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Invasive Management of Acute Coronary Syndrome - 10/11/2012

posted Oct 11, 2012, 7:56 AM by Rohit Das   [ updated Dec 27, 2012, 6:44 AM by Purnema Madahar ]

At intern report today, one of our sub-interns presented a case of a woman who had an inferior wall myocardial infarction (MI), complicated by 2nd degree AV-block and hemodynamic compromise. Overall it was a very interesting case. MI is an extensively studied, vast topic that I cannot possibly summarize adequately in this daily. However, I did want to touch a bit upon the literature that help to answer a central question in acute management of MI – when should we send patients to the CASH lab?

As a quick overview, the term acute coronary syndrome (ACS) is applied to any patient in which myocardial ischemia is suspected. Within ACS, there exists a spectrum of diagnoses, which I’m sure you all know – ST elevation MI (STEMI), non-ST elevation MI (NSTEMI), and unstable angina (UA). They each have their own definitions, and occur with relatively equal frequency – approximately 30%, 25%, and 40% respectively. These distinctions are also important for management reasons, particularly for invasive intervention.

For patients with NSTEMI/UA, an important part of their evaluation includes early risk stratification. The most widely used tool to do this is the “TIMI risk score,” a clinical prediction tool developed at the Brigham by Antman et. al., in 2000. Let’s go over some of the important details of this paper (attached):

·         The TIMI risk score was devised from a cohort of 1957 patients from the TIMI 11B trial, a study in which patients with NSTEMI/UA presented within 24 hours of symptom onset, received standard medical therapy, and then randomized to either unfractionated heparin or LMWH (Enoxaparin in this study). The primary outcome in this study was a composite of all-cause mortality, recurrent MI, or recurrent ischemia that required revascularization. The cohort used was the unfractionated heparin group.

·         Multivariate regression models were then used to identify certain dichotomous variables as predictive for the above composite outcome – the summary of these findings are depicted in Table 1. The score was then validated in the other arm of the TIMI 11B Trial, as well as both arms of the “ESSENCE” trial – another phase III trial for LMWH in NSTEMI/UA (Figure 2). Figure 1 has some interesting numbers – the rate of the primary composite outcome was ~5% in patients with the lowest TIMI scores, and as high 40% in patients with the highest TIMI scores.

·         Subsequent studies have shown that the TIMI score also correlates with severity of angiographic disease (an analysis from the PRISM-PLUS study), and predicts benefit from early invasive intervention (TACTICS-TIMI 18 study). Recent analyses have also shown that elevated cardiac enzymes and the degree of ST segment deviation are independent predictors of poor outcome.

So, in summary, the TIMI risk score is a relatively well studied clinical prediction tool that predicts prognosis and benefit from invasive intervention. Keep it in the back of your mind when you encounter your UA/NSTEMI patients…though I’m sure it’s in that red book…

Moving on to STEMI…the management of this beast is quite different, with a clear emphasis on invasive intervention ASAP. Studies have clearly shown that PCI is better than fibrinolysis, that benefit is best attained with a less than 90 minute “door to balloon” time, and that patients gain the most bang for their buck if presenting within <12 hours (ideally <3 hours) after symptom onset. So, I’ll focus on a much less defined, from an evidence standpoint, topic – management of STEMI with a delayed presentation (i.e., >12 hours).

Approximately 10-30% of STEMI patients have a delayed presentation. This is more common with elderly, female, and/or diabetic patients who have more atypical symptoms, and not the typical angina that brings patients to the ED more expediently. Importantly, in most of the primary PCI trials, patients with a delayed presentation were EXCLUDED, and the true benefit of PCI >12 hours after onset is not known. Though observational trials have suggested a benefit, randomized trials have only shown an improvement in left ventricular function, but NOT hard clinical outcomes. Let’s go over the largest of these trials – the Occluded Artery Trial (OAT; attached), published in the NEJM in 2006.

·         The OAT study recruited around 2200 stable patients who, 3-28 days after having a STEMI, were found to have a completely occluded infarct-related artery (IRA) – which happens in over 90% of patients with a STEMI - and met criterion for increased risk for adverse events. They were then randomized to PCI or no PCI, along with standard medical therapy.

·         The investigators looked at a composite outcome of all-cause mortality, reinfarction, or heart failure symptoms requiring admission to a CCU. Though a subgroup analysis did show that PCI, at repeat angiography in 1 year, lead to a higher prevalence of IRA patency as compared to the no PCI group (not really surprising), there was no overall difference in the 4-year cumulative event rate between the two groups. 

·         Based on the OAT study, as well as other related randomized trials, the ACC/AHA strongly recommend AGAINST late PCI of a totally occluded IRA. However, since most of the randomized trials for late PCI have been in patients presenting >24 hours after onset, the therapeutic benefit of PCI presenting 12-24 hours after onset is not as well defined.

Well…there's a lot of literature on this topic, but I think the two summarized above are some key ones to be familiar with. Have a good weekend…and oh yeah…KEEP READING!!


The TIMI Risk Score for Unstable Angina/Non-ST Elevation MI
Antman et. al., JAMA 2000, Volume 284 (7): 835-42

Hochman et. al., NEJM 2006, Volume 355 (23): 2395-407