During the 1970s, emphasis increased in clinical practice on early ambulation and exercise-based rehabilitation after myocardial infarction and other cardiac illnesses or procedures. This shift was based on the belief that exercise and improved conditioning would improve prognosis. We examine the evidence supporting this assertion. Most of the reports on cardiac rehabilitation are about patients who have coronary artery disease and a history of myocardial infarction. The review, therefore, is focused primarily on the patient who has had a myocardial infarction. Effects of cardiac rehabilitation, emphasizing exercise treatment and conditioning, are reviewed with regard to patient outcomes, including changes in functional (work) capacity, psychosocial functioning and health-related knowledge, risk factor modification, morbidity and mortality, and cardiac function. The safety of cardiac exercise programs is reviewed, and the use of telemetry monitoring is considered. We also discuss the role of cardiac rehabilitation in categories of patients other than those with myocardial infarction and the application of newer approaches to rehabilitation such as programs based in the patient's home.

To review the history, basic defect, pathogenesis, clinical manifestations, diagnosis, and treatment of nephropathic cystinosis.

During the past decade, the therapy for stable angina pectoris has greatly expanded with the introduction of the calcium-channel blockers. Initially studied as monotherapy, these agents have been regularly used in combination with other antianginal medications, most notably the beta-adrenergic blockers. Although there are pharmacologic rationales for combining these agents, in daily practice, the major impetus for combination therapy is continuing angina during monotherapy. At least one well-conducted double-blind study was done to confirm that diltiazem, verapamil, and nifedipine each can markedly improve both subjective and objective measures of efficacy when used in combination with a beta-blocker. However, individual patient responses are of chief importance. Many persons do better with monotherapy than with combination treatment. The offsetting hemodynamic effects of nifedipine and a beta-blocker generally work well together; however, minor side effects are not infrequent. In the patient with underlying conduction system disease, this combination is clearly preferable. Diltiazem with a beta-blocker is usually well-tolerated, with a low incidence of adverse effects, similar to the experience with diltiazem monotherapy. Verapamil in conjunction with a beta-blocker warrants the greatest concern; approximately 10% to 15% of patients will have significant bradycardia, heart block, hypotension, or congestive failure. When these agents are used concurrently, reduced dosages, especially of the beta-blocker, will likely result in a lower incidence of adverse effects with maintained efficacy.

Recent developments in health care are strikingly congruent with a Marxist paradigm. For many years small scale owner producers (physicians) dominated medicine, and the corporate class supported the expansion of services. As health care expanded, corporate involvement in the direct provision of services emerged. This involvement is reflected not only in the rise of for-profit providers, but also in the influence of hospital administrators, utilization review organizations, insurance bureaucrats, and other functionaries unfamiliar with the clinical encounter, but well versed on the bottom line. Corporate providers' quest for increasing revenues has brought them into conflict with corporate purchasers of care, whose employee benefit costs have skyrocketed. This intercorporate conflict powerfully shapes health policy and has caused the rapid proliferation of health maintenance organizations and other forms of prospective payment. Corporate purchasers of care favor the incentives under prospective payment for providers to curtail care and its costs. For corporate providers, prospective payment has allowed increased profits even in the face of constrained revenues, because reimbursement is disconnected from resource use. Unfortunately, this corporate compromise serves patients and physicians poorly. Alternative policy options that challenge corporate interests could save money while improving care.

Thirty-two studies (2889 subjects) that investigated the prevalence of the causes of dementia were critically reviewed. Particular attention was paid to potential and actual reversibility. Although dementia manifests itself primarily in old age (particularly age 75 and older), the mean age of patients for the studies that reported age data (56%) was 72.3 years. Twenty-five studies originated from secondary or tertiary centers, and four were community-based. Dementias consisted of Alzheimer disease, 56.8%; multi-infarct, 13.3%; depression, 4.5%; alcoholic, 4.2%; and drugs, 1.5%. No single other cause contributed more than 1.6% of the cases. Potentially reversible causes made up 13.2% of all cases. However, the more important question of whether patients with potentially reversible causes were followed and reversal actually seen was not always examined. In 11 studies (34%) that provided follow-up, 11% of dementias resolved, either partially (8%) or fully (3%). The commonest reversible causes were drugs, 28.2%; depression, 26.2%; and metabolic, 15.5%. Due to the presence of various biases (selection, lack of "blinded" investigators, and others) in the surveyed works, it is probable that the true incidence of reversible dementias in the community is even lower than that reported. Research implications as well as a conservative approach to the workup of a new case of dementia are offered.

Cardiovascular disease is a major clinical problem in the elderly, with coronary heart disease the most frequent cause of death and with hypertension present in as many as 50% of these patients. The cardiovascular manifestations of aging must be differentiated from those due to disease. There are clinical manifestations and responses to therapy in the elderly that differ from those in younger patients. The extent of diagnostic and therapeutic procedures undertaken should be based on the patient's physiologic age, the presence and severity of concomitant diseases, mental status and cognitive ability, and the patient's expectations from medical care. Preventive approaches are also warranted.

