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Biomedical subjects

B Magnani

Publications and source records attributed to B Magnani.

At least 127 records · Page 7Linked to original sources
PubMed1991

[Comparative effects of doxazosin and enalapril in patients with arterial hypertension and exercise-induced acute myocardial ischemia].

The effects of doxazosin (alpha-1-inhibitor) and enalapril (ACE-inhibitor) on blood pressure and exercise stress test were assessed in 10 hypertensive patients (8 M, 2 F, age 58 +/- 9 years) with coronary artery disease and exertional myocardial ischemia. A single blind, cross-over, placebo controlled trial was performed. Placebo was administered for 2 periods of 2 weeks, doxazosin and enalapril for at least 3 weeks. The sequence of the active drugs was randomized and the single daily dose, obtained by titration, was 7 +/- 5 mg for doxazosin and 18 +/- 13 mg for enalapril. Blood pressure measurements and treadmill tests (Bruce protocol) were performed at the end of each period. Rest systolic and diastolic pressures after placebo were respectively 173 +/- 15 and 106 +/- 9 mmHg and were reduced to 153 +/- 11 and 93 +/- 12 mmHg (p less than 0.05) after doxazosin and to 150 +/- 24 and 93 +/- 12 mmHg (p less than 0.05) after enalapril. Total exercise time was 473 +/- 91 s after placebo and increased to 545 +/- 84 s (p less than 0.05) after doxazosin and 529 +/- 100 s (p less than 0.05) after enalapril. Time to 1 mm ST depression (ST1) was 297 +/- 102 s after placebo and increased to 414 +/- 96 s (p less than 0.05) after doxazosin and to 396 +/- 133 s (p less than 0.05) after enalapril. Double product at peak exercise and at ST1 were respectively 26.3 +/- 2.8 and 22.1 +/- 2.8 x 10(3) and remained unchanged after enalapril and doxazosin. Peak exercise diastolic blood pressure was 107 +/- 5 mmHg after placebo, was reduced to 94 +/- 15 mmHg (p less than 0.05) after doxazosin and was unchanged after enalapril (101 +/- 10 mmHg, NS). Thus, doxazosin and enalapril induced a comparable decrease of rest blood pressure and a similar increase of exercise time in hypertensive patients with exertional myocardial ischemia. Doxazosin but not enalapril reduced exercise diastolic blood pressure.

Adrenergic alpha-Antagonists↗
PubMed1991

A double-blind crossover comparison of flecainide and slow-release mexiletine in the treatment of stable premature ventricular complexes.

In 24 patients with stable premature ventricular contractions (PVCs) greater than or equal to 100/h, Lown class greater than or equal to 2 the relative anti-arrhythmic efficacy of flecainide 150 mg twice daily and slow-release mexiletine 360 mg twice daily was evaluated in a double-blind placebo-controlled randomized crossover study. All the patients had normal ventricular function. Criteria of efficacy were: reduction greater than or equal to 70% of PVCs or reduction greater than or equal to 50% with abolition of Lown class greater than 2 arrhythmias or suppression of non-sustained ventricular tachycardias (nSVT). Twenty-two patients completed the study protocol. The placebo phases showed comparable results and no carry over effect. The criteria of efficacy were fulfilled in 20 of the 22 patients (91%) on flecainide and in 12 of the 22 (55%) on mexiletine. The absolute reductions of PVCs, couplets and nSVT obtained on flecainide and mexiletine, in comparison to the placebo, were statistically significant (p less than 0.01 for flecainide, p less than 0.05 for mexiletine). Flecainide was superior to mexiletine in overall PVC reduction (p less than 0.05). In the 17 patients with couplets the reduction obtained with flecainide was superior to mexiletine (p less than 0.05). Both drugs were highly effective on nSVT. At steady state, the mean plasma levels of both drugs were within the range of clinical efficacy. The drugs were well tolerated and no patient withdrew because of side-effects. It was concluded that at the dosages employed flecainide was superior to mexiletine in reducing premature ventricular contractions and in abolishing couplets. The efficacy of both drugs for non-sustained ventricular tachycardias was comparable. Both drugs were highly effective by comparison with the placebo.

Cardiac Complexes, Premature↗
PubMed1991

[Restenosis after coronary angioplasty: its pathogenesis and prevention].

