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Accelerated graft coronary artery disease: diagnosis and prevention
J S Schroeder1, S Z Gao, S A Hunt
1Division of Cardiovascular Medicine, Stanford University School of Medicine, CA 94305.
Insights
Accelerated graft coronary artery disease (CAD) significantly impacts heart transplant survival. This study investigates if diltiazem can prevent this condition, using quantitative coronary angiography to monitor progression.
Area of Science:
- Cardiology
- Transplantation Immunology
- Vascular Biology
Background:
- Accelerated graft coronary artery disease (CAD) is a primary limitation for long-term heart transplant recipient survival.
- Current triple therapy shows high rates of angiographically apparent accelerated graft CAD at 1, 3, and 5 years post-transplant.
- Cardiac allografts are denervated, leading to silent myocardial infarction, heart failure, or arrhythmias as primary presentations of accelerated graft CAD.
Purpose of the Study:
- To evaluate the efficacy of diltiazem in preventing accelerated graft CAD in heart transplant recipients.
- To assess the impact of calcium channel blocker therapy on the progression of graft vasculopathy.
Main Methods:
- A randomized study comparing diltiazem to no calcium blocker was initiated.
- Patients undergo early postoperative and annual quantitative coronary angiography.
- Intravascular ultrasound imaging is used to detect early intimal thickening.
Main Results:
- Quantitative arteriography is crucial for assessing accelerated graft CAD progression.
- Routine angiography may underestimate disease severity due to its diffuse nature.
- CAD risk factor modification has shown limited impact on overall incidence.
Conclusions:
- Accelerated graft CAD presents unique challenges in heart transplant recipients.
- Further research is needed to identify effective preventative strategies.
- Diltiazem's role in preventing accelerated graft CAD requires ongoing investigation.
Abstract:
Accelerated graft coronary artery disease (CAD) has become a major factor limiting survival among long-term heart transplant survivors. Currently 14%, 37%, and 50% of patients treated with triple therapy have angiographically apparent accelerated graft CAD at 1, 3, and 5 years after transplantation. Because cardiac allografts are denervated, transplant recipients generally do not experience angina pectoris. Therefore accelerated graft CAD may present as silent myocardial infarction, congestive heart failure, or ventricular arrhythmia leading to syncope or sudden death. Noninvasive tests for CAD have been insensitive for the detection of accelerated graft CAD because of the diffuse nature of the disease. Coronary arteriographic characteristics of accelerated graft CAD are a mixture of typical focal atherosclerotic lesions and unusual diffuse, concentric, and longitudinal narrowing prominent in middle to distal coronary vessels, with distal vessel obliteration and lack of collateral vessel formation. The presence and severity of accelerated graft CAD may be underestimated by routine angiography because of its diffuse and concentric nature. Quantitative arteriography has become an important technique to assess the progression of accelerated graft CAD. Intravascular ultrasound imaging can detect even earlier development of intimal thickening. CAD risk factor modification has had little impact on the overall incidence. We initiated a randomized study of diltiazem versus no calcium blocker to determine if this may prevent accelerated graft CAD. Patients have undergone early postoperative and annual quantitative coronary angiography since inception of the study.(ABSTRACT TRUNCATED AT 250 WORDS)