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REVIEW ARTICLE Table of Contents  
Ahead of print publication
Sudden cardiac death and chronic kidney disease


 Department of Nephrology, Command Hospital Air Force, Bengaluru, Karnataka, India

Click here for correspondence address and email

Date of Submission23-Oct-2021
Date of Acceptance13-Jan-2022
Date of Web Publication25-Jun-2022
 

  Abstract 


Sudden cardiac death (SCD) is responsible for approximately one fourth of all cause mortality in dialysis patients. In chronic kidney disease (CKD) patients, unlike general population, traditional coronary artery disease associated risk factors are not the major determinants of SCD. The adverse cardiomyopathic and vasculopathic milieu in CKD predispose these patients to arrythmias, conduction abnormalities, and sudden cardiac death. In advanced kidney disease, these conditions may be further exacerbated by electrolyte shifts, divalent ion abnormalities, sympathetic overactivity, decreased baroreflex sensitivity, iron toxicity, and chronic inflammation. The outcomes after cardiac arrest in CKD patients particularly those on dialysis are poor. The decision to implant a cardioverter- defibrillator deppends on the patient's age and stage of CKD. In this review, we will discuss the definition, pathophysiology, risk factors and preventive strategies of SCD in the setting of CKD.

Keywords: Arrythmia, cardiomyopathy, hemodialysis, sudden cardiac death


How to cite this URL:
Jha VK. Sudden cardiac death and chronic kidney disease. APIK J Int Med [Epub ahead of print] [cited 2022 Sep 25]. Available from: https://www.ajim.in/preprintarticle.asp?id=348288





  Introduction Top


Sudden cardiac death (SCD) is a sudden, unexpected death caused by cessation of heart function. These events are defined as those deaths that are either preceded by a witnessed collapse, or occur within 1 h of an acute change in clinical condition, or occur within 24 h since the deceased individual was known to be in his or her usual state of health.[1] It is usually from an unexpected circulatory arrest, usually from a cardiac arrhythmia. The 2006 American College of Cardiology/American Heart Association/Heart Rhythm Society to establish data standards for electrophysiology defined sudden cardiac arrest (SCA) and SCD as- SCA is the sudden cessation of cardiac activity so that the victim becomes unresponsive, with no normal breathing and no signs of circulation. If corrective measures are not taken rapidly, this condition progresses to sudden death. Cardiac arrest should be used to signify an event as described above, that is reversed, usually by Cardiopulmonary resuscitation and/or defibrillation or cardioversion, or cardiac pacing. SCD should not be used to describe events that are not fatal.[2] In the general population, SCD was recently estimated to be about 8% of the out-of-hospital cardiac arrests treated by emergency medical services personnel.[3]

In chronic kidney disease (CKD) patients, putting the diagnosis of SCD could be problematic-since deaths frequently occur at home and unwitnessed. Other noncardiac causes of sudden death, as well as cerebrovascular event, would also contribute to overall mortality in these patients. Some potentially true SCDs are excluded due to the time limits set by the definition. According to US Renal Data System,[4],[5] approximately 22% of all deaths are caused by SCD, and the incidence increases with age: 2% per year for ages 20–44 years, 3.7% per year for ages 45–64 years, and 7% per year for ages 65 years and older.

Nondialysis-dependent CKD patients are also at increased risk of SCD, have a poorer prognosis postcardiac arrest compared to the normal population, and the likelihood of survival decreases with a declining glomerular filtration rate (GFR) Even mild reductions in kidney function, demonstrated by higher cystatin C levels, increase the risk of SCD particularly in susceptible populations such as elderly patients.[6] As per current estimate, SCD is accountable for 27% ± 2% of all-cause mortality in dialysis patients.[7] Compared with the average risk of SCD, there is a 50% increased frequency of SCD on the first hemodialysis session after the long weekend interval. The risk is also increased threefold in the 12 h period before the end of the long weekend interval and increased 1.7 times in the 12 h following commencement of the dialysis procedure after this long interval.[8]


  Pathophysiology of Sudden Cardiac Death in Chronic Kidney Disease Top


Pathophysiology of SCD in CKD is depicted as in [Figure 1].
Figure 1: Pathophysiology of sudden cardiac death in chronic kidney disease

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Cardiomyopathy due to left ventricular pressure and volume overload and vasculopathy due to atherosclerosis and arteriosclerosis predispose patients with CKD to cardiovascular disease. The adverse cardiomyopathic and vasculopathic milieu predisposes these patients to arrhythmias, conduction abnormalities, and SCD. This is likely to be exacerbated by electrolyte shifts, divalent ion abnormalities, diabetes, sympathetic overactivity, inflammation and iron deposition. Impaired baroreflex effectiveness and sensitivity, as well as obstructive sleep apnea might also contribute to the risk of SCD.


