scholarly journals The Contribution of Known Familial Cardiovascular Disease Genes to Sudden Cardiac Death in Patients Undergoing Hemodialysis

2021 ◽  
pp. 1-10
Author(s):  
Tae-Hwi Schwantes-An ◽  
Matteo Vatta ◽  
Marco Abreu ◽  
Leah Wetherill ◽  
Howard J. Edenberg ◽  
...  

<b><i>Introduction:</i></b> Patients with chronic kidney disease experience high rates of cardiovascular mortality and morbidity. When kidney disease progresses to the need for dialysis, sudden cardiac death (SCD) accounts for 25–35% of all cardiovascular deaths. The objective was to determine if rare genetic variants known to be associated with cardiovascular death in the general population are associated with SCD in patients undergoing hemodialysis. <b><i>Methods:</i></b> We performed a case-control study comparing 126 (37 African American [AfAn] and 89 European ancestry [EA]) SCD subjects and 107 controls (34 AfAn and 73 EA), matched for age, sex, self-reported race, dialysis duration (&#x3c;2, 2–5 and &#x3e;5 years), and the presence or absence of diabetes mellitus. To target the coding regions of genes previously reported to be associated with 15 inherited cardiac conditions (ICCs), we used the TruSight Cardio Kit (Illumina, San Diego, CA, USA) to capture the genetic regions of interest. In all, the kit targets 572-kb regions that include the protein-coding regions and 40-bp 5′ and 3′ end-flanking regions of 174 genes associated with the 15 ICCs. Using the sequence data, burden tests were conducted to identify genes with an increased number of variants among SCD cases compared to matched controls. <b><i>Results:</i></b> Eleven genes were associated with SCD, but after correction for multiple testing, none of the 174 genes were identified as having more variants in the SCD cases than the matched controls, including previously identified genes. Secondary burden tests grouping variants based on diseases and gene function did not produce statistically significant associations. <b><i>Discussion/Conclusions:</i></b> We found no associations between genes known to be associated with ICCs and SCD in our sample of patients undergoing hemodialysis. This suggests that genetic causes are unlikely to be a major pathogenic factor in SCD in hemodialysis patients, although our sample size limits definitive conclusions.

2021 ◽  
Vol 4 (57) ◽  
pp. 8-11
Author(s):  
Szymon Warwas ◽  
Marta Jagosz ◽  
Beata Średniawa ◽  
Michał Mazurek ◽  
Ewa Jędrzejczyk-Patej

The most common cause of death among dialysis patients with end-stage kidney disease are cardiovascular diseases. It is estimated that 18-27% of all deaths in dialysis patients are sudden cardiac deaths due to arrhythmias and conduction disturbances. The most common arrhythmias in dialysis patients, often leading to sudden death, are not ventricular arrhythmias but bradyarrhythmias. The article below discusses the most common arrhythmias in dialysis patients and methods of preventing sudden cardiac death in this group of patients.


ESC CardioMed ◽  
2018 ◽  
pp. 981-984
Author(s):  
Thomas F. Mueller ◽  
Valerie Luyckx

Chronic kidney disease (CKD) encompasses a spectrum of diseases that are identified by a glomerular filtration rate below 90 mL/min/1.73m2 or the presence of proteinuria, or both of these, persisting for over 3 months. In population-based studies, mortality in patients with CKD is consistently several-fold higher than that in patients without CKD, and the risk increases as the severity of renal function worsens. Mortality risk is, not surprisingly, highest among those with end-stage kidney disease. In developed countries, patients with CKD and end-stage kidney disease do not die of renal disease, but die primarily of non-renal causes, the relative proportions of which change across the spectrum of renal function. In the early stages of CKD, malignancy tends to be the predominant case of death; however, as renal function worsens, the proportion of deaths related to cardiovascular disease increases. Coronary artery disease contributes to most cardiac deaths in those with milder CKD. The proportions of cardiac and overall deaths from heart failure and sudden cardiac death increase progressively as renal function declines. Sudden cardiac death is a major cause of death among patients with end-stage kidney disease. Multiple factors including underlying coronary artery disease, left ventricular hypertrophy, valvular heart disease, arrhythmias, volume and electrolyte abnormalities, uraemia, and inflammation all likely contribute to the increased risk of cardiovascular death. Much work is needed to understand the pathophysiology and develop strategies to prevent cardiovascular deaths especially in the CKD population.


PLoS Genetics ◽  
2011 ◽  
Vol 7 (6) ◽  
pp. e1002158 ◽  
Author(s):  
Dan E. Arking ◽  
M. Juhani Junttila ◽  
Philippe Goyette ◽  
Adriana Huertas-Vazquez ◽  
Mark Eijgelsheim ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Charlotte Strandhave ◽  
My Svensson ◽  
Henrik Krarup ◽  
Jeppe Hagstrup Christensen

Sudden cardiac death and atherosclerosis have a major impact on cardiovascular mortality in chronic kidney disease (CKD). Inflammation with elevated high-sensitive C-reactive protein (hs-CRP) is involved in both sudden cardiac death and atherosclerosis, and decreased heart rate variability (HRV) is a predictor of both sudden cardiac death and atherosclerosis. Haptoglobin (Hp) is characterised by three genotypes (1-1, 2-1, and 2-2) with different antioxidant abilities. The aim was to examine whether HRV and hs-CRP were associated with Hp genotype in CKD patients. Fifty-six patients with CKD stage 2–5 were included. Hp genotype was determined by high-performance liquid chromatography. HRV was analysed from the 24 h Holter recordings. Hs-CRP was measured using an immunoturbidimetric assay. The results show that the HRV indices SDNN and SDANN were significantly lower in the Hp 2-2 patients (P=0.02and 0.04, resp.). In an adjusted linear regression model, Hp 2-2 was associated with both SDNN (P=0.005) and SDANN (P=0.01). Hs-CRP was higher in the Hp 2-2 patients (P=0.002). In an adjusted linear regression model, the association between Hp 2-2 and hs-CRP remained significant (P=0.003). In conclusion, a negative association was observed between Hp 2-2 and HRV, and Hp 2-2 was positively associated with hs-CRP in CKD patients.


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