Hypothyroidism and Heart Disease: The Saga Continues

Well, saw the endocrinologist this morning and he confirmed my self-diagnosis; I have Hashimoto's Thyroiditis a condition where my own antibodies are attacking and slowly destroying my thyroid. I am starting tomorrow on a daily regimen of 25mcg of levothyroxine (synthetic T4). I lobbied for Armour Thyroid (a natural compound made from pig thyroids that contains both T4 and T3) but, despite the company's assurances, the doc belives there is too much variation in composition from lot to lot. He also pointed out that 80% of the body's T3 is synthesized from T4 anyway. He wanted to start me out at 75mcg but I insisted we go more slowly. No sense taking more than I need and any additive treatment will get me moving in the right direction. I can always take more and will probably have to as my thyroid self-destructs!

Now for some fun! I actually made appointments with TWO endocrinologists and see the second one tomorrow. Won't it be interesting to compare notes. I'll keep you posted on the "dueling endos" and my treatment results. Of particular interest will be how it affects my rising Lp(a) and homocysteine.

Regards, HeartHawk

Hypothyroidism and Heart Disease: An Update

OK, folks, read 'em and weep. My thyroglobulin antibody test was a whopping 37.9 IU/ml (0-14.4 reference range) and my thyroid peroxidase antibody test was worse at 22.8 IU/ml (0-3.9 reference range). Guess what, I likely have a thyroid autoimmune disease, probably Hashimoto's Thyroiditis. Well, at least I now KNOW (think I know anyway) what is causing my symptoms!

Next step, find a doctor to confirm my own diagnosis and properly treat me. Good luck. I called the top endocrinologists in my area and the wait is out one to two months or more. So, I took what I could get and will see somebody this week. Hopefully, the doc can get me started on a thyroid hormone replacement strategy so I can see how it affects my lipoproteins as well as my general well-being. However, I kept my appointment with the other guy - just in case I need a second opinion.

You know, it's funny. When I started this gig seven years ago (well before this blog) I thought I would be researching the heart and its arteries and peripherally the liver (as it makes most lipoproteins). Now, I'm digging around in my neck! Go figure. Well, you go where the cure takes you. The lesson to be learned here is to take matters into your own hands, be proactive, leave no stone unturned, and keep searching until you unearth all the root causes of your disease.

I'll heep you posted on my journey!


HeartHawk

P.S. The good news is we won't have to start our own foundation as we are with Lipoprotein(a). There are LOTS of thyroid groups!

Hypothyroidism and Heart Disease: The Plot Thickens

Wow! This rabbit hole goes a lot deeper than I could have ever imagined. It seems hypothyroidism is clearly connected with heart disease, is largely undiagnosed/misdiagnosed, and generally misunderstood. If anything, the real problem is, because thyroid hormones are used in just about every body tissue, hypothyroidism is connected with a huge list of symptoms and conditions. Now, on to my sad story.

Here I am, feeling like crap, disgestive problems, myalgias, fatigue, anemia, rising lipoprotein(a) and homocysteine, palpitations, mild depression, lack of concentration - yeah all that fuzzy, amorphous, undifferentiated, "feel like a truck hit" me stuff. One day I am so fatigued that I drop by the local walk-in clinic (because I can't get a freakin' appointment with my internist for a month - sound familiar) where they find me to be anemic. I luck out and finally get in to see my "regular" doc and he orders tests that show I have a moderately high TSH (4.5) and a lower (but in range) Free T4 (1.0ng/dl) and T3 (2.68 pg/ml). Of course, the internist's staff won't give me the results because they want me to schedule another appointment in ANOTHER MONTH! With a little subterfuge, I get them to fax the results "elsewhere" for "continued care" (the magic words) where I retrieve them. (DON'T GET ME STARTED ON THIS PET PEEVE - THAT WAS MY GODDAM BLOOD AND MY TEST RESULTS THAT I PAID FOR. HOW DARE THEY WITHHOLD MY HEALTH DATA FROM ME!)

So armed with this data I start my investigation. It seems that the new upper limit for TSH is really around 3.0 (not 4.5 or 5.5). Upper and lower limits form test "Reference ranges" and are not absolutes. They are set by testing lots of people who are categorized as "healthy" and determining their blood levels. The problem is you can have a lot of people who are subjectively categorized as healthy but are really not. That appears to be the case with hypothyroidism. It is likely there were numerous undiagnosed subjects included in the old "normal" range. As I mentioned in my last post on this subject, the more enlightened docs in the medical community now use these tests as guides rather than absolutes and treat based on symptoms rather than blood levels.

