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38 results on '"Magrini F."'

2. Effects of anthiipertensives treatment on ultrasound measures of myocardial fibrosis in hipertensives patientes with left ventriculare hypertrophy:results of a randomized trial comparing the angiotensin receptor antagonist, candesartan and the angiotensin-converting enzyme inhibitor, enalapril

Author

Ciulla, M, Paliotti, R, Esposito, A, Cuspidi, C, Muiesan, M, Rosei, E, Magrini, F, Zanchetti, A, Ciulla M, Paliotti R, Esposito A, CUSPIDI, CESARE, Muiesan ML, Rosei EA, Magrini F, Zanchetti A., Ciulla, M, Paliotti, R, Esposito, A, Cuspidi, C, Muiesan, M, Rosei, E, Magrini, F, Zanchetti, A, Ciulla M, Paliotti R, Esposito A, CUSPIDI, CESARE, Muiesan ML, Rosei EA, Magrini F, and Zanchetti A.

Abstract

OBJECTIVE: To compare the effects of the angiotensin II receptor antagonist candesartan with the angiotensin-converting enzyme inhibitor enalapril on myocardial fibrosis evaluated by echoreflectivity analysis. METHODS: Hypertensive patients (n = 196) with echocardigraphically documented left ventricular hypertrophy were randomized to candesartan 8-16 mg/day (n = 91) or enalapril 10-20 mg/day (n = 105) with possible addition of hydrochlorothiazide (12.5-25 mg/day) for 48 weeks. Echoreflectivity analysis was performed on ultrasound two-dimensional tracings of the midapex septum with a specifically designed and validated software. Colour histograms were obtained; the primary outcome variable was the treatment-related change in histogram width (broadband), previously shown to correlate with collagen volume on endomyocardial biopsy; changes in mean colour scale were secondary outcome variable. RESULTS: Echoreflectivity analysis was feasible in 84 patients (48 candesartan, 36 enalapril). Broadband decreased significantly in the candesartan (-8.0 colour levels) and in the enalapril group (-12.9 colour levels) with no significant difference between treatments (P = 0.409); no significant changes occurred in mean colour scale. Patients under monotherapy (n = 46) showed similar trends as the larger intention to treat cohort, without significant difference between treatments. CONCLUSION: In hypertensive patients with left ventricular hypertrophy, both candesartan and enalapril induce a moderate but statistically significant reduction in an echoreflectivity index of myocardial fibrosis.

Published
2009

4. Effects of antihypertensive treatment on ultrasound measures of myocardial fibrosis in hypertensive patients with left ventricular hypertrophy: results of a randomized trial comparing the angiotensin receptor antagonist, candesartan and the angiotensin-converting enzyme inhibitor, enalapril.

Author

Ciulla MM, Paliotti R, Esposito A, Cuspidi C, Muiesan ML, Rosei EA, Magrini F, Zanchetti A, Ciulla, Michele M, Paliotti, Roberta, Esposito, Arturo, Cuspidi, Cesare, Muiesan, M Lorenza, Rosei, Enrico Agabiti, Magrini, Fabio, and Zanchetti, Alberto

Published
2009
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6. Prevalence and correlates of left atrial enlargement in essential hypertension: role of ventricular geometry and the metabolic syndrome: the Evaluation of Target Organ Damage in Hypertension study.

Author

Cuspidi C, Meani S, Fusi V, Valerio C, Catini E, Sala C, Sampieri L, Magrini F, Zanchetti A, Cuspidi, Cesare, Meani, Stefano, Fusi, Veronica, Valerio, Cristiana, Catini, Eleonora, Sala, Carla, Sampieri, Lorena, Magrini, Fabio, and Zanchetti, Alberto

Published
2005
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12. Cardiogenic hypertension in maturing dogs.

Author

MAGRINI, FABIO, ROBERTS, NERYS, BRANZI, GIOVANNA, MONDADORI, CRISTINA, REGGIANI, PAOLO, CIULLA, MICHELE, MEAZZA, ROBERTO, Magrini, F, Roberts, N, Branzi, G, Mondadori, C, Reggiani, P, Ciulla, M, and Meazza, R

Published
1988

33. Effects of anthiipertensives treatment on ultrasound measures of myocardial fibrosis in hipertensives patientes with left ventriculare hypertrophy:results of a randomized trial comparing the angiotensin receptor antagonist, candesartan and the angiotensin-converting enzyme inhibitor, enalapril

Author

A. Esposito, M. Lorenza Muiesan, Enrico Agabiti Rosei, Fabio Magrini, Michele M. Ciulla, Cesare Cuspidi, Roberta Paliotti, Alberto Zanchetti, Ciulla, M, Paliotti, R, Esposito, A, Cuspidi, C, Muiesan, M, Rosei, E, Magrini, F, and Zanchetti, A

