Abnormal Coronary Arteriograms Research Articles

A precise, three-dimensional atlas of myocardial perfusion correlated with coronary arteriographic anatomy

To map precise myocardial perfusion anatomy, we correlated detailed coronary arteriographic anatomy for every coronary artery and all secondary branches in the heart that had flow-limiting stenosis with corresponding specific, circumscribed, myocardial perfusion defects by positron emission tomography. Eight hundred ninety-five patients with abnormal coronary arteriograms showing any visible coronary artery narrowing of greater than 10% diameter stenosis underwent positron emission tomography perfusion imaging at rest and after dipyridamole stress; the data obtained were processed automatically into 3-dimensional topographic displays of relative radionuclide uptake in anterior, septal, left lateral, and inferior quadrant views, without attenuation artifacts, depth-dependent resolution, or spatial distortion of polar displays. The selection criterion for detailed anatomic analysis was the presence of a discrete, localized, moderate to severe, dipyridamole-induced perfusion defect, defined by automated algorithms as 1 quadrant view outside 2 SDs of healthy control subjects with which a specific stenotic coronary artery and/or its secondary branches could be correlated unequivocally on the coronary arteriogram for mapping precise perfusion anatomy, not for determining sensitivity or specificity. Because the anatomy of myocardial perfusion is inherently not statistical data, the results are presented as a summary atlas and series of individual cases that illustrate myocardial perfusion anatomy. Because the patterns of myocardial perfusion anatomy were derived from a large number of subjects, the atlas provides generalized information, not previously published, that correlates detailed arteriographic anatomy with perfusion anatomy including secondary diagonal, marginal, and posterior descending branches of the coronary arteries. (J Nucl Cardiol 2001;8:580-90.)

Nonpharmacologic validation of the intrinsic heart rate in cardiac transplant recipients.

The maximum sinus rate during exertion in humans is inversely related to age. However, the sinus rate at rest is quite variable. The intrinsic heart (IHR) following pharmacologic blockade of autonomic tone with propranolol and atropine has been proposed as a test of sinus node function and is related to age by the linear regression equation: IHR = 118.1 - (0.57 x age). Whether this relationship exists for transplanted hearts for which the donor sinus node is denervated has not been determined. The relationship between the resting heart rate and the age of the donor heart was examined in 103 patients 1 year following orthotopic cardiac transplantation in the absence of rejection or intercurrent illness. Patients receiving beta-blockers, calcium blockers, antiarrhythmic drugs, digitalis, theophylline, or with biopsy evidence of rejection or abnormal coronary arteriograms were excluded from analysis. The recipient age, left ventricular ejection fraction, pulmonary capillary pressure, cardiac index, donor heart ischemic time and cardiopulmonary bypass time did not correlate with the rate of the resting donor sinus node. The resting heart rate was inversely related to age of the donor heart by the linear regression equation: HR = 112.0 - (046 x age). The resting rate of the denervated sinus node is related to donor age with a regression equation that is similar, though slightly slower, than that predicted after pharmacologic autonomic blockade.

Variant angina: Comparison of patients with and without fixed severe coronary artery disease

To determine if the clinical features of variant angina are predictive of the severity of underlying coronary artery disease, 43 patients with variant angina who had less than 50% fixed coronary luminal diameter narrowing (group 1) were compared with 65 patients with variant angina who had 70% or greater diameter narrowing (group 2). Statistically significant differences were found in 3 clinical features between group 1 and group 2: (1) a more than 3-month history of angina at rest before diagnosis (80% vs 23%, p less than 0.001); (2) an abnormal electrocardiogram at rest (19 vs 48%, p less than 0.01); and (3) an abnormal stress test (26% [8 of 30] vs 84% [15 of 18], p less than 0.01). However, these features were not clinically reliable in separating patients with variant angina with and without fixed severe obstructions because of overlap between the 2 groups. No difference was found between the 2 groups in age, sex, predominant symptom at the time of catheterization, history of exertional angina, syncope with angina, prolonged angina, previous myocardial infarction or risk factors for coronary artery disease. There was also no difference in the location of ST elevation or occurrence of major arrhythmias during angina. Thus, among patients with Prinzmetal's variant angina, those with normal or mildly abnormal coronary arteriograms cannot be differentiated reliably by clinical features from those with fixed severe coronary obstructions. Coronary arteriography should be performed to define the underlying coronary anatomy and to determine optimal therapy in patients with variant angina.

