[Specific IgE in the lacrimal secretion: a comparative evaluation with serum levels].
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Biomedical subjects
Publications and source records attributed to G Cocco.
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18 patients with acute myocardial infarction and sustained arrhythmias were treated with a new Ca2+ antagonist, Ro 11-1781, at the dose of 1.0 mg/kg i.v. The drug was effective in reducing heart rate to less than 90 beats/min in 9/10 patients with atrial fibrillation, in 3/4 patients with atrial flutter and in 3/4 patients with supraventricular tachycardia. The peak effect was observed within 2--5 min after the intravenous administration of Ro 11-1781. In cases with recurring tachyarrhythmias, the drug was also effective in repetitive administration. Systolic blood pressure was reduced, but severe hypotension (less than 90 mm Hg) was not observed. The atrioventricular conduction in these patients remained unimpaired and asystole did not occur. The drug appears to be an effective and a well tolerated antiarrhythmic agent.
The electrophysiological effect of dimeditiapramine (Ro 11-1781), a Ca2+ antagonist, was evaluated in 20 patients with coronary heart disease. Electrophysiological measurements, including sinus cycle length, sinoatrial conduction time, intra-atrial conduction time, atrial, atrioventricular, nodal and ventricular refractory periods and intraventricular conduction time were recorded before and after the intravenous administration of Ro 11-1781. At a dose which is effective against cardiac arrhythmias, Ro 11-1781 produced no statistical significant changes in the sinoatrial and intraventricular conduction time. Similarly, neither the sinoatrial nor the ventricular refractory period was affected. Ro 11-1781, however, increased the atrioventricular conduction time and decreased the systolic blood pressure to a statistically significant extent. The tolerance was very good.
The vascular system of 30 old asymptomatic patients (average age 62.5 years) was studied by reflection plethysmography. The plethysmogram (PTG) was recorded from the forefinger of the left hand at rest, during two postural tests (+45 degrees arm-up and -45 degrees arm-down), after physical work, and during the infusion of nitroglycerin and the beta-agonist metaproterenol. 50% of the subjects presented a normal PTG under basal conditions. However, pathological PTGs were recorded after the various tests: 23.3% with the arm-up test, 6.6% with the arm-down test, 52% with the effort test, 31% with the nitroglycerin test and 73.9% with the metaproterenol test. Clearly, the effort and metaproterenol tests are pathological in the majority of cases, both tests inducing physiologically vasodilation and increase in the peripheral pulse. The arm-down test, which usually induces vasoconstriction, is almost always normal. Since the percentage of pathological responses to the nitroglycerin test is significantly smaller than that to the effort and metaproterenol tests, it is concluded that the vascular changes induced by aging are primarily functional, at least in asymptomatic subjects. Aging more negatively influences the vasodilating than the vasoconstricting ability.
A single blind randomized parallel study designed to assess the anti-anginal efficacy of pindolol and nifedipine was carried out in 42 ambulatory coronary patients with stable angina pectoris. Drug efficacy was assessed in terms of (a) pain, (b) frequency of anginal episodes, (c) nitroglycerin consumption, (d) exercise tolerance and (e) ST-segment changes. The effect of these drugs on asymptomatic resting myocardial ischemia was also assessed by means of 24-h dynamic electrocardiography (DCG). All patients were checked at weekly intervals. At the end of a 4-wk placebo period, the patients were randomly assigned either to the pindolol or nifedipine group. The treatment lasted for 45 days. During the placebo period, ischemic ECG changes and symptoms of coronary insufficiency were detected in all patients. Furthermore, 12 out of 42 patients had asymptomatic myocardial ischemia at rest. One patient from each group was dropped because of tolerance. At the end of the 45-day study, pindolol and nifedipine were equi-effective on spontaneous and effort-related angina. There were, however, some differences: increased tolerance to exercise appeared earlier with pindolol: the pindolol group showed a slightly reduced while the nifedipine group showed a slightly increased heart rate. Furthermore, nifedipine reduced or eliminated asymptomatic myocardial ischemia in 6 out of 7 patients while only 1 out of 5 improved in the pindolol group.
