Circulating endothelial cells (CECs) have been detected in association with endothelial injury and therefore represent proof of serious damage to the vascular tree. Our aim was to investigate, using the technique of immunomagnetic separation, whether the pathological events in unstable angina (UA) or acute myocardial infarction (AMI) could cause desquamation of endothelial cells in circulating blood compared with effort angina (EA) and noncoronary chest pain. A high CEC count was found in AMI (median, 7.5 cells/mL; interquartile range, 4.1 to 43.5, P < .01 analysis of variance [ANOVA]) and UA (4.5; 0.75 to 13.25 cells/mL, P < .01) within 12 hours after chest pain as compared with controls (0; 0 to 0 cells/mL) and stable angina (0; 0 to 0 cells/mL). CEC levels in serial samples peaked at 15.5 (2.7 to 39) cells/mL 18 to 24 hours after AMI (P < .05 repeated measures ANOVA), but fell steadily after UA. Regardless of acute coronary events, the isolated cells displayed morphologic and immunologic features of vascular endothelium. The CECs were predominantly of macrovascular origin. They did not express the activation markers intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, and E-selectin, although some were positive for tissue factor. CECs failed to exhibit characteristics of apoptosis (TUNEL assay) excluding this event as a possible mechanism of cell detachment. The presence of CECs provides direct evidence of endothelial injury in AMI and UA, but not in stable angina, confirming that these diseases have different etiopathogenic mechanisms.

The results of this study allowed us to determine a high-risk group for SMI in the diabetic population. SMI with significant lesions occurs in 20.9% of type 2 diabetic male patients who are totally asymptomatic for CAD. Based on these findings, we recommend routine screening for male patients in whom the duration of type 2 diabetes is >10 years or even less when more than one cardiovascular risk factor is present.

Most studies on the natural course of coronary artery spasm in patients with normal or nearly normal coronary arteries are based on medium-term follow-up in small populations. The present series includes 277 successive patients with a median follow-up of 89 months (range: 1 to 198 months). There were 206 men and 71 women whose mean age was 53.6 +/- 9.3 years. They were all assessed with coronary arteriography which revealed no stenoses greater than 50%. Spasm was confirmed during the coronary arteriography in 157 patients (56.7%), by a positive provocation test following the arteriography in 113 patients (40.8%), and by an electrocardiogram which showed Prinzmetal's variant angina in seven patients (2.5%). The majority of patients, 264 (95.3%) were treated with calcium channel blockers. At the end of this study: 35 patients (12.6%) were lost to follow-up; 20 patients (7.2% died) including 10 (3.6%) from cardiac causes; 18 patients (6.5%) experienced myocardial infarction in 11 of whom repeat coronary arteriography consistently demonstrated one or more significant stenoses (greater than 70%); 109 patients (39%) had persistent angina, in 52 of whom the severity (more than one episode per month) warranted repeat coronary arteriography which detected significant stenosis in 19 cases; 95 patients (34.3%) were asymptomatic. Multivariate statistical analyses showed that only predictors of major coronary events (death, myocardial infarction or angina requiring repeat coronary arteriography) were systemic hypertension or the finding of minor parietal irregularities on the initial coronary arteriogram. Conclusion. Despite treatment with calcium channel blockers, persistent or recurrent episodes of angina are frequently observed whereas complications such as myocardial infarction or death are rare.

