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--- home:diseases:cardiovascular [02.11.2019] – [Cardiovascular diseases] sallieq
+++ home:diseases:cardiovascular [09.14.2022] (current) – external edit 127.0.0.1
@@ Line 7: / Line 7: @@
 Heart disease or cardiovascular diseases is the class of diseases that involve the heart or blood vessels (arteries and veins). While the term technically refers to any disease that affects the cardiovascular system, it is usually used to refer to those related to arteriosclerosis (hardening of the arteries).
-Macrophages are central to atherogenesis because they regulate cholesterol traffic and inflammation in the arterial wall. <blockquote>Excess 25-hydroxyvitamin D3 exacerbates tubulointerstitial injury in mice by modulating macrophage phenotype. (({{pubmed>long:26579677}})) </blockquote>
+Macrophages are central to atherogenesis because they regulate cholesterol traffic and inflammation in the arterial wall. <blockquote>Excess 25-hydroxyvitamin D3 exacerbates tubulointerstitial injury in mice by modulating macrophage phenotype. (({{pmid>long:26579677}})) </blockquote>
 According to the Marshall Pathogenesis, cardiovascular diseases result from the combined effects of communities of microbes that people gradually accumulate over time via the process of successive infection. In fact, there is some evidence that arterial plaque may at least be partly composed of biofilm, a community of diverse microbes that work together.
-While many more pathogens will likely be identified in patients with cardiovascular diseases, certain easily cultured and readily identifiable microbes have been repeatedly identified in people with such conditions including //H. pylori//, cytomegalovirus, and //Chlamydia pneumoniae//.(({{pubmed>long:10204048}})) (({{pubmed>long:16490835}}))
+While many more pathogens will likely be identified in patients with cardiovascular diseases, certain easily cultured and readily identifiable microbes have been repeatedly identified in people with such conditions including //H. pylori//, cytomegalovirus, and //Chlamydia pneumoniae//.(({{pmid>long:10204048}})) (({{pmid>long:16490835}}))
 One of the best known links between two different inflammatory diseases – and a prototypical illustration of successive infection – is the relationship between cardiovascular diseases such as heart attack and stroke, and periodontal disease.
@@ Line 24: / Line 24: @@
   * **congestive heart failure** – Develops when the heart’s pumping ability diminishes due to blockages or restriction of blood flow. With heart failure, the weakened heart can’t supply the cells with enough blood. This results in fatigue and shortness of breath.
   * **coronary artery disease (CAD)** – Refers to atherosclerosis in the coronary arteries, which supply the heart muscle with blood.
-  * **heart attack (coronary thrombosis, myocardial infarction [MI])** – When the heart muscle, or myocardium, stops functioning due to loss of blood flow, nutrients, or electric signal. (({{pubmed>long:27589046}}))
+  * **heart attack (coronary thrombosis, myocardial infarction [MI])** – When the heart muscle, or myocardium, stops functioning due to loss of blood flow, nutrients, or electric signal. (({{pmid>long:27589046}}))
   * **high blood pressure (hypertension)** – Besides being a measure of poor cardiovascular health, high blood pressure forces your heart and arteries to work harder, and your major organs are affected. You can live for a long time with no signs of high blood pressure, until the whole system begins to collapse under the workload. //Reviewed in [[home:diseases:hypertension|Hypertension (high blood pressure)]]//
   * **hypercholesterolemia (hyperlipidemia)** – Chronic high levels of cholesterol in the blood. //Reviewed in [[home:tests:lipids|Tests: cholesterol and triglycerides (lipids)]].//
@@ Line 31: / Line 31: @@
-[{{ :home:diseases:ottlesions.png?300|**In samples collected from patients with coronary artery disease, more than 50+ species were found in coronary artery plaque.** The arrows point to groups of bacteria emitting a fluorescent signal. Source: [[http://www.ncbi.nlm.nih.gov/pubmed/16490835|Ott et al.]]}}]
+[{{ :home:diseases:ottlesions.png?300|**In samples collected from patients with coronary artery disease, more than 50+ species were found in coronary artery plaque.** The arrows point to groups of bacteria emitting a fluorescent signal. Source: [[https://www.ncbi.nlm.nih.gov/pubmed/16490835|Ott et al.]]}}]
 ===== Evidence of infectious cause=====
 <blockquote>Immunoinflammatory processes due to chronic infection are thought to be one of the definitive atherogenetic processes.
-//**K. Ayada** et al.//(({{pubmed>long:17894024}}))</blockquote>
+//**K. Ayada** et al.//(({{pmid>long:17894024}}))</blockquote>
@@ Line 48: / Line 48: @@
 <blockquote>Reconsidering exposure as an "infectious burden" (IB) aligns with our understanding that the totality of pro-inflammatory agents can contribute to atherosclerosis and vascular risk. We define IB as the cumulative life-course exposure to infectious agents that elicit strong inflammatory responses....
-//**Elkind** et al.//((Mitchell S.V. Elkind //et al.// [[http://www.touchneurology.com/files/article_pdfs/elkind.pdf|"'Infectious Burden' – New Insights into Stroke Prevention."]] //European Neurological Review//, 2010;5(1):34–38.))
+//**Elkind** et al.//((Mitchell S.V. Elkind //et al.// [[https://www.touchneurology.com/files/article_pdfs/elkind.pdf|"'Infectious Burden' – New Insights into Stroke Prevention."]] //European Neurological Review//, 2010;5(1):34–38.))
 </blockquote>
@@ Line 55: / Line 55: @@
 ==== Arterial plaque may contain biofilm====
-Arterial plaque may contain and/or be caused by biofilm, that is, a community of diverse microbes that work together. Ott //et al.//'s work which showed a diverse groups of bacterial "signatures" in atherosclerotic lesions of patients with coronary heart disease. Using 16S rDNA sequencing, the team was able to identify over 50 different species including //Staphylococcus species, Proteus vulgaris, Klebsiella pneumoniae,// and //Streptococcus// species in plaque. The team concluded, "Detection of a broad variety of molecular signatures in all [coronary heart disease] specimens suggests that diverse bacterial colonization may be more important than a single pathogen."(({{pubmed>long:16490835}}))
+Arterial plaque may contain and/or be caused by biofilm, that is, a community of diverse microbes that work together. Ott //et al.//'s work which showed a diverse groups of bacterial "signatures" in atherosclerotic lesions of patients with coronary heart disease. Using 16S rDNA sequencing, the team was able to identify over 50 different species including //Staphylococcus species, Proteus vulgaris, Klebsiella pneumoniae,// and //Streptococcus// species in plaque. The team concluded, "Detection of a broad variety of molecular signatures in all [coronary heart disease] specimens suggests that diverse bacterial colonization may be more important than a single pathogen."(({{pmid>long:16490835}}))
 In a commentary following Ott's paper, Katz and Shannon concluded that his work suggested that atherosclerotic plaques are composed of "functional biofilm." The team noted that the characteristics of a "mature" arterial wall make it well-suited for biofilm formation. These findings further suggest:
@@ Line 62: / Line 62: @@
 <blockquote>A "conspiracy" of bacterial pathogens as opposed to a single infection is involved in atherogenesis, which may help to explain the inefficacy of antibiotics, such as macrolides or fluoroquinolones, in clinical trials.
