Why the study?
Does heart transplantation improve respiratory dysfunction in patients with severe chronic congestive heart failure?
Does heart transplantation improve respiratory dysfunction in patients with severe chronic congestive heart failure?
Heart transplantation reverses the restrictive ventilatory defect induced by severe congestive heart failure, but does not normalize the lung transfer factor for carbon monoxide (TLCO), suggesting permanent changes in lung vasculature.
Severe chronic congestive heart failure (CCHF) is known to induce a restrictive ventilatory defect, with a small decrease in lung transfer factor for carbon monoxide (TLCO). The aim of the present work was to assess the reversibility of this dysfunction. We studied a group of 47 patients with CCHF, before and one year after heart transplantation. The measurements included static and dynamic lung volumes, TLCO and cardiac function. On initial evaluation, vital capacity (VC), total lung capacity (TLC) and TLCO were reduced to 76, 79 and 64% of the predicted value (% pred), respectively. Forced expiratory volume in one second (FEV1) was decreased to 69% pred, with a FEV1/VC ratio below 0.70 in 13 out of 47 patients. One year after transplantation, cardiac function had markedly improved, as shown by a normalized left ventricular ejection fraction (from 18% preoperatively to 59% postoperatively), and mean pulmonary wedge pressure (from 26 to 12 mmHg). At this time, VC (94% pred) and TLC (98% pred) were within the normal range, whereas TLCO remained low (67% pred). The FEV1/VC ratio did not change, even in the subgroup with an initial low value. Smoking habits did contribute to the low TLCO and FEV1/VC ratio. In conclusion, respiratory dysfunction induced by CCHF is reversible, with the exception of the reduction in TLCO, which probably reflects permanent changes in the lung vasculature. CCHF does not induce an obstructive ventilatory pattern.
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Niset et al. (1993) studied this question.
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