Subjects
Adult, Male, medicine.medical_specialty, echocardiography tissue characterization, left ventricular hypertrophy, Hypertension, ultrasonography, Humans, Hypertension, Physiology, Tetrazoles, Angiotensin-Converting Enzyme Inhibitors, Angiotensin II receptor antagonist, Left ventricular hypertrophy, Muscle hypertrophy, Myocardial fibrosi, Enalapril, Internal medicine, Internal Medicine, medicine, Humans, Angiotensin receptor blocker, Aged, Echoreflectivity, biology, business.industry, Myocardium, Biphenyl Compounds, Angiotensin-converting enzyme, ultrasonography, Hypertrophy, Middle Aged, medicine.disease, Fibrosis, Angiotensin II, Candesartan, Treatment Outcome, Endocrinology, Angiotensin-converting enzyme inhibitor, ACE inhibitor, biology.protein, Cardiology, Benzimidazoles, Female, Hypertrophy, Left Ventricular, Cardiology and Cardiovascular Medicine, business, Angiotensin II Type 1 Receptor Blockers, medicine.drug
Abstract

Objective To compare the effects of the angiotensin II receptor antagonist candesartan with the angiotensin-converting enzyme inhibitor enalapril on myocardial fibrosis evaluated by echoreflectivity analysis. Methods Hypertensive patients (n = 196) with echocardigraphically documented left ventricular hypertrophy were randomized to candesartan 8-16 mg/day (n = 91) or enalapril 10-20 mg/day (n = 105) with possible addition of hydrochlorothiazide (12.5-25 mg/day) for 48 weeks. Echoreflectivity analysis was performed on ultrasound two-dimensional tracings of the midapex septum with a specifically designed and validated software. Colour histograms were obtained; the primary outcome variable was the treatment-related change in histogram width (broadband), previously shown to correlate with collagen volume on endomyocardial biopsy; changes in mean colour scale were secondary outcome variable. Results Echoreflectivity analysis was feasible in 84 patients (48 candesartan, 36 enalapril). Broadband decreased significantly in the candesartan (-8.0 colour levels) and in the enalapril group (-12.9 colour levels) with no significant difference between treatments (P = 0.409); no significant changes occurred in mean colour scale. Patients under monotherapy (n = 46) showed similar trends as the larger intention to treat cohort, without significant difference between treatments. Conclusion In hypertensive patients with left ventricular hypertrophy, both candesartan and enalapril induce a moderate but statistically significant reduction in an echoreflectivity index of myocardial fibrosis.

Published
2009

34. Acute effects of cilazapril on coronary hemodynamics in patients with renovascular hypertension.

Author

Magrini F, Reggiani P, Fratianni G, Morganti A, and Zanchetti A

Subjects
Adult, Angiotensin-Converting Enzyme Inhibitors therapeutic use, Blood Pressure drug effects, Cilazapril, Humans, Hypertension, Renovascular physiopathology, Middle Aged, Oxygen Consumption drug effects, Physical Exertion physiology, Pyridazines therapeutic use, Vascular Resistance drug effects, Angiotensin-Converting Enzyme Inhibitors pharmacology, Coronary Circulation drug effects, Hemodynamics drug effects, Hypertension, Renovascular drug therapy, Pyridazines pharmacology
Abstract

The effects of converting enzyme inhibition on coronary and systemic hemodynamics in the presence of a chronically activated renin-angiotensin system were investigated in five renovascular hypertensive patients with no ECG/echocardiographic evidence of left ventricular hypertrophy. Coronary blood flow (CBF, thermodilution technique), intra-arterial blood pressure, AVO2 difference (coronary sinus), heart rate, and coronary vascular resistance were measured at rest, during isometric exercise (handgrip to 50% of maximal effort for 3 min) before and 60 min after 2.5 mg of oral cilazapril. The drug induced a prompt, significant decrease in mean arterial pressure and a sustained increase in CBF. The performance of handgrip after cilazapril resulted in higher increases in CBF for a given increase in myocardial oxygen requirements. These observations suggest that angiotensin II (Ang II) maintains the ability to alter the control mechanisms of CBF even under long-term conditions and that converting enzyme inhibition reverses the Ang II-induced effects on coronary hemodynamics.

