Effects of calcium channel blocking agents on reperfusion arrhythmias

The effect of the calcium antagonists nifedipine (NF) and diltiazem (DT) on reperfusion after release of circumflex coronary artery (CX) occlusion was studied in open-chest dogs. Dogs were randomized to receive a bolus of 5 μg/kg NF (seven dogs), 1 μg/kg NF (nine dogs), or vehicle (nine dogs). After bolus, high and low dose NF dogs were infused with 1 μg/kg/min NF. All dogs then underwent 30 minutes CX occlusion followed by reperfusion. Dogs that did not develop ventricular fibrillation (VF) in the first 10 minutes of reperfusion were considered survivors. NF caused a dose-related increase in CX blood flow and decrease in mean arterial pressure (MAP), significant at the higher dose. Reperfusion VF occurred in five of nine low dose NF dogs, five of seven high dose NF dogs, and five of nine controls. Another 21 dogs were randomized to receive a bolus of 0.2 mg/kg DT (11 dogs) or vehicle (10 dogs). Infusion rates (and an additional bolus injection, if necessary) were chosen to produce a 10 to 20 mm Hg drop in MAP. CX occlusion and reperfusion were performed as above. Reperfusion VF occurred in 9 of 11 DT dogs vs 8 of 10 controls. Thus neither nifedipine nor diltiazem enhanced survival during reperfusion of myocardium previously subjected to 30 minutes of ischemia.     

Muscle protein catabolism in diabetes: 3-Methylhistidine excretion in the spontaneously diabetic “BB” rat

The muscle protein lost in uncontrolled diabetes may be due to decreased synthesis, increased catabolism, or to any combination of alteration in these rates that results in net loss. Differing methods of examining these rates in vivo and in vitro have given conflicting results. We assessed the rate of catabolism of proteins containing 3-methylhistidine (3-MH) by measurement of its urinary excretion in spontaneously diabetic “BB” Wistar rats. Prior to overt diabetes, rates of excretion were appropriate to the age of the rats (1.46 ± 0.15 μmole/day), with 34%–47% as the nonacetylated form. Accompanying diabetes there was an increase in urine urea nitrogen of two to threefold over 4–14 days, and an increase in ammonium nitrogen of sixfold. 3-MH excretion doubled by 4 days, and 81%–96% was excreted as the nonacetylated form. Subcutaneous insulin in doses sufficient to improve glycosuria and hyperglycemia was associated with normalized total 3-MH excretion (N-acetyl 3-MH plus 3-MH) but a greater proportion than normal appeared in the nonacetylated form. These results suggest that muscle protein catabolism increased with insulin deficiency and that this defect can be corrected by therapy. Both untreated and treated diabetic rats appear to have a limited capacity for acetylation of 3-MH prior to its excretion.     

Long-term endocardial atrial pacing in children with postoperative bradycardia-tachycardia syndrome and limited ventricular access

Permanent pacing in children, including those with postoperative bradycardia-tachycardia syndrome, has been compromised by the availability of pulse generators, electrode leads and implantation techniques designed for the adult patient. Recent technologic improvements and simplified implantation techniques have reduced many of these barriers and have made endocardial as well as epicardial ventricular pacing more feasible. However, in some children, ventricular pacing may be impeded by anatomic abnormalities due to congenital anomalies or prior cardiac operations. In these instances, endocardial atrial pacing may provide an alternative therapeutic approach in selected patients. This report describes the use of endocardial atrial demand pacing in four children with postoperative bradycardia-tachycardia syndrome and restricted ventricular access. This approach controls symptomatic bradycardia, helps prevent and convert paroxysmal intraatrial tachycardia and overcomes the problem of limited ventricular access.     

