scholarly journals Uraemic Cardiomyopathy: A Review of Current Literature

2021 ◽  
Vol 15 ◽  
pp. 117954682199834
Author(s):  
Kartheek Garikapati ◽  
Daniel Goh ◽  
Shaun Khanna ◽  
Krishna Echampati

Uraemic Cardiomyopathy (UC) is recognised as an intricate and multifactorial disease which portends a significant burden in patients with End-Stage Renal Disease (ESRD). The cardiovascular morbidity and mortality associated with UC is significant and can be associated with the development of arrythmias, cardiac failure and sudden cardiac death (SCD). The pathophysiology of UC involves a complex interplay of traditional implicative factors such as haemodynamic overload and circulating uraemic toxins as well as our evolving understanding of the Chronic Kidney Disease-Mineral Bone Disease pathway. There is an instrumental role for multi-modality imaging in the diagnostic process; including transthoracic echocardiography and cardiac magnetic resonance imaging in identifying the hallmarks of left ventricular hypertrophy and myocardial fibrosis that characterise UC. The appropriate utilisation of the aforementioned diagnostics in the ESRD population may help guide therapeutic approaches, such as pharmacotherapy including beta-blockers and aldosterone-antagonists as well as haemodialysis and renal transplantation. Despite this, there remains limitations in effective therapeutic interventions for UC and ongoing research on a cellular level is vital in establishing further therapies.

2001 ◽  
Vol 10 (4) ◽  
pp. 285-293 ◽  
Author(s):  
LG Futterman ◽  
L Lemberg

HF is a prevalent and debilitating disease, affecting nearly 5 million patients and perhaps an equal number with asymptomatic left ventricular dysfunction who are at high risk of atrial fibrillation developing. An estimated 550,000 new cases occur every year. HF is the most common diagnosis in hospitalized patients aged 65 and over and is a major cause of death. The median survival after onset is 1.7 years in men and 3.2 years in women. The majority of cardiac deaths in patients with HF are sudden and arrhythmogenic: the rest are due to progressive hemodynamic deterioration. A significant advance in the past decade has been the recognition of the importance of inhibiting the neurohormonal action in HF with the use of beta-blockers, angiotensin receptor, and aldosterone antagonists. In addition, a new concept in HF therapy has evolved. The view that chronic HF is an irreversible, end-stage process is being supplanted by the fact that it is possible to effect biological improvement in the intrinsic defects of function and structure in hearts afflicted with chronic HF. Reversibility of HF has been reported by (1) unloading the failing heart using an LVAD, (2) the sophisticated use of diuretic combinations and neurohormonal blocking drugs, or (3) employing continuous arteriovenous hemofiltration. Thus it is now possible to reverse a process that has long been considered irreversible. Exercise programs designed for patients with HF that have been advocated recently can be difficult to apply. Fine tuning of an exercise regimen is required because a reduction in cardiac work is mandatory when treating HF, where the concern is that the heart may not be capable of supplying the metabolic needs of the body, even in resting states. Finally, although not emphasized in the recent literature on HF, the use of diuretics and sodium restriction continue to be the mainstays of therapy without which compensation of HF is not possible.


2006 ◽  
Vol 6 ◽  
pp. 1262-1273
Author(s):  
Néstor H. García ◽  
Luis I. Juncos

The most important goal of antihypertensive therapy is to prevent the complications associated with hypertension (stroke, myocardial infarction, end-stage renal disease, etc). For this, secondary targets such as left ventricular hypertrophy, proteinuria, dementia, and other signs of hypertension-induced organ damage help the physician to assess risks and monitor treatment efficacy. New treatment targets may be arising, however. One such target may be endothelial dysfunction. In effect, endothelial dysfunction not only may precede the elevation of blood pressure, but may also pave the way to conditions often associated with hypertension, such as diabetes, arteriosclerosis, microalbuminuria, congestive heart failure, and tissue hypertrophy. Because inflammation often accompanies endothelial dysfunction, approaches to counteract inflammation are now being evaluated. For this, antagonists of the renin-angiotensin-aldosterone system, statins, and beta blockers are all being tested. All of these agents seem to prevent or delay the induction of proinflammatory molecules aside from, and in addition to, their specific effects on blood pressure. The focus of this review is to update some of the animal and human research showing that hypertension sets off an inflammatory state and also to consider some of the anti-inflammatory approaches that may prevent the development of endothelial dysfunction, and the subsequent renal and cardiovascular damage.


