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Biomedical subjects

A Branzi

Publications and source records attributed to A Branzi.

At least 127 records · Page 7Linked to original sources
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↗
PubMed1990

Reduced oxidative activity of circulating neutrophils in patients after myocardial infarction.

Circulating neutrophils isolated from patients 3-4 h after a myocardial infarction produced less O2-. compared with controls, when stimulated with phorbol myristate acetate or formyl-methionine-leucine-phenylalanine. Three days after the infarction the O2-. generation elicited by both stimuli further decreased markedly. Seven and 15 days after infarction the O2-. stimulated production was only slightly lower than or similar to the control values. The neutrophils of infarcted patients showed an augmented latency period before O2-. production compared with controls in response to exogenous stimuli, particularly three days after infarction. Electron microscopy revealed that the neutrophils isolated from the infarcted patients displayed signs of cell exhaustion with few alterations of the plasma membranes when stimulated with phorbol ester. In contrast, control neutrophils displayed alterations of the plasma membranes characteristic of active neutrophils. The results of this study indicate that the circulating neutrophils appear exhausted and functionally inhibited immediately after myocardial infarction.

Aged↗
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

[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↗
PubMed1989

Myocardial, coronary, and peripheral effects of xamoterol (ICI 118,587) in open-chest pigs.

The hemodynamic and coronary effects of increasing doses of xamoterol, a beta-adrenoceptor partial agonist, were assessed in an anesthetized pig preparation in which cardiovascular reflexes were abolished and sympathetic tone was modified by infusion of noradrenaline (NA). Xamoterol, in basal conditions, increased heart rate (HR) from 104 +/- 12 to 120 +/- 13 beats/min (p less than .001); systolic, diastolic, and mean blood pressure, respectively, from 77 +/- 8 to 103 +/- 17 mmHg (p less than .01), from 48 +/- 7 to 70 +/- 12 mmHg (p less than .01), and from 58 +/- 7 to 84 +/- 14 mmHg (p less than .01); left ventricular dP/dT max from 2098 +/- 564 to 4205 +/- 937 mmHg/sec (p less than .001); and systemic vascular resistance (SVR) from 1745 +/- 564 to 2270 +/- 739 dynes sec cm-5 (p less than .01). The increase in HR and dP/dT max brought about by xamoterol was about 37% and 56%, respectively, of the maximum increase produced by NA. At the highest level of sympathetic tone, xamoterol reduced HR from 148 +/- 11 to 122 +/- 11 beats/min (p less than .001) and no significant change was observed in dP/dT max. The increase in blood pressure and SVR induced by xamoterol was maintained at each level of sympathetic tone. On the contrary, SVR did not change after NA, as expected, since receptors were fully blocked. For a given inotropic effect, xamoterol and NA produced a similar increase in coronary blood flow and myocardial O2 consumption.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1989

[Idiopathic restrictive cardiomyopathy: clinical, hemodynamic, histologic and prognostic profile].

Idiopathic restrictive cardiomyopathy is a rare myocardial disease characterized by restrictive physiology without a specific histologic basis. To assess its clinical, hemodynamic, morphologic and prognostic details we retrospectively evaluated all the patients hospitalized in our Institute from 1974 to 1988. Nine patients, aged 42 +/- 16 years, M/F ratio = 0.29, who represent 64% of all the restrictive myocardial diseases biopsied were identified. Severe cardiac heart failure (3-4 NYHA) and arrhythmias (ventricular and supraventricular) were extremely common. The electrocardiogram showed several non specific signs: low voltage of QRS in peripheral leads (4/7), pseudo-infarctional aspects (3/7), mono or biventricular hypertrophy (3/7) disturbance of ventricular conduction (3/7), aspecific abnormalities of ventricular repolarization (3/7). All patients showed a prolonged QTc. M-mode and 2-dimensional echocardiography demonstrated in 6 cases biatrial enlargement, normal or slightly enlarged ventricles, normal or moderately depressed fractional shortening; biventricular concentric hypertrophy was detected in 3 cases, asymmetrical septal hypertrophy in 1. Five patients showed pericardial effusion. Cardiac catheterization disclosed an increase of left and right ventricular end-diastolic pressures (8/8) with a dip-plateau pattern and/or characteristic W waveform in the atrial pressure tracing (9/9). Passive pulmonary hypertension was detected in 6/9 cases. The cardiac index was decreased in 4/8 cases. Left ventricular angiography showed mitral regurgitation in 5/8 patients, tricuspidal in 5/8. Ejection fraction was decreased in 3/8 cases. Endomyocardial biopsy showed interstitial fibrosis (8/9), cellular hypertrophy and/or nuclear alterations (7/9), slight endocardial thickening (2/9). At a mean follow-up of 22 +/- 15 months 3 patients died and 2 underwent heart transplantation. In conclusion idiopathic restrictive cardiomyopathy is one of the most frequent forms of restrictive myocardial diseases in our geographic area. Severe congestive heart failure and arrhythmias are extremely common. The disease can be suspected by clinical, electrocardiographic and echocardiographic features, but the final diagnosis requires cardiac catheterization and endomyocardial biopsy. Prognosis is severe and heart transplantation must be considered in the cases with severe heart failure.

Adolescent↗
PubMed1988

Haemodynamic effects of short term intravenous amiodarone for hypertrophic cardiomyopathy.

