Normal Coronary Arteriographic Findings Research Articles

Diffuse disorder of coronary artery vasomotility in patients with coronary spastic angina: Hyperreactivity to the constrictor effects of acetylcholine and the dilator effects of nitroglycerin

We examined the vasomotility of the entire epicardial coronary artery system in patients with and without coronary spastic angina. The coronary arteries of patients with variant angina are hyperreactive to diverse constrictor stimuli. It is unclear whether the abnormal responses to constrictive or dilative stimuli, or both, result from a localized or diffuse disorder in the coronary artery tree. Coronary artery diameter responses to intracoronary acetylcholine and nitroglycerin were examined at the proximal, middle and distal segments of three principal coronary arteries in 36 patients with coronary spastic angina without significant stenosis and in 12 young (< or = 30 years old) and 20 older control subjects (> 30 years old) with normal coronary arteriographic findings. In 10 patients with significant coronary stenosis, the responses of the prestenotic segments were also examined. In patients with coronary spastic angina, coronary spasm was induced in 23 left anterior descending, 13 left circumflex and 17 right coronary arteries by acetylcholine. Multivessel spasm was observed in 15 patients. Acetylcholine had a dilator effect on most segments in young control subjects and a mild constrictor effect in older control subjects and in patients with significant stenosis. Comparison of the responses to acetylcholine among groups demonstrated that the constrictor response of the artery with spasm was enhanced significantly and diffusely. That of the artery without spasm also tended to be enhanced. Coronary artery diameters after nitroglycerin did not differ in any segment among patients with coronary spastic angina and both control groups. In patients with coronary spastic angina, nitroglycerin significantly enhanced dilation in all segments of the artery with spasm compared with that observed in both control groups and in most segments of the artery without spasm. Patients with significant coronary stenosis had a reduced response compared with that in control subjects. Hyperreactive responses not only to the constrictor effects of acetylcholine, but also the dilator effects of nitroglycerin were detected diffusely in the epicardial coronary arteries of patients with coronary spastic angina. This finding indicates that a diffuse, not localized, disorder in vasomotility is involved in the pathogenesis of coronary spastic angina.

Lack of a Thrombotic Tendency in Patients with Acute Myocardial Infarction and Angiographically Normal Coronary Arteries

The hematological profile of 12 patients with acute myocardial infarction and normal coronary arteriographic findings was compared to that of 8 patients with acute myocardial infarction associated with obstructive coronary artery disease, and of 12 patients with no evidence of myocardial infarction and normal coronary arteriographic and left ventriculographic findings who served as control. There were no significant differences in the hematological profile among the 3 groups, suggesting lack of a thrombotic tendency in patients with acute myocardial infarction and normal coronary arteriographic findings.

Acetylcholine-induced coronary vasoconstriction in young, heavy smokers with normal coronary arteriographic findings

purpose: Cigarette smoking is a major coronary risk factor. Acetylcholine dilates coronary arteries in normal subjects, but acetylcholine-induced coronary constriction has been reported in patients with normal coronary arteriographic findings and other risk factors for coronary artery disease. The purpose of the present study was to evaluate the epicardial coronary artery response to acetylcholine in young, heavy smokers. subjects and methods: Responses to stepwise infusion of acetylcholine (10 –8M, 10 –7M,10 –6M, and 10 –5M) into the left coronary artery were studied in five young, heavy smokers and in five age-matched nonsmokers. All subjects were normotensive and had normal left ventricular function and coronary arteriographic findings. Levels of serum cholesterol, triglycerides, and low-density lipoprotein levels were within normal ranges. Vessel dimensions were measured on four different segments in each subject, with quantitative digital-substracted arteriography. results: In smokers, no change was produced at the 10 –8M and 10 –7M concentrations of acetylcholine, but progressive diameter reduction was observed at 10 –6M and 10 –5M acetylcholine (–26.6% ± 13.6%, p <0.001;–42.2% ± 9.5%, p <0.001, respectively). In nonsmokers, a progressive diameter dilation was produced from 10 –8M to 10 –6M acetylcholine (+5.3% ± 3.6%, p <0.001; +12.4% ± 6.5%, p <0.001; +15.9% ± 6.9%, p <0.001, respectively), and no change was observed at 10 –5M acetylcholine. In the two groups, all segments dilated after infusion of intracoronary isosorbide dinitrate. conclusion: The abnormal coronary vasoconstriction induced by acetylcholine in young, heavy smokers with angiographically normal coronary arteries suggests an endothelial vasodilator dysfunction. This mechanism may contribute to the pathogenesis of coronary artery disease in cigarette smokers.

