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Program Information. Cardiogenic Shock, Acute Coronary Syndromes and Heart Failure. Fredric Ginsberg, M.D. Joseph Parrillo, M.D. Cardiogenic Shock. Inadequate tissue perfusion resulting from cardiac dysfunction

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  1. Program Information

  2. Cardiogenic Shock, Acute Coronary Syndromes and Heart Failure Fredric Ginsberg, M.D. Joseph Parrillo, M.D.

  3. Cardiogenic Shock • Inadequate tissue perfusion resulting from cardiac dysfunction • Clinical definition: decreased cardiac output and tissue hypoxia in the presence of adequate intravascular volume • Hemodynamic definition: Sustained systolic BP<90 mmHg, cardiac index <2.2 L/min/m2, PCWP > 15 mm Hg Parrillo, J. 2005

  4. Causes of Cardiogenic Shock • Acute MI • Pump failure • Mechanical complications • Right ventricular infarction • Other conditions • End-stage cardiomyopathy • Myocarditis (Fulminant Myocarditis) • Myocardial contusion • Prolonged cardiopulmonary bypass • Septic shock with myocardial depression • Valvular disease • Stress cardiomyopathy

  5. CARDIOGENIC SHOCK Evolution of the Disease •Frequently, shock develops after presentation for myocardial infarction. -SHOCK Registry •At presentation 25% in shock •Within 24 hours 75% (median delay = 7 hours) -GUSTO Trial •At presentation11% in shock •After admission89% SHOCK Registry, Circulation 1995;91:873-81 GUSTO J Amer Coll Cardiol 1995;26:668-74

  6. Schematic Diagram of Stunned Myocardium Clamp Wall motion abnormality Wall motion abnormality during occlusion Coronary occlusion Coronary reperfusion Persistent wall motion abnormality (despite reperfusion and viable myocytes) Return of function Gradual return of function (hours to days) From Kloner, R.A., Am J Med 1986;86:14.

  7. Hibernating Myocardium Wall motion abnormality Atherosclerotic narrowing Wall motion abnormality due to chronic ischemia without infarction From Kloner, R.A., Am J Med 1986;86:14.

  8. Ischemic Myocardium Cell death Reperfusion Significant residual stenosis Segments withmyocardialstunning Segments withboth stunningand hibernation Segments withhibernatingmyocardium Inotropicsupport Relief of ischemia No returnof function Return ofmyocardial function

  9. Initial Approach: Management • Assure Oxygenation • Intubation and ventilation if needed • Venous access • Pain relief • Continuous EKG monitoring • Hemodynamic support • Fluid challenge if no pulmonary edema • Vasopressors for hypotension • Dopamine • Norepinephrine

  10. Intra-Aortic Balloon Counterpulsation • Reduces afterload and augments diastolic perfusion pressure • Beneficial effects occur without increase in oxygen demand • No improvement in blood flow distal to critical coronary stenosis • No improvement in survival when used alone • May be essential support mechanism to allow for definitive therapy

  11. 1.0 Overall 30-Day Survival in the Study 0.8 Revascularization (n=152) Survival= 53% 0.6 Proportion Alive 0.4 Medicaltherapy (n=150) Survival =44% 0.2 Hochman, J.S., et al, N Engl J Med 1999;341:625-34. p =0.11 0.0 0 5 10 15 20 25 30 Days after Randomization Revascularization in Acute Myocardial Infarction Early revacularization in Acute Myocardial Infarction complicated by cardiogenic shock

  12. SHOCK Trial Mortality 100 P = 0.11 P = 0.027 P < 0.03 80 66.4 63.1 % 56 60 54.3 50.3 46.7 40 Revasc Med Rx 20 0 30 days 6 months 1 year

  13. ACC/AHA Class I Indication • Patients with ST segment elevation MI who have cardiogenic shock and are less than 75 years of age should be brought immediately or secondarily transferred to facilities capable of cardiac catheterization and rapid revascularization (PCI or CABG) if it can be performed within 36 hours of onset of shock. (Level of Evidence: A)

  14. National Registry of MI • National Registry of MI early Revascularization is Underutilized in Cardiogenic Shock • Despite ACC/AHA recommendation to treat patients <75 years of age aggressively with early mechanical revascularization, • In 2001, 2 years after the guidelines were published, only 41% of patients with cardiogenic shock complicating AMI were treated with primary PTCA and only 3.1% underwent early CABG. • These data demonstrate significant underutilization of guideline recommended therapy. Babaev A et al Circ 2002 106(19):1811 (abstract)

  15. Pathophysiology of Cardiogenic Shock • The following are observations from the SHOCK Trial and Registry that Challenge the Classic Paradigm • LVEF is only moderately depressed (30%), with a wide range of EFs and LV sizes noted. • Systemic vascular resistance (SVR) on vasopressors is not elevated (~ 1350), with a very wide range of SVRs measured. • A clinically evident systemic inflammatory response syndrome is often present in patients with CS. • Most survivors (85%) have NYHA functional Class I-II CHF status. Hochman JS. Circ .2003;107:2998-3002.

