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(Chest. 2005;128:1620-1622.)
© 2005 American College of Chest Physicians

Association of Reduced Carbon Monoxide Diffusing Capacity With Moderate or Severe Left Ventricular Diastolic Dysfunction in Obese Persons*

Gautham Ravipati, MD; Wilbert S. Aronow, MD, FCCP; Jasdeep Sidana, MD; George P. Maguire, MD, FCCP; John A. McClung, MD; Robert N. Belkin, MD and Stuart G. Lehrman, MD

* From the Pulmonary and Critical Care (Drs. Aronow, Sidana, Maguire, and Lehrman) and Cardiology Divisions (Drs. Ravipati, McClung, and Belkin), Department of Medicine, Westchester Medical Center, New York Medical College, Valhalla, NY.

Correspondence to: Wilbert S. Aronow, MD, FCCP, Cardiology Division, New York Medical College, Macy Pavilion, Room 138, Valhalla, NY 10595; e-mail: WSAronow{at}aol.com


   Abstract
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Study objectives: To determine the association of reduced diffusing capacity of the lung for carbon monoxide (DLCO) with moderate or severe left ventricular diastolic dysfunction (LVDD) in obese persons.

Design: We investigated the association of DLCO with LVDD in 105 patients with a mean ± SD body mass index of 49 ± 5 kg/m2. An abnormal DLCO was < 80%. LVDD was investigated by Doppler and by tissue Doppler echocardiography. The Doppler echocardiographic data were analyzed blindly without knowledge of the clinical characteristics or whether the DLCO was normal or abnormal.

Setting: A university hospital.

Patients: The 105 patients included 19 men and 86 women (mean age, 45 ± 9 years).

Results: An abnormal DLCO was present in 62 of 105 patients (59%). Moderate or severe LVDD was present in 35 of 105 patients (33%). Moderate or severe LVDD was present in 25 of 62 patients (40%) with an abnormal DLCO and in 10 of 43 patients (23%) with a normal DLCO (p < 0.05).

Conclusion: Obese patients with a decreased DLCO have an increased prevalence of moderate or severe LVDD.

Key Words: carbon monoxide diffusing capacity • diastolic dysfunction • echocardiography • obesity


   Introduction
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Materials and Methods
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Reduced lung diffusion contributes to symptoms and exercise limitation in patients with congestive heart failure. Decreased gas diffusion occurs as a result of reduction in global lung perfusion and in the alveolar-capillary conductance,123 as well as across the alveolar capillary interface at rest.145 Diffusing capacity of the lung for carbon monoxide (DLCO) is lower in patients with congestive heart failure than in control subjects after maximal exercise.5 Patients with congestive heart failure exhibit a reduction in DLCO that is proportional to the severity of their heart disease.123456

We have reported that in obese persons with obstructive sleep apnea, an increased prevalence of moderate-to-severe left ventricular diastolic dysfunction (LVDD) that predisposes them to diastolic heart failure.7 This correlation of LVDD with obstructive sleep apnea was also demonstrated by Fung et al.8

To the best of our knowledge, the prevalence of LVDD in patients with reduced DLCO has not been previously reported. This article reports a higher prevalence of moderate or severe LVDD in morbidly obese patients with reduced DLCO than in morbidly obese patients with a normal DLCO.


   Materials and Methods
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We investigated the prevalence of LVDD measured by Doppler and tissue Doppler echocardiography prior to gastric bypass surgery in 19 obese men and in 86 obese women (mean age, 45 ± 9 years; mean body mass index, 49 ± 5 kg/m2) who underwent pulmonary function studies.

Pulmonary function tests were conducted by one of two technicians using standardized equipment. Pulmonary function data were recorded with the patients in the sitting position. The DLCO was calculated with a single-breath test. An abnormal DLCO was considered < 80%. Global Initiative for Chronic Obstructive Lung Disease guidelines9 were used to evaluate the presence of obstructive lung disease. The DLCO was measured without knowledge of whether LVDD was present or absent.

