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MTE 2012

State of the Art: Critical Conditions Cardiogenic Shock


7th Interventional Symposium on High Risk Coronary Interventions Lugano June 28, 2012
Raban Jeger Cardiology University Hospital Basel rjeger@uhbs.ch

Cardiogenic Shock The Invincible

Cardiogenic Shock How to Defeat


G G G G Know your enemy Treat underlying disease Support hemodynamics Be fast

Cardiogenic Shock: Know Your Enemy Definition


G Systolic blood pressure <90 mmHg or a value 30 mmHg below basal levels for >30 minutes or catecholamines required to maintain pressure >90 mmHg during systole G Clinical signs of pulmonary congestion or pulmonarycapillary wedge pressure >15 mmHg G Signs of impaired organ perfusion (at least 1)
Altered mental status Cold, clammy skin and extremities Oliguria with urine output <30 mL/h Serum lactate >2.0 mmol/L

G Arteriovenous oxygen difference >5.5 ml/dL G Cardiac index <2.2 L/min/m2


Califf RM and Bengtson JR. N Engl J Med 1994; 330:1724-1730

Cardiogenic Shock: Know Your Enemy Incidence in Acute Myocardial Infarction

Goldberg RJ et al. N Engl J Med 1999;340:1162-8

Cardiogenic Shock: Know Your Enemy Mortality in Acute Myocardial Infarction

Goldberg RJ et al. N Engl J Med 1999;340:1162-8

Cardiogenic Shock: Know Your Enemy SHOCK: Non-Cardiac Cause of Death


4

n=14

Number of Deaths

3 2 1 0 Sepsis Multiorgan Failure Stroke Major Bleeding

n = 14

Hypoxic LifeBrain support Injury Removed

Jeger RV et al. Acute Card Care 2007;9:25-33.

Cardiogenic Shock: Know Your Enemy Current Pathophysiological Concept

Reynolds HR et al. Circulation 2008;117:686-697

Cardiogenic Shock: Treat the Disease SHOCK: Long-Term Survival

Hochman JS et al. JAMA 2006;295:25112515

Cardiogenic Shock: Treat the Disease Meta-analysis of Randomized Trials


1-Year Survival

Jeger RV et al. Acute Cardiac Care, March 2011; 13(1): 1420

Cardiogenic Shock: Treat the Disease TRIUMPH: Tilarginine Acetate

Tilarginine (L-NMMA) 1-mg/kg bolus and 5-hour infusion

Alexander JH et al. JAMA. 2007;297:1657-66

Cardiogenic Shock: Treat the Disease TRIUMPH: Tilarginine Acetate

Tilarginine (L-NMMA) 1-mg/kg bolus and 5-hour infusion

Alexander JH et al. JAMA. 2007;297:1657-66

Cardiogenic Shock: Treat the Disease ACC/AHA Guidelines on Revascularization

Reynolds HR et al. Circulation 2008;117:686-697

Cardiogenic Shock: Hemodynamic Support Intra Aortic Balloon Counterpulsation (IABP)

P Ao

P balloon

1 Systole: Balloon deflated, decrease in afterload and facilitation of left ventricular ejection 2 Diastole: Balloon inflated, increase in coronary flow

Cardiogenic Shock: Hemodynamic Support IABP-SHOCK Trial

G Prospective, multicenter, randomized, open-label, controlled trial (IABP vs. no IABP) G Sample size: 45 patients with acute myocardial infarction and cardiogenic shock G Primary endpoint: change in APACHE II scores (severity of illness)
Prondzinsky R et al. Crit Care Med 2010; 38:152160

Cardiogenic Shock: Hemodynamic Support IABP-SHOCK II Trial

G Prospective, multicenter, randomized, open-label, controlled trial G Sample size: 600 patients G Primary endpoint: 30-day all-cause mortality
Thiele H et al. Am Heart J 2012;163:938-45

