Abstract
A 63 year-old female with multiple atherosclerotic risk factors presented with newly diagnosed heart failure. Clinical presentation and initial work-up studies (e.g. laboratory findings, ECG, and echocardiography) were indeterminate for ischemic or non-ischemic etiology. As she developed contrast-induced nephropathy, coronary angiography was deferred and cardiac MRI was performed instead. Cardiac MRI elegantly demonstrated non-ischemic cardiomyopathy that was subsequently confirmed by invasive coronary angiography. This case emphasizes the important role of cardiac MRI in establishing the etiology of cardiomyopathy, ultimately altering the clinical management of the patient with newly diagnosed heart failure.
A 63 year-old female with hypertension, hypercholesterolemia and active cigarette smoking presented with orthopnea and dyspnea on exertion that had worsened over the previous 2 months. Pulmonary embolism was ruled out with chest CT angiogram. ECG showed new T-wave inversion in the lateral wall when compared to an old tracing (Figure 1). Laboratory data showed severely elevated pro-BNP (23,615 pg/mL). Initial troponin T was undetectable. Her renal function worsened secondary to contrast-induced nephropathy (Cr 1.5 mg/dL [baseline 0.9 mg/dL], eGFR 42 ml/min/1.73 m2 [baseline 71 ml/min/1.73 m2]). Echocardiography showed biventricular dilatation and decreased systolic function with regional wall motion abnormalities (Video 1). As the etiology of the cardiomyopathy was not clear, CMR was performed for further evaluation.
Cardiac MRI cine imaging showed severely dilated LV with severely decreased systolic function (LVEF 17%) with global hypokinesis (Video 2). On late gadolinium enhancement imaging, there was patchy myocardial fibrosis in the anterolateral papillary muscle and a small portion of the mid lateral wall, mid-wall fibrosis in the basal anteroseptal segment, and fibrosis at both anterior and inferior right ventricular insertion sites (Figure 2A). Cardiac MRI findings were compatible with non-ischemic cardiomyopathy. Invasive coronary angiography performed subsequently revealed normal coronaries (Figure 2B). Antiplatelet therapy was discontinued. She was discharged home with low dose furosemide, carvedilol, losartan, isosorbide dinitrate, and hydralazine. Sacubitril/valsartan was subsequently initiated as an outpatient, once renal function stability has been confirmed.
Coronary artery disease is the most common cause of systolic heart failure in Western countries. Ischemic cardiomyopathy is associated with decreased survival when compared to non-ischemic cardiomyopathy (1). If feasible, surgical coronary revascularization improves survival when compared to medical management (2). This case emphasizes the important role of cardiac MRI in establishing the etiology of cardiomyopathy, ultimately altering the clinical management of the patient with newly diagnosed heart failure.