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Biomedical subjects

O Visioli

Publications and source records attributed to O Visioli.

At least 91 records · Page 5Linked to original sources
PubMed1990

Assessment of peak oxygen consumption, lactate and ventilatory thresholds and correlation with resting and exercise hemodynamic data in chronic congestive heart failure.

To determine the clinical value of respiratory gas analysis during exercise, oxygen consumption (VO2) at peak exercise and at lactate and ventilatory threshold was assessed in 34 patients with chronic heart failure who underwent maximal exercise testing with expiratory gas monitoring and serial determinations of mixed venous lactate and hemodynamics by Swan-Ganz catheterization. A lactate threshold, defined as the point of abrupt increment of blood lactate, could be identified in every patient; the ventilatory threshold, detected on the basis of the respiratory changes, was found in 26 patients (77%). Lactate and ventilatory thresholds were significantly related to each other (r = 0.94; p less than 0.001) and to peak VO2 (r = 0.89; p less than 0.001 in both). Among the resting hemodynamic measurements, peak VO2 was significantly related only to total pulmonary resistances (r = -0.35). Among the parameters at maximal exercise, it was positively related to cardiac index, stroke work, stroke volume index and mean arterial pressure (r = 0.89, 0.74, 0.74 and 0.56, respectively) and inversely related to systemic vascular and total pulmonary resistances (r = -0.74 and -0.63). Using multivariate stepwise regression analysis only maximal cardiac index and, to a lesser degree, total pulmonary resistance were related to peak VO2. Similar correlations were found between the hemodynamics and the lactate and ventilatory threshold. Thus, peak VO2, lactate and ventilatory thresholds can be detected in most patients with chronic heart failure. These parameters are highly correlated to each other and bear similar relations to the hemodynamic response to exercise. The cardiac index is the main central hemodynamic determinant of exercise capacity.

Adult↗
PubMed1990

Beta 1- and beta 2-receptors are differentially desensitized in an experimental model of heart failure.

Recent reports suggested that a complex alteration in beta-receptor function occurs in failing human myocardium. We evaluated beta-receptor-subtype activity in an experimental model of monocrotaline (MCT)-induced cardiomyopathy in the rat. Through pulmonary hypertension, MCT causes right ventricular hypertrophy (RVH), either associated with heart failure or not, beta-Receptor function was evaluated in both failing-hypertrophic and hypertrophic hearts in binding studies with [125I]iodocyanopindolol (ICYP) and by measuring adenylate cyclase (AC) activity. In the right failing ventricle, beta 1- but not beta 2-receptor density was decreased. Lesion-associated modifications in the adenylate cyclase system were also observed: isoproterenol- and guanosine 5' [beta, gamma-imido]triphosphate [Gpp(NH)p]-stimulated cyclic AMP formation was reduced in the right failing ventricle, while the cyclic AMP responses to NaF and forskolin were unchanged. On the other hand, no changes in either beta-receptor density or function were found in hypertrophic ventricles. MCT-induced heart failure in the rat is thus associated with a selective decrease of beta 1-receptor density and function. These results suggest that MCT-induced cardiac failure may be an appropriate model in which to investigate heart insufficiency further.

Adenylyl Cyclases↗
PubMed1990

Occurrence of oxidative stress during reperfusion of the human heart.

We have investigated the relation between occurrence of myocardial oxidative stress and functional recovery during postischemic reperfusion in 20 selected patients subjected to aortocoronary bypass grafting. Patients were selected for having normal percent ejection fraction and left ventricular end-diastolic pressure before the operation. Occurrence of oxidative stress was assessed by measuring the formation and release of oxidized glutathione (GSSG) in the coronary sinus immediately before aortic cross-clamp, 1, 5, 10, and 20 minutes after removal of aortic cross-clamp, and 10 and 20 minutes after the end of cardiopulmonary bypass. Reduced glutathione (GSH), lactate, and creatine phosphokinase release were also monitored with the same timing. Standard hemodynamic measurements were recorded by means of a triple-lumen thermodilution pulmonary artery catheter before sternotomy, 15 minutes after the end of cardiopulmonary bypass, and during the 24 hours after termination of cardiopulmonary bypass. Reperfusion in patients after a short period of ischemia (less than 30 minutes; group 1) resulted in a small and transient release in the coronary sinus of GSSG and GSH and in a progressive improvement of hemodynamic parameters reaching a stable state 4 hours after the operation. In patients with a period of ischemia longer than 30 minutes (group 2), reperfusion induced a marked and sustained release of lactate, GSH, and GSSG; the arteriocoronary sinus difference for GSSG was still negative after the end of cardiopulmonary bypass. The arteriocoronary sinus difference for creatine phosphokinase also remained negative for as long as 20 minutes after cardiopulmonary bypass, and the rate of functional recovery was significantly delayed, reaching the values of group 1 only 12 hours after the operation. In these patients there was a positive correlation (r = 0.88, p less than 0.01) between the duration of ischemia and the myocardial arteriovenous difference for GSSG. In addition, there was a negative correlation between the arteriocoronary sinus difference for GSSG and cardiac index measured 2, 4, and 6 hours after the operation. These data suggest for the first time that, depending on the severity of the ischemic period, oxidative stress occurs during reperfusion of patients with coronary artery disease who are subjected to heart surgery and that it may be linked with a delay in postoperative recovery of cardiac function.

