Diffusion Capacity in Heart Transplant Recipients

Groen, Harry J.M.; Bogaard, J. M.; Balk, A. H. M. M.; Kho, Siang G.; Hop, Wim C. J.; Hilvering, C

doi:10.1378/chest.102.2.456

Cited by 33 publications

(16 citation statements)

References 14 publications

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“…Some of the potential causes for the fall in the transfer coefficient after HT include bypass, changes in cardiac function, CMV infection [4], early immunosuppression (i.e. RATG/cyclosporin) and maintenance immunosuppression, especially cyclosporin [1,2]. Cardiopulmonary bypass might have resulted in microvascular/alveolar injury expressed as a fall in KCO but these changes were not seen in the CABG group nor was there any correlation between the change in KCO and the duration of bypass.…”

Section: Discussionmentioning

confidence: 99%

“…Alternatively, as has been suggested before [1,2] but remains unproven, the physiological changes could be caused by cyclosporin, which is introduced at the same time as RATG. Cyclosporin can affect the microvascular structure of the kidney causing nephrotoxicity, with two histological patterns, either an arteriolaropathy with narrowing of the vascular lumen or an interstitial fibrosis [29].…”

Section: Discussionmentioning

confidence: 99%

“…Several different hypotheses have been advanced as an explanation, including cyclosporin [1,2], persistent changes associated with pulmonary venous hypertension [3], and cytomegalovirus (CMV) infection [4]. All of these studies were retrospective without control groups.…”

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confidence: 99%

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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%

Section: Discussionmentioning

confidence: 99%

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Pulmonary diffusion impairment following heart transplantation: a prospective study

Egan

Lowe²,

Yonan³

et al. 1996

Eur Respir J

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“…In good agreement with this hypothesis, persisting abnormalities in the diffusion capacity and the resolution of restrictive and obstructive changes have been observed following successful heart transplantation [4, 18,20,401. This has been attributed to a thickening of the alveolo-capillary membrane [9, 40, 451.…”

Section: Discussionmentioning

confidence: 76%

“…Recently, we could confirm these findings in 642 patients followed up to 11 years after heart transplantation [15]. Concering potential causes hCMV infection and/or immunosuppressive drugs, such as cyclosporin A controversial findings exist [18,22,34,431. In our patients after heart transplantation we were unable to demonstrate that different immunosuppressive regimens or hCMV infection were significantly correlated to the presence of pulmonary diffusion abnormalities [14].…”

Section: Discussionmentioning

confidence: 79%

High prevalence of pulmonary diffusion abnormalities without interstitial changes in long-term survivors of liver transplantation

Ewert¹,

Mutze²,

Schachschal³

et al. 1999

Transplant International

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Abnormalities in lung function are frequent findings in patients with terminal stage chronic liver disease. While spirometric parameters improve early after liver transplantation, a reduction in diffusion capacity has been reported up to 15 months after transplantation. It is unknown to what extent this disturbance in gas exchange occurs among long term survivors after liver transplantation. We assessed lung function in terms of spirometry, and gas exchange as well as pulmonary morphology by high resolution computed tomography (HRCT) in 40 patients 38 months (median, range 20-147 months) after liver transplantation. The prevalence of restrictive or obstructive changes was not different from predicted values. For the whole group of longterm survivors the carbon monoxide transfer coefficient (KCO) was reduced to 71.3 + 12.0 % predicted ( P < 0.05). HRCT revealed interstitial changes in only 2/40 (5.0 %), emphysematous bullae in 2/40 (5.0 %) and pleural thickening in 9/40 (22,s Yo). Diffusion abnormalities are prevalent in the majority of patients after liver transplantation, whereas spirometric abnormalities are absent also in the long term. The high prevalence of impaired gas exchange and the absence of interstitial lesions imply that changes in pulmonary blood vessels are the most likely cause.

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Exercise Limitation Following Transplantation

Williams

McKenna

2012

Comprehensive Physiology

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Organ transplantation is one of the medical miracles or the 20th century. It has the capacity to substantially improve exercise performance and quality of life in patients who are severely limited with chronic organ failure. We focus on the most commonly performed solid‐organ transplants and describe peak exercise performance following recovery from transplantation. Across all of the common transplants, evaluated significant reduction in o 2 peak is seen (typically renal and liver 65%‐80% with heart and/or lung 50%‐60% of predicted). Those with the lowest o 2 peak pretransplant have the lowest o 2 peak posttransplant. Overall very few patients have a o 2 peak in the normal range. Investigation of the cause of the reduction of o 2 peak has identified many factors pre‐ and posttransplant that may contribute. These include organ‐specific factors in the otherwise well‐functioning allograft (e.g., chronotropic incompetence in heart transplantation) as well as allograft dysfunction itself (e.g., chronic lung allograft dysfunction). However, looking across all transplants, a pattern emerges. A low muscle mass with qualitative change in large exercising skeletal muscle groups is seen pretransplant. Many factor posttransplant aggravate these changes or prevent them recovering, especially calcineurin antagonist drugs which are key immunosuppressing agents. This results in the reduction of o 2 peak despite restoration of near normal function of the initially failing organ system. As such organ transplantation has provided an experiment of nature that has focused our attention on an important confounder of chronic organ failure‐skeletal muscle dysfunction. © 2012 American Physiological Society. Compr Physiol 2:1937‐1979, 2012.

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Diffusion Capacity in Heart Transplant Recipients

Cited by 33 publications

References 14 publications

Pulmonary diffusion impairment following heart transplantation: a prospective study

Pulmonary diffusion impairment following heart transplantation: a prospective study

High prevalence of pulmonary diffusion abnormalities without interstitial changes in long-term survivors of liver transplantation

Exercise Limitation Following Transplantation

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