Restenosis after coronary angioplasty is due to a proliferation of smooth muscle cells growing in the vascular lumen, beneath the residual fragments of the atherosclerotic plaque, as seen in necropsy studies and examination of the specimens removed by atherectomy. At the histological analysis thrombi or their fibrocellular organization are not usually detectable. Smooth muscle cell proliferation leading to restenosis is very similar to the one observed in the experimental models of response-to-injury, so that these models are used to investigate into the pathogenetic mechanisms of restenosis. The main stimulus to the loss of the contractile phenotype and to the start of the smooth muscle cell proliferation is represented by the growth factors delivered by platelets adhered to the disendothelialized wall and by the smooth muscle cells themselves, stretched during the dilatation. Other stimuli can be growth factors delivered by monocytes and fibroblasts, by thrombin, endothelin, angiotensin and interleukin 1. The elastic recoil of the vessel wall, the plaque debris and the regional wall shear stress can also contribute to restenosis. The restenosis tissue is different from the atheromatous plaque in that it is almost only constituted by smooth muscle cells and intercellular matrix, while atheroma is much more complex due to the presence of various kinds of cells, of necrotic debris and lipid substances. The smooth muscle cells proliferation also contributes to the pathogenesis of atherosclerosis, but the stimuli starting this process have not been clarified yet; moreover this process is much slower than restenosis, interacting with several factors. Encouraging results have been achieved in the prevention of restenosis after angioplasty in experimental models, but not in man. In order to reduce the incidence of restenosis one should improve the results of angioplasty, even by the use of atherectomy and intracoronary stents. Among pharmacologic approaches anticoagulants, heparin, antiplatelet agents, calcium-channel blockers, corticosteroids all proved ineffective. Studies are in progress evaluating the effect of inhibitors of platelet-derived growth factor (PDGF), antitumor agents and radiation therapy, hirudin, angiotensin-converting enzyme inhibitors and HMG-CoA reductase inhibitors.

Angioplasty, Balloon, Coronary↗
PubMed1991

[Heart failure in patients with valve prostheses].

Congestive heart failure in patients with prosthetic valves is a complex syndrome which poses difficult clinical and therapeutical problems. In order to identify etiologic factors, pathophysiologic substrates, clinical pictures and natural history we retrospectively evaluated 124 consecutive patients (mean age 61 +/- 11 years) with prosthetic valves, hospitalized during the 1984-1990 period because of congestive heart failure. The following main etiologies were identified: acute prosthetic valve failure (19%), chronic prosthetic failure (15%), preexisting left ventricular dysfunction (9%), newly acquired left ventricular dysfunction (8%), associated valve diseases (15%), chronic constrictive pericarditis (2%), multiple causes (31%). At a mean follow-up of 8.9 +/- 4.5 years, mortality was 8.8%/patients/year in the whole group, 3% in the subgroup with chronic prosthetic failure and 19% among the cases with preexisting left ventricular dysfunction. Among the patients who underwent reoperation because of prosthetic failure, the following were incremental risk factors: mechanical (vs biological) failing prosthetic valve, mitral prosthesis, emergency operations, mitral and or aortic insufficiency as the initial diagnosis. The preliminary knowledge of the possible etiologies and of the pathophysiologic substrates can help the physician while treating the single patient with heart failure after valve replacement. Many implications derived from this kind of patients are also useful in order to select surgical candidates among patients with valve disease.

Aortic Valve↗
PubMed1991

[Significance of the degree of oxidative hepatic metabolism in conditioning the pharmacokinetics and the pharmacodynamics of propafenone].

