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Biomedical subjects

P Capone

Publications and source records attributed to P Capone.

At least 19 recordsLinked to original sources
PubMed2001

Atypical pathogens and asthma: can they influence the natural history of the disease?

The association between respiratory infections and asthma exacerbations was first observed in the early '70s. In particular, the role of viral upper respiratory tract infections has been evaluated both in pediatric and adult populations. More recently, evidence of Mycoplasma and Chlamydia pneumoniae involvement in asthma attacks has been reported. These pathogens are also involved in chronic asthma, and both in vitro and animal model studies indicate that atypical agents may play a role in the pathogenesis of the disease. Further research is required to determine whether specific antibiotic treatment may alter the natural history of asthma.

Adult↗
PubMed1997

[Right atrial thrombosis and pulmonary embolism: role of echocardiography].

The echocardiographic detection of a right thromboembolus, although rare, should be considered as a cardiological emergency that could lead to death for massive pulmonary embolism. The case of a 70 year-old man admitted to our Institution with the suspicion of pulmonary embolism is described. The echocardiogram performed showed a large mobile thrombus in the right atrium prolapsing through the tricuspid valve during diastole. After thrombolytic therapy with r-TPA, the patient faced a progressive hemodynamic deterioration and died of electromechanical dissociation.

Aged↗
PubMed1996

Clinical and hormonal effects of the new angiotensin II receptor antagonist LRB081.

The renin-angiotensin system is a major contributor to the pathophysiology of cardiovascular diseases such as congestive heart failure and hypertension. Antagonizing angiotensin (Ang) II at the receptor site may produce fewer side effects than inhibition of the promiscuous converting enzyme. The present study was designed to assess in healthy human subjects the effect of LRB081, a new orally active AT1-receptor antagonist, on the pressor action of exogenous Ang II. At the same time, plasma hormones and drug levels were monitored. At 1-week intervals and in a double-blind randomized fashion, 8 male volunteers received three doses of LRB081 (10, 40, and 80 mg) and placebo. Blood pressure (BP) was measured at a finger by photoplethysmograph. The peak BP response to intravenous injection of a standard dose of Ang II was determined before and for < or = 24 h after administration of an oral dose of LRB081 or placebo. After drug administration, the blood BP response to Ang II was expressed in percent of the response before drug administration. At the same time, plasma renin activity (PRA), Ang II, aldosterone, catecholamine (radioassays), and drug levels (by high-performance liquid chromatography) were monitored. After LRB081 administration, a dose dependent inhibition of the BP response to Ang II was observed. Maximal inhibition of the systolic BP response was 54 +/- 3 (mean +/- SEM), 63 +/- 2, and 93 +/- 1% with 10, 40, and 80 mg LRB081, respectively. The time to peak was 3 h for 6 subjects and 4 and 6 h for 2 others. Preliminary plasma half-life (t1/2) was calculated at 2 h. With the highest dose, the inhibition remained significant for 24 h (31 +/- 5%, p < 0.05). Maximal BP-blocking effect and maximal plasma drug level coincided, suggesting that the unmetabolized LRB081 is responsible for the antagonistic effect. PRA and Ang II increased dose dependently after LRB081 intake. Aldosterone, epinephrine, and norepinephrine concentrations remained unchanged. No clinically significant adverse reaction was observed during the study. LRB081 is a well-tolerated, orally active, potent, and long-acting Ang II receptor antagonist. Unlike in the case of losartan, no active metabolite of LRB081 has been shown to be responsible for the main effects.

Adult↗
PubMed1995

[Arrhythmogenic right ventricular dysplasia. Report of a familial case].

Arrhythmogenic right ventricular dysplasia is a pathologic condition of unknown origin that primarily affects the right ventricle free wall characterized by progressive atrophy with fibrous-fatty substitution of the myocardium. The patient affected may present in childhood or as an adult with cardiomegaly or/and ventricular arrhythmias with a left bundle branch block configuration. The reports of familial occurrence suggest the etiologic role of a genetic defect with autosomal dominance and variable expression and penetrance, an alternative, myocarditis (toxic or infectious) is a possible cause. The aim of the present study is an non-invasive instrumental evaluation of the family of a young patient affected by arrhythmogenic right ventricle dysplasia. The authors evaluated 10 patients, 7 women and 3 men, all asymptomatic, with electrocardiography, exercise stress test on a bicycle ergometer, 24-hour Holter monitoring and two-dimensional echocardiography. A patient had certain ARVD diagnosis, while in the other 9 patients all the instrumental investigations were normal. This observation seem to confirm that ARVD may be familial and justify a systematic in-depth familial study in all demonstrated cases of ARVD and the follow-up of all patients identified who had arrhythmias or isolated right ventricular morphologic anomalies.

