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Biomedical subjects

L de Caprio

Publications and source records attributed to L de Caprio.

12 recordsLinked to original sources
PubMed1994

[Comparison of nisoldipine and diltiazem in the treatment of effort angina pectoris].

BACKGROUND: In order to evaluate the benefits of a calcium-antagonist medium-term treatment, 20 patients with effort stable angina pectoris were treated with nisoldipine in comparison to diltiazem. METHODS: Twenty patients with stable effort angina completed a double-blind, placebo controlled trial, comparing 10 twice daily nisoldipine per os and diltiazem 120 three times daily per os for 28 days. After wash-out, placebo and drug period, ergometer stress tests were performed. Exercise tolerance, angina frequency, nitrate consumption and side effects were evaluated. RESULTS: Our results showed that both drugs significantly increased exercise tolerance. Exercise duration was 330 +/- 107 sec after placebo, 397 +/- 106 sec after nisoldipine (p < 0.05) and 378 +/- 99 sec after diltiazem (p < 0.05). Effort angina episodes decreased from 20 after placebo to 8 after nisoldipine and diltiazem. Both drugs reduced rate-pressure product at submaximal exercise in comparison to placebo. There were no differences at peak exercise between placebo or drug periods. Both drugs similarly reduced nitrate consumption and weekly effort angina attacks. No patients referred serious side-effects. CONCLUSIONS: nisoldipine, like diltiazem, is an effective drug in the treatment of stable effort angina. Moreover, the therapeutic effects of nisoldipine during medium-term treatment are probably related to decrease in oxygen consumption.

Administration, Oral↗
PubMed1989

Relationship between QT interval duration and exercise-induced ventricular arrhythmias.

This study was performed to determine if QT prolongation before and during early exercise is related to the occurrence of exercise-induced ventricular arrhythmias (EIVA). EIVA occurred in 47 of 142 patients with angiographic evidence of coronary artery disease (CAD); no EIVA occurred among the 22 patients without CAD (OV). Resting QTc and QT intervals during early exercise were similar in patients without EIVA, irrespective of the presence or absence of CAD; however resting QTc was significantly longer in CAD patients who showed EIVA (443 +/- 40 ms; P less than 0.01) than in CAD patients without EIVA (424 +/- 37 ms) and in OV patients (421 +/- 32 ms). During early exercise, the QT interval remained significantly longer in patients with than in those without EIVA. There was a trend toward increasing resting QTc in patients who exhibited EIVA more severe than grade 3. When resting QTc was longer than 440 ms, subsequent EIVA were correctly predicted in CAD patients with a sensitivity of 43%, a specificity of 72% and a predictive accuracy of 63%. Thus, a trend toward longer resting QTc values exists in CAD patients who develop EIVA; however, a long resting QTc (greater than 440 ms) appears to be only a weak predictor of subsequent EIVA.

Adult↗
PubMed1984

Influence of heart rate on exercise-induced R-wave amplitude changes in coronary patients and normal subjects.

In order to study whether different heart rates achieved at peak exercise by normal subjects and patients with coronary artery disease (CAD) affect the results of analysis of R-wave amplitude changes (delta R), we evaluated delta R at progressively increasing heart rate (HR) steps in 60 normal subjects with negative exercise tests (ET), in 130 patients with CAD, in 88 patients with true positive and 42 with false negative ET, and in 43 patients with no CAD and false positive ET. We found that the sensitivity and specificity of delta R were HR dependent, the former decreasing and the latter increasing with progressively increasing HR steps. Mean values of delta R did not discriminate among the four groups for HRs up to 150 bpm; significant differences were found between normal subjects and CAD patients, both with true positive and false negative stress tests, at HR greater than 150 bpm. False positive patients had mean delta R similar to those found in normal subjects. We hypothesize that quantitative delta R analysis could be useful in ECG diagnosis of false negative and false positive patients at HR greater than 150 bpm.

Coronary Disease↗
PubMed1984

Quantitative and qualitative analysis of the relationship between exercise-induced R wave amplitude changes and severity of coronary artery disease.

The correlation between R wave voltage variations (delta R) and the angiographic severity of coronary artery disease (CAD) at progressively increasing heart rate (HR) steps was evaluated in 51 patients (pts) without CAD (OV), in 42 pts with single (SVD), in 43 with double (DVD) and in 59 pts with triple vessel disease (TVD). At the end of stress the sensitivity of delta R was higher in DVD and TVD pts than in SVD pts. There was no clear correlation between exercise-induced R wave changes and the angiographic severity of CAD, since the qualitative and quantitative delta R evaluation during effort showed similar changes in delta R for a wide range of HR's in the entire study population. Since different degrees of exercise tolerance were found in pts with SVD, DVD and TVD, we hypothesize that the correlation between delta R and the severity of CAD at the end of stress testing may be artifactual.

