Stimulation of coronary collateral growth represents a potential alternative therapeutic approach for patients with intractable angina pectoris who are not candidates for PCI or CABG.
Do pharmacological and mechanical modulations accelerate coronary collateral growth in patients with intractable angina pectoris?
Increased shear stress is the primary stimulus for coronary collateral growth, providing a mechanistic basis for therapies like exercise, EECP, and periodic acceleration in patients with refractory angina.
There is a tremendous body of data concerning the coronary collateral circulation in both experimental animals and humans. The functional importance of a well-developed coronary collateral circulation has now been documented. The paradigm regarding the principal stimulus for coronary collateral growth has shifted from myocardial ischemia to increased shear stress at the site of pre-existing collateral arterioles. Numerous experimental and clinical studies have contributed to elucidation of the mechanisms of coronary collateral growth. Stimulation of coronary collateral growth is an alternative therapeutic approach to patients with intractable angina pectoris who are not indicated for percutaneous coronary intervention and/or coronary artery bypass grafting. Pharmacological and mechanical modulations accelerating coronary collateral growth have been challenged. Because it is conceivable that a well-developed coronary collateral circulation attenuates myocardial ischemia upon exercise, further research addressing coronary collateral growth is needed in both experimental models of myocardial ischemia and human coronary artery disease.
Fujita et al. (Fri,) conducted a review in Coronary Artery Disease. Stimulation of coronary collateral growth was evaluated. Stimulation of coronary collateral growth represents a potential alternative therapeutic approach for patients with intractable angina pectoris who are not candidates for PCI or CABG.