18 patients with non-ischemic heart disease have been studied with reference to the kinetocardiographic changes before and after i.v. administration of dopamine (DOP) (Revivan) or Isoproterenol (ISP) (Aleudrin). For this purpose a simultaneous registration of ECG (lead D2), Kinetocardiogram (KCG) in K25 and K45 was performed. Volume curves were considered as a normal features of KCG, curves showing systolic outward movements during the ejection phase were classified as pathologic. The reduction or disappearance of the systolic movements during the drug administration, were considered as kinetic improvement, the increase of their site was judged as kinetic worsening. During the infusion, 17 KCGs maintained a normal morphological pattern; out of 19 pathological KCGs, 4 did not show any change, and 15, 5 reached a complete normalization. It is pointed out the overlap of the precordial kinetics in the ventricular hypertrophies and in the normal subjects (kinetic improvement), and the possibility to differentiate a systolic outward movement due to synergic contraction of hypertrophied ventricle from a systolic outward movement to be reffered to a diskynetic contraction in the myocardial ischemia (kinetic worsening).
11 coronary patients, 8 with mild hypertension, were treated with clonidine, at a dose of 75 micrograms b.i.d. per os for a week. The effect of the drug on coronary heart disease was assessed by means of a symptom-limited multistage exercise test on the cycloergometer. Clonidine was effective in reducing the exercise-induced increases in blood pressure (by 15.5 +/- 6.1%), the double product (by 34.8 +/- 20.8%) and the electrocardiographic ischemic changes. In 2/4 patients, effort related ventricular extrasystoles were reduced by greater than 50% after clonidine. The drug worsened the anginal pain in 3 and relieved the pain in 3 patients. However, it reduced the exercise-induced ST-T segment downsloping in 7 patients. The tolerance was good, since only 3/11 patients reported slight dry mouth, sedation and pyrosis. In view of the electrocardiographic effect, further studies with clonidine on myocardial ischemia should be performed.
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Lorcainide is a promising antiarrhythmic agent that belongs to the class of local anesthetics. It was tested in 7 patients with malignant ventricular arrhythmias that were resistant to other antiarrhythmic agents. Lorcainide was effective in all cases (complete disappearance of arrhythmias in 6 cases and more than 50% disappearance in the 7th case), and the tolerance was within acceptable limits. The drug was effective at rest, as assessed by 24-h dynamic electrocardiographic monitoring, and during physical exercise. Longer studies with more patients are warranted, since the drug appears to be a promising antiarrhythmic agent.
The pharmacological methods used to assess the intrinsic sympathomimetic activity (ISA) of beta-blockers are discussed. The clinical relevance of ISA to respiratory function, peripheral resistance and cardiac function is reviewed. It appears doubtful whether ISA is always of predominant clinical significance and an alternative explanation is offered for many clinical effects observed with certain beta-blockers, e.g. pindolol, oxprenolol, tolamolol, metoprolol, etc. Some effects of these beta-blockers resemble those of labetalol, a new drug with both alpha and beta-blocking activity. Some clinical effects of certain beta-blockers are more likely to be due to alpha-blocking activity than to their ISA.
The cardiovascular (blood pressure, heart rate, central venous pressure) and ECG changes caused by dibenzepine-infusion (720 mg/day for 48 hours) have been assessed. Mean blood pressure and heart rate did not show significant changes. In some patients, however, distinct changes in both variables were observed. Central venous pressure was not affected. The infusion elicited changes in the repolarisation phase of the ECG: it did not, however, alter either the automaticity or the conductivity of the heart. These results were obtained in 40 depressive patients, whose general conditions and cardiovascular state were excellent and must not be extrapolated for cardiopathic patients. The risks inherent in this therapeutic approach are discussed.
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The most important cardiovascular interactions between cardioactive drugs and monoamino-oxidase inhibitors or tricyclic antidepressants are reviewed. Post-ganglion blocking agents (e.g., guanethidine), clonidine, reserpine, and alpha-methyl-dopa should not be used in patients needing antide-present therapy. For hypertension, diuretics, beta-blokkers, and vasodilators should be used. In patients with cardiac disease negative interactions between membrane-stabilizing antiarrhythmic agents and tricyclic antidepressants may be observed. Caution is recommended when using both drugs. On the other hand, the use of digitalis is relatively free of negative interactions. Some of the mechanisms possibly involved are discussed. The practical implications of such effects are presented and some clinically useful guidelines are suggested.
50 patients, 20 without heart disease and 30 with coronary heart disease (CHD), were studied by kinetocardiography (KCG), before and after administration of isoproterenol (initial dose 2 microgram/min, maximum dose 6 microgram/min). In the control subjects the KCG was unaffected by the drug. In contrast, in most of the patients with CHD isoproterenol induced the appearance or the increase of paradoxical systolic bulges, which are regarded as the expression of ventricular dyskinesia resulting from isoproterenol-induced transient regional ischemia. This test is recommended as a valuable noninvasive method for the diagnosis of ischemic ventricular dyskinesia.