how and why to clots form?

[mile high]

I am wondering how and why blood clots form and where for that matter.
Are we talking about clots forming on our mechanical valves or clots coming from somewhere else and getting attached to or blocking our valves?
If clots are forming on valves, why does this occur? What are the circumstances surrounding this? Is it our blood is too thick?

Since this seems to be quite a fear for many of us, it would be helpful for me anyhow to know more.

Any thoughts or where information might be found that is relevant to our situations?

thanks

mile high

 

[JimL]

This is a good question, and I'd like to hear a good, reliable answer.

I remember being told that the hemodynamics of the mechanical valve are not as good as those of the valve God gave me. In other words, at least the way I understood it, the blood tends to pool and swirl around more with the mechanical valve, favoring the formation of clots. Hence the necessity for coumadin.

But quite possibly someone knows the real answer to this question.

 

[Christina]

Mile High..

Mile High..

My blood clot formed underneath the mechanical valve 11 days after my AVR surgery as a result of mismanagement of my Coumadin. What was not known at the time was that I am a fast metabolizer. INR was 1.4 when the clot occurred.
The first time I was implanted with a Sultzer Carbomedics (21mm) but this valve was replaced with a St. Jude's (19mm).
I am on 22-23 mg of Coumadin (summers require more) daily to stay between 2.5 - 3.5.
I've been hometesting with the Protime for 4 years.

 

[tobagotwo]

If you're taking your warfarin properly, this is pretty much just an intellectual discussion. The times it becomes more real for you are when you're being transferred on or off of it for medical procedures, including the initial valve implantation.

I've endeavored some light research on this, but would appreciate any substantial corrections or additions. (I gotta wonder if Al Lodwick will be grading this...) It is an extremely complex series of processes, with numerous triggers and chemical feedback pathways (not all of which are completely understood), so anything made readable (by me, anyway) is going to be sincerely and severely simplified. If you really wanna know, and you're not afraid of some chemistry, here is one of the better sites I found:
http://ntri.tamuk.edu/homepage-ntri/lectures/clotting.html .


As I see it, where mechanical valves are concerned, there are four main contributing factors for thrombosis (blood clots).

- Vascular wall damage (tissue damage to the aorta caused by required cutting during surgery for valve replacement; by extension, also necessary surgical damage to the site of the mitral valve). This is a notable risk at the time of valve replacement, as the site of explantation and implantation requires cutting. This is a critical time for ACT to be handled carefully. As the site heals, this rapidly becomes less of a factor.

Blood platelets bind to the collagen that is exposed on the damaged epithelial walls. A variety of chemicals are released by this, which cause other parts of the process to follow. Some main players are prothrombin, which chemically alters to thrombin, and causes integrin, a binding agent, to be able to bond fibrinogen to the platelets as fibrin. The fibrin helps bind other blood elements together, ending up in a blood clot. Another chemical, which is seen as a regulator of the clotting reaction, is called von Willebrandt factor.

There are numerous other trigger chemicals and sub-factors of them, but I chose these as having the greatest significance. All of it, however, seems keyed by that first taste of collagen at the implant site.

- Changes in Blood Flow (eddies or semistagnant areas). This is the greatest long-term issue. Basically, blood naturally clumps, if it's not moving. While there are built-in mechanisms to keep blood from stagnating on most mechanical valves (e.g. agitation "ears" at the pivots, curved leaflet designs intended to create a "wash" effect), there are inevitably eddies in the flow, due partially to the fact that the parts don't flex, and the surrounding tissue does. I believe this is the main causation that creates the requirement for anticoagulation therapy (sodium warfarin).

In at least one interesting study, the On-X valve claims to have some superiorities in this area, due to its design and its material composition ( http://www.mcritx.com/news_south_africa_study.htm ).

- Rough or Foreign Surfaces ("rough" is a relative term, but may include sutured areas, or even the surface of the valve). Most mechanical valves are still seen by the body as foreign substances, and are thus occasionally subject to defensive clotting. A favorite spot for clots is around the leaflet pivot points.