No abstract

SummaryVascular disease is a multifactorial disease that involves atherosclerotic and thrombotic factors. Genetic polymorphisms have been associated with myocardial infarction and angina pectoris. The aim of the present study was to assess the relationship between some genetic polymorphisms and myocardial infarction (MI) or vasospastic angina pectoris in a population from southern France. Genetic polymorphisms of the renin angiotensin system (the D/I polymorphism of the ACE gene and the A1166C polymorphism of the angiotensin II type 1 receptor [AT1R]) and of haemostatic factors (the -675 4G/5G polymorphism of the plasminogen-activator inhibitor 1 [PAI-1] gene, and the G to T common point mutation in exon 2, codon 34 of the Factor XIII A-subunit gene) were examined.We assessed the genotype distribution in consecutive coronary artery disease (CAD) patients with MI (n = 201) and vasospastic angina pectoris (n = 43) and in 244 healthy controls comparable in age, sex, body mass index and total cholesterol level.The genotype distribution of AT1R polymorphism was significantly different between controls and patients, the prevalence of the C allele carriers being higher in patients with MI after the age of 45 than in control individuals (61 vs 45%, p <0.01), leading to an odds ratio (OR) of 2 (CI: 1.2-3.4). When looking at the group of patients with vasospastic angina the difference was even higher (76 vs 45%, p <0.01) yielding an OR of 4.3 (CI: 1.4-17.4). Genotype distributions of ACE, PAI-1 and Factor XIII polymorphisms were similar in patients and in controls.This study is in favor of a role of AT1R gene polymorphism in myocardial infarction and vasospastic angina.

Introduction-Objectives

A n 11-year-old boy with a past history of asthma was admitted to the pediatric intensive care unit (ICU) for a non-Q-wave myocardial infarction that occurred during sustained exercise (a handball match). He presented with chest pain, anterior ST-segment depression on the ECG (Figure 1), and elevation of creatinine kinase (peak, 2580 mU; MB, 240). Initial physical examination was normal, and his ICU course was uncomplicated. He was discharged to the ward after 2 days, and cardiac catheterization was performed 8 days after admission. Left ventriculography ( Figure 2) revealed mild apical hypokinesia with an ejection fraction of 55%. Selective coronary arteriography showed no atherosclerotic lesion but hypoplasia of the distal left anterior descending (LAD) and right coronary (RCA) arteries (Figures 3 and 4). There was no supply of the inferior aspect of the interventricular septum by a posterior branch from the RCA or left circumflex coronary artery (LCx). The proximal LAD was normal, with welldeveloped septal branches but no diagonal branches filled by contrast on the anterolateral free wall of the left ventricle ( Figure 4). Intracoronary infusion of nitroglycerin showed no significant changes in coronary artery diameter ( Figure 5). Total cholesterol, HDL, sedimentation rate, serological studies for connective-tissue diseases, antithrombin III, protein C, protein S, endogenous tissue plasminogen activator, and plasminogen activator inhibitor were normal. The patient was discharged home on diltiazem after a normal maximal exercise test 16 days after admission.In 85% of patients, the coronary circulation is rightdominant, and the RCA supplies the inferior aspect of the interventricular septum by giving rise to the posterior descending artery. The LCx, which is often small, does not reach the crux of the heart. Conversely, when the LCx is the dominant coronary artery, it courses to the crux of the heart and the RCA is often small. 1 In Ϸ7% of patients, there is a codominant or balanced system in which both RCA and LCx give rise to a posterior descending branch. Hypoplastic coronary artery disease (HCAD) occurs rarely and refers to the underdevelopment of Ն1 coronary arteries or their major branches. 2 Most of the patients reported were young adults and experienced sudden cardiac death without antecedent symptoms. Diagnosis is often made at autopsy. 1,2 Although reversible myocardial ischemia has previously been angiographically documented in an infant, it is unusual to see a patient with myocardial infarction and isolated HCAD diagnosed at coronary angiography, as in our patient. 3 Hypoplasia of the RCA and LCx with no posterior descending artery supplying the inferior aspect of the interventricular septum is more commonly found. 1 Hypoplasia of the LAD has also been reported. 2,3 In addition, HCAD was found in several cases of myocardial infarction distal to atherosclerotic or thrombotic occlusions. 2 References1. Roberts WC, Glick BN. Congenital hypoplasia of both right and left circumflex coronary arteries. Am ...

The authors report a case of pseudocoarctation of the aorta associated with a retro-aortic left brachiocephalic vein. This exceptional congenital malformation, never described before, was studied by aortography, computed tomography and magnetic resonance imaging.