-//**Joel T. Katz, MD and Richard P. Shannon, MD**// (({{pubmed>long:16490832}}))</blockquote>
+//**Joel T. Katz, MD and Richard P. Shannon, MD**// (({{pmid>long:16490832}}))</blockquote>
-Immune cells are abundant in the walls of the arteries even during the initial stages of plaque formation.(({{pubmed>long:18276989}})) Macrophages have been shown to infiltrate arterial plaque and express a variety of matrix-degrading enzymes that weaken and sometimes break apart the fibrous caps which holds the plaque intact.(({{pubmed>long:1872926}})) (({{pubmed>long:15337206}})) A portion of arterial plaque consists of apoptized (dead) macrophages.
+Immune cells are abundant in the walls of the arteries even during the initial stages of plaque formation.(({{pmid>long:18276989}})) Macrophages have been shown to infiltrate arterial plaque and express a variety of matrix-degrading enzymes that weaken and sometimes break apart the fibrous caps which holds the plaque intact.(({{pmid>long:1872926}})) (({{pmid>long:15337206}})) A portion of arterial plaque consists of apoptized (dead) macrophages.
 ==== Individual pathogens already implicated in cardiovascular disease ====
 While many more pathogens will likely be identified in patients with cardiovascular diseases, certain easily cultured and readily identifiable microbes have been repeatedly identified in people with such conditions. These include:
-  * **//Chlamydia pneumoniae//** – //C. pnuemonia// can readily switch between reproductive and latent forms(({{pubmed>long:19220338}})) – and, as an intracellular gram-negative bacterium, has been shown to infect macrophages responsible for degrading plaque.(({{pubmed>long:12663369}})) //Mycoplasma pneumoniae//, another intracellular pathogen, has also been associated with atherosclerosis.(({{pubmed>long:16983590}})) A number of studies have been conducted to determine the specific association between //C. pneumoniae// and the development of atherosclerotic plaque. This association was first suggested in 1988, when it was discovered that patients with cardiovascular disease or acute myocardial infarction (AMI) were more likely to have antibodies to //C. pneumoniae// in their blood.(({{pubmed>long:2902492}})) Arcari //et al.//(({{pubmed>long:15791511}})) studied the link between //C. pneumoniae// seropositivity and AMI in males aged 30 to 50. The authors found a significantly higher risk of AMI in patients who had high titers to C. pneumoniae immunoglobulin A (IgA) within the previous one to 5-year period. This risk persisted after adjusting for other cardiovascular risk factors. //C. pneumoniae// has been detected in more than 40% of atherosclerotic plaques,(({{pubmed>long:10193317}})) (({{pubmed>long:9866733}})) and has been shown (along with cytomegalovirus) to directly disseminate into the arterial vessel walls.(({{pubmed>long:14662717}})) Smoking, an independent risk factor for cardiovascular disease, has also been shown to be an independent risk factor for //C. pneumoniae// seropositivity. It has also been suggested that an exacerbation of //C. pneumoniae// infection through smoking cigarettes may increase the potential for a systemic infection and therefore increase the chance for development of atherosclerosis.(({{pubmed>long:10839723}}))
+  * **//Chlamydia pneumoniae//** – //C. pnuemonia// can readily switch between reproductive and latent forms(({{pmid>long:19220338}})) – and, as an intracellular gram-negative bacterium, has been shown to infect macrophages responsible for degrading plaque.(({{pmid>long:12663369}})) //Mycoplasma pneumoniae//, another intracellular pathogen, has also been associated with atherosclerosis.(({{pmid>long:16983590}})) A number of studies have been conducted to determine the specific association between //C. pneumoniae// and the development of atherosclerotic plaque. This association was first suggested in 1988, when it was discovered that patients with cardiovascular disease or acute myocardial infarction (AMI) were more likely to have antibodies to //C. pneumoniae// in their blood.(({{pmid>long:2902492}})) Arcari //et al.//(({{pmid>long:15791511}})) studied the link between //C. pneumoniae// seropositivity and AMI in males aged 30 to 50. The authors found a significantly higher risk of AMI in patients who had high titers to C. pneumoniae immunoglobulin A (IgA) within the previous one to 5-year period. This risk persisted after adjusting for other cardiovascular risk factors. //C. pneumoniae// has been detected in more than 40% of atherosclerotic plaques,(({{pmid>long:10193317}})) (({{pmid>long:9866733}})) and has been shown (along with cytomegalovirus) to directly disseminate into the arterial vessel walls.(({{pmid>long:14662717}})) Smoking, an independent risk factor for cardiovascular disease, has also been shown to be an independent risk factor for //C. pneumoniae// seropositivity. It has also been suggested that an exacerbation of //C. pneumoniae// infection through smoking cigarettes may increase the potential for a systemic infection and therefore increase the chance for development of atherosclerosis.(({{pmid>long:10839723}}))
 <blockquote>Taken together [the large variety of demonstrated proatherogenic changes set into motion by //Chlamydia pneumoniae//] suggested that Cpn infections could contribute to the initiation and progression of atherosclerosis leading to atherosclerotic plaque growth and increased arterial stenosis. Moreover, Cpn infection may also play a role in the development of an unstable atherosclerotic plaque leading to acute cardio- and/or cerebrovascular events.
