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Biomedical subjects

M Guazzi

Publications and source records attributed to M Guazzi.

At least 37 records · Page 2Linked to original sources
PubMed2000

Non-invasive measurement of stroke volume during exercise in heart failure patients.

The objective of the present study was to determine the variability of the arterio-venous O(2) concentration difference [C(a-v)O(2)] at anaerobic threshold and at peak oxygen uptake (VO(2)) during a progressively increasing cycle ergometer exercise test, with the purpose of assessing the possible error in estimating stroke volume from measurements of VO(2) alone. We sampled mixed venous and systemic arterial blood every 1 min during a progressively increasing cycle ergometer exercise test and measured, in each blood sample, haemoglobin concentration and blood gas data. Ventilation, VO(2) and CO(2) uptake were also measured continuously. We studied 40 patients with normal haemoglobin concentrations and with stable heart failure due to ischaemic or idiopathic cardiomyopathy. Mean values (+/-S.D.) for C(a-v)O(2) were 7.8+/-2.6, 13.0+/-2.4 and 15. 0+/-2.7 ml/100 ml at rest, anaerobic threshold and peak VO(2) respectively. The patients with heart failure were divided into classes according to their peak VO(2). Classes A, B and C contained patients with peak VO(2) values of>20, 15-20 and 10-15 ml.min(-1). kg(-1) respectively. At anaerobic threshold, C(a-v)O(2) was 12.3+/-1. 3, 13.1+/-2.7 and 13.5+/-2.6 ml/100 ml for classes A, B and C respectively (class A significantly different from classes B and C; P<0.05). At peak exercise C(a-v)O(2) was 13.6+/-1.4, 15.6+/-2.5 and 15.4+/-3.2 ml/100 ml for classes A, B and C respectively (class A significantly different from classes B and C; P<0.05). Stroke volume was estimated for each subject using the mean values of the measured C(a-v)O(2) in each functional class and individual values of VO(2) and heart rate using the Fick formulation. The average difference between the stroke volume estimated from mean C(a-v)O(2) and that obtained using the patient's actual C(a-v)O(2) value was 9.2+/-9.7, 1.0+/-8.8 and -0.2+/-6.1 ml at anaerobic threshold, and -1.9+/-11.3, 0.9+/-10.0 and -2.3+/-8.5 ml at peak exercise, in classes A, B and C respectively. Among the various classes, the most precise estimation of stroke volume was observed for class C patients. We conclude that stroke volume during exercise can be estimated with the accuracy needed for most purposes from measurement of VO(2) at the anaerobic threshold and at peak exercise, and from population-estimated mean values for C(a-v)O(2) in heart failure patients.

Adult↗
PubMed2000

Impedance to gas transfer across the alveolar-capillary membrane in chronic cardiac failure.

One of the consequences of an elevation of the pulmonary capillary pressure in chronic heart failure is the occurrence of structural and functional changes at the level of the alveolar-capillary interface. These changes are called "stress failure" of the membrane, and consist of thickening of the interstitium, increase in capillary permeability to water and ions, and disruption of local regulatory mechanisms for gas exchange. Functional correlates are an augmented impedance to gas transfer (DL), a reduction in the alveolar-capillary membrane conduction (DM) and an increase in the volume of the pulmonary capillary blood (VC). DM and VC are the two subcomponents of DL. DM has been identified as the strongest respiratory predictor of oxygen uptake at peak exercise in patients with chronic heart failure, suggesting that impeded lung diffusion may significantly contribute to exercise limitation and ventilatory abnormalities. The evidence relating to the pathophysiological and clinical significance of the impairment in lung diffusion capacity in patients with chronic heart failure, as well as the response to treatment are the main subjects of this review.

Animals↗
PubMed2000

Alveolar-capillary membrane dysfunction in chronic heart failure: pathophysiology and therapeutic implications.

Chronic heart failure (CHF) disturbs the alveolar-capillary interface and increases the resistance to gas transfer. Alveolar-capillary membrane conductance (D(M)) and capillary blood volume (V(c)) are subcomponents of the lung diffusion capacity. Elevation of the capillary pressure causes alveolar-capillary membrane stress failure (i.e. increase in capillary permeability to water and ions, and disruption of local regulatory mechanisms for gas exchange), leading to a decrease in D(M), an increase in V(c) and subsequent impairment of diffusion capacity. Renewed recent interest in abnormalities in lung diffusion in patients with CHF has brought about new pathophysiological insights. A significant contribution of the altered gas transfer to the pathogenesis of exercise limitation and ventilatory abnormalities has been reported, and D(M) has been identified as the best lung function predictor of oxygen uptake at peak exercise. This review examines the pathophysiological and clinical significance of assessing lung diffusion capacity in patients with CHF.