Adolescent↗
PubMed1994

Angiotensin-converting enzyme inhibition by hydroxamic zinc-binding idrapril in humans.

The new angiotensin-converting enzyme (ACE) inhibitor idrapril acts by binding the catalytically important zinc ion to a hydroxamic group. We investigated its pharmacodynamic and pharmacokinetic properties in 8 healthy men: Increasing doses of 1, 5, and 25 mg idrapril as well as placebo or 5 mg captopril were administered intravenously (i.v.) at 1-week intervals. Six of the subjects received 100 mg idrapril orally (p.o.) last, and two ingested oral placebo as a double-blind control. Blood pressure (BP) and heart rate (HR) remained unchanged. No serious side effects were observed. ACE inhibition in vivo was evaluated by changes in the ratio of specifically measured plasma angiotensin II (AngII) and AngI concentrations determined by high-performance liquid chromatography/radioimmunoassay (HPLC/RIA) techniques. Plasma ACE activity in vitro was estimated by radioenzymatic assay; it was suppressed by > or = 93% at 15 min after injection of 25 mg idrapril or 5 mg captopril and by 96% 2 h after idrapril intake. Mean AngII levels were decreased dose dependently at 15 min after idrapril injections. At the same time, plasma renin activity (PRA) and AngI increased according to the doses. The AngII/AngI ratio was clearly related to plasma idrapril levels (r = -0.88, n = 60). Oral idrapril inhibited ACE maximally at 1-4 h after dosing, when < 7% of initial ACE activity was observed in vitro and in vivo. Idrapril is a safe and efficient ACE inhibitor in human subjects. It is well absorbed orally. Besides having a slightly slower onset of action, idrapril has pharmacodynamic effects comparable to those of captopril.

Adult↗
PubMed1992

[Iatrogenic torsade de pointes induced by thioridazine].

Torsade de pointes is a form of polymorphous ventricular tachycardia in which the polarity of the QRS complex exhibits phasic alterations in both axis. Traditionally, torsade de pointes has been described in association with a congenital or acquired (including drug and metabolic) causes of QT prolongation. Clinical outcomes range from asymptomatic, self-terminating arrhythmias to ventricular fibrillation resulting in cardiac arrest. For the treatment of torsade de pointes, the conventional antiarrhythmic drugs cannot be relied on, cardiac pacing should be instituted as soon as possible; however, as this technique may not always be immediately available, isoproterenol infusion may be the first-choice treatment. Potassium and magnesium repletion appear to be essential in abolishing drug-induced torsade de pointes. This report describes a case of thioridazine-induced torsade de pointes treated efficaciously with magnesium sulphate and overdrive right ventricular pacing.

Cardiac Pacing, Artificial↗
PubMed1986

A comparison of celiprolol and chlorthalidone in hypertensive patients with reversible bronchial obstruction.

The objective of this study was to evaluate the effects of celiprolol, a new beta-blocking drug, on the clinical condition and pulmonary function of hypertensive patients with reversible bronchial obstruction. Celiprolol was compared with chlorthalidone, an antihypertensive drug without known effect on bronchial tone. The study consisted of a 4-week placebo run-in period and a 12-week titration period in which the dose of both drugs was increased at 4-week intervals if blood pressure was not reduced adequately. The doses of celiprolol were 200, 400, or 600 mg once daily; those for chlorthalidone 12.5, 25, or 37.5 mg once daily. Entry criteria were a diastolic blood pressure between 90 and 115 mg Hg, and FEV-1 between 40% and 80% of predicted value, increasing by 15% or more after salbutamol, and a need for occasional bronchodilator therapy. Prophylactic medication for asthma was given in constant dosage for a month before the study and throughout the study. Preliminary results on 66 patients demonstrate that neither drug had a clinically significant effect on FEV-1, FEF 25-75, or FVC. Clinical variables were not significantly changed by either drug: the average monthly asthma attacks fell from 18 to 13 with celiprolol and from 11 to 7 with chlorthalidone. FEF was reduced by more than 50% in two patients on celiprolol and three on chlorthalidone. Monthly asthma attacks increased by more than 100% in five patients on celiprolol and four on chlorthalidone. Thus, preliminary results are unable to demonstrate adverse effects from celiprolol in patients with asthma and hypertension.

