Cardiac MRI in Identifying Myopericarditis Mimicking STEMI in a Patient with HIV: A Case Report

Introduction

Myopericarditis is an underrecognized cardiac complication in people living with HIV (PLWH), particularly in those with untreated or advanced disease. Although subclinical myocardial and pericardial involvement is frequently observed, clinically overt myopericarditis remains uncommon and diagnostically challenging due to its overlap with acute coronary syndromes (ACS) [1,2]. This overlap, especially in electrocardiographic findings, can lead to misdiagnosis, unnecessary invasive procedures, and delayed targeted therapy.

In untreated HIV patients, acute myopericarditis carries added risk due to impaired immune surveillance, higher viral loads, and coexisting opportunistic infections. Moreover, progression to HIV-associated cardiomyopathy (HIVAC), a stage IV AIDS-defining illness, remains a serious consequence of missed or delayed diagnosis [1].

This report presents a diagnostically complex case of myopericarditis mimicking ST-elevation myocardial infarction (STEMI) in a patient with untreated HIV. Despite ST elevations prompting activation of a STEMI protocol, advanced imaging ultimately revealed an inflammatory rather than ischemic etiology. The case underscores the value of cardiac magnetic resonance imaging (CMR) in differentiating ACS from inflammatory pathology, and highlights the importance of high clinical suspicion and a multidisciplinary approach in managing cardiac presentations in PLWH.

Case Report

A 62-year-old white man with a history of untreated HIV, heart failure with reduced ejection fraction (HFrEF), apical LV thrombus, hypertension, and prior pontine stroke presented with chest pressure and progressive dyspnea over 3 days. The pain was a pressure sensation in the mid-chest radiating to the jaw and upper back, intermittent and not related to physical activity. He denied positional changes in pain character or intensity. His social history included homelessness, active substance use (fentanyl and methamphetamine), and noncompliance with antiretroviral therapy (ART). Initial pre-hospital ECG showed ST-segment elevations in the inferolateral leads, prompting STEMI code activation and administration of aspirin and nitroglycerin. Upon arrival to the emergency room (ER), examination revealed bilateral air entry with crackles in the right upper lobe. Cardiac examination demonstrated displaced apical impulse, no murmur, rubs or gallop, minimal pedal edema, and absence of jugular vein distention.

Initial lab work showed leukocytosis, mild anemia, thrombocytosis, and elevated high-sensitivity troponin T at 25 ng/L. Chest radiography noted right apical opacity and cardiomegaly. ECG showed sinus rhythm, rate 102/m, normal axis, borderline QRS, and widespread ST elevations in II, III, aVF, and V4–V6 (Figure 1). Differentials included acute coronary syndrome (STEMI), aortic dissection, acute myopericarditis, acute-on-chronic systolic heart failure, pulmonary embolism, and pneumonia. Cardiology was consulted and review of the ECG noted no distinct reciprocal changes and PR segment elevation in aVR, raising suspicion of pericarditis. However, given the patient’s HFrEF history and chest pain that was atypical for pericarditis, the risk of missing STEMI outweighed left heart catheterization (LHC) risks. Therefore, the STEMI code was activated and the patient was taken to the cardiac catheterization suite.

LHC revealed multivessel coronary disease: left anterior descending (LAD) proximal-to-mid 80% stenosis at bifurcation, first diagonal with ostial 80% stenosis, mid 50% stenosis left circumflex (LCX), and proximal 50% stenosis in the right coronary artery (RCA). TIMI-3 anterograde flow was noted in all vessels, without acute flow-limiting thrombotic occlusion, which can require immediate percutaneous intervention (PCI) (Figure 1; Videos 1, 2). Transthoracic echocardiography (TTE) displayed global LV hypokinesis (EF 24%) and moderate pericardial effusion without tamponade physiology (Figure 3; Videos 3, 4). A multidisciplinary team approach with interventional cardiologist, general cardiologist, internist, and infectious disease (ID) specialist was undertaken. The patient was non-compliant with ART as evidenced by CD4 count 187 and viral load 61 000 copies/ml. Revascularization as staged PCI has its own risks, including type 4 MI. Therefore, the decision to proceed with revascularization would depend on the patient’s symptoms, medication compliance, substance abstinence, and follow-up. Hence, dual anti-platelet therapy, high-dose statin, and GDMT were initiated with future evaluation for LAD/diagonal angioplasty based on close out-patient follow-up. Pericardial effusion workup was recommended. Pericardiocentesis was considered but deemed too high-risk, as non-invasive modalities could guide treatment. Cardiac magnetic resonance imaging (CMRI) was chosen as the next diagnostic step.

