Case 11

Published on 02/03/2015 by admin

Filed under Internal Medicine

Last modified 22/04/2025

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Case 11

A 36-year-old man with a history of hypertension presented to the ED with the sudden onset of left-sided weakness. He also described a 6-month history of exertional dyspnea and leg edema. He had stopped taking his antihypertensive medications several months ago. He admitted to consuming a “moderate” amount of alcohol on a daily basis.

Baseline ECG

The baseline ECG demonstrates sinus rhythm, increased QRS voltage consistent with left ventricular hypertrophy (LVH), and nonspecific ST-T abnormalities possibly related to LVH. There is also evidence of biatrial conduction abnormality.

Echocardiogram

Parasternal long-axis and short-axis images demonstrate left ventricular dilation, increased left ventricular wall thickness, and severe global left ventricular systolic dysfunction with an estimated left ventricular ejection fraction of 20% to 25%. These findings are consistent with ischemic or nonischemic cardiomyopathy.

He was referred for adenosine stress ^99mTc-sestamibi SPECT MPI to evaluate for ischemic cardiomyopathy as the cause for the left ventricular systolic dysfunction.

He underwent a 4-minute adenosine infusion without supplemental low-level treadmill exercise. No adenosine-induced symptoms were reported. Baseline blood pressure was elevated, but the blood pressure response to adenosine was normal. The ECG response was nondiagnostic owing to baseline LVH and ST-T abnormalities.

Raw Planar Images

The rotating raw planar images demonstrate left ventricular enlargement. Lateral projections demonstrate reduced inferior wall tracer activity possibly due to diaphragmatic attenuation artifact.

SPECT Images

The SPECT images demonstrate left ventricular enlargement. There is a moderate to severe fixed inferior perfusion defect extending from the base to the apex. These findings could be consistent with inferior infarction or nonischemic cardiomyopathy with inferior wall attenuation artifact. The inferior wall attenuation artifact in nonischemic cardiomyopathy is typically attributed to diaphragmatic attenuation, though photons emitted by the inferior region may be attenuated by the enlarged heart itself. “Heart attenuation” may be the predominant mechanism of the inferior wall artifact.

Polar Maps

When the tracer distribution is compared to a male-specific normal database, there is a predominantly fixed reduction in tracer activity in the inferior and inferoapical regions.

Gated SPECT Images

The poststress gated SPECT images demonstrate severe global left ventricular hypokinesis, with a computed left ventricular ejection fraction (LVEF) of 23%. The left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) were markedly increased at 335 and 259 mL, respectively.

Teaching Points

SPECT MPI in Cardiomyopathy (See Chapter 30)

1. In this case, the left ventricular systolic dysfunction was more severe than the observed perfusion abnormalities. These findings favor nonischemic cardiomyopathy, with untreated hypertension and alcohol abuse as possible etiologies. Medical therapy for cardiomyopathy and abstinence from alcohol were recommended.

2. Patients with nonischemic cardiomyopathy frequently demonstrate fixed inferior wall perfusion defects due to attenuation by the enlarged heart.

3. Reversible perfusion defects are occasionally observed in patients with nonischemic cardiomyopathy, presumably due to myocardial fibrosis and microvascular disease. Perfusion abnormalities can also be seen in other “noncoronary heart diseases,” including hypertrophic cardiomyopathy, sarcoidosis, scleroderma, myocarditis, Duchenne’s muscular dystrophy, cardiac lymphoma, left bundle branch block, and right ventricular pacing.

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