[dropcap]A[/dropcap]ortic vasculitis is an inflammatory disease of the aorta that causes dilation of the aorta wall with narrowing of the inside passageway and results in widespread impairment of blood flow to tissues served by the aorta.
Q: What is the result of inflammatory disease of the aorta?
A: The aorta is the largest artery in the body. It extends from the left ventricle (lower chamber) of the heart and carries blood out of the heart with each beat to rest of the body. Narrowing of the aorta’s inside diameter due to swelling from inflammation causes elevated blood pressure and enlarged heart because of back pressure of blood unable to be fully pumped out of the heart with each beat. The heart enlarges because the difficulty of pumping blood out makes it work harder than normal.
Vasculitis that causes midaortic syndrome is a variety of aortic coarctation (narrowing) located in the lower thoracic aorta, the abdominal aorta or both, involving the intestinal and renal vessels (kidney). It usually presents with arterial hypertension.1
What Is Aortic Vasculitis In Celiac Disease and/or Gluten Sensitivity?
Sources:
Massel D. n-3 polyunsaturated fatty acids reduced mortality and morbidity after recent myocardial infarction. Therapeutics. Jan-Feb 2000:6 [↩]
[dropcap]R[/dropcap]eversible hypertension is a pressure disorder of arteries associated with increased systemic (body wide) blood vessel resistance to blood flow due to endothelial (cell) dysfunction of arterial blood vessels that can improve with nutritional treatment.
Hypertension itself is defined as a systolic blood pressure (SBP) of 140 mm Hg (mercury) or greater and/or diastolic blood pressure (DBP) of 90 mm Hg or greater.
Q: What is blood vessel (vascular) resistance to blood flow?
A: Vascular resistance to blood flow means the arteries carrying blood away from the heart cannot relax or dilate when needed to lower blood pressure but stay constricted, which in turn, keeps the pressure high.
Here’s an analogy: if you replace your garden hose having a one inch inside diameter with one that has a smaller half inch diameter and open the water valve as usual, the result would be water shooting out with more force.
What Is Reversible Hypertension In Celiac Disease and/or Gluten Sensitivity?
[dropcap]C[/dropcap]erebral vasculitis, also called vasculitis of the central nervous system (CNS), is an autoimune attack against elastin fibers in the walls of arteries that bring blood to the head. Early recogniton may reduce poor outcomes.1
Cerebral vasculitis is characterized by inflammation of large, medium, or small blood vessels which is often segmental with scattered foci (sites) of intense inflammation, and results in necrosis (death) of affected tissues with scarring that occludes, or blocks, blood flow.
Q: What happens when an artery is occluded by scarring?
A: When an artery is occluded by scarring, blood cannot flow through it thus preventing the body tissues it supplies with oxygen and nutrition. Depending on vessels that are affected, blindness, TIA (transient ischemic attack) or stroke may result from blockage or rupture (hemorrhage).
Blood flow through arteries can be seen by angiography procedure. The diagnosis is made by biopsy. Additionally, contrast-enhanced MRI, proven to be sensitive to extradural arteritis, for the identification of intracranial vessel wall inflammation shows that wall thickening and intramural contrast uptake are frequent findings in patients with active cerebral vasculitis affecting large brain arteries.2
Vasculitis may develop with autoimmune diseases, such as celiac disease, lupus eythematosis and rheumatoid arthritis due to immune complexing, and possibly severe infection and drug sensitivity.
What Is Cerebral Vasculitis In Celiac Disease and/or Gluten Sensitivity?
Sources:
Salvarani C, Brown RD Jr, Calamia KT, Christianson TJ, Weigand SD, Miller DV, Giannini C, Meschia JF, Huston J 3rd, Hunder GG. Primary central nervous system vasculitis: analysis of 101 patients. Ann Neurol. 2007 Nov;62(5):442-51. [↩]
Küker W, Gaertner S, Nagele T, Dopfer C, Schoning M, Fiehler J, Rothwell PM, Herrlinger U. Vessel wall contrast enhancement: a diagnostic sign of cerebral vasculitis. Cerebrovasc Dis. 2008;26(1):23-9. doi: 10.1159/000135649. Epub 2008 May 30. [↩]
Figure on right shows how atherosclerosis impedes blood flow through coronary arteries while blood clots block blood flow. Courtesy Google.
What Is Coronary Artery Disease (CAD)?
[dropcap]C[/dropcap]oronary artery disease (CAD), also called ischemic heart disease, is a gradual narrowing of medium and large arteries of the heart by fatty buildups, called atherosclerotic plaques.
It is characterized by slowly developing interference with blood flow to heart tissue itself, resulting in oppressive chest pain called angina and, ultimately, thrombosis (clot) causing heart attack.
The heart is a muscular organ that is working all the time, so it needs a constant supply of oxygen. Oxygen is brought to the working heart tissue by the coronary arteries with each beat of the heart. When heart muscle has to work harder, it needs more oxygen delivered to itself. Lack of oxygen causes pain.
In fact, failure of diseased coronary arteries to deliver adequate oxygen to heart tissue is the most common cause of angina pectoris – substernal pain (under breastbone) or pressure brought on by exertion and relieved by rest.