The aim of this study was to evaluate plasma concentrations of propafenone (P) and 5-hydroxy-propafenone (5-OH-P) at steady state in 36 patients with ventricular premature beats, Lown class greater than or equal to 2, submitted to antiarrhythmic treatment with propafenone either in acute administration (AA) (300-450 mg) or in chronic administration (CA) (150-300 mg t.i.d. for 14-21 days followed by a wash out), and to define the relationship existing between metabolic oxidative capacity and P and 5-OH-P pharmacokinetics and pharmacodynamics. Antiarrhythmic treatment resulted efficacious in 31/36 cases (86%) during AA and in 28/36 cases (78%) during CA. At steady state a wide interindividual variability was observed in plasma concentrations of P (mean = 835 +/- 619 ng/ml, coefficient of variation = 74%), in plasma concentrations of 5-OH-P (mean = 142 +/- 93 ng/ml, coefficient of variation = 65%) and of their ratio (mean = 6.51 +/- 8.53, coefficient of variation = 131%), without significant differences between responders and nonresponders. In a subgroup of 14 subjects, characterized as extensive oxidizers of dbrisoquine, a significant correlation (r = 0.97, p less than 0.001) was observed between the ratio of P and 5-OH-P plasma concentrations at steady state and oxidative metabolic capacity (expressed as debrisoquine/4-hydroxy-debrisoquine ratio). Oxidative metabolic capacity was also correlated with P half life (r = 0.82, p less than 0.002 in AA and in CA) and with the ratio of P and 5-OH-P area under curve (r = 0.91, p less than 0.001 in AA and r = 0.90) changes at the electrocardiogram (mean values = + 20% for QRS, +26% for PR). In conclusion, oxidative metabolic pathway is a crucial point in propafenone metabolization; indeed the extent of metabolic oxidative capacity, evaluable by analysis of debrisoquine oxidation, is responsible for a wide interindividual variability of P and 5-OH-P plasma concentrations, present even in a population of debrisoquine extensive oxidizers and, moreover, influences the extent of electrocardiographic changes of PR and QRS intervals, which are related to 5-OH-P plasma levels, but not to P plasma levels.

Adult↗
PubMed1991

Dipyridamole technetium-99m-2-methoxy isobutyl isonitrile tomoscintigraphic imaging for identifying diseased coronary vessels: comparison with thallium-201 stress-rest study.

A same-day double injection protocol employing 99mTc-methoxyisobutyl isonitrile (MIBI) and myocardial single-photon emission computed tomography (SPECT) for detecting coronary artery disease (CAD) was assessed in 30 patients. SPECT was performed 1 hr after a first injection (250 MBq) of 99mTc-MIBI, given after 0.56 mg/kg dipyridamole (DPD) infusion. Patients were then reinjected at rest (750 MBq) and were reimaged 1 hr later. Within 1 wk, all patients underwent a complete stress-rest SPECT thallium study. Of the 330 myocardial segments evaluated, 25 were judged ischemic by both techniques, while persistent defects were demonstrated in 50 and in 47 with 99mTc-MIBI and 201TI, respectively. Six regions were considered for diseased vessels identification. Sensitivity and specificity for CAD were 100% and 75%, respectively, for both 201TI and 99mTc-MIBI. Sensitivity for identification of diseased vessels by 201TI was 68% for LAD, 89% for RCA, and 80% for LCX as opposed to 75%, 89% and 80%, respectively, by 99mTc-MIBI. Specificity was 93% in both cases for LAD, 73% and 63% for RCA, and 53% and 46% for LCX.

Adult↗
PubMed1990

Usefulness of nicorandil in congestive heart failure.

Rest and exercise hemodynamic and hormonal effects of nicorandil, a nicotinamide-nitrate vasodilator, were assessed in 9 patients with New York Heart Association class II or III congestive heart failure (CHF) and left ventricular ejection fraction less than or equal to 40%. Single oral doses of placebo and 40 and 60 mg of nicorandil were given in a double-blind, randomized trial. Hemodynamic measurements were assessed at rest, up to 8 hours after dose and at peak exercise performed on an upright cycloergometer 1 hour after the dose. Forearm blood flow and venous capacitance were measured by plethysmography 45 minutes after dose. Plasma noradrenaline and plasma renin activity were assessed 1 hour and 2 hours after dose, respectively. Data were analyzed by analysis of variance. Peak effects were observed between 30 and 60 minutes after dose. Mean blood pressure decreased from 86 +/- 7 mm Hg after placebo to 78 +/- 7 mm Hg after 40 mg (p less than 0.05) and to 78 +/- 7 mm Hg after 60 mg (p less than 0.05) of nicorandil. Mean pulmonary artery pressure decreased from 24 +/- 11 to 15 +/- 17 mm Hg (p less than 0.05) and to 17 +/- 7 mm Hg (p less than 0.05) and mean pulmonary wedge pressure decreased from 15 +/- 8 to 9 +/- 4 mm Hg (p less than 0.05) and to 10 +/- 5 mm Hg (p less than 0.05). The changes were significant up to 6 to 8 hours after both doses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Captopril improves hemodynamic response to static exercise in patients with congestive heart failure: a double-blind, placebo-controlled, randomized trial.

