The idea that animal fat consumption causes heart disease is perhaps the most controversial component of the standard preventative advice given to reduce heart disease. This association is based upon the research of Ancel Keyes, who compared heart disease rates in the United States, Canada, Australia, England, Italy, and Japan and found that lower rates of heart disease were manifested in countries with less saturated fat consumption. However, there are many examples of tribes that ate diets high in animal fats and protein yet had low rates of heart disease until exposed to a Western diet: the lifestyle practices of the industrialized world clearly seems more apt to contribute to heart disease but exactly how remains uncertain. There is a complex interplay of genetics and other metabolic factors in the development of atherosclerosis (Teicholz 2007).

Total cholesterol alone has a limited value in predicting the tendency to develop heart disease: the…...

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References

Atherosclerosis. (2012). American Heart Association. Retrieved:

 http://www.heart.org/HEARTORG/Conditions/Cholesterol/WhyCholesterolMatters/Atherosclerosis_UCM_305564_Article.jsp 

Atherosclerosis disease. (2012). Ultrasound services. Retrieved:

http://prosono.ieasysite.com/patho_chapter_atherosclerotic_disease.pdf

Though this work focuses specifically on the risk factors of atherosclerosis for A patients and how to better identify them prior to clinical presentation of atherosclerosis the work is also insightful in that it builds a case for the connection between A clinical presentations and atherosclerosis, in general. To move forward from this progressive idea is the fact that research has indicated that there is an even greater connection between A patients and increased Carotid intima-media thickness (cIMT), which has served as a preclinical predictor in non-A patients for cardiovascular events, but has now been shown to be even greater in progressive severity in A patient, but especially in those with A symptomology that has lasted longer than 20 years. This high grade of cIMT is also an indication of increased inflammation, in addition to increased plaque deposits in the carotid arteries.
A cIMT has previously been found to be…...

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Resources

Hannawi, S. Haluska, B. Marwick, T.H. & Thomas R. (2007) Atherosclerotic Disease is Increased in Recent-onset Rheumatoid Arthritis: a Critical role for Inflammation Arthritis Research & Therapy 9:R116doi:10.1186/ar2323 Retrieved September 28, 2008.  http://arthritis-research.com/content/9/6/R116 .

Margolis, S. (February 2007) Atherosclerosis and Rheumatoid Arthritis. Johns Hopkins Medicine NP Retrieved September 28, 2008.  http://health.yahoo.com/experts/heartdisease/3614/atherosclerosis-and-rheumatoid-arthritis/ 

Montecucco, F. & Mach, F. (October 16, 2008) Common Inflammatory Mediators Orchestrate Pathophysiological Processes in Rheumatoid Arthritis and Atherosclerosis. Rheumatology, doi:10.1093/rheumatology/ken395 Retrieved October 28, 2008.  http://rheumatology.oxfordjournals.org/cgi/content/abstract/ken395 

Pasceri, V., Yeh, E.T.H. (1999) a Tale of Two Diseases: Atherosclerosis and Rheumatoid Arthritis Circulation: Journal of the American Heart Association, 100, 2124-2126. Retrieved October 2, 2008.  http://circ.ahajournals.org/cgi/content/full/100/21/2124

Pathogenesis of Atherosclerosis
Artery diseases are of immense concern to medical researchers due to the cause and effect relationship shared with heart disease and cardiovascular mortality. Atherosclerosis is one of the diseases earning such focus from researchers because of its multifactorial nature, and its period of development which typically occurs years before clinical symptoms are apparent. Atherosclerosis is a disease of the arterial wall that promotes several common causes of cardiovascular mortality, including myocardial infarction and cerebrovascular disease (Channon 2002). The term "atherosclerosis" was traditionally used to describe an abnormality in lipid metabolism, an end-stage degenerative disease, and vessel stiffening. Further studies have caused a rapid increase in knowledge of the pathogenesis of atherosclerosis, and suggest the inciting event of atherosclerosis is more likely an inflammatory event which occurs years before evidence of the disease clinically manifests (Crowther 2005).

