I have posted before and am still searching for the "
smokingQuitting smoking
Smoking - tips on how to quit
Smoking and copd (chronic obstructive pulmonary disorder)
Smoking and smokeless tobacco
Smoking hazards gun" in my heart disease. At age 54 I was diagnosed with severe
blockagePeripheral artery disease of LAD and
firstFirst progesterone mc10
First progesterone mc5
First-progesterone vgs 100
First-progesterone vgs 200
First-progesterone vgs 25
First-progesterone vgs 400
First-progesterone vgs 50
First-testosterone
First-testosterone mc diagonal which was treated with CABG. This was a total
shockAcute respiratory distress syndrome
Cardiogenic shock
Electroconvulsive therapy
Hepatic ischemia
Hypoglycemia
Hypovolemic shock
Lithotripsy
Shock
Toxic shock syndrome to everyone familiar with me as I have a
benignBenign ear cyst or tumor
Benign positional vertigo familyBirth control and family planning
Choosing a primary care provider
Ewing’s sarcoma
Family troubles - resources history for heart disease, have been a heavy runner/bike racer for 30 years, and a non smoker, 130 LDL/60 HDL, and normal BP. Since surgery I have found that my homocysteine was high and I am now treating it with folic acid/B6/B12. I am also taking 40 mg Pravachol which has my LDL down to 80. 18 months post surgery I am back to all my former activities and feel that my exercise capacity is as high as ever.
My problem is that I don't know whether I have found the root cause of my disease which must be rather agressive to cause problems at an early age in light of my positive risk profile. I was wondering whether there has ever been any association made or suggested between severe seasonal allergies (hay fever) and CAD risk. I have such allergies and for 15 years was having desensitization shots every week. I know that inflamation
(inflammation) is a big player in progression of artery disease and wondered whether irritation/inflammation from the allergic response could also be significant. Am I "off the deep end here"?
Ok there is
Cholestorol
Hypertension
Diabetes
Family History
Obesity
Sedentary lifestyle
Homocysteine
C-reactive protein
Smoking
What else is there?? Ive heard that low testosterone levels is also a risk factor, ive read that on Life Extension Magazine.
I have a question....Does chronic inflammation cause CAD or does the CAD develop from other risk factors and the inflammation causes a piece of plaque to break free, which is which??
There is Smoking
High Cholesterol
Hypertension
Diabetes
Family History
HomoCysteine
CRP
what else am i missing? Is there any other risk factors out there that are being investigated?
I don't think there is general agreement at this point whether CRP and homocysteine are independant risk factors or they are actually markers of something else going on. For example, CRP is an inflamation (inflammation) marker that goes up from other inflamation (inflammation) in the body from infection or whatever.
Blumoon
I know with the blood pressure for so many years they said 120/80 now they are saying thats hypertensive its suppose to be 115/75! Man can you guys get a last number already! Sheez!!
Ahhh i say lets live life, and whatever happens happens right?
I also have run into an number of long term heavy exercisers that have experienced the LAD blockage. I for a while had a theory that the heavy turbulence associated with great extended periods of max blood flow thought this artery (especially at the point of the bifurcation) may have something to do with the blockage. I had this theory partially validated for me when my surgeon told me that stenting at this point was very risky due to the high turbulence and likelihood of early restenosis.
In my case, the occurrance of the blockage seemed so perverse in light of my doing everything that should be cardio protective, I was feeling I was in some way responsible due to my overdoing the exercise thing. I have yet to get any cardiologist to agree with this. I have been saying that I am the American Heart Association's worst nightmare-someone who is following all their guidelines yet still get early heart disease while so many couch potatoes doing all the wrong things get away with it.
See JA Pantano & RJ Oriel, Prevalence & Nature of Arrythmias in Apparently Normal Well-Trained Runners, AM Heart Journal 104, 762-768 (1982). ~40% of runners showed some symptoms.
Thickening of the heart wall and enlargement of the heart in endurance atheletes makes more heart muscle volume. The increase volume of heart muscle, in turn, may increase the probability of chance foci to misfire and cause an arrhythmia.
I have never exercised at the high level for fitness purposes. I do it because I like to do it. It makes me feel good. Racing used to be a goal but I seldom do it now. I like to feel the fitness that you could never get from walking, no matter how fast. Walking a brisk pace gets my pulse to about 80, not even in my "target zone".
I guess I will never know whether my exercise cause my problem or saved me from it. It was transient shortness of breath in the first 1/4 mile of running that got me to the doctor asking for an inhaler. The SOB would go away after that and I could run 7 minute pace without pain for any distance after that 1/4 mile. I had no clue of any problem on the bike, even when hitting pulse rates of 175+ on difficult hills. The angiogram showed impressive collateral development that was apparently sustaining me that no doubt developed due to the heavy exercise.
I have read replies to postings similar to mine where the doctor suggested that bypass may not have been necessary if there was not pain and the heart function was not being impacted. Unfortunately, I had not read these prior to my bad news and felt like I had a time bomb inside my chest and wanted the surgery that day. My cardio had in fact told me that he was not letting me out of the hospital without surgery.
In retrospect, I'm glad I had the surgery and I am very thankful to know I have artery disease. I am now on guard and will listen to my body even more than before.I may never know the exact risk factor responsible, but I think its very unlikely that any single factor working alone would be responsible. Thus, I can monitor and hopefully control the remaining recognized risk factors and hopefully match the longevity of the rest of my family.
