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Published on: July 9, 2020
The future of collateral artery research
Nazanin Hakimzadeh, Hein J Verberne, Maria Siebes
1Department of Cardiology, Room B2-250, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. j.j.piek@amc.uva.nl.
Insights
Research on coronary artery disease (CAD) shifts from promoting collateral vessel growth to blocking inhibitory pathways. New imaging methods are crucial for evaluating these therapeutic strategies.
Area of Science:
- Cardiovascular Research
- Vascular Biology
- Medical Science
Background:
- Obstructive coronary artery disease (CAD) necessitates collateral arteries for myocardial perfusion.
- Monocytes influence collateral vessel function through growth factors and enzymes.
- Previous therapeutic approaches targeting monocyte enhancement for arteriogenesis yielded disappointing clinical results.
Purpose of the Study:
- To explore a paradigm shift in arteriogenesis research, moving beyond monocyte-centric strategies.
- To investigate genetic predispositions in CAD patients with insufficient collateral vessel development.
- To identify new therapeutic targets by focusing on blocking arteriogenesis-inhibiting pathways.
Main Methods:
- Analysis of genetic heterogeneity in CAD patients with varying collateral vessel development.
- Identification of overexpressed arteriogenesis-inhibiting signaling pathways in specific patient groups.
- Evaluation of advanced diagnostic imaging modalities for assessing collateral vessel growth.
Main Results:
- Genetic predispositions contribute to poor collateral vessel development in some CAD patients.
- Overexpression of inhibitory pathways is linked to insufficient arteriogenesis.
- Advanced imaging shows promise in detecting therapeutic effects on collateral vessels.
Conclusions:
- Arteriogenesis research is shifting towards inhibiting negative regulatory pathways.
- Understanding genetic factors is key to developing effective arteriogenesis therapies.
- Improved diagnostic imaging is essential for validating pro-arteriogenic treatments.
Abstract:
In the event of obstructive coronary artery disease, collateral arteries have been deemed an alternative blood source to preserve myocardial tissue perfusion and function. Monocytes play an important role in modulating this process, by local secretion of growth factors and extracellular matrix degrading enzymes. Extensive efforts have focused on developing compounds for augmenting the growth of collateral vessels (arteriogenesis). Nonetheless, clinical trials investigating the therapeutic potential of these compounds resulted in disappointing outcomes. Previous studies focused on developing compounds that stimulated collateral vessel growth by enhancing monocyte survival and activity. The limited success of these compounds in clinical studies, led to a paradigm shift in arteriogenesis research. Recent studies have shown genetic heterogeneity between CAD patients with sufficient and insufficient collateral vessels. The genetic predispositions in patients with poorly developed collateral vessels include overexpression of arteriogenesis inhibiting signaling pathways. New directions of arteriogenesis research focus on attempting to block such inhibitory pathways to ultimately promote arteriogenesis. Methods to detect collateral vessel growth are also critical in realizing the therapeutic potential of newly developed compounds. Traditional invasive measurements of intracoronary derived collateral flow index remain the gold standard in quantifying functional capacity of collateral vessels. However, advancements made in hybrid diagnostic imaging modalities will also prove to be advantageous in detecting the effects of pro-arteriogenic compounds.