Blood-Air Barrier↗
PubMed1999

Synergistic efficacy of enalapril and losartan on exercise performance and oxygen consumption at peak exercise in congestive heart failure.

Oxygen consumption at peak exercise (peak VO2) is a strong independent predictor of the outcome in congestive heart failure (CHF). Renin-angiotensin system inhibition with either ACE or AT1 receptor blockers is effective on peak VO2. We evaluated whether mechanisms are similar for the 2 categories of drugs and whether their combination is able to produce a synergistic effect. Twenty CHF patients were randomized to receive, in a double-blind fashion, placebo + placebo (P+P), enalapril (20 mg/day) + placebo (E+P), losartan (50 mg/day) + placebo (L+P), and enalapril + losartan (E+L) or the same preparations in a reverse order, each for 8 weeks. Two patients did not complete the trial. Pulmonary function, cardiopulmonary exercise test, plasma neurohormones, and quality of life were assessed at the end of each treatment. Compared with P+P, E+P, and L+P similarly (16% and 15%, respectively) and significantly (p <0.01) augmented peak VO2. Enalapril improved lung function (reduced slope of ventilation vs carbon dioxide production and dead space to tidal volume ratio, and increased alveolar membrane conductance and tidal volume). Losartan likely activated the exercising muscle perfusion (raised delta VO2/delta work rate, which is a measure of aerobic work efficiency). In combination, they further increased peak VO2, 10% from E+P (p <0.05) and 11% from L+P (p <0.05). Compared with run-in, E+P and L+P significantly reduced plasma norepinephrine by 70 +/- 14 pg/ml and 100 +/- 16 pg/ml and aldosterone by 1.6 +/- 0.7 ng/dl and 1.6 +/- 0.8 ng/dl. These changes were significantly greater when the drugs were combined (140 +/- 20 pg/ml for norepinephrine, and 5.6 +/- 0.9 ng/dl for aldosterone). Quality-of-life score did not improve significantly at each treatment step. Thus, lorsartan and enalapril similarly increased peak VO2 in CHF patients, but mediators of this effect were, at least in part, different therapeutic targets that may be synergistic when the 2 drugs are combined.

Adult↗
PubMed1999

Exercise-induced hemoconcentration in heart failure due to dilated cardiomyopathy.

Exercise-induced hemoconcentration is a useful mechanism, particularly in heart failure, because it increases oxygen content of blood, perfusing the working muscles; in 50 normal subjects and 50 patients with congestive heart failure, hemoglobin at peak exercise increased by 7 +/- 3% and 5 +/- 3%, respectively. Hemoconcentration was due to fluid flux out of the vascular bed, likely through oncotic forces related to intracellular lactate accumulation and not to red blood cell recruitment from other organs (spleen), because hemoglobin increase, as a percentage, was similar to plasma protein increase.

Adult↗
PubMed1999

Aspirin worsens exercise performance and pulmonary gas exchange in patients with heart failure who are taking angiotensin-converting enzyme inhibitors.