Coronary Artery Bypass↗
PubMed1990

[The adrenergic beta system in an experimental model of heart failure].

Reports in the literature have suggested that a complex alteration in beta-receptor pathway takes place in failing human myocardium. The purpose of our study was to evaluate the beta-adrenergic receptor system in an experimental model of heart failure induced by monocrotaline in rats. Monocrotaline, administered with a single intraperitoneal injection (50 mg/Kg), causes pulmonary hypertension and right ventricular hypertrophy, associated with congestive heart failure. beta 1 and beta 2-receptors were characterized in the right ventricle by direct radioligand binding utilizing [125I] Iodocyanopindolol and selective beta 1-(CGP 20712A) and beta 2-(ICI 118551) antagonists. Adenylate cyclase was measured in basal condition and in the presence of different stimulators as isoproterenol with ICI 118551 (beta 1-receptor-stimulated activity), isoproterenol with CGP 20712A (beta 2-receptor-stimulated activity), Gpp(NH)p, NaF and forskolin. In the right ventricle of the failing hearts the beta 1-receptor density decreased selectively (-55.8%) while the beta 2-receptor density was unchanged. Modifications in the adenylate cyclase system were demonstrated: a reduction in the basal and beta 1- and beta 2-stimulated adenylate cyclase activity; a decrease in adenylate cyclase activation elicited by Gpp(NH)p, but not by forskolin and NaF. In conclusion, these data suggest that in monocrotaline-induced heart failure in the rat there is a selective beta 1-receptor down-regulation and an impaired coupling efficiency of G proteins. These results are in line with biochemical changes found in patients with heart failure.

Adenylyl Cyclases↗
PubMed1990

Hormonal response in untreated myocardial infarction.

Plasma levels of a variety of hormones have been measured in patients within two hours of the onset of symptoms of myocardial infarction and before commencement of any treatment. Increased plasma concentrations were found for norepinephrine, epinephrine, glucagon, aldosterone, vasopressin, atrial natriuretic peptide, corticotrophin, prolactin, cortisol and substance P while plasma renin activity was raised. The plasma concentrations of insulin, growth hormone, neurotensin, bombesin and vasointestinal peptide were normal.

Female↗
PubMed1989

Diagnosis of acute myocardial infarction by indium-111 antimyosin antibodies and correlation with the traditional techniques for the evaluation of extent and localization.

This clinical study evaluated the accuracy of planar myocardial scintigraphy with antimyosin monoclonal antibodies radiolabeled with indium-111 (AMA-Fab) in the detection and localization of acute myocardial infarction (AMI). Fifty-seven patients admitted for suspected AMI were studied; 17 patients underwent thrombolytic therapy with intravenous streptokinase and 11 had clinical signs of reperfusion; 9 had had a previous myocardial infarction. Fifty of 57 patients were discharged from the coronary care unit with a confirmed diagnosis of AMI. The AMA-Fab study results were positive for AMI in 49 patients (98%) and negative in 1 (2%). Among the 7 patients without AMI, 5 had unstable angina, 1 had Prinzmetal's variant angina and 1 had acute pancreatitis. AMA-Fab results were negative in 6 of 7 patients (85%) and positive in 1 (15%). Therefore, the sensitivity and specificity of AMA-Fab scintigraphy were 0.98 and 0.85, respectively. To assess accuracy in defining the extent and location of AMI, AMA-Fab results were compared with those of the electrocardiogram, echocardiogram, technetium-99m pyrophosphate myocardial scintigraphy and coronary angiography and left ventriculography. AMA-Fab scintigraphy showed a good concordance with the traditional techniques in the topographic definition of the infarcted regions. No uptake of AMA-Fab was seen in the regions of previous old infarcts. Ten healthy volunteers also underwent AMA-Fab scintigraphy. No evidence of myocardial tracer uptake was noted in them. No adverse reactions or side effects were noted after injection of AMA-Fab in any patient. It is concluded that planar myocardial scintigraphy with AMA-Fab is a reliable method for AMI detection and location.

