Aa
Is this possible
I am a 50 year old caucasian male. I have had four major heart attacks since August of 07. I currently have five stents in various coronary arteries. I have my medical records since July of 08 when I suffered a heart attack while in the cardiologists office. The records state, among other things, that I have 100% occluded blockage of my right anterior descending artery. I'm not real sure what this means, is it possible to have this condition (twice now the surgeons have tried to pass a wire(catheter "m guessing) through it and failed, its too calcified) without having a MI? If I had a heart attack( I recall chest pain radiating out to my left arm and up my neck in 2005 but didn't act on it since I was taking care of my mother,; new job and a previous hospitlization for an intusseption where I underwent the 14th major surgery of my life... didn't want to lose the job so I just suffered). But the question remains, is it possible to have a coronary artery completely blocked and not suffer a heart attack?
ha, speak of the devil :) I had just made a little post on the history of nitro and then I read your reply here. I myself (with some unusual case of sudden onset HTN) tried nitro to see what would happen.
The first time, the results were super powerful. I felt it strongly in my aorta. My BP dropped like a rock. (I even experienced nitrogen narcosis.) The next day, I took 500mg niacin and wham, it was almost as powerful in vasodilating as the NTG had been. I had taken niacin many times before but it was not like that previously. The NTG seemed to have potentiated the niacin, or else the niacin released the NTG from some tissue where some had been stored.
I also got hold of some Imdur, which I take infrequently when BP is up and I can't get it down by other means.
As you know, the "real" NO is made in the endothelium, via endothelial Nitric Oxide Synthase. But nitrates are direct donors for NO, and the conversion takes place right in the mitochondria of the smooth muscle, without eNOS. Apparently there is some oxidative stress arising, which results in tolerance, and that's why vit C is suggested. Have you experienced tolerance, and does vit C ameliorate the tolerance?
(My father had used isosorbide mononitrate, and had a very pronounced tolerance. But I didn't know about vit C back then.)
The first time, the results were super powerful. I felt it strongly in my aorta. My BP dropped like a rock. (I even experienced nitrogen narcosis.) The next day, I took 500mg niacin and wham, it was almost as powerful in vasodilating as the NTG had been. I had taken niacin many times before but it was not like that previously. The NTG seemed to have potentiated the niacin, or else the niacin released the NTG from some tissue where some had been stored.
I also got hold of some Imdur, which I take infrequently when BP is up and I can't get it down by other means.
As you know, the "real" NO is made in the endothelium, via endothelial Nitric Oxide Synthase. But nitrates are direct donors for NO, and the conversion takes place right in the mitochondria of the smooth muscle, without eNOS. Apparently there is some oxidative stress arising, which results in tolerance, and that's why vit C is suggested. Have you experienced tolerance, and does vit C ameliorate the tolerance?
(My father had used isosorbide mononitrate, and had a very pronounced tolerance. But I didn't know about vit C back then.)
Thanks for your input. I have a positive outlook, and I have no symptoms, accept when I workout and that is corrected with a nitrate. Frankly, I consider myself fortunate not to have the symptoms expressed by many on the forum.
I compliment your contribution to the forum with your views and information. Take care.
I compliment your contribution to the forum with your views and information. Take care.
geez, I'm sorry to hear that, Ken. That prognosis must give you an outlook on life that few have.
I'm sure there's not much that you haven't thought of already, but hopefully it won't be irksome if I mention something that might merit a few words: whenever a risk figure is given, it's for the general population. Your own individual risk can vary, sometimes a lot, depending on your own modifiable risk factors.
I was just listening earlier today to a roundtable with Dr Ridker (the JUPITER study chair), where he mentioned the thought that will likely become commonplace within a few years... that lipid levels have to do with plaque formation, but rupture is more a function of inflammation. Naturally, Ridker would likely say that potent statins are the way to achieve lowering of inflammation, at least of CRP.
Somewhere along the line, though, I'd come across the notions that arginine does the same as statins... and that the likely mechanism is via increased Nitric Oxide, which itself is anti-inflammatory. For all-around increasing of NO, maybe the person to look to is Dr Ignarro, who was 1 of 3 to get the Nobel Prize for work on NO and arteries.
Anyway, I don't mean to step on any toes. Best of luck to you.
I'm sure there's not much that you haven't thought of already, but hopefully it won't be irksome if I mention something that might merit a few words: whenever a risk figure is given, it's for the general population. Your own individual risk can vary, sometimes a lot, depending on your own modifiable risk factors.
I was just listening earlier today to a roundtable with Dr Ridker (the JUPITER study chair), where he mentioned the thought that will likely become commonplace within a few years... that lipid levels have to do with plaque formation, but rupture is more a function of inflammation. Naturally, Ridker would likely say that potent statins are the way to achieve lowering of inflammation, at least of CRP.
