Chronic kidney disease and cardiac remodelling in patients with mild heart failure: Results from the REsynchronization reVErses Remodeling in Systolic Left vEntricular Dysfunction (REVERSE) study

Division of Cardiovascular Medicine, University of Pennsylvania, Philadelphia, PA, USA.
European Journal of Heart Failure (Impact Factor: 6.53). 09/2012; 14(12). DOI: 10.1093/eurjhf/hfs135
Source: PubMed


AimsChronic kidney disease (CKD) is a risk factor for left ventricular hypertrophy (LVH) and heart failure. We evaluated the effect of CKD on left ventricular (LV) remodelling among patients with mild heart failure.Methods and resultsREVERSE was a randomized, controlled trial evaluating cardiac resynchronization therapy (CRT) in patients with New York Heart Association (NYHA) class I/II heart failure. CKD was defined as an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2. We compared changes in LV function and size over the course of 12 months by CKD status using linear mixed models adjusted for demographics, co-morbidities, medications, cardiomyopathy aetiology, and CRT status. Finally, we evaluated the effect of CKD on cardiac remodelling among patients randomized to CRT on or off. CKD was associated with worsening LV function and dilation compared with the non-CKD group adjusted, 12-month β coefficients for the CKD group compared with the non-CKD referent group: LV ejection fraction (%) [-1.80, 95 confidence interval (CI)-3.36 to-0.24], LV end-systolic volume (mL) (14.16, 95 CI 3.96-24.36), LV end-diastolic volume (mL) (14.88, 95 CI 2.88-26.76), LV end-systolic diameter (cm) (0.36, 95 CI 0.12-0.48), LV end-diastolic diameter (cm) (0.24, 95 CI 0.012-0.36), mitral regurgitation () (3.12, 95 CI 0.48-5.76), and LV shape (0.036, 95 CI 0.012-0.060). In participants assigned to CRT, those without CKD had significantly greater improvements in LV structural parameters compared with the CKD group.Conclusions
In comparison with participants with normal kidney function, CKD is an independent risk factor for ventricular dysfunction and dilation. CRT improves LV function and structure to a lesser extent in patients with CKD than in those with normal kidney function.

