2010 - TTS International Congress


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Complications Cardiovascular

31.12 - Subclinical left ventricular echocardiographic abnormalities one year after kidney transplantation are associated with graft function and future cardiovascular events

Presenter: Miha, Arnol, Ljubljana, Slovenia
Authors: Arnol M., Knap B., Oblak M., Buturović-Ponikvar J., Bren A., Kandus A.

SUBCLINICAL LEFT VENTRICULAR ECHOCARDIOGRAPHIC ABNORMALITIES ONE YEAR AFTER KIDNEY TRANSPLANTATION ARE ASSOCIATED WITH GRAFT FUNCTION AND FUTURE CARDIOVASCULAR EVENTS

COMPLICATIONS - CARDIOVASCULAR

M. Arnol, B. Knap, M. Oblak, J. Buturovi?-ponikvar, A.F. Bren, A. Kandus
Department Of Nephrology, University Medical Centre Ljubljana, Ljubljana/SLOVENIA

Body: Introduction. Cardiovascular events (CVE) are the leading cause of morbidity and mortality in kidney transplant recipients. Increased left ventricular mass (LVM) is a risk factor for CVE. This studyinvestigated the associations of subclinical left ventricular echocardiographic abnormalities with impaired kidney graft function expressed as lower glomerular filtration rate (GFR) at 1 year aftertransplantation and future CVE beyond 1 year post-transplant. Methods. A prospective cohort study included 68 consecutive non-diabetic recipients of a kidney transplant between January 1, 2004 andDecember 31, 2005 who underwent a transthoracic echocardiographic investigation at 1 year after transplantation. LVM, LVM index and left ventricular hypertrophy (LVH) were assessed usingtwo-dimensional M-mode echocardiography. GFR was estimated (eGFR) by the four-variable Modification of Diet in Renal Disease formula. Cox proportional-hazards analysis was used to estimate cardiacCVE (new-onset angina pectoris, acute myocardial infarct, coronary angioplasty or by-pass surgery, or sudden cardiac death) hazard ratios (HR) for patients who fulfilled the criteria for LVH versuscontrols with no LVH at 1 year after transplantation. Results. All patients had normal systolic function (ejection fraction > 50%) with no symptoms or signs of heart failure. LVH was present in 44patients (65%). LVM and incidence of LVH were increased in 28 patients with eGFR < 60 ml/min/1.73 m2 compared with 40 patients with eGFR >= 60 ml/min/1.73 m2 (248 +/- 61 g and 86% vs. 210 +/-46 g and 50%, respectively; P < 0.01). After adjustment for age, gender, systolic and diastolic blood pressure, and length of prior dialysis, each 5-ml/min/1.73 m2 lower eGFR was associated with agreater LVM (regression coefficient beta 7 g, 95% confidence interval [CI] 1-12 g; P = 0.007). After a median follow-up of 4.5 years, there were 18 (26.5%) cardiac CVE. The incidence of cardiac CVEwas significantly higher in patients with LVH than in patients with no LVH at 1 year post-transplant (36.4% vs. 8.3%; P = 0.02). In adjusted analyses, LVH was associated with increased risk forfuture cardiac CVE (HR 4.69, 95% CI 1.02-21.5, P = 0.037). At 1 year after transplantation 13.2% of patients were taking anti-platelet aggregation medication, 20.6% were using ACE inhibitors orangiotensin II receptor blockers, and 29.4% were treated with beta-adrenergic blockers. Conclusion. In kidney transplant recipients, a lower eGFR at 1 year post-transplant was associated with greaterLVM and higher incidence of LVH. Presence of LVH was associated with an increased risk for future cardiac CVE. Only a minority of patients was treated with anti-platelet aggregation medication,beta-adrenergic blockers, ACE inhibitors or angiotensin II receptor blockers. These findings may explain, in part, the link between impaired kidney graft function, greater LVM and increased risk forfuture CVE.

Disclosure: All authors have declared no conflicts of interest.


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