Now here is where it gets good (or bad depending on whether you are manic or depressive today). I also mentioned that hypothyroidism is connected with rising Lipoprotein(a) and now discover it is also connected with rising homocysteine (that would be me on both counts) as well as other hyperlipidemias. It also seems that certain drugs and supplememts can interfere with thyroid production (like niacin - also me). The link in the previous sentence is a multi-page article I would recommend reviewing. I also recommend this well-reasoned discussion on the treatment of hypothyroidism (especially the undiagnosed and border-line variety).

Hypothyroidism, it is real and it can screw you up. But it is easy to detect and treat. If you have symptoms or suspect it, get a doc to test your TSH, T4 and T3. To reduce delays try to get them done all at once. Many docs will do just the TSH and then only do T4 and T3 if your TSH is elevated. This is just medical "crank turning" by docs who don't like to think. In my NOT so humble opinion, you really have to look at all three and interpret the results. I'll post my results once I start treatment.

Regards from the human guinea pig,


HeartHawk

Track Your Plaque: Continued Validation!

OK, since I am now pretty much a full-fledged flack for Track Your Plaque (ya gotta love the alliteration and rhyming), I don't feel quite as bashful about saying, "I told you so." Dr. William R. Davis continues his unbroken record of prognostication and retains the title I gave him as the "Nostradamus of curing heart disease" as I find yet another vindication of the Track Your Plaque principles, in particular the 60/60/60 precept (LDL/HDL/Triglycerides).

A new report from the Stop Atherosclerosis in Native Diabetics (SANDS) study suggests that aggressive lowering of LDL (<70mg/dl) and blood pressure (<115mmHG) regresses heart disease as compared to standard targets (100mg/dl and 130mmHg respectively). Admittedly, the researchers used carotid intima media thickness (CIMT) which is the easiest surrogate end point to regress. Also, the study only looked at Native American diabetics but diabetics are traditionally the TOUGHEST group to treat. It is also possible this result only applies to persons with Native American genetics but I doubt it. Either way, it is good news and pushes us closer to a cure.

The other nugget to come away with is the TYP principle that says plaque growth rates below 10% are nearly as effective as reversal (in terms of clinical events) is also supported by SANDS. While not a cure for all, this is still great news and another win for the lower is better philosophy.

The Lipoprotein(a) Foundation: An Update

Here is a synopsis of what is going on to establish the Lipoprotein(a) Foundation (LF).

1. I met with Mary Lou Ballweg, the head of the Endometriosis Association, an extremely successful group with many similarities to our proposed foundation. She informed me that the Milwaukee, WI area is a hotbed of start-up medical fiundations so I hope to take advantage of my location. Mary Lou provided a wealth of information and, I think, a powerful idea for jump starting LF. She recounted the key event in the growth of EA was the establishment of a database of self-reported information about endometriosis sufferers. The method they used was a simple brochure she mailed with instructions to fill it out and return it with a dollar to cover data-entry costs (this was the 1980's, no Internet). Universities like Dartmouth and Vanderbuilt were eager to get this type of research data as it was not available anywhere else and, voila, the research began in earnest. We should do the same and it will be a whole lot easier with the Internet (see next item).

2. Dr. Davis has formally agreed to donate all the necessary Track Your Plaque web resources to implementing the LF website. I now have admin privileges on the new development site and will begin to implement a web-based data collection tool within the TYP framework. Doc Davis also offered to donate the 501(c)(3) non-profit filing fee. When he mentioned the effort on his blog, several commenters offered their assistance as well (as they did on this blog). I would request that anyone still interested in donating skills or making contributions to contact me directly at hearthawk(at)wi.rr.com with their contact information. I have helped start two other non-profits but I am not an expert and could use all the help I can get. (see next item).

3. In addition to the web work I have also started the IRS filing process. I guess the only thing I can say is I'll work as fast as time will allow. Obviously, anyone with knowledge of this process would be extremely helpful. We do have to form a board of directors at some point. Major contributors of time, talent, and financial resources are always prime candidates for these roles.

4. If we can attract an "angel" investor we can obviously move a lot faster! I have broached the subject of investment capital with a professional fundraiser that would consider helping us at a reduced fee as time permits but she is booked for at least six month to a year. Whether it's a million people with one dollar or one person with a million dollars we will need to start raising money to fund research. Frankly, at the risk of appearing mercenary (I am), our best bets are people plagued (or "plaqued") with Lp(a)! The beauty of medicals breakthroughs is that once a cure is found for/by one person's efforts, it cures almost everybody.

