If patient is symptomatic then revascularization  may be consider.

We published the study relationship this question.

Collaterals are usually not able to replace normal flow in dilated coronary arteries or in bypasses. Therefore, it seems to be reasonable to revascularize these pts.

no

Collaterals can provide approximately 30% flow of normal coronary artery. Then, angina pectoris can often take place when a patient has strenuous exercise or is overworked.Even though  no symptom, the heart can be gradually bigger and remodeled,eventualy provoking heart failure. Therebefore,revascularization should be recommended.

My views are same as expressed by Dr. Joseph Veselka.

In the asymptomatic subject probably not. The medical treatment is good.

An occluded coronary artery receiving collateral circulation should be regarded in terms of coronary flow as a 90% stenosis. The reason is that the flow in the collateral vessels cannot increase according to myocardial oxygen demand. It is therefore logical that patients may have anginal symptoms that indicate revascularisation.

two important questions are viability and ischemia.

If the anterior territory is viable - then the question of ischemia arises - either stress echo/Nuclear or CMR would be useful - in the case of a large deficit - revascularization could be considered - there is little evidence that this gives better outcomes in terms of mortality - it's really an extrapolation of the nuclear data that suggests that revasc. is better when >10 ischemia is present.

we found that good collaterals were associated with viability (Rentrop 2-3), but were not able to provide sufficient perfusion at stress (using CMR).

What about a patient with multiple coronary lesions not amenable to any significant bypass but the patient is carrying on his life? Ant measure short of transplant?

An 80 yr old patient, or one inactive for other reasons--no.  However, one should not forget that for the first few years of CABG (1967-±'77), the main indication  for surgery was ANGINA, especially "disabling"; so, patient's activity level and desires are paramount in this situation.

Is coronary revascularization necessary for patients with well-developed coronary collaterals and coronary artery disease? May 31, 2015

This Q deserves clever comments:

First, Ersan Tatli et al. (2012) found identical 5-years survival in patients with well-developed coronary collaterals and CABG (80%) or medical treatment (84%), no different from PCI with intensive pharmacologic therapy vs intensive pharmacologic therapy alone (Courage Trial 2007) suggesting that coronary interventions are not better that drug treatment. Corollary: Think beyond the major 3-coronary arteries (Delgado-Almeida A. Recent Pat Cardiovasc Drug Discov. 2010).

Second, what’s next? Baroldi Giorgio was an international recognized experts and author: Coronary Circulation in the Normal and Pathologic Heart. Pp. 304; illustrated. Washington, D.C.: Armed Forces Institute of Pathology, 1967. He wrote “What I have learned by monitoring my own ischemia. Ital Cardiol. 1999; Oct.29 (10):1212-27.” Corollary: Coronary collateral anastomosis even with spontaneous bypass in the obstructed artery, improve blood flow but do not imply increased oxygen diffusion to the ischemic heart.

At the same time, Likoff William found the paradox of normal coronary arteriograms in unmistakable coronary heart disease, suggesting microcirculatory alterations or impaired oxygen diffusion (NEJM 1967). This syndrome attributed to coronary microvascular dysfunction (CMD) prevalent in women (The NHLBI-Sponsored Women's Ischemia Syndrome Evaluation, WISE Study), has been documented in both sexes, despite normal stress perfusion imaging in coronary arteries, and appears to be a major factor involved on the pathogenesis of hypertension and CHD.

Third, although it is evident that each part of the heart vascular system have a well known function, the incontrovertible fact is that O2 supply is only possible at the capillary bed, involving capillary endothelial function, flow-mediated relaxation substances, and the critical role for RBC H/K and O2/CO2 exchanges and K-O2 binding by oxyhemoglobin (Delgado-Almeida A. FASEB J, 2002). In this context, any defect inherited or acquired should have direct impact on the fine control of capillary blood flow and O2 delivery, probably involved on the pathogenesis and management of hypertension and CHD (Delgado-Almeida, A. J Am Coll Cardiol. Dec. 2014; 64(24):2710-12). Corollary: A carefully attention to RBC-K function could prevent or improve angina, ACS or heart infarcts.

Cardiovascular Drugs (Pro and Cons): While prescribed drugs are intended to relief the angina, which imply increasing O2 supply according to myocytes demand, the first line drug should be given by S.L. administration, improving RBC-K uptake and preparing hemoglobin for maximal K-O2 binding. This principle excludes direct intracoronary nitrates or similar bypassing lung capillary-RBC O2 exchanges, β-blocker as propranolol inducing “massive” RBC-K efflux and decreasing hemoglobin O2Sat% (Science, Agostoni A and Oski FA, in vitro assay, confirmed in our laboratory in hypertensive patients). However, Lichtman MA et al documented abrupt in vitro RBC-K efflux and marked RBC deformability by propranolol in venous blood from two hypertensive patients, with unexplained omission of the same studies when they received the propranolol tablets for 48-hour (Circulation 1974). Finally, similar K-depletion in RBC will require omission of Diuretics, Digoxin and inhibitors of gastric H-K ATPase exchange (Not K, no Acid. Physiology Review 2007).

Second, Calcium Channel Blockers  may affects Ca-dependant K channels in erythrocytes, although such effects has not been determined in acute or chronic angina, while drugs improving coronary dilatation will shift blood flow through non-disease arteries. In brief, non-satisfactory approaches? but if were active reversing angina would never sustain the effects on long-term treatment. At the end, AHA and New York Times (May 31, 2015) disclosed similar guidelines, confirming that we are far from our goals to reverse this problem.

The last but not the less, since the regulation of the entire capillary bed is critical dependent of K-ATP synthesis and release by RBC in the presence of low pH or low PO2 (Ellsworth ML et al, 2009), any drug improving RBC-K uptake and function would serve as the bases for new therapeutic approach in CHD. In this context, our novel drug Amiloride HCl Dihydrate simple reverse angina (72-hrs) with no recurrence (2-3 years), except for omission, reversing ST-T alteration while inducing new electrical voltages in areas of old infarcts, regardless of the years of infarction. How and why? Amiloride HCl Dihydrate enhances RBC-K uptake (30-40 min), inducing K-O2 binding by human hemoglobin and increasing O2Sat% by in vitro studies in humans venous blood. In our Laboratory no other CV have similar effects. Now, AHD stands as the first line drugs for CHD (Delgado-Almeida A., et al. ICCAD 2011, 2013; Recent Pat on CV Drug Discovery 20120, 2012 (not Recent Advances in CV Drug Discovery). 

Corollary: Reevaluate CV drugs on clinical symptoms and cardiology events, along with the drug effects on RBC-K content and function and O2Sat%, by in vitro venous blood studies. 

Look at myocardial perfusion nuclear or MRI study to resolve the question

Antonio R. Delgado-Almeida ·has given a superb analysis of the situation.  Unfortunally, many young surgeons "operate upon angiographic shadows' rather than live human organisms.  My clinical summary stands: what is the disease doing to the patient? and, can I really improve his function &/or prognosis? Never as clear as a picture on x-ray.

I am in agreement with Dr James Pate although we do not have the facilities for detail investigation for everybody but that 'live human organism' gives a lot of data. I have myself gone through that when my colleagues could not decide and I told them to keep that LIMA for future. That was about 15 years back and I am normally active.