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Causes of death in patients with STEMI treated with fibrinolysis (Kashani et al,JACC,2004) VariableInhospital Death (N=913) 30 Days Death (N=1006) 31-180.

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Presentation on theme: "Causes of death in patients with STEMI treated with fibrinolysis (Kashani et al,JACC,2004) VariableInhospital Death (N=913) 30 Days Death (N=1006) 31-180."— Presentation transcript:

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3 Causes of death in patients with STEMI treated with fibrinolysis (Kashani et al,JACC,2004) VariableInhospital Death (N=913) 30 Days Death (N=1006) Days Death (N=303) CHF Recurrent M Rupture Intracranial Hemorrhage Other Cardiovascular Dysrhythmia Other Non-Cardiac Unobserved Unknown Improve myocardial salvage &more aggressive treatment of post- MI CHF Numbers in table represent percentages of death

4 Cardiogenic Shock The impaired ability of the heart to pump blood Pump failure of the right or left ventricle Most common cause is LV MI (Anterior) Occurs when > 40% of ventricular mass damage Mortality rate of 80 % or >

5 Cardiogenic Shock Etiologies Mechanical: complications of MI: Papillary Muscle Rupture!!!! Ventricular aneurysm Ventricular septal rupture Other causes: Cardiomyopathies tamponade tension pneumothorax arrhythmias valve disease

6 Cardiogenic Shock Pathophysiology Pathophysiology Impaired pumping ability of LV leads to…Impaired pumping ability of LV leads to… +Decreased stroke volume leads to….. +Decreased CO leads to ….. +Decreased BP leads to….. +Compensatory mechanism which may lead to … +Decreased tissue perfusion !!!!

7 CRITERIA of C.S. (1)Hypotension(SBP 30 minutes (2) Hypoperfusion (3) Hemodynamic confirmation ( PCWP > 15 mmHg + C.I. < 2.2 L /min./m ) ( Hochmman J.S.etal, Am H.J.,1999) 2

8 Mortality :Major shock categories Mortality % Incidence 78.5%3.9%6.9%2.8%1.4%6.7% (Hochman et al,JACC,2000)

9 Clinical profile of C.S. with L.V.F. (Hochmman et al, JACC, 2000) P.congestionHypoper-fusion N % MortalityGp.A--14(3%)21% Gp. B +-32(6%)22% Gp. C -+158(28%)70% Gp.D++367(64%)60%

10 In –hospital event rates by angiographic findings in patients with LV or RV failure (Wong et al,JACC, 2000)

11 Implications of the timing of onset of C.S. after AMI (John& Webb et al,JACC,2000)

12 Clinical correlates,management and outcome in M.T. complicated by C.S. at hospital admission : A report from the shock trial and registry A report from the shock trial and registry. C.S.A. have a more severe haemodynamic derangement and higher mortality, benefit equally from E.R.V. (Raban V. Teger,JACC, 2005) C.S. admissionC.S. delayed In hospital mortality 75%56%P< Early revascularization 60%46% Initial medical stabilization 82%62%

13 C.S. with NSTEMI Percent Vessel disease (Jacobs et al, JACC,2000)

14 C.S. with NSTEMI Percent Rates of in-hospital coronary angiography and revascularization after diagnosis of CS caused by LV failure. (Jacobs et al,JACC, 2000)

15 Cardiogenic shock complicating NSTEMI Data from Rico survey 1945 AMI 148 (7.6 % had C.S.) C.S. + NSTEMI have higher risk profile than STEMI,more recurrent angina IMJ, higher revascularization,mortality equally higher. (Marianne Zeller etal,JACC,2005) NSTEMISTEMIP No:35(23%)113 (76%) Age7873P <0.001 D.M.49%27%P=0.025 PVD29%3%P<0.01 LVEF45%34%P=0.048 IN hospital mortality 46%58%P=0.032

16 D.M. in CS complicating AMI Shindler et al,JACC, 2000 Survival benefit in diabetes (black bars) and non diabetics (white bars) In-Hospital survival(%)

