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Coronary CT Angiogram
From Irshad Khan, New Delhi, India
I have taken last week CT Angiogram and its findings are worrisome. The main impressions are:
Calcium score: 18, Soft plaques seen in proximal LAD and D1 segment.
LEFT CORONARY ARTERY
LM - Normal
LAD - (Prox/Middle/Distal)- Type -III LAD with normal course. Focal Eccentric non-calcified plaque seen with moderate luminal narrowing.
Diagonals----
D1 ----- Single large D1 branch seen with normal course. Mid vessel reveal plaquing with moderate luminal narowing.
Obtuse Marginal Branches
OM1 --- Normal
OM 2 --- Large OM2 artery seen with distal branching. Proximal vessel reveal focal luminal narrowing with approx 60-65 % stenosis.
Please advise me what course of treatment is advisable.
I have taken last week CT Angiogram and its findings are worrisome. The main impressions are:
Calcium score: 18, Soft plaques seen in proximal LAD and D1 segment.
LEFT CORONARY ARTERY
LM - Normal
LAD - (Prox/Middle/Distal)- Type -III LAD with normal course. Focal Eccentric non-calcified plaque seen with moderate luminal narrowing.
Diagonals----
D1 ----- Single large D1 branch seen with normal course. Mid vessel reveal plaquing with moderate luminal narowing.
Obtuse Marginal Branches
OM1 --- Normal
OM 2 --- Large OM2 artery seen with distal branching. Proximal vessel reveal focal luminal narrowing with approx 60-65 % stenosis.
Please advise me what course of treatment is advisable.
Q: Coronary artery disease is not caused by stents, it is caused by a few possibilities, but certainly not stents."
...Turbulance has a role to produce a site for a lesion. A good example is the branching of the LAD and ICX from the main. Increased blood velocity increases turbulance. Blood velocity is a function of pressure and resistence both which will enable an occlusion.
Q: "If a patient has high risk and progressive disease, eventually the coronary arteries will not be able to open and support collateral feeds in any form".
Collateral vessels develop from the gradient pressure of the occluding vessel. When collaterals are in place and functioning the end point of the occluded vessel can/will terminate and collateral vessels will hopefully supply the deficit area for sufficient blood flow. Your comment seems to suggest you believe there is a bridge from the proximal side of the blockage and a direct link to distal side of the occluded vessel....that is not necessarily so and frankly I don't believe that happens because the pressures down stream on the same occluded vessel won't happen for the reason you stated and that makes sense. If I understand the comment!
Q: "Collaterals have to get their feed from somewhere. Stenting doesn't cause lesions in other vessels or distal in the same vessel, turbulence in a stent can cause clots in that stent though which is why plavix is so important, especially combined with aspirin".
...It is my understanding plavix relates to blood clots not plaque, whatever. But that is another subject. It is my understandiong the distal end of the occluded vessels ends and contributory paths for blood flow dry up from the distal end of the occluded vessel. That is why to open an occluded vessel redistributes blood flow through the newly open occlusion and that puts pressure on other vulnerable segments of the cariovascular system and possilbly shut down the collateral flow and not that not effectively open the closed vessels. It changes the hemodynamics of the system associated directly and indirectly to other segments. If one envisions a closed circuit, it would be obvious for every element of the hemodynamics of blood flow and fluid physics there will be a reaction to the changing dynamics of the closed circuit that doesn't have infinite blood volume and must maintain the equilibrium of right and left side of the heart. Every hemodynamic action is compensated by a reaction and that may decrease blood flow to vulnerable heart locations, increase compensatory resistence, velocity and pressure.
Also, I don't know if I have said this on another occasion but a stent props open a segment of the occluded vessel and that does not constrict with the normal response of the proximal or distal portions of the vessel. This would increase the gradient pressure and turbulance, etc. etc. Just thinking about now, it could cause an aneursym.
...Turbulance has a role to produce a site for a lesion. A good example is the branching of the LAD and ICX from the main. Increased blood velocity increases turbulance. Blood velocity is a function of pressure and resistence both which will enable an occlusion.