Cellular and molecular mechanisms that underlie atherosclerosis demonstrate the roles of the endothelium,…...

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References

Channon, K. (2002), 'The endothelium and the pathogenesis of atherosclerosis', Medicine.

Medicine Publishing Company Ltd., Oxford.

Crowther, M. (2005), 'Pathogenesis of atherosclerosis', Hematology, pp. 436-441.

Cunningham, K. & Gotlieb, A. (2005), 'The role of shear stress in the pathogenesis of atherosclerosis', Laboratory Investigation, vol. 85, pp. 9-23.

AtherosclerosisAtherosclerosis is one of the major causes of premature disability and death in developed nations. It is estimated that this condition will become the leading cause of total disease burden in the near future because its development is fueled by multiple generalized or systemic risk factors. ao & Kiranmayi1 note that the condition is a dynamic and progressive disease that is brought about by an injury to endothelium and its associated inflammatory response. Since atherosclerosis is likely to become the leading cause of disease burden in developed countries, an understanding of the condition is essential to enhance prevention. Insights into the biochemical basis and clinical implications of atherosclerosis are essential to promote a better understanding and management of the condition.Biochemical Basis and Clinical Implications of AtherosclerosisAtherosclerosis is a disease brought by various causes and is regarded as the primary underlying cause of cardiovascular diseases and cerebrovascular accidents. The biochemical mechanisms…...

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References1. Rao PS, Kiranmayi, VS. Biochemical mechanisms underlying atherogenesis. The J. of Clin and Sci. Res. 2012;01(01):24-34.2. Alfarisi HAH, Mohamed ZBH, Ibrahim MB. Basic pathogenic mechanisms of atherosclerosis. Egyptian J. of Basic and App. Sci. 2020;7(1):116-125.3. Kwak BR, Back M, Bochaton-Piallat, M, et al. Biomechanical factors in atherosclerosis: Mechanisms and clinical implications. European Heart J. 2014;35(43):3013-3020.

3. Growth factors can induce apoptosis by binding to their respective receptors (TKs). When activated, TKs in turn activate the as, af, MEK, MAPK, MKK, EK, Fos, JNKs, and Jun pathway, which can lead to the induction of AF via gene upregulation. AF in turn suppresses mdm2, a suppressor of p53 activity. The resulting increase in p53 activity can induce Bax, Mt, and thus apoptosis.

4. Adenomatous familial polyposis is caused by a truncated APC protein, which results from inherited mutations in the APC gene (Segditsas and Tomlinson, 2006). However, the activity of the wild-type or normal APC allele is usually sufficient to maintain tumor suppressor activity. For this reason, and because the wild-type allele is often found to have acquired somatic mutations, it is assumed that both alleles must be mutated before tumors can form. The vast majority of mutations found in colorectal tumors have retained 0 to 3 20-amino…...

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References

Libby, Peter, Ridker, Paul M., and Hansson, Goran K. (2011). Progress and challenges in translating the biology of atherosclerosis. Nature, 473, 317-325.

Segditsas, S. And Tomlinson, I. (2006). Colorectal cancer and genetic alterations in the Wnt pathway. Oncogene, 25, 7531-7537.

Minde, David P., Anvarian, Zeinab, Rudiger, Stefan G.D., and Maurice, Madelon M. (2011). Messing up disorder: How do missense mutations in the tumor suppressor protein APC lead to cancer? Molecular Cancer, 10, 1-9.

AASThe AAS helps in regulating blood pressure and fluid balance. In heart failure, the reduced cardiac output and systemic blood pressure stimulate the AAS as a compensatory mechanism, which in turn leads to increased retention of sodium and water, vasoconstriction, and elevated blood pressure. This activation of the AAS is at first adaptive, but it basically contributes to the progression of heart failure and exacerbates atherosclerosis by promoting endothelial dysfunction, inflammation, and vascular remodeling.It works this way: in response to heart failure, the AAS system is activated as a compensatory mechanism (Pugliese et al., 2020). The process begins when the kidneys, sensing reduced blood flow and pressure, release the enzyme renin into the bloodstream. enin converts angiotensinogen, a liver-produced protein, into angiotensin I, which is then converted into angiotensin II by angiotensin-converting enzyme (ACE) primarily in the lungs. Angiotensin II is a potent vasoconstrictor, which increases blood pressure by narrowing…...