The haemodynamic effects of an intravenous amiodarone infusion (5 mg/kg for 10 minutes) were measured in ten patients with hypertrophic cardiomyopathy (two with a left ventricular outflow gradient at rest) five, 15, and 30 minutes after drug administration. Mean (SD) pulmonary capillary wedge pressure rose significantly at five and 15 minutes (from 12.3 (6.2) mm Hg to 17.6 (9.2) and to 16.2 (8.6] with a subsequent tendency to fall to control values at 30 minutes. Mean right atrial and right ventricular end diastolic pressures increased from 3.6 (1.8) mm Hg to 7.3 (3.1) and from 6.3 (2.4) to 9.8 (3.2) mm Hg respectively at 30 minutes. The increase in filling pressures was paralleled by a decrease of left ventricular max dP/dt from 1522 (414) to 1372 (327) to 1316 (338) and to 1326 (379) five, 15, and 30 minutes after infusion. Despite this slight negative inotropic effect, cardiac index and stroke volume index were unchanged or slightly increased, possibly because of the decrease in systemic vascular resistance (from 1326 (330) dyn s cm-5/m2 to 1152 (285]. In both patients with outflow gradient the pressure gradient at rest decreased (from 110 to 65 and from 85 to 65 mm Hg) through a reduction of left ventricular systolic pressure. Thus short term intravenous infusion of amiodarone is safe in patients with hypertrophic cardiomyopathy. The main changes were a mild depression of ventricular contractility, which was well tolerated and adequately compensated for by a decrease in afterload.

Adult↗
PubMed1987

The effects of enoximone (MDL-17043) on forearm venous circulation in healthy volunteers and patients with heart failure.

The effect of intravenous enoximone on forearm venous circulation was studied in ten healthy volunteers (group A) and in ten patients with NYHA class III-IV congestive heart failure (group B). Distensibility of the forearm capacitance vessels was assessed from pressure-volume curves by venous occlusion plethysmography using a mercury-in-rubber strain gauge. Three recordings each at 3-min intervals were obtained before the infusion and again 20 min after completion of the infusion. Venous volume changes (VV) at congesting pressures of 10, 20, and 30 mmHg before and after enoximone were compared. Forearm muscle blood flow was also measured by venous occlusion plethysmography; electrocardiogram, heart rate, and cuff blood pressure were recorded throughout. Enoximone at a dose of 1 mg/kg body weight was infused over 10 min through a peripheral vein in group A and via a central line in group B. In group A, the effect of the injection vehicle was also assessed. VV10, VV20, and VV30 did not differ from baseline values after enoximone in both groups A and B. The vehicle caused a small but significant degree of venoconstriction in group A (VV20, 2.64 +/- 0.9 to 2.48 +/- 0.83 ml/100 ml, P less than 0.05; VV30, 3.47 +/- 1.27 to 3.33 +/- 1.20 ml/100 ml, P less than 0.05), which could be explained by an acute response to local pain from the infusion. This effect was not evident following enoximone, perhaps as a result of its counterbalancing vasodilating action to venoconstriction induced by acute pain.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Hemodynamic effects of felodipine in congestive heart failure.

The hemodynamic effects of increasing dosages of felodipine, a new calcium antagonist with selective vasodilator properties, were studied in 13 patients with chronic cardiac failure. A Swan-Ganz thermodilution catheter was positioned in the pulmonary artery and hemodynamic parameters were monitored from 9 am to 6 pm for five days. On the first and the fifth day patients received placebo (P) and on the second, third, and fourth day patients received felodipine 5, 10, and 20 mg, respectively. Symptom-limited exercise tests with a bicycle ergometer were performed on both days of P and on the fourth day. A marked reduction of systemic vascular resistance (SVR) and a significant increase of cardiac index without increments of heart rate (HR) were observed after felodipine at rest. A dose response effect could be demonstrated. During exercise a significant increment of cardiac index and decrease of pulmonary wedge pressure was observed after felodipine. Felodipine showed a potent vasodilator action on systemic circulation with significant changes on both stroke volume and filling pressures at rest and during exercise without side effects.

Exercise↗
PubMed1987

Haemodynamic effects of metoprolol and intravenous nitroglycerin versus metoprolol alone in patients with acute myocardial infarction.

Among the various treatments adopted to protect the acutely ischaemic myocardium, favourable results have been reported for beta-blockers. Nitrates can also reasonably be expected to exert favourable effects in acute myocardial infarction considering their haemodynamic action. In this study we compared the haemodynamic effect of metoprolol alone with the effect of metoprolol plus nitroglycerin. Fourteen patients, admitted within 12 hours from the clinical onset of acute myocardial infarction, were initially given intravenous metoprolol (5 + 5 + 5 mg) followed 15 minutes later by an additional 50 mg oral dose. Thereafter, they were randomly allocated to a treatment with metoprolol alone (Group 1) or metoprolol plus intravenous nitroglycerin (Group 2). The two groups were comparable with regard to age, sex, time to admission, time to therapy, site of necrosis, Killip class, and infarct size. Acute beta-blockade induced a marked decrease of cardiac output, systolic blood pressure and heart rate along with a small increase of pulmonary wedge pressure and a marked systemic vasoconstriction. In Group 1 patients these haemodynamic changes persisted up to twelve hours after randomization; in Group 2 patients the addition of nitroglycerin induced a prompt decrease of pulmonary wedge pressure and peripheral vascular resistance whereas the double product was unchanged. In conclusion, intravenous nitroglycerin induces a beneficial haemodynamic effect after early beta-blockade with metoprolol.

Aged↗