Acetylcholine-induced constriction of angiographically normal coronary arteries is not time dependent in transplant recipients: Effects of stepwise infusion at 1,6,12 and more than 24 months after transplantation

Objectives. The aim of this study was to evaluate whether acetylcholine may be a useful tool for detection of early angiographically undetectable coronary atherosclerosis in heart transplant recipients.Background. Coronary artery disease is the main determinant of long-term prognosis in transplant recipients. Acetylcholine-induced constriction of angiographically normal coronary arteries in heart transplant recipients could be due to early atherosclerosis, and acetylcholine has been proposed for early detection of coronary artery disease.Methods. The responses of large coronary arteries to stepwise intracoronary infusion of acetylcholine (10−8to 10−5mol/liter) were compared in five control subjects and in four groups of transplant recipients 1, 6, 12 and >24 months postoperatively (group 1, n = 6; group 2, a = 7; group 3, n = 6; group 4, n = 6, respectively). All patients had normal coronary arteriographic findings. Vessel dimensions were measured in four segments in each patient.Results. In control subjects, acetylcholine increased diameters significantly at 10−8, 10−7and 10−6mol/liter (all p < 0.001 vs. basal value). No significant variation was observed at 10−5mol/liter. Intracoronary isosorbide dinitrate increased diameters of all segments (p < 0.001). In transplant recipients, vessel diameters did not vary significantly from baseline at 10−8and 10−7mol/liter concentrations in groups 1 and 3 and at 10−8mol/liter in group 4. Vessels constricted significantly in all the other cases. Comparisons of each group with control subjects showed that responses were significantly different for all concentrations but 10−8mol/liter in groups 3 and 4. Intracoronary isosorbide dinitrate elicited coronary vasodilation similar to that of control subjects in all groups of transplant recipients.Conclusions. This study indicates that the acetylcholine response is persistently abnormal is transplant recipients compared with that in normal control subjects and that this abnormality may not be related simply to the presence of atherosclerosis. Thus, acetylcholine may not be a useful tool for early detection of coronary atherosclerosis in heart transplant recipients.

Syndrome X

The problem of anginalike chest pain with normal coronary arteriographic findings is briefly reviewed. This common clinical presentation (ca. 20% of patients investigated by coronary arteriography) is usually due to noncardiac causes (e.g., thoracic root or esophageal pain) but may represent myocardial ischemia attributable to reduced coronary dilator capacity downstream from the epicardial vessels and of unknown pathogenesis--Syndrome X (? less than 0.1% of such patients).

Effects of intracoronary injection of acetylcholine on coronary arterial hemodynamics and diameter

To examine the effects of intracoronary injection of acetylcholine on coronary blood flow and on coronary arterial diameter in humans, acetylcholine was injected into the left coronary artery in 32 adult patients (21 men and 11 women with a mean age of 54 years, range 37 to 65) with normal or almost normal coronary arteriographic findings. Patients with angina pectoris, myocardial infarction and severe cardiac diseases were excluded. Temporary right ventricular pacing was set at a rate of 60 beats/min to prevent transient bradyarrhythmias during intracoronary injection of acetylcholine. Measurements of coronary sinus blood flow and coronary vascular resistance and quantification of coronary arterial diameters using a computer-assisted technique were performed before and after each injection of 20, 50 and 100 μg of acetylcholine. Significant increase in coronary sinus blood flow and significant decrease in coronary vascular resistance occurred after intracoronary injection of acetylcholine. In contrast, mean diameter of normal epicardial coronary artery tended to decrease and that of irregular epicardial coronary artery decreased significantly after intracoronary injection of acetylcholine. Intracoronary injection of acetylcholine increases coronary blood flow, suggesting vasodilation in the coronary arteriolar bed, while it induces vasoconstriction in most of epicardial coronary arteries in adult humans.

Simultaneous multivessel coronary artery spasm demonstrated by quantitative analysis of thallium-201 single photon emission computed tomography

Thallium-201 myocardial scintigraphy with quantitative analysis of emission computed tomography was performed during episodes of angina in 19 patients with variant angina and nearly normal coronary arteriographic findings. Eleven patients (group I) were shown by arteriography to have spasm in 2 or more large coronary arteries. Eight patients (group II) had spasm in only 1 coronary artery. In 7 patients in group I, significant diffuse perfusion defects simultaneously appeared in multiple coronary artery regions on the scintigram (group IA). The extent and severity of the perfusion defect as measured by thallium-201 tomography were significantly greater in group IA than in group II (p < 0.001 and p < 0.01, respectively). The duration of transient ST-segment elevation during the attack in group IA was significantly longer than in group II (p < 0.001). The incidence of ventricular arrhythmias, including ventricular tachycardia, or complete atrioventricular block during the anginal attack was significantly higher (p < 0.05) in group IA than in group II. In all study patients, neither attack nor scintigraphic perfusion defect appeared on the repeat test after oral administration of nifedipine. In conclusion, multivessel coronary artery spasm simultaneously appears and causes the attack in many patients with variant angina and nearly normal coronary arteriographic findings, and myocardial ischemia due to simultaneous multivessel coronary spasm is likely to be more extensive and severe, persist longer and have a higher frequency of potentially dangerous arrhythmias than that due to spasm of only 1 coronary artery.

