Acute coronary syndromes Šimek S
PŘÍMÁ PTCA UZÁVĚRU RIA ANTERO- EXTENZIVNÍ AIM
PŘÍMÁ PTCA UZÁVĚRU RIA ANTERO- EXTENZIVNÍ AIM
PŘÍMÁ PTCA UZÁVĚRU RIA ANTERO- EXTENZIVNÍ AIM
PŘÍMÁ PTCA UZÁVĚRU RIA ANTERO- EXTENZIVNÍ AIM
PŘÍMÁ PTCA UZÁVĚRU RIA ANTERO- EXTENZIVNÍ AIM
CHD = insufficient blood supply to myocardium LCA LAD CXA Stenosis Occlusion RCA
The Evolution of Atherosclerosis Foam Cells Fatty Streak Intermediate Lesion Atheroma Fibrous Plaque Complicated Lesion/Rupture Endothelial Dysfunction From 1st Decade From 3rd Decade From 4th Decade Growth Mainly by Lipid Accumulation Adapted From Stary HC et al. Circulation. 1995;92:1355-1374 Smooth Muscle & Collagen Thrombosis, Hematoma
Risk factors SMOKING HLP HT DIABETES MELLITUS POSITIVE FH OBESITY, PHYSICAL INAKTIVITY
CHD - SYMPTOMS AP CHEST PAIN HEART FAILURE - DYSPNEA ARRHYTMIAS
CHD ACUTE FORMS (CHANGING 1 m, DANGEROUS) CHRONIC FORMS (LONG LASTING UNCHANGED, RISK SMALLER)
Acute coronary syndromes Cause: coronary vessel thrombosis due to rupture of unstable plague
STABLE VERSUS UNSTABLE PLAQUE Falk E, et al. Circulation. 1995;92:657-671.
PLAQUE RUPTURE
RIZIKOVÉ FAKTORY RUPTURY PLÁTU Lokální Faktory fatique of the cap smoking Cholesterol Systémové Faktory content of the plaque inflamation thickness of the cap Diabetes Mellitus Homocystein Fibrinogen impaired Fibrinolysis Ruptura plátu Fuster V, et al. N Engl J Med. 1992;326:310-318. Falk E, et al. Circulation. 1995:92:657-671.
Acute coronary syndromes SymptomS Chest pain change in frequence, intensity or duration Atypical symptoms up to 50% (pain in neck, back, ear, abdomen, dyspnoea, dizziness)
Acute coronary syndromes final classification UNSTABLE ANGINA PECTORIS (flow limiting stenosis), <20 min ACUTE MYOCARDIAL INFARCTION (occlusion), >20 min SUDDEN DEATH
Acute coronary syndromes Newer Final CLASSIFICATION UNSTABLE ANGINA PECTORIS (UAP) Minimal myocardial lesion=microinfarct ( Troponin T+I, 1g of myocardium) MI without ST elevations (NSTEMI) MI with ST elevations(stemi) Sudden death
Eur Heart J 2000;21:1502-1513 NEW CLASSIFICATION OF ACS Acute coronary syndromes orking diagnosis according to EKG ACS without STE (NSTE-ACS) cardiomarkers negative ACS with STE (STEMI) cardiomarkers pozitive NSTEMI DEFINITIVE DIAGNOSIS UAP non QIM QIM
TREATMENT NSTE - AKS AIMS: TO PREVENT DEVELOPEMENT OF OCCLUSIVE TROMBUS TO PREVENT MYOCARDIAL NECROSIS
TREATMENT OF NSTE ACS FARMACOTHERAPY Antiischemic REST IN BED, oxygenotherapy Nitrates, betablockers, Calcium channel blockers ACE inhibitors (HT,SS,DM), sartans Opiates Antithrombotic ASA, Clopidogrel, Ticlopidin Heparin, LMWH Inhibitors of GP IIb/IIIa Stabilisation of plaque statins
NSTE ACS Interventional treatment
InvazivE vs Conservative strategy VANQWISH ICTUS léčby NAP/NSTEMI MATE TIMI IIIB ISAR- COOL RITA-3 VINO TRUCS TACTICS- TIMI 18 FRISC II conservative Invasive
Unstable plague trombus
PTCA + stent
concentric stenosis
PTCA + stent
STEMI In 90% thrombus on ruptured plaque occlusion of entire vessel Aims: to open the artery as soon as possible De Wood M.,NEJM 1980;303:897-902
MAin tasks Treatment of STEMI 1. To open IRA as soon as possible aspirin heparin (10 000j. I.V., Clexane 1ml i.v. nebo s.c.) Fibrinolytics or primary PCI 2. prevent death due to mallignant arrhytmias = ECG monitor 3. lover oxygen demands (decrease pain,activity,hr) 4. increase oxygen supply (O2) 5. improve collateral supply
FIBRINOLYSIS - EASY FAST CHEAP - SUCCES recanalisation of IRA 50-70% normal flow 30-55% 10-20% reoklusion risk of serious bleeding 1,8%
Metaanalysis od 23 randomized studies PCI versus fibrinolýsis (n=7739) 8 7 p=0,003 p=0,001 7 6,8 % 6 5 4 3 2 1 0 5 2,5 p=0,004 1 2 p=0,001 0,05 1,1 PTCA FIBRINOLÝZA ÚMRTÍ re IM CMP hemorh CMP
Transfer to PCI vs fibrinolýza úmrtí ReMi CMP Úmrtí/MI/CMP
FIBRINOLYSIS Streptokináza 1500 000 j i.v. 30-60 min + Hydrocortizon 200mg i.v. Altepláza, Actilyse, tpa 60mg i.v. 30 min + + 40mg i.v. 60 min
Distální protekce FilterWire (BS)
FREQUENT MISTAKES TIME LOOSING IV. PORT ABSENT KPR NOT SUFFICIENT CONCLUSIONS MADE FROM FIRST ENYZMES Aspirin NOT GIVEN MI OF POSTERIOR WALL NOT RECOGNIZED
WHY THE POSTERIOR MI NOT RECOGNIZED? ST elevations present mostly in posterior ECG leads V7-V9 (v 68%) Kulkarni AU, Brown R, Ayoubi M. Clinical use of posterior electrocardiographic leads: a prospective electrocardiographic analysis during coronary occlusion. Am Heart J. 1996 Apr;131(4):736-41. In some patients only in V7,V8,V9)
55 letá exkuřačka, leta HT, leta ICHS přijata pro 2 hod trvající bolest na hrudi EKG hodnoceno jako koronární insuficience, kardioenzymy negativní, léčena konzerativně po 6 hodinách pro neúspěch konzervativní léčby přeložena k SKG jako NSTE AKS
Nováková
55 letá exkuřačka, leta HT, leta ICHS přijata pro 2 hod trvající bolest na hrudi EKG hodnoceno jako koronární insuficience, kardioenzymy negativní, léčena konzerativně po 6 hodinách pro neúspěch konzervativní léčby přeložena k SKG jako NSTE AKS
ACS - DISCHARGE MEDICATION Anopyrin 100 mg FOR EVER Clopidogrel (6-12M) Betablocker (FOR EVER) Antisclerotic diet + statin ACEI if EF<0.40, HF, HT, DM