I thought I'd try to begin a thread on the very important issue of collateral circulation as it realated to cardiac survival.
It's a remarkable process where myriad routes of tiny arterioles and capillaries expand in size and number to carry blood around an arterial blockage (and presumbably in venous blockage also!)
The collateral circulation can be from the top of a blockage (proximal) to a point beyond the blockage at the bottom (distal) thus mititgating the effect of an otherwise damaging and often deadly cessation of blood flow.
Amazingly sometimes the routing is even from one artery to another often spanning accross the heart from the left decending system to the circumflex or even RCA (right) system.

Obviously the blockage spurs the circulation and it becomes a race to see if the collateralization keeps up or a heart attack occurs!

I survived for at least a decade with collaterals around a virtually complete RCA blockage from top proximal to distal right artery (same one.) I only noticed the deficiency of blood flow during peak stress....maybe 5-10 minutes a day max!

Now, HOW do we make the collateralization progress faster than the blocking? Neither drug companies nor cardiologists really seem to care about the topic (quite naturally- we live in a capitalist society.)
But WE MUST care! We MUST find a way to enhance this process.

Let me throw a couple of my thoughts out ("Partially baked ideas", if you will: an old Mensa term for decent thoughts not fleshed out...NEVER to be confused with HALF baked ideas :D )

I'm an engineer and I know that hydraulics demonstrates that a way to push a new channel through is higher pressure. Is perhaps high blood pressure a way that evolution has blessed mankind in its need for coronary and cerebral collaterals...not likely that the everpresent hypertension developed from cave man days solely to enrich doctors and drug manufacturers...or to give us red faces when we get angry! :D

This line of thinking also goes to the subject of hard cardiac workouts to get BP up so high that it can safely force through some new arteries when needed (without blowing any out :eek: )...I'm thinking Ubernier's peak exercising (and mine lately as well :bouncing: )

It has always struck me a wrong-thinking to use drugs that weaken the heart's pumping ability and strength (beta and calcium channel blockers) in an effort to develop cardiac health. Lessening of pain frequency may be admirable but what if it's at the cost of slowing down auto-revascularization.
Perhaps all the studies that show that people with high blood pressure are at higher risk of heart disease have it asp backwards. Maybe the growing blockages are putting the body into a state where it it most able to revascularize with higher hydraulic pressure to force new channels! If this is correct then perhaps ALL methods of BP overcontrol are counterproductive for cardiac health, fighting the body's best efforts to survive!

Of course, it would seem any method to stop clotting (such as daily aspirin) which will prevent catastrophic total blockage, or any any anti inflammatories (also aspirin) which will prevent plaques from becoming unstable and blowing open...also causing clotting and blocking are HIGHLY desirable to buy time for the slow coollateraliztion.

I've seen some research last week on drugs that hope to stop cancer's ability to "call" vascularization from adjoining vessels, a process which allows the tumor to feed. These drugs might be effective at blocking certain receptors on blood vessels so they don't grow over to the nearby tumor, thus starving it.

Maybe we should be learning from the cancer cell and develop some of it's chemical devices to SPUR vascularization where needed...perhaps in people with 40% blockages, or some arbitrary break even point between benefit and risk.

Any thoughts?

There are two sources I found when I was researching noninvasive alternatives to treatment for CAD. One is from the journal Circulation. 2002;105:666 and the other is from Reviews in Cardiovascular Medicine 2002;3:5.

The Veterans Affairs Non-Q-Wave Infarctions Strategies in Hospital (VANQWISH) trial showed the noninvasive strategies not only to be more economical, but those who were treated medically had better survival 76% of the time.

This is one of the more recent studies I cited to Dr. Wayne's detractors on this board and that no one was able to effectively refute. But that is an old discussion from another flood.

Thanks for renewing the debate Zip2play. I will review what is written here faithfully and perhaps even contribute now and then. However, I am far from a candidate for MENSA, so I will probably be more of an observer.

