【正文】 θi:li?l] function. ?polarized solution (potassium, magnesium） ?Others: vitamine, FDP ?Routine use of calcium antagonist increase the risk of death in AMI patients STEMI treatment Key concepts ?Atherosclerosis is the leading cause of death and disability, also the main cause of CHD ?Risk factors and prevention of atherosclerosis ?CHD is due to the imbalance between myocardial oxygen supply and demand ?Two large groups of CHD: chronic(stable angina pectoris) and ACS ?ACS posed of UAP/NSTEMI and STEMI, resulting from the plaque rupture or erosion, with differing degree of thrombosis and distal embolization, with different obstruction of the coronary artery. ? reperfusion eit。blocker: reduce HR, decrease BP, decrease myocardial oxygen consumption, decrease Vf 3. Antiplatelet: ?aspirin： first dosage 300mg， chewing, 100mg/d forever for patients without contraindication ?Clopidogrel: 300mg loading, 75mg/d STEMI treatment : antithrombin, heparin, LMWH of infarct size: reperfusion: ?Fibrinolytic treatment: intravenous， intracoronary ?rtPA： 100mg， in 90 min, use heprin before infusion ?Streptokinase (SK)： 1500,000U， iv in 60min, allergic reaction ?Urokinase (UK)： ,000 U， iv fusion in 30min ?give heprin after intravenous thrombolysis therapy ?Primary Percutaneous Coronary Intervention(PCI) ?CABG STEMI treatment AMI PTCA Stenting STEMI treatment Primary stenting Criteria for thrombolysis in STEMI indication： pain: consistent with AMI changes: ?ST elevation in at least two contiguous leads。?:tik] dissection： sever chest pain with (tearinglike), radiated to back， with aortic regurgitation[:d?i39。ristik] of chest pain, time course of chest pain and fever, ECG changes pulmonary embolization[emb?lai39。daitis]：characteristics[.k230。θr?mb?s] cause arterial embolization ?DVT (deep vein thrombus) cause pulmonary embolization aneurysm： ?persistant ST elevation ?cause mural[‘mju?r?l]附 壁 thrombus, heart failure, and arrhythmias syndrome(Dressler syndrome)： ?fever, chest pain, repeated pericarditis, pleuritis[plu?39。 rupture of interventricular septum [emb?lai39。p?lm?n?ri] edema[i:39。pil?ri] muscle： ?rare but fatal plicationcause acute massive mitral regurgitation[:d?i39。l?]蒼白 ?Cardiac examination: ?HR: bradycardia, tachycardia, irregular ?heart sound: S1 muffled[39。?k??s] , distress, cold perspiration[.p?:sp?’rei??n]冷汗 , skin pallor[39。di:m?], rales over 50% of lung fields ?Class IV: cardiogenic shock ?Classification based on invasive hemodynamic monitoring ?Class I： Normal, PCWP 18. CI； ?Class II: Pulmonary congestion, PCWP 18. CI ； ?Class III: peripheral hypoperfusion, PCWP 18, CI 。v?miti?]嘔吐 , ?arrhythmias： VPs、 AV block, atrial arrhythmias occurred more often in patients with HF ?Heart failure: mainly acute LV failure, may develope[di39。stri?m]腹上部 pain and abdominal disorders STEMI Clinical manifestation symptoms ?General： fever、 HR increase、 WBC ?， ESR fasting ?Gastrointestinal symptom： nausea[39。li?gw?l ] nitroglycerin, ?retrosternal[retr?u39。tei??n] Symptom ?Chest pain ?sever, sometimes intolerable[in39。pr?udr?um?l ] symptoms前驅(qū)癥狀 ： ?weakness, chest disfort, restlessness煩躁不安 , ?new onset AP and accelerating AP ?Circadian periodicity晝夜周期律 : ?peak incidence:612am STEMI Clinical manifestation[.m230。si:d??] ?fever, tachycardia, respiratory infection, hypoxemia[.haip?k39。plai?ns]: decrease in the peak rate最大速率 of decline in LV pressure (dP/dt) ?rise in LV enddiastolic pressure and volume STEMI pathophysiology LV function ?Predisposing[.pri:di39。d?ksik?l] expansion矛盾性膨脹 , systolic bulging ?Diastolic function: ?reduction [ri39。sei??n] of shortening ?dyskinesis運動障礙 : paradoxical[.p230。d?eisnt] segment ?hypokinesis[haip?uki39。p?uz] lifethreatening ventricular arrhythmias. STEMI Ventricular remodeling[ri39。ri:p?ul?rai39。di??nl ]額外 myocardial necrosis”. . ventricular dilatation： ? shift of pressurevolume curve of LV to the right ? larger LV volume at any given diastolic pressure ? Compensatory[k?m39。lei??n] tissue removal of necrosis tissue collagenization firm connective tissue scar OMI 12hr 23d 12 weeks 6－ 8 weeks STEMI STEMI Pathology: myocardial diseases Ventricular remodeling ?concept: ? the changes in LV size, shape, and thickness ? involving both the infarcted and noninfarcted segments ?Determinants: ?the size of infarction ?Ventricular loading conditions ?Infarct related artery patency[39。kr?usis ] ( coagulation necrosis) coronary occlusion necrotic muscle fibres dissolved granulation[.gr230。mek?niz?m of the chronic CAD to ACS 炎癥 細胞 少量平滑肌 細胞 激活的巨噬細胞 血栓 Pathology: Coronary diseases Occlusion[?39。ns39。ni??n ] ： in USA, 71‰ in male between 3584 yrs, 22‰ in female, 1 attack in about 20 second 2. mortality： ?decreased in 30% recent 10 years ?still 1/3 of the patients died ?50% of the death occured within 1 h after the onset MI ?most deathes result from ventricular fibrillation epidemiology STEMI Cause of the decreased mortality new drug therapy ?223。zist](through not nessarily sever) atherosclerotic plaque。θr?mb?s] at the site of a preexisting [39。blockers, Statin, ACEI,aspirin clopidegrel(12m) UAP and nonSTEMI ST elevation myocardial infarction STEMI Acute Coronary Syndrome(ACS) Resting ischemia NonST elevation STelevation Unstable angina NonQ wave AMI Q wave AMI *positive serum cardiac markers * * * * occasionally variant angina ?ischemic necrosis of myocardium ?results from the prolonged myocardial ischemia ?precipitated 促成 by an occlusive[?39。k230。 ticlopidine: ADP receptor antagonists: ?Cilostazol: phosphodiesterase inhititor,50100mg bid b. Lipidlowering angents: statins c. Angiotesinconv