Perfusion artifacts caused by marked RV enlargement
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Thomas Jefferson University, Philadelphia, PA
Received Mar 13, 2019; accepted May 3, 2019 doi:10.1007/s12350-019-01757-1
A 64-year-old woman with a prior kidney transplantation for focal segmental glomerulosclerosis and graft failure was referred for pharmacologic stress testing as part of preoperative evaluation prior to a second kidney transplant. In the year prior, she had been evaluated for pulmonary hypertension that had been discovered on routine echocardiography. The patient was diagnosed with autoimmune-associated pulmonary hypertension and started on bronchodilators, tadalafil, and ambrisentan with marked improvement in her symptoms. Later, selexipag was added but she could not tolerate this. She was documented to have an elevated jugular venous pressure and a positive hepatojugular reflux. A right-sided sternal heave was described but no murmurs or gallops. Her lungs were clear. There was a fistula in her right arm. Her EKG (Figure 1) was remarkable for right ventricular hypertrophy and diffuse ST-T abnormalities. A regadenoson stress was performed; imaging was done using a standard SPECT orbit, which was performed from RAO to LPO. Perfusion images showed marked RV dilatation and a large, mild, fixed septal defect (Figure 2). Incidental note was made of significant clockwise rotation of the heart (Figure 3). Gated images (supplemental movie 1) revealed vigorous contraction of the septum suggesting that the defect was due to artifact instead of infarction. Review of the raw projection images (supplemental movie 2) also showed the marked clockwise rotation of the heart.
Electronic supplementary material The online version of this article (doi:https://doi.org/10.1007/s12350-019-01757-1) contains supplementary material, which is available to authorized users. Reprint requests: Christopher L. Hansen, MD, MASNC, Thomas Jefferson University, 925 Chestnut St, Philadelphia, PA 19107; [email protected] J Nucl Cardiol 1071-3581/$34.00 Copyright Ó 2019 American Society of Nuclear Cardiology.
An echocardiogram was performed which demonstrated marked RV enlargement with decreased function (supplemental movie 3). Both supplementary movies 2 and 3 show markedly reduced RV function. The patient later underwent right heart catheterization (Table 1). Calculated Fick cardiac index was 3.12 L/min/m2 and pulmonary vascular resistance 2.99 Wood units. RV systolic pressure was only moderately elevated at that time. Her symptoms are well controlled on medications and she is awaiting kidney transplantation. DISCUSSION The patient had marked RV enlargement felt most likely due to long-standing pulmonary hypertension. The fact that her pulmonary pressures were only moderately elevated on her right heart catheterization is most likely due to a failing right ventricle and aggressive treatment of her pulmonary hypertension with both tadalafil and ambrisentan. This study highlights several important points that are summed up in a single concept: what is ‘normal’ can change dramatically when the underlying anatomy chan
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