Gopal Das

Esmolol versus verapamil in the acute treatment of atrial fibrillation or atrial flutter

The effects of esmolol, an ultrashort-acting beta blocker, and verapamil were compared in controlling ventricular response in 45 patients with atrial fibrillation or atrial flutter, in a randomized, parallel, open-label study. Patients with either new onset (less than 48 hours, n = 31) or old onset (greater than 48 hours, n = 14) of atrial fibrillation or flutter with rapid ventricular rate were stratified to receive esmolol (n = 21) or verapamil (n = 24). Drug efficacy was measured by ventricular rate reduction and conversion to sinus rhythm. The heart rate declined with esmolol from 139 to 100 beats/min (p less than 0.001) and with verapamil from 142 to 97 beats/min (p less than 0.001). Fifty percent of esmolol-treated patients with new onset of arrhythmias converted to sinus rhythm, whereas only 12% of those who received verapamil converted (p less than 0.03). Mild hypotension was observed in both treatment groups. Esmolol compares favorably with verapamil with respect to both efficacy and safety in acutely decreasing ventricular response during atrial fibrillation or flutter. Moreover, conversion to sinus rhythm is significantly more likely with esmolol.

Intravenous sotalol for the termination of supraventricular tachycardia and atrial fibrillation and flutter: A multicenter, randomized, double-blind, placebo-controlled study

Sotalol is an antiarrhythmic agent with combined beta-blocking and class III antiarrhythmic properties. This study was designed to assess the safety and efficacy of sotalol in terminating supraventricular tachycardia (SVT), atrial fibrillation (AFib), and atrial flutter (AFl). Ninety-three patients with spontaneous or induced SVT (n = 45) or AF (AFib or AFl; n = 48) with a ventricular rate of > or = 120 beats/min were studied. In the first phase, the double-blind phase, patients were randomly assigned to receive placebo or intravenous (i.v.) sotalol, 1.0 or 1.5 mg/kg. If SVT or AF did not convert to sinus rhythm or if the ventricular rate did not slow to < 100 beats/min within 30 minutes, patients then entered the second phase, the open-label phase, which also lasted 30 minutes, and were given 1.5 mg/kg iv sotalol. In the SVT group, during the double-blind phase conversion to sinus rhythm occurred in 2 (14%) of 14 of patients who received placebo, 10 (67%) of 15 who received sotalol, 1.0 mg/kg (p < 0.05 vs placebo), and 10 (67%) of 15 who received 1.5 mg/kg sotalol (p < 0.05 vs placebo); during the open-label phase, 1.5 mg/kg i.v. sotalol converted 7 (41%) of 17 of patients. In the AF group, during the double-blind phase conversion to sinus rhythm occurred in 2 (14%) of 14 of patients who received placebo, 2 (11%) of 18 who received 1.0 mg/kg sotalol (p not significant [NS] vs placebo), and 2 (13%) of 16 who received 1.5 mg/kg sotalol (p = NS vs placebo); in these groups, a > 20% reduction of ventricular rate without conversion to sinus rhythm occurred in 0 (0%) of 14, 13 (72%) of 18 (p < 0.05 vs placebo), and 12 (75%) of 16 of patients (p < 0.05 vs placebo), respectively; during the open-label phase, 1.5 mg/kg i.v. sotalol converted 7 (30%) of 23 of patients. The most common adverse events were hypotension and dyspnea. During the double-blind phase they occurred in 10% of patients who received placebo, 9% of those who received 1.0 mg/kg i.v. sotalol (p = NS vs placebo), and 10% of those who received 1.5 mg/kg i.v. sotalol (p = NS vs placebo). Most of these events were mild to moderate, but all were transient and clinically manageable.(ABSTRACT TRUNCATED AT 400 WORDS)

Comparison of the efficacy and safety of esmolol, a short-acting beta blocker, with placebo in the treatment of supraventricular tachyarrhythmias

