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.