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home:diseases:cardiovascular [12.26.2018] – [Effect of olmesartan on cardiovascular diseases] + ref. & Jigsaw quote sallieq | home:diseases:cardiovascular [09.14.2022] (current) – external edit 127.0.0.1 | ||
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- | ====== Cardiovascular diseases ====== | + | ====== Cardiovascular diseases ====== |
- | <relatedarticle> [[home: | + | <relatedarticles> [[home: |
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). | 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. < | ||
According to the Marshall Pathogenesis, | According to the Marshall Pathogenesis, | ||
- | 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, | + | 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, |
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. | 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. | ||
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* **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. | * **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. | * **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> | + | * **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> |
* **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: | * **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: | ||
* **hypercholesterolemia (hyperlipidemia)** – Chronic high levels of cholesterol in the blood. //Reviewed in [[home: | * **hypercholesterolemia (hyperlipidemia)** – Chronic high levels of cholesterol in the blood. //Reviewed in [[home: | ||
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- | [{{ : | + | [{{ : |
===== Evidence of infectious cause===== | ===== Evidence of infectious cause===== | ||
< | < | ||
- | //**K. Ayada** et al.//(({{pubmed> | + | //**K. Ayada** et al.//(({{pmid> |
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< | < | ||
- | // | + | // |
</ | </ | ||
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==== Arterial plaque may contain biofilm==== | ==== 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.//' | + | Arterial plaque may contain and/or be caused by biofilm, that is, a community of diverse microbes that work together. Ott //et al.//' |
In a commentary following Ott's paper, Katz and Shannon concluded that his work suggested that atherosclerotic plaques are composed of " | In a commentary following Ott's paper, Katz and Shannon concluded that his work suggested that atherosclerotic plaques are composed of " | ||
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< | < | ||
- | //**Joel T. Katz, MD and Richard P. Shannon, MD**// (({{pubmed> | + | //**Joel T. Katz, MD and Richard P. Shannon, MD**// (({{pmid> |
- | Immune cells are abundant in the walls of the arteries even during the initial stages of plaque formation.(({{pubmed> | + | Immune cells are abundant in the walls of the arteries even during the initial stages of plaque formation.(({{pmid> |
==== Individual pathogens already implicated in cardiovascular disease ==== | ==== 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: | 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: | ||
- | * **// | + | * **// |
< | < | ||
- | //**Frank R. Stassen**// (({{pubmed> | + | //**Frank R. Stassen**// (({{pmid> |
</ | </ | ||
- | * **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, | + | * **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, |
- | * **// | + | * **// |
- | * **// | + | * **// |
==== Other evidence ==== | ==== 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, | + | * **Common infections predispose a person to stroke and heart attack** – In a prospective cohort study, a composite measure of //Chlamydia pneumoniae, Helicobacter pylori//, cytomegalovirus, |
- | * **Common infections and cardiovascular diseases share the same inflammatory markers** – As Costa //et al.// have pointed out,(({{pubmed> | + | * **Common infections and cardiovascular diseases share the same inflammatory markers** – As Costa //et al.// have pointed out,(({{pmid> |
- | * **[[home: | + | * **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> |
- | * **prenatal exposure to influenza and cardiovascular disease** – Prenatal exposure to the 1918 influenza pandemic | + | * **[[home: |
+ | |||
+ | [[https:// | ||
==== A causal relationship between periodontal disease and cardiovascular disease? ==== | ==== 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: | + | One of the best known links between two different inflammatory diseases – and a prototypical illustration of [[home: |
- | A 2010 study using pyrosequencing compared the bacterial diversity of atherosclerotic plaque, oral, and gut samples of 15 patients with atherosclerosis, | + | A 2010 study using pyrosequencing compared the bacterial diversity of atherosclerotic plaque, oral, and gut samples of 15 patients with atherosclerosis, |
- | 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 // | + | 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 // |
- | Work by Kozarov //et al.// strongly suggests that "the key step [towards systemic infection] is the persistence of intracellular bacteria in phagocytes." | + | Work by Kozarov //et al.// strongly suggests that "the key step [towards systemic infection] is the persistence of intracellular bacteria in phagocytes." |
< | < | ||
- | // | + | // |
</ | </ | ||
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- | < | + | < |
- | //**R. Han**// (({{pubmed> | + | //**R. Han**// (({{pmid> |
< | < | ||
- | //Richard P. Bazinet, PhD and Michael W.A. Chu, MD MEd// (({{pubmed> | + | //Richard P. Bazinet, PhD and Michael W.A. Chu, MD MEd// (({{pmid> |
Key points | Key points | ||
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< | < | ||