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ReferencesLaranjo, L., Lanas, F., Sun, M. C., Chen, D. A., Hynes, L., Imran, T. F., ... & Chow, C. K. (2024). World Heart Federation Roadmap for Secondary Prevention of Cardiovascular Disease: 2023 Update. Global Heart, 19(1).   Pugliese, N. R., Masi, S., & Taddei, S. (2020). The renin-angiotensin-aldosterone system: a crossroad from arterial hypertension to heart failure. Heart Failure Reviews, 25, 31-42.Romero-González, G., Rodríguez-Chitiva, N., Cañameras, C., Paúl-Martínez, J., Urrutia-Jou, M., Troya, M., ... & Bover, J. (2024). Albuminuria, Forgotten No More: Underlining the Emerging Role in CardioRenal Crosstalk. Journal of Clinical Medicine, 13(3), 777.  https://doi.org/10.3390/jcm13030777  Senatore, F., Balakumar, P., & Jagadeesh, G. (2021). Dysregulation of the renin-angiotensin system in septic shock: mechanistic insights and application of angiotensin II in clinical management. Pharmacological Research, 174, 105916.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10809857/ 

Metabolic syndrome is significant for our patient for several reasons. As we have noted, the syndrome is associated with a higher risk of cardiovascular disease. Those patients who have metabolic syndrome tend to develop coronary atherosclerosis at a higher rate than those who have coronary risk factors alone. Obesity increases the risk of metabolic syndrome but so does pre-obesity, or BMI ranging from 25-30. Women who have been diagnosed with polycystic ovarian syndrome are noted to be at increased risk of hypertension, dylipidemia, insulin resistance, impaired glucose tolerance and Type II diabetes. Because of all these comorbidities, women with PCOS also tend to be at greater risk for patients with subclinical carotid atherosclerosis, especially in the premenopausal population (Talbot, et al., 2000). For these same reasons, women diagnosed with PCOS have a 5 fold increased risk for the development of complications of coronary and cerebrovascular atherosclerosis.

Mrs. Stiller has many concerns…...

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Reference:

Reaven G. (2002) Metabolic syndrome. Pathophysiology and implications for management of cardiovascular disease. Circulation.106:286-288

Manson JE, Willet WC, Stampfer MJ, Colditz GA, Hunter DJ, Hankinson SE, et al. (2005) Body weight and mortality among women. N Eng J. Med 333:677-85

Juahan-Vague I, Alessi MC. (1997) PAI-1, obesity, insulin resistance and risk of cardiovascular events. Thromb Haemost 78:656-60

Wilson PW. (2004) Estimating cardiovascular disease risk and the metabolic syndrome: a Framingham view. Endocrinol Metab Clin N. Am. 33:467-81

New Suppliers of Health Supplements
A promising new addition to the company's current line of health supplements was identified during a recent trip to Bangkok, Thailand, to meet suppliers of a promising antioxidant, coenzyme Q10. A growing body of research suggests this antioxidant is effective in improving cardiovascular function and may also be useful in alleviating the symptoms of angina pectoris, cardiac arrhythmia, high blood pressure, moderate gingival disease, congestive heart failure, dilated cardiomyopathy and severely impaired immune systems. Based on the documented efficacy, high quality and low costs of the health supplement offered by this vendor, this report provides the background and an overview of the supplier, a description of the health supplement, and current applications for coenzyme Q10. A summary of the business trip and meeting with the company's president is followed by recommendations and a brochure illustrating various aspects of the product.

esults of Business Trip to Thailand

Background…...