Fibrinopeptide A, Platelet Factor 4, and β-Thromboglobulin Levels in Coronary Heart Disease

In vivo platelet alpha-granule release and fibrin I formation were measured in 82 patients with ischemic heart disease by radioimmunoassay of platelet factor 4, beta-thromboglobulin, and fibrinopeptide A. The presence and extent of coronary artery disease were determined by coronary arteriography, and the extent of left ventricular regional dysfunction was assessed by contrast left ventriculography. In patients with abnormal coronary arteriograms without previous myocardial infarction, mean levels of platelet factor 4, beta-thromboglobulin, and fibrinopeptide A were not elevated. In patients in whom myocardial infarction had occurred more than 6 mo previously, platelet factor 4 (8.3 ng/ml; p less than 0.01) and beta-thromboglobulin (33.2 ng/ml; p less than 0.001) levels were significantly elevated, but fibrinopeptide A levels were normal. Levels of platelet factor 4 and beta-thromboglobulin were unrelated to the extent of coronary artery disease. In the patients with prior infarction, beta-thromboglobulin correlated directly with extent of left ventricular regional dysfunction (r = 0.53; p less than 0.01) and inversely with ejection fraction (r = -056; p less than 0.05). In a small group of patients with left ventricular aneurysm, mean fibrinopeptide A levels were also elevated. We interpret these findings as indicating that platelet release in patients with ischemic heart disease results from platelet reaction with previously infarcted myocardium rather than with the atherosclerotic coronary arteries.

Fibrinopeptide A, platelet factor 4, and beta-thromboglobulin levels in coronary heart disease

In vivo platelet alpha-granule release and fibrin I formation were measured in 82 patients with ischemic heart disease by radioimmunoassay of platelet factor 4, beta-thromboglobulin, and fibrinopeptide A. The presence and extent of coronary artery disease were determined by coronary arteriography, and the extent of left ventricular regional dysfunction was assessed by contrast left ventriculography. In patients with abnormal coronary arteriograms without previous myocardial infarction, mean levels of platelet factor 4, beta-thromboglobulin, and fibrinopeptide A were not elevated. In patients in whom myocardial infarction had occurred more than 6 mo previously, platelet factor 4 (8.3 ng/ml; p less than 0.01) and beta-thromboglobulin (33.2 ng/ml; p less than 0.001) levels were significantly elevated, but fibrinopeptide A levels were normal. Levels of platelet factor 4 and beta- thromboglobulin were unrelated to the extent of coronary artery disease. In the patients with prior infarction, beta-thromboglobulin correlated directly with extent of left ventricular regional dysfunction (r = 0.53; p less than 0.01) and inversely with ejection fraction (r = -056; p less than 0.05). In a small group of patients with left ventricular aneurysm, mean fibrinopeptide A levels were also elevated. We interpret these findings as indicating that platelet release in patients with ischemic heart disease results from platelet reaction with previously infarcted myocardium rather than with the atherosclerotic coronary arteries.

Leukocyte ascorbic acid and its relationship to coronary artery disease in man

The ascorbic acid level of the leukocytes in patients with coronary artery disease was compared to the ascorbic acid level of the leukocytes in patients without coronary artery disease as demonstrated by coronary arteriography. The leukocyte ascorbic acid level was found significantly lower in patients with coronary arteriography. The leukocyte ascorbic acid level was found significantly lower in patients with coronary atherosclerosis (P < 0.001). There was also significant difference in the leukocyte ascorbic acid levels among patients with abnormal coronary arteriograms who smoked compared to those who did not. The anatomical changes secondary to atherosclerotic disease, and mainly those changes related to the ground substance, have been shown to be the changes that have been observed in patients with ascorbic acid deficiency. From the present study, with its limitations, it is suggested that ascorbic acid may play a role in the pathogenesis of atherosclerosis, and although not implicated as an etiological factor in coronary artery disease, it suggests that a closer look at its possible role in the pathogenesis and progression of coronary artery disease is warranted.

Clinical course of patients with normal or slightly or moderately abnormal coronary arteriograms: 10-year follow-up of 521 patients.

