- The risk of ACS in patients with negative biomarkers and normal ECGs approaches 0.2%.
- Prior risk scores, such as TIMI and GRACE, provide little, if any benefit, in risk stratification for ED chest pain patients.
- The HEART score and pathway can risk stratify patients into three separate categories: low (0-3), moderate (4-6), and high score (> 7).
- Low-risk patients on the HEART pathway demonstrate likelihood of ACS that approaches < 1%, and it is easy to use in the ED.
- Risk factors, history, ECG, troponin, follow up, gestalt, patients with points 3 or 4, and research design are areas of potential weakness.
- Further improvement of the HEART pathway at this time is difficult, but in patients at moderate risk, CCTA may hold promise for evaluation of risk. This requires further study.
A cohort of 446 763 individuals including 61 460 with acute myocardial infarction was acquired. Taking any dose of NSAIDs for one week, one month or more than a month was associated with an increased risk of myocardial infarction. With use for one to seven days, the probability of increased myocardial infarction risk (posterior probability of odds ratio >1.0) was 92% for celecoxib, 97% for ibuprofen, and 99% for diclofenac, naproxen, and rofecoxib. The corresponding odds ratios (95% credible intervals) were 1.24 (0.91 to 1.82) for celecoxib, 1.48 (1.00 to 2.26) for ibuprofen, 1.50 (1.06 to 2.04) for diclofenac, 1.53 (1.07 to 2.33) for naproxen, and 1.58 (1.07 to 2.17) for rofecoxib. Greater risk of myocardial infarction was documented for the higher dose of NSAIDs. With use for longer than one month, risks did not appear to exceed those associated with shorter durations.
This ECG assessment is designed to evaluate your ability to use simply the 12-Lead ECG to make the diagnosis of a coronary artery occlusion. It uses a standardized list of 36 ECG’s from McCabe JM, et al. Physician Accuracy in Interpreting Potential ST-Segment Elevation Myocardial Infarction Electrocardiograms. J Am Heart Assoc. 2013;2:e000268.
There is obvious inferior ST elevation, with reciprocal ST Depression in aVL (inferior STEMI). There is also ST Depression in lead I. This is good evidence that the inferior STEMI is caused by an RCA occlusion. There is ST depression maximal in lead V2. Thus, there is a posterior STEMI. There is also ST depression in V5 and V6.
Where else is there evidence of STEMI?