- | A high level of blood serum homocysteine (known as " | + | A high level of blood serum homocysteine (known as " |
Because supplementation of the B vitamins lower levels of homocysteine, | Because supplementation of the B vitamins lower levels of homocysteine, | ||
- | * 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> | + | * 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> |
- | * 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> | + | * 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> |
- | Marino //et al.// showed that eradication of // | + | Marino //et al.// showed that eradication of // |
- | The role of hyperhomocysteinemia in coronary artery disease (CAD) patients remains unclear. | + | The role of hyperhomocysteinemia in coronary artery disease (CAD) patients remains unclear. |
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< | < | ||
- | As is the case with the antivirals, | + | As is the case with the antivirals, |
{{section>: | {{section>: | ||
- | < | + | < |
===== Other treatments ===== | ===== Other treatments ===== | ||
- | * **statins** – As the 2008 ENHANCE trial illustrates, | + | * **statins** – As the 2008 ENHANCE trial illustrates, |
* **[[home: | * **[[home: | ||
- | * **[[home: | + | * **[[home: |
* **high-dose antibiotics** – //See above section, [[home: | * **high-dose antibiotics** – //See above section, [[home: | ||
- | * **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> | + | * **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> |
- | * **anti-arrhythmics** – Ventricular arrhythmia is correlated with an almost 400% increase in the risk of death from cardiac complications, | + | * **anti-arrhythmics** – Ventricular arrhythmia is correlated with an almost 400% increase in the risk of death from cardiac complications, |
- | * **vitamin D** – According to results shared at a [[http:// | + | * **vitamin D** – According to results shared at a [[https:// |
- | 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. | + | 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. |
{{section> | {{section> | ||
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neurosarcoidosis, | neurosarcoidosis, | ||
- | Read the [[http:// | + | Read the [[https:// |
< | < | ||
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sarcoidosis of the heart, coronary artery disease, atrial fibrillation | sarcoidosis of the heart, coronary artery disease, atrial fibrillation | ||
- | Read the [[http:// | + | Read the [[https:// |
< | < | ||
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===== More information ===== | ===== More information ===== | ||
- | | + | 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. |
- | * [[http:// | + | |
- | * [[http:// | + | 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> |
+ | |||
+ | | ||
+ | * [[https:// | ||
+ | * [[https:// | ||
* [[https:// | * [[https:// | ||
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| | ||
+ | < | ||
===== Notes and comments ===== | ===== Notes and comments ===== | ||
--- //Sallie Q 08.25.2017// | --- //Sallie Q 08.25.2017// | ||
- | * [[http:// | + | * [[https:// |
- | * [[http:// | + | * [[https:// |
--- //Sallie Q 06.04.2017// | --- //Sallie Q 06.04.2017// | ||
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< | < | ||
- | http:// | + | https:// |
- | http:// | + | https:// |
- | http:// | + | https:// |
- | http:// | + | https:// |
FDA Drug Safety Communication: | FDA Drug Safety Communication: | ||
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< | < | ||
- | See this too: http:// | + | See this too: https:// |
Lancet. 2009 Nov 28; | Lancet. 2009 Nov 28; | ||
- | Effects of high-dose versus low-dose losartan on clinical outcomes in patients with heart failure (HEAAL study): a randomised, double-blind trial.(({{pubmed> | + | Effects of high-dose versus low-dose losartan on clinical outcomes in patients with heart failure (HEAAL study): a randomised, double-blind trial.(({{pmid> |
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. | 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. | ||
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< | < | ||
- | http:// | + | https:// |
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, | 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, | ||
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< | < | ||
- | http:// | + | https:// |
Adipocyte fatty acid binding protein (A-FABP) has been reported to be involved in insulin resistance, lipid metabolism, and atherosclerosis; | Adipocyte fatty acid binding protein (A-FABP) has been reported to be involved in insulin resistance, lipid metabolism, and atherosclerosis; | ||
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</ | </ | ||
< | < | ||
- | http:// | + | https:// |
"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," | "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," | ||
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< | < | ||
- | http:// | + | https:// |
Concurrent with this rise in vitamin D ingestion in Canada, United States, Sweden, Israel, and England were the epidemic onsets of atherosclerosis and osteoporosis, | Concurrent with this rise in vitamin D ingestion in Canada, United States, Sweden, Israel, and England were the epidemic onsets of atherosclerosis and osteoporosis, | ||
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1. Moon J, Bandy B, Davison AJ. Hypothesis: etiology of atherosclerosis and osteoporosis: | 1. Moon J, Bandy B, Davison AJ. Hypothesis: etiology of atherosclerosis and osteoporosis: | ||
- | 2. | + | 2. |
3. | 3. | ||
4. Demer LL. Vitamin D supplementation and atherosclerosis, | 4. Demer LL. Vitamin D supplementation and atherosclerosis, | ||
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</ | </ | ||
- | ===== References ===== | + | ===== References =====</ |