5. If anyone has any medical/research/academic contacts they would be useful to help form our advisory board. The University of Wisconsin is a top medical research facility and I have scheduled a meeting with a blood researcher there. As luck would have it, my daughter is a biochem major at UW working on here senior research thesis and is searching for addtional contacts (I oughta get something back for all those tuition payments!).

That's where we are. Let's slay the Lp(a) dragon!

Regards,


HeartHawk

Hypothyroidism and Heart Disease: Here we go!

Now what?! I just finished clearing up a low blood count and a mild case of anemia (watch your aspirin intake folks - it's hard on the tummy) only to find my Thyroid Stimulating Hormone (TSH) was above normal. TSH is excreted by the pituitary gland and stimulates the thyroid gland (nice video here - after the ad ends) to produce the hormones thyroxine (T4) and triiodothyronine (T3) which in turn is used by various organs and tissues of the of the body. Suffice to say your whole body pretty much needs the stuff (follow or Google these blog links if you want to dig into this stuff). The key here is to realize that a high TSH means low thyroid function or hypothyroidism. The pituitary essentially tries to kick-start the thyroid to secrete more of its hormones by overproducing TSH.

Hypothyroidism has a number of irritating symptoms (severe cases can result in a life threatening condition known as myxedema coma). The most common are fatigue and depression. Here is the list of symptoms from the American Association of Clinical Endocrinologists (AACE) for all of us hypochondriacs:

• Dry skin and cold intolerance
• Yellow skin
• Coarseness or loss of hair
• Hoarseness
• Goiter
• Reflex delay, relaxation phase
• Ataxia
• Constipation
• Memory and mental impairment
• Decreased concentration
• Depression
• Irregular or heavy menses and infertility
• Myalgias
• Hyperlipidemia
• Bradycardia and hypothermia
• Myxedema fluid infiltration of tissues

There is also additional evidence (About.com, American Thyroid Association) to suggest hypothyroidism (as well as hyperthyroidism) can have negative effects on the heart.

The real problem here is when and how to treat sub-clinical or mild hyperthyroidism. AACE has waffled in the past but their most recent statement is typical of head-in-the-sand traditional medicine; esentially, do nothing (gee, thanks, I was already doing that, slowly dying of heart disease, and feeling crappy in the process). Others disagree. Amazingly, the American Academy of Family Physicians (AAFP) makes a cautiously worded statement that suggests treating patients based on their symptoms rather than their TSH levels (what a concept). Mary Shomon (perhaps the "ThyroidHawk" of bloggers) takes a shot at the medical establishment in this article. Doubtlessly, the indifference and incompetence heart disease sufferers face is common among all the halls of traditional medicine.

I'll continue to update you on what happens in my "heart disease and thyroid saga." This is of particular importance to me since I discovered this article that suggests T3 rapidly lowers lipoprotein(a)! Oh, and you know darn well I'll be pestering Doctor Davis to chime in on the subject.

Regards,

HeartHawk

P.S. My next blog will update everyone on how the formation of the Lipoprotein(a) Foundation is coming. Suffice to say I am moving forward.

Vitamin D: The Evidence Keeps Rolling In

I guess I shouldn't be surprised but Dr. Davis of Track Your Plaque continues to demonstrate he is the Nostradamus of heart disease prevention medicine. For the last year he has trumpeted the powerful effects of Vitamin D in regressing plaque and presented his findings in early April at the Experimental Biology Symposium in San Diego.

Now, researchers using data from the National Health and Nutrition Examination Survey (NHANES) study have presented their similar findings at the Arteriosclerosis, Thrombosis and Vascular Biology Annual Conference. They found that persons with low Vitamin D levels have a higher incidence of Peripheral Artery Disease (PAD). PAD, also known as intermittent claudication, is a condition where blood vessels in the extremities become narrowed or occluded by plaque.

Once again, Dr. Davis proves to be ahead of the curve!

Regards,


HeartHawk

More on the Lipoprotein(a) Foundation

Looks like we may be on to something here. We have already had interest from several blog readers about keeping this idea going (see previous blog entry). Here is what has transpired in the past day.

1. Track Your Plaque (TYP) has graciously offered to host the Lipoprotein(a) website. I am meeting with their head web programmer on April 18th to lay the ground work.

2. I am meeting with Mary Lou Ballweg one of the founders of the Endometriosis Association (EA) on April 23rd to pick her brain on how to start and run a successful medical Foundation. Endometriosis was a little known disease and, similar to Lp(a), had little or no research or funding. Mary Lou grew (EA) from a humble start of one person working from her living room to an international association with its own headquarters building. She will be a fantastic resource for us.

