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Progressive Rapid Atherosclerotic Plaque Formation and Early Stent re-Stenosis in an Untreated CLL Patient; A Case
Mohammad Shojae1, Hosseinali Rostamipour2, Aref Ghanaatpisheh1,3
1Cardiology Department Jahrom University of Medical Sciences Jahrom Iran.
Insights
This case study shows a rare link between chronic lymphocytic leukemia (CLL) and rapid coronary artery disease (CAD) progression. Patients with CLL may require closer cardiac monitoring due to accelerated atherosclerosis risks.
Area of Science:
- Cardiology
- Hematology
- Oncology
Background:
- Chronic lymphocytic leukemia (CLL) is a hematologic malignancy.
- Coronary artery disease (CAD) is a leading cause of mortality.
- The association between CLL and accelerated CAD is not well-established.
Purpose of the Study:
- To report a case of a patient with CLL experiencing rapid CAD progression.
- To explore potential mechanisms linking CLL and accelerated atherosclerosis.
- To emphasize the importance of cardiac evaluation in CLL patients.
Main Methods:
- Case report of a 66-year-old male with CLL and recurrent myocardial infarction.
- Review of coronary angiography findings before and after percutaneous coronary intervention (PCI).
- Analysis of laboratory results, including white blood cell (WBC) counts.
Main Results:
- The patient experienced two non-ST elevation myocardial infarctions (NSTEMI) within six months.
- Coronary angiography revealed progression from two-vessel to three-vessel disease, including in-stent restenosis.
- White blood cell counts significantly increased, correlating with disease progression.
Conclusions:
- CLL may be associated with accelerated CAD, potentially due to leukocyte aggregation, endothelial injury, or amyloid deposition.
- Thorough cardiac evaluation is crucial for CLL patients.
- Further research is needed to understand and manage this high-risk association.
Abstract:
A 66 year-old male with a history of hypertension and poor follow-up for chronic lymphocytic leukemia (CLL) experienced two episodes of non-ST elevation myocardial infarction (NSTEMI) within a 6 month period. Initial coronary angiography showed two-vessel disease, and percutaneous coronary intervention (PCI) was performed on the left anterior descending artery (LAD). Six months later, repeat angiography revealed rapid progression to three-vessel disease, including in-stent restenosis and new severe lesions, which required urgent coronary artery bypass grafting (CABG). Laboratory tests indicated persistent leukocytosis, with white blood cell (WBC) counts increasing from 38.6 × 103/μL to 75.7 × 103/μL. This case highlights a rare but clinically significant association between CLL and accelerated coronary artery disease (CAD), suggesting potential mechanisms such as leukocyte aggregation, endothelial injury, and amyloid deposition contributing to rapid atherosclerosis. The findings underscore the importance of thorough cardiac evaluation in CLL patients and the need for further research into the underlying mechanisms and optimal treatment strategies for this high-risk group.
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