  Risk Factors of Sudden Cardiac Death in Chronic Kidney Disease Top


Risk factors of SCD in CKD are as in [Figure 2].
Figure 2: Risk factors for sudden cardiac death in chronic kidney disease

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Uremic cardiomyopathy

In predialysis CKD patients, left ventricular hypertrophy (LVH) increases as GFR falls. LVH is present in almost 75% of patients starting dialysis.[9] Hypertension, anemia, volume overload and other risk factors can partly explain the progression of LVH. Even after initiation of dialysis, progressive left ventricular dilation and LVH continues and is associated with the subsequent development of heart failure.[10] LVH predisposes individuals to sudden death through prolongation of corrected QT (QTc) interval or by increasing arrhythmogenesis. The QTc interval is longer in hemodialysis patients than in those with normal kidney function. Premature ventricular complexes (PVCs) occur more during hemodialysis in patients with LVH compared with those without it. In uremic patients, activation of growth factors, proto-oncogenes, plasma noradrenaline, cytokines and angiotensin II regulate intracellular processes which accelerate cardiac hypertrophy and myocardial fibrosis.[11] Both LVH and myocardial fibrosis increase risk of sustained ventricular arrhythmias and predisposition to SCD.[12]

Ischemic heart disease

In dialysis dependent patients, severe coronary stenosis is associated with the induction and lengthy persistence of ventricular arrhythmias during and after hemodialysis.[13] The number of PVCs during and after hemodialysis is higher in patients with ischemic heart disease.[14] Ischemia modified albumin (IMA), novel biomarker of acute ischemia has high sensitivity and moderate specificity. Cardiac mortality risk was increased sevenfold in patients with combined elevated IMA and cardiac troponin levels.[15] Severely impaired myocardial fatty acid metabolism occurring as a result of recurrent myocardial ischemia, can also identify patients on hemodialysis who are at high risk of SCD.[16] Paraoxonase-1 (PON-1) is a calcium-dependent esterase which protects against oxidative damage of various cells and lipoproteins. Low serum levels of PON-1 have been detected in HD and non-HD dependent CKD patients.[17] The actual association of the roles of these cardiac biomarkers-PON-1 and IMA to SCD related to CKD is still unknown.

Corrected QT interval lengthening

QTc interval prolongation is associated with several manifestations of uremic cardiomyopathy including LVH, left ventricular dilatation, and reduced left ventricular ejection fraction. In patients with CKD, prolonged QTc interval results from inappropriate myocardial depolarization and repolarization due to LVH and intercardiomyocytic fibrosis.[18] Prolongation of QT interval, an increase of QT dispersion, and an alteration in the capacity to adapt QT interval to heart rate changes (QTc) have been reported during HD session.[19],[20],[21] In HD patients, prolongation of QTc interval was inversely correlated with intradialytic variation of Ca++.[20] Hemodialysis increased QTc intervals from 421 ± 26 ms before hemodialysis to 434 ± 29 ms after hemodialysis (P = 0.005).[22] QT dispersion is also associated with increased risk of ventricular arrhythmias and mortality in patients with congestive heart failure (CHF) and in the general population.[23] Elevated QT dispersion in patients on dialysis was significantly higher than in with healthy controls. QT dispersion that occurred for longer than 74 ms is an independent predictor of all-cause mortality, cardiovascular mortality, and arrhythmia-related mortality.[24] QT variability index (QTvi) calculated as the logarithm of the ratio between the variances of the normalized QT and rr intervals–can provide an estimation of the temporal variability in the myocardial repolarization process.[25] The elevated QTvi in patients with advanced CKD is the result of both reduced rr interval variance (secondary to reduced autonomic control of heart rate) and increased QT-interval variance.[26] QTvi ≥0.1 was significantly associated with a higher risk of arrhythmias and SCD.[25]

Inflammation

Serum levels of proinflammatory cytokines increases with declining GFR. High C-reactive protein (CRP) and cytokine (such as interleukin [IL]-6 and platelet-activating factor) levels are associated with ventricular arrhythmias via modulation of ion channel function and sympathetic nervous system hyperactivity.[9],[27] These proinflammatory cytokine (CRP and IL-6) are associated with a doubled risk of SCD.[27] Premature atherosclerosis and cytokines induce plaque instability resulting in direct effect on the myocardium and the electrical conduction system.[7],[27] Myocardial fibrosis associated with an inflammatory process causing a delay in repolarization leading to ventricular arrhythmias and SCD.[27] High levels of inflammatory mediators in CKD induce production of reactive oxygen species resulting in an accelerated vascular atherosclerosis and arterial calcification.[9] High homocysteine levels are common in CKD patients and are associated with atherothrombolic events and incidents of cardiovascular mortality.[28] The accumulation of asymmetric dimethylarginine in CKD inhibits nitric oxide synthesis in endothelial cells inducing endothelial dysfunction, vasoconstriction, and atherosclerosis.[29] In patients with end-stage renal disease (ESRD) elevated levels of calcification promoters and reduced levels of calcification inhibitors, in addition to abnormal calcium–phosphate metabolism, hyperparathyroidism, and oxidant stresses promote myocardial fibrosis and metastatic vascular calcification, which results in diminished coronary flow during diastole.[30]

