NSTEMI

NSTEMI differs from UA in that ischemia is severe enough to produce myocardial necrosis, resulting in release of detectable amounts of biochemical markers, primarily troponin I or T and creatine kinase myocardial band (CK-MB) from the necrotic myocytes into the bloodstream. 

Unstable Angina (UA) and Non-ST-Segment Elevation Myocardial Infarction (NSTEMI) are important situations which may cause SCD or ML Treatment is aimed at the prevention of these events, mainly by revascularization after the immediate medical treatment. In this section, the medical therapy will be separately discussed for the hospital care and posthospital discharge care. 

ACS can be classified into UA, myocardial infarction (Ml) without ST-segment elevation [non-ST-elevation Ml (NSTEMI)], or STEMI. The presence of cardiac troponin in ACS indicates worse prognosis than the absence of troponin (9). 

In the ESSENCE trial, the LMWH enoxaparin led to a relative risk reduction of 15% to 16% in the rate of death, Ml, or refractory ischemia as compared to unfractionated heparin at 30 days in UA/NSTEMI patients (38). Nadroparin [FRAXIS study (39)] and dalteparin [FRIC study (40)] did not demonstrate superiority against unfractionated heparin. Human pharmacokinetic data indicate that these differences in clinical efficacy might be explained by different elimination half-lives of antifactor Xa activity (dalteparin 2.8 hours, nadroparin 3.7 hours, enoxaparin 4.1 hours) (41). 

Several direct thrombin inhibitors have been studied in NSTEMI and STEM I patients and were compared to unfractionated heparin. In the GUSTO lib- and OASIS-2 trial (42,43), hirudin was studied versus heparin in patients with ACS. Despite early benefits, no statistical significance could be demonstrated at 30 days. Together with the OASIS-1 data, a combined analysis indicated a 22% relative risk reduction in cardiovascular death or Ml at 72 hours, 17% at 7 days, and 10% at 35 days (42). 

This grouping of clinical syndromes are compatible with myocardial ischemia, and a prompt visit to the emergency department is indicated. Electrocardiograms in the emergency department would differentiate a NSTEMI from a STEMI, the latter suggesting a greater degree of myocardial ischemia. 

Multiple biomarkers are under study. Well-studied and commercially available biomarkers include CK-MB, troponin I or T CRR and BNR and recently, myeloperoxidase, Each of these biomarkers is an independent predictor of death, myocardial infarction, or congestive heart failure. Utilizing the opus TIMI 16 patients, Sabatine et al. studied CRP BNP and troponin in 450 patients. These authors found a 30-day risk of death increased in proportion to the number of these biomarkers that were elevated at baseline (25). They validated the concept in the tactics TIMI 18 patients (26). These two trials of over 2000 patients with NSTEMI, troponin, CRR and BNP provided independent prognostic information. 

Clopidogrel STEMI (10), NSTEMI (11) Elective PCI (l 2) 300 mg loading dose (10-12) unless PCI to be performed within eight hours in which case 600 mg recommended As effective as ticlodipine in preventing stent thrombosis (9) Reduced incidence of adverse hematologic reactions compared to ticlodipine (9)... 

Glycoprotein In the case of unstable angina or NSTEMI, the preferred... 

Abbreviations ACS, acute coronary syndrome ACT, activated clotting time BP, blood pressure CTO, chronic total occlusion i.v., intravenous MI, myocardial infarction NSTEMI, non-ST-segment elevation myocardial infarction PCI, percutaneous coronary intervention RCA, right coronaiy artery STEMI, ST-segment elevation myocardial ... 

Patients with persistent angina pectoris who lack an elevated ST segment in the ECG but show an elevated blood level of troponin may have a non-STEMI ("NSTEMI ). The most frequent cause is thrombi that have moved from the larger coronary arteries into smaller branches to produce a blockage there. If neither ST segment elevation nor biochemical MI markers can be ascertained, unstable angina pectoris is present, which is initially treated with antiplatelet drugs. 

Total loss of coronary blood flow results in a clinical syndrome associated with what is known as ST segment elevation AMI (STE AMI). Partial loss of coronary perfusion if severe also can lead to necrosis as well—which is generally less severe and is loiown as NSTEMI (non-ST-elevation myocardial infarction), and other events of still lesser severity may be missed entirely or called angina, which can range from stable to unstable. 

A major determinant of mortality and morbidity is the amount of myocardial damage. With STE AMI, most of it is acute whereas with NSTEMI, it may evolve because of repetitive events over many months, thus interrupting the process improves survival. 

TABLE 44-9 Studies of BNP and NT-proBNP for Risk Assessment in UA/NSTEMI ... 

Substudy of RCT (Opus—TIMI 16) 1698 BNP 10 months RR 12.5 for mortality in highest vs. lowest quartile in NSTEMI, RR 7.9 for mortality in highest vs. lowest quartile in UA... 

Observational 405 NT-proBNP 52 months RR 5.6 for mortality above vs. below median in NSTEMI... 

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