BACKGROUND: Pulmonary function abnormalities participate in causing exercise disability in patients with congestive heart failure (CHF). Impaired pulmonary gas transfer is one of these abnormalities. Angiotensin-converting enzyme (ACE) inhibitors improve diffusion for carbon monoxide and exercise capacity, an effect that is seemingly mediated through prostaglandin activation because it is inhibited by cyclooxygenase blockade with aspirin. This suggests the possibility that aspirin may disturb the pulmonary function and exercise ability in CHF, at least in those patients who are taking ACE inhibitors. This study was aimed at probing this hypothesis. METHODS: A dose of 325 mg aspirin was given daily for 8 weeks to 26 consecutive patients with primary dilated cardiomyopathy (New York Heart Association class II or III) whose current outpatient antifailure therapy included (group 1, 18 cases) or did not include (group 2, 8 cases) an ACE inhibitor in addition to digoxin and furosemide. During the study ACE inhibition was continued in group 1 by giving enalapril 20 mg daily. RESULTS: Tests repeated at 8 weeks proved that aspirin was deleterious in group 1. Compared with run-in, rest carbon dioxide, peak exercise oxygen uptake (peak VO(2 )), and tidal volume levels were diminished in this group; the ratio of exercise minute ventilation to carbon dioxide production (VE/VCO(2)) was augmented and its variations were inversely related to those of peak VO(2). Similar results were not observed in group 2; however, once this part of the study was completed and enalapril was included in the current therapeutic regimen, an inhibitory effect of aspirin on carbon dioxide, peak VO(2), peak tidal volume, and VE/VCO(2) at 1 L levels became evident and was similar to that observed in group 1. CONCLUSIONS: Aspirin does not affect ventilation efficiency and peak VO(2 ) in patients with CHF not taking ACE inhibitors, but it worsens the pulmonary diffusion for carbon monoxide, VO(2 ), and the ventilatory response to exercise in the presence of ACE inhibition. This may be relevant in patients with CHF from ischemic heart disease. Whether the same may be true of smaller aspirin doses was not investigated in this study.

Aged↗
PubMed1999

Pulmonary function, cardiac function, and exercise capacity in a follow-up of patients with congestive heart failure treated with carvedilol.

BACKGROUND: Chronic heart failure causes disturbances in ventilation and pulmonary gas transfer that participate in limiting peak exercise oxygen uptake (VO(2p )). The beta-adrenergic receptor blocker carvedilol improves left ventricular (LV) function and not VO(2p). This study was aimed at investigating the pulmonary response to changes in LV performance produced by carvedilol in patients with chronic heart failure. METHODS: Twenty-one patients with New York Heart Association class II to III heart failure were randomly assigned (2 to 1) to carvedilol (25 mg twice daily, n = 14) or placebo (n = 7) for 6 months. Rest forced expiratory volume (FEV(1)), vital capacity, total lung capacity, carbon monoxide diffusing capacity, its alveolar-capillary membrane component, pulmonary venous and transmitral flows (for monitoring changes in LV end-diastolic pressure), LV diastolic and systolic dimensions, stroke volume, ejection fraction, and fiber shortening velocity were measured at baseline and at 3 and 6 months. VO(2p), peak ratio of dead space to tidal volume (VD/VT(p)), ventilatory equivalent for carbon dioxide production (VE/VCO(2)), and VO(2) at anaerobic threshold (VO(2at)) were also determined. RESULTS: FEV(1), vital capacity, total lung capacity, carbon monoxide diffusing capacity, and the alveolar-capillary membrane component were impaired in chronic heart failure compared with 14 volunteers and did not vary with treatment. Carvedilol reduced end-diastolic pressure, end-diastolic diameter, and end-systolic diameter and increased ejection fraction, stroke volume, and fiber shortening velocity without affecting VO(2p), VO(2at), VD/VT(p), or VE/VCO(2) at 3 and 6 months. Placebo did not produce significant changes. CONCLUSIONS: In chronic heart failure carvedilol ameliorates LV function at rest and does not significantly affect ventilation and pulmonary gas transfer or functional capacity. These results suggest that improvement in cardiac hemodynamics with carvedilol does not reverse pulmonary dysfunction. Persistent lung impairment might have some role in the failure of carvedilol to improve exercise performance.

Adrenergic beta-Antagonists↗
PubMed1999

Angiotensin-converting enzyme inhibition facilitates alveolar-capillary gas transfer and improves ventilation-perfusion coupling in patients with left ventricular dysfunction.

OBJECTIVE: The backward effects of left ventricular dysfunction include alterations in alveolar-capillary gas transfer and ventilation-perfusion coupling. Because the angiotensin-converting enzyme (ACE) is highly concentrated in the vascular endothelium of the lungs, we examined whether ACE inhibitors may influence the pulmonary function in patients with congestive heart failure. METHODS: In 20 patients with idiopathic cardiomyopathy, pulmonary function and exercise capacity were evaluated at baseline and 6 and 12 months after treatment with enalapril (10 mg twice a day) was started. The study also included 19 age- and sex-matched control subjects with mild primary hypertension and normal left ventricular function who were given enalapril as a standard treatment of high blood pressure. RESULTS: In congestive heart failure, forced expiratory volume in 1 second, vital capacity, and total lung capacity did not vary significantly with enalapril; alveolar-capillary diffusion of carbon monoxide (DL(CO)) increased toward normal; exercise tolerance time, peak exercise oxygen uptake (peak VO2), minute ventilation and tidal volume (peak VT) also increased; and the ratio of volume of dead space (VD) to VT (peak VD/VT) at peak exercise reduced. Changes in peak VO2 showed a direct correlation with those in DL(CO) and an inverse correlation with those in peak VD/VT. Results at 6 and 12 months were comparable. Enalapril did not affect these variables in the control population. CONCLUSIONS: In patients with idiopathic cardiomyopathy heart failure, but not in control subjects, gas transfer and ventilation-perfusion improved with ACE inhibition. These pulmonary changes may contribute to the associated increase in exercise tolerance.

