Prognostic significance of global longitudinal strain in chronic kidney disease: the evidence is building

Abstract

This article refers to 'Prevalence of left ventricular systolic dysfunction in pre-dialysis and dialysis patients with preserved left ventricular ejection fraction' by L.C.R. Hensen et al., published in this issue on pages 560-568.Chronic kidney disease (CKD) is a major health burden affecting roughly 11% of the population with a disproportionally increased propensity to develop cardiovascular disease and events. 1 CKD perpetuates systemic inflammation and oxidative stress, well-known instigators in cardiovascular disease. Proposed mechanisms by which renal dysfunction causes cardiac dysfunction include uraemic toxins, altered levels of renal endocrine factors, and haemodynamic overload. There is mounting evidence to support that CKD patients have an accelerated disease process with premature atherosclerosis, calcification, and cardiac remodelling resulting in left ventricular (LV) hypertrophy and diastolic dysfunction in early stages of the disease. LV systolic function when measured by LV ejection fraction (LVEF) is often preserved. We have a limited understanding of how to use echocardiographic parameters to risk stratify these patients. Although the relative risk of adverse events and death increases with decreasing estimated glomerular filtration rate and increasing proteinuria, patients within the same CKD classification may have very different absolute risks, while there is substantial overlap between the categories. In patients with heart failure and preserved LVEF, CKD is independently associated with increased cardiac remodelling (high LV mass, impaired diastolic relaxation), significantly worse cardiac mechanics (impaired LV longitudinal, left atrial, and right ventricular free wall strain), and worse outcome. 2,3 However, the role of CKD in patients with heart failure and preserved LVEF remains controversial as it was recently reported that although CKD is more common among these patients, it is less important with a weaker association and a less discriminatory power for mortality compared to heart failure with reduced or mildly reduced LVEF. 4 The opinions expressed in this article are not necessarily those of the Editors of the European Journal of Heart Failure or of the European Society of Cardiology.

Relationship between Microfibrillar-Associated Protein 4 Levels and Subclinical Myocardial Damage in Chronic Kidney Disease

“…In the present research, GLS was lower in the CKD patient group than in the control group, although no significant difference was determined between the groups in terms of GCS. The majority of previous studies have involved stage 3-5 CKD, and significant decreases in both GLS and GCS have been shown, particularly toward the final stage [3,21,22]. The median GFR in the present study was approx-imately 43 mL/min/1.73 m 2 , and our patients had predominantly stage 3 CKD.…”

“…Numerous similar studies have shown preserved EF in CKD and decreased GLS associated with hospitalization and cardiovascular mortality [3]. Studies have also shown decreased GCS in CKD, although others have reported no difference compared to control groups [3,22]. In the present research, GLS was lower in the CKD patient group than in the control group, although no significant difference was determined between the groups in terms of GCS.…”

“…Hensen et al [21] investigated EF in normal patients with stage 3-5 end-stage renal failure and revealed decreased GLS in this patient group, which they associated with a higher risk of heart failure-related hospitalization and mortality. Numerous similar studies have shown preserved EF in CKD and decreased GLS associated with hospitalization and cardiovascular mortality [3]. Studies have also shown decreased GCS in CKD, although others have reported no difference compared to control groups [3,22].…”

“…Potential reasons for an increased risk of LV hypertrophy and ischemic coronary artery disease from the early stages of CKD may include hypertension, volume loading, impaired calcium and phosphorus metabolism, increased inflammation, and oxidative stress. Early identification of systolic and diastolic dysfunction in CKD is therefore of vital importance in terms of appropriate precautions and therapeutic approaches [1][2][3][4]13]. The search for early biomarkers and imaging techniques capable of acting as early markers of myocardial damage in CKD is still continuing.…”

“…These processes lead to accelerated atherosclerosis, vascular calcification, and cardiac remodeling. Left ventricular (LV) hypertrophy and diastolic dysfunction begin to develop in the early stages of kidney disease in CKD, while ejection fraction (EF), an echocardiographic marker of LV systolic function, is usually preserved [3,4]. The search for early markers of cardiac functional impairment in CKD is therefore still continuing in terms of both biomarkers and echocardiographic markers.…”