Feasibility of myocardial tissue mapping and stress perfusion imaging using wideband cardiac magnetic resonance in a patient with an implantable cardioverter defibrillator (QF_FR_106)

A 51-year-old male with heart failure with reduced ejection fraction and an implantable cardioverter defibrillator was admitted with decompensated heart failure. An echocardiogram showed an acute decline in left ventricular ejection fraction (LVEF) from 45% to 10%. He was subsequently referred for stress perfusion cardiac magnetic resonance (CMR) imaging.

Diagnostic Techniques and Their Most Important Findings:

To assess for potential contributors of the patient’s acute reduction in systolic function, including ischemia and inflammation, vasodilator-induced stress perfusion CMR imaging was performed using a 1.5-T (SIGNA Artist, GE HealthCare) scanner. The CMR protocol included cardiac cine, parametric mapping (T1, T2) and late gadolinium enhancement acquisitions with wideband parameters. For stress imaging, regadenoson 0.4 mg (injected over approximately 10 seconds into a peripheral vein) was administered, followed by perfusion imaging during the first pass of the gadolinium-based contrast agent (Gadovist). Aminophylline 75 mg was administered intravenously for reversal of hyperemia after stress. Ten minutes after stress imaging, rest perfusion was performed during the infusion of a gadolinium-based contrast agent (Gadovist), followed by a saline flush (50 mL). For perfusion imaging, three short axis (SAX) slices were obtained during stress and resting conditions with the following imaging parameters: slice thickness 8 mm, flip angle 15°, NEX 0.75, parallel imaging factor 2, acquired matrix 192x148 pixels, FOV 38-42 cm x 29-32 cm, and TR/TE 3.1/1.5 ms. Pre- and post-contrast T1 mapping in 3 SAX planes were acquired using a wideband inversion recovery SPGR modified look-locker inversion recovery (MOLLI) sequence, and T2 mapping was acquired by a multi-echo fast spin echo sequence before contrast administration. Stress perfusion CMR was well tolerated, and image quality for perfusion and LGE was excellent and diagnostic in all segments. Device integrity was preserved without significant alterations of lead impedance, pacing capture threshold, and sensing amplitude.

In addition to severe LV dysfunction, CMR showed a fixed perfusion defect in the inferior and inferoseptal segments corresponding with areas of transmural LGE (Figure 1). Additional segments also displayed mid/subepicardial LGE suggesting non-ischemic fibrosis. A subsequent coronary angiogram revealed non-obstructive disease, and work-up for sarcoidosis was pursued.

Learning Points from this Case:

Vasodilator stress perfusion CMR remains limited in patients with ICD due to potential device-induced image artifacts. Although the development of wideband protocols have recently enabled LGE and T1 imaging, the feasibility and diagnostic utility of myocardial T2 mapping and stress perfusion imaging is largely unknown. This case illustrates the clinical usefulness of wideband stress perfusion CMR in a patient with an ICD, suggesting potential diagnostic and therapeutic value of stress perfusion CMR in this high-risk patient population.