#4 - Knowing What to Expect from an Anterior versus Inferior Wall Myocardial Infarction

Inferior Wall MIs Don’t Get Systemic Emboli

Figure of a Subtle IMI with only slight inferior ST elevation.

The last several posts have discussed the differences in the clinical course of acute inferior wall Mis (IMI) vs. anterior wall Mis (AWMI). The point is to know what to expect so that you can look for other causes if the clinical course is not as expected. Those posts have addressed hypotension, heart rate and pulmonary edema. This post addresses systemic emboli.

The incidence of left ventricular thrombus and systemic emboli after an acute MI has decreased with the advent of thrombolytic therapy and acute angioplasty and because of the use of anticoagulants and platelet inhibitors. Nevertheless, the prevalence of LV thrombi after a completed, “high risk” AWMI remains between 3 and 9%.(1) High risk is generally defined as an AWMI with wall motion abnormalities and/or an ejection fraction of <40%. The prevalence of LV thrombi also depends on when the echocardiogram was performed with fewer thrombi being detected if the echo is done within 5 days of the infarct.(1) That means that if no observed LV thrombi are seen early after the infarct, they may develop later. Systemic emboli can occur after AWMI’s from LV thrombus especially when there are severe wall motion abnormalities. Systemic emboli are unusual after an IMI, and if they occur, should prompt an examination for other sources such as an atrial septal defect with paradoxical emboli. “Paradoxical emboli” refer to emboli originating in the venous system, that cross to the arterial side of the circulation via an atrial septal defect.

The 2013 guidelines for managing acute MIs state that “Anticoagulant therapy may be considered for patients with STEMI and anterior apical akinesis or dyskinesis”, (2) but this is a Level II B recommendation with a level of evidence of C, so not a strong recommendation. Nevertheless, I have a low threshold for starting oral anticoagulation in patients with a completed AWMI and wall motion abnormalities, even if their echo soon after the event did not show a thrombus. That’s because of the rule that “one stroke ruins your whole day if it’s yours” and because the thrombus may develop later after the echo. This decision depends on multiple factors including the individual patient’s risk of bleeding from the therapy. I prefer factor Xa inhibitors over coumadin for this purpose. There are not yet conclusive studies that factor Xa inhibitors work for LV thrombi, but they probably do (3) and they work quicker with less intracerebral bleeding risk than warfarin. The treatment should be for only 3 months.

The rule – Consider other, non-cardiac sources of the embolus in a patient with an IMI and have a low threshold for briefly anticoagulating a patient with a completed AWMI.

1. Shavadia, JS. et al. Outcomes and Prognostic Impact of Prophylactic Oral Anticoagulation in Anterior ST-Segment Elevation Myocardial Infarction Patients With Left Ventricular Dysfunction. J Am Heart Assoc. 2017 Jul 3;6(7):e006054. PMID: 28673899.

2. O’Gara PT, et.al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. JACC. 2013;127(4):e362-425. PMID: 23247304

3. Pradham A, et. Al. Anticoagulation for Left Ventricle Thrombus—Case Series and Literature Review for Use of Direct Oral Anticoagulants. J Cardiovasc Dev Dis. 2023 Jan 23;10(2):41. PMID: 36826537

#myocardialinfarction #cardiology #medicine #inferiorwallMI #anteriowallMI #heartattach #heart attackcomplications #stroke #emboli

Francis Kiernan, my colleague at Hartford Healthcare, provided advice for this post.