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References

Cerrato, P.L. (1999, June). Coenzyme Q. And heart disease. RN, 62(6), 61 -- 62.

Chalmers, A.H., Blake-Mortimer, J.S. & Winefield, A.H. (2003). The prooxidant state and psychologic stress. Environmental Health Perspectives, 111(1), 16.

Complete-Pharma Co., Ltd. (2011). Retrieved from   / th107560976.html.http://www.alibaba.com/member 

Freeman, M.S. & June, C. (2005). The Harvard Medical School guide to lowering your cholesterol. New York: McGraw-Hill.

Discussion Qs1Atherosclerosis is disease in which cholesterol and lipids gather on the walls of a persons arteries (Jebari-Benslaiman et al., 2022). These substances form plaque, which prevents normal blood flow by restricting the space through which blood can move. The arteries become tighter and tighter like a clogged pipe, making it harder for the heart to pump the same amount of blood throughout the body. This process begins with injury to the endothelium, which is the inner lining of the artery. Injury can occur as a result of smoking or diabetes or some other problem. Lipids accumulate on the endothelium as a result of permeability caused by the injury. Oxidation follows, triggering inflammation.Next, monocytes begin to affix to the endothelium and produce foamy, fatty cells (Mehu et al., 2022). More inflammation occurs due to cytokine build-up, and plaque formation then results. Lipids, foam cells, new cell growth combine to facilitate…...

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ReferencesDuckett, L. J. (2021). Quantitative research excellence: Study design and reliable and valid measurement of variables. Journal of human Lactation, 37(3), 456-463.Hunziker, S., Blankenagel, M., Hunziker, S., & Blankenagel, M. (2021). Experimental research design. Research Design in Business and Management: A Practical Guide for Students and Researchers, 221-234.

Carl must be psychologically prepared to make such changes, however. Thus, as well as taking Carl's blood pressure and submitting a blood sample to have his cholesterol screened (getting his blood glucose level assessed, even though there were no problems in the past with this reading might also be wise), the nurse should try to obtain a full assessment of Carl's lifestyle. When and what does he eat? What are his work habits? His sleep habits? Has anything changed recently in his life? All of these factors could make a potentially meaningful impact upon both the test results and the eventual prescription for Carl to improve his health.
Carl is still very young to run the risk of having a heart attack: the risk of having a heart attack increases dramatically after age 65) so engaging in positive changes now is wise and prudent (Heart health screening, 2013, AHA). It…...

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References

Drug therapy for cholesterol. (2013). AHA. Retrieved:

 http://www.heart.org/HEARTORG/Conditions/Cholesterol/PreventionTreatmentofHighCholesterol/Drug-Therapy-for-Cholesterol_UCM_305632_Article.jsp 

Heart health screening. (2013). AHA. Retrieved:

 http://www.heart.org/HEARTORG/Conditions/Heart-Health-Screenings_UCM_428687_Article.jsp

Vascular Disease
andy Jackson

Geriatric Nursing

The disease known as Peripheral Vascular Disease (PVD), according to the American Heart Association (AHA, 2004), involves the blood vessels "outside the heart and brain." This disease refers to a narrowing of those vessels that carry blood to one's leg and arm muscles.

In particular, the AHA states that there are two forms of PVD: one is "Functional Peripheral Vascular Disease," and the other is "Organic Peripheral Vascular Disease." The first, Functional PVD, does not allude to actual defects in the structure of the blood vessel, but rather refers to "short-term effects" caused by cold temperatures, stress caused by emotions, smoking, or handling machinery that vibrates powerfully.

The second form of PVD - "Organic" - is actually caused by "structural changes" in blood vessels. These changes may be inflammation, tissue damage, or the buildup of fatty substances in the arteries, called "atherosclerosis" - which restricts good blood flow…...

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References

American Medical Association (2004). "Peripheral Vascular Disease." Retrieved June 17, 2004, at  http://www.americanheart.org/presenter.jhtml?identifier=4692 .