2021 ◽  
Author(s):  
Wailesy Adam ◽  
Tumaini Nagu ◽  
Reuben Mutagaywa ◽  
Onesmo Kisanga

Abstract BackgroundArrhythmias are responsible for almost 2 out of 3 cardiac deaths among patients on hemodialysis. We report the prevalence and risk factors for clinically significant arrhythmias among end stage renal disease (ESRD) patients on maintenance dialysis at a tertiary dialysis facility in Tanzania. MethodsCross-sectional study, involving consenting adults with ESRD was conducted September 2019 to February 2020. Arrhythmias were assessed using standard 5-leads Holter electrocardiography placed 15 minutes before dialysis and connected throughout dialysis. Clinically Significant Arrhythmias (CSA) was defined as ectopic beats in excess of 10 per hour or any of the ventricular tachycardia or Pause lasting for at least 2.5 seconds or paroxysmal supraventricular tachycardia or atrial flutter or atrial fibrillation. ResultsA total of 71 (44.4%) participants had CSA. Factors associated with increased risk for CSA were: age older than 60 years (OR 34; 95% CI: 5.15-236; P< 0.001), intradialytic blood pressure change of ≥ 10mmHg (OR 3.85; 95% CI: 1.27-11.7; P=0.017) and the presence of Left Ventricular Hypertrophy (OR 5.84; 95% CI: 1.85-18.4; P< 0.01). On the contrary, three dialysis sessions per week (OR 0.14; 95% CI: 0.03-0.67; P=0.013) and use of beta-blockers (OR 0.18; 95% CI: 0.05-0.68; P=0.011) were significantly associated with a decreased risk of CSA. ConclusionClinically significant arrhythmias are not uncommon in ESRD patients undergoing maintenance haemodialysis. We recommend increasing vigilance for CSA among older patients (>60 years) as well as those with left ventricular hypertrophy. Beta blockers among hypertensive ESRD patients with ventricular hypertrophy could be helpful.


2004 ◽  
Vol 4 (1) ◽  
pp. 34-40 ◽  
Author(s):  
Senija Rasić ◽  
Indira Kulenović ◽  
Azra Haracić ◽  
Amra Catović

Cardiovascular diseases are the major cause of mortality in uraemic patients treated by hemodialysis. Left ventricular hypertrophy (LVH) is considered to be a major cardiac risk factor.AIM: To investigate the presence of some potential adverse risk factors in hemodialysis patients with developed LVH echocardiography verified and determine their relative contribution to the LVH in comparison with patients with normal LV.METHOD: The study included 50 patients with end-stage renal disease in the first 2 years of hemodialysis treatment, who were followed up during one year. All participants have the echocardiography performed as well as serial measurements of potential modifiable cardiovascular risk factors.RESULTS: This investigation showed that LVH is present in high percentage (72%) in uraemic patients, even at the beginning of hemodialysis treatment. This LV morphological abnormality is statistically significantly related to anaemia (p<0,001), systolic (p<0,001) and diastolic hypertension (p<0,001)), elevated mean arterial pressure (p<0,001) and hyperparathyroidism (p=0,002).CONCLUSION: Modification of existing risk factors in uraemic patients could contribute to prevention and treatment of LV hypertophy and thus reduce cardiovascular morbidity and mortality.