Adult↗
PubMed1999

The influence of diastolic and systolic function on exercise performance in heart failure due to dilated cardiomyopathy or ischemic heart disease.

BACKGROUND: Peripheral adaptations and ventricular abnormalities influence physical performance in chronic heart failure. However, the role of the heart in determining exercise capacity has not been completely elucidated. AIMS: To define cardiac determinants of exercise capacity in patients with dilated cardiomyopathy. METHODS: In 101 patients with heart failure (NYHA class II-III) due to primary or ischemic dilated cardiomyopathy we measured peak exercise oxygen consumption (Pvo2), left ventricular ejection fraction (EF), left and right atrial and ventricular cavity dimensions, mitral and tricuspid flows. Patients were subdivided in class A (Pvo2 > 20 ml/min per kg; n = 44), class B (Pvo2 16-20 ml/min per kg; n = 42) and class C (Pvo2 < 16 ml/min per kg; n = 15). RESULTS: Left ventricular diastolic and systolic dimensions, left atrial diameter, right atrial and ventricular areas were greater in class C than in class B and A; EF was lower in class C than in the other two classes; mitral peak flow velocity at early diastole (PFVE) and the ratio between early and late peak flow velocity (PFVE/PFVA) were higher in class C; mitral and tricuspid deceleration time (DT) in class B and A significantly exceeded those in class C. Peak vo2 was correlated with left and right ventricular dimensions, left atrial diameter, EF, mitral PFVE and PFVE/PFVA, mitral and tricuspid DT. Left ventricular EF, DT of the mitral valve and left ventricular diastolic diameter were independent predictors of peak vo2 at multivariate analysis. CONCLUSIONS: In patients with dilated cardiomyopathy Pvo2 is related to left and right ventricular dimensions, left and right ventricular filling pattern and EF. Both systolic and diastolic dysfunction influence functional capacity.

Blood Flow Velocity↗
PubMed1999

Impeded alveolar-capillary gas transfer with saline infusion in heart failure.

The microvascular pulmonary endothelium barrier is critical in preventing interstitial fluid overflow and deterioration in gas diffusion. The role of endothelium in transporting small solutes in pathological conditions, such as congestive heart failure (CHF), has not been studied. Monitoring of pulmonary gas transfer during saline infusion in CHF was used to probe this issue. Carbon monoxide diffusion (DL(CO)), its membrane diffusion (D(M)) and capillary blood volume (V(C)) subcomponents, and mean right atrial (rap) and mean pulmonary wedge (wpp) pressures after saline or 5% D-glucose solution infusions were compared with baseline in 26 moderate CHF patients. Saline was also tested in 13 healthy controls. In patients, 750 mL of saline lowered DL(CO) (-8%, P<0.01 versus baseline), D(M) (-10%, P<0.01 versus baseline), aldosterone (-29%, P<0.01 versus baseline), renin (-52%, P<0.01 versus baseline), and hematocrit (-6%, P<0.05 versus baseline) and increased V(C) (20%, P<0.01 versus baseline), without changing rap and wpp. Saline at 150 mL produced qualitatively similar results regarding DL(CO) (-5%, P<0.01 versus baseline), D(M) (-7%, P<0.01 versus baseline), V(C) (9%, P<0.01 versus baseline), rap, wpp, aldosterone (-9%, P<0.05 versus baseline), and renin (-14%, P<0.05 versus baseline). Glucose solution (750 mL), on the contrary, increased DL(CO) (5%, P<0.01 versus 750 mL of saline) and D(M) (11%, P<0.01 versus 750 mL of saline) and decreased V(C) (-9, P<0.01 versus 750 mL of saline); aldosterone (-40%), renin (-41%), hematocrit (-3%), rap, and wpp behaved as they did after saline infusion. In controls, responses to both saline amounts were similar to responses in CHF patients regarding aldosterone, renin, hematocrit, rap, and wpp, whereas DL(CO), D(M), and V(C) values tended to rise. Hindrance to gas transfer (reduced DL(CO) and D(M)) with salt infusion in CHF, despite an increase in V(C) and no variations in pulmonary hydrostatic forces, indicates an upregulation in sodium transport from blood to interstitium with interstitial edema. Redistribution of blood from the lungs, facilitating interstitial fluid reabsorption, or sodium uptake from the alveolar lumen by the sodium-glucose cotransport system might underlie the improved alveolar-capillary conductance with glucose.

