Late Gadolinium Enhancement of the Anterolateral Papillary Muscle in a Patient With Acute Myocardial Infarction, Atrial Fibrillation and Hypertrophic Cardiomyopathy

Papillary muscle (PM) fibrosis is most commonly secondary to coronary atherosclerosis [1]. The anterolateral papillary muscle (ALPM) is less prone to infarction due to its dual blood supply. Hypertrophic cardiomyopathy (HCM) is an uncommon cause of PM fibrosis, with late gadolinium enhancement (LGE) of PM seen in only 6% of HCM patients during cardiac magnetic resonance (CMR) imaging [2]. We report a case of a patient presenting initially with acute myocardial infarction (AMI) and later found to have HCM and ALPM LGE.

A 43-year-old Chinese male with no past medical history presented with palpitations and acute chest pain. Apart from tachycardia, vital signs and physical examination were unremarkable. A 12-lead electrocardiogram showed rapid atrial fibrillation (AF) and right bundle branch block. High-sensitivity cardiac troponin I was 87 ng/L (reference range: 0–18 ng/L), rising to 1874 ng/L 8 hours later, consistent with a diagnosis of AMI. Coronary catheterisation revealed severe distal left circumflex artery (LCx) and moderate proximal right coronary artery (RCA) stenoses (Fig. 1). The left anterior descending artery (LAD) only had minor luminal irregularities. Notably, the first diagonal (D1) and first obtuse marginal (OM1) arteries were disease free and had early take-offs. Percutaneous coronary intervention was performed to the distal LCx with a drug-coated balloon. The moderate RCA lesion was not haemodynamically significant and was conservatively managed.

Fig. 1
Coronary angiogram. A: AP caudal view showing severe stenosis of the distal left circumflex artery. B: RAO cranial view showing minor irregularities in the left anterior descending artery. AP, anteroposterior; RAO, right anterior oblique; LCx, left circumflex artery.

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Transthoracic echocardiography was done three days into admission. It showed normal ejection fraction, no regional wall motion abnormalities and only trivial mitral regurgitation without mitral valve prolapse (MVP). However, there was severe concentric left ventricular hypertrophy (LVH) and mild systolic anterior motion of the anterior mitral leaflet with a resting mid-cavitary gradient of 11 mm Hg, raising the suspicion of HCM. CMR, done five months after the initial presentation, showed asymmetrical LVH in the basal-to-mid anterior, anteroseptal and mid-inferoseptal walls with a maximal wall thickness of 24 mm. Diffuse mid-wall LGE typical of HCM was present particularly in areas of LVH and the inferior right ventricular insertion point. Hypertrophy of the ALPM with associated focal LGE was seen (Fig. 2).

Fig. 2
Representative steady-state free precession (top row) and corresponding delayed gadolinium enhancement images (bottom row) obtained during cardiac magnetic resonance in the basal short axis (A and B), mid short axis (C and D) and 2-chamber (E and F) views demonstrating asymmetrical septal hypertrophy particularly in the basal antero-septum with patchy areas of mid wall delayed gadolinium enhancement in the thickened myocardium (asterix) as well as the antero-lateral papillary muscle (arrows).

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We report a case of ALPM LGE in a patient presenting with AMI, AF and HCM. This case presents an imaging diagnostic challenge as there may be several reasons for the finding. AMI with associated ALPM infarction may be possible. However, studies employing superselective contrast injections during studies employing superselective contrast injections during coronary bypass demonstrated that the ALPM had dual blood supply from the LCx (typically OM1) and LAD (typically D1) 71% of the time, with the remaining having single-vessel supply from either OM1 or D1 [3]. As such, cases of ALPM rupture following anterolateral AMI from OM1/D1 occlusion are rarely reported. Even if our patient had the uncommon single-vessel supply variant, his culprit vessel was the distal LCx which does not supply the ALPM. Notably, both his OM1 and D1 branches were free of disease.

Given the presence of AF, cardio-embolism to the ALPM’s blood supply vessel may be possible. However, we did not observe infarct pattern LGE over multiple coronary territories, which would be expected with cardio-embolism from AF [4].

HCM is associated with PM abnormalities such as hypertrophy, anteroapical displacement and anomalous insertion [5]. Specifically, ALPM dysfunction can occur secondary to mid-septum thickening [1]. Myocardial LGE is typically inhomogenous, patchy and involves the most hypertrophied segments [6]. Limited existing literature suggests that patchy PM LGE indicating interstitial fibrosis can be seen in 6% of patients [1, 2]. Other causes of PM fibrosis include shock, infective endocarditis, acute valvular regurgitation, anaemia, left ventricular outflow tract obstruction, and anomalous origin of coronary arteries from the pulmonary arteries [1], all of which were not present in our patient. Although it is well known that LGE burden in HCM correlates with arrhythmic risk, the prognostic implications of having PM LGE are unknown. Extrapolating data from other causes of PM fibrosis such as MVP and mitral annular disjunction, PM LGE was significantly associated with development of ventricular arrhythmias [7].

In summary, HCM associated PM LGE is a rare finding. PM infarct from coronary stenosis and cardio-embolism are possibilities, but less likely in our patient. Cardiac imagers should be aware of this finding which may have added prognostic implications.