1.
Long-term cardiac allograft valves after heart transplant are functionally and structurally preserved, in contrast to homografts and bioprostheses.
Wilhelmi, MH, Bara, C, Kofidis, T, Wilhelmi, M, Pichlmaier, M, Haverich, A
The Journal of heart valve disease. 2006;(6):777-82
Abstract
BACKGROUND AND AIM OF THE STUDY Homograft valves undergo degenerative changes over time, which finally lead to functional deterioration. Immunological events are believed to play a pivotal role in this process. To further evaluate this hypothesis, the valvular morphology and function, as well as comorbidities predisposing to deteriorative processes, were evaluated in patients who had undergone heart transplant more than 10 years previously. METHODS In a consecutive cohort of 146 patients (125 males, 21 females; mean age at transplant 43.8 +/- 11.2 years), heart and valve function were assessed by color Doppler echocardiography at a mean of 5306 +/- 987 days after heart transplant. Evaluated parameters included chamber dimensions, cardiac function, valvular morphology/function, and concomitant diseases. RESULTS Atrial and ventricular dimensions were within normal ranges for the left atrium (LA; n=7), right atrium (RA; n=7), left ventricle (LV; n=143) and right ventricle (RV; n=119). Slight enlargements occurred in the LA (n=138), RA (n=137), LV (n=1) and RV (n=11), while significant enlargements were seen in the LA (n=1), RA (n=2), LV (n=2), and RV (n=16). With regard to cardiac function, the ejection fraction (EF) was 63.9 +/- 4.9%, left ventricular isovolumic relaxation time (IVRT) 85.04 +/- 14.64 ms, fractional shortening (FS) 34 +/- 12%, and pulmonary artery systolic pressure (PASP) 29.81 +/- 6.4 mmHg. Valvular regurgitation (grade > or =2) was present in 34 patients (31 tricuspid valves, three mitral valves). No patients presented with aortic valve regurgitation. Concomitant conditions with a potential impact on calcium balance/valvular deterioration included immunologic/chronic inflammatory diseases (n=6), malignancies (n=12), kidney (n=41), cardiovascular system (n=39) and thyroid/parathyroid (n=12). CONCLUSION During the long term after heart transplant, heart valves were characterized by normal morphology and function in the majority of cases. Although most patients presented with concomitant conditions strongly predisposing for valvular deterioration/calcification, sole immunosuppressive/anti-inflammatory therapy appears to prevent these processes in heart transplant patients.
2.
High-dose angiotensin-converting enzyme inhibition restores body fluid homeostasis in heart-transplant recipients.
Braith, RW, Mills, RM, Wilcox, CS, Davis, GL, Hill, JA, Wood, CE
Journal of the American College of Cardiology. 2003;(3):426-32
Abstract
OBJECTIVES We tested the hypothesis that salt and fluid retention in heart-transplant recipients (HTRs) is caused by a failure to reflexively suppress the renin-angiotensin-aldosterone system (RAAS). BACKGROUND It is known that extracellular fluid volume is expanded (12% to 15%) in HTRs who develop hypertension. METHODS Responses to volume expansion were measured in eight HTRs (ages 57 +/- 6 years) and six liver-transplant recipients (LTRs) (ages 52 +/- 2 years) both before and after treatment with captopril (225 mg/day). After three days of a standardized diet, 0.154 mol/l saline was infused at 8 ml/kg/h for 4 h. Blood pressure, hormones, and renal function were monitored for 48 h. After four months, the same subjects received captopril (225 mg/day), and the protocol was repeated. RESULTS Before captopril, saline infusion suppressed the RAAS in LTRs but not in HTRs, resulting in elimination of 86 +/- 12% versus 50 +/- 11% of the sodium load by 48-h postinfusion. Blood pressure increased only in the HTRs (+16 +/- 5/9 +/- 3 mm Hg) and remained elevated for 48 h (p < or = 0.05). After captopril, sodium elimination was comparable in the liver (87 +/- 13%) and heart groups (86 +/- 12%) and blood pressure did not change in either group. CONCLUSIONS; Heart transplant recipients have blunted diuretic and natriuretic responses to volume expansion that is mediated by their inability to suppress the RAAS. Pharmacologic suppression of the RAAS normalized defects in blood pressure and fluid homeostasis. These findings indicate that hypertension in HTRs is caused, in part, by a failure to reflexively suppress the RAAS when these patients become hypervolemic.
3.
Better late than never? Experience with intravenous pamidronate treatment in patients with low bone mass or fractures following cardiac or liver transplantation.
Dodidou, P, Bruckner, T, Hosch, S, Haass, M, Klar, E, Sauer, P, Ziegler, R, Leidig-Bruckner, G
Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA. 2003;(1):82-9
Abstract
Organ transplantation is associated with a high turnover of bone metabolism, and an increased loss of bone mass and incidence of osteoporotic fractures. Established therapies for osteoporosis after organ transplantation are still lacking, however. We report on an intravenous bisphosphonate therapy initiated in transplant patients because of a high rate of bone loss or incident osteoporotic fractures. Twenty-one patients after liver transplantation and 13 patients after heart transplantation received 30 mg pamidronate intravenously every 3 months, combined with 1000 mg calcium and 1000 IU vitamin D per day. The median time interval between transplantation and start of pamidronate treatment was 1.9 years in cardiac patients and 2.3 years in liver patients. Lumbar spine bone mineral density (LS BMD) and femoral neck BMD (FN BMD) were measured before and every 6 months after pamidronate therapy was initiated. Spinal radiographs were performed annually. Biochemical markers of bone metabolism were determined every 3 months, immediately before pamidronate administration. From a previous observational study, 58 patients treated only with calcium and vitamin D were matched for age, sex, pretransplantation LS BMD and time interval between transplantation and the first pamidronate treatment. In the pamidronate-treated patients, the mean increase in LS BMD adjusted for baseline values amounted to 0.080 +/- 0.038 g/cm(2) (8.6 +/- 4.0 %) after 1 year and 0.091 +/- 0.058 g/cm(2) (10.4 +/- 6.1%) after 2 years compared with 0.001 +/- 0.037 g/cm(2) (0.26 +/- 4.0%) after 1 year and 0.015 +/- 0.057 g/cm(2) (1.8 +/- 6.0%) after 2 years in the historical control group (absolute LS BMD changes pamidronate group vs historical group p < 0.0001 after 1 and 2 years). The changes of FN BMD were 0.024 +/- 0.043 g/cm(2) (3.2 +/- 6.1%) after 1 year and 0.046 +/- 0.052 g/cm(2) (7.0 +/- 6.1%) after 2 years in the pamidronate group compared with -0.012 +/- 0.043 g/cm(2) (-1.6 +/- 6.1%) after 1 year and -0.013 +/- 0.052 g/cm(2) (-1.1 +/- 6.1%) after 2 years in the historical control group (absolute FN BMD changes pamidronate group vs historical group p = 0.003 after 1 year and p = 0.001 after 2 years). From a total of 287 application cycles of pamidronate treatment, no severe side effects were observed and non-severe side effects were seen in only 39 cycles (13.6%). We conclude that cyclic intravenous pamidronate treatment is beneficial to patients with low bone mass or osteoporotic fractures following transplant, even when not immediately initiated.