Basics
Description
- Collateral blood vessels are anastomotic connections that offer an important source of blood supply when original vessels fail to provide sufficient blood, and are extremely important in the coronary circulation.
- Coronary collateral vessels limit myocardial ischemia during coronary occlusion and may minimize the infarct area.
- 2 types of coronary collateral vessels include:
- Capillary size collaterals: These vessels do not have vascular smooth muscle, are observed in all layers of the ventricular muscle (but have a predilection for the subendocardium where they form a plexus), and develop via angiogenesis.
- Larger muscular collaterals: These vessels are located epicardially, develop from preexisting arterioles (arteriogenesis), and can be angiographically classified into 4 types: Septal, atrial, branch-branch in ventricular free walls, and bridging across lesions.
Epidemiology
- Collateral arteries that prevent signs of myocardial ischemia are present in 1/3 of patients with coronary disease and 1/5 of patients without coronary disease.
- A reduction in coronary collaterals has been reported in the elderly and diabetics and is associated with a reduction in the expression of angiogenic factors.
Pathophysiology
- Angiogenesis:
- Stimulated by hypoxia via biochemical signals including vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-β, and basic fibroblast growth factor (b-FGF).
- Arteriogenesis:
- Not stimulated by hypoxia.
- Stimulated by an increase in shear stress (ie, hemodynamically relevant stenosis of coronary artery creates a decrease in arterial pressure distal to the stenosis and blood flow is redistributed through preexistent arterioles from high-pressure to low-pressure area. This creates increase in flow velocity and shear stress, which leads to morphological changes and vascular remodeling.
- Major biochemical factors include: GM-CSF, monocyte chemoattractant protein-1 (MCP-1), TGF-β
Etiology
- Ischemia
- Pressure gradients and shear stress
Associated Conditions
- Coronary artery disease
- Peripheral vascular disease
Diagnosis
Tests
Imaging
- Coronary angiography
- Myocardial contrast echo
- Spiral CT scan
- MRI
- PET scan
Surgery
Coronary angiography reveals grades of collateral filling:
- 1 = filling of side branches of the artery without visualization of the epicardial segment
- 2 = partial filling of the epicardial segment
- 3 = complete filling of the epicardial segment
Treatment
Additional Treatment
Additional Therapies
Therapeutic angiogenesis:
- A pharmacological agent that could stimulate collateral vessel growth could have a major impact on morbidity and mortality.
- Experimental studies have been promising; clinical research is ongoing.
Ongoing Care
Prognosis
- Beneficial effects of collaterals include:
- Decrease the severity of myocardial ischemia
- Decreased infarct size
- Improve LV function
- Reduce the likelihood of LV aneurysm formation
- Improve survival
- Only rarely provides blood flow increases adequate to meet maximal physical exercise
Additional Reading
1Cohen M, Rentrop KP. Limitation of myocardial ischemia by collateral circulation during sudden controlled coronary artery occlusion in human subjects: a prospective study. Circulation. 1986;74:469-476. [View Abstract]2Fukai M, Ii M, Nakakoji T. Angiographically demonstrated coronary collaterals predict residual viable myocardium in patients with chronic myocardial infarction: a regional metabolic study. J Cardiol. 2000;35:103-111. [View Abstract]3Isner JM, Pieczek A, Schainfeld R. Clinical evidence of angiogenesis after arterial gene transfer of phVEGF165 in patients with ischemic limbs. Lancet. 1996;348:370-374. [View Abstract]4Kern M. Atherosclerotic cardiovascular disease: Coronary blood flow and myocardial ischemia. In: Zipe D Braunwald's Heart Disease, 7th ed. Philadelphia: Elsevier Saunders, 2005;1103-1127.5Koerselman J, van der Graaf Y, de Jaegere PP. Coronary collaterals: An important and underexposed aspect of coronary artery disease. Circulation. 2003;107:2507-2511. [View Abstract]6Meier P, Gloekler S, Zbinden R. Beneficial effect of recruitable collaterals. A 10 year follow up study in patients with stable coronary artery disease undergoing quantitative collateral measurements. Circulation. 2007;116:975-983. [View Abstract]7Rentrop KP, Cohen M, Blanke H. Changes in collateral channel filling immediately after controlled coronary artery occlusion by angioplasty balloon in human subjects. J Am Coll Cardiol. 1985;5:587-592. [View Abstract]8Rockstroh J, Brown G. Coronary collateral size, flow capacity, and growth. Estimates from the angiogram in patients with obstructive coronary disease. Circulation. 2002;105:168-173. [View Abstract]9Schaper W. Collateral vessel growth in the human heart. Role of fibroblast growth factor-2 editorial. Circulation. 1996;94:600-601. [View Abstract]10Schirmer SH, Nooijen FC, Piek JJ. Stimulation of collateral artery growth: Travelling further down the road to clinical application. Heart. 2009;95:191-197. [View Abstract]
Codes
ICD9
459.89 Other specified circulatory system disorders
SNOMED
59093008 venous collateral circulation, any site (disorder)
Clinical Pearls
- The capillary-sized vessels are observed in all layers of the ventricular muscle, but have a predilection for the subendocardium where they form a plexus. The larger muscular collaterals are found epicardially.
- There are two main types of collateral blood vessels: Capillary-sized vessels without smooth muscle and larger muscular vessels. The capillary-sized vessels form through angiogenesis stimulated hypoxia via biochemical signals including: VGEF, TGF-β, and b-FGF. The larger muscular vessels are nonfunctional pre-existing conduits that become functional in the setting of a hemodynamically significant stenosis. These larger vessels then undergo vascular remodeling in the setting of shear stress.
- Studies have found a decrease in the severity of myocardial ischemia, a decreased infarct size, improved LV function, a reduction in the likelihood of LV aneurysm formation, and improved survival.