Could perivascular inflammation detected by CMR and CT be associated with acute myocardial infarction in a heart transplant patient?

Description of Clinical Presentation: A 30-year-old female with a history of orthotropic heart transplant in 2017, presented in December 2023 with nausea, vomiting and palpitations. Bloods revealed elevated CRP (113 mg/L) and WBC (11.4 10⁹/L), and was treated empirically as infection. ECG showed complete heart block and 2D echocardiography revealed an impression of overall borderline low systolic function (EF~50%). As troponin T was elevated (934ng/L, Normal = 11ng/L), the patient was scheduled to have invasive coronary angiography. This revealed occlusion of the mid right coronary artery (RCA) for which percutaneous intervention (PCI) was performed.

Diagnostic Techniques and Their Most Important Findings: The patient had CMR scans at 4 and 8 months following the PCI, to assess ventricular function and myocardial viability. The CMR scans showed partial thickness infarct in the RCA territory, preserved left ventricular systolic function, and increased native myocardial T1.

In addition, the CMR demonstrated increased signal intensity in the RCA perivascular fat on the STIR sequence and T2 mapping with lack of fat suppression in this region. The T2 time in the RCA perivascular fat was prolonged (160ms) compared to the epicardial fat elsewhere (54ms) . Additionally, there was post contrast enhancement in the RCA perivascular fat on the T1 mapping sequence (Figure 2d).



Although, no CMR scan was performed before the acute event, a CCTA scan from 8 months earlier revealed increased fat attenuation (35 HU) around the RCA with normal value (-103 HU), 24 months earlier.

Learning Points from this Case: CMR scans are now increasingly being performed in patients post heart transplantation with myocardial T1 and T2 mapping to exclude rejection.⁵ This provides an opportunity to assess the perivascular tissue for changes in signal intensity and, T1 and T2 times multi-parametric mapping sequences, that may represent oedema and thus PVI.

This picture demonstrates the patient's first presentation with acute MI, pre and post PCI is shown
This picture is a collective of the CMR findings of the RCA perivascular inflammation, as shown to have high signal in the STIR and T2 map, suppression on T1 sequence enhancement in the T2 post contrast
this picture shows the incresed RCA perivascular fat in a CCTA done 8 months before the acute MI compared with normal RCA perivascular fat in a CCTA done 2 years prior (both are done as a routine follow up and the patient had no symptoms at time)