-//**Frank R. Stassen**// (({{pubmed>long:18276989}}))
+//**Frank R. Stassen**// (({{pmid>long:18276989}}))
 </blockquote>
-  * **Cytomegalovirus** – Cytomegaloviruses (CMV) can cause acute, persistent and latent infections in both humans and animals. Of all herpes viruses, CMV has been most frequently associated with atherosclerosis in epidemiological, experimental and clinical studies.(({{pubmed>long:18276989}})) First evidence for a role for CMV in cardiovascular disease comes from studies demonstrating the presence of CMV antigens or nucleic acids in the diseased vascular wall.(({{pubmed>long:6136795}})) Likewise, CMV nucleic acids have repeatedly been detected in arteries obtained from atherosclerotic patients. More importantly, viral presence was higher in arterial biopsies of patients undergoing reconstructive vascular surgery as compared to patients with early atherosclerosis.(({{pubmed>long:2541613}})) (({{pubmed>long:2153348}})) Also, a positive correlation between CMV and cardiovascular disease has been demonstrated in a variety of studies examining blood markers in diseases.(({{pubmed>long:9259669}})) Several studies showed the level of CMV antibodies to be gradually related to increased intimal-medial thickening (a measure of the thickness of artery walls). No association were found between low CMV antibody titers and cardiovascular disease, but a clear association was found when the height of the titers was taken into account. Stassen //et al.// conclude, "In summary, a large variety of data support the hypothesis that CMV contribute to atherogenesis."(({{pubmed>long:18276989}}))
+  * **Cytomegalovirus** – Cytomegaloviruses (CMV) can cause acute, persistent and latent infections in both humans and animals. Of all herpes viruses, CMV has been most frequently associated with atherosclerosis in epidemiological, experimental and clinical studies.(({{pmid>long:18276989}})) First evidence for a role for CMV in cardiovascular disease comes from studies demonstrating the presence of CMV antigens or nucleic acids in the diseased vascular wall.(({{pmid>long:6136795}})) Likewise, CMV nucleic acids have repeatedly been detected in arteries obtained from atherosclerotic patients. More importantly, viral presence was higher in arterial biopsies of patients undergoing reconstructive vascular surgery as compared to patients with early atherosclerosis.(({{pmid>long:2541613}})) (({{pmid>long:2153348}})) Also, a positive correlation between CMV and cardiovascular disease has been demonstrated in a variety of studies examining blood markers in diseases.(({{pmid>long:9259669}})) Several studies showed the level of CMV antibodies to be gradually related to increased intimal-medial thickening (a measure of the thickness of artery walls). No association were found between low CMV antibody titers and cardiovascular disease, but a clear association was found when the height of the titers was taken into account. Stassen //et al.// conclude, "In summary, a large variety of data support the hypothesis that CMV contribute to atherogenesis."(({{pmid>long:18276989}}))
-  * **//Helicobacter pylori//** – //H. pylori// is a known causal agent of several gastrointestinal diseases and has also been implicated in ischemic heart disease (reduced blood supply to the heart muscle). Researchers have proposed a number of mechanisms by which //H. pylori// may accelerate cardiovascular disease. Ayada states that local inflammatory and immune responses against //H. pylori// in the stomach can induce systemic (including atherosclerotic lesions) immune reactions due to the chronic nature of the infection.(({{pubmed>long:17894024}})) There is also speculation that //H. pylori// may act directly on atherosclerotic plaques, because studies have found its DNA in arterial plaque.(({{pubmed>long:17215796}})) Other studies suggest that //H. pylori// may induce platelet aggregation, and thereby play a role in the acute phase of ischemic heart disease.(({{pubmed>long:18607339}})) A recent meta-analysis indicates that infection with certain more virulent strains of //H. pylori// may provoke an intense immune response and precipitate coronary events.(({{pubmed>long:18599062}}))
+  * **//Helicobacter pylori//** – //H. pylori// is a known causal agent of several gastrointestinal diseases and has also been implicated in ischemic heart disease (reduced blood supply to the heart muscle). Researchers have proposed a number of mechanisms by which //H. pylori// may accelerate cardiovascular disease. Ayada states that local inflammatory and immune responses against //H. pylori// in the stomach can induce systemic (including atherosclerotic lesions) immune reactions due to the chronic nature of the infection.(({{pmid>long:17894024}})) There is also speculation that //H. pylori// may act directly on atherosclerotic plaques, because studies have found its DNA in arterial plaque.(({{pmid>long:17215796}})) Other studies suggest that //H. pylori// may induce platelet aggregation, and thereby play a role in the acute phase of ischemic heart disease.(({{pmid>long:18607339}})) A recent meta-analysis indicates that infection with certain more virulent strains of //H. pylori// may provoke an intense immune response and precipitate coronary events.(({{pmid>long:18599062}}))
-  * **//Porphyromonas gingivalis//** – //P. gingivalis// appears to have an important role in the initiation and progression of atherosclerosis.(({{pubmed>long:18829178}})) Gibson //et al.// showed that immunizing mice against //P. gingivalis// prevents acceleration of atherosclerosis.(({{pubmed>long:18220804}})) For more on //P. gingivalis// and other known periodontal pathogens, [[home:diseases#a_causal_relationship_between_periodontal_disease_and_cardiovascular_disease|see below]].
+  * **//Porphyromonas gingivalis//** – //P. gingivalis// appears to have an important role in the initiation and progression of atherosclerosis.(({{pmid>long:18829178}})) Gibson //et al.// showed that immunizing mice against //P. gingivalis// prevents acceleration of atherosclerosis.(({{pmid>long:18220804}})) For more on //P. gingivalis// and other known periodontal pathogens, [[home:diseases#a_causal_relationship_between_periodontal_disease_and_cardiovascular_disease|see below]].
 ==== Other evidence ====
-  * **Common infections predispose a person to stroke and heart attack** – In a prospective cohort study, a composite measure of //Chlamydia pneumoniae, Helicobacter pylori//, cytomegalovirus, and herpes simplex virus 1 and 2 infection, were associated with a higher risk of stroke and other vascular events.(({{pubmed>long:19901154}})) Diarrhea as an infant (the primary cause of which is microbial infection) has been associated with later cardiovascular disease.(({{pubmed>long:11281409}})) Further, influenza vaccination was associated with a 50% reduction in the incidence of sudden cardiac death, acute myocardial infarction (heart attack), and ischemic stroke. Both heart attack and stroke have their peak incidence in winter months, which correspond to the time of year when cases of influenza also peak.(({{pubmed>long:12573201}}))
+  * **Common infections predispose a person to stroke and heart attack** – In a prospective cohort study, a composite measure of //Chlamydia pneumoniae, Helicobacter pylori//, cytomegalovirus, and herpes simplex virus 1 and 2 infection, were associated with a higher risk of stroke and other vascular events.(({{pmid>long:19901154}})) Diarrhea as an infant (the primary cause of which is microbial infection) has been associated with later cardiovascular disease.(({{pmid>long:11281409}})) Further, influenza vaccination was associated with a 50% reduction in the incidence of sudden cardiac death, acute myocardial infarction (heart attack), and ischemic stroke. Both heart attack and stroke have their peak incidence in winter months, which correspond to the time of year when cases of influenza also peak.(({{pmid>long:12573201}}))