Q: "If a patient has high risk and progressive disease, eventually the coronary arteries will not be able to open and support collateral feeds in any form".
Collateral vessels develop from the gradient pressure of the occluding vessel. When collaterals are in place and functioning the end point of the occluded vessel can/will terminate and collateral vessels will hopefully supply the deficit area for sufficient blood flow. Your comment seems to suggest you believe there is a bridge from the proximal side of the blockage and a direct link to distal side of the occluded vessel....that is not necessarily so and frankly I don't believe that happens because the pressures down stream on the same occluded vessel won't happen for the reason you stated and that makes sense. If I understand the comment!
Q: "Collaterals have to get their feed from somewhere. Stenting doesn't cause lesions in other vessels or distal in the same vessel, turbulence in a stent can cause clots in that stent though which is why plavix is so important, especially combined with aspirin".
...It is my understanding plavix relates to blood clots not plaque, whatever. But that is another subject. It is my understandiong the distal end of the occluded vessels ends and contributory paths for blood flow dry up from the distal end of the occluded vessel. That is why to open an occluded vessel redistributes blood flow through the newly open occlusion and that puts pressure on other vulnerable segments of the cariovascular system and possilbly shut down the collateral flow and not that not effectively open the closed vessels. It changes the hemodynamics of the system associated directly and indirectly to other segments. If one envisions a closed circuit, it would be obvious for every element of the hemodynamics of blood flow and fluid physics there will be a reaction to the changing dynamics of the closed circuit that doesn't have infinite blood volume and must maintain the equilibrium of right and left side of the heart. Every hemodynamic action is compensated by a reaction and that may decrease blood flow to vulnerable heart locations, increase compensatory resistence, velocity and pressure.
Also, I don't know if I have said this on another occasion but a stent props open a segment of the occluded vessel and that does not constrict with the normal response of the proximal or distal portions of the vessel. This would increase the gradient pressure and turbulance, etc. etc. Just thinking about now, it could cause an aneursym.
agrajjain, Thanks for your response and sharing your experience. I agree with irshad for his assessment that stress test would be better for you and others with a similar condition. Why? If I remember correctly you do not have angina with exercise and you don't know your capacity for the most beneficial cardio workout (with angina one knows the limitation). A stress test lets your doctor know how well your heart muscle is being supplied with blood, its functionality, etc. and the test will provide your heart/respiratory capacity for a workout and what are your limitations based on the vital signs and it will also establish a basis for future tests.
A cath would observe if there are any blockages and whether or not a stent implant is necessary (my opinion at that time of intervention cardiologist is inclined to implant a stent rationalizing the patient would need a stent later and might as well do it now for occlusions that really do not require immediate treatment and possibly never.
About 8 years ago, I had stent implant in my RCA and a 72% ICX blockage and not stented at that time. About 2 months later the cardiologist wanted to stent the ICX, and could not answer my question why a stent now and not at the time of the angioplasty. The doctor left the employment a few weeks later...my current and subsequent cardiolost has never suggested an angioplasty!? In my opinion the first interventional cardiologist was attempting to double dip and somewhat evident he could not answer my question, why now?.
Take care and I wish you well going forward.
A cath would observe if there are any blockages and whether or not a stent implant is necessary (my opinion at that time of intervention cardiologist is inclined to implant a stent rationalizing the patient would need a stent later and might as well do it now for occlusions that really do not require immediate treatment and possibly never.
About 8 years ago, I had stent implant in my RCA and a 72% ICX blockage and not stented at that time. About 2 months later the cardiologist wanted to stent the ICX, and could not answer my question why a stent now and not at the time of the angioplasty. The doctor left the employment a few weeks later...my current and subsequent cardiolost has never suggested an angioplasty!? In my opinion the first interventional cardiologist was attempting to double dip and somewhat evident he could not answer my question, why now?.
Take care and I wish you well going forward.