Jeff
:jester:

The thing about the beta blockers is what about the person who was not on beta blockers until after they already had the heart attack? Why did their blood pressure not go up and create collateral arteries if that is it's mission. Another question is why do you need the collateral arteries if it has been bypassed or stented? I realize these can block again, but will collateral arteries that form around a bypassed blockage help in any way? And will collateral arteries even form if the blockage is bypassed?
I take a small dose of ToprolXl and I've wondered if slowing down the heart is good for it as well? They tell me it will make my heart not have to work so hard but I'm not so sure that is a good idea either.

NineLives,

I'd probably consider a person who had extensive plaques WITHOUT High Blood Pressure anomalous. Of course a heart attack can hit out of the blue from a rogue clot formed near or in the heart chamber, even from pooling because of some rhythm defect. Pre-collateralization doesn't enter this picture at all.
But my guess is the rule of thumb is that HBP (treated or not) preceeds heart disease? I might be wrong here. But even in the presence of normal blood pressure measured by arm cuff, fluid dynamics indicates an extremely high pressure MUST exist immediately above a constricting plaque and a very low BP immediately below it. IDEAL conditions to force new channels between the pressure differentials <pardon the engineering jargon sneaking out:D>.

I would think that a stent or a bypass would pretty much stop the collateralization in it's tracks. (I hope my extensive network REMAINS though, because I might need it in the future for other plaques (vessel to vessel) or indeed for passing around a clogging stent <please lord, no!>

In the sad event of a heart attack with death of a portion of the heart (nothing can reclaim it), the pressure above the total block must be enormous (squeeze a hose shut!) This would force collaterals that might save the margin of the heart that hasn't died but is VERY short of food...this marginal area MUST exist! Also the pressure can force the network into other areas of the heart for future protection from local plaques (where there's one there's often many.)

Jeff,
I will see what the NYPublic Library has in Circulation circulation:D:D! Are you doing anything geared specifically to revascularize. It seems most of your regimen is a high dosage approach to BP lowering and heart exertion easing. Have I missed something?
Are you getting CIRCULATION on-line/is there a fee?

Consider this.
How about a plan where a person with angina works to the point of pain maybe twice a day WITHOUT heart slowing meds and then CONTINUES to work through the pain instead, at a rate that JUST holds the pain slight but present...say, 5 to 10 minutes (maybe longer.)

My partially baked theory would have this as the point where revascualarization occurs most readily. A test on the effectiveness of the work would be whether or not exercise ability before pain increases at a noticeable pace over a few weeks or months.

SCARY though, eh? I know the natural tendency is to stop immediately til the pain abates and then sit quietly...and PANIC!:D

But again, medications like beta blockers and calcium channel blockers would seem to prevent the whole process from occurring. The accepted theory being basically, if there's pain take more drugs! <Can't imagine WHO dreamt THAT up?:D:D>

As an aside:
My first hand experience was with my mother with 3 big blockages. Her options were to have a bypass (before the age of stenting- plain vanilla angioplasty was rarely done on women[smaller vessels??]) or to take the betas, ccbs, ACEinhib, thiazides, nitrites and REST. She opted for fistfuls of drugs and survived less than 10 years...and it was not a good 10 years with progressive weakening and more and more frequent and debilitating pain (and drugs) and hospitalizations.

Hi Zip:
Your partially-baked idea sounds plausible. It reminds me of some of the stuff I've read on neuroplasticity, where new neural pathways (bifurcations) develop in response to damage (stroke, etc.). It seems the body is capable of repairing itself to some degree, given the incentive to do so. In your example, that incentive would be the difference in pressure gradients between two sections of a blocked artery. The new pathway, given its original orientation with respect to flow, would continue along the same orientation until it merged with the same artery, or one in close proximity. Would this suggest that a blockage that occurs at the proximal end of the artery would develop more pathways than one that occurs at the distal end? In any event, I agree that the use of drugs ("dampers") would disrupt this self-regulating system, assuming that some critical threshold in pressure is the trigger that sets things in motion. You pose some interesting questions about the true "efficacy" of drug therapy.