  16. Overproduction of Nitric Oxide Thus, excess nitric oxide and peroxy nitrites may be a major contributor to cardiogenic shock complicating MI. The Overproduction of Nitric Oxide May Cause Both Myocardial Depression and Inappropriate Vasodilatation. Cotter, Eur Heart J. 2003:24:1287-1295

  17. Acute Coronary Syndromes: Definitions Acute coronary syndrome: Constellation of clinical symptoms compatible with acute myocardial ischemia 1. ST-segment elevation MI (STEMI) 2. Non-ST-segment elevation MI (NSTEMI) 3. Unstable angina Unstable angina: • angina at rest (usually >20 minutes) • new-onset of class III or IV angina • increasing angina (from class I or II to III or IV) Braunwald. Circulation 2002; 106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  18. Hospitalizations in the US Due to Acute Coronary Syndromes Acute Coronary Syndromes ~1.8 Million Hospital Admissions UA/NSTEMI 1.42 Million Admissions Per Year STEMI 0.41 Million Admissions Per Year National Hospital discharge survey 1999. National Center for health Statistics/Centers for Disease Control and Prevention. Series 13, No. 14. September 20000.

  19. Pathogenesis of Acute Coronary Syndromes Plaque rupture Platelet adhesion Platelet activation Partially occlusive arterial thrombosis & unstable angina Microembolization & non-ST-segment elevation MI Totally occlusive arterial thrombosis & ST-segment elevation MI White HD. Am J Cardiol 1997;80 (4A):2B-10B.

  20. Structure of ThrombusFollowing Plaque Disruption STEMI:Occlusive thrombus (platelets, red blood cells, and fibrin) UA/NSTEMI:Partially-occlusive thrombus (primarily platelets) Intra-plaque thrombus (platelet-dominated) Plaque core Plaque core Intra-plaque thrombus (platelet-dominated) SUDDEN DEATH UA = Unstable Angina NSTEMI = Non-ST-segment Elevation Myocardial Infarction STEMI = ST-segment Elevation Myocardial Infarction White HD. Am J Cardiol 1997;80 (4A):2B-10B.

  21. + Troponinor + CK-MB &/or ST-segment elevation MI Non-ST Elevation ACS* Non-ST Elevation MI Therapeutic goal: rapidly break apart fibrin mesh to quickly restore blood flow Therapeutic goal: prevent progression to complete occlusion of coronary artery and resultant MI or death Consider fibrinolytic therapy, if indicated, or primary percutaneous coronary intervention (PCI) Consider GP IIb-IIIa inhibitor + aspirin + heparin before early diagnostic catheterization Diagnostic Algorithm Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf.

  22. Risk of MI & Death During Treatment 0.25 0.20 Placebo 0.15 Probabilityof Death or MI 0.10 0.05 Aspirin 75 mg Risk ratio 0.5295% CL 0.37 - 0.72 0.00 0 3 6 9 12 The following graph displays the risk of MI and death during treatment with low-dose aspirin and iv heparin in men with unstable cad Wallentin LC, et al. J Am Coll Cardiol, 1991;18:1587-93. Months

  23. Low Molecular Weight Heparin (LMWH) vs. Unfractionated Heparin (UFH) Day: Trial: FRIC (Dalteparin; n = 1,482) FRAXIS (nadroparin; n = 2,357) ESSENCE (enoxaparin; n = 3,171) TIMI 11B (enoxaparin; n = 3,910)  6  14 (p= 0.032) 14  (p= 0.029) 14  .751.0 1.5 LMWH Better UFH Better The following chart displays the low molecular weight heparin (LMWH) vs. unfractionated heparin (Ufh) in non-st elevation ACS: effect on death, MI, recurrent ischemia. Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  24. % 14 11.4% Placebo + ASA 12 9.3% 10 8 Clopidogrel + ASA Death, MI, or Stroke 6 4 20% RRR P < 0.001 N = 12,562 N Engl J Med. 2001;345:494-502. 2 0 0 3 6 9 12 Months of Follow-Up Effects of Clopidogrel This graph demonstrates the effects of Clopidogrel in addition to Aspirin in patients with ACS without ST-Segment Elevation