3. I have talked briefly with Dr. Davis of TYP and while he cannot become directly involved due to time constraints, he has agreed to help us in any way he is able. He can be our "in" in the medical community.

4. I am about to contact other Lp(a) researchers such as Drs. Marcovina and Scanu to get their input.

The rest is pretty much up to us to keep the "viral marketing" campaign going and build a list of potential members and contributors. I will also attempt to start scaring up a few bucks and will talk to the programmer on the 18th about setting up a PayPal online contributions page as well. The oft repeated bromide is true here, "If every Lp(a) sufferer kicked in just $1, we would have millions." Finally, anybody know any non-profit lawyers and accountants who suffer from Lp(a) and want to help save their own lives? Sooner or later we will have to form a board of directors if we get this thing off the ground. Say, you don't suppose Warren Buffet or Bill Gates has Lp(a) do you?

The Lipoprotein(a) Foundation: Time to Start One?

I just received some disheartening news from Dr. Sally McCormick one of the world's few Lipoprotein(a) researchers. I had asked her how her lead anti-Lp(a) compound was fairing in trials and the answer was not good, "some of the animals were quite sick after dosing with the peptide, we think due to the peptide being unstable and aggregating in the circulation."

On the bright side she also mentioned she is about to publish some preliminary research on DMPC (dimyristoylphosphatidylcholine which is not to be confused with PPC or phosphatidylcholine being studied in the Track Your Plaque Virtual Clinical Trial). Additionally, Dr. McCormick does have one other lead compound in the pipeline but it is not in trials yet.

Sally did make one other statement at the end of her letter that stuck with me, "Sorry I can't be of more help to you and other high Lp(a) sufferers as yet, we are trying to develop something but its just really slow when time and funding is limited." This reminded me of a woman I know (right here in my hometown) with another neglected medical condition called endometriosis. Like Lp(a), few people were doing any research and fewer companies were investing any money in finding a cure. She started the Endometriosis Association to provide support and create pressure to find remedies for persons with her condition and was immensely successful.

Perhaps all of us Lp(a) sufferers should do the same. I have started a 501(c)(3) educational charity in the past - it's not fast or easy thanks to the U.S. government. It takes lawyers (or really knowledgeable people) at least a little money (the filing fee alone is around $500) , and a lot of work to grow the organization. My vision would also include raising a boat load of money to fund independent medical research similar to what is being done by some of the pioneers like Dr. McCormick (I'll bet there are as many wealthy people as poor people slowly dying of Lp(a)).

So there you have it, the Lipoprotein(a) Foundation! I know Track Your Plaque will front us the web presence and let us use their new community/networking software they are developing. Dr. Davis as well as several other professionals associated with Track Your Plaque have expressed interest but they are too busy to start it or run it. Now, can the rest of us develop the critical mass to put something like this together and cure ourselves?!

Regards,

HeartHawk

More on Vitamin D and Testosterone

Lot's of great comments on my last blog concerning Vitamin D and testosterone. A few commenters rightly took me to task for my less than rigorous data regarding the association between my Vitamin D intake and my testosterone level. So, here is what we can say.

1. For my "n of one" study there is an "association" between between Vitamin D and testosterone levels. However, it cannot be concluded it is causative. It could be that can of "Coke Zero" I drink every day that's doing the trick!

2. It is not outrageous to speculate that there could be a link between Vitamin D and testosterone given chemistry. We just cannot prove it with my results. There is some excellent material on Vitamin D pharmacology put out by the Vitamin D Council (really level-headed stuff not marketing hyperbole) and for those who lean toward the "geeky" side this cite from AACC is nice.

3. It is unlikely my low testosterone stayed high several years after stopping my use of topical testosterone. What I really need to do is stop the Vitamin D for several months and re-check my testosterone to see if it goes lower. The problem is that Vitamin D is good for so many other things that it does not seem appropriate to discontinue it. Perhaps a new Track Your Plaque Virtual Clinical Trial might be useful where we measure "before" and "after" testosterone levels.

We certainly need more clinical data on the relationship between Vitamin D and testosterone. We have chicken data (and more chicken data here - what is it with chickens anyway) and we have rat data that suggests Vitamin D increases male (rat) fertility but we just do not have anything that says Vitamin D increases human testosterone (yet).