Systemic and peripheral hemodynamic response to isometric exercise by handgrip test at 30% maximal voluntary contraction (MVC) for 3 minutes was assessed in 16 patients with congestive heart failure (CHF) after short-term treatment with either captopril or placebo given according to a double-blind, randomized, cross-over sequence. During placebo, isometric exercise increased blood pressure (BP) and total peripheral vascular resistance (TPVR) and decreased cardiac index (CI). Captopril reduced the pressor response to exercise (mean +/- SD) (% systolic: from 14.7 +/- 6 to 11.7 +/- 3; p less than .05/% diastolic: from 12.4 +/- 4 to 8 +/- 3; p less than .005) and increased CI (from 2.3 +/- .6 to 2.6 +/- .9 liters/min/m2; p less than .01) whereas TPVR remained virtually unchanged (from 1479 +/- 597 to 1594 +/- 692 U; NS). The changes in mean BP after exercise were inversely related to the early increase in forearm blood flow (FBF) in exercising forearm during both placebo (r = .67) and captopril (r = .71). The extent of reduction in mean BP response after captopril was inversely related to the extra increase in exercising FBF determined by the drug when compared to placebo (r = .73). We conclude that captopril is able to improve the hemodynamic response to static exercise in patients with CHF, probably by increasing the blood supply to exercising muscles during contraction, thus blunting the extent of reflex pressor response.

Blood Pressure↗
PubMed1990

Minimal effective concentration values of propafenone and 5-hydroxy-propafenone in acute and chronic therapy.

We evaluated the antiarrhythmic efficacy and the minimal effective concentrations of propafenone and its metabolite 5-hydroxy-propafenone during a) acute intravenous infusion (1.5 mg/kg in bolus followed by 45 minutes infusion), b) an acute oral single-dose test (450 mg), and c) 14-day chronic therapy (300 mg tid) followed by a washout. Oxidative metabolism was assessed by a debrisoquine oral test in every patient. Eleven patients with stable ventricular premature beats (VPBs) greater than or equal to 300/hr and Lown class greater than or equal to 3 completed the study. The main results emphasized a certain discrepancy between the clinical effect of the acute intravenous infusion (efficacy in 5 out of 11 patients) and of the acute oral test and chronic therapy (efficacy in 11/11), with a time lag of the ECG changes during the acute intravenous infusion. The minimal effective concentrations were lower after acute oral administration compared with chronic treatment both for propafenone (200 +/- 189 ng/ml vs. 492 +/- 530 ng/ml; p less than 0.05) and for 5-hydroxy-propafenone (82 +/- 40 ng/ml vs. 149 +/- 80 ng/ml; p less than 0.02). A linear correlation was demonstrated between drug/metabolite ratios of propafenone and debrisoquine, either after acute oral (r = 0.91) or after chronic administration (r = 0.84). The pharmacokinetics of propafenone was nonlinear and showed wide interindividual variations.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

Idiopathic restrictive cardiomyopathy in the young: report of two cases.

Two cases of idiopathic restrictive cardiomyopathy in young age are reported. This rare kind of restrictive cardiomyopathy is characterized by the absence of specific histologic features of myocardial abnormalities. In both cases (aged 12 and 9 years at diagnosis), the clinical picture was characterized by severe and slowly progressive congestive heart failure. The electrocardiogram showed biventricular hypertrophy, right bundle branch block and pseudoinfarctional Q waves. Echocardiography revealed moderate pericardial effusion, biatrial enlargement, and normal or nearly normal biventricular dimensions and systolic function. Cardiac catheterization disclosed the typically restrictive filling pattern. Right ventricular endomyocardial biopsy demonstrated moderate interstitial fibrosis and cellular hypertrophy without any evidence of infiltrative or storage myocardial disease or endocardial pathology. One patient underwent cardiac transplantation, whereas in the other, transplantation was contraindicated because of longstanding pulmonary hypertension and liver cirrhosis. The knowledge of this rare entity may correctly orient the diagnostic process in children suspected of having restrictive myocardial disease. Heart, or even heart-lung, transplantation must be considered in cases with congestive heart failure before irreversible damage occurs in many organs.