Cardiogenic Shock: Hemodynamic Support Left Ventricular Assist Devices

Thiele H et al. Eur Heart J 2007;28:20572063

Cardiogenic Shock: Hemodynamic Support Abiomed Impella Support System

Cardiogenic Shock: Hemodynamic Support ISAR-SHOCK Trial


Myocardium Device

G Prospective, multicenter, randomized, open-label, controlled trial (Impella vs. IABP) G Sample size: 26 patients with acute myocardial infarction and cardiogenic shock G Primary endpoint: change of the cardiac index (CI)
Seyfarth M et al, J Am Coll Cardiol 2008;52:15848

Cardiogenic Shock: Hemodynamic Support TandemHeart

Cardiogenic Shock: Hemodynamic Support TandemHeart in Cardiogenic Shock After PCI

G Prospective, multicenter, randomized, open-label, controlled trial (VAD vs. IABP) G Sample size: 42 patients G Primary endpoint: change in cardiac power index
Thiele H et al, Eur Heart J 2005;26:12761283

Cardiogenic Shock: Be Fast AMIS Plus: Treatment of Cardiogenic Shock


80 70 60 50 PCI (p<0.01) Thrombolysis (p<0.01) IABP (p<0.01) CABG

% 40
30 20 10 0 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006

Jeger RV et al. Ann Intern Med 2008;149:618-626

Cardiogenic Shock: Be Fast AMIS Plus: Mortality of Cardiogenic Shock


80 70 60 50

% 40
30 20 10 0 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006
Jeger RV et al. Ann Intern Med 2008;149:618-626

Cardiogenic Shock Overall (p=0.01) Cardiogenic Shock on Admission (p=0.009) Cardiogenic Shock During Hospitalization (p=0.094)

Cardiogenic Shock: Be Fast AMIS Plus: Incidence of Cardiogenic Shock


16 14 12 10 Cardiogenic Shock Overall (p<0.01) Cardiogenic Shock on Admission Cardiogenic Shock During Hospitalization (p<0.01)

% 8
6 4 2 0
1997 1998 1999 2000 2001 2002 2003 2004 2005 2006

Jeger RV et al. Ann Intern Med 2008;149:618-626

Cardiogenic Shock: Be Fast AMIS Plus: Predictors of Cardiogenic Shock

Intra-aortic counterpulsation ST-elevation ACS Age (per year increase) Heart rate (per beat per minute increase) Systolic blood pressure (per mmHg increase) Primary PCI Lipid-lowering drug

Odds Ratio 16.6 2.89 1.03 1.02 0.99 0.59 0.52

95% Confidence Interval 11.2-24.6 1.97-4.22 1.02-1.05 1.01-1.02 0.98-1.00 0.39-0.89 0.37-0.73

p <0.001 <0.001 <0.001 <0.001 0.002 0.012 <0.001

Jeger RV et al. Ann Intern Med 2008;149:618-626

Cardiogenic Shock: How to Defeat Conclusion


G Modest decrease of mortality rates due to higher rates of early PCI and IABP use G A systemic inflammatory response syndrome may play a major role in the pathogenesis of cardiogenic shock, but therapeutic large-scale randomized trials have been negative G Newer mechanical hemodynamic support devices are promising but exhibit high complication rates G Today, the prevention of cardiogenic shock using early PCI and statins may be the best way to save lives

Thank You For Your Attention


rjeger@uhbs.ch

Cardiogenic Shock: Treat the Disease Nitric Oxide and the Myocardium
G Low levels of NO (eNOS-derived) protect against ischemiareperfusion injury G Large quantities of NO (iNOS-derived) contribute to cardiac reperfusion injury through superoxide and peroxynitrite formation G Myocardial ischemia increase iNOS and NO production G The overproduction of NO may cause both myocardial depression and inappropriate vasodilatation G Thus NO may be a major contributor to cardiogenic shock complicating myocardial infarction

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