Collateralization
In medicine, collateralization, also vessel collateralization and blood vessel collateralization, is the growth of a blood vessel or several blood vessels that serve the same end organ or vascular bed as another blood vessel that cannot adequately supply that end organ or vascular bed sufficiently.
Coronary collateralization is considered a normal response to
Collateral or anastomotic blood vessels also exist even when blood supply is adequate to an area, and these blood vessels are often taken advantage of in surgery. Some notable areas where this occurs include the abdomen, rectum, knee, shoulder, and head.
Coronary collateralization
Coronary collateralization exists latently in the normal
The functional significance of the coronary collateral vessels is a matter of continuing experimental investigation although their existence has been known for over three centuries and been documented repeatedly in man and beast over the past seven decades. Although a now-classic series of
The native collaterals are small vessels, with a narrow endothelial lining, a layer or two of
Schaper summarizes the status-2009 knowledge of coronary collateral transformation in a recent review:
Kolibash's 1982 study of the effect of collaterals on rest and stress myocardial perfusion, left ventricular function, and myocardial infarction prevention was most influential in turning the tide of professional opinion toward acknowledging the impact of these vessels on the jeopardized heart.
Since Kolibash's study, newer techniques have been used effectively to investigate the issues he raised and to characterize both the mechanism of the transformation of the native collaterals and assess their impact on myocardial perfusion and function—among them percutaneous transluminal coronary angioplasty (PTCA), ergovine-provocative spasm tests, and myocardial perfusion studies. Using PTCA, Rentrop demonstrated that collateral vessel filling jumps dramatically during coronary occlusion by balloon inflation—within ninety seconds of total occlusion.[12] Filling improved in 15 of 16 patients; neither chest pain nor pre-inflation angina correlated with the extent of collateral filling, and coronary spasm did not occur. Rentrop did not generalize about the functional significance of these collaterals, which he said was "unknown," but their existence suggests that they may exert a preemptive, protective effect.
Subsequently, Rentrop's associate Cohen prospectively evaluated 23 patients undergoing PTCA and observed that during balloon inflation, the mean grade of collateral filling increased dramatically. Nineteen of 23 patients showed improvement (p=0.01) but post-PTCA arteriography[13] revealed no visible collaterals in any patient. The functional effect of filling was dramatic: using an index of ischemia (based on the percent of hypocontractile perimeter of myocardium, sum of ST segment elevation, and time of onset of angina), Cohen found that grade 0 or 1 filling confers only nominal protection from ischemia (i.e., filling is non-existent or of side branches only), but partial filling (i.e. grade 2 or greater) of these segments provides almost complete preservation of the affected myocardium from the asynergy associated with critical coronary stenosis.[13] Pain was observed in all nine patients with 0 or 1 filling, but in only five of 14 patients with grade 2 or 3 filling. Thus, the severity of symptoms correlated inversely with the degree of observed collateral filling.
In another often-cited study,[9] Freedman focused on the issue of MI prevention by selecting 121 patients with severe single vessel disease. 64 had Q-wave infarction and 57 did not; 32 had unstable angina or subendocardial infarction. 74 totally occluded vessels and 47 subtotally occluded vessels were identified in this study, and the presence of total occlusion was the most significant predictor of the existence of collaterals. 63 of 74 (85%) of the "totalled" vessels were accompanied by evidence of collaterals, compared to 8 of 47 (17%) of the subtotalled vessels (p=0.001). Collaterals were completely absent beside arteries with less than 90% stenosis. Totally occluded arteries were found in 29 of 57 patients in the group without Q-wave myocardial infarctions, and all 29 showed collaterals. In comparison, 76% of those who lacked totally occluded arteries showed collaterals (p is less than 0.005). In contrast, all 24 of those 57 patients without Q-wave MI's who did not have collaterals had subtotal stenosis of their diseased vessel. Though smoking, cholesterol levels, and the presence of angina did not differ between the groups, the presence of subendocardial infarction was significantly greater in those with collaterals, suggesting either that subendocardial infarction precipitates the formation of collaterals to an extent comparable to Q-wave infarcts, or that preexisting collaterals prevent subendocardial infarctions from becoming transmural infarctions.
Among several Japanese studies utilizing the ergovine-provocative spasm test to simulate ischemia in man and beast, including those of Takeshita
Whether angina causes collateral development is still debatable, but at least one investigator, Fujita, believes that angina is either symptomatic of, or somehow promotes the development of, collateral circulation, and, in any case, sometimes precedes, and often prevents, infarction by relieving the critically occluded vessel before thrombosis can occur.[17] Examining 37 patients who underwent intercoronary thrombolysis within six hours of MI, Fujita found that 2 of 19 patients without preinfarct angina had collaterals and 9 of 18 patients with angina had them. No other variables pertaining to collateral development distinguished the groups. Fujita therefore suggests that the absence of symptomatic angina may not always portend favorable developments, and infarct prevention must surely be targeted to those with coronary disease who are without symptoms, as they may be without the protective effects of collateral development provoked by the presence of angina.
Relation to angiogenesis
Collateralization differs from angiogenesis in that several blood vessels supply one vascular bed and these vessels are maintained (one does not involute/regress).
See also
- Angiogenesis
- Atherosclerosis
- Axonal collateralization and its dependence on Dendritic arborization
References
- PMID 15100419. Free Full Text.
- PMID 12131019.
- ^ Schaper W, The collateral circulation of the heart, New York, N.Y.: Elsevier, 1971.
- ^ Kolibash AJ, et al., "Coronary collateral vessels: spectrum of physiologic capabilities with respect to providing rest and stress myocardial perfusion, maintenance of left ventricular function, and protection against infarction," American Journal of Cardiology 1982; 50: 230-238.
- ^ See notes 5-15 in Kolibash, op. cit., for relevant studies with this perspective. (Note that the most recent is from 1977.)
- ^ Kolibash, op. cit., 232. See also Yamagsihi M, "The functional significance of transient collaterals during coronary artery spasm," American Journal of Cardiology 1985; 56: 407-12.
- ^ Yamagsihi M, "The functional significance of transient collaterals during coronary artery spasm," American Journal of Cardiology 1985; 56: 411.
- ^ This information is cited for the record only.
- ^ a b Freedman SB, et al., "Influence of coronary collateral blood flow on the development of exertional ischemia and Q wave infarction in patients with severe single-vessel disease," Circulation 1985; 71 (4): 681-6.
- ^ Schaper W. Basic Research in Cardiology. 2009 Jan;104(1):5-21. Epub 2008 Dec 20.
- ^ Hypoxia appears to initiate dilation by causing release of an as yet unknown and yet-to-be-isolated substance.
- ^ Rentrop KP, et al., "Changes in collateral filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subjects," Journal of the American College of Cardiology 1985; 5: 587-92.
- ^ a b Cohen M and KP Rentrop, et al., "Limitation of myocardial ischemia by collateral circulation during sudden controlled coronary artery occlusion in human subjects: a prospective study," Circulation 1986; 74 (3): 469-76.
- ^ Takeshita A, et al., "Immediate appearance of coronary collaterals during ergovine-induced arterial spasm," Chest 1982; 3: 319-22.
- ^ Tada M, et al., "Transient collateral augmentation during coronary arterial spasm associated with ST-segment depression," Circulation 1983; 67 (3): 693-8.
- ^ Yamagsihi M, "The functional significance of transient collaterals during coronary artery spasm," American Journal of Cardiology 1985; 56: 407-12.
- ^ Fujita M, "Importance of angina for development of collateral circulation," British Heart Journal 1987; 57: 139-43.