I took Thallium (MIBI) test today which has the following report:
"Quantitative Gated Mycardial Perfusion Study performed using 99mTc Tetrofosmin in the one day Stress/Rest Protocol. The maximum Heart Rate achieved during stress on TMT was 147 BPM (91% THR). Max. Blood Pressure 134/82 mmHg, duration of exercise was 6.10 minutes (5 METS) on Bruce Protocol. Exercise terminated on as Target HR was attained.
LV cavity appears normal in size.
Tracer distribution in the entire left ventricular myocardium is within normal physiological limits at both stress and rest.
Quantification using the QGS/QPS Protocol shows no evidence of haemodynamically significant reversible Ischemia.
Functional Information: Multi Gated resting SPECT images show good wall motion and systolic thickening in all regions of the LV myocardium with good global LVEF.
Impression
• No scan evidence of stress induced reversible ischemia noted in the LV myocardium.
• Good resting LV systolic function as estimated by quantitative Gated SPECT."
I saw the Cardiologist and he ruled out necessity of cath angio as MIBI test showed good blood flow/circulation in my coronary arteries and there is no reversible ischemia. However, to deal with narrowing and preventing further narrowing I will be on statin and aspirin and no beta blocker.
My conclusion is first, CT angio is not very accurate. Second, one should not rush for cath angio if there are no symptoms of angina. Third, always take second and/third opinion if a Dr decares you having heart disease or on may have heart attack.
Thanks for all the members of this group for their useful opinions that helped me in avoiding cath angio intervention. It is goof forum and I will continue to participate and shere my experience and learn from yours.
"Quantitative Gated Mycardial Perfusion Study performed using 99mTc Tetrofosmin in the one day Stress/Rest Protocol. The maximum Heart Rate achieved during stress on TMT was 147 BPM (91% THR). Max. Blood Pressure 134/82 mmHg, duration of exercise was 6.10 minutes (5 METS) on Bruce Protocol. Exercise terminated on as Target HR was attained.
LV cavity appears normal in size.
Tracer distribution in the entire left ventricular myocardium is within normal physiological limits at both stress and rest.
Quantification using the QGS/QPS Protocol shows no evidence of haemodynamically significant reversible Ischemia.
Functional Information: Multi Gated resting SPECT images show good wall motion and systolic thickening in all regions of the LV myocardium with good global LVEF.
Impression
• No scan evidence of stress induced reversible ischemia noted in the LV myocardium.
• Good resting LV systolic function as estimated by quantitative Gated SPECT."
I saw the Cardiologist and he ruled out necessity of cath angio as MIBI test showed good blood flow/circulation in my coronary arteries and there is no reversible ischemia. However, to deal with narrowing and preventing further narrowing I will be on statin and aspirin and no beta blocker.
My conclusion is first, CT angio is not very accurate. Second, one should not rush for cath angio if there are no symptoms of angina. Third, always take second and/third opinion if a Dr decares you having heart disease or on may have heart attack.
Thanks for all the members of this group for their useful opinions that helped me in avoiding cath angio intervention. It is goof forum and I will continue to participate and shere my experience and learn from yours.
Exactly right. Each case is independent and there is no ONE rule for every patient. This is why it's important to weigh everything up before agreeing to anything.
Each person can speak about his own case only and should not be generalised. With the help of doctor intelligent peoples can find out better ways for their own treatment. Probliem with some doctors is due to ignorance they do not want to share the procedure with patients particularly intelligent patient. Here doctor is missing opportunity of further research in the subject. Of course things depend upon the time available. How much desire I may have still I can not exchange all the information with me about my disease with you or even with doctor some time. Sufficient time is needed which does not come free. But due to that opportunity of knowing some thing new is lost. Still I am happy that discussions here are going on smoothly and with understanding.In my case I am disputing the results of catherter angiography because I discussed with doctor how percentages of blockages are caulated. I am sure doctor is wrong and i will be going for catherter angiography again some time next year or two. Thank you. I hope I will come back to you then to report.