Zip2play,

The two references I gave you are available free. Do a Google search on "revascularization techniques" or "revascularization medication." One article hits on stents specifically, but it gives the high rates of restenosis after stenting, which sounds too high for me to want to go that route.

As for my medication regimen, what I wrote is what I am on. I am not certain how these meds enahnce revascularization, but I am told by Dr. Wayne that they will. I need to study the issue a lot more and I appreciate your efforts.

How about a plan where a person with angina works to the point of pain maybe twice a day WITHOUT heart slowing meds and then CONTINUES to work through the pain instead, at a rate that JUST holds the pain slight but present...say, 5 to 10 minutes (maybe longer.)

I know I did essentially this during the seven months prior to treatment. I do believe the pain is our body's way of telling us to slow down and do something about the problem. I'll tell you what I would suggest, go to Dr. Howard H. Wayne's website (I know I can't post it here, but you can do a Google search on "noninvasive heart center') and e-mail a question or two to him. He is an excellent correspondent. He answered each of three rather long e-mails I sent him before becoming his patient and he did so within a day or two each time.

Jeff
:jester:

Tschuess,

Yes, I'd assume that proximal auto-revascularization occurs much more readily than distal. And thank God for that because a blockage in a tiny distal artery might not cause more than a little cramp if anything. By the time you are at the end of the arterial chain, very little damage can occur. The ever shrinking tiny arteries and arterioles provide the resistance to keep lowering pressure until at capillary level it's near nil.
If, however you mean distal vs. proximal on an unbranched artery...well then pressures would be similar (fluid through an unrestricted liquid is constant throughout it's volume.)

Jeff,
I'll see if I can find those freebie CIRCULATION articles. Did they give you the option of stenting?

Hi guys. I had four vessel blockage with normal blood pressure. Not even a slight rise. I did have a resting pulse of 80 to 85, but that has been the same for years. As you know if you have read my previous posts I also had no symptoms before quad bypass. All problems were found on a routine screening stress EKG followed up by stress EKG with echo and then cardiac catheterization. At the time of my bypass I was walking two miles five days a week, pushing a mower for an hour at a time--uphill at times and continuing on with my activities of daily living. I asked the cardiac surgeon before my bypass if I had this much blockage (I felt surely he was looking at someone else's results!) wouldn't I have had symptoms. He said that because I was diabetic it was very common for them to have extensive blockage without symptoms. Why? Do we (diabetic) have no nerve endings or what? Why was I not short of breath, have swelling in my legs, etc. On echo stress test the technician told me my heart looked great. I had exercised to full limits and as far as she could tell everything looked great. When they called to tell me that the cardiologist felt it was abnormal I was confused. He told me that my heart looked good, except that it looked like I might have a little blockage in the front, otherwise it was pumping well. Imagine his and my surprise when three vessels were 95% blocked and one was 70% blocked. So your theory might be correct. Maybe collateral arteries develop and carry the oxygenated blood to the heart. My endocrinologist says this happens in the legs if you walk on a regular basis. Diabetic develop problems with circulation in their legs, but if you continue to walk it forces blood to flow through other collateral smaller vessels. Interesting.

Fascinating stuff, KShortie.
Gee, I can imagine how horrible you must have felt when told of the symptomless need for such extensive surgery!:(

I think your doctor was "full of it" when he extrapolated the leg numbness from nerve damage to foot nerves that is common to advanced diabetes to your lack of heart pain. You felt no heart pain for the same reason I was able to go 10 painless years the with my right coronalry artery completely closed suffering nothing more than occasional heartburn...you had developed an extensive collateral circulation.

I really think there's a Nobel prize and a $billion bucks out there for someone who can enhance the process!