17 CS due to acute severe MR Valve surgery (n=43) No valve surgery (n=51) P value Left heart cathterization 9361<0.001 Intra-aortic ballon pump 9843<0.001 Angioplasty attempted Bypass surgery868,0.001 Angioplasty or by pass surgery 8826<0.001 Transfusion9340<0.001 In-hospital mortality (Thompson et al,JACC, 2000)

18 Patient characteristics :VSR vs. acute severe MR in shock trial registery patients characteristicsVSRSevere MRP value n5497 History of MI Diabetes LV ejection fraction In-hospital survival <0.001 (Menon et al,JACC, 2000)

19 C.S. due to free – wall rupture or tamponade (Slater etal, JACC,2000) Intervention in subacute possible Incidence : 2.7% of all C.S. Less P. Edema,D.M. prior MJ. Pericardial effusion in 75% 27/28 had surgery or pericardiocetesis Survival rate 39.3% as the overall group

20 Mortality by revascularization status No LH CATH N=334(38%) 88.6% Mortality No revascularization attempt N=146(17%) 59.6% Mortality CABG < 18 hours post –CS N= % Mortality PTCA< 18 hours post-CS N= % Mortality LH CATH N=550(62%) 44.9% Mortality CABG N=136(15%) 27.9% Mortality PTCA N=268(30%) 45.5% Mortality (Hochman et al,JACC,2000)

21 Thrompolysis, Ballon counter pulsation in the shock trial registry (Sanborn et al,JACC, 2000)

22 Thrombolysis and JABPC in C.S. (Sanborn etal,JACC,2000) Mortality No. T.T. no IABP N=285 33% 77% IABP only N=279 33% 52% TT only N=132 15% 63% + TT + JABP N= % 47%

23 Intra-Aortic Balloon Pump Inflatable cc balloon Triggered to inflate with helium immediately after aortic valve closure Triggered to deflate with opening of the aortic valve

24 Intra-Aortic Balloon PumpIntra-Aortic Balloon Pump

25 VAD reverse C.s. more effectively than IABP With more complications (Thiele etal EHJ,2005) VAD IABO Days from randomization Cumulative survival % Log –rank P=0.80

26 Pharmacological support Dopamine Norepinphrine 31.6% Epinephrine 41.9% Dobutamine in 70.1% Shock trial ®istry (Hochman etal,JACC, 2000)

27 A comparison of continous I.V. arginine Vasopressin to dopamine in the treatment Of cardiogenic shock AVP is safe and might have some clinical and haemodynamic advantages over DOA in the treatment of C.S. (Masehisa Janane etal,JACC,2005) AVP(N=16)DOA(N=16)P Dose IU/HR mcg/Kg/min. H.R BPM BPM TIMI 3 94%81%0.285 Meaning time hrs hrs month survival 81.2%13/ % 10/

28 L- NAME :N-Monomethyl L- arginine:anitric oxide synthesis inhibitor 1 mg/kg bolus than 1mg/kg/hr for 5 hs versus placebo in 30 patients with refractory C.S. 1 month survival 73% versus 33% in placebo (Cotlar etal,EHJ,2003)

29 One month survival in the two treatment groups ( after Cotler etal,EHJ,2003) Survival time (Days) 1 No treatment 2 L-Name 1 No treatment 2 L-Name 1 Survival(%) Survival (%) One –month survival in the two treatment arms One-week survival in the two treatment arms

30 Levosimendan is safe and effective in patients with severe LCOP failure and critical hypotension (Franco etal,JACC,2004) (Franco etal,JACC,2004) * Mean + SD; †P < 0.05 Clinical parameter*/ Outcome Group 1 Levo, Dob/Dop (n=15) Group 2 Dob/Dop (n=11 Baseline Baseline 48 h. Baseline 48 h. Baseline 48 h. Systolic BP (mmHg) † Heart Rate (beats/min) † Diuresis (mL/hr) † † Creatinine (mg/dL) † In-hospital mortality (%)