-  * **Common infections and cardiovascular diseases share the same inflammatory markers** – As Costa //et al.// have pointed out,(({{pubmed>long:17686992}})) inflammatory markers that are risk factors for heart attack and stroke are also elevated during lower respiratory tract infections as well as during infections such as rheumatic fever, syphilis, diarrhea, malaria, and tuberculosis.(({{pubmed>long:15375259}})) (({{pubmed>long:5755517}})) (({{pubmed>long:14614368}})) (({{pubmed>long:12413502}}))
+  * **Common infections and cardiovascular diseases share the same inflammatory markers** – As Costa //et al.// have pointed out,(({{pmid>long:17686992}})) inflammatory markers that are risk factors for heart attack and stroke are also elevated during lower respiratory tract infections as well as during infections such as rheumatic fever, syphilis, diarrhea, malaria, and tuberculosis.(({{pmid>long:15375259}})) (({{pmid>long:5755517}})) (({{pmid>long:14614368}})) (({{pmid>long:12413502}}))
-  * **[[home:pathogenesis:evolution|evolutionary analysis]] suggests cardiovascular disease is not caused by lifestyle or genetic factors** – Atherosclerosis has been identified in Egyptian mummies.(({{pubmed>long:10495769}})) This suggests that whatever factors cause atherosclerosis has existed for at least several millenia. If it were true that a factor such as a harmful allele for a gene or the consumption of fatty foods caused atherosclerosis, the human species would have had several millenia to evolve a defense for this vulnerability to disease or, at the very least, to weed this trait out of the population.(({{pubmed>long:10839723}}))
+  * **prenatal exposure to influenza and cardiovascular disease** – Prenatal exposure to the 1918 influenza pandemic (Influenza A, H1N1 subtype) is associated with >/=20% excess cardiovascular disease at 60 to 82 years of age, relative to cohorts born without exposure to the influenza epidemic, either prenatally or postnatally. These findings suggest novel roles for maternal infections in the fetal programming of cardiovascular risk factors that are independent of maternal malnutrition.(({{pmid>long:20198106}}))
-  * **prenatal exposure to influenza and cardiovascular disease** – Prenatal exposure to the 1918 influenza pandemic (Influenza A, H1N1 subtype) is associated with >/=20% excess cardiovascular disease at 60 to 82 years of age, relative to cohorts born without exposure to the influenza epidemic, either prenatally or postnatally. These findings suggest novel roles for maternal infections in the fetal programming of cardiovascular risk factors that are independent of maternal malnutrition.(({{pubmed>long:20198106}}))
+  * **[[home:pathogenesis:evolution|evolutionary analysis]] suggests cardiovascular disease is not caused by lifestyle or genetic factors** – Atherosclerosis has been identified in Egyptian mummies.(({{pmid>long:10495769}})) This suggests that whatever factors cause atherosclerosis has existed for at least several millenia. If it were true that a factor such as a harmful allele for a gene or the consumption of fatty foods caused atherosclerosis, the human species would have had several millenia to evolve a defense for this vulnerability to disease or, at the very least, to weed this trait out of the population.(({{pmid>long:10839723}}))
+[[https://www.amjmedsci.org/article/S0002-9629(15)30809-0/fulltext|Infections May be Causal in the Pathogenesis of Atherosclerosis]]
 ==== A causal relationship between periodontal disease and cardiovascular disease? ====
-One of the best known links between two different inflammatory diseases – and a prototypical illustration of [[home:pathogenesis:successive_infection|successive infection]] – is the relationship between cardiovascular diseases such as heart attack and stroke, and periodontal disease. A //BMJ// paper showed a correlation between dental disease and systemic disease (stroke, heart disease, diabetes). After correcting for age, exercise, diet, smoking, weight, blood cholesterol level, alcohol use and health care, people who had periodontal disease had a significantly higher incidence of heart disease, stroke and premature death. More recently, these results were confirmed in studies in the United States, Canada, Great Britain, Sweden, and Germany. The magnitude of the association is striking: one study found that people with periodontal disease had a two times higher risk of dying from cardiovascular disease.(({{pubmed>long:10197286}}))
+One of the best known links between two different inflammatory diseases – and a prototypical illustration of [[home:pathogenesis:successive_infection|successive infection]] – is the relationship between cardiovascular diseases such as heart attack and stroke, and periodontal disease. A //BMJ// paper showed a correlation between dental disease and systemic disease (stroke, heart disease, diabetes). After correcting for age, exercise, diet, smoking, weight, blood cholesterol level, alcohol use and health care, people who had periodontal disease had a significantly higher incidence of heart disease, stroke and premature death. More recently, these results were confirmed in studies in the United States, Canada, Great Britain, Sweden, and Germany. The magnitude of the association is striking: one study found that people with periodontal disease had a two times higher risk of dying from cardiovascular disease.(({{pmid>long:10197286}}))
-A 2010 study using pyrosequencing compared the bacterial diversity of atherosclerotic plaque, oral, and gut samples of 15 patients with atherosclerosis, and oral and gut samples of healthy controls.(({{pubmed>long:20937873}})) The team concluded that there was a high degree of correlation between the presence of certain bacteria in the oral cavity (and to a somewhat lesser extent the gut) with bacteria in the gastrointestinal tract. Interestingly, several bacterial taxa in the oral cavity and the gut correlated with plasma cholesterol levels. A 2011 study that [[http://www.reuters.com/article/2009/04/01/us-heart-mouth-idUSTRE5300RU20090401|compared heart attack victims]] to healthy volunteers found the heart patients had higher numbers of bacteria in their mouths.(({{pubmed>long:21375559}})) Their tests on 386 men and women who had suffered heart attacks and 840 people free of heart trouble showed two types – //Tannerella forsynthesis// and //Prevotella intermedia// – were more common among the heart attack patients. Interestingly, the total number of species that could be identified in the saliva was the best indicator that somebody was likely to have had a heart attack.
+A 2010 study using pyrosequencing compared the bacterial diversity of atherosclerotic plaque, oral, and gut samples of 15 patients with atherosclerosis, and oral and gut samples of healthy controls.(({{pmid>long:20937873}})) The team concluded that there was a high degree of correlation between the presence of certain bacteria in the oral cavity (and to a somewhat lesser extent the gut) with bacteria in the gastrointestinal tract. Interestingly, several bacterial taxa in the oral cavity and the gut correlated with plasma cholesterol levels. A 2011 study that [[https://www.reuters.com/article/2009/04/01/us-heart-mouth-idUSTRE5300RU20090401|compared heart attack victims]] to healthy volunteers found the heart patients had higher numbers of bacteria in their mouths.(({{pmid>long:21375559}})) Their tests on 386 men and women who had suffered heart attacks and 840 people free of heart trouble showed two types – //Tannerella forsynthesis// and //Prevotella intermedia// – were more common among the heart attack patients. Interestingly, the total number of species that could be identified in the saliva was the best indicator that somebody was likely to have had a heart attack.
