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smoking

My blood presure has always been 117/78. I quit smoking last year and my blood presure is now 140/90 the only thing that changed is that I quit smoking and I have gained 20 lbs. The very thing has happened to my supervisor. We both have not smoked in 11 months. Any ideas.
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Avatar_n_tn
Congratulations for kicking the habit...The increase in your blood pressure may well be due to the 20# weight gain. I would work on cutting back on high calorie snacks and high calorie desserts if you've been eating them (subsitute fresh fruits) and try to increase your walking and physical activity. Good luck!
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976897_tn?1379171202
That seems strange to me because smoking normally raises blood pressure.
I gave up when I had my heart attack and then 9 months later I was told I would be having a triple bypass which scared the hell out of me. I went outside the hospital and lit up a cigarette. I had to sit down quickly because I went so light headed. I'm not sure how I managed to get back to the ward without falling over, but the nurse took my BP which was suddenly very high. It took an hour to drop.
What about your diet? you say you have gained weight, but this can be through a higher fluid intake often associated with quiters. Are you consuming lots of caffeine? or maybe salt?
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Avatar_f_tn
When you quit smoking your lungs immediately start repairing themselves, but the damage to your coronary artery system is forever!  The weight gain plays a role, I'm sure you're more stressed with not smoking, and you need to exercise and avoid caffeine and salt.  Regardless, you need to address this with your doctor.  It's awesome that you are being vigilant with watching your BP as this will prevent future problems.  Your BP is only slightly elevated, but talk to your doctor about it.  My husband is suffering very badly from his smoking days that ended 27 years ago.  I have a sister-in-law who is dying from emphysema and still smokes, I guess to hurry up the process.  Kudos to you for quitting!!!
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976897_tn?1379171202
"but the damage to your coronary artery system is forever!"

That statement is actually far from true. In fact, everyone develops tiny fractures in arteries which are quickly repaired by the body. Maybe you are referring to disease rather than damage?
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Avatar_f_tn
NO!! This is fact!  I see and speak with several cardiologists on a regular basis regarding this issue and those are their words.  My husbands problems are a direct result of his smoking many years ago.  They call it damage which maybe leads to disease, but they still use the word "damage."
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976897_tn?1379171202
Im just saying that the way you state it is not entirely accurate. It's like saying if you cut yourself and damage an artery, it will never repair and you will bleed to death. Also, as I stated above, damage to everyones arteries, even healthy people, occurs all the time. This is why eating a healthy diet is important, to give the body what it needs to repair them. I believe you have misunderstood the cardiologists. They are probably stating the situation with your Husbands arteries, not everybodys in general.
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Avatar_f_tn
This is how it's been said to me many times....once one stops smoking, their lungs start to repair themselves immediately, but the damage to their cardiovascular system is forever.
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Avatar_f_tn
Here is a direct quote out of a textbook.  Smoking "damages" the innermost layer of the coronary arteries, known as the endothelium.  Causing the arteries to have difficulty expanding in response to increased blood flow.  Endothelial dysfunction may occur in teenagers and young adults as a result of tobacco use.  Endothelial dysfunction, or the loss of proper endothelial function, is a hallmark for developing vascular "disease" and often leads to artherosclerosis.

The "damage" leads to "disease."  It doesn't heal itself.
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976897_tn?1379171202
You are really missing my point. You first stated that artery 'damage' is for life. I stated that arteries can heal themselves because we witness that when we are cut. You then state that smoking causes artery disease and quote some text. So now we have slightly changed the subject from artery damage is for life, to , smoking causes artery damage which is for life, or disease which is for life.
I still don't agree that either of those are the case with everyone. In fact, through medication it has been witnessed in many people that atherosclerosis stops in its tracks and in some people it actually improves. However, in some people it continues to worsen. The problem is, atherosclerosis can be caused by several factors and unless you find the specific cause for your own body, then it will never slow down or stop.
If someone smokes and then packs in the habit, their arteries will obviously start to improve to some extent. However, if they are a stressful person, which is perhaps why they smoked, then the disease will continue. All the risk factors have to be removed.
If reports say that atherosclerosis has improved in some people through the use of drugs such as statins, then I don't know why your cardiologist is contradicting this?
This is another classic situation where contradictions in the medical profession arise and confusion is the result. I'm not looking for an argument Mammo, I'm simply saying that there are obviously two views on this and I'm not sure why.
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159619_tn?1318997813
"If reports say that atherosclerosis has improved in some people through the use of drugs such as statins, then I don't know why your cardiologist is contradicting this?"

