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Biomedical subjects

W Chalak

Publications and source records attributed to W Chalak.

4 recordsLinked to original sources
PubMed1993

Torsade de pointe. Report of 18 cases.

Eighteen patients with long QT interval and recurrent ventricular tachycardia, torsade de pointe, were studied. Fourteen patients had an underlying heart disease. The factors involved in the appearance of this arrhythmia were: antiarrhythmic drugs (55.5%), complete heart block (33.5%), Romano-Ward syndrome (5.5%) and hypokalemic periodic paralysis (5.5%). In drug-induced torsade de pointe the QT interval was moderately prolonged. Seven patients (70%) had hypokalemia and 5 patients were bradycardic (50%). In patients with heart block-induced torsade de pointe, the QT interval was markedly prolonged. The ventricular rate was markedly slow (38 beat/min +/- 6 SD), and hypokalemia was less obvious (33.3%). In all cases there were ventricular extrasystoles with bigeminy, couplets or polymorphism on the basic ECG. Long-short sequence initiating the torsade de pointe was observed in 83 out of the 92 episodes. The withdrawal of the offensive drug or the correction of a treatable cause was sufficient to prevent torsade de pointe while the use of isoproterenol was effective in 7 patients who received this drug alone or prior to the ventricular pacing which was successfully used in 9 patients. Lidocaine was ineffective or had deleterious effects in 15 patients where electrical cardioversion required repeated use with an average of 5 times/patient.

Adult↗
PubMed1991

Decrease in pulmonary artery pressure with slow release nifedipine in Saudi patients with primary pulmonary hypertension.

We studied the acute and short-term hemodynamic effects of vasodilators in three Saudi patients with primary pulmonary hypertension. The study protocol included the measurement of pulmonary artery pressure, resistance and cardiac output at baseline and at 15, 30, 45 and 60 minutes after 10 mg sublingual nifedipine. These hemodynamic studies repeated at 3 and 6 months follow-up. A 24 hour profile of pulmonary artery and aortic pressures were recorded to evaluate the effect of 20 mg of slow release nifedipine, after 25 mg of captopril and 5 mg of sublingual isordil. After nifedipine there was a marked reduction in systolic pulmonary artery pressure from 85 +/- 18 to 55 +/- 8 mmHg and the pulmonary resistance decreased from 1422 +/- 367 to 954 +/- 69 dynes-sec/cm-5. The cardiac output increased from 2.9 +/- 0.2 to 0.2 to 4.0 +/- 0.4 l/min after nifedipine. The patients were discharged on nifedipine 10 mg qid, except for patient #3 who was a non-responder. At follow-up there was a symptomatic improvement and a favourable hemodynamic response was maintained, though patient #2 required a higher dose of nifedipine. The pulmonary artery 24 hour pressure profile revealed that 20 mg slow release adalat reduced pulmonary artery pressure for a 6 hour period. Whereas, regular nifedipine decreased pulmonary artery pressure for a period of less than 90 minutes. There was no favourable hemodynamic response to either captopril 25 mg oral of isordil 5 mg administered sublingually. We conclude that slow release nifedipine decreases the pulmonary artery pressure for longer periods compared to regular nifedipine in patients with primary pulmonary hypertension.

Adolescent↗