-Successive infection dictates that as a person accumulates pathogens in one area of the body, those pathogens likely have mechanisms that allow them to slow the immune response. So, if people harbor greater number of pathogens in their mouths, the immune response may slow in the heart and arteries, making it easier for microbes to spread their as well. The same can be said for the opposite scenario. Also, it may be possible that microbes in the mouth spread toward the heart and arteries, although this has yet to be completely confirmed. However, some of the same bacteria identified in the salivary microbiome, such as //Actinobacillus actinomycetemcomitans// and //Porphyromonas gingivalis// - both of which cause tooth decay(({{pubmed>long:10699021}})) - have also been identified in atherosclerotic plaque.(({{pubmed>long:15662025}})) (({{pubmed>long:17981690}}))
+Successive infection dictates that as a person accumulates pathogens in one area of the body, those pathogens likely have mechanisms that allow them to slow the immune response. So, if people harbor greater number of pathogens in their mouths, the immune response may slow in the heart and arteries, making it easier for microbes to spread their as well. The same can be said for the opposite scenario. Also, it may be possible that microbes in the mouth spread toward the heart and arteries, although this has yet to be completely confirmed. However, some of the same bacteria identified in the salivary microbiome, such as //Actinobacillus actinomycetemcomitans// and //Porphyromonas gingivalis// - both of which cause tooth decay(({{pmid>long:10699021}})) - have also been identified in atherosclerotic plaque.(({{pmid>long:15662025}})) (({{pmid>long:17981690}}))
-Work by Kozarov //et al.// strongly suggests that "the key step [towards systemic infection] is the persistence of intracellular bacteria in phagocytes." Bacterial strains, they conclude, "once in the circulation, are internalized by phagocytic cells, at which stage selected species avoid immediate killing and spread and colonize distant sites."(({{pubmed>long:20972353}})) The group also showed that older patients, when compared to younger controls, have atheromas (plaques) which contain greater proportions of pathogens traditionally associated with periodontitis.(({{pubmed>long:16513386}}))
+Work by Kozarov //et al.// strongly suggests that "the key step [towards systemic infection] is the persistence of intracellular bacteria in phagocytes." Bacterial strains, they conclude, "once in the circulation, are internalized by phagocytic cells, at which stage selected species avoid immediate killing and spread and colonize distant sites."(({{pmid>long:20972353}})) The group also showed that older patients, when compared to younger controls, have atheromas (plaques) which contain greater proportions of pathogens traditionally associated with periodontitis.(({{pmid>long:16513386}}))
 <blockquote>Our data demonstrate that the elderly individuals (mean age 67 years) have higher incidence of periodontopathogens in their plaques than the younger individuals.... Species from the //Bacteroides// family were found in about 17% of the young but in about 80% of the elderly patients, as expected given the association of this family with adult and refractory periodontitis.
-//**Kozarov** et al.//(({{pubmed>long:16513386}}))
+//**Kozarov** et al.//(({{pmid>long:16513386}}))
 </blockquote>
@@ Line 121: / Line 123: @@
-<blockquote>The cumulative evidence suggests that infections may induce or promote atherosclerosis.(({{pubmed>long:12196340}})) (({{pubmed>long:16490835}})) (({{pubmed>long:17295657}})) (({{pubmed>long:17967778}})) (({{pubmed>long:18551190}})) (({{pubmed>long:16781371}})) (({{pubmed>long:16277580}})) From our point of view, scientists might readily explain the correlation between infections and atherosclerosis on the basis of the double-edged sword property of the anti-infective immune effects of lipoproteins, and might be able to design more rational and systemic experiments to test this correlation.
+<blockquote>The cumulative evidence suggests that infections may induce or promote atherosclerosis.(({{pmid>long:12196340}})) (({{pmid>long:16490835}})) (({{pmid>long:17295657}})) (({{pmid>long:17967778}})) (({{pmid>long:18551190}})) (({{pmid>long:16781371}})) (({{pmid>long:16277580}})) From our point of view, scientists might readily explain the correlation between infections and atherosclerosis on the basis of the double-edged sword property of the anti-infective immune effects of lipoproteins, and might be able to design more rational and systemic experiments to test this correlation.
-//**R. Han**// (({{pubmed>long:20377753}}))</blockquote>
+//**R. Han**// (({{pmid>long:20377753}}))</blockquote>
 <blockquote>much confusion has arisen from unclear nomenclature with regard to polyunsaturated fatty acids and the lack of reporting of food sources in prospective cohorts. Data from prospective cohort studies and randomized controlled trials generally support the replacement of saturated fats with mixed polyunsaturated fatty acids to reduce the risk of death from coronary artery disease. However, it is unclear whether oils rich in omega-6 linoleic acid but low in omega-3 α-linolenic acid also reduce this risk.
-//Richard P. Bazinet, PhD and Michael W.A. Chu, MD MEd//  (({{pubmed>long:24218530}}))
+//Richard P. Bazinet, PhD and Michael W.A. Chu, MD MEd//  (({{pmid>long:24218530}}))
 Key points
@@ Line 139: / Line 141: @@
 <relatedarticle> [[home:food:folic|Folic acid and folate]]</article>
-A high level of blood serum homocysteine (known as "homocysteinemia") is a strong risk factor for cardiovascular disease,(({{pubmed>long:12015248}})) This has led some to conclude homocysteine "has many deleterious cardiovascular effects."(({{pubmed>long:11872979}})) However the amino acid does not appear to cause disease.
+A high level of blood serum homocysteine (known as "homocysteinemia") is a strong risk factor for cardiovascular disease,(({{pmid>long:12015248}})) This has led some to conclude homocysteine "has many deleterious cardiovascular effects."(({{pmid>long:11872979}})) However the amino acid does not appear to cause disease.
 Because supplementation of the B vitamins lower levels of homocysteine, one common intervention for altering this risk factor is to supplement patients at risk for cardiovascular disease with folic acid (B<sub>9</sub>), pyridoxine (B<sub>6</sub>), and cyanocobalamin (B<sub>12</sub>). In fact,  interventions designed to lower levels of homocysteine with high-dose supplementation of the B vitamins been equivocal, in some cases, seeming to exacerbate disease.
-  * A 2010 study by House //et al.// has shown substantial adverse outcomes associated with high-dose B vitamins in patients with advanced diabetic nephropathy.(({{pubmed>long:20424250}})) These side effects included myocardial infarction, stroke, revascularization, and all-cause mortality. According to [[http://www.medscape.com/viewarticle/731177|one commentator]], unless other explanations come to light in further analyses of the study, these findings make repetition of a similar trial in this high-risk patient group unethical.
+  * A 2010 study by House //et al.// has shown substantial adverse outcomes associated with high-dose B vitamins in patients with advanced diabetic nephropathy.(({{pmid>long:20424250}})) These side effects included myocardial infarction, stroke, revascularization, and all-cause mortality. According to [[https://www.medscape.com/viewarticle/731177|one commentator]], unless other explanations come to light in further analyses of the study, these findings make repetition of a similar trial in this high-risk patient group unethical.
-  * The Heart Outcomes Prevention Evaluation (HOPE-2) study, involved 5,522 patients with vascular disease or diabetes mellitus and found no effect of high-dose B6, B9 and B12 cosupplementation on death from cardiovascular disease, whereas the risk of stroke was decreased and the risk of unstable angina requiring hospitalization was increased.(({{pubmed>long:16531613}}))
+  * The Heart Outcomes Prevention Evaluation (HOPE-2) study, involved 5,522 patients with vascular disease or diabetes mellitus and found no effect of high-dose B6, B9 and B12 cosupplementation on death from cardiovascular disease, whereas the risk of stroke was decreased and the risk of unstable angina requiring hospitalization was increased.(({{pmid>long:16531613}}))
-Marino //et al.// showed that eradication of //Helicobacter pylori// associated with gastritis reduced abnormally high levels of homocysteine.(({{pubmed>long:17005765}}))
+Marino //et al.// showed that eradication of //Helicobacter pylori// associated with gastritis reduced abnormally high levels of homocysteine.(({{pmid>long:17005765}}))
-The role of hyperhomocysteinemia in coronary artery disease (CAD) patients remains unclear.  (({{pubmed>long:26762617}}))
+The role of hyperhomocysteinemia in coronary artery disease (CAD) patients remains unclear.  (({{pmid>long:26762617}}))
@@ Line 159: / Line 161: @@
 <mainarticle> [[home:protocol:olmesartan|Science behind olmesartan]]</article>
-As is the case with the antivirals,(({{pubmed>long:18276989}})) antibiotics such as [[home:othertreatments:antibacterials:highdose#high-dose_clarithomycin_is_ineffective|clarithomycin]] have consistently failed to reduce the rate of cardiovascular disease.(({{pubmed>long:16096289}})) However, these failures are not conclusive evidence that cardiovascular diseases are not caused by infections nor do they show that these diseases cannot be treated as a chronic infection. These trials did not induce immunopathology and they did not use high dose olmesartan, which has several benefits beyond its role in activating the innate immune system.