Adrenergic beta-Antagonists↗
PubMed1986

A placebo-controlled double-blind multicenter study of celiprolol in the treatment of mild and moderate hypertension.

This study evaluated the 24-h antihypertensive effect of single daily doses of celiprolol, a beta-1 adrenoceptor antagonist. Patients with supine diastolic BP between 95 and 114 mm Hg started on placebo or celiprolol 200 mg daily for 2 weeks; non-responders received 400 mg daily for 2 weeks and then 600 mg daily for another 2 weeks. Response was defined as a reduction of diastolic BP to 90 mm Hg or below. One hundred ninety patients were evaluated for efficacy, 114 in the celiprolol group and 76 in the placebo group, 84 men and 106 women, mean age 52 years. Blood pressure after 6 weeks fell from 165/103 to 149/92 on celiprolol and from 162/103 to 157/97 on placebo. The fall in systolic and diastolic BP after celiprolol is statistically different (p less than 0.001) from that after placebo. The pulse rate was reduced to a similar extent by the two treatments. The percent of patients with supine diastolic BP either reduced by at least 10 mm Hg or to 90 mm Hg or below, was 66% after celiprolol and 38% after placebo (p less than 0.001). The incidence of adverse reactions was comparable in the two groups: 31% during celiprolol, 25% during placebo. The most frequent reactions observed in both groups were gastrointestinal symptoms, dizziness, fatigue, headache. In conclusion, celiprolol proved to be a safe and effective beta-blocker in the treatment of mild and moderate hypertension.

Adrenergic beta-Antagonists↗
PubMed1986

Celiprolol in angina pectoris: a controlled study.

This double-blind, placebo-controlled, parallel, multicenter study was designed to evaluate the anti-anginal and anti-ischemic effects of celiprolol in patients with stable, exercise-induced angina pectoris. The study began with a 4-week single-blind, placebo run-in, followed by 4 weeks of double-blind active treatment with celiprolol 200, 400, or 600 mg once daily or placebo, and 1 week of a placebo run-out. Patients studied had a history of chronic, stable angina pectoris and myocardial ischemia (greater than or equal to 1.0 mm ST segment depression) within 3-12 min of treadmill exercise (modified Bruce) after 3 and 4 weeks of placebo. After 2 weeks treatment, treadmill testing results indicated a mean time to myocardial ischemia for patients receiving placebo increased by 0.5 min (8%), whereas the increases for celiprolol 200, 400, and 600 mg were 0.8 min (11%), 2.1 min (33%), and 1.1 min (16%) respectively. Mean time to anginal symptoms for placebo patients was increased by 0.6 min (10%), and for celiprolol patients by 1.8 min (27%), 1.5 min (19%), and 1.0 min (14%) respectively at the 3 dose levels. The maximum exercise double product (heart rate X systolic BP) 24 h after medication, was increased by a mean of 373 (2%) after placebo, but decreased by 3301 (-15%), 3400 (-17%), and 3549 (-16%) for celiprolol 200, 400, and 600 mg respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Celiprolol in the treatment of exercise induced angina pectoris.

A multicenter, double-blind placebo controlled study was designed to examine the efficacy of celiprolol in exercise induced angina pectoris. The study consisted of a 4-week placebo run-in period, 6-week titration, 4-week maintenance, 2-week tapering and a 2-week placebo run-out period. Entry criteria were a history of stable angina with chest pain and 1 mm ST segment depression between 3 and 12 min after start of treadmill exercise stress test. Patients started with celiprolol 200 mg daily for 2 weeks; non-responders received 400 mg daily for 2 weeks and then if necessary 600 mg daily for another 2 weeks. A 20% increase over baseline in exercise stress test to onset of angina was considered a response. Ninety-two patients were evaluated, 54 in the celiprolol group and 38 in the placebo group; 63 men and 29 women, mean age 57 years. The celiprolol group was significantly different from placebo after 6 weeks. In particular, exercise time increased by 4.3 min (placebo increased by 0.3 min), ST segment depression reduced by 0.4 mm, notwithstanding the increase in exercise time (placebo increased by 0.2 mm), maximum exercise heart rate reduced by 6 beats per min (placebo increased by 3 beats per min), maximum exercise systolic BP reduced by 14 mm Hg (placebo decreased by 1 mm Hg). The therapeutic success rate based on a 20% increase of exercise time was 85% after celiprolol and zero after placebo. Reduction in weekly angina attacks and nitroglycerin consumption was from 8 to 3 after celiprolol and from 9 to 6 after placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