10th Anniversary Themed Article y Disorders of the Myocardium
Editorial
Is uremic cardiomyopathy a direct consequence of chronic kidney disease? Expert Review of Cardiovascular Therapy Downloaded from informahealthcare.com by Selcuk Universitesi on 01/30/15 For personal use only.
Expert Rev. Cardiovasc. Ther. 12(2), 127–130 (2014)
Shanmugakumar Chinnappa Author for correspondence: Leeds Institute of Biomedical and Clinical Sciences, University of Leeds and Leeds General Infirmary, Leeds, UK and Sheffield Kidney Institute, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK Tel.: +44 113 225 5296 Fax: +44 113 225 5296 [email protected]
Sandeep S Hothi Physiological Laboratory and Murray Edwards College, University of Cambridge, Cambridge, UK and Glenfield Hospital, Leicester, UK
Lip-Bun Tan Leeds Institute of Biomedical and Clinical Sciences, University of Leeds and Leeds General Infirmary, Leeds, UK and Department of Cardiology, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK
Heart failure is a major cause of morbidity and mortality in chronic kidney disease (CKD). Rather than merely secondary to traditional vascular factors, CKD is also an independent risk factor for heart failure, termed uremic cardiomyopathy (UCM). Echocardiography commonly reveals structural left ventricular hypertrophy in CKD, without clarifying whether it is adaptive or maladaptive. Corresponding functional assessments have been mostly conducted at rest. To unravel the extents and mechanisms UCM, a next step involves the adoption of direct measurements of CKD-induced cardiac pumping incapacity at peak exercise. This could potentially lead to future novel interventions to ameliorate or reverse UCM.
Chronic kidney disease (CKD) carries a high burden of morbidity and mortality. Recent registry data from the US Renal Data System show that >40% of endstage renal disease (ESRD) deaths were due to cardiovascular disease (CVD) [1]. Indeed, 50% of ESRD patients suffer from heart failure (HF), thus forming the predominant cardiac abnormality observed in CKD [1]. It is a common perception that HF in CKD is secondary to vascular comorbid conditions such as ischemic heart disease (IHD), hypertension and diabetes mellitus, but it is becoming apparent that primary CKD is an independent risk factor for incident HF even in nondiabetic and normotensive patients [2]. It is also becoming clearer that CVD in CKD is more than just accelerated atherosclerosis [3]. Thus, nontraditional risk factors such as uremic toxins, anemia, calcium phosphate imbalance, renin–angiotensin–aldosterone system (RAAS) activation, sympathetic activation, inflammation and oxidative stress are gaining recognition for their roles in the pathogenesis of cardiac disease in CKD [4]. A recent Kidney Disease: Improving Global Outcome report emphasized the need for improving our understanding of cardiac dysfunction in CKD and highlighted the need for research that is capable of evaluating asymptomatic left ventricular (LV) dysfunction [5]. Of the five
subtypes of cardiorenal syndromes so far classified [6], it is the fourth subtype, CKD directly leading to cardiac dysfunction, which will form the focus of this brief editorial, and for simplicity, we shall ascribe the term uremic cardiomyopathy (UCM) to this type of dysfunction. Structural & ultrastructural abnormalities of UCM
By far the commonest, easily accessible method of studying the structural abnormalities of UCM is echocardiography, with which it is observed that a predominant feature in CKD is LV hypertrophy (LVH). A recent large observational study has demonstrated a graded relationship between the severity of CKD and the prevalence and severity of LVH [7]. The prevalence increased from 32 to 75% as one moved from patient groups with estimated glomerular filtration rate (eGFR) >60 to
Editorial
Is uremic cardiomyopathy a direct consequence of chronic kidney disease? Expert Review of Cardiovascular Therapy Downloaded from informahealthcare.com by Selcuk Universitesi on 01/30/15 For personal use only.
Expert Rev. Cardiovasc. Ther. 12(2), 127–130 (2014)
Shanmugakumar Chinnappa Author for correspondence: Leeds Institute of Biomedical and Clinical Sciences, University of Leeds and Leeds General Infirmary, Leeds, UK and Sheffield Kidney Institute, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK Tel.: +44 113 225 5296 Fax: +44 113 225 5296 [email protected]
Sandeep S Hothi Physiological Laboratory and Murray Edwards College, University of Cambridge, Cambridge, UK and Glenfield Hospital, Leicester, UK
Lip-Bun Tan Leeds Institute of Biomedical and Clinical Sciences, University of Leeds and Leeds General Infirmary, Leeds, UK and Department of Cardiology, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK
Heart failure is a major cause of morbidity and mortality in chronic kidney disease (CKD). Rather than merely secondary to traditional vascular factors, CKD is also an independent risk factor for heart failure, termed uremic cardiomyopathy (UCM). Echocardiography commonly reveals structural left ventricular hypertrophy in CKD, without clarifying whether it is adaptive or maladaptive. Corresponding functional assessments have been mostly conducted at rest. To unravel the extents and mechanisms UCM, a next step involves the adoption of direct measurements of CKD-induced cardiac pumping incapacity at peak exercise. This could potentially lead to future novel interventions to ameliorate or reverse UCM.
Chronic kidney disease (CKD) carries a high burden of morbidity and mortality. Recent registry data from the US Renal Data System show that >40% of endstage renal disease (ESRD) deaths were due to cardiovascular disease (CVD) [1]. Indeed, 50% of ESRD patients suffer from heart failure (HF), thus forming the predominant cardiac abnormality observed in CKD [1]. It is a common perception that HF in CKD is secondary to vascular comorbid conditions such as ischemic heart disease (IHD), hypertension and diabetes mellitus, but it is becoming apparent that primary CKD is an independent risk factor for incident HF even in nondiabetic and normotensive patients [2]. It is also becoming clearer that CVD in CKD is more than just accelerated atherosclerosis [3]. Thus, nontraditional risk factors such as uremic toxins, anemia, calcium phosphate imbalance, renin–angiotensin–aldosterone system (RAAS) activation, sympathetic activation, inflammation and oxidative stress are gaining recognition for their roles in the pathogenesis of cardiac disease in CKD [4]. A recent Kidney Disease: Improving Global Outcome report emphasized the need for improving our understanding of cardiac dysfunction in CKD and highlighted the need for research that is capable of evaluating asymptomatic left ventricular (LV) dysfunction [5]. Of the five
subtypes of cardiorenal syndromes so far classified [6], it is the fourth subtype, CKD directly leading to cardiac dysfunction, which will form the focus of this brief editorial, and for simplicity, we shall ascribe the term uremic cardiomyopathy (UCM) to this type of dysfunction. Structural & ultrastructural abnormalities of UCM
By far the commonest, easily accessible method of studying the structural abnormalities of UCM is echocardiography, with which it is observed that a predominant feature in CKD is LV hypertrophy (LVH). A recent large observational study has demonstrated a graded relationship between the severity of CKD and the prevalence and severity of LVH [7]. The prevalence increased from 32 to 75% as one moved from patient groups with estimated glomerular filtration rate (eGFR) >60 to