+As is the case with the antivirals,(({{pmid>long:18276989}})) antibiotics such as [[home:othertreatments:antibacterials:highdose#high-dose_clarithomycin_is_ineffective|clarithomycin]] have consistently failed to reduce the rate of cardiovascular disease.(({{pmid>long:16096289}})) However, these failures are not conclusive evidence that cardiovascular diseases are not caused by infections nor do they show that these diseases cannot be treated as a chronic infection. These trials did not induce immunopathology and they did not use high dose olmesartan, which has several benefits beyond its role in activating the innate immune system.
 {{section>:home:protocol:olmesartan#cardiovascular_disease&noheader}}
- <blockquote>//Jigsaw wrote// Since Elizabeth Blackburn won a Nobel prize for telomerase in 2009, I have wondered what effect olmesartan might have on it. //Are our telomeres getting shorter and shorter, so we just go POP?//  while getting healthier and healthier in other respects.     This report (({{pubmed>long:27079876}})) is re-assuring. Olmesartan raises ACE2 which converts angII to Ang 1-7</blockquote>
+ <blockquote>//Jigsaw wrote// Since Elizabeth Blackburn won a Nobel prize for telomerase in 2009, I have wondered what effect olmesartan might have on it. //Are our telomeres getting shorter and shorter, so we just go POP?//  while getting healthier and healthier in other respects.     This report (({{pmid>long:27079876}})) is re-assuring. Olmesartan raises ACE2 which converts angII to Ang 1-7</blockquote>
 ===== Other treatments =====
-  * **statins** – As the 2008 ENHANCE trial illustrates, while high cholesterol is //correlated// with increased incidence of diseases, lowering cholesterol does not appear to improve human health.(({{pubmed>long:18376000}})) Indeed, there is some evidence this type of intervention does the opposite.(({{pubmed>long:14631060}})) The statins have a range of documented negative effects, some of which may be immunopathological. Because statins may interfere with the Marshall Protocol, these drugs are contraindicated.
+  * **statins** – As the 2008 ENHANCE trial illustrates, while high cholesterol is //correlated// with increased incidence of diseases, lowering cholesterol does not appear to improve human health.(({{pmid>long:18376000}})) Indeed, there is some evidence this type of intervention does the opposite.(({{pmid>long:14631060}})) The statins have a range of documented negative effects, some of which may be immunopathological. Because statins may interfere with the Marshall Protocol, these drugs are contraindicated.
   * **[[home:othertreatments:diuretics|diuretics]]** – A diuretic is any drug that elevates the rate of urination and thus provides a means of forced diuresis. There are several categories of diuretics. All diuretics increase the excretion of water from bodies, although each class of diuretic does so in a distinct way. Some diuretics are contraindicated for MP patients.
-  * **[[home:alternate:environment|diet and exercise]]** – It has been widely hypothesized that a poor diet and a lack of exercise are driving the recent surge in obesity and cardiovascular disease – diseases which are closely linked. But, even the most ambitious intervention programs, which have gone to great lengths to increase rates of exercise and improve eating habits of a population, have failed. One 1999 $200,000 NIH-funded intervention, known as the Pathways program, was performed on two groups of children. Pathways involved a substantial increase in physical education programs, classes about nutrition, significant reduction in fat and calorie content of all school meals, and several other health related measures - and all as part of a randomized controlled trial, the gold standard in studies. The primary goal of the study was to reduce the rate of body fat (a risk factor for cardiovascular disease) in the intervention group, but after the three-year intervention the percent of body fat in both groups was essentially identical. The researchers were unable to explain the failure of their intervention.(({{pubmed>long:14594792}})) Other such trials for obesity have been equally unsuccessful.(({{pubmed>long:17028105}}))
+  * **[[home:alternate:environment|diet and exercise]]** – It has been widely hypothesized that a poor diet and a lack of exercise are driving the recent surge in obesity and cardiovascular disease – diseases which are closely linked. But, even the most ambitious intervention programs, which have gone to great lengths to increase rates of exercise and improve eating habits of a population, have failed. One 1999 $200,000 NIH-funded intervention, known as the Pathways program, was performed on two groups of children. Pathways involved a substantial increase in physical education programs, classes about nutrition, significant reduction in fat and calorie content of all school meals, and several other health related measures - and all as part of a randomized controlled trial, the gold standard in studies. The primary goal of the study was to reduce the rate of body fat (a risk factor for cardiovascular disease) in the intervention group, but after the three-year intervention the percent of body fat in both groups was essentially identical. The researchers were unable to explain the failure of their intervention.(({{pmid>long:14594792}})) Other such trials for obesity have been equally unsuccessful.(({{pmid>long:17028105}}))
   * **high-dose antibiotics** – //See above section, [[home:diseases#effect_of_olmesartan_on_cardiovascular_diseases|Effect of olmesartan on cardiovascular diseases]]//
-  * **beta-blockers** – In the aftermath of a heart attack, a beta-blocker will reduce consumption of limited oxygen supplies by slowing a straining heart. This intervention appears to be a sensible one in light of the assumption that heart failure is caused by the heart over-exerting itself. Yet the best study to date has shown that this routinely prescribed class of drugs increases heart failure and overall death.(({{pubmed>long:16271643}})) ((Newman, D. H. (2008). //Hippocrates' shadow: secrets from the house of medicine.// New York, NY, Scribner.))
+  * **beta-blockers** – In the aftermath of a heart attack, a beta-blocker will reduce consumption of limited oxygen supplies by slowing a straining heart. This intervention appears to be a sensible one in light of the assumption that heart failure is caused by the heart over-exerting itself. Yet the best study to date has shown that this routinely prescribed class of drugs increases heart failure and overall death.(({{pmid>long:16271643}})) ((Newman, D. H. (2008). //Hippocrates' shadow: secrets from the house of medicine.// New York, NY, Scribner.))
