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Biomedical subjects

J F Spann

Publications and source records attributed to J F Spann.

At least 109 records · Page 6Linked to original sources

The hyperlipoproteinemias. A simplified classification and approach to therapy.

It is now clear that the various hyperlipidemias represent a heterogenous group of disorders, each having various clinical and laboratory characteristics, prognosis and treatment. The three disorders commonly associated with premature atherosclerotic vascular disease are Type II (hyperbetalipoproteinemia), Type III ("broad beta" or "floating beta" disease) and Type IV (hyperprebetalipoproteinemia or, endogenous hypertriglyceridemia). The diagnosis of each of these three disorders can be suggested by the fasting serum cholesterol level and the appearance of the fasting serum after it has remained overnight in a refrigerator. Type II disease is characterized by a clear serum and a pronounced to moderate hypercholesterolemia. It is treated by reducing dietary cholesterol and saturated fats, increasing dietary polyunsaturated fats, and cholestyrmine. Type IV disease is characterized by a turbid serum indicating hypertriglyceridemia and a normal or only slightly elevated serum cholesterol level. It is treated with weight reduction, a low carbohydrate diet and clofibrate. Type III disease is characterized by both a turbid serum and increased cholesterol levels. It is treated with weight reduction, a low cholesterol diet and clofibrate. With the treatment of all disorders the lipid values should improve; however, with the treatment of Type III disorder both triglyceride and cholesterol levels return to normal, xanthoma resorb and there is an improvement in the peripheral blood flow, indicating that there has been amelioration of the atherosclerotic process.

Blood Protein Disorders↗

New trends in the treatment of angina pectoris.

Traditionally when considering the pharmacologic basis of therapy in angina pectoris, attention is focussed on alterations of coronary blood flow. Yet the diseased coronary arteries in these patients often do not appear to be capable of responding to vasodilatory drugs. Since the pain of myocardial ischemia is relieved by a number of interventions without an increase in coronary blood flow, the concept herein considered is that angina pector is best viewed as an unfavorable relation between myocardial oxygen requirements and availability. Thus, the clinical value of the major antianginal agents is thought to be based importantly upon their actions to reduce myocardial oxygen consumption rather than to increase coronary blood flow. Sublingual nitroglycerin possesses a powerful dilator effect on veins which reduces venous return and thereby the size of the heart and intra-myocardial tension; thus myocardial oxygen requirements are diminished. The beta-adrenergic receptor blocking drug, propranolol (Inderal(R)), inhibits sympathetic stimulation of the heart at rest and during exercise. Thus, myocardial oxygen requirements are diminished by the reduction in heart rate and diminished contractility. As a result of this latter action, cardiac output is reduced and thereby arterial pressure and intramyocardial tension is lowered. In patients with advanced heart disease and borderline cardiac compensation, propranolol is hazardous because it removes the availability of one of the important reserve mechanisms for maintaining cardiac compensation-the sympathetic support of the failing heart. The introduction of electrical stimulation of the carotid sinus nerves as a means of therapy in patients with angina pectoris has provided a powerful tool for the treatment of patients with refractory ischemic pain.

Angina Pectoris↗

Defective lipid metabolism in the failing heart.

The metabolism of long chain fatty acids was investigated in the failing heart of guinea pigs with chronic constriction of the ascending aorta. Homogenates prepared form failing hearts exhibited (a) a decreased capacity to oxidize palmitic acid (failure = 0.50 +/- 0.06 mumole/g of protein per 20 min; control = 1.09 +/- 0.10); (b) a reduced level of carnitine, a myocardial constituent which serves to control the oxidation rate of long chain fatty acids in the heart (failure = 0.91 +/- 0.10 mumole/g wet weight; control = 1.69 +/- 0.10); and (c) an increased rate of palmitate incorporation into triglycerides and lecithin. Exogenous carnitine effected a restoration of the defective palmitate metabolism of the homogenates towards normal. In contrast to long chain fatty acid oxidation, glucose oxidation by the failing heart was not impaired. As a consequence of this selective lesion in energy substrate utilization, the failing heart might be forced to rely on substrates other than long chain fatty acids for its major energy supply.

Animals↗