Effects of intracoronary injection of acetylcholine on coronary arterial diameter

The effects of intracoronary injection of acetylcholine on coronary arterial diameter was examined by coronary arteriography in 30 adult patients (13 men, 17 women), aged 23 to 67 years (mean 51), with normal or almost normal coronary arteriographic findings. Patients with angina pectoris, myocardial infarction and other severe cardiac diseases were excluded. Two minutes after injection of 30 to 100 μg of acetylcholine into the left coronary artery, significant diffuse narrowing (more than 25% reduction in diameter) of the left main trunk, the proximal, mid- and distal left anterior descending artery, and the proximal, mid- and distal left circumflex artery occurred in 1 (4%), 5 (20%), 3 (12%), 9 (36%), 6 (24%), 8 (32%) and 3 (12%) of 25 patients, respectively. After injection of 30 to 50 μg of acetylcholine into the right coronary artery, significant diffuse narrowing of the proximal, mid- and distal right coronary artery occurred in 5 (25%), 7 (35%) and 10 (50%) of 20 patients, respectively. However, significant diffuse dilatation (more than 25% increment in diameter) appeared in the left main trunk, left anterior descending, left circumflex and right coronary arteries in a few patients. These results indicate that acetylcholine induces coronary vasoconstriction in a significant number and coronary vasodilatation in a small number of adult humans, and that response of the coronary artery to acetylcholine varies along the course of the coronary artery.

Panconductional Defect in Mixed Connective Tissue Disease: Association with Sjogren's Syndrome

A patient in whom mixed connective tissue disease in association of Sjögren's syndrome had previously been diagnosed, experienced a syncopal attack. Electrocardiographic monitoring revealed periods of profound sinus bradycardia, sinus arrest with slow junctional escape rhythm, and first degree atrioventricular block during several episodes of dizziness. Complete right bundle branch block was a constant finding in this patient. Sinoatrial conduction time and sinus node recovery time were prolonged. Coronary heart disease was excluded by normal coronary arteriographic findings. This patient represents a rare case of cardiac involvement in mixed connective tissue disease.

Myocardial infarction in patients with normal patent coronary arteries as visualized by cinearteriography

Myocardial infarction with normal coronary arteriographic findings is rare. Three patients are presented who had typical clinical and laboratory findings of acute myocardial infarction and normal coronary arteriograms. Two patients were male, 16 and 24 years old, respectively, and 1 was female, aged 36 years. None had major predisposing factors to precocious coronary atherosclerosis. Thrombocytosis was considered to be the etiologic factor in 1 male patient; no etiologic factor could be traced in the other male patient; estrogen therapy may be considered as the cause of the myocardial infarction in the female patient.

The fate of women with normal coronary arteriograms and chest pain resembling angina pectoris

The clinical and laboratory findings and subsequent fate of 100 women with unexplained chest pain, having some or all of the features of angina pectoris, and normal selective coronary arteriographic findings were studied. Some basis for the chest pain was discovered in only 14 percent (14 of 100) and included the unusual conditions of systolic click syndrome, primary myocardial disease, rheumatic heart disease and a cystic duct neuroma. Of the remaining 86 patients with no readily apparent cause for their symptoms, the average age was 44 years. Atypical angina was noted in 76 percent (65 of 86); 46 percent (40 of 86) gained relief of pain from nitroglycerin, and 40 percent (34 of 86) manifested anxiety neurosis. Of 44 patients who exercised, 16 had a positive electrocardiographic response of S-T segment depression of more than 1 mm, yet this group did not differ significantly from those with a negative response to exercise. Follow-up study of these 86 patients from 6 months to 2 1 2 years revealed that 50 percent had a decrease or disappearance of pain. More important, there was no instance of sudden death or myocardial infarction. It is suggested that chest pain with normal coronary arteriographic findings should be clearly distinguished, especially as to its benign prognosis, from the angina pectoris associated with large vessel obstructive atherosclerosis and that it most likely is related to neurocirculatory asthenia, although other possible explanations are discussed.