Regadenoson Stress Perfusion Cardiac Magnetic Resonance Imaging Before and After Coronary Revascularization in Kawasaki Disease (RF_SA_464)

Presenting Author(s)

• AK

  Alexander Kiener, MD, MPH

  Post-Doctoral Clinical Fellow
  Baylor College of Medicine / Texas Children's Hospital

Primary Author(s)

• AK

  Alexander Kiener, MD, MPH

  Post-Doctoral Clinical Fellow
  Baylor College of Medicine / Texas Children's Hospital

Co-Author(s)

• CA

  Carolyn Altman, MD

  Professor
  Baylor College of Medicine
• KS

  Kristen Sexson, MD, PhD

  Assistant Professor
  Baylor College of Medicine
• 

  Tam T. Doan, MD

  Assistant Professor
  Baylor College of Medicine / Texas Children's Hospital

Background: Stress perfusion cardiac magnetic resonance imaging (spCMR) has been increasingly used to guide management in patients with Kawasaki Disease (KD) with elevated AHA risk levels. Data on spCMR in patients who have undergone coronary revascularization is sparse. We aimed to study the utility of spCMR in patients with KD who underwent coronary revascularization.

Methods: We performed a retrospective case series at a single tertiary institution. We included consecutive patients with KD who underwent coronary revascularization (with either coronary bypass grafting or stent placement) and had spCMR before and after coronary procedure. Pharmacologic spCMR was performed with regadenoson. Baseline demographic and clinical data were collected along with spCMR findings (coronary artery anatomy, ventricular function, myocardial delayed enhancement, and first pass perfusion). Most recent clinical follow-up data was assessed for relevant outcomes including activity restriction.

Results: There were 7 patients who met inclusion criteria  (Table 1) with a median age of 9.2 years at the time of pre-revascularization spCMR (range 2.2-15.4). All patients were male and had AHA risk scores of 5.1. Six patients underwent surgical revascularization (3 LIMA to LAD, 2 RIMA to RCA/PDA, 1 double bypass) and 1 patient underwent coronary stent recanalization. All patients had inducible perfusion defects with pharmacologic stress prior to undergoing revascularization. Following revascularization 3 patients had complete resolution of stress perfusion defects and 4 patients had persistent stress perfusion defects (Figures 1 and 2). Of the 4 patients with persistent inducible defects, 2 had significant improvement in the extent of “at-risk” myocardium, 1 patient had inducible defects in coronary branches not addressed with revascularization and underwent further revascularization with coronary artery stenting of additional branches, and 1 patient had persistent inducible defects which persisted on subsequent spCMR with progressive left ventricular systolic dysfunction. No patients had new development of late gadolinium enhancement following revascularization.

Conclusion: In a series of patients with KD who required coronary revascularization, spCMR provided important information to guide management, including the effect of revascularization, activity restriction, and the need for additional intervention. Patients with improvement or resolution of inducible perfusion defects on post-interventional spCMR did not need additional revascularization procedures or develop compromised ventricular function. Future large studies are needed to validate our observation from this case series.

Table 1. Stress perfusion cardiac magnetic resonance imaging among a series of patients with Kawasaki Disease who underwent coronary revascularization. KD, Kawasaki disease; LAD, left anterior descending artery; LCx, left circumflex artery; LIMA, left internal mammary artery; LGE, late gadolinium enhancement; LVEF, left ventricular ejection fraction; PDA, posterior descending artery; RCA, right coronary artery; RIMA, right internal mammary artery; spCMR, stress perfusion cardiac magnetic resonance imaging; SVG, saphenous vein graft

Figure 1. Patient with coronary angiography revealing severe stenosis proximal to right coronary artery aneurysm (A). Stress perfusion CMR showed inducible perfusion defect in the right coronary artery territory (B). Following coronary revascularization there was resolution of the inducible perfusion defect (C).

Figure 2. Patient with inducible perfusion defect in the territories of the left anterior descending artery and the right coronary artery (A). There was a small area of late gadolinium enhancement on baseline CMR (B). Following coronary revascularization there was persistent perfusion defects in the right coronary artery territory (C). This patient required subsequent revascularization procedures.