Adult↗
PubMed1989

Prolonged protective effect of the calcium antagonist anipamil on the ischemic reperfused rabbit myocardium: comparison with verapamil.

To assess whether pretreatment with the calcium antagonist anipamil protects the heart against ischemic and reperfusion damage and to establish how long the protection persists after cessation of the therapy, rabbits were injected subcutaneously twice daily for 5 days with 2 mg/kg body weight of this drug. The heart was then isolated 2, 6, or 12 hours after the last injection and was perfused by the Langendorff technique during a control period and 90 minutes of total ischemia (37 degrees C), followed by 30 minutes of reperfusion. Diastolic and developed pressure was monitored; coronary effluent was collected and assayed for creatine phosphokinase (CPK); mitochondria were harvested and assayed for respiratory activity, ATP production, and calcium content; and tissue concentration of adenosine triphosphate (ATP) and creatine phosphate were determined. The data obtained with anipamil were compared with those obtained with verapamil administered to the rabbit at the same dose and following the same procedure. Pretreatment with anipamil induced a negative inotropic effect under normoxic conditions; reduced the rate and extent of depletion of ATP and creatine phosphate during ischemia, with an incomplete restoration of the nucleotides after reperfusion; maintained mitochondrial function and calcium homeostasis during ischemia and reperfusion; reduced the rate of CPK release; and improved the recovery of ventricular function on reperfusion. The protective effects of anipamil persisted for as long as 12 hours after the last administration. In contrast, the protective and negative inotropic effects of verapamil were no longer apparent in heart isolated 6 or 12 hours after the last dose of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1989

Electrophysiological evaluation of the sinus node in patients with atrioventricular and/or intraventricular conduction defects.

The authors evaluated retrospectively sinoatrial conduction time (SACT), sinus node recovery time (SNRT), and corrected sinus node recovery time (CSNRT) in 272 patients with atrioventricular and/or intraventricular conduction defects without evidence of overt sinus node dysfunction. The study was designed to determine the prevalence of electrophysiologic sinus node abnormalities in patients with overt atrioventricular and/or intraventricular conduction defects. One or more sinus node electrophysiological abnormalities were observed in 133 cases (48.9%). There was a significant prevalence of electrophysiologic sinus node abnormalities only in patients older than 71 years of age. The data suggest that the involvement of the specialized conduction system is much more diffuse than one might expect simply observing the single recorded ECG defect and that the prevalence of associated defects of the conduction system increases with increasing age of patients.

Adolescent↗
PubMed1989

Efficacy of ibopamine treatment in patients with advanced heart failure: purpose of a new therapeutic scheme with multiple daily administrations.

Eighteen patients with severe unstable heart failure who presented with hemodynamic deterioration after withdrawal of i.v. dopamine were treated with high doses of ibopamine (100 mg eight times a day, orally) in association with digitalis, diuretic, and vasodilator therapy. Ibopamine, used at these dosages, could effectively substitute for the i.v. infusion of dopamine in 15 of the 18 studied patients. Each patient was studied by right heart Swan-Ganz catheterization and two-dimensional echocardiography before and during ibopamine infusion, after dopamine withdrawal, and after acute ibopamine administration; measurements were then made after 3 months of chronic ibopamine treatment (100 mg eight times a day). Blood samples for plasma dopamine and epinine concentrations were obtained at the time of the hemodynamic measurements. Both drugs did not induce any significant change in arterial pressure whereas heart rate was slightly reduced after dopamine and chronic ibopamine. Cardiac index and stroke volume index were significantly increased by dopamine (from 1.81 to 2.24 L/min/m2 and from 20.3 +/- 6.5 to 27.7 +/- 8.1 ml/beat/m2) and acute and chronic ibopamine (from 1.80 to 2.15 and 2.23 L/min/m2 and from 22.4 +/- 6.8 to 28.2 +/- 7.5 and 30.3 +/- 7.0 ml/beat/m2, respectively); these changes were attended by a decrease in systemic vascular resistance; pulmonary pressures were not significantly modified. No significant change of the echocardiographic parameters was noted. During dopamine infusion, mean dopamine plasma concentrations were 211.8 +/- 32.4 pmol/ml; after acute and repeated administration of ibopamine, free epinine plasma concentrations averaged 45.1 +/- 14.5 and 62.2 +/- 12.7 pmol/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1989

