Double infarct syndrome: Simultaneous subacute ST-segment elevation myocardial infarction involving the right coronary and the left circumflex arteries

Khalil A. Kaid, MD

Marc Cohen, MD: From Newark Beth Israel Medical Center, Newark, New Jersey.

Cardiology Review® Online, February 2008, Volume 25, Issue 2

Ruptured or vulnerable plaques exist not only at the culprit lesion but also in the whole coronary artery in some acute coronary syndrome (ACS) patients.Goldstein et al found features of instability of nonculprit plaques in nearly 40% of patients by angiography,1 whereas actual rupture in a remote site other than the angiographic culprit lesion was found in approximately 13% to 79% of cases when evaluated by intravascular ultrasound.

Presentation and Evaluation

A 61-year-old male smoker with history of hyperlipidemia, peripheral vascular disease, and a family history of coronary artery disease presented to the emergency room with chest pain of 2 hours duration, complicated by ventricular tachycardia requiring defibrillation. On physical examination, blood pressure was 95/75 mm Hg and heart rate was regular at 80 beats/minute. There were no abnormal findings on cardiac or other systemic examinations.


Initial electrocardiogram showed ST-segment elevations in leads II, III, aVF, and tall R waves in V1 and V2 (Figure 1). A diagnosis of ST-segment elevation myocardial infarction was made.

Figure 1. Electrocardiogram at presentation, with signs of acute inferior myocardial

infarction (ST-segment elevation in II, III, aVF, and ST-segment depression in aVL, V1-V6).

Patient management and outcome

After administering aspirin 325 mg, clopidogrel 600 mg, heparin 10,000 U bolus IV followed by 1000 U infusion, and eptifibatide double bolus infusion, the patient was referred for direct angioplasty. Coronary angiography showed a left-dominant system. There was 99% occlusion of the right coronary artery (RCA) with a Thrombolysis in Myocardial Infarction (TIMI) grade 2 (Figure 2A), and a total occlusion of the left circumflex artery (LCx) with TIMI grade 0 flow (Figure 2B). Percutaneous coronary intervention of the RCA was performed first and a 3.0 x 28-mm Cypher stent was implanted, yielding a TIMI grade 3 flow. Intervention of the LCx was then performed without any difficulty. The guidewire passed easily through the fresh occlusion and implantation of a 3.0 x 18-mm Cypher stent resulted in TIMI grade 3 flow. The patient was continued on eptifibatide for 18 more hours. A postintervention echocardiogram revealed evidence of mild mitral regurgitation (not shown).

Figure 2. 99% Occlusion of the right coronary artery (A) and 100% occlusion of the left circumflex

artery (B)


On postangioplasty day 2, the patient started developing shortness of breath. Physical examination showed bilateral rales and a new-onset holosystolic murmur radiating to the axilla. Transthoracic echocardiogram revealed an eccentric, posterior jet with moderate mitral regurgitation (not shown). Transesophageal echocardiogram revealed papillary muscle dysfunction with increasing severity of the mitral regurgitation (Figure 3A and B). There was no papillary muscle or chordal rupture. Magnetic resonance imaging showed infarction in the territory of the RCA and LCx. There was a 75% infarcted inferomedial papillary muscle and severe mitral regurgitation (Figure 4). The patient underwent mitral valve replacement, and was subsequently discharged home without any complications.

Figure 3. Transesophageal echocardiography image with a thickened and elongated

posteromedial papillary muscle (arrow) (A), and severe mitral regurgitation (B).

Figure 4. Magnetic resonance image showing

a normal anterolateral papillary muscle, and

a posteromedial papillary muscle that is 75%

infarcted (arrow).

Primary angioplasty has become the mainstay therapy for acute myocardial infarction (MI). More often than not, a single-vessel occlusion—the so-called "culprit" vessel—is present. We describe an uncommon occurrence of simultaneous occlusion of 2 major vessels treated successfully with percutaneous transluminal coronary angioplasty.


The above case is an example of the so-called "double infarct syndrome."1 It is not uncommon to find more than 1 occluded vessel; however, 1 artery is usually chronically occluded. Although rare, this phenomenon has been described previously to involve mostly the right coronary and the left anterior descending arteries.2,3 To our knowledge, this is the first described case involving the RCA and the LCx.

The rare observation of 2 or more culprit vessels is possibly due to the fact that acute MI with acute obstruction of multiple major vessels causes extensive myocardial damage, which may kill the patient before presentation to a medical facility. It has been hypothesized that the double infarct syndrome may be due to the global prothrombotic and inflammatory conditions associated with acute MI.4

It is well known in coronary intervention that during an acute MI, the "culprit" artery should be intervened upon first, with intervention on the nonculprit vessel deferred to an alternative time. In the setting of simultaneous acute occlusions, we have described successful angioplasty of 2 arteries in 1 procedure.

Moreover, this case presents yet another interesting phenomenon—ischemic mitral regurgitation. Ischemic mitral regurgitation can very often follow myocardial infarction or ischemia of the papillary muscles.

The posterior papillary muscle (PPM) in patients with right-dominant coronary arteries is supplied by the RCA 68% of the time. The terminal branches of the left circumflex system supply the PPM in the remaining percentage of patients and in patients with a left-dominant coronary system. The anterior papillary muscle is supplied primarily by the circumflex coronary arterial system.5,6

The PPM more often than not is the most likely culprit in ischemic mitral regurgitation. Either the entire muscle or one of the heads to which the chordae are attached may be ischemic. The attachments of the papillary muscles—arising from the trabeculae carneae lining and not from the heart wall—may possibly make them vulnerable to rupture.7 Partial rupture is not uncommon, and may occur up to 90 days postinfarction. Complete rupture occurs most commonly within the first 7 days after an acute event.8-12 Ischemic mitral regurgitation has a 30-day mortality of 24%.13 The treatment is usually surgical and should be employed early rather than late.