ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation Subsequent management and therapies Marco Valgimigli, MD, PhD University of Ferrara ITALY
Disclosures Served as a speaker, an advisor or consultant for: AstraZeneca Pharmaceuticals LP; Bayer Health Care Pharmaceuticals; Daiichi Sankyo, Inc.; Eli Lilly and Company; The Medicines Company; Abbott; St Jude; Terumo; CID; Cordis; Boston Scientific; Merck;
Logistical issues during hospital stay
Number of beds in ICCU: 4-5 beds for each 100 000 inhabitants,, 10 beds for every 100,000 visits/year in ER ICCU equipment: IABP (one console every 3 beds up to 6) Mechanical ventilation system Haemodyalisis/haemofiltration machine External and Temporary pacemakers Echocardiography Defibrillator Mechanical compression devices for groin homeostasis (optional) (Continuous) monitoring for: a) EKG b) Invasive and non invasive pressure 3) Sp02 4) End tidal C02 5) Body temperature 6) Cardiac output 7) Glucose 8) ACT 9) Blood gasses and electrolyte analyser
Logistical issues during hospital stay
Low Risk patients selection Criteria for early ( day 3) discharge PAMI II Criteria: (J Am Coll Cardiol. 1998;31(5):967-72) Age <70 years, Left ventricular ejection fraction >45%, One- or two-vessel disease, Successful PTCA, No persistent arrhythmias Zwolle Criteria (Circulation 2004; 109:2737 2743) Total score 3 Zwolle Risk score for STEMI Killip Class Points 1 0 2 4 3-4 9 TIMI Flow post 3 0 2 1 0-1 2 Age <60 0 60 2 3-Vessel Disease No 0 Yes 1 Anterior MI No 0 Yes 1 Ischemic time>4 hours No 0 Yes 1
Summary of indications for imaging and stress testing
Routine therapies in the acute, subacute and long term phase of STEMI Observational studies show that patients who stop smoking reduce their mortality in the succeeding years compared with continued smokers. Stopping smoking is potentially the most effective of all secondary prevention measures, and much effort should be devoted to this end. Patients do not smoke during the acute phase of a STEMI and the convalescent period is ideal for health professionals to help smokers to quit. However, resumption of smoking is common after discharge, and continued support and advice are needed during rehabilitation. Nicotine replacement, bupropione and antidepressants may be useful. Nicotine patches have been demonstrated to be safe in ACS patients.
Randomized data supporting 6 month DAPT duration after DES 12 10 8 P=0.001 for noninferiority P=0.91 for superiority 6 Mo DAPT 12/24 mo DAPT 6 4 2 0 STEMI 3.1% STEMI 33% Excellent Circ 2012;125(3):505-13 Prodigy Circ 2012;125(16):2015 Prodigy: II III,V BARC: 3.5% vs. 7.4%, p<0.001 Non-CABG TIMI Major: 0.6% vs. 1.6%, p=0.041
Routine therapies in the acute, subacute and long term phase of STEMI
Estimated Cumulative Rate (%) PRIMARY EFFICACY ENDPOINT: CV Death / MI / Stroke* (Ischemic + Hemg.) 12 Placebo 10.7% 10 8.9% 8 6 4 Rivaroxaban (both doses) HR 0.84 (0.74-0.96) ARR 1.7% mitt p = 0.008 ITT p = 0.002 2 STEMI ~50% of overall patient population NNT = 59 0 0 4 8 12 16 20 24 Months After Randomization
Estimated Cumulative incidence (%) PRIMARY EFFICACY ENDPOINT*: 2.5 mg PO BID 12% CV Death / MI / Stroke* HR 0.84 mitt p=0.020 ITT p=0.007 5% Cardiovascular Death Placebo HR 0.66 HR 0.68 10.7% 9.1% mitt p=0.002 ITT p=0.005 Placebo 5% 4.1% 2.7% All Cause Death mitt p=0.002 ITT p=0.004 Placebo 4.5% 2.9% Rivaroxaban 2.5 mg BID NNT = 63 12 0 12 24 12 Months Months 1 Months 0 24 Rivaroxaban 2.5 mg BID NNT = 71 Rivaroxaban 2.5 mg BID NNT = 63 0 24
PRIMARY EFFICACY SUBGROUP RESULTS HR (95% CI) P interaction Overall 0.84 (0.74 0.96) ASA 0.69 (0.45-1.05) ASA + thienopyridine 0.86 (0.75-0.98) 0.34 <65 Years 65 Years STEMI NSTEMI UA Male Female Weight <60 kg Weight 60 to <90 kg Weight 90 kg Prior MI No Prior MI Diabetes Mellitus No Diabetes Mellitus Creatinine Cl <50 ml /min Creatinine Cl > 50 ml /min North America South America Western Europe Eastern Europe Asia Other 0.83 (0.70-0.99) 0.84 (0.70-1.01) 0.85 (0.70-1.03) 0.85 (0.68-1.06) 0.82 (0.62-1.07) 0.87 (0.75-1.01) 0.77 (0.60-0.99) 0.83 (0.56-1.25) 0.85 (0.72-0.99) 0.83 (0.64-1.08) 0.83 (0.68-1.01) 0.85 (0.72-1.01) 0.96 (0.77-1.20) 0.78 (0.67-0.92) 0.88 (0.62-1.26) 0.84 (0.73-0.96) 0.57 (0.33-0.97) 0.89 (0.59-1.34) 0.90 (0.59-1.37) 0.83 (0.69-1.00) 0.86 (0.63-1.17) 0.92 (0.60-1.39) 0.94 0.96 0.40 0.98 0.80 0.14 0.82 0.80 0.5 0.8 1.0 1.25 2.0 European Rivaroxaban Heart Better Journal 2012 - doi:10.1093/eurheartj/ehs215 Placebo Better
