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If there is one constant in this still rapidly evolving field, it is the major impact that the time from symptom onset to effective coronary reperfusion has in modulating patient outcome.Effective reperfusion therapy initiated within the first hour of symptom onset saves lives. Hence, whereas 65 of 1000 patients so treated are saved, this benefit declines over time, within the second hour, to 37 of 1000 patients treated. Less than half the benefit found in the first hour is achieved, if reperfusion is delayed 4 to 6 hours after symptom onset.Effective fibrinolytic therapy and percutaneous coronary intervention (PCI) are administered with antithrombotic therapy (aspirin; an antithrombin, usually unfractionated heparin or low molecular weight heparin).When faced with a patient with ST-elevation myocardial infarction (STEMI), the physician should pose the following key questions: What is the time from symptom onset to first medical contact?What is the baseline risk of the myocardial infarction, based on incorporation of the 12-lead electrocardiogram (ECG)?What is the risk of fibrinolysis?What is the time required to transport the patient and achieve PCI by a skilled operator?Percutaneous coronary intervention is superior to fibrinolytic therapy in circumstances where there is immediate access to skilled facilities and physician/health care teams. If this is not available, fibrinolytic therapy is an effective alternative, usually consisting of tPA, TNK-tPA, or rPA. Care should be exercised in balancing the risk of the myocardial infarction (MI) with the risk of fibrinolysis, paying particular attention to those with a prior cerebrovascular accident, systemic arterial hypertension, recent major surgery, and known bleeding diathesis.Overcoming undertreatment and applying reperfusion therapy promptly is likely more important than the choice of which reperfusion therapy is employed.It is essential that community hospitals develop or enhance effective communication strategies with fully equipped tertiary care centers to ensure that timely transfer of high-risk patients as well as those not responding to fibrinolytic therapy can occur.Secondary prevention after MI begins on admission and consists of pharmacologic therapy with beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, statins, aspirin, and often clopidogrel. This, plus appropriate lifestyle modifications and rehabilitation are important determinants of longer term outcome. [ABSTRACT FROM AUTHOR]

Unstable angina and non-ST-elevation myocardial infarction (NSTEMI) are usually caused by coronary artery atherosclerotic plaque fissuring or ulceration with subsequent transient and repetitive thrombosis and vasoconstriction with unstable angina, and slightly more prolonged but still transient or subtotal coronary artery occlusion and vasoconstriction in the patient with NSTEMI.Patients with increased serum levels of C-reactive protein (CRP) or of a troponin should be referred for coronary arteriography and percutaneous coronary intervention (PCI) or surgical revascularization when their coronary artery anatomy is appropriate. Recent data suggest referral for PCI or coronary artery bypass graft (CABG) is also appropriate for patients with elevations of multiple serum biomarkers, for example, CRP, troponin, and brain naturetic peptide (BNP) and for those with elevated Thrombosis in Myocardial Infarction (TIMI) risk scores (three or more of the following: age of 65 years or older, at least three risk factors for coronary heart disease, prior coronary artery stenosis of 50% or greater, ST segment deviation on the electrocardiogram (ECG) on presentation, at least two anginal events in prior 24 hours, use of aspirin in prior 7 days, and elevated serum cardiac markers).Recent studies have suggested that many patients with these coronary artery syndromes have coronary arterial plaque inflammation and a vulnerable atherosclerotic plaque(s).Initial medical treatment of these acute coronary syndromes includes aspirin, heparin (either low molecular weight or unfractionated), clopidogrel (Plavix), and a betablocker if blood pressure or heart rate are elevated. A platelet glycoprotein IIb/IIIa inhibitor is added in those with continuing angina at rest or in those with known or suspected complex coronary anatomy and in the diabetic patient undergoing PCI. Angiotensin-converting enzyme (ACE) inhibitors and beta-blockers are added to the acute and chronic medical management regimen when there are no contraindications. [ABSTRACT FROM AUTHOR]

Atherosclerotic plaque fissuring or ulceration generally cause the development of the acute coronary artery disease syndromes.Vulnerable or "unstable" atherosclerotic plaques have temperature and pH heterogeneity, thin fibrous caps, inflammatory cells primarily macrophages, and activated T cells on their surface, and an adjacent lipid pool. Some patients have multiple unstable atherosclerotic plaques simultaneously.Several serum markers when elevated help identify patients at increased risk for future vascular events, including C-reactive protein (CRP), CD40SL, pregnancyassociated protein, serum amyloid protein (SAP), brain natriuretic peptide (BNP), vascular cell adhesion molecule (VCAM), intracellular adhesion molecule (ICAM), and interleukin-6.Unstable angina and non-ST segment elevation myocardial infarction (NSTEMI) are associated with atherosclerotic plaque fissuring or ulceration, adherence of platelets at the same sites, the accumulation of thromboxane A2, serotonin, adenosine diphosphate (ADP), thrombin, tissue factor, oxygen-derived free radicals, and endothelin promoting growth of the thrombus and dynamic vasoconstriction with transient (unstable angina or NSTEMI) or permanent coronary artery occlusion (ST segment elevation MI, STEMI).The functional absence or diminished effect of nitric oxide (NO), tissue-type plasminogen activator (t-PA), and prostacyclin at sites of vascular injury contributes to dynamic thrombosis, vasoconstriction, fibroproliferation, and inflammation at sites of coronary artery atherosclerosis and plaque fissuring and ulceration.Unstable angina, NSTEMI, and STEMI represent a continuum of thrombosis and vasoconstriction in that unstable angina is often caused by transient and recurrent coronary artery thrombosis and vasoconstriction, NSTEMI by slightly more prolonged but still usually transient thrombosis and vasoconstriction or subtotal coronary artery occlusion, and STEMI by prolonged and usually permanent coronary artery occlusion.Power failure complications of MIs occur in patients with ≥40% irreversible damage to the left ventricle (LV) and include cardiogenic shock, medically refractory congestive heart failure (CHF), and medically refractory arrhythmias.Even with relatively small MIs, mechanical problems, such as acute mitral regurgitation (MR), ventricular septal defects (VSDs), and ventricular aneurysms may lead to shock and CHF. [ABSTRACT FROM AUTHOR]