31 COMMIT: Effects of METOPROLOL on Death by attributed cause(s) MetoprololPlaceboOdds ratio & 95% CI Metop. betterPlacebo better Cause(s) (22,927)(22,922) Arrhythmia388498(1.7%)(2.2%) 22% SE 6 Shock496384(2.2%)(1.7%) -29% SE 8 Other causes892916(3.9%)(4.0%) 3% SE 5 ANY DEATH (7.7%)(7.8%) 1% SE 3 (2P > 0.1; NS)

32 COMMIT: Absolute effects of METOPROLOL on Re-MI, VF, Shock and Death by KILLIP class Killip at entry Absolute differences per 1000 Re-MIVFShockDeath I II III Any

33 COMMIT: Effects of METOPROLOL on Cardiogenic Shock by day of event MetoprololPlaceboOdds ratio & 95% CI Metop. betterPlacebo better Day of event (22,927) (22,922) (2.1%)(1.4%) (1.2%)(0.9%) (1.7%)(1.6%) ALL (5.0%)(3.9%) -29% SE 5 (2P < )

34 COMMIT: Effects of METOPROLOL on Cardiogenic Shock by Killip class MetoprololPlaceboOdds ratio & 95% CI Metop. betterPlacebo better Baseline Killip class (22,927) (22,922) I611487(3.5%)(2.8%) II362296(7.9%)(6.5%) III155100(16.2%)(10.4%) ALL (5.0%)(3.9%) -29% SE 5 (2P < )

35 The CAPTIM Had a lower incidince of cardiogenic shock in the pre-hospital thrombolysis arm than in the primary PCI arm (Bonnefoy E et al, Lancet, 2002)

36 C.S. death predictors (1)Previous MI (2) Age > 70 Y. (3) Failed thrombolysis (Suttor et al, BMJ,2005)

37 B-Tpe Natriuretic Peptide Strongly Predicts Mortality in Intensive Care Unit Shock (Tung et al,JACC,2004)

38 (Hassan Kafri et al,JACC, 2005)

39 C.S. with preserved L.V. systolic function (Nayar etal,JACC,2004) Shock trial : 24 patient had EF > 37% Had non-dilated L.V. + abnormal vascular tone C.S.

40 Long term outcome of patients with CS complicating AMI (Holmes et al,JACC,2004) GUSTOI 9 years F.U. 47% 30d survival, 53% 9 Y. survival N Alive 457 Dead 402P Male 66.5% 65.7%.793 Age (yrs)60.6 +/ / <.001 Diabetes9.9% 20.6%<.001 Prior MI10.8% 26.8%<.001 Anterior MI 37.7% 50.3%<.001 Inferior M 60.1%47.8%<.001 Revasc within 30 days PTCA 42.7% 28.9%<.001 CABG 21.9%21.1%.763 PTCA or CABG 58.3% 46.3%<.001

41 Low output cardiogenic shock Check blood pressure Systolic BP Greater than 100 mm HG Systolic BP 70 to 100 mmHg No signs/symptoms Of shock Systolic BP 70 to 100 mmHg signs/symptoms Of shock Systolic BP Less than 70 mmHg signs/symptoms Of shock Nitroglycerine 10 to20 mcg/min IV Dobutamine 2 to 20 mcg/kg Per min. IV Dopamine 5 to 15 mcg/kg Per min. IV Norepinephrine 0.5 to 30 mcg/min. IV Further diagnostic /therapeutic considerations (should be considered in nonhypovolemic shock) Dignostic Therapeutic Pulmonary artery catheter intra-aortic ballon pump Echocardiography reperfusion Angiography for MI/ischemia revascularization Additional diagnostic studies ACC/AHA Guidelines further management of STEMI Antman et al,JACC, 2004

42 Conclusion (1)Invasive strategy with early revascularization is associated with a better long term outcome than continued medical treatment. Intensive medical treatment (ventilation,JABP,late revascularization action) is associated with a better outcome than previously experienced with a conservative medical approach. (2) Intensive medical treatment (ventilation,JABP,late revascularization action) is associated with a better outcome than previously experienced with a conservative medical approach.

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