Anecdotally Yours,

HeartHawk

Vitamin D and Testosterone: Another "Fountain of Youth" Find

When Dr. Davis of Track Your Plaque first reported his phenomenal success using Vitamin D to reverse coronary plaque I pretty much blew it off as coincidental and too good to be true. But, once again, Dr. Davis has proven to be the "Nostradamus of Heart Disease Reversal" as breaking data continues to support his prediction and clinical evidence.

After much brow beating, I finally decided to try Vitamin D. With some rather interesting results. Let's first set the table for my experience.

When I first became a follower of Dr. Davis (long before there was a Track Your Plaque) I had my testosterone tested and it was fairly low (near the bottom end of normal). Because testosterone can be an effective Lp(a) remedy (my scourge) I tried using a testosterone cream to raise my level and it promptly went up to the high end of normal. But, for various reasons (no effect on Lp(a), lowering of HDL, and it's inconvenient as hell to use) I stopped. But look at my Testosterone (T) blood levels since I started using Vitamin D!

Date	T (ng/dL)	Vit D (ng/mL)	Notes
10/18/01	328	Unknown	Baseline testosterone
02/06/03	774	Unknown	Started topical testosterone
08/04/06	792	53.0	Stopped T 1 year earlier/started 2100IU D
12/26/07	735	40.7	8000IU Vitamin D (increased for winter)
03/06/08	728	69.2	10000IU Vitamin D (needed more to hit TYP threshhold)

As you can see the Vitamin D was just as effective at raising my endogenous testosterone as was using synthetic, topically applied testosterone cream. Also note that I had to signficantly raise my D dosage in winter months to offset the lack of sun. The other goofy thing is that for some reason there is a threshhold effect at around 50ng/mL (although mine kicked in at 40). This Vitamin D stuff is damn interesting. The numbers do not lie and for a numbers guy like me its all the proof I need.

Regards,

HeartHawk

Mammography and Calcium: More Steadfast Denial

It is often absolutely stunning how tradition medicine continues to remain in a state of denial over the efficacy of calcium scoring as a measure of heart disease risk. A new study revealed that women who display arterial calcification on their mammograms are over twice as likely to develop cardiovascular disease. Ya think?!

Dr. Michelle A. Rotter (University of Connecticut School of Medicine, Farmington) and colleagues reported their findings in the March/April 2008 issue of Menopause. Dr. Rotter went on to comment, "it has yet to be determined whether screening for BACs is an effective tool in screening for CAD." But that is not the point as the evidence continues to mount and doctors continue to ignore it. Arterial calcium is the strongest predictor of heart disease and future events - period - and it appears that detection via routine mammography can be an important predictive tool much like heart scans.

Although the link between arterial calcification, especially calcification in coronary arteries, has long been established as the single greatest predictor of heart disease, the traditional medical community continues to dither over supportive findings such as this lastest study. It is not as though this were the first time such a study came up with this discovery. Another study published in 2000 found a similar association between breast arterial calcifications and atherosclerosis.

When is traditional medicine going to 'fess up to the truth and stop letting people become so sick they have no choice but to pay big bucks to be butchered on their operating tables. This is utterly repugnant! We already know that arterial calcium is the greatest predictor of future heart disease in asymptomatic individuals and the COURAGE trial proved that non-surgical therapies are just as effective as surgical therapies in non-acute patients. One day, this is going to come back to bite these negligent hospitals, doctors, and insurers in the butt to the tune of billions!

Still holding my nose and holding out hope,


HeartHawk

Additional commentary on this study from Medscape, heartWire

More on Aspirin Resistance, NSAIDs, and Stroke

In an earlier blog I discussed aspirin resistance as a factor in heart attack. A new study now confirms similar results in stroke victims. You are 14 times more likely to have a recurrence of stroke if you are aspirin resistant.

Similar to previous studies, 20% of partcipants were found to be resistant to the effects of aspirin on the interruption of the arachodonic acid cascade that inhibits platelet aggregation (clotting). Of the 87 patients who had recurrent strokes while taking aspirin, 57 (66%) were nonresponsive to aspirin. That an odds ratio of more than 14 times greater. Put another way, of the patients who were aspirin responsive, only 5% were among those who suffered recurrent symptoms while taking aspirin.

In another paper in the Journal of Clinical Pharmacology, the same researchers found an interesting association between people taking both aspirin and NSAIDs (ibuprofen for example). All of the participants who took both aspirin along with some other NSAID showed signs of aspirin resistance. However, when they stopped taking the NSAID, the aspirin resistance disappeared.

Dr. Gengo, one the head researchers commented in a Heartwire interview, "There are many people out there who are taking an NSAID while on aspirin and therefore putting themselves at increased risk of ischemic events (e.g. heart attack and stroke - HH). This study shows that there are many strokes every year that could be prevented."