The efficacy and safety of esmolol, a short-acting intravenous beta-adrenergic-blocking agent, and placebo were compared in patients with supraventricular tachyarrhythmias (heart rate greater than 120 bpm) in a multicenter, double-blind, partial-crossover study. Seventy-one patients were randomized to receive either esmolol (n = 36) or placebo (n = 35) as initial treatment. Therapeutic failures were crossed over to the other study medication. Therapeutic response was defined as greater than or equal to 20% reduction in heart rate, heart rate less than 100 bpm, or conversion to normal sinus rhythm. The therapeutic response to esmolol during the initial treatment period (72%) was similar to that obtained when esmolol was given as a second agent. The average esmolol dosage producing a therapeutic response was 97.5 micrograms/kg/min. Four patients (6%) converted to normal sinus rhythm during esmolol infusion. In the majority of patients (80%), therapeutic response was lost within 30 minutes following discontinuation of esmolol infusion, a finding indicative of rapid reversal of beta-adrenoceptor blockade. The most prevalent adverse effect during esmolol infusion was hypotension which occurred in eight patients (12%). Hypotension and associated symptoms resolved within 30 minutes after discontinuation of esmolol infusion, which is consistent with the short duration of action of esmolol (elimination half-life of 9.2 minutes).

Cocaine Abuse in North America: A Milestone in History

The euphoric effects of coca leaves have been known to mankind for thousands of years. Yet the first epidemic of cocaine use in America occurred during the late 19th century. Initially, there were no laws restricting the consumption or sale of cocaine. In fact, cocaine was freely available in drug stores, saloons, from mail‐order vendors, and even in grocery stores, it is reported that one drug manufacturer, in 1885, was selling cocaine in 15 different forms, including cigarettes, cheroots, inhalants, cordials, crystals, and solutions. Many famous imported wines, such as “Vin Mariani,” contained a mixture of wine and coca. For consumers on budgets, the wonder drug was available as Coca‐Cola and dozens of other soda pops and pick‐me‐up drinks. One of them even had a simple and direct name, Dope. Soon enough, the ill effects of cocaine became apparent, and by the 1920s cocaine was the most feared of all illicit drugs. Most states began enacting laws against cocaine use. President William Taft proclaimed cocaine as Public Enemy No. 1, and in 1914 the Congress passed the Harrison act, which tightly regulated the distribution and sale of cocaine. By the late 1950s, cocaine use in the United States was simply considered a problem in the past. Unfortunately, the people who were aware of the nations first cocaine epidemic gradually passed away, and America once again was ready for its fling with cocaine in the 1960s. Today, it is estimated that upwards of 50 million Americans, that is one in four, have used cocaine. In addition, another fifty thousand people use this substance for the first time each day. More than 6 million Americans use cocaine on a regular basis. Little wonder, then, that America as well as the other countries have declared a “War on Drugs.” In this review, pharmacology of cocaine, major complications arising from its use, and efforts to curb its abuse are discussed.

QT interval and repolarization time in patients with intraventricular conduction delay

A prolonged QT interval is an important prognostic indicator for cardiac arrhythmias and sudden death. The conventional QT interval measurement, however, includes in its measure the cardiac depolarization (QRS) as well as the cardiac repolarization (JT) intervals. To evaluate the relative contribution of the depolarization and the repolarization time prolongation to the prolonged QT interval in patients with intraventricular conduction delay (IVCD), the QRS, QT, and JT intervals were measured in 72 subjects with various types of IVCD. The observed intervals in IVCD subjects were compared to similar intervals in 33 healthy individuals in whom there was no evidence for intraventricular conduction abnormalities. The QTc (QT interval corrected for heart rate) in subjects with IVCD were 445 +/- 6.8 msec (mean +/- SEM) in those with LAD, 470 +/- 9.1 msec with RBBB, and 489 +/- 6.9 msec with LBBB. All of these intervals were significantly prolonged compared to 430 +/- 4.3 msec in the control group. The prolongation of QTc interval in each category of IVCD subjects was entirely secondary to a prolonged depolarization time, as the repolarization intervals were not significantly different from those observed in the control group (F = 0.5, p = NS). These observations may provide an explanation for the differential prognosis for subjects with prolonged QT interval with prolonged repolarization time as compared to those with prolonged QT interval with prolonged depolarization time.

Treatment of Thyrotoxic Storm with Intravenous Administration of Propranolol

Abstract Thyrotoxic storm is a rare but serious complication of thyrotoxicosis. Proper preoperative preparation of the thyrotoxic patient and the therapeutic use of radioactive iodine (131I) have r...

