BACKGROUND To determine whether or not a moderate genetic defect of homocysteine metabolism is associated with the development of coronary artery disease, we studied the prevalence of thermolabile methylenetetrahydrofolate reductase, which is probably the most common genetic defect of homocysteine metabolism. METHODS AND RESULTS Three hundred thirty-nine subjects who underwent coronary angiography were classified into three groups: (1) patients with severe coronary artery stenosis (> or = 70% occlusion in one or more coronary arteries or > or = 50% occlusion in the left main coronary artery), (2) patients with mild to moderate coronary artery stenosis (< 70% occlusion in one or more coronary arteries or < 50% occlusion in the left main coronary artery), and (3) patients with non-coronary heart disease or noncardiac chest pain (nonstenotic coronary arteries). The thermolability of methylenetetrahydrofolate reductase was prospectively determined in all subjects. Plasma homocyst(e)ine levels were then measured in those with thermolabile methylenetetrahydrofolate reductase. The traditional risk factors for coronary artery disease were thereafter ascertained by chart review of all subjects. The prevalence of thermolabile methylenetetrahydrofolate reductase was 18.1% in group 1, 13.4% in group 2, and 7.9% in group 3. There was a significant difference between the prevalence of thermolabile methylenetetrahydrofolate reductase in groups 1 and 3 (P < .04). All individuals with thermolabile methylenetetrahydrofolate reductase irrespective of their clinical grouping had higher plasma homocyst(e)ine levels than normal (group 1, 14.86 +/- 5.85; group 2, 15.36 +/- 5.70; group 3, 13.39 +/- 3.80; normal, 8.50 +/- 2.8 nmol/mL). Nonetheless, there was no statistically significant difference in the plasma homocyst(e)ine concentrations of these patients with or without coronary artery stenosis. Using discriminant function analysis, thermolabile methylenetetrahydrofolate reductase was predictive of angiographically proven coronary artery stenosis. The traditional risk factors--age, sex, diabetes, smoking, hypercholesterolemia, and hypertension--were not significantly associated with the presence of thermolabile methylenetetrahydrofolate reductase. CONCLUSIONS Thermolabile methylenetetrahydrofolate reductase is a risk factor for coronary artery disease and is unrelated to other risk factors.

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We determined the sequence and timing of inward ventricular wall motion by least-square phase analysis of radionuclide cineangiograms in 10 patients with left bundle branch block (LBBB), five patients with right bundle branch block (RBBB) and 11 patients with normal conduction. All LBBB and RBBB patients had normal coronary arteries and no segmental wall motion abnormalities. The left ventricle (LV) was divided into eight segments and the right ventricle (RV) into three; sequence and timing were scored by three observers. In normal subjects, wall motion begins in either or both ventricles and ends in the LV or both ventricles. In patients with LBBB it begins in the RV and ends in the LV; in patients with RBBB is begins in the LV and ends in the RV or both ventricles. The intraventricular wall motion is also altered in the ventricle ipsilateral to a bundle branch block. In LBBB, the mean time of onset of LV wall motion is delayed 1.9 frames (38 msec), whereas RV wall motion is normal. In RBBB, the onset of RV wall motion is delayed 1.3 frames (26 msec), whereas LV wall motion is not delayed.

Aneurysmal dilatations in saphenous vein grafts are rare complications of coronary artery bypass surgery that mostly represent thin-wall pseudoaneurysms at anastomotic sites. We describe a case of an enlarging distal saphenous vein graft aneurysm in which intravascular ultrasound (IVUS) and computerized three-dimensional reconstruction (3DR) of the IVUS images was performed to conclusively demonstrate true aneurysm morphology. Although both atherosclerotic and nonatherosclerotic mechanisms for vein graft aneurysm formation have been previously suggested, IVUS images and 3DR of the aneurysm in this case did not reveal any of the features typical for atherosclerotic lesions. Further, the IVUS images and 3DR suggest that progressive atherosclerosis is not the likely cause of aneurysm formation in this case. This application of IVUS and 3DR provides detailed information about saphenous vein graft aneurysm structure, clues to aneurysm formation, and suggests a natural history that may differ from that of pseudoaneurysms.