Termination of ventricular tachycardia with bursts of rapid ventricular pacing

Bursts of rapid ventricular pacing used during 573 episodes of ventricular tachycardia in 23 patients terminated 5 12 episodes (89 percent), with burst rates averaging 56 beats/min above the ventricular tachycardia rate, for 5 to 10 captures. Tachycardia was accelerated by pacing bursts to rates below 300 beats/min in 16 episodes (3 percent); 10 of these terminated spontaneously or responded to further bursts. Acceleration of heart rate to more than 300 beats/min or ventricular fibrillation occurred six times (1 percent), each episode requiring direct current cardioversion. Pacing bursts had no effect in 38 instances (7 percent), mostly in patients with terminal cardiogenic shock. Implantable pacemakers delivering bursts of rapid ventricular pacing were placed in two patients who have used these units at home. No deaths were associated with bursts of rapid ventricular pacing, which is an effective, rapid, pleasant alternative to repeated direct current cardioversion and a useful tool during electrophysiologic testing in patients with recurrent tachycardia.     

Alteration of type A behavior and reduction in cardiac recurrences in postmyocardial infarction patients

Eight hundred sixty-two postmyocardial infarction patients volunteered to be randomly selected and enrolled into: (1) a control section of 270 patients, who received group cardiologic counseling; and (2) an experimental section of 592 patients, who received group type A behavior counseling in addition to group cardiologic counseling. Reduction in type A behavior at the end of 3 years was observed in 43.8% of the 592 participants, who initially were enrolled to receive group cardiologic and type A behavioral counseling. This degree of behavioral reduction was significantly greater than that observed in participants who initially were enrolled to receive only group cardiologic counseling. The 3-year cumulative cardiac recurrence rate was 7.2% in participants who initially were enrolled to receive group cardiologic and type A behavioral counseling. This was significantly less (p less than 0.005) than that (13%) observed in participants who initially were enrolled to receive only cardiologic counseling. This difference in recurrence rates was due to a lesser incidence of nonfatal infarctions in the patients who had been enrolled in the section receiving type A behavioral as well as cardiologic counseling. These data suggest that type A behavior can be altered in a sizable fraction of postinfarction patients and that such alteration is associated with a significantly reduced rate of nonfatal myocardial infarctions.     

Influenza A/Philippines/2/82 outbreak in a nursing home: Limitations of influenza vaccination in the aged

The failure of the 1982-1983 influenza vaccine to protect elderly NHCU residents from clinical infection with influenza A/Philippines/2/82 resulted primarily from antigenic drift of the epidemic strain, inasmuch as the attack rates in the vaccinated and nonvaccinated patients were not significantly different. This experience supports the decision to replace A/Bangkok/1/79 with A/Philippines/2/82 virus antigen in the 1983-1984 influenza vaccine.     

Reactive hypoglycemia.

The hypoglycemoses include a large category of distinctly unique entities. Guidelines for a clinical, physiological approach to these disorders is presented. Within this diagnostic spectrum of hypoglycemia lies the reactive hypoglycemic disorders that are characterized by their postprandial onset, adrenergic mediated symptoms, and relatively benign causes. The spectrum of reactive hypoglycemia includes early alimentary-reactive hypoglycemia, late diabetic-reactive hypoglycemia, hormonal deficiency states, and idiopathic hypoglycemia. A new postprandial hypoglycemic disorder, fructose 1-6 diphosphatase, can be added to this list. The frequent sampling of blood-glucose values in the postprandial state will frequently lead to the finding of a biochemically low blood-glucose value of below 50 ml/100 ml, and these individuals show no hypothalamic-pituitary-adrenal stress to the low blood sugar and do not manifest adrenergic symptoms. Their low blood-glucose value simply reflects the transition in intermediary metabolism between the fed and fasting state and provides a biochemical marker of this event. We refer to this asymptomatic biochemical event as transitional low blood-glucose state. It has no clinical implication and may frequently be confused with the bona fide reactive hypoglycemic disorders. Using a symptomatic, counter-regulatory model to define hypoglycemia as a bona fide disorder, findings are presented in patients with the varying types of reactive hypoglycemia, and their results are compared to normal controls and to a weight-matched and disease patient controls. Abnormalities in insulin secretion are discussed as relating to the pathophysiology causal in the hypoglycemia. An approach to therapy is presented based upon the classification of the patient as to the type of hypoglycemia and their abnormalities in insulin secretion.