Vascular Cardiotoxicity of Ponatinib
Trial Snapshot
- Phase
- Not Applicable
- Enrollment
- 32
- Locations
- 1
- Primary Endpoint
- Carotid plaque size
Study Overview
Brief Summary
Pre-clinical studies suggest that the third generation tyrosine kinase inhibitor ponatinib can result in microvascular angiopathy and acceleration of atherosclerosis. This study is intended to examine for myocardial microvascular angiopathy and changes in carotid plaque in patients receiving ponatinib as part of their clinical care.
Detailed Description
In this study, we will perform serial echocardiography for ventricular function, myocardial contrast echocardiography for microvascular perfusion assessment, blood analysis for myocardial injury, and carotid US for plaque or IMT progression in subjects receiving ponatinib. This series of tests is intended to provide information on the presence of clinically-evident or subclinical microvascular angiopathy and plaque acceleration.
Study Design
- Study Type
- Observational
- Observational Model
- Cohort
- Time Perspective
- Prospective
Eligibility Criteria
- Ages
- 18 Years to 100 Years (Adult, Older Adult)
- Sex
- All
- Accepts Healthy Volunteers
- No
Inclusion Criteria
- •Diagnosis of CML or ALL
- •Prescribed ponatinib
Exclusion Criteria
- •pregnancy or lactation
- •major medical illness involving the heart or vasculature (CAD, PAD, DCM).
- •hemodynamically unstable
- •allergy to ultrasound contrast agents.
Outcomes
Primary Outcomes
Carotid plaque size
Time Frame: 12 months
Changes in IMT or plaque size
Presence versus absence of any myocardial perfusion defect assessed by visual analysis for any abnormalities of microvascular flux rate (beta function) or microvascular blood volume during an infusion of ultrasound microbubble contrast agents.
Time Frame: 12 months
Contrast ultrasound perfusion imaging will be performed using power-modulation imaging and infusion of an ultrasound contrast agent. Destruction replenishment kinetics will be assessed visually by examination of delayed replenishment of signal intensity (\>5 seconds) after a high-mechanical index burst sequence, or abnormalities in plateau intensity reflecting regional abnormalities in myocardial microvascular blood volume.
Secondary Outcomes
No secondary outcomes reported
Investigators
Jonathan R. Lindner, MD
Assistant Professor
Oregon Health and Science University