After cardiac transplant, there is often development of restrictive cardiac physiology. Little is known about the factors that contribute to this physiology and its correlation with pathology. Heart retransplantation provides a valuable opportunity to further understand this relationship. In this study, we investigated the correlation of myocardial fibrosis and restrictive physiology, and possible risk factors utilizing data from all retransplants at our center. A retrospective review of the 30 patients who underwent retransplantation at our institution between 1994 and 2004 was performed. Hemodynamic and imaging data were reviewed for the presence of restrictive physiology. Pathology reports were reviewed for the presence of myocardial fibrosis in the explanted hearts. The cohort with restrictive physiology preceding redo heart transplant had significantly more patients exhibiting myocardial fibrosis compared with the non-restrictive physiology group (94.1% vs. 15.4%, p < 0.001). We found no difference in the immunosuppressive regimen, history of rejection, and reason for transplant. In our study, we observed that myocardial fibrosis is an important contributor to the development of restrictive physiology. Further work needs to be done for risk stratification and the mechanism of fibrosis development.

BackgroundIntense interest surrounds the recent expansion of US National Institutes of Health (NIH) budgets as part of economic stimulus legislation. However, the relationship between NIH funding and cardiovascular disease research is poorly understood, making the likely impact of this policy change unclear.MethodsThe National Library of Medicine's PubMed database was searched for articles published from 1996 to 2006, originating from U.S. institutions, and containing the phrases “cardiolog,” “cardiovascular,” or “cardiac,” in the first author's department. Research methodology, journal of publication, journal impact factor, and receipt of NIH funding were recorded. Differences in means and trends were tested with t-tests and linear regression, respectively, with P≤0.05 for significance.ResultsOf 117,643 world cardiovascular articles, 36,684 (31.2%) originated from the U.S., of which 10,293 (28.1%) received NIH funding. The NIH funded 40.1% of U.S. basic science articles, 20.3% of overall clinical trials, 18.1% of randomized-controlled, and 12.2% of multicenter clinical trials. NIH-funded and total articles grew significantly (65 articles/year, P<0.001 and 218 articles/year, P<0.001, respectively). The proportion of articles receiving NIH funding was stable, but grew significantly for basic science and clinical trials (0.87%/year, P<0.001 and 0.67%/year, P = 0.029, respectively). NIH-funded articles had greater journal impact factors than non NIH-funded articles (5.76 vs. 3.71, P<0.001).ConclusionsNIH influence on U.S. cardiovascular research expanded in the past decade, during the period of NIH budget doubling. A substantial fraction of research is now directly funded and thus likely sensitive to budget fluctuations, particularly in basic science research. NIH funding predicts greater journal impact.

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