The New Hub-Bub Over Metabolic Syndrome

Metabolic Syndrome has long been identified as a risk factor for heart disease. However, idientifying exactly what it is and what its cause or causes are has been a subject of much debate. Now, a new study published in Cell Metabolism has thrown the issue into a full-fledged brouhaha over whether Metabolic Syndrome is a multi-cause condition or more simply a single cause condition with multiple symptoms. For example, is small-LDL a contributor to a diagnosis of Metabolic Syndrome or is some other single root cause driving a host of symptoms such as small-LDL to appear.

The Multi-Cause camp has labored long and hard at defining what group of causes is sufficient to render a diagnosis of Metabolic Syndrome. Different organizations have different standards but all require having some combination of common symptoms such as:

• Presence of diabetes
• Microalbuminuria
• High blood pressure
• High triglycerides
• Low HDL
• Overabundnace of small-LDL
• Insulin resistance
• High fasting blood glucose
• High waist to hip ratio

Here are links to the various guidelines NCEP ATP III (what most U.S. doctors use), American Heart Association, World Health Organization (pages 32 and 33), European Group on Insulin Resistance (EGIR).

This latest study by the Joslin Diabetes Center focuses on insulin resistance in the liver as the key factor in the cause of metabolic syndrome and its association with heart disease. It advances the theory that metabolic syndrome is not simply a collection of abnormalities that should be treated independently but a group of closely linked disturbances in glucose and cholesterol metabolism that stem from a defect in insulin signaling in the liver. This thinking suggests the cure for Metabolic Syndrome is not to treat a variety of symptoms but rather to find and treat the underlying cause perhaps with a single "magic bullet." This is tantatmount to treating and eliminating a cold virus rather than treating the associated symptoms aches, sore thoat, congestions, and sniffles associated with the cold.

OK, great! Now let's find that magic bullet!

HeartHawk

Do YOU Worship at the Alter of LDL Cholesterol?

Many years ago, doctors would simply measure total cholesterol and call it a day. As the snail-slow medical community progressed it identified LDL Cholesterol as the "bad" guy and basically did little else for decades but beat up on LDL and develop LDL lowering drugs like statins and, more recently, ezetimibe. But a funny thing happened on the way to the temple.

Much like the COURAGE trial delivered a much different than expected result on stenting (it's not much better than drug therapy for non-acute heart disease) , the ENHANCE trial found that lowering LDL with ezetimibe provided little improvement in outcomes. Track Your Plaque proponent Dr. William Davis often opines, "The average LDL Cholesterol of a heart attack victim is 134mg/dl, the average LDL Cholesterol for someone who does not have a heart attack is 131mg/dl." It is a statistical dead heat!

The latest theory is that what matters most is not merely how low you drive LDL Cholesterol but how you go about lowering it (statins deliver pleiotropic effects beyond simply lowering LDL). Ezetimibe can dramatically lower LDL when taken in combination with a statin. You have probably seen the commercials for Vytorin (simvastatin plus ezetimibe) that proclaim it treats the "two sources of cholesterol" (genetic and dietary). The ENHANCE studiers naturally expected to prove ezetimibe was a blockbuster drug that whose LDL lowering effects would earn billions. But it didn't happen. Moreover, the researchers were accused of delaying publication of the bad news.

Dr. Eric Topol has an interesting Video Blog on the subject that is worth the 4-1/2 minutes of your time to see and hear. He suggests that the true cuplrit is oxidized LDL. It makes a lot of sense as we begin to "peel back the onion" on LDL Cholesterol. Stay tuned! You know my next move. Find a test for it so I can hang on number on it!

Regards,


HeartHawk

Is Your Aspirin Resisting You?

Like most of you I take aspirin daily, 325mg. Even traditional cardiologists recommend aspirin for heart disease sufferers. Aspirin works by interfering with the generation of thromboxane A2 (TXA2) which is needed for platelet aggregation (clotting). The COX-1 enzyme acts on arachidonic acid (AA) to produce endoperoxides that in turn produce TXA2 . Aspirin interferes with the generation of TXA2 by irreversably acetylating the platelet COX-1 enzyme thereby blocking its access to AA. Because platelets are anucleate, they cannot generate additional COX-1. In the absence of TXA2, platelet aggregation does not occur. Got all that?!

