Sarin Exposure and Late Onset Heart Damage

Having tracked the early deaths of Gulf War Veterans in their 30-50’s and having talked to many thousands of Gulf War Veterans and some of their survivors the answer coming from the mice study from Wright State University on sarin affects.  Leads to the appeal for Gulf War Veterans and their families to report cardiac symptoms one of which is palpitation and chest pains.  Please do not ignore these symptoms report them to your physician immediately and ask to see a cardiologist for further work up.  Take a copy of this article and share it with the health care professionals.  Keep a copy in your records!  Please veterans widely distribute this information!  Those veterans that were exposed at multiple weapons locations when those were ordered destroyed need to pay even closer attention.    This is an urgent health alert that should be mass distributed.

The VA needs to review this research and also look at the early cardiac deaths of Gulf War Veterans and Gulf War Veterans that are experiencing Cardiac Problems.  WE need service connection made!  WE need the survivors that are fighting for DIC in relationship to an early death need assistance!  Their cases need administrative review and a fast track response.  See the article below.

Gulf War Nerve Agent Tied to Late-Onset Heart Damage in Mice

Signs appeared 10 weeks after exposure to low-dose sarin, researchers found

By — Robert Preidt


WEDNESDAY, Oct. 13 (HealthDay News) — Low-dose exposure to the chemical warfare agent sarin may lead to long-term heart damage, a new study suggests.

Sarin is known to affect the nervous system and can cause convulsions, breathing difficulties and death. In this study, researchers examined how sarin affected the hearts of mice. The chemical was injected into the animals at doses too low to produce visible symptoms and the mice were checked 10 weeks after exposure.

“The two-month period was used to simulate the late-onset effect of sarin/nerve agents in Gulf War veterans. There are suggestions that Gulf War illness, in which symptoms are long-lasting, may be related to exposure to low-dose chemical warfare agents,” Mariana Morris, of the Boonshoft School of Medicine at Wright State University in Dayton, Ohio, said in a news release from the American Heart Association.

Heart damage that was noted in the mice 10 weeks after exposure to sarin, but not earlier, included: enlargement of the left ventricle; an electrical conduction problem that could lead to heart rhythm abnormalities; and reduced ability of the ventricles to contract and pump blood, the researchers found.

“These results have implications for the military in terms of conflict and for civilian populations in cases of environmental or occupational exposure,” Morris said in the news release.

The study results are scheduled for presentation Wednesday at the American Heart Association’s High Blood Pressure Research 2010 Scientific Sessions, held in Washington, D.C.

More information

The U.S. Centers for Disease Control and Prevention has more about sarin.

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Next articleAnother New Gulf War Illness Research Finding
Maj. Denise Nichols, Vietnam era and Gulf War veteran, retired nurse, MSN, retired US Air Force Flight Nurse Clinical specialist in cardio-vascular nursing, served on the nursing faculty of several universities around the country. Denise has been active in research and advocacy in the areas of Gulf War Illness and Agent Orange. Denise has testified before congress many times, has been interviewed nationally and internationally and is an outspoken advocate for Americas veterans.


  1. Have you been diagnosed with Pericarditis? I am having issues as well and would like to see if there is a commonality. What years did you serve? Any progress with your claim?

  2. Guess who went to see a cardiologist earlier this year?! Guess who was diagnosed with atrial fibrillation? Guess who’s on metoprolol? Yay…between that and the ALS risk, and my genetics of heart attacks and Alzheimers, I’d say the next 20yrs are going to be a hoot!…if I live that long.

  3. Damn! sorry to hear.

    “NBC correspondent David Bloom died of ? in 2003 after spending days inside a tank while covering the invasion of Iraq.” Vibrated to death!

  4. Prior to deployment no cardiac problems, no family med history. Upon return fluid was seen around my pericardium. Told by all MD’s seen at the time leave it alone it’s not bothering you. 07/00 had mulitple syncople episodes in 24hr period. One captured episode(cardiac monitor)of asystole (1 min). Wound up in OR 250cc fluid removed and demand pacemaker implanted. Was assigned to the 1st ID and was within 5km of Kamasiayia(sp) All claims with VA to this point in time denied. Was given an Honorable Discharge (not a Medical) after being told I was medically unfit to serve further. Hopefully this research will change my DAV claim and those of us out there still paying the price. This is our generations Agent Orange Battle.

