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Approximately 80% of all patients with diabetes die of cardiovascular disease. The traditional management of type 2 diabetes has been ineffective in altering this dismal prognosis. Insulin resistance is the fundamental defect of type 2 diabetes. Insulin resistance often leads to hyperinsulinemia, which is associated with hypertension, atherogenic dyslipidemia, left ventricular hypertrophy, impaired fibrinolysis, visceral obesity, and sedentary lifestyle. Although all these conditions are associated with atherosclerosis and adverse cardiovascular events, the therapeutic efforts in patients with diabetes have focused predominantly on normalizing glucose levels. Improved insulin sensitivity through lifestyle modifications or pharmacologic therapy (troglitazone and metformin) will lower both insulin and glucose levels as well as diminish dyslipidemia and hypertension. In contrast, sulfonylurea agents lower glucose by increasing insulin levels and may increase the risk of cardiovascular events. Therapy including aspirin, lipid agents (for example, statins), angiotensin-converting enzyme inhibitors, beta-adrenergic blockers, postmenopausal estrogen replacement, and vitamin E should be considered for patients with type 2 diabetes. In most patients with diabetes who have multivessel coronary artery disease, coronary artery bypass grafting is superior to coronary angioplasty for improving long-term cardiovascular prognosis. This superiority is mediated in part by the use of a left internal mammary graft to the left anterior descending coronary artery. Urgent coronary angioplasty or thrombolytic therapy should be considered for all patients with diabetes who have acute myocardial infarction.

Objective: To present information about risk factor clustering and the oxidation hypothesis of atherosclerosis and attempt to synthesize these facts into a clinically relevant approach to patients with or at risk for coronary artery disease (CAD)., Material and Methods: The total cholesterol level is a relatively weak marker for the risk of CAD. The levels of both high-density lipoprotein (HDL) cholesterol and remnants of triglyceride-rich lipoproteins and the inherent susceptibility of the low-density lipoprotein (LDL) particles to oxidative modification may be as important as the total or LDL cholesterol levels. LDL cholesterol must undergo oxidative modification by means of oxygen free radical processes before it becomes atherogenic. Patients with high levels of oxidative stress include those with risk factor clustering or insulin resistance (or both). Such patients are characterized by hypertension, truncal obesity, hypertriglyceridemia, depressed HDL cholesterol levels, and increased insulin levels. They also have increased levels of triglyceride-rich remnant lipoproteins and LDL particles that are characterized by their small dense nature and pronounced predisposition to oxidative modification., Results: Biologic antioxidants seem to be promising therapy for the prevention of atherogenesis. Although long-term prospective data are not yet available, vitamin E has been shown to be effective in both animal and human models in preventing LDL oxidation, and it may have a role in the prevention of CAD. A healthy diet of fresh fruits, vegetables, and whole grains is beneficial because it improves the lipid levels and provides high levels of natural antioxidants. The atherogenic potential of hydrogenated polyunsaturated fats is approximately equivalent to that of saturated fats. Monounsaturated fat is inherently resistant to oxidation and may be protective against CAD. Niacin may be effective in patients with clustered risk factors. It has been found to convert the easily oxidized small dense LDL pattern to the large buoyant oxidation-resistant particles. Hydroxymethylglutaryl-coenzyme A reductase inhibitors are well tolerated and highly effective in decreasing LDL cholesterol, but they are expensive. Estrogen has multiple potentially beneficial effects relative to cardiovascular disease., Conclusion: Persons with or at high risk for CAD should be identified early and aggressively treated with a program that involves lifestyle changes, alterations in dietary intake, and pharmacologic therapy.

Eight men, 45 to 50 years of age, with mild stable angina pectoris, participated in a graduated exercise program. Coronary arteriography, left ventriculography, left ventricular hemodynamics at rest and during supine leg exercise, treadmill testing with electrocardiographic monitoring, and measurement of oxygen uptake were obtained before and 1 year after the exercise training program. No change was noted in the arteriographic appearance of coronary artery lesions or of collateral circulation. Left ventricular performance, assessed by qualitative left ventriculography and the hemodynamic response of the left ventricle to supine leg exercise, was unchanged after the training program. Oxygen consumption for a given repetitive work load during treadmill exercise decreased. Two patients with a pretraining exercise ECG positive for ischemia reverted to a normal response after the exercise program. All had a decrease in angina, an increase in self-esteem, and a more positive attitude toward their work and their disability.