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Cardiovascular Disaster in Hemodialysis patients
Pattaraporn MD.
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Causes of death in prevalent dialysis patients 2008-2010
41.6%
26.5%
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Cardiovascular Disaster
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Sudden death
• Unexpected natural death• Within a short time period >> 1-24 h• Due to cardiac etiology• New or more serious symptoms
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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
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Left ventricular Hypertrophy and Heart failure
Concentric LV hypertrophy Eccentric LV hypertrophy
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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.
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Myocardial Interstitial fibrosis and Microvessel disease
Inadequate capillary density + increased oxygen demand >> relative hypoxia >> fibrosis
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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
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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
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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
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• 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
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Other factors
• Rapid electrolyte shifts• Hypervolemia • Anemia • Dyslipidemia • Hypertension • Calcium/phosphate deposition
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Prevention of Sudden Death
Beta-blocker
Implantable defibrillators
Avoiding low Kdialysate & rapidelectrolyte shifts
ACEI andARBs
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Beta-blocker
• Reduction of– Cardiac hypertrophy & fibrosis– Antifibrillary activity– Ventricular arrhythmia– Reduced risk of acute MI
• Improve Heart rate variability• Increase in baroreflex sensitivity
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ACEI andARBs
• Reduction of– Cardiac hypertrophy & fibrosis– Fatal arrhythmia
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Avoiding low K dialysate & rapidelectrolyte shifts:
• To avoid– QT dispersion– Re entrant arrhythmias‐– Premature ventricular extrasystole (VES)
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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
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• 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)
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Herzog CA et al. Kidney Int. 2005;68:818-825.
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Thank You