Barker, Jason; & Meletis, Chris D. "Peripheral Vascular Disease and Stasis Ulcers:

Treatment from a Naturopathic Perspective." Townsend Letter for Doctors and Patients. i241-242, 76-79.

Health & Medicine Week (2003). "Peripheral Vascular Disease Treatment Slated to Begin Phase II Trials." NewsRX, 123.

M.K., a 45-year-old female who has a history of Type II diabetes mellitus and primary hypertension. In addition to this, M.K. is overweight and persists with a poor diet. The patient has also been smoking for the past 22 years, and has recently been diagnosed with chronic bronchitis. Current symptoms include chronic cough, which tends to be more severe in the mornings and productive with sputum, light-headedness, distended neck veins, excessive peripheral edema, and increase urination at night. The patient is currently on several medications including Lotensin and Lasix for the hypertension, along with Glucophage for the Type II diabetes mellitus. From an analysis of M.K.'s lab results, this report will offer clinical findings and treatment recommendations, as well as suggestions for what other conditions M.K. may be at risk for given her health history, lifestyle, and lab results as follows:
Vitals

BP

158/98 mm Hg

CBC

Hematocrit

57%

Glycosylated hemoglobin (HbA1c)

Arterial Blood Gas Assessment

PaCO2

52 mm…...

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References

American Heart Association (2015). Types of heart failure. Retrieved online:  http://www.heart.org/HEARTORG/Conditions/Heartfailure/Aboutheartfailure/Types-of-Heart-Failure_UCM_306323_Article.jsp#.WEy-h6IrKRs 

CDC (2016). High blood pressure facts. Retrieved online:  http://www.cdc.gov/bloodpressure/facts.htm 

Cheung, M.M. & Li, C. (2012). Diabetes and Hypertension: Is There a Common Metabolic Pathway? Curr Atheroscler Rep. 2012 Apr; 14(2): 160 -- 166.

Elliot, W.J. (2003). The economic impact of hypertension. J Clin Hypertens (Greenwich). 2003 May-Jun;5(3 Suppl 2):3-13.

When evaluating completions rates involved with PWA, radial tonometry had a 66% and carotid tonometry had a 99%. The radial tonometry was determined to be easier on the patient.
Laser Doppler Imaging (LDI)

Laser Doppler Imaging (LDI) has increased significance over previous single probe techniques. lood flow is no longer measured at a single site but between an area and the LDI due to being non-contact cannot interfere with the final results. LDI is a 1mm laser beam that uses a mirror to scan in two dimensions. A small amount of light penetrates the skin; the depth depends on wavelength and absorption, of area scanned and interacts with cells and tissues. Speed and density of moving cells determine the signal sent to detector. Discovery Technology International defines the amount of tissue measured as:

we have estimated that for well-perfused tissue such as muscle, the mean sampling depth for our probes is in…...

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Bibliography

Arnett, D. (n.d.). Arterial Stiffness and Hypertension. Retrieved on April 12, 2010 from  http://www.fac.org.ar/scvc/llave/hbp/arnett/arnetti.htm 

Bailey, B.; Jacobsen, D.; LeCheminant, J.; Kirk, E.; & Donnelly, J. (2003). The Effect of Analysis Method in Determining Change in Post Exercise Oxygen Consumption.

Retrieved on April 12, 2010 from  http://journals.lww.com/acsm-msse/Fulltext/2003/05001/The_Effect_of_Analysis_Method_in_Determining.1004.aspx 

Balmain, S., Padmanabhan, N., Ferrel, W., Morton, J. & McMurray, J. (2007). Differences in arterial compliance, microvascular function and venous capacitance between patients with heart failure and either preserved or reduced left ventricular systolic function. Retrieved on April 12, 2010 from http://eurjhf.oxfordjournals.org/content/9/9/865.full

2010; Chorny et al. 2010). This research is still quite new, however, and the question remains as to whether or not nanoparticles can truly serve as a replacement for stents by prohibiting plaque growth through a variety of means, including more targeted and longer-range delivery of pharmaceutical substances that destroy such build-ups and inhibit plaque deposits from forming. The efficacy of this approach has already been preliminarily demonstrated, but the long-term viability and safety of this intervention method as well as attendant risks have not yet been fully determined (Chan et al. 2010; Chorny et al. 2010).
IV. Motivation for esearch

Despite the numerous advancements that have been made in treating plaque build-up in arteries and the general treatment and control of other cardiac issues, coronary artery disease is still the leading cause of death in North America and is a significant problem in other parts of the world, as well…...

