Glucocorticoid treatment in patients with septic shock: effects on vasopressor use and mortality.

Corticosteroids were proposed for the treatment of sepsis as early as 1940. Several RCTs cast serious doubts on the usefulness of high dose corticosteroids and doubt still persists regarding the efficacy of replacement therapy. Adrenal insufficiency (non-responders to the 250 microg corticotropin test: increase in cortisol < 9 microg/dl) is present in about half of patients with septic shock and is associated with higher rates of refractory hypotension and mortality. Peripheral glucocorticoid resistance, which may even occur more frequently, can be easily assessed at bedside using skin tests. Cortisol antagonizes the migration of inflammatory cells, the synthesis or action of virtually all proinflammatory mediators, promotes virtually all anti-inflammatory components and enhances humoral immunity by means of transcriptional interference between its receptor and both AP-1 and NF-kappaB. Cortisol mediates cardiovascular tolerance to endotoxin and the maintenance of vascular sensitivity to catecholamines. Low doses (about 300 mg daily for 5 days or more) of hydrocortisone increase vasoconstrictor response to catecholamines in animals, in healthy volunteers challenged with LPS and in several RCTs. Hydrocortisone also increases arterial pressure and decreases the duration of shock. A meta-analysis of all available clinical controlled studies showed a reduction in 28 days, all-cause mortality with glucocorticoids (RR = 0.88, 95% CI: 0.78 - 1.00; p = 0.04). However, there was a significant heterogeneity across the trials (p = 0.006). On the other hand, analysis of studies where low doses of glucocorticoids were given for prolonged periods showed a 24% reduction in the risk of all-cause mortality at 28 days in treated patients (RR = 0.76, 95% CI: 0.64 - 0.90; p = 0.002) without heterogeneity across the trials (p = 0.28). In conclusion, in severe sepsis, high doses of corticosteroids should not be given. Septic shock should be treated with a replacement dose of hydrocortisone.

The impact of transtelephonic documentation of arrhythmia on morbidity and mortality rate in sudden death survivors.

A post hospital follow-up system based on predetermined antiarrhythmic strategies and telephone transmitters used to record ECGs was helpful in managing post hospital course and improved survival in patients with a history of out-of-hospital sudden death. All patients underwent therapy guided by serial electrophysiologic testing. Of the 47 patients, 19 used the telephone transmitter system and 28 did not. During follow-up, residual symptomatic and silent ventricular arrhythmia was documented in 78% of patients using telephone transmitters. Ventricular tachycardia was transmitted in six patients--all survived. During an average 15-month follow-up, 1 of 19 patients using the telephone transmitter system died vs 12 deaths among the 28 patients who did not use the system (p less than 0.005). These results were independent of ejection fraction, presence of congestive heart failure, amiodarone therapy, and the outcome on electrophysiologic therapy. Thus, patients with a history of out-of-hospital sudden death, discharged following electrophysiologic guided therapy, require repeated antiarrhythmic dose titration for side effects or residual ventricular arrhythmia. Prompt diagnosis and treatment of potentially fatal arrhythmia is crucial and feasible, especially with regular ECG checks through telephone transmission.

Effect of propranolol after acute myocardial infarction in patients with congestive heart failure.

The incidence of congestive heart failure was studied in the Beta Blocker Heart Attack Trial in which postmyocardial infarction patients between the ages of 30 and 69 years, with no contraindication to propranolol, were randomly assigned to receive placebo (n = 1921) or propranolol 180 or 240 mg daily (n = 1916) 5 to 21 days after admission to the hospital for the event. Survivors of acute myocardial infarction with compensated or mild congestive heart failure, including those on digitalis and diuretics, were included in the study. A history of congestive heart failure before randomization characterized 710 (18.5%) patients: 345 (18.0%) in the propranolol group and 365 (19.0%) in the placebo group. The incidence of definite congestive heart failure after randomization and during the study was 6.7% in both groups. In patients with a history of congestive heart failure before randomization, 51 of 345 (14.8%) in the propranolol group and 46 of 365 (12.6%) in the placebo group developed congestive heart failure during an average 25 month follow-up. In the patients with no history of congestive heart failure, 5% in the propranolol group developed congestive heart failure and 5.3% in the placebo group developed congestive heart failure. Baseline characteristics predictive of the occurrence of congestive heart failure by multivariate analyses included an increased cardiothoracic ratio, diabetes, increased heart rate, low baseline weight, prior myocardial infarction, age, and more than 10 ventricular premature beats per hour.(ABSTRACT TRUNCATED AT 250 WORDS)

