Bundle branch block in acute myocardial infarction. Current concepts and indications.

The blood supply to the conducting system is reviewed. As a result of discrete lesion in individual coronary arteries, specific patterns of conduction disturbances arise during myocardial infarction. Inferior wall infarctions produce relatively benign arrhythmia with blocks proximal to the bundle of His. Anterior infarctions tend to produce malignant arrhythmias, with blocks distal to the bundle of His. The appearance of intraventricular conduction blocks and bundle branch blocks may often be the only indication of the development of high grade atrioventricular block. The mortality of patients post-myocardial infarction with different conduction disorders increases but varies according to the nature of the conduction disturbance. Based upon such information, recommendations for temporary and permanent pacing are developed.

Capillary Ultrastructure in Thermally Stressed Paired Digital Biopsies in Man.

Two digital biopsies were removed from the fingertips of each of 5 subjects--one in a cold environment and the other in a warm environment. Electronmicroscopic examination of the capillaries within the dermis revealed a pleated, contracted endothelial lining in the cold, with encroachment of the lumen by projecting nuclei and cytoplasm. Biopsies from the warm fingertips were dilated in appearance and had more microvillous processes and vesicles.Contraction and dilation of capillaries under physiologic thermal variation would appear to result from swelling of endothelium and consequent occlusion of the lumen.

Potassium metabolism in the normal and ischemic heart cell.

Potassium is an important electrolyte in heart cells and has the greatest membrane permeability in the unexcited state. Hence it is responsible for th generation of the resting membrane potential. Clinical disorders of conduction and impulse formation occur within physiological values of serum potassium. Potassium is indirectly involved in excitation-contraction coupling, and its relation to intracellular calcium metabolism is reviewed. While potassium movements within the cell are metabolic-dependent, it is also true that the activity of metabolic pathways is affected by changes in potassium concentration. During anoxia and ischemia, sodium and calcium are gained by the myocyte, and potassium and magnesium are lost by the cell. At the same time, the action potential duration is abbreviated, the slope of the action potential downstroke (phase 2) is increased, and the resting membrane potential may be reduced. A relationship between disturbances in intracellular potassium and ischemic arrhythmias appears likely.

Reduction in myocardial infarct size: prevention of heart cell death.

The course of myocardial necrosis, the clinical syndrome, and methods of treatment are presented. Heart cell death may be prevented by maintaining the balance between myocardial oxygen and energy supply and consumption. New technics of improving this balance by reducing myocardial energy demand, altering metabolism, increasing myocardial substrate supply, and protecting cellular integrity are discussed.

Glucose-insulin-potassium (GIK) therapy for ischemic heart disease.

In 1912 Goulston advocated glucose therapy for several different kinds of heart disease, and in 1933 Shirley-Smith recommended glucose and insulin for coronary artery disease. Thirty years later, Laborit noted that treatment of rabbits with glucose and insulin prevented ventricular fibrillation induced by potassium chloride solutions. Sodi-Pallares et al, pioneers in glucose-insulin-potassium (GIK) therapy for heart disease, showed not only that potassium may be a major excitant in the genesis of ventricular tachycardia in the ischemic heart but that GIK solution was capable of enhancing oxidative phosphorylation in the ischemic heart. Interest in GIK therapy for ischemic heart disease has been renewed as the effects of GIK solutions on myocardial infarct size, metabolism and electrical properties are better understood. In this paper, selected new information regarding the actions of GIK and the clinical applications will be reviewed.

Insulin: fundamental mechanism of action and the heart.

Insulin accelerates the entry of glucose and amino acids into muscle cells by acting upon the 'carrier-facilitated' transport mechanism. For glucose this process is passive and leads to equilibration of intracellular and extracellular concentrations. In heart muscle, glucose transport is a rate-limiting step for glucose uptake. During hypoxia and ischemia the heart turns to anaerobic glycolysis for energy production and therefore, maximal glucose transport becomes important. Insulin is necessary to insure proper protein synthesis, probably at the level of membrane-bound polyribosomes. However, during myocardial hypoxia, insulin alone cannot restore the associated depression in protein synthesis. Although insulin hyperpolarizes the cell, a change in the ratio of intracellular to extracellular activities of potassium is not its primary mode of action. An insulin-induced configurational change in the plasma membrane could simultaneously account for the effects of insulin on sodium and potassium permeability and the action on facilitated transport. Intracellular levels of cyclic adenylate may be reduced by insulin in adipose tissue because of inhibition of adenyl cyclase or stimulation of phosphodiesterase. However, at this time there is little evidence that insulin alters cyclic AMP levels in the heart. Insulin secretion is depressed in patients with heart disease in proportion to the reduction of cardiac index sustained. Since the ischemic heart is dependent upon glucose as the major fuel, insulin lack may deprive the heart of adequate substrate.

Glucocorticoid therapy for acute myocardial infarction.

Several uncontrolled early studies established that corticosteroid administration to patients with ischemic heart disease and cardiogenic shock was relatively safe. Whether or not the glucocorticoids were of benefit or not remained unclear when mortality was used as an index of efficacy. Hemodynamically, glucocorticoids may decrease peripheral vascular resistance, increase cardiac output and coronary blood flow, but leave myocardial contractility unchanged. The mean arterial pressure may vary unpredictably. The increase in coronary blood flow may certainly be advantageous in treating patients with acute myocardial infarction. The decrease in infarct size recently reported, if confirmed in man, would also be desirable. However, there is a paucity of good data concerning the effects of corticosteroids in man postinfarction. In addition, through unproved mechanisms, the corticosteroids decrease the extent and severity of myocardial ischemic injury. While these fundamental actions may not result in improved mortality, ongoing studies suggest that minimization of ischemic injury may ultimately prove to be most rewarding in the prevention of cardiogenic shock.