Diagnosis
Careful clinical history, physical examination, resting 12-lead and serial EKG-marked symmetrical T-wave inversion in precordial leads, various cardiac markers. For patients unlikely to have coronary artery disease, AHRQ guidelines recommend a treadmill test without imaging, recording an EKG both during symptoms and after symptom relief; recurrent symptom or a change in clinical status; ST-elevation ACS, which requires immediate reperfusion, must be rapidly excluded.
Risk factors
Diabetes, smoking, hypertension, increased cholesterol.
Types
ST-elevation ACS is essentially the same as Q-wave infarction; non-ST-elevation ACS encompasses a broader range of disease—e.g., rest angina, new-onset angina, increasing angina, post-infarction angina, variant angina, and non-Q-wave infarction.
Early management
Bed rest, control of precipitating factors, initiation of medical therapy with IV access.
Prognosis
Most ACS patients stabilise; 10% suffer in-hospital MI; some patients die suddenly; patients with cardiomegaly and non-responders to initial medical therapy have a higher risk for subsequent cardiac events.
Clinical trials
Randomised clinical trials have provided data on the incidence of subsequent cardiac events in non-ST-elevation ACS patients with unstable angina: ESSENCE, GUSTO II, PARAGON, PURSUIT trials reported death rates between 2.9% and 4.7%, reinfarction rates of 5% to 12%, and stroke rates of 0.4% to 0.9%; other risk factors associated with adverse outcomes include male sex, older age, HTN, left ventricular hypertrophy, poor performance on exercise stress testing, and extensive disease on angiography or nuclear testing.
Antagonists
Thrombogenic stimuli (i.e., ulcerated plaques and intimal tears) can persist for prolonged periods, and the haemostatic system may remain activated for months after ACS decreased in patients treated with GP IIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban, lamifiban); agents that directly inhibit thrombin, including hirudin and bivalirudin, are being explored as alternatives to unfractionated heparin in ACS and during percutaneous coronary interventions.
Theoretical advantages
Inhibit clot-bound thrombin, decreased variability in dosing, eliminate risk of HIT and thrombocytopenic purpura.
Next generation treatments
IV VEGF (vascular endothelial growth factor), fibroblast growth factor; laser revascularisation, external counterpulsation; gene therapy with various molecules, IV GP IIb/IIIa (efficacy of these last agents has not been strong).