CMRI showed elevated T1 myocardial time, mild fibrosis, and subclinical edema suggesting myocarditis, dilated LV with end-diastolic volume index (EDVI) of 108 ml/m2, LVEF 17%, and normal indexed RV with EF 33%. Normal T2 time was noted and the lack of late gadolinium enhancement ruled out ischemic heart disease (IHD) (Figure 4). The myopericarditis diagnosis was confirmed. Given the patient’s geographic residence in the southwestern United States, where Coccidioides species are endemic and have been associated with cardiomyopathy, the infectious disease (ID) team requested serum coccidioidomycosis titers in addition to a viral panel and tuberculosis workup to evaluate for potential co-infections contributing to his presentation. He was discharged on colchicine and ibuprofen per acute pericarditis guidelines. Aspirin and high-dose statin continued for underlying CAD along with GDMT for HFrEF, along with resumption of ART and prophylactic treatment of opportunistic infections (Figure 5; Video 5).

Discussion

Cases of myopericarditis mimicking STEMI in ART-naïve HIV patients are exceedingly rare. A 2018 case series by Peters et al [3] described 3 patients presenting with inferolateral ST elevations who were found to have myocarditis on CMRI, but none had multivessel coronary disease on angiography. Unlike those reports, our patient’s concomitant non-occlusive coronary stenoses and substance use disorder added diagnostic ambiguity, underscoring the uniqueness of this presentation. People living with HIV-1 infection (PLWH) have increased cardiovascular disease risk [4]. PLWH present with CAD at about 10 years younger than those without HIV [4]. When adjusting for ASCVD risk factors, PLWH have a 1.5-fold to 2-fold increased CAD risk [4]. This risk persists with ART, and cardiovascular disease (CVD) remains the leading cause of mortality in PLWH [5]. When presentations overlap, differentiating between the 2 conditions is crucial, as their management differs. Our patient’s pressure-like pain without positional changes suggested ACS rather than myopericarditis, which typically presents with pleuritic pain improving when sitting up.

The pathogenesis of myopericarditis in HIV involves direct viral invasion, immune-mediated injury, and opportunistic infections converging to inflame myocardial and pericardial tissues. In our patient, untreated HIV with high viral load and CD4 suppression likely intensified cytokine-driven damage (via gp120/Tat pathways), chronic inflammation, and autoantibody formation, manifesting as diffuse inflammation rather than focal ischemia [6–9]. Immune activation by microbial translocation due to impaired intestinal barrier function in HIV infection has been proposed; however, its influence on HIV-associated myopericarditis remains unclear [10]. Recognizing these mechanisms explains the global hypokinesis on echocardiography and the absence of regional wall-motion abnormalities typical of coronary occlusion.

CMR is the standard imaging modality for diagnosing myopericarditis. The American College of Cardiology and American Heart Association recommend CMR with gadolinium contrast for patients with acute chest pain and myocardial injury with nonobstructive coronaries, helping distinguish myopericarditis from conditions like myocardial infarction with nonobstructive coronary arteries (MINOCA) [11]. CMR also provides prognostic information, identifying myocardial involvement extent, with late gadolinium enhancement patterns indicating higher risk, while negative CMR suggests a favorable prognosis [12]. CMR findings of elevated native T1, subclinical edema, and diffuse pericardial enhancement confirmed inflammation and ruled out infarction in our patient. Pericardiocentesis is not a diagnostic tool for myopericarditis; it is reserved for therapeutic drainage of significant pericardial effusions causing hemodynamic compromise (eg, tamponade) or for fluid analysis in suspected infectious or malignant pericarditis. It does not provide information about myocardial inflammation or fibrosis and is not recommended for routine evaluation of myopericarditis.

Biomarker evaluation in this case could have been strengthened by calculating a CRP/troponin ratio. A CRP/troponin ratio >250 suggests myopericarditis, while >500 may confirm diagnosis [13]. In emergency settings, integrating rapid CRP assays with ECG patterns (lack of true reciprocal changes, PR segment deviations) can expedite differentiation and guide early CMRI utilization. Treatment with NSAIDs and colchicine followed ACC pericarditis guidelines to suppress inflammation and prevent recurrence. Corticosteroids are not a first-line treatment and are used only when NSAIDs are contraindicated or first-line therapy fails. While anti-platelet therapy and statins are not typically recommended, our patient received aspirin and high-dose atorvastatin due to underlying CAD. Finally, ART resumption and opportunistic infection prophylaxis targeted the root cause of HIV-driven immune dysregulation.

Conclusions

This case highlights the challenge of distinguishing acute myopericarditis from STEMI in ART-naïve HIV patients, where overlapping symptoms and ECG findings can lead to unnecessary invasive procedures. Cardiac magnetic resonance imaging proved critical, confirming inflammation through elevated native T1, diffuse pericardial enhancement, and absence of ischemic late gadolinium uptake. Accurate diagnosis is essential for appropriate therapy and preventing HIVAC. Future research should investigate early CMR and biomarker-driven diagnostic algorithms, and refine management guidelines for HIV-associated cardiac inflammation.