the left anterior descending artery, 55% and 51% vs 32% (p less than 0.05). The anterior MI group had, on the average, larger left ventricular scars than the posterior MI group (20% vs 9%, p greater than 0.002) and more frequent scarring of the ventricular septum, 16 patients (73%) vs six patients (16%) (p less than 0.001).
The amount of cross-sectional area (XSA) narrowing in each 5 mm long segment of each of the four major epicardial coronary arteries was determined in each of five patients with type III hyperlipoproteinemia (HLP) and symptomatic, fatal atherosclerotic coronary disease (CAD). Four had angina pectoris; two had acute myocardial infarcts which healed, and two died suddenly. Of the four major epicardial coronary arteries, all four were narrowed 76% to 100% in XSA by atherosclerotic plaques in two patients, three were narrowed to this degree in two patients, and two were so narrowed in one patient. Three patients had severe narrowing of the left main coronary artery. The percent of 5 mm long segments of coronary artery narrowed to various degrees was as follows: 96% to 100%, 0 to 37 (mean 14); 76% to 95%, 14 to 61 (mean 35); 51% to 75%, 9 to 41 (mean 24); 26% to 50%, 0 to 42 (mean 16), and 0% to 25%, 0 to 27 (mean 11). Utilizing a scoring system of 1 to 4 for the four categories of narrowing (1 = 0% to 25%, 2 = 26% to 50%, 3 = 51% to 75% and 4 = 76% to 100% XSA narrowing), scores per 5 mm segment for each patient ranged from 2.5 to 3.9 (mean 3.1). Thus these five type III HLP patients had severe diffuse coronary narrowing by atherosclerotic plaques.