Serum, red blood cell and whole blood magnesium in patients with uncomplicated acute myocardial infarction.

Serum, whole blood and red blood (intracellular) magnesium determinations were made in 52 patients, without other factors predisposing to hypomagnesemia, admitted to a coronary care unit. Acute uncomplicated myocardial infarction was documented in 31 and the serum cardiac enzymes as well as the electrocardiogram remained nondiagnostic in 21 patients. There was no significant difference in the serum magnesium level in the two groups. An increasing trend with time was noted in the serum (p less than 0.001) and whole blood magnesium (p less than 0.005) during the first 4 days postmyocardial infarction. The whole blood magnesium as well as the red blood (intracellular) magnesium was higher (p less than 0.01) in myocardial infarction patients. There was no significant difference in the hematocrit or other electrolytes during this time.

Clinical hypomagnesemia, coronary spasm and cardiac arrhythmia.

The case report demonstrates another case of hypomagnesemia with electrocardiographic evidence of acute myocardial ischemia due to coronary spasm. The patient was successfully treated with intravenous, followed by oral, magnesium sulfate. Magnesium therapy may be justified especially in patients with prolonged QT intervals, cardiac arrhythmias and hypokalemia with hypomagnesemia.

Efficacy and safety of esmolol vs propranolol in the treatment of supraventricular tachyarrhythmias: a multicenter double-blind clinical trial.

The efficacy and safety of intravenous esmolol infusion was compared to that of intravenous propranolol injection in patients with supraventricular tachyarrhythmias (SVT) in a multicenter double-blind parallel study. A total of 127 patients were randomized to either the esmolol (n = 64) or propranolol (n = 63) group. Therapeutic response was achieved in 72% of esmolol and 69% of propranolol patients (p = NS). The average dose of esmolol in responders was 115 +/- 11 micrograms/kg/min. Therapeutic response was sustained in the 4-hour maintenance period in 67% of esmolol and 58% of propranolol patients (p = NS). Rate of conversion to normal sinus rhythm was similar in the two treatment groups. After discontinuation, rapid recovery from beta blockade (decrease in heart rate reduction) was observed in esmolol patients (within 10 minutes) compared to propranolol patients (no change in heart rate up to 4.3 hours). The principal adverse effect was hypotension, reported in 23 esmolol (asymptomatic in 19) and four propranolol (asymptomatic in three) patients. In the majority of esmolol patients, hypotension resolved quickly (within 30 minutes) after esmolol was discontinued. It was concluded that esmolol was comparable in efficacy and safety to propranolol in the treatment of patients with SVT. Unlike propranolol, because of the short half-life of esmolol, rapid control of beta blockade is possible with esmolol in clinical conditions when required.

Relationship of psychologic factors to frequent symptomatic ventricular arrhythmia.

Since there is very little available systematic information on the psychological profile of patients with cardiac arrhythmia, a battery of 12 standardized personality inventories was administered to 102 patients ranging in age from 19 to 69 years. Thirty-eight patients with frequent ventricular premature beats (more than 30 per hour) without myocardial infarction were significantly more psychologically symptomatic than 34 age- and sex-matched general medical/surgical patients. The variables found to be significant portray the patient with frequent ventricular premature beats without myocardial infarction: high scores for hysteria, less moral orientation, more anxiety, depression and social alienation, and an inhibited and low respectful style. This combination of psychological variables produced a discriminant function (p less than 0.001) that accounted for 53 percent of the variance between the arrhythmia/no myocardial infarction group and the medical/surgical control group and could correctly predict group membership in 83.3 percent of cases. These results may have further implications in nonpharmacologic and psychotropic adjuncts to antiarrhythmic therapy.