  5. “Cardiovascular System
    The cardiovascular response to vibration is well
    studied. This system reacts to vibration as it does
    to any stress, with an increase in heart rate and
    blood pressure. Several limited Scandinavian stud-
    ies indicate a rise in blood lipids.
    vibration results in hand-arm vibration syndrome,
    in which segmental vibration results in endothelial
    damage to the small arterioles. Patients present with
    vasospasm of the digits, especially in response to

    Military Preventive Medicine: Mobilization and Deployment, Volume 1
    P. Smith, Colonel, Medical Corps, US Army, Occupational Environmental Medicine Staff Officer, Proponency Officer for Preven-
    tive Medicine, Office of The Surgeon General, 5109 Leesburg Pike, 6 Skyline Place, Falls Church, VA 22041-3258

  6. I am a 37 year old gulf Veteran who has had, three MI’s (Heart Attacks), One TIA, (Mini Stroke) with no family History, No drug Use,just long exhausting answers from Drs stating that I need to stay calm and take my pills LMAO> I would love someone, anyone to recognize that these symptons are coming from somewhere (AKA PERSIAN GULF), but I have my doubts. So I say, we are all dying it’s just a matter of when….Good Luck Vets, and If anyone hears of an answer or solution hit me up and let me know.

  7. FYI—Blood work to be aware of…if you go in with chest pain. Blood work and EKG!!!
    If no MI then Stress Treadmill test….

    Have you all had these??
    Strokes(Brain) could occur re if you have Atrial Fib, and blood clot…..

    Deep Vein Thrombous is also a possible problem! Remember David Bloom(Bloom Mobile) the young reporter MSNBC re invasion of Iraq 2003 died suddenly…re Vaccines?, Sand inhalation?, Chems? DU?—- problem with blood flow re legs in cramped position….then it breaks loose and causes Pulmonary Embolism, I think is what they determined re his death.

    BE ASSERTIVE and ask for second opinions…

    ———–more info below—Cardiac____
    Troponins will begin to increase following MI within 3 to 12 hours, about the same time frame as CK-MB. However, the rate of rise for early infarction may not be as dramatic as for CK-MB.
    Troponins will remain elevated longer than CK–up to 5 to 9 days for troponin I and up to 2 weeks for troponin T. This makes troponins a superior marker for diagnosing myocardial infarction in the recent past–better than lactate dehydrogenase (LDH).


    Cardiac Enzymes
    – CPK: – normal values: – men: less than 174 Units/liter – women: less than 140 Units/liter –

    MM 100%,
    MB (cardiac)
    and BB (brain) normally comprise 0%;
    – abnormal values: –

    myocardial infarct –

    CPK levels begin to rise 4-6 hours after MI has started and reaches its peack values within 30 hrs; – look for an elevation of the CPK MB isoenzymes at 4-6 hours (in MI the CPK MB is more than 5% of total CPK);
    – post surgical elevation: there will be an elevation of the CPK level, but the CPK MB percentage should be close to 0; – polymyositis –
    Troponin I and T: – these are cardiac specific muscle proteins which are elevated with cardiac muscle damage; –

    Cardiovascular Evaluation

    Test Includes Triglycerides, cholesterol, HDL cholesterol, LDL cholesterol, HDL/cholesterol ratio

    Specimen Blood
    Volume 7 mL

    Collection Routine venipuncture
    Patient Preparation A 12- to 14-hour fast is required. The patient should be on his/her normal diet for several days prior to having the blood drawn.
    Reference Range

    Total cholesterol
    -Desirable: <200 mg/dL
    -Borderline-high: 200-239 md/dL
    -High: = 240 mg/dL

    HDL cholesterol
    -Low (major risk factor): <35 mg/dL
    -High (negative risk factor): : = 60 mg/dL

    For secondary prevention in adults with evidence of coronary heart disease, the optimum LDL cholesterol level is <100 mg/dL.
    LDL cholesterol
    -Desirable: <130 mg/dL
    -Borderline-high: 130-159 mg/dL
    -High: : = 160 mg/dL
    -Normal 1000 mg/dL