-  * **anti-arrhythmics** – Ventricular arrhythmia is correlated with an almost 400% increase in the risk of death from cardiac complications, but a large randomized controlled trial showed that the drugs encainide and flecainide tripled the risk of death from other causes when compared with placebo.(({{pubmed>long:15863552}}))
+  * **anti-arrhythmics** – Ventricular arrhythmia is correlated with an almost 400% increase in the risk of death from cardiac complications, but a large randomized controlled trial showed that the drugs encainide and flecainide tripled the risk of death from other causes when compared with placebo.(({{pmid>long:15863552}}))
-  * **vitamin D** – According to results shared at a [[http://www.telegraph.co.uk/health/healthnews/8891327/High-dose-vitamin-D-pills-can-double-heart-condition-risk.html|2012 conference]], patients with 25-D levels above 100 nanograms per 100ml, were 2.5 times more likely to have atrial fibrillation as those with more moderate levels (41-80ng/100ml). A 2012 randomized controlled trial conducted over four months showed that daily doses of 2500 IU of vitamin D do not protect against cardiovascular disease risk.(({{pubmed>long:22586483}}))
+  * **vitamin D** – According to results shared at a [[https://www.telegraph.co.uk/health/healthnews/8891327/High-dose-vitamin-D-pills-can-double-heart-condition-risk.html|2012 conference]], patients with 25-D levels above 100 nanograms per 100ml, were 2.5 times more likely to have atrial fibrillation as those with more moderate levels (41-80ng/100ml). A 2012 randomized controlled trial conducted over four months showed that daily doses of 2500 IU of vitamin D do not protect against cardiovascular disease risk.(({{pmid>long:22586483}}))
-The level of vitamin D in our blood should neither be too high nor to low. Scientists have now shown that there is a connection between high levels of vitamin D and cardiovascular deaths.  [[http://www.sciencedaily.com/releases/2015/03/150310105222.htm|vitamin D is suspected of increasing mortality rate]]
+The level of vitamin D in our blood should neither be too high nor to low. Scientists have now shown that there is a connection between high levels of vitamin D and cardiovascular deaths.  [[https://www.sciencedaily.com/releases/2015/03/150310105222.htm|vitamin D is suspected of increasing mortality rate]]
 {{section>home:diseases:cancer#Are There Concerns About Over-supplementing with Vitamin D&noheader}}
@@ Line 200: / Line 202: @@
 neurosarcoidosis, systemic sarcoidosis; spasticity, myasthenia, CNS dysfunction, joint pain, pulmonary, splenic and cardiac involvement
-Read the [[http://bacteriality.com/2008/03/02/interview17/|interview]]
+Read the [[https://bacteriality.com/2008/03/02/interview17/|interview]]
 <html></div></div></html>
@@ Line 213: / Line 215: @@
 sarcoidosis of the heart, coronary artery disease, atrial fibrillation
-Read the [[http://bacteriality.com/2008/01/18/interview15/|interview]]
+Read the [[https://bacteriality.com/2008/01/18/interview15/|interview]]
 <html></div></div>
@@ Line 252: / Line 254: @@
 ===== More information =====
-  * [[http://www.medicalnewstoday.com/articles/91894.php|Olmetec Is First Angiotensin Receptor Blocker (ARB) To Suggest Atherosclerosis Regression (in Hypertensives With Cardiovascular Risk)]]
+Hyperuricaemia was associated with an unfavourable cardiovascular risk profile in HF patients. Treatment with low doses of allopurinol did not improve the prognosis of HF patients.  (({{pmid>long:    31119751}}))
-  * [[http://www.medscape.com/viewarticle/714592|Links Between Infectious Diseases and Cardiovascular Disease: A Growing Body of Evidence]] (registration required)
-  * [[http://news.bbc.co.uk/2/hi/health/8363200.stm|Ancients had heart disease too]]
+Increased risks per 10 000 person-years found in estrogen plus progestin therapy for 16608 healthy postmenopausal women (studied over 5 years) were 7 more CHD events, 8 more strokes, 8 more PEs, and 8 more invasive breast cancers. (({{pmid>long:12117397}}))
+  * [[https://www.medicalnewstoday.com/articles/91894.php|Olmetec Is First Angiotensin Receptor Blocker (ARB) To Suggest Atherosclerosis Regression (in Hypertensives With Cardiovascular Risk)]]
+  * [[https://www.medscape.com/viewarticle/714592|Links Between Infectious Diseases and Cardiovascular Disease: A Growing Body of Evidence]] (registration required)
+  * [[https://news.bbc.co.uk/2/hi/health/8363200.stm|Ancients had heart disease too]]
   * [[https://www.youtube.com/watch?v=p-aNRQNRtaI|Extra load which radiation from a Smart Meter makes on even a healthy heart]]
@@ Line 270: / Line 276: @@
  {{tag>diseases}}
+<nodisp>
 ===== Notes and comments =====
 --- //Sallie Q 08.25.2017// removed broken links
-  * [[http://www.cosmosmagazine.com/features/print/3477/can-you-catch-a-heart-attack|Can you catch a heart attack?]] – Trevor Marshall, PhD interviewed in COSMOS magazine article
+  * [[https://www.cosmosmagazine.com/features/print/3477/can-you-catch-a-heart-attack|Can you catch a heart attack?]] – Trevor Marshall, PhD interviewed in COSMOS magazine article
-  * [[http://www.medconnect.com.au/tabid/84/s2/Endocrinology/p6/Parathyroid/ct1/c335474/Skepticism-Grows-Regarding-Widespread-Vitamin-D-Supplementation/Default.aspx|Skepticism Grows Regarding Widespread Vitamin D Supplementation]]
+  * [[https://www.medconnect.com.au/tabid/84/s2/Endocrinology/p6/Parathyroid/ct1/c335474/Skepticism-Grows-Regarding-Widespread-Vitamin-D-Supplementation/Default.aspx|Skepticism Grows Regarding Widespread Vitamin D Supplementation]]
 --- //Sallie Q 06.04.2017// adding uTube on smart meter effect
@@ Line 286: / Line 293: @@
 <blockquote>Benicar and cardiovascular events:
-http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789932/?tool=pubmed
+https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789932/?tool=pubmed
-http://clinicaltrials.gov/ct2/show/NCT00185159?term=ROADMAP&rank=2
+https://clinicaltrials.gov/ct2/show/NCT00185159?term=ROADMAP&rank=2
-http://clinicaltrials.gov/ct2/show/NCT00141453?term=ORIENT+olmesartan&rank=1
+https://clinicaltrials.gov/ct2/show/NCT00141453?term=ORIENT+olmesartan&rank=1
-http://www.biosciencetechnology.com/News/Feeds/2010/06/sections-regulatory-news-fda-drug-safety-communication-ongoing-safety-revi/
+https://www.biosciencetechnology.com/News/Feeds/2010/06/sections-regulatory-news-fda-drug-safety-communication-ongoing-safety-revi/
 FDA Drug Safety Communication: Ongoing safety review of Benicar and cardiovascular events
@@ Line 310: / Line 317: @@
 <blockquote>
-See this too: http://www.theheart.org/article/1024539.do
+See this too: https://www.theheart.org/article/1024539.do
 Lancet. 2009 Nov 28;374(9704):1840-8. Epub 2009 Nov 16.