I don't think anyone is taking the position that statins repair artery damage, they only reduce Low-density lipoprotein (LDL), just one of the three components of  atheromatous plaques, which in turn helps prevent atherosclerosis. Perhaps I have missed it, but I've never read anything about statins repairing damaged arteries. I have read that they appear to be potent and effective cardioprotective agents however.

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976897_tn?1379171202
Something taught to everyone in cardiac rehabilitation in the UK. I will try to find out where they got this information.
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976897_tn?1379171202
Here are some interesting articles.

http://www.sciencedaily.com/releases/2007/02/070207091532.htm#

The newest statin, rosuvastatin, has been the first to demonstrate regression of atherosclerotic plaque within the coronary arteries by IVUS (intravascular ultrasound evaluation)

Actually the internet is full of reports on this, it would take a whole forum to list them all. There are also some reports that claim through trials, that lowering LDL-c enough along with raising HDL has produced regression of Atherosclerosis.
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976897_tn?1379171202
However, I still stand by my personal viewpoint that a singular therapy regime is not adequate to treat everyone. I still firmly believe that if someone leads a high stress lifestyle that statins or lowering cholesterol through other means will not slow the progression of the disease. The initial cause of the disease, the primary cause, has to be the target for treatment first, everything else should be secondary.
I still believe there are many studies needed to fully understand how some people are immune to the believed risk factors. some very obese people have no problems with their coronary arteries. Some heavy smokers have very clear vessels. Some people with high blood pressure have no disease. So, perhaps the whole underlying cause needs to be examined more closely and the relationships between Atherosclerosis and Lipids certainly needs to be understood if we stand a chance of combating the disease. There are still so many blanks in the book of knowledge for Atherosclerosis. We probably have ten pages filled in a 50 page manual, the rest are blank.
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Avatar_f_tn
I agree that there is a lot to be learned regarding this.  But it has always been my understanding that statins merely prevent further plaque build-up and do nothing for the existing plaque, and this is why we have stenting and surgeries for this.  The cardiologists said my husband's two blockages were like concrete and the only way to remove it was with surgery.  Then you also run the risk of a piece breaking loose and going into the blood stream.  I can't imagine anything effective enough to start dissolving something as hard as plaque can be, or if there was it would have to take a very long time to see any effect of it working. Since most plaque build-ups are at a later age, who would have the time for this?  I wish I had the answers.
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976897_tn?1379171202
"I can't imagine anything effective enough to start dissolving something as hard as plaque can be, or if there was it would have to take a very long time to see any effect of it working. Since most plaque build-ups are at a later age, who would have the time for this?  I wish I had the answers"