Electrolyte shifts

The rapid change in the extracellular concentration of electrolytes during a dialysis session effect cellular membrane polarization and stability. Dialysis with a potassium dialyzate concentration of 0 mmol/l or 1 mmol/l was considered a significant risk factor for cardiac arrest.[31] Cardiac arrests were more frequent during dialysis sessions carried out on a Monday compared with a Wednesday and Friday.[31] It may be due to increased potassium concentrations or increased blood volume. Complex arrhythmias were observed more frequently during and after hemodialysis in those with a decreasing potassium profile compared with individuals whose potassium levels were kept constant.[32] Hypocalcemia after hemodialysis is associated with prolonged corrected QTc interval and SCD.[29] Hypomagnesmia observed after hemodialysis was not correlated with corrected QTc dispersion.[21]

Divalent ion abnormalities

Hyperphosphatemia is associated with hyperparathyroidism, smooth muscle proliferation, vascular calcification, and coronary atherosclerosis.[33] All these could alter microcirculatory hemodynamics, raise extravascular resistance and impair myocardial perfusion.[34] Hyperphosphatemia and elevated Ca++ x PO4 product were correlated with an increase in the risk of death related to coronary artery disease (CAD) and SCD.[34]

Rapid ultrafiltrate removal during hemodialysis

Ultrafiltrate removal may contribute to an acute reduction of circulating volume, hypotension, tissue ischemia, maladaptive cardiac structural changes, arrhythmias and SCD.[35] There is a small increase in all-cause mortality without an increase in cardiac mortality in patients undergoing a UF rate higher than 10 ml/h/kg.[36] Higher UF rates are associated with greater CV mortality. Intradialytic recurrent myocardial stunning due to hypotension secondary to rapid ultrafiltrate removal may over time lead to irreversible fibrotic changes and CHF, arrhythmias and SCD.[37]

Iron overload

Iron overload can promote reactive oxygen species and free radical production resulting in intercardiomyocytic fibrosis leading to conduction abnormalities and prologed QTc dispersion.[38],[39] Also, it has been associated with elevated rates of hospitalization and mortality in patients with ESRD.[39]

Sympathetic overactivity

Augmented sympathetic activity is seen during hemodialysis sessions.[40] This could aggravate hypertension, ventricular hypertrophy, and heart failure and result in increased risk of SCD.[40] There is also reduced amount of renalase (which metabolizes catecholamines) secretion by inured kidneys in CKD resulting in augmented sympathetic drive.[41]

Baroreflex effectiveness and sensitivity

Impaired arterial baroreflex function in CKD is associated with an increased risk of ventricular arrhythmia and SCD.[42] Patients with CKD and diabetes had a greater reduction in both baroreflex sensitivity and effectiveness than patients with CKD who did not have diabetes. Reduced baroreceptor effective index is an independent predictor of all-cause mortality, while reduced baroreflex sensitivity is an independent predictor of SCD.[43]

Obstructive sleep apnea

Episodes of nocturnal arterial oxygen desaturation, has been reported to affect 21%–47% of patients undergoing dialysis compared with 2%–4% of the general population.[44]

Strategies to prevent sudden cardiac death are as in [Table 1].
Table 1: Strategies to prevent sudden cardiac death

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β-Blockers

Use of the β-blocker carvedilol reduces morbidity, and all-cause and cardiovascular mortality in patients with ESRD and dilated cardiomyopathy who are undergoing dialysis.[45] In a retrospective study, HD patients using beta-blockers had a lower rate of SCD.[46]

Calcium channel blockers

Calcium channel blocker (CCB) may have potential cardioprotective effects by preventing coronary artery spasm, normalizing intracellular Ca++ concentration, limiting injury after cardiac arrest and preventing fatal arrhythmias. While CCB may be beneficial for patients with CKD due to their antihypertensive effects, there is only limited data about the effects of CCB on SCD.[47]

Digoxin

In digoxin therapy, there is risk of narrow therapeutic window, long half-life, and the potential risk for lethal arrhythmias in presence of hypokalemia. Hemodialysis involves large potassium fluxes, so digoxin is not a good choice in these patients.

