Abstract

Background: Chronic kidney disease (CKD) is associated with increased cardiovascular (CV) risk. Cardiac abnormalities have been studied in severe CKD but not in the most prevalent stage 3 (s3), often under-diagnosed. We evaluated whether s3-CKD is associated with abnormalities of CV system. Methods: 39 asymptomatic patients with s3-CKD (GFR = 45 ± 10 ml/min/1.73m2), free of prevalent CV disease, from the outpatient clinic of the Department of Nephrology, were compared with 44 control subjects with GFR>60 ml/min/1.73m2 (GFR = 84 ± 14 ml/min/1.73m2) and comparable prevalence of hypertension (66% vs 69 in s3-CKD). In addition to standard echocardiographic parameters of left ventricular (LV) geometry and function, we computed non-invasive effective arterial elastance (EAe in mmHg/mL/beat, using an estimate of end-systolic pressure), systolic LV elastance (LVe, in mmHg/mL) and myocardial mechanic efficiency (MME, in mL/sec), using previously reported formulas. Results: s3-CKD and controls were comparable for age, sex, lipid profile, prevalence of diabetes and smoking habit. LV mass, LV geometry and stroke work were similar in the two groups, but both ejection fraction and midwall shortening (mS) were significantly reduced in s3-CKD (both p < 0.001), with 36% s3-CKD with clear-cut depressed mS. EAe and peripheral resistance were higher in s3-CKD than in controls (both p < 0.002), without significant difference in LVe, resulting in an apparently favorable vascular ventricular coupling. However MME was substantially reduced in CKD (p < 0.004). For comparable levels of LV mass, MME was substantially reduced in s3-CKD, compared to controls, with the difference increasing with increasing values of LV mass (p < 0.001 for slope). Similarly, at a given level of peripheral resistance, LV geometry was less concentric in s3-CKD than in controls (p < 0.05). Conclusions: We conclude that s3-CKD asymptomatic patients present with a peculiar CV phenotype, characterized by impaired mechano-energetic efficiency and reduced midwall mechanics, in the absence of compensating LV concentric remodeling, to avoid fall in ejection fraction. How much these characteristics might impact evolution toward more pronounced LV abnormalities in more advanced CKD and incident heart failure should be investigated.

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