    FOR MI
    Creatine Kinase – Total:
    The total CK is a simple and inexpensive test that is readily available using many laboratory instruments. However, an elevation in total CK is not specific for myocardial injury, because most CK is located in skeletal muscle, and elevations are possible from a variety of non-cardiac conditions.
    Creatine Kinase – MB Fraction:
    Creatine kinase can be further subdivided into three isoenzymes: MM, MB, and BB. The MM fraction is present in both cardiac and skeletal muscle, but the MB fraction is much more specific for cardiac muscle: about 15 to 40% of CK in cardiac muscle is MB, while less than 2% in skeletal muscle is MB. The BB fraction (found in brain, bowel, and bladder) is not routinely measured.
    Thus, CK-MB is a very good marker for acute myocardial injury, because of its excellent specificity, and it rises in serum within 2 to 8 hours of onset of acute myocardial infarction. Serial measurements every 2 to 4 hours for a period of 9 to 12 hours after the patient is first seen will provide a pattern to determine whether the CK-MB is rising, indicative of myocardial injury. The CK-MB is also useful for diagnosis of reinfarction or extensive of an MI because it begins to fall after a day, dissipating in 1 to 3 days, so subsequent elevations are indicative of another event.
    A “cardiac index” can provide a useful indicator for early MI. This is calculated as a ratio of total CK to CK-MB, and is a sensitive indicator of myocardial injury when the CK-MB is elevated.
    CK-MB Isoforms:
    The CK-MB fraction exists in two isoforms called 1 and 2 identified by electrophoretic methodology. The ratio of isoform 2 to 1 can provide information about myocardial injury.
    An isoform ratio of 1.5 or greater is an excellent indicator for early acute myocardial infarction. CK-MB isoform 2 demonstrates elevation even before CK-MB by laboratory testing. However, the disadvantage of this method is that it is skilled labor intensive because electrophoresis is required, and large numbers of samples cannot be run simultaneously nor continuously. False positive results with congestive heart failure and other conditions can occur.
    Troponin I and T are structural components of cardiac muscle. They are released into the bloodstream with myocardial injury. They are highly specific for myocardial injury–more so than CK-MB–and help to exclude elevations of CK with skeletal muscle trauma. Troponins will begin to increase following MI within 3 to 12 hours, about the same time frame as CK-MB. However, the rate of rise for early infarction may not be as dramatic as for CK-MB.
    Troponins will remain elevated longer than CK–up to 5 to 9 days for troponin I and up to 2 weeks for troponin T. This makes troponins a superior marker for diagnosing myocardial infarction in the recent past–better than lactate dehydrogenase (LDH). However, this continued elevation has the disadvantage of making it more difficult to diagnose reinfarction or extension of infarction in a patient who has already suffered an initial MI. Troponin T lacks some specificity because elevations can appear with skeletal myopathies and with renal failure.
    Myoglobin is a protein found in skeletal and cardiac muscle which binds oxygen. It is a very sensitive indicator of muscle injury. The rise in myoglobin can help to determine the size of an infarction. A negative myoglobin can help to rule out myocardial infarction.. It is elevated even before CK-MB. However, it is not specific for cardiac muscle, and can be elevated with any form of injury to skeletal muscle.
    Lactate dehydrogenase:
    The LDH has been supplanted by other tests. It begins to rise in 12 to 24 hours following MI, and peaks in 2 to 3 days, gradually dissipating in 5 to 14 days. Measurement of LDH isoenzymes is necessary for greater specificity for cardiac injury. There are 5 isoenzymes (1 through 5). Ordinarily, isoenzyme 2 is greater than 1, but with myocardial injury, this pattern is “flipped” and 1 is higher than 2. LDH-5 from liver may be increased with centrilobular necrosis from passive congestion with congestive heart failure following ischemic myocardial injury.

  8. My comment after reading David W, Adam, Phillip, Samuel, Karen, and Bryant.

    Dr Cheney re CFS and cardiac.

    Also Hypercoagulation articles

    Suggest arterial and Venous simultaneous blood draw for actual O2 level and not just the finger monitor.

    Also do not ignore! get treadmill stress test, referral re cardiac cath.
    Have too many GWVets with cardiac stints and also early deaths Cardiac?

    Keep your weight down! Exercise, change your diets, check to be sure no diabetes.

    YOU HAVE TO BE YOUR OWN ADVOCATE!!! Get your SS rating or use tricare get to second opinions experts!!!

  9. Adam,

    I have tingling/numbness around my lips & chin. They don’t know why it is happening so they say. They also say its not MS or TIA-related. Then what is it?

    It happens to me, I know it & they (the physicians) know it; so what clinically could it be?

    Still, no answers! Terribly frustrating!

    All the best,


  10. Dave,

    I have a very similar condition.

    My records state, an enlarged heart (many years now). An echocardiogram done at the DCVAMC-WRIISC Clinic last year demostrated left ventricle enlargement. I have gone to Acute Care (ER) at the Durham VAMC (NC) for chest pains for years, until I became tired of traveling for no answers; they hook me up to the “echo” & send me home…it comes out normal according to them!