Renin-angiostensin-aldosterone system blockers

High aldosterone levels are reported to be an independent risk factor for SCD in non-CKD patients. In the Fosinopril in Dialysis Trial[48] there was no reduction in cardiovascular events in the treated patients group. The use of ACE inhibitors and ARBs was associated with a significantly reduced risk of SCD after 6 months of treatment in survivors of a cardiac arrest.[49] Increased availability of angiotensin II in the tissues of incident hemodialysis patients with genotype D of the ACE gene has been associated with an increased risk of cardiovascular death.[50]

Statin

Benefit in reducing all cardiac events was observed, but no effect on CV deaths or all-cause mortality was reported.[51]

Dialysate

K + dialyzate concentration from 0 mmol/l to 1 mmol/l is associated with increased risk of cardiac arrest. K + dialysate of <2 mmol/l (or <3 mmol/l if pre-HD serum K + is <5 mmol/l) confers an increased risk of SCD.[32],[52] Serum and dialysate Ca++, and serum-dialysate Ca++ gradients should be monitored in determining the optimal dialysate Ca prescription.[52]

Ultrafiltration

Daily dialysis or nocturnal hemodialysis therapies can prevent prolonged myocardial damage by removing excessive fluid in a longer session. In a randomized controlled study,[53] patients treated 2.5 h for six times a week, showed more favorable survival and decreased left ventricular mass index compared with those treated 3.5 h three times a week. Similarly, in another study,[54] patients undergoing nocturnal HD showed better survival rates compared with patients. Higher dialysis dose may control volume overload, improve the uremic milieu, diminish levels of inflammatory markers and reduce LVH and left ventricular dilation, thereby reducing the risk of SCD.

Coronary revascularisation

Risk of long-term repeated revascularization, myocardial infarction, and SCD is more in patients with CKD than in those with normal kidney function.[55] A significant reduction in repeat revascularization and a trend toward reduced mortality was observed in drug eluting stent compared with bare metal stent treated dialysis patients.[56] Existing data are inadequate to make a determination on the optimal strategy of coronary revascularization–coronary artery bypass graft versus percutaneous coronary intervention for dialysis patients.[57]

Implantable cardioverter defibrillator

There is no general consensus on the use of implantable cardioverter-defibrillator (ICD) devices in CKD patients, as data in these patients are lacking. There is a significant reduction in the risk of all-cause mortality and SCD risk in CKD patients with estimated glomerular filtration rate (eGFR) ≥35 ml/min per 1.73 m2 treated with ICD compared with those in the no ICD therapy.[58] No significant difference was found in outcomes between the two treatment groups for patients with eGFR <35 ml/min per 1.73 m2. In dialysis patients hospitalized for ventricular fibrillation/cardiac arrest who received ICD implantation within 30 days of admission, there was a 42% reduction in overall death risk of death.[59] In a recent prospective randomised controlled ICD2 trial it was concluded that in a well screened and well treated population undergoing dialysis, prophylactic ICD therapy did not reduce the rate of SCD or all cause mortality.[60] Advanced stages of CKD and older age favor the “no ICD” strategy.[61]


  Conclusion Top


About one fourth of hemodialysis patients will die from SCD. Among CKD patient, CAD risk factors play very small role as compared to the general population. Cardiomyopathy and ischemic heart disease predispose to conduction abnormalities and arrythmogenesis, which can be exacerbated by electrolyte shifts, excess ultrafiltrate removal, iron overload, divalent ion abnormalities, sympathetic overactivity, and baroreflex abnormalities. Beta-blockers, CCB and Renin angiotensin aldosterone system blockers have been associated with a survival benefit after an arrhythmic cardiac arrest. Both low potassium dialysate and extremes of serum potassium levels, as well as low calcium dialysate and large serum to dialysate calcium gradients, have been shown to increase risk of SCD. It is also important to avoid excessive rates of fluid removal per HD session, as high UF volumes have been associated with SCD. Short daily-HD or nocturnal-HD may be considered, especially for patients with several comorbidities or those with hemodynamic instability. Recommendation regarding revascularisation should be individualised, and other supportive therapies may be needed to prevent SCD in CAD patients. The survival following cardiac arrest is very poor in the setting of CKD. The decision to implant a cardioverter-defibrillator should be influenced by age and CKD stage. In a recent ICD2 trial, prophylactic ICD therapy did not reduce the rate of SCD or all cause mortality.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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Correspondence Address:
Vijoy Kumar Jha,
Command Hospital Air Force, Bengaluru - 560 007, Karnataka
India
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajim.ajim_114_21



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