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<title>Endothelial dysfunction</title>

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Endothelial dysfunction

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In <a href="Vascular_disease" title="Vascular disease">blood vessel diseases</a>, endothelial dysfunction is an unhealthy state of <a href="Endothelium" title="Endothelium">the cells that line the blood vessels (endothelium)</a>. The main cause of endothelial dysfunction is impaired bioavailability of <a href="Nitric_oxide" title="Nitric oxide">nitric oxide</a>.<a href="#cite_note-pmid31354915-1">[1]</a>

In addition to acting as a <a href="Semipermeable_membrane" title="Semipermeable membrane">semipermeable membrane</a>, the endothelium is responsible for maintaining <a href="Vascular_tone" class="mw-redirect" title="Vascular tone">vascular tone</a> and regulating <a href="Oxidative_stress" title="Oxidative stress">oxidative stress</a> by releasing mediators, such as nitric oxide, <a href="Prostacyclin" title="Prostacyclin">prostacyclin</a> and <a href="Endothelin" title="Endothelin">endothelin</a>, and by controlling local <a href="Angiotensin" title="Angiotensin">angiotensin</a>-II activity.<a href="#cite_note-2">[2]</a><a href="#cite_note-3">[3]</a>

Dysfunctional endothelium is characterized by <a href="Vasoconstriction" title="Vasoconstriction">constricted blood vessels</a>, increased <a href="Vascular_permeability" title="Vascular permeability">ability of chemicals to flow through blood vessel walls</a>, <a href="Thrombosis" title="Thrombosis">blood clots</a>, and <a href="Inflammation" title="Inflammation">inflammation</a>. This pathological state is often associated with elevated levels of <a href="Biomarker" title="Biomarker">biomarkers</a> such as <a href="Prothrombin_time" title="Prothrombin time">prothrombin time</a>, <a href="D-dimer" title="D-dimer">D-dimer</a>, <a href="Von_Willebrand_factor" title="Von Willebrand factor">von Willebrand factor</a>, <a href="Fibrin_degradation_product" title="Fibrin degradation product">fibrin degradation products</a>, <a href="C-reactive_protein" title="C-reactive protein">C-reactive protein</a> (CRP), <a href="Ferritin" title="Ferritin">ferritin</a>, <a href="Interleukin_6" title="Interleukin 6">Interleukin 6</a> (IL-6), and plasma <a href="Creatinine" title="Creatinine">creatinine</a>. The result of this endothelial dysregulation is a cascade of harmful effects, including tightened blood vessels, <a href="Capillary_leak_syndrome" title="Capillary leak syndrome">small blood vessel leakage</a>, blood clots, high levels of inflammation, and a disrupted <a href="Immune_response" title="Immune response">immune response</a> against <a href="Virus" title="Virus">viruses</a>. These changes contribute to the progression of blood vessel (vascular) diseases.<a href="#cite_note-:0-4">[4]</a>

In a healthy state, the endothelium exhibits <a href="Vasodilation" title="Vasodilation">wider blood vessels</a>, tightly-controlled blood vessel permeability, and anti-thrombotic and anti-inflammatory properties. This balance ensures the smooth functioning of the vascular system.<a href="#cite_note-:0-4">[4]</a>

<div class="mw-heading mw-heading2"><h2 id="Research">Research</h2></div>

<div class="mw-heading mw-heading3"><h3 id="Atherosclerosis">Atherosclerosis</h3></div>

Endothelial dysfunction may be involved in the development of <a href="Atherosclerosis" title="Atherosclerosis">atherosclerosis</a><a href="#cite_note-jh-5">[5]</a><a href="#cite_note-pmid24222847-6">[6]</a><a href="#cite_note-botts-2021-7">[7]</a> and may predate vascular pathology.<a href="#cite_note-jh-5">[5]</a><a href="#cite_note-pmid18382884-8">[8]</a> Endothelial dysfunction may also lead to increased adherence of <a href="Monocyte" title="Monocyte">monocytes</a> and <a href="Macrophage" title="Macrophage">macrophages</a>, as well as promoting infiltration of <a href="Low-density_lipoprotein" title="Low-density lipoprotein">low-density lipoprotein</a> (LDL) in the vessel wall.<a href="#cite_note-9">[9]</a> <a href="Low-density_lipoprotein#Oxidized_LDL" title="Low-density lipoprotein">Oxidized LDL</a> is a hallmark feature of atherosclerosis,<a href="#cite_note-pmid25804383-10">[10]</a> by promoting the formation of <a href="Foam_cell" title="Foam cell">foam cells</a>, <a href="Monocyte" title="Monocyte">monocyte</a> <a href="Chemotaxis" title="Chemotaxis">chemotaxis</a>, and platelet activation, leading to <a href="Atheroma" title="Atheroma">atheromatous plaque</a> instability and ultimately to rupture.<a href="#cite_note-pmid35722128-11">[11]</a> <a href="Dyslipidemia" title="Dyslipidemia">Dyslipidemia</a> and <a href="Hypertension" title="Hypertension">hypertension</a> are well known to contribute to endothelial dysfunction,<a href="#cite_note-12">[12]</a><a href="#cite_note-13">[13]</a> and lowering blood pressure and LDL has been shown to improve endothelial function, particularly when lowered with <a href="ACE_inhibitor" title="ACE inhibitor">ACE inhibitors</a>, <a href="Calcium_channel_blocker" title="Calcium channel blocker">calcium channel blockers</a>, and <a href="Statin" title="Statin">statins</a>.<a href="#cite_note-pubmed.ncbi.nlm.nih.gov-14">[14]</a> Steady laminar flow with high shear stress in blood vessels protects against atherosclerosis, whereas disturbed flow promotes atherosclerosis.<a href="#cite_note-pmid31354915-1">[1]</a>

