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Gaia Cattadori

Publications and source records attributed to Gaia Cattadori.

9 recordsLinked to original sources
PubMed2006

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↗
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↗
PubMed2005

Work-rate affects cardiopulmonary exercise test results in heart failure.

AIMS: Cardiopulmonary exercise test (CPET) is used to evaluate patients with chronic heart failure (HF) usually by means of a personalized ramp exercise protocol. Our aim was to evaluate if exercise duration or ramp rate influences the results. METHODS AND RESULTS: Ninety HF patients were studied (peak V (O(2)): >20 ml/min/kg, n=28, 15-20 ml/min/kg, n=39 and <15 ml/min/kg, n=23). Each patient did four CPET studies. The initial study was used to separate the subjects into three groups, according to their exercise capacity. In the remaining studies, work-rate was increased at three different rates designed to have the subjects reach peak exercise in 5, 10 and 15 min from the start of the ramp increase in work-rate, respectively. The order was randomized. The work-rate applied for the total population averaged 22.7+/-8.0, 11.6+/-3.7, 7.5+/-2.9 W/min with effective loaded exercise duration of 5 min and 16 s+/-29 s, 9 min and 43 s+/-49 s and 14 min and 32 s+/-1 min and 12 s for the 5-, 10- and 15-min tests, respectively. Peak V (O(2)) averaged 16.9+/-4.3*, 18.0+/-4.4 and 18.0+/-5.4 ml/min/kg for the 5-, 10- and 15-min tests, (*=p<0.001 vs. 10 min). The shortest test had the lowest peak heart rate and ventilation and highest peak work-rate. Peak V (O(2)) and heart rate were lowest in 5-min tests regardless of HF severity. The DeltaV (O(2))/Deltawork-rate was lowest in 5-min tests and highest in 15-min tests. At all ramp rates, DeltaV (O(2))/Deltawork-rate was lower for the subjects with the lower peak V (O(2)). The V (e)/V (CO(2)) slope and V (O(2)) at anaerobic threshold were not affected by the protocol for any grade of HF. CONCLUSIONS: In chronic HF, exercise protocol has a small effect on peak V (O(2)) and DeltaV (O(2))/Deltawork but does not affect V (O(2)) at anaerobic threshold and V (e)/V (CO(2)) slope.

Anaerobic Threshold↗
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↗
PubMed2003

Exercise-induced pulmonary edema in heart failure.

BACKGROUND: In heart failure (HF) patients, exercise may increase pulmonary capillary hydrostatic pressure and thereby generate pulmonary edema. If pulmonary edema developed, alveolar-capillary membrane conductance (Dm), measured immediately after exercise, would decrease. To test this hypothesis, we measured Dm before and at 2 and 60 minutes after exercise. METHODS AND RESULTS: We studied 10 HF patients with exercise-induced periodic breathing, 10 with peak o2 < or =15 mL x min(-1) x kg(-1) (severe HF), 10 with o2=15 to 20 mL x min(-1) x kg(-1) (moderate HF), and 10 normal subjects (control). Using the Roughton-Forster technique, we measured carbon monoxide diffusion capacity (DLco) and its components, capillary blood volume (Vc) and Dm, at rest and 2 and 60 minutes after exercise. At rest, DLco and Dm were lowest in periodic breathing and highest in control subjects. Dm decreased in periodic breathing, severe HF, and moderate HF (-7.83+/-3.98, -5.57+/-2.03, and -3.85+/-3.53 mL x min(-1) x mm Hg(-1), respectively; P<0.01) at 2 minutes after exercise but not in control subjects. Vc increased in all groups at 2 minutes and remained elevated at 60 minutes only in periodic breathing. Dm/Vc was decreased in periodic breathing, severe HF, and moderate HF at 2 minutes but not in control subjects. Dm and Dm/Vc remained low at 60 minutes only in periodic breathing. CONCLUSIONS: Dm decreases after exercise in HF patients but not in control subjects, which suggests a decrease in conductance across the alveolar-capillary barrier, as with pulmonary edema. The reductions were most marked in HF patients with periodic breathing and less reduced in less severe HF.

Aged↗
PubMed2002

[T-wave alternation: a new method for identifying patients at risk of malignant ventricular tachyarrhythmia].

T wave alternans (TWA) is a change, in the microvolt range, of T wave amplitude on ABABAB sequence. TWA depends on heart rate, being optimally analyzed at a target frequency of 110 b/min. Initial studies used atrial pacing to reach the target frequency and reported a sensitivity and specificity of 89% for TWA in predicting tachyarrhythmic events. Subsequently, similar results were obtained using ergometric test to reach the target frequency, a less invasive and more "physiologic" approach to increase heart rate. This method became therefore the elective system to increase heart rate in order to evaluate the presence of TWA by means of spectral analysis. At present, various groups of high arrhythmic risk patients have been evaluated, including those with a recent myocardial infarction, congestive heart failure, implantable cardiac defibrillator and clinical indication to programmed ventricular stimulation. In all clinical conditions analyzed, TWA analysis demonstrated a good diagnostic accuracy, suggesting a possible clinical use of the test in these settings.

Electrocardiography↗