Pacemaker Malfunction Following Transthoracic Countershock

Electrical cardioversion or defibrillation may be necessary in patients with implanted artificial cardiac pacemakers. Sudden discharge of high electrical energy employed in DC transthoracic countershock procedures may damage the sensitive pacemaker circuitry and result in malfunction. We report a case in which, following synchronized DC countershock, a non‐programmable demand pacemaker functioned in the R‐wave triggered mode rather than the R‐wave inhibited mode as designed. Further, the pacemaker output voltage was reduced to about half its specified output. Such a malfunction may not be readily apparent, and requires careful analysis following electric shock. (PACE, Vol. 4, September‐October, 1981)

Selective Dysfunction of Ventricular Electrode-Endocardial Junction Following DC Cardioversion in a Patient with a Dual Chamber Pacemaker

A patient with a dual chamber pacemaker received two transthoracic (anterior‐anterior paddle position) shocks for VF. Subsequent analysis of stimulation thresholds revealed a marked rise in the ventricular threshold only. Later, she received three additional shocks (anterior‐posterior paddle position) during electrophysiological study to terminate episodes of induced VT. Following these, the ventricular stimulation threshold was > 10 Vat 2.0 ms. The selective damage at the ventricular site in this patient led us to carry out in vitro studies that revealed a preferential shunting of high electrical energy into the ventricular lead, as compared to the atrial lead, following a DC shock. These observations may explain the selective pacing malfunction observed in our patient.

Efficacy of Esmolol in the Treatment and Transfer of Patients with Supraventricular Tachyarrhythmias to Alternate Oral Antiarrhythmic Agents

The efficacy and safety of esmolol, a titratable intravenous beta‐adrenergic blocking agent with a short elimination hall‐life (t1/2 = 9.0 min) was evaluated in a multicenter open‐label study for the treatment of supraventricular tachyarrhythmias (heart rate greater than 100 bpm). The study also investigated the feasibility of transferring patients from esmolol to alternate oral antiarrhythmic agents without loss of therapeutic response. Of the 113 patients studied, 95 (84%) achieved therapeutic response (reduction in heart rate of 15% or more or conversion to sinus rhythm). Most of these patients (93%) achieved the therapeutic response at esmolol doses of 200 μg/kg/min or lower. Transfer from esmolol to an oral antiarrhythmic agent(s) was studied in 76 patients. Alternate antiarrhythmic agents used in this study were digoxin (N = 25), propranolol (N = 21), verapamil (N = 10), metoprolol (N = 11), quinidine (N = 2), and a combination of two antiarrhythmic agents (N = 7). Sixty‐seven (88%) patients were successfully transferred to oral antiarrhythmic agents without loss of the therapeutic response obtained with esmolol. The most frequent adverse effect observed during the study was hypotension, which resolved quickly (16 ± 14 min) either by decreasing the dose or by discontinuation of esmolol infusion. This study supports previous observations concerning the safety and efficacy of esmolol in the treatment of supraventricular tachyarrhythmias. Furthermore, it demonstrates that the majority of patients successfully treated with esmolol can be safely and effectively transferred to oral therapy with alternate antiarrhythmic agents.

You and Your Drinking Water: Health Implications for the Use of Cation Exchange Water Softeners

F or most of us, turning on the faucet and getting safe drinking water is as natural as getting up in the morning and going to bed at night. However, there is a growing concern about the quality of the water we consume especially that which has been softened with the use of in home water softeners. It seems a curious fact that, while water is an absolute necessity for life, little has been recorded by ancient historians on the quality of the drinking water. Description of water filtration to improve water quality first appeared in 1771.1 Hippocrates, the father of medicine (460-354 B.C.), stressing the linkage between the water quality and its importance for health, suggested that the water be boiled and strained prior to consumption to achieve better health.2 The standards for water quality are notably absent from historical records up to and including much of the nineteenth century. In this country, the first standards for drinking water were established in 1914. These standards primarily dealt with bacteriological impurities. Since then however, standards for drinking water have been revised periodically and a Federal Safe Drinking Water Act was enacted in 1974. Most states have also enacted similar laws governing their “public water supplies” and have designated the Department of Health to monitor and to enforce the compliance with the regulations. The current standards regulate most of the contaminants (physical, chemical, biological and radiological) in the public water supplies. “Potable water” is defined as water that is free from impurities sufficient to cause disease or harmful physiological effects. The states, among other things strictly regulate a maximal limit for inorganic compounds (Table I) in the drinking water.4 Sodium concentration in the water though is routinely measured (for information purposes), its concentration however, is not regulated.5 The Environmental Protection