Published
1992

35. Converting-enzyme inhibition and coronary blood flow.

Author

Magrini F, Shimizu M, Roberts N, Fouad FM, Tarazi RC, and Zanchetti A

Subjects
Adult, Animals, Furosemide therapeutic use, Hemodynamics drug effects, Humans, Male, Middle Aged, Rats, Rats, Inbred Strains, Renin blood, Angiotensin-Converting Enzyme Inhibitors, Captopril therapeutic use, Coronary Circulation drug effects
Abstract

The effects of converting-enzyme inhibition (25 mg oral captopril) on coronary hemodynamics in the presence and absence of activation of the renin-angiotension system were studied in 10 patients with mild essential hypertension with no evidence of ischemic heart disease. Coronary blood flow was determined by thermodilution before and after 1 week of diuretic therapy in six patients and before and after placebo in four patients. The diuretic (50 mg/day furosemide) reduced coronary blood flow and increased coronary vascular resistance; in these same patients, captopril reduced mean arterial pressure and the rate-pressure product but increased coronary flow significantly. There was no change in any of these variables after captopril in the placebo group. Similar results were obtained in normotensive rats treated with hydrochlorothiazide; the increase in coronary flow after captopril correlated significantly with the control plasma renin activity. These results in hypertensive humans and normotensive experimental animals indicate that diuretic therapy reduces coronary blood flow significantly, and angiotensin can play a significant role in modulating coronary vascular resistance under conditions associated with activation of the renin-angiotensin system.

Published
1987

36. The effects of a microgravitational environment on the blood pressure maturation curve in normotensive rats.

Author

Magrini F, Ciulla M, Meazza R, and Reggiani P

Subjects
Animals, Heart Rate physiology, Immersion physiopathology, Male, Rats, Rats, Inbred Strains, Urine physiology, Blood Pressure physiology, Environment, Controlled, Gravitation
Abstract

In order to determine whether gravity influences the growth of terrestrial mammals, systolic blood pressure, heart rate, urinary output and body weight were measured at 10-day intervals from the age of 30 days (weaning) to 150 days in 12 male Sprague-Dawley rats. Six rats were grown in a gravitational environment. 'Dry' water immersion was used to subject six rats to a microgravitational environment between the ages of 30 and 90 days. A downward shift in systolic blood pressure and body weight maturation curves was observed in the microgravitational group from the age of 60 days. After the 'dry' water immersion was stopped, the fully developed rats showed a significant increase in systolic blood pressure, which returned to control values, but not in body weight. We conclude that the physiological increase in systolic blood pressure taking place in rats during growth is partly dependent on gravity.

Published
1989
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37. Systemic and pulmonary hemodynamic effects of indapamide in patients with mild arterial hypertension.

Author

Magrini F, Buzzetti G, De Giovanni F, Cerati D, Macchi G, and Mondadori C

Subjects
Adult, Humans, Male, Middle Aged, Posture, Diuretics pharmacology, Hemodynamics drug effects, Hypertension physiopathology, Indapamide pharmacology, Pulmonary Circulation drug effects
Abstract

We studied the hemodynamic mechanism responsible for the antihypertensive effect of indapamide in eight patients with mild essential hypertension. Systemic and pulmonary hemodynamics were measured using direct techniques (right heart catheterization and thermodilution method), before and 7-10 days after oral treatment with indapamide (2.5 mg/day). Indapamide reduced mean arterial blood pressure from 120 +/- 1.6 (mean +/- SE) to 101 +/- 1.4 mm Hg (p less than 0.01), and mean pulmonary artery pressure from 21 +/- 0.59 to 17 +/- 1.05 mm Hg (p less than 0.01). Total peripheral vascular resistance (TPR) and pulmonary vascular resistance were reduced from 36 +/- 0.85 to 29 +/- 0.72 U/m2 (p less than 0.01) and from 4.3 +/- 0.17 to 3.8 +/- 0.18 U/m2 (p less than 0.01), respectively. Indapamide did not change cardiac index (CI) (3,311 +/- 61.6 vs. 3,325 +/- 72.1 ml/min/m2), heart rate (HR) (75 +/- 1.7 vs. 75 +/- 9 beats/min), mean rate of left ventricular ejection index 140 +/- 2.04 vs. 139 +/- 1.99 ml/s/m2, and stroke index (44 +/- 5.6 vs. 43 +/- 5.8 ml/m2). Mean pulmonary wedge pressure decreased from 7 +/- 0.6 to 5 +/- 0.5 mm Hg (p less than 0.05). Body weight, 24-h urinary volume, and hematocrit were unchanged after treatment. We conclude that the hemodynamic mechanism responsible for the antihypertensive action of indapamide is a reduction in TPR without changes in CI and HR.

Published
1985
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38. Selective reduction of renal perfusion pressure and blood flow in man: humoral and hemodynamic effects.

Author

Fiorentini C, Guazzi MD, Olivari MT, Bartorelli A, Necchi G, and Magrini F

Subjects
Adult, Arterial Occlusive Diseases physiopathology, Cardiac Output, Female, Heart Rate, Humans, Hypertension physiopathology, Kidney blood supply, Male, Middle Aged, Regional Blood Flow, Renal Artery physiopathology, Renin blood, Time Factors, Vascular Resistance, Blood Pressure, Hemodynamics, Kidney physiopathology, Perfusion
Published
1981
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