    I want answers, enough of this “little bit of info at a time” stuff!

    We share common issues; some worse than others; what is it going to take for REAL action & health care concerning Gulf War Veterans! I am so frustrated!

    Great work, Denise! Thanks for your comment, Dave, it inspired me to write…!


  11. You know what, I have a slight heart arrhythmia and never paid much attention to it. I have constant muscle pain and joint pain, my skin it blotched with white spots (vitiligo-about 20% of my entire body), PTSD, depression and constant headaches. All of this is from being in the Gulf 20 yrs ago. I hope that I get compensated as my case it pending but I really want my health back. Once it is gone it is over. I try my best to eat healthy foods and very little exercise, I do believe that this has mad a lot of difference but when your DNA has been altered and your body is constantly trying to fight off foreign matter in your body it is pretty hard to stay positive. Let’s just pray to God that we are vendicated here in this life and our assailants-our own govn’t be dealt with from the Most High

  12. Great to see the article. Had an angio done at a civilian hospital after the VA in Philly said nothing was wrong from a stress test. The Angio showed 2 blocked arteries at 80 – 90 %. You all hang in there.

  13. @Dave Winnett,Adam Smith, and Phillip Nelson: I don’t know if you read about the patient-driven Ad campaign going on at

    or at the (new) website:

    but we are including GWI, and veterans are needed to help us!

    Please check out the information on these sites; in just under 3 months, we have enlisted 1412 Members and $8,365 for our first AD coming out in the Washington Post very, very soon now; and MEMBERS GET TO VOTE on which ad they want to run, from a field of 4-5. We will have more than one AD in the Wash. Post. Fundraising will begin soon for the next one: they are $8500 each, for charity/advocacy ones.

    Your Voices will be vital to this effort; GWI has so many of the symptoms of CFS (aka Myalgic Encephalomyelitis) that we want your voices included in all our discussions and the media storm that is going to happen as soon as this ad runs.

    If you’re not on FB, I encourage you to use the
    website to join the discussions; it doesn’t have much traffic yet, but it will, after this Ad runs.

    I hope you will join us, the ME/CFS Worldwide Patient Alliance (MCWPA). We must join all of our patient voices together and make sure our VA and government research and health agencies are doing the right thing by us all, and we think public scrutiny and alarm will do that.

    There’s no way to thank you, Denise, for the carefully vetted articles you post, and your columns of information and encouragement to us all…thank you!

    I am a 100% Army Vet (1974-1980), served only in-country at WRAMC, Brooks AFB, and Ft. Sam Houston, but I still got 3 mycoplasmas by PCR and CFS and FM…and now Myasthenia Gravis. I had vaccines for overseas duty, got pneumonia in Basic, and they wouldn’t send me, said I was too ‘fragile’…served as Sec. to Chief, Personnel, WRAMC and then in Cancer Registry at Brooks AFB, then ran Medical Outprocessing at FT SAM and interim aide to Flight Surgeon there.

    Come join us at above site(s)….you’ll be glad you did!

  14. Adam T, Smith
    Your story sound a like and the same VA Medical Center in Memphis. I still have the same old e-mail address so, e-mail me.

  15. I have been to the ER twice over the past eight or so years with sever chest pains, nothing was found. The VAMC Memphis told me about ten years ago I had Hypertention which they claimed was related to my PTSD.
    Just last month on two seperate occastions I woke with complete numbness on one side of my face encluding half the inside of my mouth and my left arm, I just had a CT with dye done but have not received any results, this was symptomatic of a TIA (mini-stroke) has any other GWV had this happen to them?
    I stay weak, but not sure if it is related to my heart or cronic fatigue?
    Denise I know we have not spoke in some time, hope you are well, do you have any input as to these symptoms?

  16. I was recently told I have an enlarged heart and mitro valve regurgitation. I also experience frequent bouts of heart arrhythmia. I’m 56, a longtime runner (always 1st Class PFT during my 20-year USMC career). Stopped exercising altogether about 2 years ago due to extreme fatigue. Never smoked in my life and I’m normal body weight. I’ve been diagnosed with CFS and I have constant muscle pain throughout my body. Maybe this (sarin) is the cause? I served with 1st Marine Division Headquarters in the assault through Kuwait. We just need definitive answers. 20 years of not knowing is enough. I want my life back. Dave Winnett, Captain, USMC (Ret.).

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