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Biomedical subjects

Anna Apostolo

Publications and source records attributed to Anna Apostolo.

6 recordsLinked to original sources
PubMed2006

Cardiopulmonary interaction in heart failure.

In heart failure lung dysfunction is frequent and is greater the greater the heart failure severity. It can be evaluated in terms of lung mechanics and gas diffusion. Indeed heart-lung interaction is related to heart dimensions and lung fluid content; furthermore heart-lung interaction is influenced by the body position. Lung diffusion is also altered in patients with chronic heart failure, and a low gas diffusion is associated with a reduced performance. During exercise, heart-lung interaction becomes more evident. Heart failure patients show an abnormal hyperventilation due to a progressively increased respiratory rate, and a lower tidal volume; hyperventilation is due to different causes including enhanced responses from chemo- and metabolo-receptors, increased CO(2) production and increased dead space ventilation. Several drugs affect the ventilatory pattern in heart failure patients: ACE-inhibitors and anti-aldosteronic drugs improve lung diffusion and ventilatory efficiency during exercise; beta-blockers reduce exercise-induced hyperventilation. Furthermore, ultrafiltration improves lung mechanics, both at rest and during exercise, through body fluid content reduction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

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↗
PubMed2006

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↗
PubMed2005

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↗
PubMed2004

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↗