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

Marco Guazzi, Roberto Brambilla, Gianluca Pontone, Piergiuseppe Agostoni, Maurizio D. Guazzi

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish
Pages (from-to)191-197
Number of pages7
JournalThe American Journal of Cardiology
Volume89
Issue number2
DOIs
Publication statusPublished - Jan 15 2002

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Exercise Tolerance
Type 2 Diabetes Mellitus
Heart Failure
Carbon Monoxide
Lung
Exercise
Oxygen
Pulmonary Ventilation
Architectural Accessibility
Pulmonary Wedge Pressure
Tidal Volume
Left Ventricular Dysfunction
Glycosylation
Carbon Dioxide
Heart Diseases
Diabetes Mellitus
Gases
Control Groups
Membranes
Proteins

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

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abstract = "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.",
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N2 - 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.

AB - 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.

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