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Mauro Contini

Publications and source records attributed to Mauro Contini.

8 recordsLinked to original sources

Gas diffusion and alveolar-capillary unit in chronic heart failure.

AIMS: Alveolar gas diffusion (DLCO) is impaired in chronic heart failure (CHF). Diffusion depends on membrane diffusion (DM) and the amount of blood participating in gas exchange (VC). How DM, VC, and the alveolar-capillary unit behave in relationship to CHF severity is unknown. METHODS AND RESULTS: We measured pulmonary function, including DLCO, DM, VC, and alveolar volume (VA), in 191 CHF patients in NYHA class I-III. CHF patients were grouped accordingly to peak exercise oxygen uptake (pVO(2)): group <12 mL/min/kg (n=24), group 12-16 (n=76), group 16-20 (n=64), and group >20 (n=27). DLCO, DM, VC, and VA were lowest in severe CHF and were linearly related to pVO(2) (DLCO, r=0.577, P<0.001; DM, r=0.490, P<0.001; VC, r=0.216, P<0.01; VA, r=0.565, P<0.01). DM/VC ratio, an index of the alveolar-capillary unit efficiency, was higher in group <12 (0.49+/-0.39 mL/min/mmHg/mL) and >20 (0.46+/-0.29), compared with 12-16 (0.34+/-0.19) and 16-20 (0.35+/-0.17). CONCLUSION: DLCO progressively worsens as CHF severity increases due to reduction in lung tissue participating to gas exchange (low VC and VA). In severe CHF, the few working alveolar-capillary units are the most efficient as shown by the high DM/VC. This is useful for maintaining gas exchange efficiency in severe CHF.

Capillaries↗

Carvedilol reduces exercise-induced hyperventilation: A benefit in normoxia and a problem with hypoxia.

AIMS: To evaluate whether carvedilol influences exercise hyperventilation and the ventilatory response to hypoxia in heart failure (HF). METHODS AND RESULTS: Fifteen HF patients participated to this double blind, randomised, placebo controlled, cross-over study. Patients were evaluated by quality of life questionnaire, echocardiography, pulmonary function and cardiopulmonary exercise tests (ramp and constant workload) both in normoxia (FiO2 = 21%) and hypoxia (FiO2 = 16%, equivalent to a simulated altitude of 2000 m). Carvedilol improved clinical condition and reduced left ventricle size, but had no effect on lung mechanics. In normoxia during exercise, ventilation was lower, V(CO2) unchanged and PaCO2 (constant workload) or PetCO2 (ramp) higher with carvedilol, exercise capacity was unchanged (peak workload 92+/-22 and 90+/-22W for placebo and carvedilol, respectively). Abnormal V(E)/V(CO2) slope was reduced by carvedilol. Hypoxia increased ventilation but less with carvedilol; exercise capacity decreased to 87+/-21W (placebo) and to 80+/-11 W (carvedilol, p < 0.01). With hypoxia, carvedilol decreased V(E)/V(CO2) slope. At constant workload exercise with hypoxia, PaO2 decreased to 69+/-6 mm Hg (placebo) and to 64+/-5 (carvedilol, p < 0.01). CONCLUSION: Carvedilol reduced hyperventilation possibly by reducing peripheral chemoreflex sensitivity as suggested by PaCO2 increase with normoxia and PaO2 decrease with hypoxia without V(CO2) and V(D)/V(T) changes. Lessening hyperventilation is beneficial when breathing normally, but detrimental when hyperventilation is needed for exercise at high altitude.

Adrenergic beta-Antagonists↗

Cardiopulmonary evidence of exercise-induced silent ischaemia.

BACKGROUND: Exercise-induced ST changes, suggestive of cardiac ischaemia, are found in asymptomatic patients. METHODS: Gas exchange kinetics were studied during exercise to help to separate patients affected by epicardial coronary disease from those without. Forty-eight patients, without angina symptoms and showing significant changes of ST during exercise, underwent a coronarography and maximal cardiopulmonary exercise test. Thirty-five healthy individuals of matched age and sex underwent a cardiopulmonary exercise test as controls. RESULTS: Patients were grouped according to the presence (group 1, n = 35) or the absence (group 2, n = 13) of significant coronary lesions at angiography. When corrected for predicted oxygen consumption (VO2) at peak exercise and at anaerobic threshold, results showed a low VO2 at peak exercise and anaerobic threshold in group 1 (68 +/- 19 and 84 +/- 17% of predicted, respectively) compared with normal subjects (91 +/- 19 and 96 +/- 24% of predicted VO2) and group 2 patients (86 +/- 17 and 96 +/- 18%). Also the ischaemic threshold, when normalized for predicted workload at peak exercise, occurred earlier in group 1 (67 +/- 22%) than in group 2 (87 +/- 19%). The time-related (Delta)VO2/Deltawork relationship showed a significant flattening above the anaerobic threshold in group 1 (7.4+/-2.2 versus 9.4+/-1.4 ml/watt per minute, P < 0.01), but not in controls or in group 2. Also the DeltaVO2/Deltawork relationship, above the ischaemic threshold, flattened in group 1, but not in group 2. CONCLUSION: The suggestion of major coronary disease in patients with exercise-induced ST changes is given by: (i) a flattening of the DeltaVO2/Deltawork relationship, above both the ischaemic and anaerobic thresholds; and (ii) low VO2 values at anaerobic and ischaemic thresholds.

Aged↗

Cardiopulmonary exercise test evidence of isolated right coronary artery disease.