SAFETY ENDPOINTS 2,5 HR 3.46 p<0.001 HR 4.47 p<0.001 Placebo Riva 2.5 Riva 5 2 1,5 1 0,5 p=0.009 Riva Vs Placebo p=ns for Riva vs Placebo p=0.044 for 2.5 mg vs 5.0 mg 0 Non-CABG TIMI Major NNH: 83 for Riva 2.5 mg ICH Fatal Bleeding
Routine therapies in the acute, subacute and long term phase of STEMI
Routine therapies in the acute, subacute and long term phase of STEMI The benefit of long-term treatment with beta-blockers after STEMI is well established, although mostly from trials pre-dating the advent of modern reperfusion therapy and pharmacotherapy. The benefits In contemporary of statins trials in secondary utilizing prevention primary PCI, have betablockers been unequivocally demonstrated, have not been and specific investigated, trials have although demonstrated it is not unreasonable the benefit of early and intensive to extrapolate statin their therapy. benefit The to recent this setting. meta-analysis of trials comparing more- vs. less-intensive LDL-cholesterol lowering with statins indicated that, compared with less-intensive regimes, more-intensive statin therapy produced reductions in the risks of cardiovascular death, non-fatal myocardial infarction, ischaemic stroke and coronary revascularization. For every 1.0 mmol/l reduction in LDL cholesterol, these further reductions in risk were similar to the proportional reductions in the trials of statin vs. control. Therefore, statins should be given to all patients with acute myocardial infarction, irrespective of cholesterol concentration. This treatment should be started early during admission, as this increases patient adherence after discharge, and given at high doses, as this is associated with early and sustained clinical benefits.
5. Complications following STEMI
Treatment of mild HF (Killip class II)
Treatment of mild HF (Killip class III)
Treatment of cardiogenic shock (Killip class IV) Evidence regarding its efficacy, in the setting of acute myocardial infarction Complicated by cardiogenic shock, has been reviewed recently for patients in the prefibrinolytic, the fibrinolytic and the primary PCI eras. Owing to the lack of randomized trials, only registries were evaluated, and showed conflicting results for the three eras, with mortality risk differences of 29% and 18% in favour of IABP in the prethrombolytic and thrombolytic eras, and an increase of 6% in mortality with IABP in the primary PCI era Another recent meta-analysis suggests a survival benefit from IABP in patients with cardiogenic shock. Overall, despite common use in clinical practice, there is somewhat conflicting evidence with respect to the benefit of IABP in cardiogenic shock, which is probably largely related to the difficulty of performing randomized trials in this setting.
Management of atrial fibrillation
Levels of evidence A 21% C 44% 35% B
Major gaps in evidence Strategies to minimize early cardiac arrest. Improving patient and public awareness of STEMI symptoms. Optimizing clinical pathways for high-quality, homogeneous early STEMI diagnosis and management. Reducing or minimizing myocardial injury and left ventricular dysfunction following STEMI. Defining the optimal management strategy for non-culprit vessels in primary PCI patients. Defining the optimal long-term antithrombotic regimen in patients receiving stents and who have an indication for oral anticoagulants. Defining the role for pre-hospital thrombolysis in patients presenting early. Defining the optimal combination and duration of antithrombotic therapies. Defining the optimal glucose-management goals and strategy in patients with known diabetes or acute hyperglycaemia. Developming percutaneous techniques for managing ventricular septal defects. Effective and safe of cell therapy to replace myocardium or minimize the consequences of myocardial injury. Strategy to minimize risk of sudden death in patients with ventricular tachycardia or ventricular fibrillation during or after STEMI. Effective strategies to achieve and maintain long-term effective risk factor control.