Biomedical subjects
Publications and source records attributed to M Chimienti.
Acute intoxication with verapamil (2400 mg) induced A-V dissociation and circulatory failure in a 38-year-old woman with no previous cardiac disease. Resumption of A-V conduction was observed after administration of orciprenalin, calcium gluconate, and dopamine, with no effect on blood pressure. Epinephrine infusion finally restored satisfactory blood pressure level and allowed a favorable outcome.
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The value of the dipyridamole test (0.75 mg/kg i.v.) in the diagnosis of angina pectoris was studied in 54 patients with angina pectoris (35 with angina on effort associated or not associated with rest angina and 19 with angina only at rest) and in 12 control subjects. The test induced electrocardiographic signs of ischemia (positive test) in 74% of patients with angina on effort, while it was negative in all cases with angina only at rest and in control subjects. All anginal patients with normal coronary arteries or less than 50% stenosis had a negative test; a positive response was observed in 36, 79 and 60% of cases with one-, two-or three-vessel disease, respectively. Hemodynamic changes with a marked arteriolar vasodilatation were observed both in the negative and in the positive tests. In the positive tests no significant change of double product, blood pressure and left ventricular end-diastolic pressure occurred before ischemia appeared. The results of the study show that dipyridamole as a diagnostic test in angina pectoris has a high specificity but a lower sensitivity than exercise test. The hemodynamic and eletrocardiographic findings in the positive tests suggest that dipyridamole-induced ischemia is due to a flow maldistribution with selective subendocardial ischemia secondary to the coronary arteriolar dilatation caused by the drug.
The absolute bioavailability of dihydroquinidine chloride (normal tablet and sustained-release capsule) was studied in 12 hospitalized patients with heart disease. A 300-mg dose of dihydroquinidine gluconate was administered to each patient by short intravenous infusion. After a single dose of two tablets of dihydroquinidine chloride (300 mg), the average peak concentration was 0.74 +/- 0.43 mg/l (+/- SD); following administration two capsules of the sustained-release form (500 mg dihydroquinidine chloride) the average peak concentration was 0.55 +/- 0.25 mg/l. Tmax was approximately 5 h with the dihydroquinidine tablet and 7 h with the dihydroquinidine capsule. The mean absolute bioavailability was 89 +/- 9% for the conventional tablet and 52 +/- 15% for the sustained-release capsule. After intravenous infusion of dihydroquinidine (2.63 +/- 0.29 mg/kg), the disposition of the drug is described by a two-compartment open model. The volume of distribution (Vd) was 4.67 l/kg. Distribution (t1/2 alpha = 18.63 +/- 15.2 h) and the apparent elimination half-life (t1/2 beta = 10.8 +/- 4.7 h) were longer than the corresponding values reported by Ueda et al. [1976]. These discrepancies are presumably due to the different sampling period that was extended to 24 h in our study, consequently evidencing a slower rate of elimination from 12 to 24 h. Mean total body clearance (Cl) was 0.28 +/- 0.057 l/h/kg. Urine sample collection for 48 h showed 21% of the dose was excreted unchanged. The renal clearance (Clr) was 0.062 +/- 0.018 l/h/kg.
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Presence of rate-dependent (RD) intraventricular conduction defects (IVCD) was documented by inducing variations in heart rate in 30 acute myocardial infarction (AMI) patients (10 right bundle branch block, six left bundle branch block, 13 left anterior hemiblocks, and two left posterior hemiblocks). Five IVCDs were tachycardia-dependent (TD), 20 were bradycardia-dependent (BD), and six were both TD and BD. In TD blocks shortest cycles showing normal intraventricular conduction ranged from 410 to 1330 msec (697 +/- 84 SE); in BD blocks longest cycles with normal intraventricular conduction ranged from 450 to 1450 msec (962 +/- 52). In 60% of cases intermittent incomplete RD blocks were also present. In one patients RD-IVCD intermittency remained until discharge; in the others it lasted from 4 minutes to 10 days. Afterwards 19 RD-IVCDs disappeared and four became stable; six patients died during RD-IVCD intermittency period. Disappearance of RD block was preceded by gradual reduction in cycle length showing TD block and lengthening of cycles stopped beats with BD block. Serial observation of RD-IVCDs provides information about sequence of electrophysiologic effects on the intraventricular conduction system in clinical AMI.
The effectiveness of nitroglycerin ointment in vasospastic angina pectoris at rest was evaluated in 10 patients selected for study. The study was performed after a 24 hour control period, and a randomized single-blind crossover experimental design was followed. Two percent nitroglycerin ointment (15 mg) or placebo ointment was administered every 6 hours for a period of 48 hours each; the first treatment period was followed by a second in which each preparation was used for a 24 hour period. All patients were hospitalized in the coronary care unit; an objective evaluation was carried out using a multichannel electrocardiographic recording to assure recognition of the painless ischemic episodes. Coronary angiography showed critical stenosis of one or two vessels in 9 of the 10 patients; spasm was demonstrated in 3. Results of the ergonovine test were positive in nine of nine patients. Nitroglycerin ointment produced a significant reduction in the mean daily number of episodes during the first (12.5 +/- 3.9 versus 0.5 +/- 0.4, p less than 0.02) as well as the second treatment period (10.6 +/- 3.8 versus 0.6 +/- 0.4, p less than 0.02). These results demonstrate that nitroglycerin ointment provides effective, long-lasting protection against angina due to coronary spasm.
A patient with intermittent tachycardia-dependent left posterior hemiblock is reported. Electrocardiographic patterns of complete and incomplete block were documented. Identification of the electrocardiographic characteristics of intraventricular conduction defects is aided when they are intermittent. The difficulty in diagnosing incomplete left posterior hemiblock, and the possible masking of the signs of previous inferior infarction by left posterior hemiblock are emphasised.
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A patient admitted for evaluation of repeated episodes of faintness not associated with chest pain is presented. The episodes were caused by marked sinus bradyarrhythmias secondary to ischemic attacks with inferior ST-segment elevation, no accompanied by anginal pain. Medical treatment with nifedipine was able to prevent both the ischemic attacks and cardiac rhythm disturbances associated with acute ischemia. This case shows that ischemic pathogenesis of syncopal attacks should not be ruled out even in the absence of chest pain and that the attacks may be prevented by treating their primary cause.
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The effectiveness of nifedipine in treating angina pectoris at rest was evaluated in 14 patients with frequent ischemic episodes associated with S-T segment elevation or depression. The trial consisted of (1) a 48 hour control period; (2) a placebo period and a period of treatment with nifedipine of 48 hours each; and (3) a second placebo period and a second period of treatment with nifedipine of 24 hours each. The efficacy of treatment was evaluated by continuous electrocardiographic recording to detect painless ischemic episodes. During coronary angiography coronary spasm was demonstrated in five patients. The ergonovine maleate test was positive in seven of eight patients. No statistically significant difference was found in the mean daily number of ischemic episodes between the control period and the first placebo period, or between the control and the second placebo periods. Nifedipine produced a highly significant reduction in the mean daily number of episodes compared with the response to placebo during the first as well as the second period. Nifedipine is effective in angina at rest caused by coronary arterial spasm. The prevention of ischemia may be related to the ability of nifedipine to decrease calcium-dependent coronary muscle tone and to prevent coronary spasm.