Osteoporosis, osteopenia, and atherosclerotic vascular disease

Older women with low bone mineral density (BMD) have a higher prevalence of atherosclerotic vascular disease (coronary artery disease, ischemic stroke, or peripheral arterial disease) than older women with normal BMD. Three coronary angiographic studies have shown that low BMD is associated with obstructive coronary artery disease. Low BMD has been shown to be associated with stress test-induced myocardial ischemia, reduced exercise capacity, and with aortic valve calcification. Women with osteoporosis have an increased risk for cardiovascular events. Treatment of osteoporosis or osteopenia should include therapeutic measures to prevent cardiovascular events

Peripheral arterial disease of the lower extremities

Persons with peripheral arterial disease (PAD) are at increased risk for all-cause mortality, cardiovascular mortality, and mortality from coronary artery disease. Smoking should be stopped and hypertension, dyslipidemia, diabetes mellitus, and hypothyroidism treated. Statins reduce the incidence of intermittent claudication and improve exercise duration until the onset of intermittent claudication in persons with PAD and hypercholesterolemia. The serum low-density lipoprotein cholesterol should be reduced to < 70 mg/dl. Antiplatelet drugs such as aspirin or clopidogrel, angiotensin-converting enzyme inhibitors, and statins should be given to persons with PAD. β-Blockers should be given if coronary artery disease is present. Cilostazol improves exercise time until intermittent claudication. Exercise rehabilitation programs should be used. Revascularization should be performed if indicated

Management of Cardiac Hemochromatosis

Iron-overload syndromes may be hereditary or acquired. Patients may be asymptomatic early in the disease. Once heart failure develops, there is rapid deterioration. Cardiac hemochromatosis is characterized by a dilated cardiomyopathy with dilated ventricles, reduced ejection fraction, and reduced fractional shortening. Deposition of iron may occur in the entire cardiac conduction system, especially the atrioventricular node. Cardiac hemochromatosis should be considered in any patient with unexplained heart failure. Screening for systemic iron overload with serum ferritin and transferin saturation should be performed. If these tests are consistent with iron overload, further noninvasive and histologic confirmation is indicated to confirm organ involvement with iron overload. Cardiac magnetic resonance imaging is superior to other diagnostic tests since it can quantitatively assess myocardial iron load. Therapeutic phlebotomy is the therapy of choice in nonanemic patients with cardiac hemochromatosis. Therapeutic phlebotomy should be started in men with serum ferritin levels of 300 mug/l or more and in women with serum ferritin levels of 200 mug/l or more. Therapeutic phlebotomy consists of removing 1 unit of blood (450 to 500 ml) weekly until the serum ferritin level is 10 to 20 mug/l and maintenance of the serum ferritin level at 50 mug/l or lower thereafter by periodic removal of blood. Phlebotomy is not a treatment option in patients with anemia (secondary iron-overload disorders) nor in patients with severe congestive heart failure. In these patients, the treatment of choice is iron chelation therapy