-Effects of high-dose versus low-dose losartan on clinical outcomes in patients with heart failure (HEAAL study): a randomised, double-blind trial.(({{pubmed>long:19922995}}))
+Effects of high-dose versus low-dose losartan on clinical outcomes in patients with heart failure (HEAAL study): a randomised, double-blind trial.(({{pmid>long:19922995}}))
 Konstam MA, Neaton JD, Dickstein K, Drexler H, Komajda M, Martinez FA, Riegger GA, Malbecq W, Smith RD, Guptha S, Poole-Wilson PA; HEAAL Investigators.
@@ Line 352: / Line 359: @@
 <blockquote>Expression of the vitamin d receptor is increased in the hypertrophic heart.
-http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2690395/?tool=pubmed
+https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2690395/?tool=pubmed
 The liganded vitamin D receptor is thought to play an important role in controlling cardiac function. Specifically this system has been implicated as playing an anti-hypertrophic role in the heart. Despite this, studies of the VDR in the heart have been limited in number and scope. In the present study we use a combination of real time PCR, Western blot analysis, immunofluorescence and transient transfection analysis to document the presence of functional VDR in both the myocytes and fibroblasts of the heart, as well as in the intact ventricular myocardium. We also demonstrate the presence of 1-α-hydroxylase and 24-hydroxylase in the heart, two enzymes involved in the synthesis and metabolism of 1,25 dihydroxyvitamin D (VD3). VDR is shown to interact directly with the human B-type natriuretic peptide (hBNP) gene promoter, a surrogate marker of the transcriptional response to hypertrophy. Of note, induction of myocyte hypertrophy either in vitro or in vivo leads to an increase in VDR mRNA and protein levels. Collectively, these findings suggest that the key components required for a functional VD3-dependent signaling system are present in the heart and that this putatively anti-hypertrophic system is amplified in the setting of cardiac hypertrophy.
@@ Line 359: / Line 366: @@
 <blockquote>Olmesartan reduces arterial stiffness and serum adipocyte fatty acid-binding protein in hypertensive patients.
-http://www.ncbi.nlm.nih.gov/pubmed/21063874
+https://www.ncbi.nlm.nih.gov/pubmed/21063874
 Adipocyte fatty acid binding protein (A-FABP) has been reported to be involved in insulin resistance, lipid metabolism, and atherosclerosis; however, little is known about the effect of medication on the change in circulating A-FABP in human subjects. We evaluated the effects of angiotensin II type 1 receptor blocker (ARB) on arterial stiffness and its association with serum A-FABP in patients with hypertension. Thirty patients newly diagnosed with essential hypertension were treated with olmesartan (20 mg/day), an ARB, for 6 months. Serum levels of A-FABP and high-sensitivity C-reactive protein (hsCRP) were examined and the cardio-ankle vascular index (CAVI), which is a marker of arterial stiffness, was also determined. Serum A-FABP at baseline was significantly correlated with the body mass index (r = 0.45, P = 0.01), homeostasis model assessment as a marker of insulin resistance (r = 0.53, P < 0.01), and systolic blood pressure (r = 0.37, P = 0.047), and tended to be correlated with low-density lipoprotein cholesterol, triglyceride, and CAVI. Olmesartan treatment resulted in a significant decrease in CAVI, serum A-FABP levels, and hsCRP, besides a significant reduction of blood pressure. Multiple regression analysis revealed that the change in CAVI was independently correlated with the change in serum A-FABP. Olmesartan ameliorated arterial stiffness in patients with hypertension, which may be involved in the reduction of serum A-FABP.
@@ Line 365: / Line 372: @@
 </blockquote>
 <blockquote>Body's Bacteria Affect Atherosclerosis
-http://www.sciencedaily.com/releases/2010/10/101018074538.htm
+https://www.sciencedaily.com/releases/2010/10/101018074538.htm
 "The causes of atherosclerosis have recently become clearer, but we know less about why the plaque in the arteries ruptures and contributes to clot formation," says Fredrik Bäckhed, researcher at the Sahlgrenska Academy's Department of Molecular and Clinical Medicine.
@@ Line 540: / Line 547: @@
 <blockquote>Controversies in Vitamin D Supplementation
-http://escholarship.org/uc/item/4m84d4fn
+https://escholarship.org/uc/item/4m84d4fn
 Concurrent with this rise in vitamin D ingestion in Canada, United States, Sweden, Israel, and England were the epidemic onsets of atherosclerosis and osteoporosis, which led Moon et al. to hypothesize that chronic vitamin D excess contributes to the development of these two illnesses (1). Moon and colleagues supported their postulate by citing 37 studies, some dated as early as 1945, which documented cardiovascular and skeletal effects similar to atherosclerosis and osteoporosis in humans and laboratory animals after high vitamin D intake. Subsequently, Haddad et al. showed in seven healthy human volunteers that while endogenously synthesized dermal vitamin D is transported on vitamin D binding protein and causes a more sustained increase in serum 25-hydroxy vitamin D, the orally administered vitamin D is absorbed from the intestinal tract via chylomicrons and carried in the circulation by lipoproteins such as VLDL and LDL, which may end up in the artery wall (3, 4). This finding supports Fraser’s earlier speculation that the toxicity of orally acquired vitamin D might be due to its unnatural route through the body and, consequently, it is less finely regulated than endogenously synthesized dermal vitamin D (5).
@@ Line 550: / Line 557: @@
 .     Moon J, Bandy B, Davison AJ. Hypothesis: etiology of atherosclerosis and osteoporosis: are imbalances in the calciferol endocrine system implicated? J Am Coll Nutr. 1992;11:567-83.
-.     Norman AW. Vitamin D and milk, Department of Biochemistry & Biomedical Sciences at the University of California, Riverside website http://vitamind.ucr.edu/milk.html December 12, 2000. Comment: Highly respected institution. Anthony Norman is a professor in the Department of Biochemistry & Biomedical Sciences at the University of California, Riverside.
+.     Norman AW. Vitamin D and milk, Department of Biochemistry & Biomedical Sciences at the University of California, Riverside website https://vitamind.ucr.edu/milk.html December 12, 2000. Comment: Highly respected institution. Anthony Norman is a professor in the Department of Biochemistry & Biomedical Sciences at the University of California, Riverside.
 .     Haddad JG, Matsuoka LY, Hollis BW, Hu YZ, Wortsman J. Human plasma transport of vitamin D after its endogenous synthesis. J Clin Invest. 1993;91:2552–5.
 .     Demer LL. Vitamin D supplementation and atherosclerosis, Personal communication. 2003. Comment: Dr. Demer is a professor in the Departments of Medicine and Physiology at the David Geffen School of Medicine at UCLA, a highly respected institution.
@@ Line 568: / Line 575: @@
 </blockquote>
-===== References =====
+===== References =====</nodisp>

home/diseases/cardiovascular.1549924620.txt.gz · Last modified: 02.11.2019 by sallieq