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cardiogenic shock

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Slide 1 :

Cardiogenic Shock Incidence Pathogenesis Diagnosis Treatment Options Pharmacologic Treatment PCI-CABG The SHOCK Trial Circulatory Support Prognosis ACC/AHA Guidelines Clinical Implications Jeffrey J. Popma, MD Boston, MA

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Within the past 12 months, I have had a financial interest/arrangement or affiliation with the organization(s) listed below. Physician Name Company/Relationship Jeffrey J. Popma, MD Research Grants: Cordis, Boston Scientific, Medtronic, Abbott-Guidant, Biosensors, Radiant, eV3 Medical Advisory Board: Cordis, Boston Scientific, Medtronic Speaker’s Bureau: Sanofi, BMS, Boston Scientific, Pfizer Conflict of Interest Statement

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Backgound Cardiogenic shock (CS) is a state of inadequate tissue perfusion due to cardiac dysfunction, and complicates 7-10% of cases of acute myocardial infarction Without treatment, cardiogenic shock is associated with a 70-80% mortality rate, and is the leading cause of death in patients hospitalized for an acute myocardial infarction Proper recognition and management of patients who develop cardiogenic shock will result in substantial improvements in early and late mortality

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Cardiogenic Shock Incidence Pathogenesis Diagnosis Treatment Options Pharmacologic Treatment PCI-CABG The SHOCK Trial Circulatory Support Prognosis ACC/AHA Guidelines Clinical Implications

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NRMI STEMI Registry1 N=25,311 Inclusion of 293,633 patients from Jan 1995-May 2004 with STEMI or new LBBB 775 US Hospitals with on-site PCI CS developed in 25,311 (8.6%) pts CS present on admission in 29% Frequency of Cardiogenic Shock 1Babaev et al JAMA 2005 294:448 Frequency of CS Has Remained Steady Over Time NRMI Registry1 Worcester Heart Attack Study2 1975-88 ? 7.5% Gusto-13 1995 ? 7.2% 3 Holmes DR JACC 1995 26:668 2Goldberg RJ NEJM 1991; 325:1117

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Hollenberg Ann Int Med 1999; 131:47-99 Pathophysiology When a critical mass of LV is necrotic and fails to pump, stoke volume and CO falls Myocardial and coronary perfusion are compromised causing tachycardia and hypotension Increased LVEDP further decreases coronary perfusion Increase LV wall stress increases myocardial oxygen demand Lactic acidosis worsens myocardial performance

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Reversible Myocardial Dysfunction Myocardial stunning represents persistent myocardial dysfunction that occurs despite the restoration of normal flow. Develops as a result of alterations in calcium homeostasis, oxidative stress, and decreased myofilament responsiveness to calcium Hibernating myocaridum is a persistent state of myocardial dysfunction at rest because of severely reduced coronary flow. Develops as an adaptive response to hypoperfusion Both conditions may indicate recovery over time as reperfusion occurs Hollenberg Ann Int Med 1999; 131:47-99

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Etiology of Cardiogenic Shock Acute Myocardial Infarction (most common) Pump Failure Large infarction Smaller infarctions with preexisting CHF Infarction extension or expansion Mechanical complications Acute MR caused by papillary muscle dysfunction Free wall rupture Pericardial tamponade Other conditions End-stage cardiomyopathy, myocarditis, prolonged cardiopulmonary bypass, aortic stenosis, mitral stenosis, left atrial mxyoma, acute aortic insufficiency Hollenberg Ann Int Med 1999; 131:47-99

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Causes of Cardiogenic Shock SHOCK Trial and Registry (N=1160) Hochman Circ 1995; 91:873-81 Acute MR LV failure VSD RV Infarct Cardiac Rupture Other 74.5% 8.3% 4.6% 3.4% 1.7% 8%

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Inferior Anterior Posterior Multiple Locations 55% 46% 21% 50% Infarct Location in Cardiogenic Shock SHOCK Trial (N=1160) Hochman Circ 1995; 91:873-81

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Recurrent ischemia, Q waves in = 2 leads LAD culprit vessel Chest pain at shock onset ST-segment elevation in two or more leads Multiple infarct locations Inferior MI Left main disease Smoking Shock onset after acute MI occurred within 24 h in 74% of the patients with predominant LV failure Predictors of Early (< 24 h) Cardiogenic Shock Predictors of Late (= 24 h) Cardiogenic Shock Webb JACC 2000; 36:1084