Thrombosis, or clot formation, occurs when blood cells within a narrowed artery can no longer get through. Trapped, blood cells pile up and block the artery thus triggering a cascade of events called heart attack. Coronary arteries that are narrowed by atherosclerotic plaques can rupture causing injury to the coronary blood vessel resulting in blood clotting which blocks the flow of blood to the heart muscle. Blood clots may form, partially dissolve, and later form again and angina can occur each time a clot blocks blood flow in an artery.1
Q: How does coronary artery disease develop?
A:Coronary artery disease slowly develops from this combination of events:
Dysfunction of epithelial cells that line the inside of arteries cause the vessels to stiffen, and subsequently
Accumulation of lipid (fat) in smooth muscle cells beneath the inside lining of arteries and in foam cells cause buildup of fatty deposits on the inside walls progressing to fibrous plaque formation.
Oxidized low-density lipoprotein (oxLDL), so-called bad cholesterol, and oxysterols play important roles in the development of atherosclerosis. OxLDL triggers the immune system to produce autoantibodies against oxLDL that are detectable in serum. These antibodies are called anti-oxLDL. Anti-oxLDL antibody and oxysterol concentrations are associated with coronary artery stenosis. Oxidative stress may be greatly increased in unstable angina.2 and Chronic inflammation in the general population is a major risk factor for ischemic heart disease.
The pathophysiology of atherosclerosis is, clearly, different in women when compared to the men. The women have a higher risk of blood coagulability making them at high risk for the blood clot formation. In a large number of women endothelial dysfunction, small vessel size and diffuse atherosclerosis have been identified as causes of ischemia without evidence of blockade in the coronary arteries.3
Also, atherosclerotic plaque in women is less fibrotic and contains more lipid filled foam cells, implying greater potential for reversibility but also potentially greater vulnerability for plaque rupture and thrombosis.4
Who is Affected in the General Population?
Coronary artery disease remains the leading cause of death in developed countries despite significant progress in primary prevention and treatment strategies.
It is the leading cause of death in women, as well as an important cause of disability.
Older patients are at particularly high risk of poor outcomes following acute coronary syndrome.5
What Is Coronary Artery Disease In Celiac Disease and/or Gluten Sensitivity?
Ischemic heart disease is the leading cause of death in the United States, making cardiovascular risk assessments and potential interventions or treatments imperative for patients with celiac disease.6
Yasunobu Y, Hayashi K, Shingu T, Yamagata T, Kajiyama G, Kambe M. Coronary atherosclerosis and oxidative stress as reflected by autoantibodies against oxidized low-density lipoprotein and oxysterosis. Atherosclerosis. Apr 2001;155(2):445-53. [↩]
Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. Epub 2013 Dec 19. [↩]
Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. Epub 2013 Dec 19. [↩]
Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. [↩]
Robinson BL, Davis SC, Vess J, Lebel, J. Primary care management of celiac disease. Nurse Practitioner. February 2015: Vol 40 – Issue 2; 28–34. [↩]
[dropcap]A[/dropcap]therosclerosis is a disease of arteries involving the buildup of fatty material called plaque along the walls of medium and large arteries characterized by patchy subintimal thickening, hardening, and loss of elasticity of blood vessels.
The intima is the innermost layer of an artery, having contact with blood. The subintima is beneath it.
Q: What happens when arteries become narrowed and less flexible?
A: Narrowing of the inside diameter of blood vessels and hardening of their walls reduce or obstruct blood flow through them which impairs their ability to supply tissues of the body with oxygen and nourishment.
When tissues are deprived of oxygen, pain and dysfunction results such as angina pectoris involving heart muscle because the heart continually needs oxygen never being able to rest.
It is thought that atherosclerosis develops from 1) epithelial cell dysfunction of the intima, and 2) lipid (fat) accumulation in smooth muscle cells and in foam cells, causing buildup of fatty deposits on the inside walls progressing to fibrous plaque formation. That is, intimal smooth muscle cells are surrounded by connective tissue and intracellular and extracellular lipids (fat build-up inside and outside of these cells).
What Is Atherosclerosis In Celiac Disease and/or Gluten Sensitivity?
[dropcap]E[/dropcap]cchymosis, or easy bruising, is a feature of impaired secondary hemostasis (blood clotting) characterized by subcutaneous bleeding (under the skin) in response to light trauma.
Q: What causes easy bruising?
A: Easy bruising is the direct result of vitamin K deficiency that develops from inadequate diet, malabsorption, dysbiosis, and vitamin K depleting medications.
What Is Easy Bruising In Celiac Disease and/or Gluten Sensitivity?
[dropcap]E[/dropcap]pistaxis, or nosebleed, is a feature of secondary hemostasis (blood clotting) characterized by fragility of a plexus of blood vessels in the antero-inferior septum (just inside nostril) and/or abnormal blood coagulation.
What Is Epistaxis In Celiac Disease and/or Gluten Sensitivity?
A feature of vitamin C deficiency that is characterized by fragility of the underlying capillaries resulting in bleeding under the nail. Click for full description.
Sustained elevated arterial blood pressure resulting from impaired absorption of essential co-factors for normal homocysteine metabolism (folate, vitamin B12, or vitamin B6) that resolves with normalization of homocysteine levels.
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