Diabetology ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 31-35
Author(s):  
Keiichiro Matoba

Diabetic kidney disease (DKD) is a global epidemic leading to end-stage renal disease (ESRD) and susceptibility to cardiovascular disease, with few therapeutic interventions. A hallmark of DKD is the activation of the renin-angiotensin-aldosterone system and hemodynamic changes in glomerulus. Although intensive therapy with agents that targets those abnormalities lowers the risk of DKD progression, it does not completely abolish the risk of ESRD and cardiovascular events. Recent studies have illustrated the importance of renal inflammation, oxidative stress, and activated Rho-associated protein kinase (ROCK) signaling as essential pathogenesis for the development of DKD. In this commentary, these topics will be discussed.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ashwin Radhakrishnan ◽  
Luke C. Pickup ◽  
Anna M. Price ◽  
Jonathan P. Law ◽  
Kirsty C. McGee ◽  
...  

Abstract Background Coronary microvascular dysfunction (CMD) is common in end-stage renal disease (ESRD) and is an adverse prognostic marker. Coronary flow velocity reserve (CFVR) is a measure of coronary microvascular function and can be assessed using Doppler echocardiography. Reduced CFVR in ESRD has been attributed to factors such as diabetes, hypertension and left ventricular hypertrophy. The contributory role of other mediators important in the development of cardiovascular disease in ESRD has not been studied. The aim of this study was to examine the prevalence of CMD in a cohort of kidney transplant candidates and to look for associations of CMD with markers of anaemia, bone mineral metabolism and chronic inflammation. Methods Twenty-two kidney transplant candidates with ESRD were studied with myocardial contrast echocardiography, Doppler CFVR assessment and serum multiplex immunoassay analysis. Individuals with diabetes, uncontrolled hypertension or ischaemic heart disease were excluded. Results 7/22 subjects had CMD (defined as CFVR < 2). Demographic, laboratory and echocardiographic parameters and serum biomarkers were similar between subjects with and without CMD. Subjects with CMD had significantly lower haemoglobin than subjects without CMD (102 g/L ± 12 vs. 117 g/L ± 11, p = 0.008). There was a positive correlation between haemoglobin and CFVR (r = 0.7, p = 0.001). Similar results were seen for haematocrit. In regression analyses, haemoglobin was an independent predictor of CFVR (β = 0.041 95% confidence interval 0.012–0.071, p = 0.009) and of CFVR < 2 (odds ratio 0.85 95% confidence interval 0.74–0.98, p = 0.022). Conclusions Among kidney transplant candidates with ESRD, there is a high prevalence of CMD, despite the absence of traditional risk factors. Anaemia may be a potential driver of microvascular dysfunction in this population and requires further investigation.


2017 ◽  
Vol 37 (4) ◽  
pp. 375-383 ◽  
Author(s):  
Charlotte E. Grantham ◽  
Katherine L. Hull ◽  
Matthew P.M. Graham-Brown ◽  
Daniel S. March ◽  
James O. Burton

Cardiovascular mortality in the end-stage renal disease (ESRD) population remains the leading cause of death. Targeting traditional cardiovascular risk factors has proven unsuccessful in this patient population, and therefore attention has turned to risk factors related to chronic kidney disease (CKD). The toxicity of high-glucose peritoneal dialysis (PD) solutions has been well documented. The breakdown of glucose into glucose degradation products (GDP) and advanced glycation end-products (AGE) has the ability to alter cell viability and cause premature apoptosis and is strongly correlated with interstitial fibrosis and microvascular sclerosis. Biocompatible solutions have been introduced to combat the hostile milieu to which PD patients are exposed.Given the considerable cardiovascular burden for PD patients, little is known about the cardiovascular impact the new biocompatible solutions may have. This review analyzes the existing literature regarding the mechanisms through which low-GDP solutions may modulate cardiovascular risk. Interventions using low-GDP solutions have provided encouraging changes in structural cardiovascular measures such as left ventricular mass (LVM), although metabolic changes from reduced GDP and AGE exposure yield inconclusive results on vascular remodelling. It is thought that the local effects of reduced glucose exposure may improve membrane integrity and therefore fluid status. Further research in the form of a robust randomized controlled trial should be carried out to assess the true extent of the cardiovascular benefits these biocompatible solutions may hold.


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