Most practitioners prescribe anywhere from 81mg to 325mg. Studies such as CURE suggest 81mg is optimal. The ISIS-2 study puts the dose at 162mg (for recent heart attack sufferers) and, frankly, since aspirin is so cheap, many (like me) simply make the leap to "more must be better." Ahh, but there are downsides to higher dose aspirin, among them bleeding and stomach problems (me again). But there is another dosing consideration, aspirin resistance, a reduced response to aspirin that one study suggests affects 27% of the general population.

Once again, like many of you, I am also a Track Your Plaque convert (see my early posts and disclaimers). As a numbers geek it appeals to me to have hard data to track and make intelligent decisions about controlling my heart disease. So the question those like me have is, "Is there any way to determine if I am aspirin resistant and if so, how resistant am I and how much aspirin do I need to take?" The biggest problem is that there is currently NO clinically valid definition or measurement of "aspirin resistance". However, here is the latest on available tests to provide some answers.

The PFA-100 is US Food and Drug Administration (FDA)-approved to detect platelet dysfunction, von Willebrand disease, and aspirin-induced platelet inhibition. The instrument measures collagen-induced platelet plug formation as time in seconds to occlude an aperture. Its sensitivity as a screen for platelet dysfunction is approximately 95%.

The VerifyNow Aspirin Assay is FDA-approved for detection of aspirin-dependent platelet aggregation. Its sensitivity as a screen for aspirin-induced platelet dysfunction is approximately 91%.

PlateletWorks is FDA-approved to detect platelet dysfunction due to inhibition secondary to diet, aspirin, and/or other drugs. PlateletWorks has limitations. There is a very short time allowed -- 10 minutes -- between sample collection and assay. Also, there may be unacceptably high false-positive rate because of interference by dietary substances such as chocolate and red wine.

AspirinWorks is FDA-approved to provide a quantitative measurement of aspirin-induced inhibition of TXA2 generation from a urine sample. Results are ranged in quartiles with different quartiles represent differing degrees of risk for heart attack. A patient whose results are in the first quartile has a relative risk 1 (average). A patient whose results are in the second quartile has a 1.3 times greater risk of heart attack than a patient in the first quartile. A patient whose results are in the third quartile has a 1.5 times greater risk, and a patient in the fourth quartile has twice the risk. As with many lipid tests, there are still problems to work out in comparing results based on different assay methods.

The bottom-line is there is no perfect way to determine to what degree you are aspirin resistant but the technology is improving. However, if you are looking for some way to put a hard number on where you stand there are several interesting tests available. For now, I simply take the high-end of the dose range until my tummy starts to hurt then take a break or reduce my dose.

Regards,


HeartHawk

New Year's Eve: A Cure for Lp(a) Sufferers?

FIRST A LITTLE NEW YEAR'S FUN & SARCASM

I, like many people with early heart disease, suffer from high lipoprotein(a) - about 140 nmol/l. Naturally, I spend a great deal of time looking for novel methods to reduce it. Unfortunately, the front line remedies like niacin and testosterone (estrogen if you are a woman) have only been marginally effective in my case. In perhaps the most twisted ignominy of Lp(a), many of the things that will reduce it will harm or kill you some other way. For Example, neomycin is an effective Lp(a) treatment but it has nasty kidney and nervous system side effects. Additionally, a relatively new study (http://circ.ahajournals.org/cgi/reprint/85/6/2034.pdf) has determined that tissue plasminogen activator (tPA) also drastically reduces Lp(a). Great, instead I'll just die from internal hemoraghing.

So what does this have to do with New Year's Eve? Well, it turns out that several other studies have found that high alcohol intake may reduce Lp(a) (for example http://invention.swmed.edu/cgi-bin/etblast/abstract_local?pmid=1827857&user=hobbs&application=2) and the same is true of severe burns and sepsis (http://invention.swmed.edu/cgi-bin/etblast/abstract_local?pmid=10764684&user=hobbs&application=2). So all I have to do to reduce my Lp(a) is get drunk on New Year's Eve and set myself on fire in a wild celebration. Lucky me!

NOW ON TO SERIOUS STUFF

All the studies I cited above are in what is the most complete compendium of research studies on Lp(a) I have ever come across. You can peruse this link http://invention.swmed.edu/frisc/faculty/hobbs/profile.shtml for hours on end to get the skinny on what is going on regarding Lp(a), both the weird and the wonderful.

Happy New Year!


HeartHawk

The Revolution Moves Forward: It's About(.com) Time

One of the most promising signs that the traditional heart disease "wait until broken and repair" medical model is slowly giving way to the prevention model is that more and more doctors are jumping on the bandwagon. Track Your Plaque recently ran an interview with Colorado prevention pioneer Dr. William Blanchet who independently arrived at the same conclusions and treatment strategies as Track Your Plaque author Dr. William Davis.