Somewhere along the line, though, I'd come across the notions that arginine does the same as statins... and that the likely mechanism is via increased Nitric Oxide, which itself is anti-inflammatory. For all-around increasing of NO, maybe the person to look to is Dr Ignarro, who was 1 of 3 to get the Nobel Prize for work on NO and arteries.
Anyway, I don't mean to step on any toes. Best of luck to you.
A recent CT scan 64-slice angio (6/24/08) impressions comments are elevated calcium score (soft plaque between inner and outer linning). Total score is 1207.1 and the prognosis is a 50% probablity of a major heart event within a year.
LAD: There is severe amount of calcium and calicified plaque in the ostium of the LAD and appears to involve the distal left main, moderatre to severe degree. Following this there is an area of non-calcified with a severe stenosis with almost sensation of contrast in the proximal LAD. This is non-calcified p;aque. In the mid LAD is a very smal vessel and is diffusely diseased as well. The distal LAD appears to be relatively free of significant disease. The first diagonal branch is a large vessel that has moderate to severe degree of calicified plaque in its ostial course and the mid course has soft calcified and non-calcified plaque with moderate degree of stenosis. The LAD appears to be completely occluded in it proximal course
Circumflex has moderate degree of stenosis, etc.
RCA: Has large amount of calcium in its proximal course with a blooming artifact that appears to be a stent in its proximal course. Cannot visualize within the stent but there is good flow present just beyond and just prior, etc.
Symptomatically, there has been regression and very little progression, if any. Prior to chf my lipid profile was within the normal range; normal weight, no smoking, alcohol, etc. Medication has reduced lipids, (chol, etc.) into the accepted level...doctor stated it could not be better.
I don't believe a totally blocked vessel can benefit from medication. If there were a drug remedy vessel occlusions, it may require blood flow as you comment.
LAD: There is severe amount of calcium and calicified plaque in the ostium of the LAD and appears to involve the distal left main, moderatre to severe degree. Following this there is an area of non-calcified with a severe stenosis with almost sensation of contrast in the proximal LAD. This is non-calcified p;aque. In the mid LAD is a very smal vessel and is diffusely diseased as well. The distal LAD appears to be relatively free of significant disease. The first diagonal branch is a large vessel that has moderate to severe degree of calicified plaque in its ostial course and the mid course has soft calcified and non-calcified plaque with moderate degree of stenosis. The LAD appears to be completely occluded in it proximal course
Circumflex has moderate degree of stenosis, etc.
RCA: Has large amount of calcium in its proximal course with a blooming artifact that appears to be a stent in its proximal course. Cannot visualize within the stent but there is good flow present just beyond and just prior, etc.
Symptomatically, there has been regression and very little progression, if any. Prior to chf my lipid profile was within the normal range; normal weight, no smoking, alcohol, etc. Medication has reduced lipids, (chol, etc.) into the accepted level...doctor stated it could not be better.
I don't believe a totally blocked vessel can benefit from medication. If there were a drug remedy vessel occlusions, it may require blood flow as you comment.
> I have had a completely blocked LAD for at least 5 years,
Ken, have you achieved any regression in any coronary vessel over the years? Have you tried to do that at all, e.g. with high doses of potent stains and/or strict diet?
Lastly, as side note, with 100% blockage in any vessel, is regression even possible because there is no flow?
Ken, have you achieved any regression in any coronary vessel over the years? Have you tried to do that at all, e.g. with high doses of potent stains and/or strict diet?
Lastly, as side note, with 100% blockage in any vessel, is regression even possible because there is no flow?
Yes, you can have a completely occluded coronary artery and not have an acute heart attack. However, if sufficient blood oxygen is not reaching heart cells as a result of ischemia the heart cells can begin to die (negrosis) and heart failure ensues. An acute heart attack usually happens when a clot quickly cuts the blood supply, and an emergency to open the vessel is required.
I have had a completely blocked LAD for at least 5 years, and collateral vessels provide a natural bypass. I had hypokinesis (heart wall movement impairment), but a stent implant 98% blocked RCA, added additional blood to the deficit area. apparently, the heart cells were what is medically trermed hibernating heart cells, and medication has returned by left ventricle to normal size and it is pumping adequately (EF 59%).
When you have angina (chest pain) that indicates your heart cellls are not getting enough blood/oxygen. This condition should be treated with at least medication to open the vessels enough not to experience angina. You can continue to have heart cell damage without angina...called silent ischemia.
I have had a completely blocked LAD for at least 5 years, and collateral vessels provide a natural bypass. I had hypokinesis (heart wall movement impairment), but a stent implant 98% blocked RCA, added additional blood to the deficit area. apparently, the heart cells were what is medically trermed hibernating heart cells, and medication has returned by left ventricle to normal size and it is pumping adequately (EF 59%).
When you have angina (chest pain) that indicates your heart cellls are not getting enough blood/oxygen. This condition should be treated with at least medication to open the vessels enough not to experience angina. You can continue to have heart cell damage without angina...called silent ischemia.
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