Heparin for Acute Coronary Syndrome: an evidence review

I don’t prescribe heparin in NSTEMI or unstable angina patients. However, if I for some reason felt compelled to, I would tell my patient: “We have this medicine, called heparin, that has traditionally been given to all patients with a heart attack. It will not change whether you live or die. It decreases heart attacks in the first week, but by one month there is no benefit to this medicine. The major side effect of this medicine is that about 1 in 33 people will have a problem with major bleeding, such as vomiting blood, bleeding in the brain, or requiring blood transfusions.” And assuming my doctor gave me the choice, I absolutely would not want to be given heparin if I happened to be having an NSTEMI

 Mythbusting: Heparin isn’t beneficial for noninvasive management of NSTEMI

The use of heparin for noninvasive management of non-ST elevation MI (NSTEMI) is one of the most deeply entrenched myths of modern medicine. Although heparin reduces reinfarction, when it is discontinued there is a rebound in infarction rates. Ultimately, short-term treatment with heparin delays reinfarction without having any sustained benefit.

 No More Heparin for NSTEMI?

Parenteral anticoagulation therapy did not decrease mortality in patients with NSTEMI undergoing PCI, but did have more bleeding events compared to non-parenteral anticoagulation therapy. As this is a retrospective review, which has methodological limitations, the findings of this study should be considered hypothesis generating, urging the need for RCTs. At this point in time, with no mortality benefit and increased bleeding risk, I would recommend holding off on parenteral anticoagulation therapy in UA/NSTEMI until I have had a discussion with my consultant cardiologist about their preference of anticoagulation prior to PCI.

 NSTEMI, STEMI, ACS

A lot of these treatments have been found to worsen outcomes. Let’s take a walk with old MONAH B for a bit. Morphine: Back in the day with the CRUSADE initiative, morphine was actually found to increase mortality (Meine et al). The thought is that by covering up the pain, concerning changes in patient’s presentation were muted. Furthermore, Morphine has been found to decrease the efficacy of other meds that patient should be getting (i.e. Ticagrelor) So use your clinical decision, if patient’s pain is not improved with Nitro and they continue to have inexhaustible extreme pain- then you might need to treat. Oxygen: Another no. It turns out that O2 has a paradoxical effect on the oxygenation of the heart, actually increasing coronary resistance, decreasing cardiac output and stroke volume and also causing reperfusion injury due to increase oxygen free radicals. In all good ol’ O2 has been shown to increase infarct size and possibly increase mortality risk. (Raut and Maheshwari) So, if they need it (i.e. Sats less than 90%) go ahead and give it- but be discerning because we may actually be doing harm here. Nitroglycerin: Definitely. Give this. See if it helps with pain. Give .4mg every 5 min, or go ahead and start a drip (40mcg per minute) especially if there are signs of heart failure. But remember the contraindications — not in posterior MI, not if taking phsophodiesterace inhibitiors. Aspirin: Yes. Do this. And add on Ticagrelor 180mg or Plavix for dual antiplatelet treatment. Heparin: This one does need a little bit of conversation with your cardiologist. If this patient is not going to undergo PCI- give lovenox instead. This will likely vary hospital to hospital- definitely don’t hold up PCI for the heparin but patient does need it. Beta-Blockers. Don’t give if bradycardia, CHF, reactive airway disease. But if there are no contraindications, go ahead with 25 mg oral metorprolol.

 Rapid Refresher: Non–ST-segment elevation ACS

Diagnosis is based on the presence of cardiac chest pain, ECG changes such as ST depression and T-wave inversions, and elevated cardiac biomarkers such as troponin. However, it is important to recognize that ECGs are normal in 30% to 50% of patients presenting with NSTE-ACS. Suspicion for ACS should be increased in patients with cardiac risk factors. Note that if you see ST depressions in the anterior leads, remember to order a 15-lead ECG, as there may be a concealed posterior STEMI, which would require prompt revascularization.

 ‘Let’s talk about N-STEMI, Let’s talk about Cath, baby, Let’s talk about all the good things and the bad things that may be…'

There are clear mortality benefits to emergent PCI for patients with STEMI. However, optimal treatment for patients presenting with unstable angina or NSTEMI remains controversial. Importantly, the goal of revascularization in STEMI is different then in NSTEMI/UA. For STEMI, PCI is intended to restore perfusion by eliminating an occlusive thrombus. In NSTEMI, thrombi typically are not occlusive – thus the focus of PCI is to improve long-term outcomes.

Current ED Management of Non-ST Segment Elevation MI (NSTEMI): A Practice Update

Atypical symptoms such as weakness and nausea should not exclude NSTE-ACS from differential diagnosis, especially in the elderly, diabetics and women.

How to Manage Suspected Non–ST-Elevation Acute Coronary Syndrome

In conclusion, patients who present with chest pain with low risk for ACS (eg, HEART score ≤3) and a normal troponin at 0 and 3 hours post-presentation may be discharged safely, with less than a 2 percent risk of subsequent 30-day MACE.

NSTEMI

There is insufficient high quality evidence for pre-hospital care or transport in NSTEMI. (Doesn’t mean it doesn’t help, just that we need more evidence). Much of what we do is extrapolated from STEMI care.

The DIFOCCULT Trial: Time to Change from STEMI/NSTEMI to OMI/NOMI?

Does shifting from a STEMI/NSTEMI paradigm to a new approach (ACO-MI/ non-ACO-MI) result in better identification of the patients who need acute reperfusion therapy?