<div class="mw-heading mw-heading3"><h3 id="Nitric_oxide">Nitric oxide</h3></div>

Nitric oxide (NO) suppresses platelet aggregation, inflammation, oxidative stress, vascular smooth muscle cell migration and proliferation, and leukocyte adhesion.<a href="#cite_note-pmid24222847-6">[6]</a> A feature of endothelial dysfunction is the inability of <a href="Arteries" class="mw-redirect" title="Arteries">arteries</a> and <a href="Arterioles" class="mw-redirect" title="Arterioles">arterioles</a> to dilate fully in response to an appropriate stimulus, such as <a href="Exogenous" class="mw-redirect" title="Exogenous">exogenous</a> <a href="Nitroglycerine" class="mw-redirect" title="Nitroglycerine">nitroglycerine</a>,<a href="#cite_note-jh-5">[5]</a> that stimulates release of <a href="Vasodilation" title="Vasodilation">vasodilators</a> from the endothelium like NO. Endothelial dysfunction is commonly associated with decreased NO bioavailability, which is due to impaired NO production by the endothelium or inactivation of NO by reactive <a href="Oxygen" title="Oxygen">oxygen</a> species.<a href="#cite_note-pmid25804383-10">[10]</a><a href="#cite_note-pmid29596860-15">[15]</a> As a co-factor for <a href="Nitric_oxide_synthase" title="Nitric oxide synthase">nitric oxide synthase</a>, <a href="Tetrahydrobiopterin" title="Tetrahydrobiopterin">tetrahydrobiopterin</a> (BH4) supplementation has shown beneficial results for the treatment of endothelial dysfunction in animal experiments and clinical trials, although the tendency of BH4 to become oxidized to BH2 remains a problem.<a href="#cite_note-pmid29596860-15">[15]</a>

<div class="mw-heading mw-heading3"><h3 id="Testing_and_diagnosis">Testing and diagnosis</h3></div>

In the <a href="Coronary_circulation" title="Coronary circulation">coronary circulation</a>, <a href="Angiography" title="Angiography">angiography</a> of <a href="Coronary_artery" class="mw-redirect" title="Coronary artery">coronary artery</a> responses to vasoactive agents may be used to test for endothelial function, and venous occlusion <a href="Plethysmography" class="mw-redirect" title="Plethysmography">plethysmography</a> and <a href="Ultrasonography" class="mw-redirect" title="Ultrasonography">ultrasonography</a> are used to assess endothelial function of peripheral vessels in humans.<a href="#cite_note-jh-5">[5]</a>

A <a href="Minimally_invasive_procedures" class="mw-redirect" title="Minimally invasive procedures">non-invasive</a> method to measure endothelial dysfunction is % <a href="Flow-mediated_dilation" title="Flow-mediated dilation">Flow-Mediated Dilation</a> (FMD) as measured by Brachial Artery Ultrasound Imaging (BAUI).<a href="#cite_note-16">[16]</a> Current measurements of endothelial function via FMD vary due to technical and physiological factors. Furthermore, a <a href="Negative_relationship" title="Negative relationship">negative correlation</a> between percent flow-mediated dilation and baseline artery size is recognised as a fundamental scaling problem, leading to biased estimates of endothelial function.<a href="#cite_note-17">[17]</a>

<a href="Von_Willebrand_factor" title="Von Willebrand factor">von Willebrand factor</a> is a marker of endothelial dysfunction and is consistently elevated in <a href="Atrial_fibrillation" title="Atrial fibrillation">atrial fibrillation</a>.<a href="#cite_note-pmid31631989-18">[18]</a>

