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Cardiovascular disease is the number one cause of morbidity and mortality in the United States, with coronary heart disease (CHD) and myocardial infarction (MI) being the leading causes of death. The 5 major risk factors for CHD—hypertension, dyslipidemia, diabetes mellitus, smoking and obesity—account for 80% of the risk for CHD. Interventions, both pharmacologic and nonpharmacologic, can improve all of these risk factors and decrease the incidence of cardiovascular disease (CVD) and its consequences such as MI, angina, congestive heart failure, and stroke. In this article, we will review the nonpharmacologic treatment of dyslipidemia. Recent guidelines by the National Cholesterol Education Program recommend more aggressive control of serum lipids to reduce the incidence of CHD. Nutritional and dietary therapy, weight loss, exercise, and scientifically proven nutritional supplementation should be used initially in appropriately selected patients to manage dyslipidemia. Hypertriglyceridemia, frequently due to obesity, insulin resistance, metabolic syndrome, and diabetes mellitus, deserves special attention. Pharmacologic therapy should be administered in those cases that are at high or very high risk for CHD or who do not respond to nondrug therapy. Many patients prefer nondrug therapies for many reasons including adverse effects of antilipid drugs, contraindications or allergic reactions to drugs, perceptions of adverse effects of drugs, or personal

This retrospective study, conducted as part of a private practice quality assurance process for patients with coronary artery disease (CAD), compares practice patterns in the LIFEHELP lipid clinic and non–lipid clinic settings at the Heart Institute of St. Petersburg. Quality assurance parameters included documentation of low-density lipoprotein (LDL) cholesterol, initiation of lipid-lowering therapy, and achievement of the Second National Cholesterol Education Program (NCEP II) goal for CAD patients of LDL cholesterol ≤100 mg/dL. A total of 934 patient charts with ICD-9 codes of 410–414 for ischemic heart disease were randomly selected and reviewed by a utilization review nurse. A higher level of documentation and treatment of elevated LDL cholesterol to NCEP II goal in CAD patients was found for those followed in the lipid clinic. Among non–lipid clinic physicians, cardiologists documented and treated elevated LDL cholesterol more frequently than primary care physicians. Women and the elderly subgroups received improved care in the lipid clinic setting. Screening activities and risk-factor management by cardiologists within a lipid clinic, therefore, demonstrated an improved standard of care that came closer to achieving national guidelines in the secondary prevention of CAD.

Aneurysm formation in saphenous vein aortocoronary bypass grafts is an extremely rare complication of coronary artery bypass surgery. Aneurysms of native coronary arteries are found in a small percentage of patients at autopsy. Reported is a case with multiple coronary artery aneurysms in which a dissecting aneurysm of the saphenous vein bypass graft also developed following coronary artery bypass surgery. This is the first report of such association.

This study correlated the location and size of posterolateral myocardial infarcts (Mls) measured anatomically with that estimated by quantitative criteria derived from the standard 12-lead ECG. Twenty patients were studied who had autopsy-proved, single, posterolateral Mls and no confounding factors of ventricular hypertrophy or bundle branch block in their ECG. Left ventricular anatomic Ml size ranged from 1 to 46%. No patient had a ≥ 0.04-second Q wave in any electrocardiographic lead and only 55% had a 0.03-second Q wave. A 29-point, simplified QRS scoring system consisting of 37 weighted criteria was applied to the ECG. Points were scored by the ECG in 85% of the patients (range 1 to 8 points). Ml was indicated by a wide variety of QRS criteria; 19 of the 37 criteria from 8 different electrocardiographic leads were met. The correlation coefficient between MI size measured anatomically and that estimated by the QRS score was 0.72. Each point represented approximately 4% Ml of the left ventricular wall.

The effects of oral prazosin (PZ), 15 to 20 mg/day, on symptoms, exercise performance and left ventricular (LV) function were assessed in a 6-month, double-blind, placebo-controlled study of patients in New York Heart Association functional class III. Ejection fraction (EF) was measured at rest and during upright bicycle exercise by equilibrium radionuclide angiography; end-diastolic volume, stroke volume and cardiac output were derived from corresponding count measurements. Although there was no statistically significant difference between clinical responses in the prazosin and placebo groups, qualitative differences suggested a clinical response to prazosin. Of the 9 patients who received PZ, 5 improved to functional class II and 2 became asymptomatic; the 2 nonresponders deteriorated to functional class IV when PZ was stopped. Four of 9 patients who received placebo improved to functional class II and 2 deteriorated to class IV. Exercise time tended to increase in the prazosin group (from 541 ± 204 to 630 ±100 seconds at 6 months) and decrease in the placebo group (from 539 ± 141 to 435 ±148 seconds at 6 months), but neither change was significant. Prazosin effected a sustained decrease in mean blood pressure of approximately 10 mm Hg at rest, and a quantitatively similar but insignificant decrease during exercise. Radionuclide EF increased and LV end-diastolic counts decreased significantly at rest and during exercise in the prazosin group, but not in the placebo group. Because changes in EF and end-diastolic counts were similar, stroke counts and count output were unchanged. Thus, long-term oral PZ therapy caused sustained changes in blood pressure and LV function in most patients in functional class III, but these changes were not uniformly translated into clinical improvement or increased exercise tolerance. Prazosin does not appear to increase cardiac output during exercise in patients with heart failure.

• Histologic pictures have been conflicting in previous cases of quinidine-associated hepatitis. We report a case of reversible granulomatous hepatitis from quinidine hypersensitivity, with granuloma induction occurring within three days after readministration of quinidine. Fever, urticaria, and mild thrombocytopenia were associated clinical findings. Both light and electron microscopic study results are reported. ( Arch Intern Med 140:395-397, 1980)