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Clinical Observations from the SHOCK Trial The average LVEF is only moderately depressed (30%) with a wide range of EFs and LV sizes noted - While most patients were on IABP support and ionotropes, hemodynamic measurements demonstrated persistent hypotension, low CO, and high filling pressures despite a 30% LVEF The SVR was not markedly elevated in many cases, with the SVR ranging from 1350-1400 dynes-sec-cm-5 despite ionotropic support - Cardiac power = CI x MAP was the most powerful hemodynamic predictor of mortality - The ability to raise SVR may be an important compensatory mechanism to support BP – Endogenous/exogenous vasodilators inhibit this response Hochman Circulation 2003; 107:2998

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Clinical Observations from the SHOCK Trial The classic notion that cardiogenic shock develops only when 40% of the myocardium is irreversibly damaged is inconsistent with: 50% survival in PCI-treated patients Improved LVEF in patients undergoing revascularization NYHA Class I symptoms in 58% of patients after survival of the cardiogenic shock Resolution of the ischemia and neurohumeral-inflammatory mediates may result in resolution of the cardiogenic shock The range of LVEFs, LV size, and SVR in patients with cardiogenic shock indicate that the pathogenesis may be multifactorial. Hochman Circulation 2003; 107:2998

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Cardiogenic Shock Incidence Pathogenesis Diagnosis Treatment Options Pharmacologic Treatment PCI-CABG The SHOCK Trial Circulatory Support Prognosis ACC/AHA Guidelines Clinical Implications

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Cardiogenic Shock: Diagnosis Clinical definition1 is a decreased cardiac output and evidence of tissue hypoperfusion in the presence of adequate filling pressures: - Marked and persistent (> 30 min) hypotension with a systolic BP < 90 mmHg - Reduction in the cardiac index (<2.2 L/min/M2) - Normal or elevated PCWP (> 15 mmHg) Circulatory shock2 is diagnosed by poor tissue perfusion, including oliguria, clouded sensorium, and cool mottled extremities 2Hollenberg Ann Int Med 1999; 131:47-99 1Forrester JS et al 1976; 295:1404-13

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VSD MR due to papillary muscle dysfunction Incidence 1-2% 1-6% 1-2% Timing 3-5 d p MI 3-6 days after MI 3-5 days after MI Phy Exam murmur 90% JVD, EMD murmur 50% Thrill Common No Rare Echo Shunt Pericardial Effusion Regurgitation Jet PA cath O2 step up > 9% Equal Diastolic Pressures c-v wave in PCW http:www.americanheart.org/stemi Images:Courtesy of W D Edwards (Mayo Foundation) Data: Lavocitz. CV Rev Rpt 1984;5:948; Birnbaum. NEJM 2002;347:1426. Free Wall Rupture Mechanical Complications Resulting in Cardiogenic Shock

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Ventricular Septal Defect: In-Hospital Mortality in the SHOCK Trial Menon V et al 2000; 36:1110-6 61% 81% 87% VSD All Shock LV Dysfunction Surgical Repair

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Right Ventricular Infarction: Diagnosis Clinical findings: Shock with clear lungs, elevated JVP Kussmaul sign Hemodynamics: Increased RA pressure (y descent) Square root sign in RV tracing ECG: ST elevation in R sided leads Echo: Depressed RV function Rx: Maintain RV preload Lower RV afterload (PA---PCW) Inotropic support Reperfusion V4R Modified from Wellens. N Engl J Med 1999;340:381. http:www.americanheart.org/stemi

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Cardiogenic Shock Incidence Pathogenesis Diagnosis Treatment Options Pharmacologic Treatment PCI-CABG The SHOCK Trial Circulatory Support Prognosis ACC/AHA Guidelines Clinical Implications

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Goldberg RJ NEJM 1999; 340:1162 Mortality Rates Have Progressively Fallen Over Time Worcester Heart Attack Registry (N=644)

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California Medicare Database (1994) 1,122 Patients with Cardiogenic Shock Edep et al AJC 2000;85:1185