Adult↗
PubMed1990

Comparative haemodynamic effects of transdermal vs intravenous nitroglycerin in acute myocardial infarction with elevated pulmonary artery wedge pressure.

The comparative haemodynamic effects of transdermal and intravenous nitroglycerin were evaluated in 16 patients with haemodynamic and radiographic left heart failure following a recent myocardial infarction. After the control period patients were randomized to transdermal (10 mg(24 h)-1) or intravenous (mean dose: 40 +/- 9 micrograms min-1) nitroglycerin. Haemodynamic parameters were recorded after 0.5,1,2,6,12,18 and 24 h during administration of the drug and 2 h after drug discontinuation. After the washout period the alternate system of nitroglycerin administration was adopted, according to a cross-over design. No differences were found in baseline measurements. Transdermal nitroglycerin reduced the pulmonary artery wedge pressure after 0.5 h (from 21 +/- 5 to 16 +/- 5 mmHg; P less than 0.05). The peak effect occurred at 2 h (12 +/- 5 mmHg). The improvement was sustained over 24 h. Transdermal nitroglycerin also significantly reduced mean pulmonary arterial and right atrial pressures (from 28 +/- 3 to 20 +/- 5 mmHg and from 6 +/- 3 to 2 +/- 2 mmHg at peak effect, respectively). Cardiac index increased from 2.5 +/- 0.6 to 2.8 +/- 0.8 l min-1 m-2 (P less than 0.05). There was no change in heart rate. Similar haemodynamic changes were observed after the intravenous infusion of nitroglycerin. Thus transdermal nitroglycerin is a safe and effective treatment of acute myocardial infarction with signs of left ventricular failure when an intravenous nitroglycerin infusion cannot be properly implemented.

Administration, Cutaneous↗
PubMed1990

Enhanced thrombolytic efficacy and reduction of infarct size by simultaneous infusion of streptokinase and heparin.

Because paradoxical increase in thrombin activity was reported after the administration of streptokinase in patients with acute myocardial infarction the velocity of reperfusion and degree of myocardial damage were studied when heparin was infused during rather than after streptokinase infusion. Thirty seven consecutive patients with acute myocardial infarction were randomised to receive intravenous heparin during (group 1, n = 18) or after (group 2, n = 19) streptokinase (1.5 megaunits over 60 minutes). Markers of reperfusion were monitored every 15 minutes for 3 hours. The serum concentration of creatine kinase was measured every 2 hours. The two groups were similar in terms of age and sex distribution, infarct site, time to treatment, and baseline myocardial ischaemia. Patients in group 1 had a significantly shorter mean (SD) reperfusion time (57 (35) minutes v 101 (47)). From 60 to 120 minutes after randomisation there were significant differences in ST segment elevation between the groups. Serum creatine kinase MB peaked earlier (8 (2) hours) in group 1 than in group 2 (10 (4) hours). The peak concentration was significantly lower in group 1 (87 (47) mU/ml) than in group 2 (134 (96) mU/ml) and infarcts were smaller (25.2 (9.8) gram equivalents/m2) in group 1 than in group 2 (35.1 (10.2) gram equivalents/m2). Simultaneous infusion of heparin and streptokinase speeds up the appearance of signs of reperfusion and reduces infarct size.

Aged↗
PubMed1990

[The clinical evaluation of the severity of chronic heart failure: a comparison between the NYHA functional class and the Goldman scale].