Clinical pharmacology of inodilators.

Recent advances in our knowledge of heart failure have shown that both a central and a peripheral factor are involved in this syndrome. Therefore, the ideal drug should combine the properties of a positive inotropic agent with those of a peripheral vasodilator; many drugs recently introduced into clinical practice have been shown to present both of these features, and the term "inodilators" has been used to characterize them. Inodilators can be further classified on the basis of their mechanism of action, i.e., phosphodiesterase inhibitors, and sympathomimetic and dopaminergic drugs. Phosphodiesterase inhibitors include bipyridine, imidazolone, and benzimidazole derivatives, which present potent inotropic and vasodilatatory actions. Despite their favorable acute effects, long-term studies have often yielded controversial, and sometimes disappointing, results as their chronic administration seems often to be associated with untoward effects and, above all, a poor prognosis. Sympathomimetic agonists act by stimulation of beta-receptors, with a consequent increase of myocardial contractility and peripheral vasodilation. Differently from the parenteral drugs (e.g., dobutamine), the oral agents present many important shortcomings including central nervous system effects, increased myocardial oxygen consumption, tachyarrhythmias, and, above all, development of tolerance during chronic administration. Dopaminergic drugs possess a unique pharmacologic profile since they add to the adrenergic stimulation their selective action on dopaminergic receptors. Dopamine is still one of the most useful drugs for the treatment of acute heart failure; the two oral drugs that more closely resemble its actions are levodopa and ibopamine. The administration of levodopa to patients with heart failure can induce a significant hemodynamic improvement that is maintained during chronic therapy. Ibopamine has been widely shown to cause a significant hemodynamic improvement in patients with heart failure. Its effects can be ascribed to a moderate increase of myocardial contractility accompanied by peripheral and renal vasodilatatory actions. This drug can also counteract some of the neurohumoral mechanisms (e.g., sympathetic stimulation and aldosterone secretion) that are activated in heart failure. These features can explain the favorable results that have also been recently obtained after the chronic administration of ibopamine.

Cardiotonic Agents↗
PubMed1989

[Effects of intravenous flecainide in the treatment of paroxysmal or recent-onset atrial fibrillations].

Intravenous flecainide (2 mg/Kg for 15 min) was used in 30 patients (18 men and 12 women aged 23 to 85 years: mean 62) with recent or paroxysmal atrial fibrillation: 5 patients returned to sinus rhythm during flecainide administration while other 23 patients did it not later than 2 hours. Treatment with intravenous flecainide proved to be safe without significant side effects. Further investigations are required to define the effects of flecainide in the treatment of atrial fibrillation; at the moment it must be admitted that flecainide acetate is a useful, safe, fast acting drug for the conversion of paroxysmal or recent atrial fibrillation to sinus rhythm.

Adult↗
PubMed1989

[Pharmacologic characterization of the internal mammary artery used in myocardial revascularization].

The aim of this study concerned the pharmacological investigation of the isolated internal mammary artery. Spirally-cut vascular segments were obtained from patients undergoing myocardial revascularization and set up in isolated baths under isometrical tension. Reactivity of internal mammary artery preparations to stimulatory and inhibitory agents was evaluated. KCl (90 mM), noradrenaline (10-8)-10(-5) M) and serotonine (10(-9)-10(-5) M) induced a tonic contraction lasting for more than 60 min. Angiotensin II (10(-6)-10(-5) M) and dopamine (10)-8)-10(4) M) resulted virtually uneffective. The serotonine-induced contractions were strongly inhibited by ketanserin (10-9)-10(-6) M), a selective S2-blocker, and also by verapamil (10(-3)-10(-6) M) and nitroglycerin (10(-7)-10(-5) M). These data suggest that internal mammary artery is sensitive to different contractile agents, in particular serotonine activates muscular contractions through S2 receptors. The knowledge of such a mechanism may be of clinical relevance.

