Adenosine-induced tachycardia: what is the mechanism?
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Biomedical subjects
Publications and source records attributed to Y Lokhandwala.
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OBJECTIVE: Paroxysmal supraventricular tachycardia (PSVT) can be effectively terminated by the intravenous administration of adenosine or verapamil. However adenosine is expensive and injectable verapamil currently is scarcely available. While intravenous diltiazem has been shown to be useful for terminating PSVT, the efficacy of esmolol in this regard has not been evaluated previously. Hence these latter two drugs were studied for their efficacy in terminating PSVT. METHODS: A prospective, randomised, crossover study was undertaken in patients presenting with hemodynamically tolerated PSVT to the ICCU. While 50 patients had been planned for the trial, the study had to be prematurely terminated after 32 patients had been enrolled due to the marked superiority of diltiazem. Two sequential doses with a 5 minute interval of either drug were administered before crossover. Diltiazem was given in a dose of 0.25 mg/kg while the esmolol dose was 0.5 mg/kg. RESULTS: Diltiazem terminated PSVT in all the 16 patients in whom it was given as the first drug. The 12 patients who did not respond to esmolol were also effectively treated with diltiazem. Thus totally 28/28 patients responded to diltiazem while only 4/16 patients responded to esmolol (p < 0.001). Of the 28 patients who responded to diltiazem, in 13 patients the second bolus of diltiazem worked after the first one had failed. No significant adverse effects were seen. CONCLUSION: Intravenous diltiazem is highly effective and safe for terminating PSVT. When the first bolus is ineffective, the second bolus given after 5 minutes usually succeeds. Esmolol in the dose of 0.5 mg/kg has poor efficacy for terminating PSVT, even when 2 boluses are administered.
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A 30-year-old woman presented with tachycardiomyopathy due to atrial flutter-fibrillation and underwent radiofrequency ablation of the AV node and VVIR pacemaker implantation. There was no evidence of any accessory pathway (AP) conduction during the AV nodal ablation or during chronic ventricular pacing. One year later, she had a transient preexcited tachycardia. A year after this, her ECG showed 1:1 AV conduction with preexcitation. Electrophysiologic study revealed a left lateral AP with anterograde and retrograde refractory periods of 280 and 240 msec, respectively. Successful radiofrequency ablation of the AP was performed. This case highlights a unique emergence of an AP in adult life.
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A mother and three of her four children, one girl and two boys, who had valvar pulmonary stenosis are described. One child had an associated septum secundum atrial septal defect, and another had an associated ventricular septal defect. An autosomal dominant mode of inheritance is likely for the valvar pulmonary stenosis. The association of additional cardiac lesions in two of the three siblings raises the possibility of closely associated genetic loci.
A double blind randomized placebo controlled clinical trial was carried out to assess the efficacy and safety of L-carnitine in patients suffering from acute anterior wall myocardial infarction with respect to left ventricular function. Sixty patients (34 men, 26 women, mean age 56+11 yr.) with acute anterior wall myocardial infarction were randomized to placebo and L-carnitine. All the patients were given intravenous L-carnitine / placebo in the dose of 6gm/day for the first seven days followed by oral L-carnitine / placebo 3 gm/day in three divided doses for a period of three months. Echocardiography was performed for regional wall motion abnormality, left ventricular end systolic volume (ESV), end diastolic volume (EDV) and ejection fraction (EF) on admission, after seven days and after three months of the infarction. Forty-four patients completed the study. There were three deaths, two in the placebo and one in the L-carnitine group (p>0.05). Thirteen patients were lost to follow up. Echo parameters in both groups were comparable (p>0.05). The duration of chest pain prior to initiation of the I.V. L-carnitine was 7.5 + 5.2 hrs in the L-carnitine group and 7 + 4 hrs in the placebo group (p>0.05). There was no statistical difference in the EF, ESV and EDV on admission, at discharge and after three months in the L-carnitine and the placebo groups (p>0.05). No significant adverse effects were noted. L-carnitine, though a safe drug, does not affect the left ventricular function in patients with myocardial infarction.
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