A non-invasive, <a href="Food_and_Drug_Administration" title="Food and Drug Administration">FDA</a>-approved device for measuring endothelial function that works by measuring <a href="Hyperaemia#Reactive_hyperaemia" title="Hyperaemia">Reactive Hyperemia</a> Index (RHI) is <a href="Itamar_Medical" title="Itamar Medical">Itamar Medical</a>'s EndoPAT.<a href="#cite_note-19">[19]</a><a href="#cite_note-pmid20972417-20">[20]</a> It has shown an 80% sensitivity and 86% specificity to diagnose <a href="Coronary_artery_disease" title="Coronary artery disease">coronary artery disease</a> when compared against the gold standard, acetylcholine angiogram.<a href="#cite_note-21">[21]</a> This result suggests that this peripheral test reflects the physiology of the <a href="Coronary_circulation" title="Coronary circulation">coronary</a> endothelium.

Since NO maintains low tone and high compliance of the small arteries at rest,<a href="#cite_note-22">[22]</a> a reduction of age-dependent small artery compliance is a marker for endothelial dysfunction that is associated with both functional and structural changes in the microcirculation.<a href="#cite_note-23">[23]</a> Small artery compliance or stiffness can be assessed simply and at rest and can be distinguished from large artery stiffness by use of pulsewave analysis.<a href="#cite_note-24">[24]</a>

<div class="mw-heading mw-heading3"><h3 id="Endothelial_dysfunction_and_stents">Endothelial dysfunction and stents</h3></div>

<a href="Stent" title="Stent">Stent</a> implantation has been correlated with impaired endothelial function in several studies.<a href="#cite_note-jte-25">[25]</a> <a href="Sirolimus" title="Sirolimus">Sirolimus</a> eluting stents were previously used because they showed low rates of in-stent <a href="Restenosis" title="Restenosis">restenosis</a>, but further investigation showed that they often impair endothelial function in humans and worsen conditions.<a href="#cite_note-jte-25">[25]</a> One drug used to inhibit restenosis is <a href="Iopromide" title="Iopromide">iopromide</a>-<a href="Paclitaxel" title="Paclitaxel">paclitaxel</a>.<a href="#cite_note-26">[26]</a>

<div class="mw-heading mw-heading3"><h3 id="COVID-19_complication_in_the_lungs">COVID-19 complication in the lungs</h3></div>

COVID-19 can present with an acute lung injury manifestation that arises from endothelial dysfunction.<a href="#cite_note-27">[27]</a>

<div class="mw-heading mw-heading3"><h3 id="Risk_reduction">Risk reduction</h3></div>

Treatment of <a href="Hypertension" title="Hypertension">high blood pressure</a> and <a href="Hypercholesterolemia" title="Hypercholesterolemia">high levels of cholesterol in the blood</a> may improve endothelial function in people taking <a href="Statins" class="mw-redirect" title="Statins">statins</a> (HMGCoA-reductase inhibitor), and <a href="Renin" title="Renin">renin</a> <a href="Angiotensin" title="Angiotensin">angiotensin</a> system inhibitors, such as <a href="ACE_inhibitors" class="mw-redirect" title="ACE inhibitors">ACE inhibitors</a> and <a href="Angiotensin_II_receptor_antagonists" class="mw-redirect" title="Angiotensin II receptor antagonists">angiotensin II receptor antagonists</a>.<a href="#cite_note-pmid17583170-28">[28]</a><a href="#cite_note-29">[29]</a> Calcium channel blockers and selective beta 1 antagonists may also improve endothelial dysfunction.<a href="#cite_note-pubmed.ncbi.nlm.nih.gov-14">[14]</a> Lifestyle modifications such as <a href="Smoking_cessation" title="Smoking cessation">smoking cessation</a> have also been shown to improve endothelial function and lower the risk of major cardiovascular events.<a href="#cite_note-30">[30]</a>

<ul><li><a href="Atherosclerosis" title="Atherosclerosis">Atherosclerosis</a></li>

<li><a href="Endothelial_activation" title="Endothelial activation">Endothelial activation</a></li>

<li><a href="Nitric_oxide" title="Nitric oxide">Nitric oxide</a></li>

<li>Endothelial <a href="Nitric_oxide_synthase" title="Nitric oxide synthase">nitric oxide synthase</a></li>

<li><a href="Prostacyclin" title="Prostacyclin">Prostacyclin</a></li>

<li><a href="Endothelium-derived_relaxing_factor" title="Endothelium-derived relaxing factor">Endothelium-derived relaxing factor</a></li>

<li><a href="Endothelin" title="Endothelin">Endothelin</a></li>

<li><a href="Integrin" title="Integrin">Integrin</a> network</li>

<li>Endothelial <a href="Shear_stress" title="Shear stress">shear stress</a></li></ul>

<div class="mw-heading mw-heading2"><h2 id="References">References</h2></div>

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