As well, the surfaces of the valve or the material of its suture skirt can create rough areas for clots to adhere on or under. Platelets and clot-attracting chemicals are attracted to these rough surfaces, where they can adhere. Again, "rough" is a relative term. To our touch, the valve surfaces would likely seem extremely smooth. It should not be discounted that the body interior is an extremely corrosive environment, loaded with water and salts, which can pit most materials that are introduced into it over time.

- Hemolysis (breakage of the blood cells by the valve, releasing chemicals that are involved in or can incite clotting). Mechanical valves, and even to a very slight extent biological valves cause some hemolysis, or damage to the blood cells. Some of the chemicals that are released can stimulate a protective clotting response.

This seems to be an unpredictable, almost whimsical causation, as hemolysis can also seemingly have an opposite effect as well. ( http://chealth.canoe.ca/health_news...53&news_id=8001 ).


Hopefully, this creates a straw dog for discussion.

Best wishes,

 

[Nan]

Hi Christina, this is on a different topic than how a blood clot can form (interesting topic)...
I was wondering if your 19mm St. Judes has caused any problems for you as it is small like mine (17mm). I think I remember seeing that you had a small one at some point, but don't remember if it causes you grief.

Just curious, as mine has/is causing problems.

Thanks.

 

[Christina]

For Nan..

For Nan..

Hi Nan,

So far so good with my St.Jude's valve. I have a cardio appointment tomorrow and we'll see what he has to say this time. It's never a long appointment and if he stays for 7 minutes in the room, that is long. It's been 9 months since I last saw him. On previous appointments everything's been okay according to him. My insurance pays for an echocardiogram once a year and the last one I had in March of this year.
One problem I still have is, I still often get very hot and sweaty in my face. Not sure if they are hotflashes or if this is a problem coming from the heart working too hard. I am 58 years old and am post menopause, but other women tell me that the hotflashes can last the rest of your life. The sweating in my face started several years before surgery. This is quite uncomfortable and embarrassing at times, especially when I am at a nice dinner with friends, and here I am fanning my face with a hand fan. But that's what I have to do.
Any input?

 

[JimChicago]

Here is one more theory of a factor that could cause clots from Dr. Mercola's site. The article implies one additional cause of clots could be infection, inflamation.
From:
http://www.mercola.com/2003/may/31/smallpox_vaccine.htm
>>>>
The presence of viruses in the blood stream has been scientifically shown to induce a physiological state called "hypercoagulability." The "hypercoagulable state" is a condition in which a person has the increased potential to develop a thrombosis, commonly called a "blood clot." Thus, the possibility that vaccinia, injected into the blood stream at the time of vaccination, caused the blood to clot. And that could have led to the sudden cardiac deaths.

There are many causes of hypercoagulability, ranging from rare genetic conditions and a variety of blood disorders, to surgical interventions, birth control pills and cancer. In addition, there is a long list of cardiovascular diseases, including valvular defects, bypass surgery and hypertension, that can lead to hypercoagulability.(ii)

The physiology of the hypercoagulable state is complex. The cascade of events begins when an irregularity develops on the inside lining of a blood vessel called the endothelial wall. As the blood flows over the turbulent surface, platelet cells are disrupted, causing the release of an enzyme called thrombin. Thrombin catalyzes the conversion of proteins called fibrinogen into molecules called soluble fibrin monomers (SFM), generally referred to as fibrin. Strands of this "sticky," insoluble protein forms a mesh that collects the other types of blood cells involved in the formation of blood clots and scars.



However, the release of fibrin doesn?t necessarily result in the formation of blood clots. As the body depletes its supply of circulating fibrinogen during the creation of fibrin, more and more fibrinogen is released into the blood stream from the liver. The combination of the additional quantities of both fibrinogen and free, non-polymerized fibrin fragments in the blood increases its viscosity, meaning the blood becomes "thicker and stickier." Over time, the excessive amounts of circulating "sticky" fibrin adhere to the walls of capillaries in the microcirculation, resulting in narrowed blood vessels. Tissues that are dependent on blood squeezing through the narrowed vessels become compromised, as the supply of both oxygen and essential nutrients is reduced. If this is occurring in the vessels delivering oxygen to the heart, the result is ischemic heart disease and heart attacks. If it is occurring in the brain, strokes can result.