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Hochman et al NEJM 1999;341:625 The Shock Trial has been the most important study for management guidelines in patients with cardiogenic shock

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The SHOCK Trial (N=302) Randomization from Apr 1993-Nov 1998 Emergency Revascularization N = 152 Angioplasty or CABG within 6 hours after randomization IABP recommended in all pts Medical Therapy N = 150 IABP Thrombolytic Therapy Delayed Revascularization after 54 hours following randomization, if appropriate Primary Endpoint: Overall 30 day mortality Seconday Endpoints: 6 month and 1 year mortality Hochman et al NEJM 1999;341:625

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SHOCK Trial: Inclusion Criteria ST Elevation, Q-wave MI, new LBBB, posterior MI STEMI complicated by shock due to LV dysfunction Hypotension - Systolic BP < 90 mmHg x 30 mins or need for supportive measures to maintain systolic BP > 90 mm Hg - End organ hypoperfusion (cool extremities, urine output < 30 cc/min, HR > 60 bpm Hemodynamic criteria - Cardiac index < 2.2 L/min/M2 - PCWP = 15 mm Hg Onset of shock < 36 hours within hospital admission Hochman et al NEJM 1999;341:625

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Hochman et al NEJM 1999;341:625 The Shock Trial: Treatment

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Hochman et al NEJM 1999;341:625 Shock Trial: 30 day mortality (1o Endpoint)

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Hochman et al NEJM 1999;341:625 Shock Trial: 30 Day and 6 Month Mortality

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Hochman et al NEJM 1999;341:625 Shock Trial: Subgroup Analyses Cautionary Note: The Elderly?

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Coronary Angiography N = 142 Emergency PCI (N=81) N = 142 Emergency CABG N = 47 CABG < 24 hours N = 6 Delayed CABG N = 1 No revascularization, N = 14 Death within 30 minutes, 2 No significant lesions, 6 Vessels no suitable, 6 PCI v. CABG in the Shock Trial White HD et al Circulation 2005; 112:1992

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PCI v. CABG in the Shock Trial White HD et al Circulation 2005; 112:1992 Despite increased patient co-morbidities, include the presence of diabetes mellitus, multivessel disease, left main disease, patients treated with CABG had similar one year outcomes to patients treated with PCI PCI successful revasc, 77.2% PCI complete revasc, 23.1% CABG complete revasc, 87.2% CABG LIMA, 15.2%

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Webb et al JACC 2003;42:1380 Shock Trial: Mortality Rates with PCI Overall Mortality = 50% 67 39 85 38 55 100 Severe MR Succ PCI Unsucc PCI TIMI Flow 3 2 0,1 N=80 with angiograms

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6 Yr Outcome of SHOCK All Patients Hochman et al JAMA 2006; 295:2511

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Intra-Aortic Balloon Pump Support Reduces afterload Augments diastolic perfusion pressure Improvement in cardiac output and coronary blood flow No change in myocardial oxygen demand Essential as a support device for PCI or bridge to CABG ACC-AHA Class I recommendation IABP support was associated with a ? in mortality: * NRMI-2 with lysis, from 67% to 49%2 * SHOCK Trial, from 63% to 47% 1Hollenberg Ann Int Med 1999; 131:47-99 2Barron AHJ 2001; 141:933

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Tandem Heart Percutaneous Device (CardiacAssist, Inc, USA) Transeptal puncture with inflow venous catheter placed in LA 17 French Arterial Cannula or two 12 Fr in both femoral arteries Delivery 4.0 L/min at 7500 rpm ACT 180-200 secs 42 Pts with Cardiogenic Shock VAD N=21 IABP N=20 Thiele et al EHJ 2005; 26:1276

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Circulatory Support Devices Left Ventricular Support (Abiomed Impella device) Windecker Kardiovaskulare Medizin 2005;8:187 Meyns B Thorac Cardiovasc Surg 2003; 51:312 12 F Microaxial pump mounted on a 9 Fr Catheter inserted via a 13 Fr sheath 2.5 L Flow