Aldosterone↗
PubMed1999

Lack of prognostic value of 99mTc MIBI rest, 18F FDG and 201TL rest/redistribution on PTCA outcome of patients with moderate left ventricle dysfunction.

BACKGROUND: The clinical work-out of patients undergoing coronary revascularization includes the assessment of myocardial viability. This approach has to be defined in the different classes of patients. The aim of this study was to evaluate the predictive prognostic value of different techniques on outcome following PTCA in patients with moderate left ventricle dysfunction (left ventricle EF > or = 40%). METHODS: Seventeen patients with EF > or = 40% and undergoing PTCA were studied by 201Tl rest/redistribution, 18F-FDG and 99mTc-MIBI rest. Regional kinesis was scored by echo, dividing left ventricle in 11 segments. The echo evaluation was repeated at 1 and 6 months after revascularization. RESULTS: Global EF was 52.5 +/- 7% and 69 segments had abnormal kinesis. Patients underwent stress/rest 99mTc-MIBI SPET, rest/redistribution 201Tl SPET and rest 18F-FDG PET. Among the 11 segments defined on echo-matched tomographic images, the one with the highest activity at stress was assumed as reference (activity = 100%). If > 50% of reference segment, 18F-FDG and 201Tl uptakes were considered significant. After PTCA, the echo-follow-up did not demonstrated significant improvement of left ventricle function at 30 days after PTCA (EF 56 +/- 6%) as well as at 6 months (EF 56 +/- 9%). The positive predictive value under these conditions resulted: 46.5% with 99mTc-MIBI rest, 47.4% with 201Tl rest-redistribution and 45.7% with 18F-FDG. CONCLUSIONS: In summary, in the class of patients with moderately compromised function, considering as reference the improved regional kinesis after PTCA, 99mTc-MIBI at rest, 201Tl rest/redistribution and 18F-FDG do not exhibit a clear predictive value; patient population is then a highly relevant point to establish the accuracy of these diagnostic procedures.

Adult↗
PubMed1999

Oxygen consumption.

It gets more and more frequent to use oxygen consumption (VO2) to evaluate exercise capacity and response to treatment in heart failure patients. The amount of VO2 is due to ventilation, oxygen transport and muscle activity. No one of these single steps can define by itself VO2, but all these physiological functions are integrated each other. In this paper we examine the modifications of cardiac output, arteriovenous oxygen content difference, and the temporal behavior of their variations during exercise in heart failure. We specifically describe changes in VO2 during simulated altitude; we also contemplate mechanisms governing oxygen diffusion from capillary bed to mitochondria and critical capillary PO2 concept.

Animals↗
PubMed1999

Angiotensin-converting enzyme inhibition restores the diffusing capacity for carbon monoxide in patients with chronic heart failure by improving the molecular diffusion across the alveolar capillary membrane.

