Kul D. Chadda

Hypomagnesemia and refractory cardiac arrhythmia in a nondigitalized patient

Abstract A case of hypomagnesemia and refractory cardiac arrhythmia is presented. The patient had no evidence of clinical heart disease and was not receiving digitalis therapy. The cardiac arrhythmia was refractory to all usual forms of therapy but was instantly abolished with intravenous magnesium therapy. The unusual nature of this relation and a possible hypothesis to explain its occurrence are discussed.

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.

Appraisal of sinus nodal recovery time in patients with sick sinus syndrome.

Abstract Right atrial pacing for 2 to 5 minutes at rates ranging from 90 to 150/ min was performed in 17 patients with the sick sinus syndrome and in 15 control subjects with no evidence of sinus node disease. The postpacing pause or the sinus recovery time was defined as the pause between the last paced atrial beat and the subsequent sinus escape beat. The corrected sinus recovery time was determined by subtracting the basic sinus cycle length from the sinus recovery time. In the 15 control subjects, the corrected sinus recovery time ranged from 0 to 375 msec (210 ± 131 [mean ± standard deviation]). In patients with the sick sinus syndrome, the corrected sinus recovery time was normal in 11 (−150 to 350 msec) and prolonged in 6 (480 to 5,690 msec). Intravenously administered atropine (0.6 to 2 mg) used in 11 patients produced an adequate increase in the sinus rate in 6 patients. Junctional escape rhythm lasting for several seconds appeared in three of seven patients who underwent repeat atrial pacing after administration of atropine. Two of these had a normal control recovery time and an adequate response of the sinus rate to atropine administration; in one, the control recovery time was slightly prolonged and the response to atropine was inadequate. In the remaining four patients, three with a normal and one with a prolonged control recovery time, no significant change in recovery time occurred after administration of the drug. We conclude that only a limited number of patients with the sick sinus syndrome have an abnormal corrected sinus recovery time. Some patients with a normal control recovery time may show an abnormal response when atrial pacing is repeated after atropine administration.

Lidocaine-induced heart block in patients with bundle branch block

Abstract His bundle electrography and atrial pacing were used to evaluate the effect on cardiac conduction of an intravenous bolus injection (50 to 100 mg) of lidocaine in 21 patients with various intraventricular conduction abnormalities and ventricular premature beats. Sixteen patients (76 percent) had prolonged His-Purkinje conduction time (H-V interval greater than 55 msec). Six patients (all with a prolonged H-V interval) had earlier shown transient second degree or complete heart block. Administration of lidocaine produced complete heart block distal to the His bundle potential in two patients. Both patients had a prolonged H-V interval (100 and 140 msec, respectively) and had shown 2:1 A-V block distal to the H deflection on atrial pacing before the injection. A third patient, with an H-V interval of 70 msec, showed second degree block distal to the H deflection during atrial pacing after administration of lidocaine but not before. An additional patient, observed clinically to have alternating right and left bundle branch block, experienced cardiac standstill after the injection. Lidocaine should be used cautiously in patients with incomplete bilateral bundle branch block, and a temporary pacemaker should be considered in patients with a prolonged H-V interval or known trifascicular disease.

Diagonal ear-lobe crease: prevalence and implications as a coronary risk factor.

THE diagonal ear-lobe crease described below appears more commonly in patients with coronary heart disease and should be regarded as a coronary risk factor. Although other risk factors may be prese...

Effects of atropine in patients with bradyarrhythmia complicating myocardial infarction. Usefulness of an optimum dose for overdrive.

Abstract The effects of 0.4 to 1.5 mg intravenously administered atropine were evaluated in 100 patients with a heart rate Thus, a relatively lower dose of atropine (

Bradycardia-hypotension syndrome in acute myocardial infarction: Reappraisal of the overdrive effects of atropine

Sixty-eight (17 per cent) of 380 patients with acute myocardial infarction had the bradycardia-hypotension syndrome (ventricular rate below 60/min and systolic blood pressure less than 100 mm Hg) during the first 24 hours of admission to a large general hospital. In 61 of the 68 patients, the administration of atropine significantly increased the heart rate (from 46 plus or minus 14 to 79 plus or minus 12/min) (p less than 0.01) and systolic blood pressure (from 70 plus or minus 15 to 105 plus or minus 13 mm Hg) (p less than 0.001). In 26 of the 68 patients, ventricular premature complexes decreased from 9.4 plus or minus 3/min to 2.4 plus or minus 0.7/min (p less than 0.001) after the administration of atropine. It is concluded that the bradycardia-hypotension syndrome is not an uncommon complication following acute myocardial infarction and that selected doses of atropine may have a beneficial effect without significant complications.

Atrioventricular block with lidocaine therapy

Abstract A case is presented of complete atrioventricular (A-V) block occurring after a 50 mg bolus injection of lidocaine. Base-line studies before administration of lidocaine showed evidence of trifascicular block manifested by complete right bundle branch block, left anterior hemiblock and a markedly prolonged H-V interval. Advanced A-V block and then complete A-V block distal to the His bundle developed after administration of lidocaine. Lidocaine should be used with caution in patients with trifascicular disease; if it is administered to such patients, insertion of a temporary pacemaker catheter should be considered.

Incidence and description of accelerated ventricular rhythm complicating acute myocardial infarction

One hundred and nineteen episodes of accelerated ventricular rhythm (less than 125/min) were noted in 37 patinets with acute myocardial infarction during a 1 year period. The incidence was 12.7 per cent. Twenty-seven episodes of fast ventricular tachycardia (less than 125/min) were noted in 16 of these patients. Eighteen patients had anterior myocardial infarction and 19 inferior myocardial infarction. The mechanism of onset of accelerated ventricular rhythm was classified as escape in 65 episodes. Ventricular premature beats were noted close to episodes of accelerated ventricular rhythm in 31 patients and fast ventricular tachycardia in 14 patients. The morphology of accelerated ventricular rhythm was similar to the ventricular premature beats in 27 patients and similar to the fast ventricular tachycardia in 12. In 11 patinets the morphology of ventricular premature beats, accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm is a relatively common complication of both anterior and inferior myocardial infarction. The high incidence of concomitant fast ventricular tachycardia, the frequency of ventricular premature beats with similar morphology and coupling time, and the instances of two arrhythmias having common rate multiples, suggest that at least in some instances accelerated ventricular rhythm may represent an ectopic focus with exit block.

Diagonal Ear-Lobe Crease and Coronary Artery Sclerosis

Excerpt We previously reported our observations concerning the relation of a diagonal ear-lobe crease and coronary heart disease (1, 2). In our present study we further examine this relation by com...