The clinical course was followed for 10 years in 521 patients whose coronary arteriograms did not show any severe obstruction. Coronary disease had been suspected in all patients before arteriography. Two of 357 patients thought to have normal arteriograms died from coronary disease and two of 101 patients died who had less than 30% estimated narrowing of at least one coronary artery. Ten deaths ascribed to coronary disease occurred in 63 patinets who had 30-50% narrowing of at least one major coronary artery. The difference in death rates between the normal or mildly diseased groups and the group that had moderate narrowing was significant (p < 0.01). Coronary events (death from coronary disease, subsequent myocardial infarction, or arteriographic evidence of progression of coronary obstruction) occurred in 2.1% of those who had normal arteriograms, 13.8% of the group with mild lesions, and 33% of those with moderate degree of coronary arterial narrowing.

Nifedipine therapy for refractory coronary arterial spasm

Nifedipine was evaluated in the management of eight patients with intractable coronary arterial spasm. All had Prinzmetal's variant angina, normal or mildly abnormal coronary arteriograms, and a positive ergonovine maleate provocative test. Anginal attacks occurred at least three times a week in all patients during isosorbide dinitrate therapy. All patients had a decrease in frequency of ischemic attacks with nifedipine. Seven patients underwent repeat Holter monitor evaluation, which confirmed the absence of ischemic changes while they were taking nifedipine. When nifedipine dosage was decreased or therapy discontinued in six patients, all experienced a recurrence of anginal attacks. Two patients had minor side effects, which required a decrease in the dose of nifedipine. Nifedipine was well tolerated, and no major complications occurred with its use. Nifedipine appears to be effective in the management of patients with symptomatic coronary arterial spasm and normal or mildly abnormal coronary arteriograms. Our data justify further investigation of nifedipine for treatment of such patients.

The prevalence of angina pectoris and abnormal coronary arteriograms in severe aortic valvular disease

In order to relate the frequency of angina pectoris to associated coronary artery disease, 66 consecutive patients with severe aortic valvular disease were studied by cardiac catheterization, including coronary angiography. Angina pectoris was found in 63 per cent of patients with predominant aortic stenosis, 62 per cent with aortic regurgitation, and 67 per cent with mixed disease. Associated coronary artery disease (larger than or equal to 75 per cent luminal stenosis) ranged from 14 to 28 per cent and averaged 20 per cent for the entire group of 66 patients. Only one patient without angina had significant coronary artery stenosis. Our studies indicate that angina pectoris is equally common in all forms of severe aortic valve disease and is usually not associated with significant coronary artery disease.

Clinical course of patients with normal, and slightly or moderately abnormal coronary arteriograms. A follow-up study on 500 patients.

In a series of 500 patients who had normal coronary arteriograms or narrowings &lt; 50% of the lumen diameter the subsequent clinical course was studied. The minimum follow-up period was 5 years. In 342 patients with entirely normal coronary arteriograms there were only two (0.6%) presumed cardiac deaths and three (0.9%) acute myocardial infarctions within 5 years; both incidences are about half the expected rates in the average unselected population of the United States matched by sex and age. In 101 patients with mild abnomalities (&lt;30% narrowing of the lumen diameter) the prognosis was less good than in the normal group but still better than in the average population. In 57 patients with moderate abnormalities (30 to less than 50% narrowing) there were three (5.3%) presumed cardiac deaths and two (3.5%) myocardial infarctions within 5 years; both incidences are higher than in the average population. Serial arteriograms were made in 20 cases and showed progression of the disease in the majority of cases with moderate narrowings, but progression or development of narrowings in only one of the cases with normal arteries or mild narrowings. Other determinants included in this study appeared to have limited predictive value regarding the clinical course. It is concluded that the coronary arteriogram contains major predictive information. Normal findings indicate an excellent prognosis regardless of other diagnostic parameters; moderate abnormalities indicate the early phase of an essentially progressive disease.

Angina pectoris in patients with normal and abnormal coronary arteriograms: Hemodynamic and clinical aspects

Ten patients with typical angina pectoris and normal coronary arteriograms were evaluated. Hemodynamic measurements and clinical features were analyzed and compared to those in a similar group of patients with angina secondary to demonstrable coronary artery disease. Both hemodynamic and clinical abnormalities were observed in those patients with angina and normal coronary arteries. However, with the exception that exercise elicited angina and electrocardiographic changes more consistently in the group with coronary artery disease, there were no significant differences between the two groups.