Cardiologists understand the phenomenon of hypercoagulability and routinely recommend a daily aspirin or other "blood thinning" drugs to reduce the risks of clot development. However, these medications are only treating the symptom, and do nothing to address the underlying cause of the hypercoagulation.

Pathogens that can activate the fibrin-forming cascade include a long list of bacteria, fungi, mycoplasma and viruses. Because these pathogens are primarily anaerobes, they thrive in tissues that are deprived of oxygen. Fibrin-narrowed vessels delivering less oxygen to tissues allow the pathogens to become embedded, creating tiny tissue "abscesses" that fester and cause inflammation.(iii) This theory provides a possible explanation for the muscle aches seen in fibromyalgia, and why aerobic exercise--which serves to deliver more oxygen to the problem areas--seems to decrease pain. (iv)

Viruses create a self-perpetuating, hypercoagulable state by adhering directly to blood vessel walls. When this occurs, circulating fibrin is deposited directly onto the virus creating a protective "coating" in an attempt to isolate the virus from the rest of the body. The result is the formation of visible "bumps" along the inside wall of the blood vessels, increasing the blood flow turbulence, releasing more thrombin, creating a perpetual thrombin-fibrin-deposition cycle, leading to hypercoagulabilty and clot formation. (v)

Conventional medicine primarily blames the narrowing of blood vessels and subsequent clot formation on elevated cholesterol and fat deposits.

But it is highly possible that the actual underlying mechanism has been overlooked. It may be the adherence of microbes--specifically viruses--to endothelial lining of the blood vessels is the underlying culprit. (vi) In a word: are heart attacks really caused by an unrecognized, underlying infection?

©Copyright 2004 Dr. Joseph Mercola. All Rights Reserved
http://www.mercola.com/2003/may/31/smallpox_vaccine.htm
>>>>
>

 

[azpam]

you want input christina? do you mean about using the hand fan? get on the table and jump up and down alot creating a breeze. therefore you won't have to hand fan yourself anymore.i'm always available for advice. trouble is no one wants it.

 

[Nan]

Hi Christina, I am going to Private Message you !

 

[Rich]

I have seen an example of what may cause a clot.
My nieghbor went to my cardiologist on my recomendation.
His heart skips beats on a pretty regular basis.
He is in his seventies and in excellent condition.
The doctor put him on a medication to try and bring his heart rate to a point where it may no longer skip beats.
He also put him on Coumadin because he says during those skipped beats clots could possibly form since no blood is being pumped during those times.

 

[Guest]

Jim's post covers most of what is known. It was thought that the clotting cascade was thoroughly understood until it was realized that what happens to people with antiphospholipid antibody syndrome isn't covered by the clotting cascade. Now there is work underway to redefine it.

The infection theory is (so far) just a theory. So far as I know, nobody has ever been able to prove as relationship between a certain infectious agent and a certain disease. It may be proven some day but right now it is just an idea.

 

[JimChicago]

That's interesting Al - "antiphospholipid antibody syndrome" - is there a blood test for that?

There is an interesting article on a study to identify risk factors for strokes for those with prosthetic heart valves at:
http://circ.ahajournals.org/cgi/content/full/108/10_suppl_1/II-68#SEC2

Apparently it was a small study that said for prosthetic heart valves infection might possibly be realted to increased risk of clots - primarily within the first months after surgery and said Chlamydia pneumoniae may be a risk factor too.