  25. Hospital Care Anti-Thrombotic Therapy I IIa IIb III Immediate aspirin Clopidogrel,if ASA contraindicated Aspirin + Clopidogrel, for up to 1 month, if medical therapy or PCI is planned Heparin (IV unfractionated, LMW) with antiplatelet agents listed above Enoxaparin preferred over UFH unless CABG is planned within 24 hours Braunwald. Circulation 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  26. Hospital Care Platelet GP IIb/IIIa Inhibitors (1) I IIa IIb III Any GP IIb/IIIa inhibitor + ASA/Heparin for all patients, if cath/PCI planned Eptifibatide or tirofiban + ASA / Heparin for high risk * patients in whom early cath/PCI is not planned. Any GP IIb/IIIa inhibitor for patients already on ASA + Heparin + clopidogrel, if cath/PCI is planned Braunwald. Circulation 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  27. Hospital Care Platelet GP IIb/IIIa Inhibitors (2) I IIa IIb III Eptifibatide or tirofiban + ASA / Heparin for patients without continuing ischemia in whom PCI is not planned. Abciximab for patients in whom PCI is not planned. Braunwald. Circulation 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  28. Hospital Care Anti-ischemic Therapy (1) I IIa IIb III β-blocker(IV►oral)ifnotcontraindicated Non-dihydropyridineCa2+antagonistifβ-blockercontraindicatedandnoLVdysfunction,forreccurrentischemia ACEinhibitorif↑BPpersistswithNTG+β–blocker,forpatientswithCHFordiabetes. Braunwald. Circulation 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  29. Hospital Care Anti-Ischemic Therapy (2) I IIa IIb III ACE inhibitor for all ACS pts Extended-releaseCA2+blockerinsteadofβ-blocker Immediate-releaseCa2+blockerwithβ-blocker Long-actingCa2+blockerforrecurrentischemia,ifnocontraindicationsandNTG+β-blockerusedfully C Braunwald. Circulation 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  30. ST-segment Depression Predicts Higher Risk of Mortality in ACS 10% 8% 6% 4% 2% % Cumulative Mortality at 6 Months ST-segment depression8.9% ST-segment elevation6.8% T-wave inversion3.4% Savonitto S. J Am Med Assoc 1999; 281: 707-711. 306090120150180 Days from randomization

  31. Mortality Rates According to Level of Cardiac Troponin

  32. Variables Used in the TIMI Risk Score • Age >65 years • At least 3 risk factors for CAD • Known prior coronary stenosis of >50% • ST segment deviation on presenting ECG • At least 2 anginal events in prior 24 hours • Use of aspirin in prior 7 days • Elevated serum cardiac biomarkers

  33. Number of TIMI Risk Factors Predicts Short-Term Recurrent Events

  34. 35 30.6 30 25 20.3 19.5 20 16.1 12.8 15 11.8 10 5 0 Low 0-2 Intermed. 3-4 High 5-7 TIMI UA Risk Score: Primary Endpoint at 6 mos OR=0.55 CI (0.33, 0.91) CONS INV OR=0.75 CI (0.57, 1.00) Death/MI/ACS Rehosp (%) % of Pts: 25% 60% 15%

  35. Troponin and ST-Segment Shift Predict Benefit of Invasive Treatment Strategy Cannon. J Invas Cardiol 2003; 15:22B

  36. Management of Patients with Unstable Angina • ACC/AHA Guideline Update for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation MI Class I • An early invasive strategy in patients with a high-risk indicator: • Recurrent angina/ischemia despite intensive anti-ischemic rx • Elevated troponin-T or troponin-I • New or presumably new ST-segment depression • Recurrent angina/ischemia with CHF sx, S3, pulmonary edema, worsening rales, or new or worsening MR • High-risk findings on noninvasive stress testing • Depressed LV systolic function (EF <40%) • Hemodynamic instability • Sustained ventricular tachycardia • PCI within 6 months • Prior CABG • Either early invasive or early conservative strategy if not high risk Braunwald, Circulation. 2002:106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pd

  37. 2002 ACC/AHA Guidelines for theManagement of High-risk NSTE ACS At presentationST-segment depression &/or elevated cardiac troponin Need to immediately arrest thrombus progression Need to eliminate occlusive ruptured plaque • Start immediate • Aspirin • Heparin or low-molecular-weight heparin • GP IIb-IIIa inhibitor Send for catheterization & revascularization within 24-48 hours • Cautionary information • No clopidogrel within 5-7 days prior to CABG surgery • No enoxaparin within 24 hours prior to CABG surgery • No abciximab, if PCI is not planned Adapted from Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf.