Controversies exist about the functional evaluation of chronic heart failure; aim of this study has been the assessment of the feasibility of the Goldman classification, based on the metabolic cost of various daily physical activities, in a cohort of patients with mild to moderate heart failure, its relation to NYHA class and to the main clinical parameters currently used. We evaluated 114 patients (mean age 61 years) with mild to moderate heart failure due to idiopathic cardiomyopathy (78%), ischemic heart disease (14%) and others (8%). Based on the Goldman classification there were 82 patients (72%) in second and 28 (24%) in third class while 83 (73%) were in NYHA II class and 31 (27%) in NYHA III class. The concordance rate between Goldman second and NYHA II class was 84% and 64% between Goldman third and NYHA III class. The cardiothoracic ratio was statistically different in all 3 Goldman classes while this happened only in NYHA IIM and III versus IIS. Double product and duration of exercise were statistically different in all Goldman classes but only in NYHA II and III class. No relation was observed with ejection fraction on echocardiogram. In the subgroups analysis there was a linear positive relation between duration of exercise versus double product and cardiothoracic ratio versus cardiac volume. We conclude that Goldman class is a feasible method to assess quality of life in chronic heart failure and is more helpful and objective than NYHA class in determining the functional class of the patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Double injection of Tc99m-methoxy isobutyl isonitrile in the same session: diagnostic accuracy in tomography compared with that of thallium-201 chloride].

Radionuclide imaging with thallium-201 is widely accepted for identifying the presence and the severity of coronary artery disease, but this radiotracer is hampered by some limitations (low-energy photons and long physical half-life) and by delivering difficulties. Therefore, various technetium 99m-labelled compounds have been proposed as myocardial perfusion agents. In particular, technetium 99m methoxy isobutyl isonitrile (Tc99m-MIBI) showed the most favourable characteristics for clinical applications. Recently a study protocol involving a split dose of the radiocompound injected in the same day has been proposed. The aim of this work has been to evaluate the diagnostic accuracy of this procedure coupled with tomographic study (SPECT-MIBI) in a group of patients with documented coronary artery disease and to compare the results with those obtained by means of Tl-201 tomographic studies (SPECT-Tl) in the same patient group. Twenty-four patients, 21 males and 3 females, entered the study: the mean age was 57 +/- 6 years (44-71). For the rest study the patients were given 250 MBq of Tc99m-MIBI. Then, after 2-3 hours, they were reinjected with a second dose of 750 MBq when exercise endpoints were reached. The studies with Tl-201 were carried out the week before or subsequent the Tc99m-MIBI studies. Sensitivity was 88% with SPECT-Tl and 78% with SPECT-MIBI for the anterior descending artery (LAD), 86% and 64% respectively for right coronary artery disease (RCA) and 69% with both procedures for the left circumflex artery (LCX). Specificity was 88% with SPECT-Tl and 78% with SPECT-MIBI LAD, 60% with both procedures for RCA and 55% and 81% respectively for LCX. Coronary artery disease, involving 2 or more vessels, was correctly identified in 93% of patients by Tl-201 studies and only in 60% of patients by Tc99m-MIBI. In several cases the high count rate obtained by Tc99m-MIBI did not allow the identification of hypoperfused segments. In conclusion, a rest-stress double injection of Tc99m-MIBI in a same-day protocol has shown a lower sensitivity for detecting coronary lesions than Tl-201. Moreover, radiation exposure for medical and technical staff is greater with Tc99m-MIBI than with Tl-201.

Adult↗
PubMed1990

[Surgical therapy for prosthetic heart valve endocarditis: immediate results and follow-up].

Between January 1980 and May 1990 17 patients underwent surgery for prosthetic valve endocarditis at Cardiosurgical Department of Bologna University. Ten patients were female and seven male, the average age was 33 years (range 19 to 67 years). The interval from valve replacement to onset of symptoms of prosthetic valve endocarditis was less than 2 months in 5 patients and longer than 2 months in 12 patients. Sixteen of 17 infected prostheses were mechanical and one biological. All patients were surgically treated and the infected prostheses replaced with new valve prostheses. The hospital mortality rate for early prosthetic valve endocarditis was 60%, for late endocarditis was 16.5%, global hospital mortality was 29.4%.

Adult↗
PubMed1990

[Effect of diazepam on mitochondrial respiration].

Our hypothesis that the strong effects of neutropic drugs on nervous system have hidden more widespread effects on all tissues and cells, is collecting evidences in our laboratory. We have essayed in vitro benzodiazepines on liver rat mitochondria. The present work deals with experiments on diazepam: it depresses the respiration coupled to phorphorylation in mitochondria having a good respiratory control; so respiratory control too is depressed. Also P/O ratio is lowered.

Animals↗