Cardiovascular Disaster in Hemodialysis patients

Cardiovascular Disaster in Hemodialysis patients

Pattaraporn MD.

Causes of death in prevalent dialysis patients 2008-2010

41.6%

26.5%

Cardiovascular Disaster

Sudden death

• Unexpected natural death• Within a short time period >> 1-24 h• Due to cardiac etiology• New or more serious symptoms

Possible Mechanisms Responsible for SD in HD

Cardiac arrest

QT dispersion

Cardiac arrhythmia

cardiomyopathy

Ischecmic heart disease

•Myocardial interstitial fibrosis•Microvessel disease•CHF•CAD/MI•LVH/LV dysfunction

Rapid electrolyte shifts/Hypervolemia

Inflammation

Sympathetic overactivity

Left ventricular Hypertrophy and Heart failure

Concentric LV hypertrophy Eccentric LV hypertrophy

Left ventricular Hypertrophy and Heart failure

• LVH is an powerful indicator of mortality in dialysis patients

• Presence of LVH >>> arrhythmia• Left ventricular systolic dysfunction >>

arrhythmia

Redaelli B: Lancet 1988;ii:305–309.

Myocardial Interstitial fibrosis and Microvessel disease

Inadequate capillary density + increased oxygen demand >> relative hypoxia >> fibrosis

Myocardial Interstitial fibrosis and Microvessel disease

• Fibrous tissue >> high electrical resistance• Development of atrial and ventricular reentry

types of arrhythmias• Risk factor for the development of

arrhythmias especially during the dialysis

QT Dispersion

• Difference between the longest and shortest QT intervals >> EKG 12 lead

• Predict an increased risk of malignant arrhythmias• Normal value of QT dispersion in normal subjects

was ≤40 ms• Dialysis patients with QT dispersion > 74 ms >>

ventricular arrhythmias or SD• Low K+ and low Ca2+ >> acquired long QT syndrome

Sympathetic overactivity

• Heart rate >> myocardial demand supply >> cardiac hypertrophy and fibrosis

• Decrease heart rate variability (reflecting autonomic dysfunction) >> increased risk for all-cause and SD in HD

• Marker : C-reactive protein, inhibit the hepatic generation of albumin

• Reflection of vascular injury VS actually promotes vascular injury ?

• High CRP level ( >6 mg/l ) : independent , predictive marker of future myocardial infarction– Herzig, K. A. et al. J. Am. Soc. Nephrol. 12, 814–821 (2001).

• Inflammation could trigger SD >> atherosclerosis or direct effect on myocardium

Inflammation

Other factors

• Rapid electrolyte shifts• Hypervolemia • Anemia • Dyslipidemia • Hypertension • Calcium/phosphate deposition

Prevention of Sudden Death

Beta-blocker

Implantable defibrillators

Avoiding low Kdialysate & rapidelectrolyte shifts

ACEI andARBs

Beta-blocker

• Reduction of– Cardiac hypertrophy & fibrosis– Antifibrillary activity– Ventricular arrhythmia– Reduced risk of acute MI

• Improve Heart rate variability• Increase in baroreflex sensitivity

ACEI andARBs

• Reduction of– Cardiac hypertrophy & fibrosis– Fatal arrhythmia

Avoiding low K dialysate & rapidelectrolyte shifts:

• To avoid– QT dispersion– Re entrant arrhythmias‐– Premature ventricular extrasystole (VES)

Implantable defibrillators or Implantable Cardioverter Defibrillators (ICDs)

• Most effective therapy for SCD in the general population• Indication – Survival of cardiac arrest due to VT or VF– Episode of sustained VT causing severe hemodynamic

compromise– Episode of sustained VT without hemodynamic compromise

+ EF 35%– MI + EF 35% + nonsustained VT on 24-h ECG + inducible VT

on electrophysiologic testing– MI + EF 30% QRS duration 120 ms on ECG

• 42% risk reduction for death in dialysis patients with ICDs implanted according to conventional guidelines

• Greater risk of device complications• No statistically increase >>> infection or

fistula thrombosis

– Kidney Int. 2005;68:818-825.

Implantable defibrillators or Implantable Cardioverter Defibrillators (ICDs)

Herzog CA et al. Kidney Int. 2005;68:818-825.

Thank You