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Aiba et al Jpn Circ J 2001;65:145 When Should Advanced Percutaneous Support Be Considered in Patients with Cardiogenic Shock? In Hospital Survival Rate in Patients with Moderately Severe Shock IABP PCPS 5% 38.5% 64 patients with CS treated with an IABP (n=38) or PCPS (n=26). The shock score (0-15) was used to quantify the severity of shock. Multivariate logistic regression analysis found that the most significant factor related to the in-hospital prognosis was the shock score (p=0.0007; OR 2.16, 95% CI: 1.37-3.39). None of the patients in either IABP or PCPS whose shock score was more than 9 survived

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Cardiogenic Shock Incidence Pathogenesis Differential Diagnosis Treatment Options Pharmacologic Treatment PCI-CABG The SHOCK Trial Circulatory Support Prognosis ACC/AHA Guidelines Clinical Implications

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NRMI STEMI Registry (N=25,311) Age, 69.4 years Women, 42.6% Hypertension, 49.7% Diabetes, 27.2% Prior MI, 23.2% Prior CHF, 15.2% Prior PCI, 9.1% Prior CABG, 12.2% Mortality Rates Over Time Babaev et al JAMA 2005 294:448 1995 2004 60.3% 47.9% P < 0.001

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Majority of CS Patients are Class I-II at 1 Year Sleeper et al JACC 2005; 46:266

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Holmes et al Circ 1999;100:2067 Prognosis Is Worse With NSTEMI likely related to the extent of underlying disease

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Multivariable Mortality Predictors Increasing age 1,2,3,4,7 and female gender7 Lower left ventricular ejection fraction 4,6 Chronic renal insufficiency7 Initial6 and Final TIMI Flow grade 14 Lower systolic blood pressure 1 Diabetes mellitus 5 Prior MI 2 Increasing time from symptom onset to PCI 1,4 Total Occlusion of the LAD 7 Mitral regurgitation Multivessel PCI (p = 0.040) 1,4,6 1 Webb et al JACC 2003;42:1380 2 Sutton Heart 2005;91:339 3 Tedesco AHJ 2003:146; 472 4 Zeymer et al EHJ 2004;25:322 5 Tedesco JV Mayo Clin Proc 2003; 78:561 6 Sanborn JACC 2003:42; 1373 7 Klein et al AJC 2005; 96:35

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Cardiac Power Is The Most Important Mortality Predictor in the SHOCK Trial Finke et al JACC 2004; 44:340

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Dzavik et al AHJ 2005; 149:1128 “The lack of benefit of emergency revascularization in elderly patients with cardiogenic shock may relate to differences in baseline left ventricular function and the smaller sample size” The Elderly with Cardiogenic Shock

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Decade-long experience in prospective registry of consecutive PCIs in Northern New England Characteristics and hospital mortality were compared for elderly (= 75 years old) versus non-elderly (<75 years old) patients. From 1990 to 2000, a total of 310 patients had PCI for cardiogenic shock, 24% of whom were elderly. Independent predictors of mortality for both groups were older age and the absence of collaterals; During the stent era, significant predictors were lack of stent placement and diabetes mellitus. New England Registry 30-Day Mortality Patients > 75 yrs Dauerman et al J Invasive Card 2003; 15: 380 46%

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ACC/AHA Guidelines for PCI in Patients with Cardiogenic Shock Primary PCI is recommended for patients less than 75 years with ST elevation or LBBB or who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock. Primary PCI is reasonable for selected patients 75 years or older with ST elevation or LBBB or who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock. http:www.americanheart.org/stemi

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Mortality rates also decreased for those pts undergoing PCI Use of PCI increased from 27.4% to 54.4% (p < 0.001) Use of PCI was the strongest independent predictor of a lower in-hospital mortality (AOR 0.46; p < 0.001) Babaev et al JAMA 2005 294:448 NRMI Revascularization Rates Over Time By Age

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Clinical Implications Although there was a general increase in the rate of primary PCI for cardiogenic shock over time that was associated with an improved survival, there was no temporal impact of the ACC Guidelines for the management of cardiogenic shock in clinical practice PCI and CABG were still underused in the NRMI Registry, potentially due to the higher mortality rates that are seen in patients with cardiogenic shock. PCI may be used more liberally in the elderly, due to the limited number of elderly patients (N=56) enrolled in the SHOCK Trial Babaev et al JAMA 2005 294:448