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Available from: Cecilia Linde, Sep 03, 2014
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    • "It is increasingly recognized that both a low glomerular filtration rate and increased urinary protein excretion are associated with an adverse cardiac or cardiovascular outcome [24, 25]. Both low eGFR [11, 18] and proteinuria [26] have been shown to be associated with cardiac remodeling. On the other hand, as compared with the relationship between eGFR and FGF23/α-Klotho, information seems to be limited regarding the relationship association between proteinuria (or albuminuria) and FGF23/α-Klotho. "
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    ABSTRACT: Background Expression and/or excretion of fibroblast growth factor-23 (FGF23) and its co-receptor Klotho are altered in patients with end-stage renal disease. The possibility that the FGF23/α-Klotho system mediates the aggravated cardiovascular outcome among patients with chronic kidney disease (CKD) has been suggested. We determined whether FGF23 and α-Klotho concentrations are altered among patients with reduced renal function and proteinuria. Methods Serum FGF23 and α-Klotho were measured in cardiology patients who were not undergoing chronic hemodialysis. Estimated glomerular filtration rate (eGFR) was correlated negatively with FGF23 and positively with α-Klotho. Results The correlation between FGF23 and the renal tubular maximum reabsorption rate of phosphate to the GFR (TmP/GFR) was not significant, but that between FGF23 and serum calcium or inorganic phosphate was significant among patients with an estimated GFR of less than 60 mL/min/m2. By stepwise multivariate regression analysis, eGFR was selected as significant predictor for FGF23 or α-Klotho among patients with an estimated GFR of less than 60 mL/min/m2; however, urine albumin/creatinine ratio was not selected as a predictor for FGF23 or α-Klotho irrespective of the eGFR levels. In patients with eGFR of <60 mL/min/1.73 m2, UACR was significantly associated with log(FGF23); but, this association did not remain statistically significant in a multivariate model. Conclusions Among cardiology patients with various stages of CKD, serum concentrations of FGF23 and α-Klotho were associated with renal function, but not with the extent of proteinuria.
    BMC Nephrology 09/2014; 15(1):147. DOI:10.1186/1471-2369-15-147 · 1.69 Impact Factor
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    • "Hypertensive target organ damage includes impaired renal function and left ventricular hypertrophy (LVH). Impaired renal function is an independent marker for LVH and a good predictor of morbidity and mortality in cardiovascular disease.[1],[2] In patients with chronic kidney disease (CKD), there is a significant association between decreased estimated glomerular filtration rate (eGFR) and LVH.[3] "
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    ABSTRACT: Serum cystatin C levels can be used to predict morbidity and mortality in patients with cardiovascular disease. However, the clinical relevance of serum cystatin C levels in patients with hypertensive left ventricular hypertrophy (LVH) has rarely been investigated. We designed the present study to investigate whether serum cystatin C levels are associated with cardiac structural and functional alterations in hypertensive patients. We enrolled 823 hypertensive patients and classified them into two groups: those with LVH (n = 287) and those without LVH (n = 536). All patients underwent echocardiography and serum cystatin C testing. We analyzed the relationship between serum cystatin C levels and LVH. Serum cystatin C levels were higher in hypertensive patients with LVH than in those without LVH (P < 0.05). Using linear correlation analysis, we found a positive correlation between serum cystatin C levels and interventricular septal thickness (r = 0.247, P < 0.01), posterior wall thickness (r = 0.216, P < 0.01), and left ventricular weight index (r = 0.347, P < 0.01). When analyzed by multiple linear regression, the positive correlations remained between serum cystatin C and interventricular septal thickness (β = 0.167, P < 0.05), posterior wall thickness (β = 0.187, P < 0.05), and left ventricular weight index (β = 0.245, P < 0.01). Serum cystatin C concentration is an independent marker for hypertensive LVH.
    Journal of Geriatric Cardiology 09/2013; 10(3):286-90. DOI:10.3969/j.issn.1671-5411.2013.03.001 · 1.40 Impact Factor
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    • "This difference however, was not statistically significant when adjusted for age, hypertension and gender. We therefore can exclude that mild kidney dysfunction is associated with a clinically relevant cardiomyopathy as recently suggested [25], and we can also exclude the possibility that these patients have a higher myocardial vulnerability to ischemic damage. Although, the presence of more subtle cardiac dysfunctions (either diastolic or detectable with more sensitive methods) in patients with mild kidney dysfunction cannot be ruled out, the available studies [5] [6] suggest that it is present in patients who had a moderate/severe kidney function reduction and it is closely related to hypertension. "
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    ABSTRACT: Background & Aims The bases of the link between reduced glomerular filtration rate (GFR) and coronary artery disease (CAD) are complex and to some extent still unclear. We performed this observational, single referral center, cohort study to evaluate whether mild to moderate GFR reduction is associated with more severe CAD and/or with a worse cardiac prognosis independently of proteinuria, diabetes and traditional risk factors. Methods and results In 1,752 consecutive non-diabetic patients without proteinuria or moderate/severe kidney disease undergoing a clinically driven coronary angiography, coronary arteries lesions, myocardial function and hypertrophy and 10-yrs incidence of cardiac events and death were evaluated in relation to classes of estimated GFR defined according the lowest eGFR value (105+, 90+, 75+, 60+, 45+). A reduced eGFR was independently associated with hypertension, myocardial hypertrophy and stress induced ischemia, while the excess coronary lesions and the worse myocardial systolic function were both largely explained by age and cardiovascular risk factors. When compared to subjects 75+, both the risk of cardiac death (1.67[1.10-2.57] and 3.06[1.85-5.10]) and non-fatal myocardial infarction (2.58[1.12-6.49] and 2.73[1.31-6.41]) adjusted for age and comorbidities were higher in eGFR 60+ and 45+ patients. Conclusions A mild-moderate reduction of eGFR is closely associated to higher rates of stress-induced ischemia, myocardial hypertrophy and higher risk of fatal and non-fatal cardiac events. The associations of reduced eGFR with coronary atherosclerosis and myocardial systolic dysfunction are both largely explained by age and traditional risk factors.
    Nutrition, metabolism, and cardiovascular diseases: NMCD 01/2013; 24(6). DOI:10.1016/j.numecd.2013.12.005 · 3.32 Impact Factor
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