Conductance of alveolar capillary membrane (DM) and capillary blood volume (VC) are the subcomponents of the pulmonary diffusing capacity for carbon monoxide (DLCO). In chronic heart failure, stress failure of the membrane provides a mechanism for reduced DM and subsequent impairment of DLCO. Angiotensin-converting enzyme inhibition improves DLCO in patients with chronic heart failure. This study was aimed at investigating which of the two subcomponents of DLCO is affected by angiotensin-converting enzyme inhibitors. Twenty-seven patients with NYHA class II to III chronic heart failure (group 1) and 13 age- and sex-matched normal subjects underwent pulmonary function testing with determination of DM and VC, while receiving placebo and 48 h and 1 and 2 months after starting enalapril treatment (10 mg twice daily). Nine similar patients (group 2) received isosorbide dinitrate (40 mg thrice daily) for a month then enalapril for another month, and underwent pulmonary function testing at 48 h and 1 month after starting treatments. Effects of angiotensin-converting enzyme inhibition in normal controls were not significant in the short- or mid-term. In group 1 patients, the only change observed at 48 h was a reduction in VC (probably due to a decrease in capillary pulmonary pressure). There was a marked increase in DM to a similar extent at 1 and 2 months, resulting in a significant improvement in DLCO despite a decrease in VC. In group 2 patients, nitrates failed to improve DLCO and DM, whereas enalapril was as effective as in group 1. These observations suggest a modulatory effect of angiotensin-converting enzyme inhibition on the membrane function which emerges gradually and persists over time and is probably dissociated from changes in pulmonary capillary pressure and VC. Chronic heart failure disturbs the alveolar capillary interface and increases gas diffusion resistance; angiotensin-converting enzyme inhibition restores the diffusive properties of the membrane and gas transfer, and protects the lung when the heart is failing.

Analysis of Variance↗
PubMed1998

Antihypertensive efficacy of angiotensin converting enzyme inhibition and aspirin counteraction.

OBJECTIVE: Blockade of bradykinin breakdown and enhancement of prostaglandin release probably participate in the antihypertensive activity of angiotensin converting enzyme (ACE) inhibitors. Cyclooxygenase blockers may attenuate the efficacy of ACE inhibitors by interfering with prostaglandin synthesis, and patients taking aspirin may not benefit from ACE inhibition. This study was designed to evaluate the incidence of the counteractive phenomenon and to define minimal aspirin dosage that causes an antagonistic effect. METHODS: These were 26 patients with mild to moderate hypertension (group 1) and 26 patients with severe untreated primary hypertension (group 2). Enalapril (20 mg twice a day) was used as a single drug in group 1 and was added to the combination of long-acting nifedipine (30 mg/day) and atenolol (50 mg/day) in group 2. Aspirin was tested at doses of 100 and 300 mg/day, and an attenuation of more than 20% of the mean blood pressure decrease produced by enalapril was the criteria that defined antagonism. RESULTS: The 100 mg dose was ineffective. However, 300 mg aspirin had an antagonistic effect in 57% of patients in group 1 and 50% of patients in group 2: mean arterial pressure was lowered by 63% and 91% less, respectively. Results were independent of the drug administration order. In "responders," aspirin significantly attenuated the renin rise associated with ACE inhibition. CONCLUSIONS: These findings suggest that a number of ACE-inhibited patients are susceptible to 300 mg/day aspirin, regardless of hypertension severity. Antagonism may be mediated through prostaglandin inhibition according to predominance, in an individual patient, of prostaglandin activation (also as a renin secretory stimulus) or angiotensin blockade by enalapril.

Adult↗
PubMed1998

[A failed improvement in pulmonary function and exercise capacity with carvedilol in congestive heart failure despite an excellent effect on left ventricular function].

This study was aimed at investigating in chronic heart failure (CHF) the effects that beta-blockade with carvedilol may have on lung function, and their relationship with left ventricular (LV) performance and peak exercise oxygen uptake (VO2p). CHF causes disturbances in ventilation and pulmonary gas transfer (stress failure of alveolar-capillary membrane) that participate in limiting VO2p. Carvedilol improves LV function and not VO2p. Twenty-one NYHA functional class II-III patients were randomized (2 to 1) to carvedilol (25 mg bid., 14 patients) or placebo (7 patients) for 6 months. Rest forced expiratory volume (FEV1), vital capacity (VC), total lung capacity (TLC), carbon monoxide diffusing capacity (DLCO), its alveolar-capillary membrane component (DM), pulmonary venous and transmitral flows (for monitoring changes in LV end-diastolic pressure, EDP), LV diastolic (EDD) and systolic (ESD) dimensions, stroke volume (SV), ejection fraction (EF), fiber shortening velocity (VCF) were measured at baseline and at 3 and 6 months. VO2p, peak ratio of dead space to tidal volume (VD/VTp), ventilatory equivalent for CO2 production (VE/VCO2), VO2 at anaerobic threshold (VO2at) were also determined. FEV1, VC, TLC, DLCO, DM were impaired in CHF compared to 14 volunteers, and did not vary with treatment. Carvedilol reduced EDP, EDD, ESD, and increased EF, SV, VCF, without affecting VO2p, VO2at, VD/VTp, VE/VCO2, at 3 and 6 months. Placebo was ineffective. In CHF, carvedilol exerts neutral effects on ventilation and pulmonary gas transfer and ameliorates LV function at rest. This proves that antifailure treatment may not be similarly effective on cardiac and pulmonary function; and does not contradict the possibility that persistence of lung impairment may contribute to lack of improvement in exercise performance with carvedilol.

