Author + information
- Received March 23, 2004
- Revision received May 28, 2004
- Accepted June 7, 2004
- Published online September 15, 2004.
- Anne B. Taegtmeyer, BMBCh*,†,
- Angela M. Crook, MSc‡,
- Paul J.R. Barton, PhD† and
- Nicholas R. Banner, FRCP*,* ()
- ↵*Reprint requests and correspondence:
Dr. Nicholas R. Banner, Royal Brompton and Harefield NHS Trust, Hill End Road, Harefield, Middlesex UB9 6JH, United Kingdom
Objectives This study was designed to test the hypothesis that heterotopic heart transplant (HHT) patients have lower blood pressure than orthotopic cardiac transplant (OCT) patients because their native heart is involved in blood pressure homeostasis.
Background Hypertension occurs more frequently after OCT than after liver or lung transplantation, suggesting that transplantation of the heart itself contributes to post-transplant hypertension.
Methods Blood pressure and related measurements in 233 OCT and 38 HHT patients were studied retrospectively post-transplant.
Results Systolic blood pressure (SBP) was persistently lower among HHT patients (means 121 vs. 137, 126 vs. 137, 125 vs. 139, and 128 vs. 143 mm Hg at month 3 and years 1, 3, and 5 respectively, p < 0.005). Left ventricular and aortic systolic pressures were also lower (130 vs. 143 mm Hg, p = 0.01 and 129 vs. 142 mm Hg, p = 0.01). Multivariable analysis with age, gender, body mass index, creatinine, steroids, cyclosporine, use of antihypertensive medication, donor left ventricular ejection fraction, donor weight, and type of transplant as covariables showed HHT to be independently associated with a lower SBP at each time point (beta-coefficients −16.2, −12.1, −13.3, and −14.2 mm Hg, p < 0.01). The adjusted hazard ratio for the development of systolic hypertension among HHT compared with OCT patients was 0.59 (95% confidence interval 0.39 to 0.91, p = 0.017).
Conclusions Heterotopic heart transplant patients had lower SBP than OCT patients, consistent with the hypothesis that the native heart continues to contribute to blood pressure homeostasis.
This study was supported by the Harefield Research Foundation and the Royal Brompton and Harefield NHS Trust.
- Received March 23, 2004.
- Revision received May 28, 2004.
- Accepted June 7, 2004.
- American College of Cardiology Foundation