Cardiac Multimodality Imaging Assessment of Dystrophic Myocardial Calcification in a Human Immunodeficiency Virus-Infected Patient With Dilated Cardiomyopathy

Abstract

Dystrophic myocardial calcification represents the sequelae of local tissue damage and cellular necrosis. We present the case of a 72-year-old man who presented with exertional chest pain. He had a medical history of human immunodeficiency virus (HIV) infection and chronic dilated cardiomyopathy with severe left ventricular (LV) systolic dysfunction and wall motion abnormalities at the inferior and lateral LV walls. A cardiac magnetic resonance (CMR) examination from 16 years ago showed a subendocardial late gadolinium enhancement (LGE) distribution consistent with prior myocardial infarction (MI). Recently, a pharmacological stress myocardial perfusion imaging by CMR had been positive for myocardial ischemia in the left descending coronary artery (LAD) territory. A cardiac CT angiography (CCTA) showed non-significant LAD obstruction <50% consistent with microvascular ischemia and the presence of dystrophic myocardial calcification as an unusual progression of a prior MI. Conservative approach and optimal medical therapy were employed in our patient, and there was no symptom progression during the two-month follow-up period.

Keywords: cardiac multimodality imaging; dystrophic myocardial calcification; hiv-infection.

Figure 1. 12-lead electrocardiogram of the patient

Figure 2. Transthoracic echocardiography findings of the patient

Two-dimensional left ventricular apical views at the A: four-chamber view, B: two-chamber view, and C: three-chamber view. D: bullseye map of left ventricular global longitudinal strain. E: three-dimensional echocardiography evaluation of left ventricular volumes and ejection fraction

Figure 3. Pharmacological stress myocardial perfusion imaging by CMR using dipyridamole

A: left ventricular short-axis views from base to apical segments in stress (upper left) and rest (bottom left) showing permanent perfusion defect at the inferior, inferolateral, and lateral left ventricle from base to apex (white arrows) and reversible perfusion defect at the mid-inferoseptal, anteroseptal, and septal apical segments (red arrows). B: cine steady-state free precession short-axis images during systole in stress (upper right) and rest (bottom right) denoting a very thinned and akinetic motion at the inferior, inferolateral, and lateral left ventricle from base to apex (orange arrows) CMR: cardiac magnetic resonance

Figure 4. Coronary CT angiography findings of the patient

A: left descending coronary artery; B: circumflex coronary artery; and C: right coronary artery with a diffuse multi-vessel disease with calcified and non-calcified plaque burden CT: computed tomography

Figure 5. CMR and CT findings

A: cardiac magnetic short-axis images showing the progression over 16 years, of the evolution of an extensive myocardial infarction with subendocardial LGE distribution (orange arrows), and a non-ischemic patchy intramyocardial LGE at the basal inferoseptal level (yellow asterisks). B: CCTA short-axis images at the same level confirming the dystrophic calcification of a part of the myocardium at the subendocardial level. C and D: comparative CMR and CCTA assessment of myocardial involvement in short-axis left ventricular views MI: myocardial infarction; LGE: late gadolinium enhancement; CCTA: cardiac computed tomography angiography; CMR: cardiac magnetic resonance