Cardiac Magnetic Resonance: One Slice, Two Different LGE Patterns.

A 56-years-old man with previous myopericarditis (10 months earlier, coronary angiography not performed) was admitted because of pericarditis pain and ST segment elevation, together with myocardial necrosis markers rise. Electrocardiogram (EKG) showed negative T waves in lateral and inferior leads; echocardiogram showed mild pericardial effusion and inferior and lateral basal hypokinesis. Cardiac magnetic resonance imaging (CMRI) on day 7 post-admission showed increased T2-short tau inversion recovery (T2-STIR) signal of inferior wall and two different noncontiguous late gadolinium enhancement (LGE) areas: Ischemic-like with about 75% transmural extension (inferior wall) and subepicardial (inferolateral wall) along with pericardial LGE (inferior and inferolateral wall). Coronary angiography showed three vessel disease. Pathogenetic hypothesis of these unexpected findings are discussed. This case shows again the ability of CMRI to unreveal unusual and unexpected pathologic patterns.

A 56-year-old man with hypertension, obesity, and type 2 diabetes mellitus was admitted because of chest pain; he had a myopericarditis 10 months earlier, diagnosed by typical pericarditis pain, and ST segment elevation, together with myocardial necrosis markers rise; coronary angiography was not performed. The actual pain was exacerbated by deep breath and supine lying. Electrocardiogram (EKG) showed negative T waves in lateral and inferior leads; echocardiogram showed mild pericardial effusion and inferior and lateral basal hypokinesis; peak I Tp was 143 pg/ml and CRP 8.6 mg/dl (normal value <14 and <0.5, respectively).

Cardiac magnetic resonance imaging (CMRI) on day 7 post-admission showed inferior-basal hypokinesis, mild pericardial effusion [Figure 1], and increased T2-short tau inversion recovery (T2-STIR) signal of inferior wall: Transmural with more extensive epicardial involvement contiguous with pericardial involvement [Figure 2a]. Two different noncontiguous late gadolinium enhancement (LGE) areas were clearly shown: Ischemic-like with about 75% transmural extension (inferior wall) and subepicardial (inferolateral wall) along with pericardial LGE (inferior and inferolateral wall) [Figure 2b].

Figure 1

Four chamber cine, endsystolic frame. Mild pericardial effusion (arrow)

Figure 2

(a) Cardiac magnetic resonance (CMR) short axis. T2-short tau inversion recovery (T2-STIR): Transmural inferior myocardial increased signal (arrow), pericardial increased signal (point arrow), and epicardial increased signal (small point arrow) (b) CMR short axis. Gadolinium-enhanced late inversion recovery sequence: Inferior infarction (arrow), inferolateral myocarditis focus (point arrow), and pericardial enhancement (point arrows)

Based on these findings, a diagnosis of inferior acute myocardial infarction (AMI), along with actual pericarditis, and previous myocarditis was formulated. Coronary angiography showed ostial, proximal and mid left anterior descending artery (LAD) critical stenosis, as well as critical stenosis of proximal and distal circumflex, and 70-90% diameter stenosis of interventricular posterior (IVP) branch of the right coronary artery; a culprit lesion was not found. The following course after coronary artery bypass surgery was uneventful.

CMRI allows accurate tissue characterization by T2 weighted sequences and LGE inversion recovery sequences.

T2 weighted sequences are water sensitive: Tissue with enhanced water content (edematous or inflamed) shows enhanced signal with respect to normal water content analogous tissue, thus appearing whiter. T2-STIR sequences (T2 triple inversion recovery sequences) are T2-weighted sequences with added nulling of myocardial and fat signal, thus allowing better differentiation between normal myocardium/fat, appearing black, and enhanced water content myocardium, appearing whitish.

LGE inversion recovery sequences are obtained at least 10 min post gadolinium (Gd) injection; Gd is retained by increased extracellular space areas, such as fibrosis, necrosis and even intense inflammation.[1] Gd concentration is a function of wash-in and wash-out kinetics of the contrast into interstitial space or extracellular matrix. Gd retaining areas show increased signal (enhancement), while normal muscles appears black. Intense fibrosis areas appear white; inflammation and necrosis areas appear whitish to white. Patchy small areas or low concentration Gd areas may be unapparent on visual inspection; software-aided signal intensity computation is commonly used, but it cannot overcome method limits. T1 mapping allows signal quantification on a standardized scale of each myocardial voxel to characterize myocardial fibrosis thus can solve the problem of quantification of density fibrosis,[1] but as yet is not widely available.

Ischemic necrosis and fibrosis typically involve endocardial muscle with variable mural extension (“ischemic pattern”), while non-coronary enhancement involves intramural and epicardial muscle (“non-ischemic pattern”), occasionally but not pre-eminently involving the endocardium, thus endocardial LGE in practice is considered synonymous of ischemic necrosis.

The same considerations are valid as to T2 increased signal, endocardial localization suggesting recent intense ischemia and intramural or epicardial localization suggesting inflammation of diverse origin, for example, myocarditis. As T2 increased, signal depends on the persistence of enhanced water tissue content, when inflammation or edema resolve, T2 signal normalizes; thus allowing estimation of time course from the index episode. In practice T2 signal normalizes a few weeks after AMI, thus coexistence of T2 increased signal and ischemic LGE stays for a recent infarction, while absence of T2 increased signal stays for an infarction at least some weeks old.

The combined presentation of two different disease patterns, such as previous myocarditis and actual AMI with concomitant pericarditis, may be due to chance or to sharing of some common pathogenetic mechanism, a debate often presenting in differential diagnostics.[2] Accordingly to chance hypothesis, previous myopericarditis and actual AMI with pericarditis should be independent events; in this case the pericarditis should be considered as early post-AMI pericarditis. Early post-AMI pericarditis, however, occurs most commonly with large transmural AMI[3] and uncommonly is the initial symptom of AMI, thus this hypothesis seems not entirely convincing. Diagnostic parsimony[2] otherwise, could stimulate an alternative unifying hypothesis, albeit speculative and unproven: The recurrence of pericarditis through inflammatory mediators might have triggered the actual AMI in this patient with severe, previously undiagnosed, coronary artery disease.[456] Furthermore the increased epicardial T2-STIR signal, contiguous with pericardial involvement could suggest associated myocarditis. Myocarditis, in turn, commonly presents with chest pain[7] and is quite often associated with inducible coronary spasm,[8] which reportedly can be clinically relevant[910] and might have contributed to ischemia.

Pathogenetic hypothesis apart, obviously impossible to prove, the fact remains that this case shows again the ability of CMRI to unreveal unusual and unexpected pathologic patterns.