Biomedical subjects

Roberto Brambilla

Publications and source records attributed to Roberto Brambilla.

4 recordsLinked to original sources

PubMed2005

Reverse ventricular remodeling and improved functional capacity after ventricular resynchronization in advanced heart failure.

BACKGROUND: Ventricular resynchronization is a non-pharmacological treatment for advanced heart failure refractory to drug therapy and with intraventricular conduction delay. We describe the time course of echocardiographic and functional recovery after resynchronization in 31 patients (mean age 67 +/- 8 years). METHODS: We evaluated NYHA class, echocardiogram, respiratory function, and cardiopulmonary test before pacemaker implantation (baseline), after 1-3 months (short-term evaluation), and 10-15 months afterwards (long-term evaluation, n = 21 patients). Mortality at 1 year was considered. RESULTS: Both at short and long-term, patients improved NYHA class, ventricular function, and ventricular volumes. Already at short-term, we observed an increase in oxygen consumption at peak exercise (12.6 +/- 0.6 vs 10.5 +/- 0.5 ml/kg/min), oxygen consumption at anaerobic threshold (9.8 +/- 0.6 vs 8.3 +/- 0.6 ml/kg/min) and oxygen pulse (8.3 +/- 0.5 vs 7.5 +/- 0.5 ml/beat). Ventilatory efficacy (VE/VCO2 slope) and alveolo-capillary diffusion (estimated by the measurement of lung diffusion capacity for carbon monoxide - DLCO) improved only at long-term (VE/VCO2: 40.7 +/- 1.6 vs 45.3 +/- 1.8; DLCO: 70.3 +/- 2.7 vs 59.4 +/- 5.9% of predicted, p = 0.05). The 1-year mortality was 9.7%. CONCLUSIONS: Ventricular resynchronization is linked to a fast and prolonged recovery of NYHA class, echocardiographic variables and stress tolerance. The improvement of indexes known to carry a prognostic value confirms that ventricular resynchronization can positively interfere with the evolution of the disease.

Aged↗

PubMed2003

Aspirin-angiotensin-converting enzyme inhibitor coadministration and mortality in patients with heart failure: a dose-related adverse effect of aspirin.

BACKGROUND: It is debated whether in patients with chronic heart failure (CHF), aspirin may contrast the clinical benefits of angiotensin-converting enzyme inhibitors (ACEIs). Two major unresolved issues in patients with CHF are whether these agents together can affect mortality and whether the interaction is related with the dose of aspirin. We aimed at exploring these possibilities. METHODS: We evaluated more than 4000 hospitalizations with a principal discharge diagnosis of CHF from January 10, 1990, to December 31, 1999. The final analysis was restricted to 344 patients taking ACEIs who satisfied the selection criteria, in whom reliable information was available concerning drug therapy during follow-up. In these patients, treatment included no aspirin in 235 (group 1), a low dose (< or =160 mg) in 45 (group 2), and a high dose (> or = 325 mg) in 64 (group 3). RESULTS: During a mean follow-up of 37.6 months, there were 84 (36%) deaths in group 1, 15 (33%) in group 2, and 35 (55%) in group 3. By the Kaplan-Meier approach, survival was similar in groups 1 and 2, and significantly (P =.009) worse in group 3 compared with groups 1 and 2. After adjusting for potential confounding factors (including treatment, cause of heart disease, age, smoking, and diabetes mellitus), a time-dependent multivariate Cox proportional hazards regression analysis showed that the combination of high-dose aspirin with an ACEI was independently associated with the risk of death (hazard ratio, 1.03; P =.01) and that the combination of low-dose aspirin with an ACEI was not (hazard ratio, 1.02; P =.18). CONCLUSION: These results support the possibility that in some patients with CHF who are taking an ACEI, a dose-related effect of aspirin may adversely affect survival.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2002

Diabetes worsens pulmonary diffusion in heart failure, and insulin counteracts this effect.

Chronic heart failure (CHF) (hydrostatic stress) and diabetes (basal laminae thickening) share the potentiality of damaging the alveolar-capillary membrane. We investigated 15 control subjects and 3 groups of 15 patients each having type 2 diabetes (Group 1), CHF (Group 2), and diabetes and CHF (Group 3), to probe whether addition of diabetes worsens lung diffusion in CHF and whether insulin counteracts this effect. Compared with control subjects, carbon monoxide diffusing capacity (DL(CO)) and diffusing capacity of the alveolar-capillary membrane at rest were increasingly depressed from Group 1 through Group 3. DL(CO) was lower than predicted in 11 patients each in Groups 1 and 2 and in all patients in Group 3. Regular insulin (10 IU) was ineffective in CHF alone, whereas it improved DL(CO) and diffusing capacity of the alveolar-capillary membrane in diabetes; changes, however, were significantly greater in the patients with both diabetes and CHF (+17.6%, +27.3%) than in those with diabetes alone (+9.2%, +13.1%). Insulin did not affect lung spirometry, volumes, and hemodynamics. Thus, gas transfer is depressed in a number of patients with diabetes or CHF; comorbidity increases the frequency and extent of this disorder. Insulin facilitates diffusion in diabetes, through an influence on alveolar-capillary conductance, and its efficacy is greater in comorbidity; diabetes is more disturbing in patients with CHF and produces a synergistic rather than a simple additive effect.

Aged↗

PubMed2002

Effect of non-insulin-dependent diabetes mellitus on pulmonary function and exercise tolerance in chronic congestive heart failure.

In chronic congestive heart failure (CHF), backward effects of left ventricular dysfunction alter pulmonary volumes and gas diffusion. Some of these disorders are detected in some patients with diabetes mellitus, possibly due to a microangiopathic process and nonenzymatic glycosylation of lung tissue proteins. We explored the possibility that coexistence of non-insulin-dependent diabetes mellitus (NIDDM) may potentiate the deterioration of lung function in CHF. In 20 normoglycemic patients (group 1) and in 20 patients with NIDDM (group 2), with New York Heart Association class II to III CHF due to idiopathic or ischemic cardiac disease, and in 20 controls (groups were age- and gender-matched), we investigated cardiac function, pulmonary volumes, carbon monoxide diffusion (DL(CO)) and its alveolar-capillary membrane (D(M)) subcomponent, oxygen uptake and dead space-to-tidal volume ratio (pVD/VT) at peak exercise (individualized ramp test), and slope of ventilation-to-carbon dioxide production ratio (VE/VCO(2)) during exercise. Although, compared with reference subjects, both patient groups had similar variations in left ventricular diastolic volume, ejection fraction, and pulmonary wedge pressure; in group 2 lung volumes, DL(CO), D(M), and oxygen uptake were significantly more reduced; in this group there was no overlap of individual results of DL(CO) and D(M) with those in controls; VE/VCO(2) slope and pVD/VT also were significantly increased, and inversely correlated with D(M). Thus, coexistence of NIDDM makes pulmonary dysfunction worse in CHF, and significantly enhances exercise intolerance.

Analysis of Variance↗