Observations on serum and red blood cell magnesium changes in treadmill exercise-induced cardiac ischemia.

To evaluate changes in magnesium levels with treadmill exercise-induced coronary insufficiency, 59 consecutive patients were studied. In addition to electrocardiographic monitoring, hematocrit, total protein, whole blood, serum and red blood cell magnesium determinations were made before and after exercise testing. Fifteen patients had positive exercise test, 18 did not complete, and 26 had negative exercise test. There was no significant difference in the serum and red blood cell magnesium on the basis of stress test results for ischemia. Although whole blood magnesium, hematocrit, and total proteins increased (P less than .05) in both groups, we did not find a significant change in magnesium homeostasis.

Effects of nadolol on the spontaneous and exercise-provoked heart rate of patients with chronic atrial fibrillation receiving stable dosages of digoxin.

Nadolol, a long-acting beta-adrenergic-blocking agent, was evaluated in 20 patients with chronic atrial fibrillation by means of a randomized, double-blind, crossover study. Patients were required either to demonstrate resting heart rates in excess of 80 bpm or to show a rate of 120 bpm or an increment of greater than 50 bpm during mild treadmill exercise provocation (3 minutes, 1.75 mph, 10% grade). With placebo the group averaged a heart rate of 92 +/- 19 bpm, determined by 24 hours of ambulatory ECG recordings; this rate was significantly reduced to 73 +/- 16 bpm (p less than 0.001) with nadolol (mean dosage, 87 +/- 43 mg/day). During standardized exercise testing, heart rates increased to 153 +/- 26 bpm with placebo and to 111 +/- 24 bpm with nadolol (p less than 0.001), representing 65% and 52% increments, respectively. Digoxin blood levels averaged 0.8 +/- 0.5 ng/ml with placebo and were similar with nadolol (0.9 +/- 0.4; p = NS). Total exercise time on a modified Bruce treadmill protocol was 466 +/- 143 seconds with placebo and was significantly decreased by nadolol (380 +/- 143; p less than 0.01). During initial dose titration with nadolol, one patient was dropped from study for intolerable fatigue and one for worsened claudication. No patients were dropped from the double-blind treatment periods, although two patients receiving nadolol and one patient receiving placebo complained of moderate fatigue. We conclude that nadolol is a safe and effective agent for the control of spontaneous and exercise-provoked heart rates in patients with chronic atrial fibrillation who were already receiving digoxin treatment.

Severe thrombocytopenia as a result of contrast left ventricular angiography.

A case report of a 29-year-old Hispanic male who developed an acute thrombocytopenic reaction immediately following a cardiac catheterization using Hypaque-M radiographic dye. Laboratory studies immediately post-catheterization revealed a platelet count of 11,000 with a subsequent further drop to a low of 4,000. A need for the prompt identification and possible causes of this unusual reaction are discussed. Recovery occurred following treatment with corticosteroids.

Characteristics of ventricular ectopic beats in patients with ventricular tachycardia. A 24-hour Holter monitor study.

A total of 99 consecutive 24-hour Holter recordings with ventricular tachycardia were reviewed. Ventricular premature beats which occurred alone, and ventricular premature beats which initiated ventricular tachycardia were examined to determine which characteristics correlated with occurrence of ventricular tachycardia and which predicted rate and duration of ventricular tachycardia. The preceding R-R interval, the coupling interval, and a ratio of the two were examined. We found that ventricular tachycardia rate and duration increase with a shorter coupling interval, and the coupling interval/preceding R-R ratio was significantly different in single beats not initiating ventricular tachycardia. The ratio for the beat initiating ventricular tachycardia was smaller, indicating more prematurity.