From:
http://circ.ahajournals.org/cgi/content/full/108/10_suppl_1/II-68#SEC2
>>>>>
Postoperative infections in this study included 13 wound infections, 2 pulmonary infections, 1 urinary-tract infection, 1 case of mediastinitis, and 1 intravenous line infection. Seven patients with postoperative infections had 10 TE events (7 ischemic stroke in 5 patients and 3 TIA). On multivariate analysis, considering time to first event in all patients, they doubled the risk of subsequent TE. This suggests that stimulation of an inflammatory response also activated the coagulation system, as the two are known to be closely linked,17 and that this effect persisted following discharge from the hospital. First events occurred within 6 months in 4 patients, 2 years in 2 patients, and within 6 years in 1 patient suggesting that the effect, if present, was predominantly related to the early postoperative months.

Among the laboratory variables identified as risk factors, evidence of chronic infection with Chlamydia pneumoniae emerged as the strongest predictor of future TE events with a hazard ratio of 2.9. Chronic Chlamydial infection as a risk factor for TE events after valve replacement is consistent with similar data for stroke in the general population.18,19 Interestingly Chlamydial infection was present in 5 out of 7 patients who had both postoperative infection and subsequent TE events and the hazard ratio for the combination of Chlamydial infection and a postoperative infection was 8.3.
>>>>

I heard someone on the radio saying dehydratiion might possibly be involved in coagulation also. There are some articles linking air travel with dehydration and blood clots - could dehydration also be a potential risk factor for clots?

From:
http://www.biospace.com/ccis/news_story.cfm?StoryID=6985215&full=1
>>>>
"Sitting in a cramped airplane seat for hours on end could result in a blood clot in a vein," said Belcaro. "Lack of mobility is the reason for the clot, but low pressure in the airplane cabin, low humidity and dehydration may also be contributing factors."
>>>>

From:
http://www.enterprisor.com/article7348.html
>>>>
So unlike a bus, car or train journey, when you travel by air you are much more likely to suffer dehydration, and this in turn increases the danger of blood clots. This is so for four reasons: i. BLOOD THICKENING. Dehydration makes the blood thicker and heavier from lack of water, and therefore more likely to settle in the legs instead of circulating freely around the body. The thicker blood allows a blood clot to form and grow more quickly. ii. VEIN CONSTRICTION. Dehydration dries the skin and constricts the surface veins. This slows down the blood circulation, also making your blood thicker, thus increasing the likelihood of a blood clot. iii. HIGHER BLOOD PRESSURE. Dehydration puts your body under greater stress because all your organs start to compete for the limited amount of water circulating in the blood. This in turn increases your blood pressure. If a blood clot is formed, the high blood pressure can dislodge the clot and carry it through the body to a point where it blocks blood to the heart, the brain, the lungs, a limb, or some other part of the body. iv. CHEMICAL CHANGES. Dehydration causes chemical changes in the body, which dramatically increase the levels of compounds associated with blood clotting. So, to reduce the risk of DVT you have to reduce passenger dehydration. Airlines can best do this by encouraging passengers to drink more water and less alcohol, and by making cabin air less dry
>>>>

 

[Guest]

Interesting posts, Jim.

I have been updating my page on air travel. Dehydration may play a part but this hasn't been proven in a study of people without other risk factors. Planes are pressurized to about the equivalent of 8,000 feet. This is about the equivalent of Colorado ski towns. The air is very dry up there (there are humidifiers in the hotel rooms), lots of alcohol flows and people have limbs immobilized, but there seems to be no epidemic of clots there. In fact the Stedman-Hawkins clinic in Vail specializes in knee surgery.

The main thing for mechanical valve patients to remember is that warfarin counteracts the other risk factors when flying.

 

[McCln]

I do not know why or eaxctly how clots are formed, when when you are taking warafin(coumadin) and you are in the normal range, you will be fine. When you are not in range, you may get a clot in many places. But the best advice, do not live so careful that you are afraid of living. We here have come to terms with the clot issues and continue daily lives. I have more chances on clots due to being diabetic, but am exercising more and keeping active is my goal everyday. You cannot live fearing clots. Please live and be sure to ask your doctor questions on this subject as well as getting educated by other sources. Keep exercising and live life.