Adrenergic beta-Antagonists↗
PubMed1998

[Effects of cardiomegaly on the anatomical and functional state of the lung in chronic heart failure].

Heart and lungs might compete for the intrathoracic space in case of heart enlargement (as in heart failure). Therefore, the pulmonary abnormalities observed in patients with chronic heart failure (restrictive pattern and reduction of diffusion capacity) might be at least in part related to cardiomegaly. In 53 patients (11 women, 42 men, mean age 65 +/- 8 years) with stable heart failure and cardiac enlargement (cardiothoracic ratio-Ctr > or = 50%) we measured carbon monoxide lung diffusion (DLCO), lung tissue content (VT, single breath, expiratory regression of acetylene), alveolar volume (Va, single breath, expiratory regression of methane) and vital capacity (VC). In 16 patients the two subcomponents of DLCO, i.e. alveolar-capillary membrane diffusion (Dm) and diffusion related to capillary volume (Cv), were analyzed. Patients were grouped for Ctr (> or = 60%, Group 1, n = 28 and < 60%, Group 2, n = 25): VT (Group 1 0.62 +/- 0.2 l; Group 2 0.76 +/- 0.2 l, p < 0.01); Va (Group 1 4.21 +/- 0.97 l; Group 2 5.37 +/- 1.12 l, p < 0.0001); VC (Group 1 2.3 +/- 0.6 l; Group 2 3.1 +/- 0.6 l, p < 0.0001); DLCO (Group 1 16.15 +/- 3.95 ml/min x mmHg; Group 2 22.24 +/- 6.57 ml/min x mmHg, p < 0.0001). An inverse correlation was observed between Dm and Ctr (r = -0.47, p < 0.02), which disappeared when Va was accounted for Dm/Va (r = -0.12, NS). Cv was lower in Group 1 vs Group 2. In conclusion, in patients with Ctr > or = 60% (Group 1) "anatomy" (VT, Va, VC and Cv) and function (DLCO) of the lungs are impeded. This is likely due to reduction of space available for the lungs in the thorax by an enlarged heart (no correlation between Dm/Va vs Ctr).

Aged↗
PubMed1998

Decrease by ACE-inhibition of the excessive alveolar-capillary membrane resistance to gas transfer in chronic heart failure.

In this study the mechanisms were investigated whereby ACE-inhibitors improve pulmonary diffusion for carbon monoxide (DLco) in chronic heart failure. The two subcomponents of DLco are the alveolar-capillary membrane conductance (DM) and the capillary blood volume (VC). Stress failure of the membrane in chronic heart failure provides a mechanism for reduction of DM and, as a consequence, impairment of DLco. In 27 patients with chronic heart failure in NYHA functional class II to III and in 13 age- and sex-matched normal subjects, we evaluated the pulmonary function and determined DM and VC, according to the classic Roughton and Forster method, while they were given placebo, at 48 hours and 8 weeks after starting enalapril treatment (10 mg bid). ACE-inhibition had no effect in controls at both short- and mid-term. In chronic heart failure patients, a reduction in VC (likely consequence of a decrease in capillary pulmonary pressure) was the only change observed at 48 hours. At 8 weeks, DM was greatly increased even when the effective alveolar volume (VA) was accounted for (DM/VA), resulting in a significant improvement in DLco, despite a decrease in VC. The slow onset DM improvement makes it likely that the modulatory effect of ACE-inhibition on the membrane function emerges gradually, suggesting that it is likely dissociated from changes in pulmonary capillary pressure and VC. Thus, derangements of the alveolar-capillary membrane in chronic heart failure increase gas diffusion resistance; ACE-inhibition restores the diffusive properties of the membrane and gas transfer, and protects the lung when the heart is failing.

Angiotensin-Converting Enzyme Inhibitors↗