976897 tn?1379167602


I think that all the literature I've so far read on this subject only seems to mention collaterals forming to feed the left side of the heart. Does anyone know if collaterals ever form to support the right side?
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976897 tn?1379167602
Thank you, I wish I was young enough to go for it.
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367994 tn?1304953593
Keep at it, you may discover useful information....with your tenacity you should be in research.
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976897 tn?1379167602
Thank you again for providing very fascinating information. It is one of those topics where the more you read, the more questions you seem to develop. For example...
It is obvious that with collateral development, you still suffer angina. I can relate to this from my own experience because my perfusion scan looked quite amazing. The level of blood reaching all areas of heart tissue is very high, even when I had a totally blocked LAD. A Cardiologist stated "If I had seen your perfusion scan, and not your angiogram, I would have put you as a very healthy individual". Even now, the discomforts I get from angina are very bad, yet I know the level of blood reaching all tissue areas is high.
I also wonder about sizes of developed collaterals. I assume they are not all the same sized vessels because I was told by a cardiologist they sometimes find one large enough which can be ballooned, making it more effective.
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367994 tn?1304953593
QUOTE: :I have read that collaterals are already in place on the heart, waiting for activation, but surely the mapping would have to be quite complex to allow for so many variations in blockages in different vessels?"

It seems the inception of the vascular system occurs early in mammalian development with the differentiation and aggregation of angiogenic precursors in the embryo culminating in the blood islands of the visceral sac. The early blood vessels of the embryo develop by aggregation of angioblasts that de novo create a primitive network of simple endothelial tubes – the process of vasculogenesis. Extensive research into the molecular mechanisms involved in vessel formation has identified proangiogenic factors such as vascular endothelial growth factor (VEGF) and the angiopoietins, together with antiangiogenic factors such as the thrombospondins and transcription factors leading to their expression.

It is arguably true to say that few researchers in the field of angiogenesis expected the growth of new blood vessels to be a simple event, nevertheless the molecular complexity of the process and the number of pathways involved has been a surprise. A significant outcome of this complexity has been the pleasing number of potential new targets available for therapeutic intervention. Studies of antiangiogenesis and vascular targeting are clearly at an exciting stage.

Angiogenesis is a normal function in the body, but it’s not always helpful. For example, while it is critical to normal embryonic development and beneficial in wound healing and recovery from heart disease, it can be harmful when it creates new feeder lines that help cancerous tumors grow and spread.

For further insight: Endothelial and smooth muscle cells interact with each other to form new blood vessels.... the cellular and molecular mechanism underlying the formation of the primary vascular plexus (vasculogenesis), the sprouting of further blood vessels (angiogenesis) and their maturation via recruitment of smooth muscle cells (arteriogenesis) during physiological and pathological conditions are summarized.  The concept of angiogenesis is studied in tumoral and cardiovascular pathology. Promoting the formation of new collateral vessels in ischemic tissues using angiogenic growth factors (THERAPEUTIC ANGIOGENESIS) is a promising approach in cardiovascular diseases. Conversely, inhibition of the action of key regulators of angiogenesis is a new pathway for the treatment of solid tumors and metastasis.

FUTURE PROSPECTS AND PROJECTS: These concepts are being tested now in clinical trials in the oncology or cardiovascular fields. Some trials are reported in this review with their potential adverse effects, limits and developments in the future.

Angiogenesis and arteriogenesis differ in morphogenesis:  "After birth, new blood vessel formation proceeds via angiogenesis or arteriogenesis. Angiogenesis (capillary sprouting) results in higher capillary density. Arteriogenesis (rapid proliferation of collateral arteries) is potentially able to significantly alter the outcome of coronary and peripheral artery disease. The processes share some growth features but differ in many aspects".

When the heart starts beating the circulation commences shortly thereafter, significant changes occur in the morphogenesis of the vascular system. Some vessels of the primary plexus remain as capillaries, whereas others differentiate into arteries or veins.

Although regression and differentiation are still unknown processes, it is believed that hemodynamic forces (blood flow, shear stress, gradient pressure, blood volume) play a central role. Cessation of blood flow into a capillary segment causes the regression of the vessel, whereas an increase in PRESSURE and SHEAR stress may be an inductive factor for the local recruitment of smooth muscle cells, leading to the differentiation of a capillary vessel into an artery or vein.
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976897 tn?1379167602
Great, thanks for this info.

Total patients in study 74 /
Total with LAD blockage - 46  (32 no collaterals - 14 with collaterals)
Total with RCA blockage - 28 (8   no collaterals - 20 with collaterals)

This at first glance makes you assume that RCA is far more common in developing collaterals, but there were nearly twice as many patients with RCA blockage. However
30% developing collaterals in the LAD is much lower than I had suspected, I feel luckier now. Can we assume a 1 in 3 chance of developing them for the LAD?

I wonder also if collaterals develop for RCA AND LAD when both have blockages. For example, my LAD was blocked at the top and my RCA is blocked just before the acute margin. Could I develop collaterals for both I wonder.

In your research, did you come across any information regarding where collaterals start from? i.e. their source. I know this is a silly example, but lets assume that a patient has a totally blocked rca and lad. The only vessel open is the lcx. Would collaterals actually come directly off of this vessel to feed others? I have read that collaterals are already in place on the heart, waiting for activation, but surely the mapping would have to be quite complex to allow for so many variations in blockages in different vessels?

Thank you again, very interesting.
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367994 tn?1304953593
Q!UOTE: "I think that all the literature I've so far read on this subject only seems to mention collaterals forming to feed the left side of the heart. Does anyone know if collaterals ever form to support the right side?"

Good question because one seldom reads anything about the RCA collaterals.  I believe you have raised that question before and my  notes on the subject at that time is as follow from a study, and it includes acute collateral development after MI. Yes, there are collaterals associated with RCA, and there can be development with acute MI.

Coronary collateral vessel development after acute myocardial infarction.  The aim of the present study was to assess the factors affecting collateral vessel development in patients with acute myocardial infarction

Only patients with total proximal occlusion in the left anterior descending coronary artery (LAD) or right coronary artery (RCA) in angiography were included in the study. Patients were separated into two groups according to the development of coronary collateral circulation (CCC). In group 1, CCC was inadequate (Rentrop 0, 1 and 2); and in group 2, CCC was adequate (Rentrop 3). Although CCC was adequate in 20 of 28 (71%) patients who had RCA occlusion (P=0.015), it was adequate in only 14 of 46 (30%) patients who had LAD occlusion (P>0.05). The presence of angina pectoris was positively correlated with the development of CCC (P=0.03). Diabetes mellitus (DM) was present in 14 of 40 (35%) patients with inadequate CCC and four of 34 (11%) patients with adequate CCC. The presence of DM was significantly higher in the group with inadequate development of CCC (P=0.017).
While DM was associated with an inadequate development of CCC, the presence of angina pectoris and RCA occlusion were associated with an adequate development of CCC.

More details are available.
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916737 tn?1243936842
I’m not sure and I have seen no proof, but I think that logically, collaterals develop everywhere in the body; many have developed collaterals in their legs. What I know, is that collaterals need time to develop, which means that they can’t form on sudden obstruction, but on gradual one. If the RCA was found obstructed completely and still well perfused, it can only mean that the obstruction was gradual giving the time for the collaterals to develop.
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