As previously stated, I am quite ready to accept the idea that "overdoing it" was involved in my disease-but please define what amounts to overdoing it. Unfortunately, I have seen absolutely no studies even suggesting the idea (other than the A-fib). If you can produce any references supporting your supposition, I would welcome them. Otherwise, I have read a number of authors proposing that greater exercise volume and intensity has a positive effect on lipid profiles and other objective measures of cardiac risk. For example, please see study of over 8000 runners finding improvement in cardiac risk profile with no point diminishing returns up to 50 miles per week.(Archives of Internal Medicine, 1997;157;191-198).
Aerobic Exercise can also successfully treat some arrhythmias. See, for example, an invited review article, "Aerobic Exercise Conditioning: A NonPharmacological AntiArrhythmic Intervention" by George Billman, J.Appl.Physiol 92, 446-454 (2002).
Experiments on dogs have shown a similar effect. In one study (referenced in above article), a number of dogs had their hearts ablated to make them susceptible to induced arrhytmias. The dogs were then split into two groups. One group was kept as controls and the other group was exercised vigorously on treadmills everyday. Although arrhythmias could be easily induced in all of the control dogs, virtually no arrhthymias (<1%)could be induced in the dogs that had daily treadmill exercise.
As is well known, some pharmalogical treatments while sucessfully preventing the arrhythmias counterintuitively actually double the incidence of SCD. So if you have any choice, exercise instead of taking drugs.
And there are many other benefits to exercise that are reviewed in a nice article by Harvard epidemiologists.
http://www.harvardmagazine.com/on-line/030407.html
Here is how the article begins:
"In the bottle before you is a pill, a marvel of modern medicine that will regulate gene transcription throughout your body, helping prevent heart disease, stroke, diabetes, obesity, and 12 kinds of cancer — plus gallstones and diverticulitis. Expect the pill to improve your strength and balance as well as your blood lipid profile. Your bones will become stronger. You'll grow new capillaries in your heart, your skeletal muscles, and your brain, improving blood flow and the delivery of oxygen and nutrients. Your attention span will increase. If you have arthritis, your symptoms will improve. The pill will help you regulate your appetite and you'll probably find you prefer healthier foods. You'll feel better, younger even, and you will test younger according to a variety of physiologic measures. Your blood volume will increase, and you'll burn fats better. Even your immune system will be stimulated. There is just one catch.
There's no such pill. The prescription is exercise."
In your case, I would feel pretty good about a negative nuclear stress test. The composite of 6 or so studies I have seen shows a sensitivity of about 95%, meaning you have only one chance in 20 of having ischemia with a negative test. Unfortunately, the test's specificity is in the range of 56%, meaning there is almost a 50% chance that a positive would be a false positive.
Could your discovery of being able to handle a higher workload later in a workout be due to a normal warmup response? I have found that on a bicycle exerciser that I find 200 Watts difficult to do in the first 10 minutes, but its much easier later and I find myself doing 250W. I have always wondered whether it was me or the machine that was getting warmed up. I have also found that my legs are really reluctant to do hard enough work in the first 10 minutes on the road to get my heart rate to 135. After I am warmed up, 160 seems to be a reasonable level of effort.
Liz
It makes sense that extensive collateralization as I had would impact the sensitivity of the nuclear stress test but I am no authority in that field and have seen no research on the subject. From the pictures I saw of the nuclear stress I had after my bypass, I cannot believe that there is enough sensitivity to see the difference between a normal heart and one that has blockages "bypassed" by collaterals. The image of the heart either "lights up" due to adequate perfusion or it does not.
An alternative promoted by Lance Gould in his writings is the PET scan that offers equivalent sensitivity to the nuclear stress and specificity approaching 95%. This is a non-invasive test but unfortunately my insurance considers it experimental and will not pay for it (in spite of the fact that its cost is about 25% of an angiogram that they would readily pay for).
There is hope in the future. A cardiologist that I have a personal connection with (my daughter is a nanny for his 9 year old daughter)was babbling he was so excited with a new technique he had just witnessed. I think it is called an EKG gated spiral CT scan. The idea is that they do a CAT scan of the heart but take pictures only when the heart is at rest. The camera gets this info from the EKG. They can image the arteries as well as an angiogram and it is completely non-invasive except for the injection of a contrast media. Within 2 years, the test should be widely available.
I've heard of the ECG gating technique, I know it is used in MRI to obtain precisely timed pictures, I believe this is done for cine MRI. Good to hear that it is being integrated into CT technology as well, I would be interested to read about it.
Liz
I have never been given a straight answer to why an angiogram was ordered for me. The cardio said that it was because of my concern over my PVCs. That sounds a bit lame to me. My GP who did the stress test on me had quite freaked when he saw the arrythmia at high effort, but that had already been seen by another cardio on my holter. My cynical side believes that this particular group of cardiologists pushes procedures as that is where the money is. In my case, it may have worked out in my favor.
I don't want to alarm you, but I was recently told a story by a friend about another cycling friend who at at 45 was having trouble keeping up with old riding companions on a specific hill. He had passed the cardiolite stress and echo with flying colors. He finally convinced his cardio to do an angiogram because he "knew" something was not right. He was found to have a 100% occluded LAD similar to mine.
You might take comfort in the fact that even if you do have a blockage, it is unlikely that they would cause an infarc. These larger, long standing occlusions seem to be stable and mostly cause angina and loss of exercise capacity.