Doppler and tissue Doppler interrogation of the mitral inflow and mitral annulus, respectively, were performed in 20 obese persons referred for echocardiography prior to gastric bypass surgery. Mitral inflow recordings were obtained with the pulsed Doppler sample volume at the level of the mitral leaflet tips during the maximal opening in diastole. Pulmonary vein recordings were obtained with the sample volume positioned in the right paraseptal vein in the apical four-chamber view. Recordings of mitral inflow with the Valsalva maneuver were not generally performed. Studies were recorded on videotape or stored digitally for off-line review.

LVDD was evaluated and classified using previously described parameters.10 Moderate LVDD was diagnosed if the peak early diastolic transmitral flow velocity (E)/peak late diastolic transmitral flow velocity ratio was 0.75 to 1.50 and one or both of the following were present: the E/peak early diastolic myocardial velocity ratio was ≥ 10, or the peak systolic pulmonary vein flow velocity/peak diastolic pulmonary vein flow velocity ratio was < 1.10 Severe LVDD was diagnosed if the E/peak late diastolic transmitral flow velocity ratio was > 1.5 and one or both of the following were present: the E/peak early diastolic myocardial velocity ratio was ≥ 10, or the peak systolic pulmonary vein flow velocity/peak diastolic pulmonary vein flow velocity ratio was < 1.10 LVDD was evaluated blindly by a single experienced echocardiographer without knowledge of the clinical characteristics or whether a normal or abnormal DLCO was present.

Hypertension was diagnosed if the patient was being treated with antihypertensive medication, or if the systolic BP was ≥ 140 mm Hg, or the diastolic BP was ≥ 90 mm Hg. Diabetes mellitus was diagnosed if the patient was being treated for diabetes mellitus or the fasting blood sugar on two occasions was ≥ 126 mg/dL. Hypercholesterolemia was diagnosed if the patient was being treated for hypercholesterolemia or if the fasting serum total cholesterol was ≥ 200 mg/dL.

Student t test were used to analyze continuous variables. {chi}2 tests were used to analyze dichotomous variables.


   Results
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Table 1 shows the baseline characteristics of the patients with abnormal vs normal DLCO. No significant difference in baseline characteristics was present in patients with abnormal vs normal DLCO. Moderate or severe LVDD was present in 25 of 62 patients (40%) with abnormal DLCO and in 10 of 43 patients (23%) with normal DLCO (p < 0.05). Two of three patients (67%) with a DLCO < 60% had moderate or severe LVDD.


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  		Table 1.. Baseline Characteristics in Patients With Abnormal vs Normal DLCO Values*

 

   Discussion
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The blood-gas barrier is responsible for gas exchange between blood and alveolar air and regulation of the solute and fluid flux between the alveolar surface, interstitium, and blood. This is dependent on the carbon monoxide conductance across the alveolar-capillary tissue membrane and plasma barrier, as well as the rate of carbon monoxide uptake by whole blood in combination with hemoglobin and the pulmonary capillary blood volume as described by the Roughton and Forster model.11

The occurrence of a gas exchange abnormality has been shown to be a powerful independent predictor of a worse prognosis in patients with stable chronic heart failure.5 In the presence of heart failure, lung capillaries are subjected to increased pressure and increased volume. An acute stepwise increase in pulmonary microvascular pressure as well as mechanical insult trigger a morphologic disruption of the alveolar-capillary barrier that leads to a transition from a hydrostatic and low-permeability form to a high-permeability form of pulmonary edema.12 This stress failure process is the result of alveolar membrane exposure to increased left ventricular end-diastolic pressure and pulmonary capillary stasis.12

However, recurrent injury to the alveolar capillary interface and contribution from neurohormonal, cytotoxic, and genetic expression may further injure lung capillary and alveolar spaces, leading to a remodeling process characterized by increased thickness of the alveolar capillary membrane. The increased amount of fluid leaking across the alveolar-capillary membrane leads to prolongation of the diffusion path for gas exchange.121314

The increased prevalence of a decreased DLCO in our patients suggests that LVDD acts in a similar mechanism at the level of the pulmonary capillary, leading to increased pressure and volume. The fact that some of our patients with LVDD did not demonstrate a reduction in DLCO is attributable possibly to the duration of their LVDD. It may also be explained by the presence of subclinical pulmonary vascular congestion leading to an acute increase in DLCO before chronic adaptive changes have developed.15

By demonstrating a decreased DLCO in morbidly obese patients with LVDD, our study highlights a possible mechanism of exercise intolerance and dyspnea in this subset of patients. It also suggests a possible role for using DLCO as a surrogate marker for prognosis to monitor progression of LVDD and for correlation with the degree of dyspnea and exercise performance. In conclusion, we found that obese patients with a reduced DLCO have an increased prevalence of moderate or severe LVDD.