"Yes, based on fluid dynamics. For instance, when a there is a stent implant the coronary wall is propped open and the other sections of the vessel normally continues to dilate and constrict when stimulated,..This wil cause turbulence when a portion that has a stent implant has a wider fixed diameter than the lumen prior and subsequent to the stent portion and is directly proportional to the length of the implant and/or end to end implants"
Oh wow. I really couldn't disagree more. This is why I asked you a question with a given scenario a while ago which you seemed reluctant to answer. Let me put it to you this way.
Coronary artery disease is not caused by stents, it is caused by a few possibilities, but certainly not stents. If a patient has high risk and progressive disease, eventually the coronary arteries will not be able to open and support collateral feeds in any form. The blood has to come from a coronary artery, but it flow/pressure is too low in all vessels over time because intervention is avoided, then nothing will develop. The patient is simply waiting to die. Collaterals have to get their feed from somewhere. Stenting doesn't cause lesions in other vessels or distal in the same vessel, turbulence in a stent can cause clots in that stent though which is why plavix is so important, especially combined with aspirin. If a patient ignores risk factors they can remove, such as prolonged stress or smoking, stents or not, they will continue to develop lesions. Collaterals closing down due to stenting is not bad thing either. The body opens collaterals in SOME patients when required, but if they are no longer required, they will close. If flow/pressure is adequate through the native vessels again, why would you need collateral vessels?
Stenting saves millions of lives every year but I still fail to see why you are so anti. When my LAD was opened, I felt fantastic and don't require nitrates, beta blockers or blood pressure meds. I have no restriction on exertion and have never felt better in 6 years.
In march this year I had to have 2 blockages stented. However, previous angiograms did reveal a small amount of disease in that area. I went through a period of high stress for 6 months due to family issues and this caused the progression. It wasn't because I had other stents, it was because of the stress. As I endured the stress I could feel problems developing and I warned Doctors. The new blockages were mid LCX and distal to this would have been the collaterals which were feeding my once blocked LAD. If my LAD hadn't been re-opened, I would have lost those collaterals, and had a blocked LCX. I would have very likely died. So it looks as though having my LAD opened was the best decision I've ever made in my life.
Oh wow. I really couldn't disagree more. This is why I asked you a question with a given scenario a while ago which you seemed reluctant to answer. Let me put it to you this way.
Coronary artery disease is not caused by stents, it is caused by a few possibilities, but certainly not stents. If a patient has high risk and progressive disease, eventually the coronary arteries will not be able to open and support collateral feeds in any form. The blood has to come from a coronary artery, but it flow/pressure is too low in all vessels over time because intervention is avoided, then nothing will develop. The patient is simply waiting to die. Collaterals have to get their feed from somewhere. Stenting doesn't cause lesions in other vessels or distal in the same vessel, turbulence in a stent can cause clots in that stent though which is why plavix is so important, especially combined with aspirin. If a patient ignores risk factors they can remove, such as prolonged stress or smoking, stents or not, they will continue to develop lesions. Collaterals closing down due to stenting is not bad thing either. The body opens collaterals in SOME patients when required, but if they are no longer required, they will close. If flow/pressure is adequate through the native vessels again, why would you need collateral vessels?
Stenting saves millions of lives every year but I still fail to see why you are so anti. When my LAD was opened, I felt fantastic and don't require nitrates, beta blockers or blood pressure meds. I have no restriction on exertion and have never felt better in 6 years.
In march this year I had to have 2 blockages stented. However, previous angiograms did reveal a small amount of disease in that area. I went through a period of high stress for 6 months due to family issues and this caused the progression. It wasn't because I had other stents, it was because of the stress. As I endured the stress I could feel problems developing and I warned Doctors. The new blockages were mid LCX and distal to this would have been the collaterals which were feeding my once blocked LAD. If my LAD hadn't been re-opened, I would have lost those collaterals, and had a blocked LCX. I would have very likely died. So it looks as though having my LAD opened was the best decision I've ever made in my life.
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