  38. Ongoing Evaluation in an Early Conservative Strategy Early medical management Patient stabilizes Recurrent Symptoms/ischemia Heart failure Serious arrhythmia Evaluate LV function EF < .40 EF .40 Stress Test Low risk Not low risk Follow on Medical Rx Immediate angiography Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf.

  39. Guideline Update • ACC/AHA Guideline Update for the Management of Patients with Unstable Angina and on-ST-Segment Elevation MI - Class I indications for revascularization with PCI or CABG • CABG for > 50% stenosis of the left main coronary artery • CABG for 3 vessel CAD • CABG for 2 vessel CAD including proximal LAD stensoes & EF < 50% • PCI or CABG for 1 or 2 vessel CAD, no proximal LAD large area of viability, high-risk noninvasive test • PCI for patients with multivessel CAD, normal EF, no diabetes • IV platelet GP IIb/IIIa inhibitior in ACS patients undergoing PCI Braunwald, Circulation. 2002:106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pd

  40. Guideline Update • ACC/AHA Guideline Update for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation MI Class IIa indications for revascularization with PCI or CABG • Repeat CABG for patients with multiple saphenous vein graft stenoses especially if LAD graft • PCI for focal saphenous vein graft lesions or multiple lesions if poor surgical candidate • PCI or CABG for patients with 1 or 2 vessel CAD, not proximal LAD, but moderate area of viability and ischemia • PCI or CABG for patients with 1 vessel CAD with proximal LAD • CABG with Internal Mammary artery for patients with multivessel CAD and diabetes Braunwald, Circulation. 2002:106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pd

  41. Recommendations for Revascularization Braunwald, Circulation. 2002:106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pd

  42. ACC/AHA REVISED GUIDELINES UA/NSTEMI ASA, Heparin/Enox.,   block., Nitrates, Clopidogrel RISK STRATIFY Low Risk High Risk * Braunwald E, et al. Circ. 2002;106:1893. * Recurrent ischemia; Trop; ST; LV failure/dysf.; hemodynamic instability; VT; prior CABG Enoxeparin. Preferred to UFH (IIa) If coronary arteriography >24 hours

  43. ACC/AHA REVISED GUIDELINES High Risk Cor. Arteriography LMCD, 3VD+LV Dys., or Diab. Mell. 1 or 2VD, Suitable for PCI Normal CABG Consider Alternative Diagnosis Clopidogrel, IIb/IIIa inhib. PCI Discharge on ASA, Clopidogrel, Statin, ACEI Braunwald E, et al. Circ. 2002;106:1893. Braunwald E, et al. Circ. 2002;106:1893.

  44. I IIa IIb III Discharge Medications ASA, if not contraindicated Clopidogrel, when ASA contraindicated Aspirin + Clopidogrel, for up to 9 months -blocker, if not contraindicated Lipid  agents (statins) + diet ACE Inhibitor: CHF, EF < 40%, DM, or HTN Braunwald, Circulation. 2002:106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pd Braunwald. Circulation 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  45. Death or Major Cardiovascular Events This graph displays the all-cause death or major cardiovascular events in all randomized subjects Cannon CP, et al. N Engl J Med. 2004:350:1495-1504.

  46. Reductions in Major Cardiac End Points Cannon CP, et al N Engl J Med. 2004:350:1495-1504

  47. Risk Factor Modification Braunwald, Circulation. 2002:106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pd

  48. Heart Failure due to LV Systolic Dysfunction • Approximately 5 million Americans have Heart Failure (male to female ratio 1:1) • 550,000 new cases annually • Hospital discharges 1,000,000 annually • 80% of men and 70% of women under the age of 65 with HF will die within 8 years Numbers based on 2000 data. American Heart Association. 2003 Heart and Stroke Statistical Update. Dallas, Tex: AHA; 2002.

  49. Neurohormonal Activation in Heart Failure Myocardial injury to the heart (CAD, HTN, CMP, Valvular disease) Initial fall in LV performance, wall stress Activation of RAS and SNS Fibrosis, apoptosis,hypertrophy, cellular/molecular alterations,myotoxicity Remodeling and progressive worsening of LV function Peripheral vasoconstriction Hemodynamic alterations Heart failure symptoms Morbidity and mortality Arrhythmias Pump failure FatigueActivity altered Chest congestionEdemaShortness of breath RAS, renin-angiotensin system; SNS, sympathetic nervous system.

  50. LV Remodeling After Anteroseptal MI 1 week 3 months EDV 189 mL ESV 146 mL EF 23% EDV 137 mL ESV 80 mL EF 41% Apical 4 Chamber View

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