Analysis of Variance↗
PubMed1984

Effects of long-term molsidomine treatment versus isosorbide dinitrate and placebo on exercise tolerance in stable angina.

A single-blind study (n = 59) was performed to assess the effect of long-term (4 week) orally administered molsidomine (2 mg 4 X daily), isosorbide dinitrate (10 mg 4 X daily), and placebo on exercise tolerance performed on the bicycle ergometer by patients with stable angina on effort and with significant coronary artery disease. Isosorbide dinitrate had similar effects to placebo, both failed to modify the pressure-rate product, the sustained work load, and the ST segment depression, but slightly decreased, although not significantly, the incidence of angina. Although not affecting the pressure-rate product and the mean blood pressure, molsidomine decreased significantly the ST segment depression (p less than .05). In conclusion, by markedly reducing preload and because of its long-lasting effect (up to 6 h), the new vasodilator drug molsidomine plays a useful role in the long-term management of stable angina on effort.

Angina Pectoris↗
PubMed1981

[Serial evaluation by effort test of the effects of coronary artery bypass on effort angina (author's transl)].

To evaluate the duration of favourable effects of coronary artery bypass (CAB) on exercise-induced angina (A), 58 patients: 13 with single 21 with double and 24 with triple vessel disease, were studied. All patients underwent CAB for stable angina on effort. Patients underwent exercise testing (ET) before surgery at one, two and three years. Heart rate peak (HR), HR x systolic blood pressure peak (DP), work load (W), exercise-induced ST segment depression (ST) and incidence of A were evaluated; the results of ET before surgery were compared with those found after CAB. Our findings show that HR, DP, W and ST were significantly improved by surgery for at least 3 years. The lowest incidence of A was found at one year ET (20.6%), while it increased at two years (27,5%) and three years ET (37.9%). Most patients with A had angiographic evidence of left ventricular abnormal wall motion and ec-graphic signs of previous myocardial infarction. Our data indicate that serial exercise testing can objectively monitor the results of CAB. Most patients show an improved exercise tolerance for up to 3 years after CAB. Some patients, with more extensive CAD, showed a progressive deterioration of the clinical pattern and a decrease of the exercise tolerance.

Angina Pectoris↗
PubMed1976

Participation of beta receptors in reflex vasodilatation in the dog.

The effects of propranolol, given by direct intraarterial injection, on the reflex vasodilatation induced in the atropinized isolated gracilis muscle by rapid intravenous administration of norepinephrine, were studied in dogs. In these studies, both atropine and atropine plus propranolol did not significantly alter the maximum fall in vascular resistance in the perfused gracilis muscle following intravenous norepinephrine; however, if the reflex responses were evaluated as integrated areas of vasodilatation, atropine attenuated the vasodilatation and the administration of propranolol further attenuated the reflex. In fact, the value of the integrated areas of vasodilatation was 52.8 +/- 9 mmHg/min in the basal state, 39 +/- 6 mmHg/min after administration of atropine, and 24 +/- 7 mmHg/min after propranolol, whereas the integrated areas of the systemic hypertension did not show any modification. These results prompt us to conclude that the adrenergic beta receptors participate in the reflex vasodilatation, although the mechanism of their action needs further elucidation.

Animals↗
PubMed1975

Studies on the hemodynamic changes induced by electrical stimulation of the vagosympathetic trunks in the dog.

The effects of electrostimulation of the cephalic endings of the vago-sympathetic trunks on the systemic and perfusion pressure of the hind limb of the dog depend upon frequency, intensity and duration of the stimulus. The electrostimulation performed with stimuli of high frequency, low intensity and moderately long duration (rectangular waves of 1.5 V, 0.7 msec, 100 Hz) consistently elicited systemic hypertension and vasoconstriction. This response was completely abolished by pretreatment with guanethidine or hexamethonium. On the other hand, electrostimulation with stimuli of low frequency, high intensity and long duration (5 V, 1 msec, 10 Hz) produced systemic hypotension and vasodilatation in the perfused hind limb. These effects were completely blocked by atropine or hexamethonium, while guanethidine was unable to induce any modification. These findings suggest that electrostimulation of vagosympathetic trunks can evoke different hemodynamic responses depending upon the characteristics of the stimulus. The occurrence of a vasodilatation specifically blocked by atropine demonstrates that a purely cholinergic mechanism underlies such a reflex response.

Animals↗