By Jim Upchurch
Our cardiology colleagues are a clever bunch.
There is a long list of amazing acronyms they have crafted for their numerous clinical trials, such as (to name just a few):
- ACME: angioplasty compared to medicine
- BATMAN: batimastat SV stent versus balloon angioplasty for the reduction of restenosis in small coronary arteries
- COOL MI: cooling as an adjunctive therapy to percutaneous intervention in patient with acute myocardial infarctions.
You can find more research acronyms here. Who said cardiologists don’t have a sense of humor?
But seriously, what is most amazing is the national and international cooperation in many of these cardiac clinical trials. This creates huge numbers of patients that increase the validity of the study findings and produces treatment recommendations at a faster pace than many other medical research fields. Good for the patient but tough on the provider trying to keep up with the rapid evolution of cardiac care.
So we’ll slow down a bit and turn to some clinical trials that are oldies but definitely goodies; but first some definitions and clarifications. As you recall, the triad of Acute Coronary Syndromes (ACS) is to be considered when your patient presents with the complaint of chest pain that you think might be coming from the heart. These include ST elevation myocardial infarct (STEMI), Non-ST elevation MI (NSTEMI) and Unstable Angina (UA). The goal is early recognition of which one of the three is occurring in your patient; this will direct further treatment. STEMI requires opening the completely plugged artery with intravenous fibrinolytics or percutaneous coronary intervention. For the NSTEMI (which used to be called a non-Q-wave MI) or UA, the problem is an incompletely obstructed coronary artery and the goal is to minimize the potential for further blood clot growth or development.
This is accomplished by making platelets less likely to stick together and inhibiting the clotting factors that produce the fibrin that sticks to the platelets that forms a web that catches the red blood cells forming a clot; that clot being useful if you need to control unwanted blood loss but potentially damaging if it is forming in your coronary artery. Treatment is initiated in the field with aspirin and continued in the receiving facility with other platelet inhibitors such as clopidogrel and glycoprotein IIb IIIa inhibitors and the use of heparin to block the clotting factors. At some point, most patients will have an angiogram to determine the extent of coronary artery pathology and need for further intervention.
If you are capable of obtaining a electrocardiogram (ECG) in the field, then the absence of ST segment elevation will tilt you toward a NSTEMI or UA. However, in the absence of an ECG there are other determinants to help elevate your suspicion that this chest pain is of cardiac origin; but of course while you ponder, you are providing the patient with aspirin, oxygen, nitroglycerine if no contraindications are present as well as timely transport.
The Thrombolysis in Myocardial Infarction (TIMI) trial from 1996-1998 and the Efficacy and Safety of Subcutanous Enoxaparin in Unstable Angina and Non-Q-Wave MI (ESSENCE) trial from 1994-1996 produced the research data for the development of the TIMI risk score in 2000.
The TIMI risk score is comprised of seven items that help determine a patient’s risk of ischemia and death from a NSTEMI or UA.
- Patient age 65 or older (1 point)
- Three or more cardiac risk factors (1 point)
(Family history, HTN, Elevated cholesterol, DM, active smoker) - Known coronary artery disease (1 point)
- Aspirin use in the past 7 days (1 point)
- Chest pain in the past 24 hours (1 point)
- Elevated Cardiac Markers (1 point)
- ST segment deviation > 0.5mm (1 point)
As the points pile up so does the risk of ischemia, MI or death.
Interestingly, five of the seven risk factors can be obtained by talking to the patient — that’s right, taking a history. Add one point if you have field ECG capability and observe ST segment changes. You may even have a microlab in your rig that can measure the cardiac markers troponin and creatine kinase (CK MB), but if not the receiving facility can add that piece of the puzzle. Troponin and CK MB are proteins normally contained within cardiac muscle cells, and when those cells are injured or die, they release troponin and CK MB which can then be detected in the blood.
The TIMI risk score may also be useful in patients who present atypically with their ACS. These patients may not have chest pain but describe chest pressure, ache or burning; or have no chest discomfort but complain of pain in the back, abdomen, shoulder or neck; or even no pain at all but report recent onset of one or more of the following symptoms: fatigue, dyspnea or shortness of breath, dizziness, or diaphoresis (sweating).
As you can tell, even if you collect only a portion of the seven TIMI risk score components, the information is useful to you in determining the patient’s risk that something cardiac is going on with their chest pain or atypical presentation. In addition, the data you collect is foundation information that will be built upon by the receiving facility.
References
1. Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA. 2000;284:835–42
2. www.timi.org