Hematologic management of adults with cyanotic congenital heart disease has received little recent attention. The lack of practical therapeutic guidelines prompted us to consolidate our observations on 124 cyanotic adults for general physicians, cardiologists, and hematologists who care for these patients. Specific attention focused on regulation of erythrocyte mass and concepts of compensated and decompensated erythrocytosis, symptoms of deficient tissue oxygen transport, hyperviscosity and iron deficiency, the potential relation between elevated hematocrit levels and brain injury, hemostasis, urate metabolism, and renal function. Cerebral infarction was not seen in any patient. Phlebotomy is best reserved for treatment of symptomatic hyperviscosity. Iron therapy is indicated for symptomatic iron deficient erythropoiesis. Abnormal hemostatic mechanisms are the rule. Antithrombotic medications have little or no role in treatment. Hyperuricemia is the result of abnormal renal uric acid excretion not urate overproduction, and serves as a marker of abnormal renal function. Drugs that promote urate excretion are the preferred maintenance treatment in symptomatic hyperuricemic patients.

Silent myocardial ischemia has emerged from a subject of mainly research interest to one with important clinical implications for practicing physicians. Although the pathophysiologic mechanisms responsible for the absence of pain are still not clear, it is apparent that episodes of silent myocardial ischemia are frequent and occur in many patients with coronary artery disease; episodes occur both in asymptomatic and symptomatic patients; episodes are detectable by various noninvasive and invasive techniques; and episodes appear to have important prognostic implications when combined with the extent of anatomic disease and degree of left ventricular dysfunction. It is expected the rapidly accumulating prognostic data, especially in patients after infarctions and patients with unstable angina, will have a profound effect on the way physicians treat their patients with coronary artery disease.

The clinical and biological features of Alzheimer disease are not uniform in their expression; heterogeneity is evident in the disease's clinical, anatomic, and physiologic characteristics. The presence of considerable intersubject and intrasubject heterogeneity suggests that subtypes of the disease exist. We define subtypes of Alzheimer disease in regard to the behavioral features (for example, predominant right or left hemisphere, or symmetrical impairment), inheritance (familial or sporadic), dosage of chromosome 21 (presence of the Down syndrome), time course of progression, age of onset (presenile or senile), and presence or absence of motor deficit (myoclonus or signs of an extrapyramidal syndrome). Studies of regional cerebral glucose metabolism with positron emission tomography and [18-fluorine] fluorodeoxyglucose show focal alterations in glucose use, with cerebral metabolic asymmetries in patients with Alzheimer disease that are related to the nature of the cognitive deficit. Serial roentgenographic computed tomographic studies show heterogeneous rates of lateral ventricle enlargement in the disease that are related to rates of cognitive decline. Similar anatomic and physiologic abnormalities are also found in persons 45 years of age or older who have the Down syndrome. Furthermore, patients with Alzheimer disease who have extrapyramidal dysfunction or myoclonus are a distinct subgroup, with specific abnormalities of central monoamine markers of dopamine metabolism, serotonin metabolism, and the hydroxylation cofactor, biopterin. The concept of subtypes in Alzheimer disease serves as a model with which the interactions of genetic influences with environmental factors can be examined.

Tamoxifen, an antiestrogen, is a competitive inhibitor of estradiol, blocking its effects on the target organs. During the 10 years it has been used in the United States it has become preferred over estrogens for treating postmenopausal women with metastatic breast cancer. Recently, tamoxifen has been used in treating premenopausal women with recurrent breast cancer, and its efficacy has been proved equal to that of ovarian ablation. In comparative trials, tamoxifen has been as effective as alternative endocrine treatments, and has greatly reduced toxicity and no irreversible side effects. Because of the high risk for systemic relapse in patients with breast cancer with regional lymph node metastases, (stage II), tamoxifen has been evaluated as adjuvant therapy after local treatment of the tumor. The results of these trials have shown a significant increase in the disease-free survival of postmenopausal women treated with tamoxifen, particularly in patients with hormone-receptor-positive tumors. Tamoxifen has not been as useful as adjuvant treatment in premenopausal women, for whom combination chemotherapy is the treatment of choice.

Modification of risk factors in patients who have had myocardial infarctions has received little attention in the literature. Yet, major modifiable risk factors for recurrent coronary heart disease, including hypertension, smoking, increased serum cholesterol levels, sedentary lifestyle, and obesity are the same risk factors for its development. Although coronary atherosclerosis is already established in patients who have had a myocardial infarction, evidence suggests that important reductions in recurrent coronary heart disease and death can be achieved through secondary prevention programs that modify risk factors. The high risk for recurrence and mortality in patients who survive a heart attack means that substantial reductions in the rates of these events can be achieved with relatively small reductions in risk factors. Patients who have had a myocardial infarction are also active participants in health care and are likely to be highly motivated to modify their risks for cardiac disease.