Those are some of the questions I have pondered over for the last two years and ones which Cardiologists tend to carefully avoid answering. I do know however that not everyone has reached the late stage of atherosclerosis before treatment because it would not be possible to balloon the plaque into the artery wall for a stent. Maybe this is one reason they decide to push for a bypass. Many stents are placed against soft fatty tissue which hasn't yet formed a calcified covering. I suppose there is also the possibility that removing some of the fats (foam cells) under the plaque covering, may help it to reduce in size because the plaque is no longer being pushed out into the artery? I agree that plaque becomes very hard over time, I witnessed it being chipped away in my LAD. However, isn't plaque mostly made up from calcium? which I believe the body has the ability to break down. I remember there were some experiments run a while ago with certain vitamins used to promote bone growth. If memory serves me right, they found that reducing the vitamins reduced plaque in the arteries, increasing them increased plaque in the arteries. However, this also reduces or increases our ability to continually replace worn bone tissue in our joints. A bigger study was going to be started to see if a better understanding of this relationship could be reached, so bone growth would not be affected but atherosclerosis could be stopped before the last stages.
I haven't heard anything more about that study and when I get time I will see if it indeed led to any new conclusions.
As a matter of interest. With your husbands plaque, have they looked at using PCI treatments such as laser or Rotablation to remove it? Have they considered a more risky procedure is becoming more common in coronary arteries, an endtype arterectomy?
I was in this situation and it took me two years to find a Doctor with enough confidence to remove the concrete. I found the Cardiologist in a research centre in London which is where many of the best seem to be. Research centres normally have equipment not yet rolled out into the general population and can prove useful.
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159619_tn?1318997813
"Actually the Internet is full of reports on this, it would take a whole forum to list them all. There are also some reports that claim through trials, that lowering LDL-c enough along with raising HDL has produced regression of Atherosclerosis".

It has long been said that an LDL under 70 may cause a regression in soft plaque build ups and slow, stop or even reverse Atherosclerosis to some degree, that I was aware of. Perhaps I misread you post, but I thought your point was that statins could help promote the repair of damaged arteries, that I was unaware of. If that were the case I would like to read that as that would be a very strong case for the use of statins beyond lowering overall cholesterol levels.
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976897_tn?1379171202
no my point was nothing to do with atheroscerosis. The statement was made that damaged arteries never repair themselves. Now, if you look at that statement in context, then we would all bleed to death. My point was that arteries do repair themselves.
However, many scientists/doctors believe that low LDL and high HDL would regress fatty deposits on the artery lining. When I look at this with the little blood chemistry I know, it seems highly impossible.
Nothing in the circulatory system can mop up fats and remove them. Blood is made up mostly from water and so it cannot dissolve the fat into it for removal. Once the fat has been stripped of the lipid, it's too late. No level of HDL can remove pure fat because it doesn't act as a vacuum cleaner. HDL has to come across a LDL lipid to signal it to return to the liver. This is one of the big problems I have. Reports are made by research centres/drug companies but in reality it seems impossible. Its enough to give you a headache and I'm sure half the stuff we read is generated by the drug companies to push their products. Statin manufacturers have been claiming that even healthy people should take the medication to lower the risk of heart disease. Think of the revenue generated from that. However, it's ridiculous to give medication to healthy people.
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367994_tn?1304957193
Damaged vessels in the post's context of atherosclerosis assumes the pathogenesis of the disease is a response to an injury hypothesis (there are 4 other theories).  Smoking relies on the hemodynamic theory for atherosclerosis and the epidemiology (study of the factors) and smoking that promotes atherosclerotic disease suggests inflammation....

Atherosclerosis is a slow, progressive disease that may begin as early as childhood. Although the exact cause is unknown, researchers suspect that atherosclerosis starts with damage or injury to the inner layer of an artery. The damage may be caused by:
■High blood pressure
■High cholesterol
■An irritant, such as nicotine
■Certain diseases, such as diabetes

Once the inner wall of an artery is damaged, blood cells called platelets often clump at the injury site to try to repair the artery, leading to inflammation. Over time, fatty deposits (plaques) made of cholesterol and other cellular waste products also accumulate at the injury and harden, narrowing the arteries.  Atherosclerosis develops as a response of the vessel wall to injury. To reverse vessel or repair wall injury would be what?  

"Careful review of epidemiological studies indicates that the classic risk factors, eg, hypercholesterolemia, cigarette smoking, and hypertension, account for the majority but not the entirety of the etiology and pathogenesis of the clinical complications of atherosclerosis, including ischemic heart disease and acute myocardial infarction.2 3 Furthermore, exact knowledge regarding the mechanisms by which the various established risk factors contribute to the development and progression of lesions is incomplete. These facts have led investigators to pursue other possible etiologies and factors that may be involved in the etiology and pathogenesis of atherosclerosis and its complications".....  Anything to add that understanding?



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