Diffusing Capacity Decreases After Heart Transplantation

Ohar, Jill A.; Osterloh, Joan; Ahmed, Nadeem; Miller, Leslie W.

doi:10.1378/chest.103.3.857

Cited by 49 publications

(18 citation statements)

References 19 publications

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“…The improvement in cardiac function following HT may influence the changes in gas transfer, with improved left atrial pressures abolishing an artificially elevated diffusion capacity prior to transplant, perhaps existing because of pulmonary vascular engorgement [23]. However, this seems unlikely for two reasons.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary diffusion impairment following heart transplantation: a prospective study

Egan

Lowe²,

Yonan³

et al. 1996

Eur Respir J

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The aim of this prospective study was to confirm whether and when a fall in gas transfer occurs following heart transplantation (HT); and to examine the potential relationship between gas transfer and haemodynamic change, immunosuppression, and cytomegalovirus (CMV) infection.The lung physiology of 34 heart transplant recipients (HTR) and 14 control patients undergoing coronary artery bypass grafting (CABG) were studied. The absolute and standardized residual values of forced expiratory volume in one second (FEV1), forced vital capacity (FVC), residual volume (RV), forced residual volume (FRC), total lung capacity (TLC), transfer factor of the lungs for carbon monoxide (TL,CO) and carbon monoxide transfer coefficient (KCO) were measured before and at 30, 60, 90, 120 and 150 days after HT. These data were compared to haemodynamic status, graft rejection, cyclosporin levels and episodes of CMV infection. Lung function was studied in a group of patients before and 4 weeks after CABG.There was a significant fall in mean KCO after HT (pre-HT=1.29 and post-HT= 1.06 mmol·min -1 ·kPa·L -1 ) but not after CABG (pre-CABG=1.49, post-CABG=1.5 mmol·min -1 ·kPa·L -1 . No relationship was observed between gas transfer and CMV.At the latest stage following HT (150 days) there was a positive correlation between TL,CO (absolute value and standardized residual) and mean cyclosporin level (r=0.48 and r=0.44, respectively) and also between the absolute KCO and actual (r=0.56) and mean (r=0.55) cyclosporin levels. Following HT, there is an early fall in gas transfer, which is independent of the effects of surgery and bypass, implicating early immunosuppression (e.g. antithymocyte globulin/cyclosporin).

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Section: Discussionmentioning

confidence: 99%

Pulmonary diffusion impairment following heart transplantation: a prospective study

Egan

Lowe²,

Yonan³

et al. 1996

Eur Respir J

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“…By contrast, DLCO has been shown to be either lower than expected or progressively deteriorate (Al-Rawas et al 1997;Groen et al 1992;Ohar et al, 1993). There is agreement that pulmonary microvascular injury may be the cause of diffusion abnormalities in HTR (Ewert et al 2000;Mettauer et al 1999).…”

Section: Lung Limitationsmentioning

confidence: 98%

Exercise after heart transplantation

Marconi¹,

Marzorati²

2003

European Journal of Applied Physiology

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Exercise intolerance in heart transplant recipients (HTR) has a multifactorial origin, involving complex interactions among cardiac, neurohormonal, vascular, skeletal muscle and pulmonary abnormalities. However, the role of these abnormalities may differ as a function of time after transplantation and of many other variables. The present review is aimed at evaluating the role of cardiac, pulmonary and muscular factors in limiting maximal aerobic performance of HTR, and the benefits of chronic exercise. Whereas pulmonary function does not seem to affect gas exchange until a critical value of diffusing lung capacity is attained, cardiac and skeletal muscle function deterioration may represent relevant factors limiting maximal and submaximal aerobic performance. Cardiac function is mainly limited by chronotropic incompetence and diastolic dysfunction, whereas muscle activity seems to be limited by impaired oxygen supply as a consequence of the reduced capillary network. The latter may be due to either immunosuppressive regimen or deconditioning. Endurance and strength training may greatly improve muscle function and maximal aerobic performance of HTR, and may also reduce side effects of immunosuppressive therapy and control risk factors for cardiac allograft vasculopathy. For the above reasons exercise should be considered an important therapeutic tool in the long-term treatment of heart transplant recipients.

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“…Pulmonary congestion, interstitial fibrosis, cardiac enlargement, and respiratory muscle weakness are responsible for the restrictive ventilatory defect (19 -22). Of note, the restrictive ventilatory defect regresses after cardiac transplantation, whereas DLCO does not improve (23).…”

Section: Lung Function In Chf and Copdmentioning

confidence: 96%

Therapeutic Update: Non-Selective Beta- and Alpha-Adrenergic Blockade in Patients With Coexistent Chronic Obstructive Pulmonary Disease and Chronic Heart Failure

Sirak

Jelić

Jemtel

2004

Journal of the American College of Cardiology

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Patients with chronic heart failure (CHF) have a resting restrictive ventilatory defect. Any type of exercise requires patients with CHF to markedly increase their minute ventilation. Patients with chronic obstructive pulmonary disease (COPD) have airflow obstruction that leads to dynamic lung hyperinflation and reduced ventilatory response to exercise. Because exercise is associated with abnormally high minute ventilation in patients with CHF and with a limited minute ventilation increase in patients with COPD, functional capacity is severely impaired in patients with coexistent CHF and COPD. Optimal treatment of both conditions is a prerequisite to maximally improve functional capacity in patients with CHF and COPD. Unfortunately, beta-adrenergic blockade, the current cornerstone of CHF therapy, is frequently omitted in patients with CHF and COPD for fear of inducing bronchoconstriction. Furthermore, when prescribed, beta-adrenergic blockade is often attempted with a moderate dose of metoprolol tartrate, a beta-1-blocker that results in lesser clinical benefits than combined non-selective beta-blockade with carvedilol at the maximally recommended dose. Recent experience indicates that combined non-selective beta- and alpha-blockade with carvedilol is well tolerated in patients with COPD who do not have reversible airway obstruction. Alpha-adrenergic blockade may promote mild bronchodilation that offsets non-selective beta blockade-induced bronchoconstriction in patients with obstructive airway disease.

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Diffusing Capacity Decreases After Heart Transplantation

Cited by 49 publications

References 19 publications

Pulmonary diffusion impairment following heart transplantation: a prospective study

Pulmonary diffusion impairment following heart transplantation: a prospective study

Exercise after heart transplantation

Therapeutic Update: Non-Selective Beta- and Alpha-Adrenergic Blockade in Patients With Coexistent Chronic Obstructive Pulmonary Disease and Chronic Heart Failure

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