Isolated right coronary artery disease is usually difficult to diagnose because of frequent negativity of standard exercise stress test. We report a case of isolated coronary artery stenosis which was not detected by standard ECG stress testing. The cardiopulmonary exercise test showed a peculiar pattern: abrupt flattening in VO2/Work relationship, plateau in O2 pulse and 90 s afterwards a plateau in heart rate, probably related to vagal afferent stimulation by ischaemia of the postero-inferior wall of the left ventricle. Multidetector computed tomography of coronary vessels and coronary angiography confirmed isolated critical stenosis of middle right coronary artery. After revascularization by PTCA, normalization of cardiopulmonary exercise test was obtained.

Angioplasty, Balloon, Coronary↗

Lateral decubitus position generates discomfort and worsens lung function in chronic heart failure.

BACKGROUND: Lateral decubitus position is poorly tolerated by heart failure patients. STUDY OBJECTIVES: To evaluated pulmonary function and lung diffusion in heart failure patients in the following five body positions: sitting, prone, supine, and left and right decubitus. SETTING: Heart failure unit of a university hospital. SUBJECTS: We studied 14 chronic heart failure patients in New York Heart Association class III and 14 healthy volunteers. MEASUREMENTS AND RESULTS: After 15 min of a selected position, subjects were evaluated by a discomfort scale, ear oximetry, and pulmonary function, which included FEV1, FVC, vital capacity (VC), alveolar volume, and diffusing capacity of the lung for carbon monoxide (D(LCO)) with subcomponent membrane resistance (DM) and capillary volume. In healthy subjects, we observed a reduction of D(LCO) and capillary volume in both lateral decubiti. Some discomfort was documented in both lateral decubiti when selected positions were compared with the sitting position. In the sitting position, pulmonary function suggested slight restriction ([mean +/- SD] FVC, 89.8 +/- 22.3% predicted; FEV1, 84.7 +/- 16.9% predicted, VC, 88.6 +/- 21.5% predicted; and FEV1/VC, 74 +/- 7) with low D(LCO) (73 +/- 19% predicted). Compared with sitting, lung mechanics were unchanged in prone and supine positions; FEV1, FVC, and FEV1/VC were lower when patients were lying on their side, with unchanged alveolar volume and VC. D(LCO) was similar when comparing sitting, prone, and supine positions, and it was lower in lateral decubitus because of the lower capillary volume (vs sitting) and DM (vs prone and supine). Body position-related FVC and D(LCO) reduction were greatest in the largest hearts (deltaFVC and deltaD(LCO) vs left ventricle diastolic volume R = 0.524, p < 0.05 and R = 0.630, p < 0.02, respectively; deltaFVC and deltaD(LCO) vs cardiothoracic index R = 0.539, p < 0.05 and R = 0.685, p < 0.01, respectively). CONCLUSIONS: In heart failure, lateral decubitus airway obstruction and lung diffusion impairment become greater as heart dimensions increase.

Aged↗

Spironolactone improves lung diffusion in chronic heart failure.

AIMS: To evaluate whether anti-aldosteronic treatment influences lung diffusion (DLCO) in chronic heart failure (HF) patients. Spironolactone improves clinical conditions and prognosis in chronic HF and reduces connective tissue matrix turnover; DLCO abnormalities in chronic HF are related to increase in fibrosis and connective tissue derangement. METHODS AND RESULTS: Thirty stable chronic HF patients, with reduced DLCO (<80% of predicted), were randomly assigned to active treatment (25 mg spironolactone daily) or placebo in addition to conventional anti-failure treatment. They were evaluated by quality of life questionnaire, laboratory investigations, cardiopulmonary exercise test, and pulmonary function test, which included DLCO and membrane diffusing capacity (DM). The evaluation was done before treatment and 6 months after. Quality of life score and standard pulmonary function tests were not significantly affected by spironolactone, while active treatment increased DLCO due to an increase of DM (DLCO: 18.3+/-3.9 vs. 19.9+/-5.5 mL/min/mmHg; DM: 28.1+/-7.7 vs. 33.3+/-8.6 mL/min/mmHg) and peak oxygen consumption (peak VO2 16.8+/-1.9 vs.18.6+/-2.2 mL/min/kg). Increments of DLCO and peak VO2 were linearly related (R=0.849, P<0.001). CONCLUSION: These data show a positive effect of spironolactone on gas diffusion and exercise capacity suggesting a novel mechanism by which anti-aldosteronic drugs improve HF clinical condition and prognosis.

Exercise Test↗

Circadian distribution of acute myocardial infarction by anatomic location and coronary artery involvement.

PURPOSE: Acute myocardial infarction follows a circadian pattern, with a morning peak ascribed to sympathetic activation. However, about 20% of myocardial infarctions occur between midnight and 6 AM; these events may have different characteristics. METHODS: We studied 1571 patients with acute myocardial infarction (866 anterior and 705 inferior myocardial infarctions) who were admitted to our coronary care units from January 1997 to February 2001. We noted the time of the infarction, its anatomic location, and the involved coronary arteries. RESULTS: Inferior myocardial infarctions were more frequent during the night (midnight to 6 AM) than during other periods of the day (n = 238, 34% of all inferior infarctions, P <0.01). When coronary angiography was performed (795 patients), 92% (127/138) of inferior infarctions were due to right coronary artery occlusion, whereas only 54% (130/242) of the remaining inferior infarctions involved that artery. CONCLUSION: Inferior myocardial infarctions occur disproportionately at night, usually due to right coronary artery occlusion. This suggests that a protective role for sleep may be limited to left coronary artery-related events.

Adult↗