Acetylcholine↗
PubMed1989

[Combination use of an automatic anti-tachycardia pacemaker and an automatic implantable cardioverter-defibrillator in sustained recurrent ventricular tachycardia resistant to drugs].

We used the combination of an antitachycardia automatic ventricular pacemaker with the automatic implantable cardioverter-defibrillator in two patients with sustained, recurrent, drug-resistant ventricular tachycardias in whom a surgical ablation was not indicated. The indications for the combined use of the two systems were the possibility to control: a) the ventricular tachycardias with ventricular programmed stimulation; b) the arrhythmias which might eventually degenerate into ventricular flutter or fibrillation (as a result of anti-tachycardia pacing) with the defibrillator. To avoid any possible interference between the two systems we used the following protocol: a) endocardial bipolar pacing; b) the sensing electrodes of the defibrillator were placed as far as possible from the endocardial one; c) a suitable programming of the pacemaker output; d) a careful selection of the anti-tachycardia pacing programme (burst rate inferior to the cut-off rate of the cardioverter-defibrillator and/or a duration of the burst pacing inferior to the arrhythmia sensing time of the defibrillator); e) use of cardioverter-defibrillators with a high cut-off rate. We never observed, during the follow-up (11 and 4 months, respectively), interference between the two systems. Both patients had ventricular tachycardia recurrences (51 and 3 episodes, respectively). The arrhythmias were correctly detected and interrupted by the pacemaker without the intervention of the defibrillator. These data confirm the feasibility of the combined use of the two systems in patients with ventricular tachycardias and, in selected cases, this approach is preferable. The anti-tachycardia pacemaker counteracts some limitations of the defibrillators available at present. It offers a protection against bradyarrhythmias and allows a more precise storage of arrhythmic events. The anti-tachycardia pacemaker often controls ventricular tachycardias without the intervention of the defibrillator, thus giving the same a longer life-span and allowing patients to avoid the shock.

Aged↗
PubMed1989

[Thromboembolus migrating into the right heart in pulmonary embolism. Echocardiographic and clinico-therapeutic aspects in 7 cases and review of the literature].

We report the clinical, echocardiographic and therapeutic aspects and the evolution of 7 cases of right cardiac migrant thromboembolus in pulmonary embolism (5 M and 2 F, aged 43 to 91). Our data are also compared with all the cases reported in the literature (77 patients). During a sample year (1987) we systematically performed two-dimensional echocardiograms (2D Echo) as early as possible in all the patients admitted to our Coronary Care Unit for suspected pulmonary embolism; among 42 patients the diagnosis of pulmonary embolism was confirmed in 30 out of 42 patients. A relatively high incidence of thromboembolus was found (5/30, 17% in 1987); this finding seems to be relative to the early execution of the 2D Echo study (thromboembolus was found in 4/5 patients when 2D Echo was performed within 20 hours and in only 1/23 when 2D Echo was performed later). The 2D Echo was always evocative of freely floating migrant thromboembolus (6 in right atrium, 1 in right ventricle) and no differential diagnosis with thrombi in situ or other masses was necessary. The therapy for 6 patients hospitalized for pulmonary embolism and surviving the first hours (1 patient died immediately) was: surgical in 1 case, medical in the other 5. Medical therapy consisted only of heparin-calcium in one patient and heparin-calcium + dipyridamole in another because of contra-indications for more aggressive therapy. One patient underwent anticoagulant therapy with i.v. heparin. The remaining two underwent fibrinolytic therapy with urokinase and, afterwards, anticoagulant therapy: in 1 case the therapy was started after the embolization of the mass in the pulmonary artery had occurred; in the other one we observed the progressive reduction of thromboembolus until its disappearance within 5 days without any signs of further embolization. All patients survived and were discharged within 25 days, despite the occurrence of lung embolization in 4 of them. The review of 77 cases reported in the literature shows good outcomes for embolectomy when compared with medical therapy, but almost half of the patients underwent surgical therapy directly. Medical therapy experience, particularly with thrombolytic agents (10 cases in all), is still too scarce to exclude its role, as indeed our experience seems to indicate.

Adult↗