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Long-term changes in left ventricular hypertrophy after renal transplantation
C Rigatto1, R N Foley, G M Kent
1Division of Nephrology, Memorial University, St. John's Newfoundland, Canada.
Insights
Left ventricular hypertrophy regression after kidney transplant continues until year two, then stabilizes. Factors like older age and hypertension predict poor regression, impacting long-term cardiac health in transplant recipients.
Area of Science:
- Nephrology
- Cardiology
- Transplantation Medicine
Background:
- Left ventricular hypertrophy (LVH) is a common, progressive complication in dialysis patients, linked to adverse cardiac outcomes.
- While partial LVH regression occurs post-transplant, its long-term trajectory remains unclear.
Purpose of the Study:
- To investigate the long-term evolution of left ventricular hypertrophy (LVH) after renal transplantation.
- To identify factors associated with the failure of LVH regression post-transplant.
Main Methods:
- A prospective cohort study of 143 renal transplant recipients from a larger dialysis patient cohort.
- Annual echocardiography and monthly laboratory assessments over four years post-transplant.
- Multiple linear regression analysis to model changes in left ventricular mass index (LVMI).
Main Results:
- LVMI decreased significantly from year 1 to year 2 post-transplant (161 g/m2 to 146 g/m2), then stabilized.
- Left ventricular volume index followed a similar pattern, declining by year 2 and stabilizing thereafter.
- Failure to regress LVMI by year 2 was associated with older age, hypertension, and specific pulse pressure characteristics relative to heart size.
Conclusions:
- LVH regression extends beyond the first year post-renal transplant, reaching a nadir at two years and persisting.
- Older age, history of hypertension, and abnormal pulse pressure dynamics are linked to incomplete LVH regression.
Background:
Concentric and eccentric left ventricular hypertrophy are common progressive disorders in dialysis patients and are associated with cardiac failure and death. Although partial regression of these abnormalities is known to occur during the first post-transplant year, their long-term evolution is unknown.
Methods:
A total of 143 of 433 dialysis patients participating in a long-term prospective cohort study received renal transplants. Laboratory parameters were assessed monthly. Echocardiography was performed annually. Left ventricular mass index (LVMI) and cavity volume index were calculated according to standard formulae. Multiple linear regression was used to model change in LVMI as a function of baseline clinical and laboratory variables.
Results:
LVMI fell from 161 g/m2 at 1 year to 146 g/m2 (P=0.009) g/m2 after 2 years. No further regression was seen in years 3 and 4. Left ventricular volume index showed similar trends, with a decline from year 1 to year 2 (P=0.05) followed by stabilization in years 3 and 4. Older age, long duration of hypertension, need for more than one antihypertensive, high pulse pressure in normal-size hearts, and low pulse pressure in dilated hearts were significantly associated with failure of regression of LVMI between the first and second years (MLR, P<0.000001, r2=0.57).
Conclusions:
Regression of left ventricular hypertrophy continues beyond the first year after renal transplantation, reaching a nadir at 2 years and persisting into the third and fourth posttransplant years. Failure to regress was associated with older age, hypertension, high pulse pressure in normal-size hearts and low pulse pressure in dilated hearts.
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