   Footnotes
 
Abbreviations: DLCO = diffusing capacity of the lung for carbon monoxide; E = peak early diastolic transmitral flow velocity; LVDD = left ventricular diastolic dysfunction

Received for publication February 16, 2005. Accepted for publication March 7, 2005.


   References
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 Abstract
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  1. Puri, S, Baker, BL, Dutka, DP, et al (1995) Reduced alveolar-capillary membrane diffusing capacity in chronic heart failure: its pathophysiological relevance and relationship to exercise performance. Circulation 91,2769-2774[Abstract/Free Full Text]
  2. Assayag, P, Benamer, H, Aubry, P, et al Alteration of the alveolar-capillary membrane diffusing capacity in chronic left heart failure. Am J Cardiol 1998;82,459-464[CrossRef][ISI][Medline]
  3. Smith, AA, Cowbum, PJ, Parker, ME Impaired pulmonary diffusion during exercise in patients with chronic heart failure. Circulation 1999;100,1406-1410[Abstract/Free Full Text]
  4. Guazzi, M, Brambilla, R, Pontone, G, et al Effect of non-insulin-dependent diabetes mellitus on pulmonary function and exercise tolerance in chronic congestive heart failure. Am J Cardiol 2002;89,191-197[CrossRef][ISI][Medline]
  5. Guazzi, M, Pontone, G, Brambilla, R, et al Alveolar-capillary membrane gas conductance: a novel prognostic indicator in chronic heart failure. Eur Heart J 2002;23,467-476[Abstract/Free Full Text]
  6. Messner-Pellenc, P, Brasileiro, C, Ahmaidi, S, et al Exercise intolerance in patients with chronic heart failure: role of pulmonary diffusing limitation. Eur Heart J 1995;16,201-209[Abstract/Free Full Text]
  7. Sidana, J, Aronow, WS, Ravipati, G, et al Prevalence of moderate or severe left ventricular diastolic dysfunction in obese persons with obstructive sleep apnea. Cardiology 2005;,(inpress)
  8. Fung, JWH, Li, TST, Choy, DKL, et al Severe obstructive sleep apnea is associated with left ventricular diastolic dysfunction. Chest 2002;121,422-429[Abstract/Free Full Text]
  9. Pauwels, R, Buist, A, Calverley, P, et al Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: NHLBI/WHO global initiative for chronic obstructive lung disease (GOLD) workshop summary. Am J Respir Crit Care Med 2001;163,1256-1276[Free Full Text]
  10. Khouri, SJ, Maly, GT, Suh, DD, et al A practical approach to the echocardiographic evaluation of diastolic function. J Am Soc Echocardiogr 2004;17,290-297[CrossRef][ISI][Medline]
  11. Roughton, FJ, Forster, RE, Cander, L Rate at which carbon monoxide replaces oxygen from combination with human hemoglobin in solution and in the red cell. J Appl Physiol 1957;11,269-276[Abstract/Free Full Text]
  12. West, J Pulmonary capillary stress failure. J Appl Physiol 2000;89,2483-2489[Abstract/Free Full Text]
  13. Guazzi, M. Alveolar-capillary membrane dysfunction in heart failure. evidence of a pathophysiologic role Chest 2003;124,1090-1102[Abstract/Free Full Text]
  14. Tomsley, MI, Fu, Z, Mathieu-Costello, O, et al Pulmonary microvascular permeability; responses to high vascular pressure after induction of pacing induced heart failure in dogs. Circ Res 1995;77,317-325[Abstract/Free Full Text]
  15. Kraemer, MD, Kubo, SH, Rector, TS, et al Pulmonary and peripheral vascular factors are important determinants of peak exercise oxygen uptake in patients with heart failure. J Am Coll Cardiol 1993;21,641-648[Abstract]




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