Back in September I took some shots at Dr. Richard Fogoros, a contributor to About.com's heart disease pages. At the time I mentioned what a pity it was because "he almost got it right!" I considered the flaw in his position to be the same as many cardiologists, a blind obsession with obstructive disease. My disparaging of Fogoros was a rehash about how traditional medicine waits until it finds coronary obstruction via stress testing, which is end stage heart disease, rather than finding - and treating - early stage heart disease after detection and tracking via heart scanning.

Despite my rather scathing accusations, Dr. Fogoros was kind enough to take the high high road and write to me explaining that his statements as posted on About.com were from 2003 and his views since then have evolved. He has more recently published a new and reasonably objective review of the traditional "repair" versus "prevent" debate that is raging in the medical marketplace.

Here it is. http://heartdisease.about.com/od/coronaryarterydisease/a/noninvasiveCAD.htm

I encourage everyone concerned with heart diease to read Dr. Fogoros' insightful analysis and decide which camp you want to be in, with the traditional "repair" folks, or the "prevention" team.

Thank you Dr. Fogoros. The Revolution continues!


HeartHawk

Great Resource for Understanding Clinical Trials

I often talk about clinical trials and, if you are not a numbers and statistics geek like me, the lingo can be downright confusing and the results difficult to properly interpret. Enter, MedPage Today to offer this little gem to bring you up to speed on understanding clinical trial geek-speak.
http://www.medpagetoday.com/Medpage-Guide-to-Biostatistics.pdf

Enjoy,


HeartHawk

Cypher Stent Commercial: Not Very COURAGE-OUS

In my last post I took Johnson & Johnson to task for their decision to push stents on the public. Kartik asked that I find and publish a video of the commercial for people to view. YouTube did not have it as of the date of this post but it is available by clicking this link.

Cypher Video

It seems I am not the only one who is having ethical concerns.

From the New York Times

"Not surprisingly, the campaign has stirred criticism among doctors who oppose direct-to-consumer advertising of drugs and devices, and especially among doctors who contend that stents are being implanted too often in patients who might do better with other treatments."

From leading doctors

"It's deplorable," said Dr. William E. Boden, a professor of medicine at the State University of New York at Buffalo. "You've got to wonder whether it's a sign of desperation."

Raymond Gibbons, M.D. Mayo Clinic, "Angiopplasty should be reserved for patients who are refractory to medical therapy for chest pain."

Judith S. Hochman, M.D., of New York University School of Medicine, and P. Gabriel Steg, M.D., of the Centre Hospitalier Bichat-Claude Bernard at the University of Paris, concluded that "patients . . . who have failed to control symptoms remain candidates for revascularization, but percutaneous coronary intervention should not play a major role as part of a secondary prevention strategy."

And, of course, we have the COURAGE trial (the inspiration for this post's title)

which found that stenting is no more effective than non-surgical methods for managing stable (not in the throes of a heart attack) heart disease.

CLICK HERE to watch a short video explaining the COURAGE trial

Stent manufactures will stop at nothing to push their product on an unsuspecting public. Remember, the American College of Cardiology and New England Journal of Medicine actually sanctioned researcher and interventional cardiologist (fancy title for some stent pushers) Dr. Martin Leon for attempting to sabotage the COURAGE trial once it was clear that, contrary to his expectations, it would not support stenting as a superior therapy. More chilling is that Dr. Leon was considered an important and well-respected cardiologist who has held titles such as Chairman Emeritus and Founder of the Cardiovascular Research Foundation, Associate Director of the Center for Interventional Vascular Therapy (CIVT) at Columbia University Medical Center, Director of Clinical Research at the Washington Cardiology Center, Clinical Professor of Medicine at Georgetown University Medical Center, Director of the Catheterization Laboratories in the Cardiology Branch of the National Heart, Lung, and Blood Institute at the National Institutes of Health (that's a mouthful), among others.

Kinda make you wonder just who you can trust! You know, if this were just two "corn flakes" manufacturers competing in the marketplace I would say, "Have at it. Sell me YOUR corn flake." But this isn't about breakfast, it is about cutting people open, it's about life and death.

We all know what is going on here. Since the COURAGE trial and revelation about stent thrombosis, Cypher stent sales have plummeted. The Cypher Stent commercial is all about trying to get past doctors who have started to put the brakes on the overzealous implantation of stents. This, in a word, is DISGUSTING!

Yuck,

HeartHawk