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References

Chan, J., Zhang, L., Tong, R., Ghosh, D., Gao, W., Liao, G….Farokhzad, O. (2010). Spatiotemporal controlled delivery of nanoparticles to injured vasculature. Proceedings of the National Academy of Sciences, January 2010.

Chorny, M., Fishbein, I., Yellen, B., Alferiev, I., Bakay, M., Ganta, S….Levy, R. (2010). Targeting stents with local delivery of paclitaxel-loaded magnetic nanoparticles using uniform fields. Proceedings of the National Academy of Sciences, April 2010.

Kohn, J. & Zeltinger, J. (2005). Degradable, drug-eluting stents: a new frontier for the treatment of coronary artery disease. Expert review of medical devices, 2(6), pp. 667-71.

Schoenhagen, P. & Nissen, S. (2003). Assessing Coronary Plaque Burden and Plaque Vulnerability:Atherosclerosis Imaging With IVUS and Emerging Noninvasive Modalities. American Heart Hospital Journal 1(2), pp. 164-9.

1958

After studying the cardiovascular effects of various catecholamines, Moran and his research partner, Perkins, are published in the same journal as Ahlquist arguing "that DCI's activity belonged to Ahlquist's 'beta-adrenergic' type, and coined the term 'beta-adrenergic blocking drug', later shortened to 'beta-blocker'"

1959

Sir James Black joins the cardiovascular team at Imperial Chemical Industries, Ltd., reads Moran's research and realizes the possibilities of synthesizing an analog to DCI that would be clinically useful.

1959

Black's ICI report contradicts Waring's arguing that the "altered fat metabolism with associated changes in blood coagulability interact, permissively, with sympathetic neurohumoural stress responses to produce fatal damage."

1962

Black synthesizes propranolol (Inderal)

1963

ICI launches Black's first beta blocker treatment -- pronethalol (Alderlin).

1964

The first clinical studies are conducted for the use of proopranolol.

1965

ICI launches propranolol, the replacement for propranolol as it was found to cause thymic tumors in mice.

1966

Propranolol is first marketed in the U.S.

1967

Lands identifies a variety of models of sensitivity to…...

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References

Altman, L. (2 Feb 1982), New class of drugs revolutionizes therapy for heart disease, [Online], Available:   [22/10/09].http://www.nytimes.com/1982/02/02/science/new-class-of-drugs-revolutionizes-therap-y-for-heart-disease.html?&pagewanted=print 

Archard, G. (2005), Beta-Blocker Use in CHF Patients: History of CHF Treatments, [Online], Available:   [22/10/09].http://www.medscape.com/viewarticle/510212_2 

Betaxolol, (2008), [Online], Available:   [22/10/09].http://www.medicinenet.com/betaxolol/article.htm 

Bisoprolol, (2008), [Online], Available:   [22/10/09].http://www.medicinenet.com/bisoprolol/article.htm 

1. Plants have developed a fascinating array of chemical defenses to protect themselves from various threats such as herbivores, pathogens, and environmental stressors. These chemical compounds not only play a crucial role in the survival of plants but also have the potential to benefit human health through their unique properties. Researchers have increasingly turned their attention to exploring the therapeutic potential of plant chemical defenses in medical treatments and therapies. By harnessing the power of these natural compounds, scientists aim to develop new drugs, supplements, and therapies that could effectively combat various diseases and improve human health.

2. One way....

1. The unique atherosclerosis risk factors in the Western region of Saudi Arabia include high consumption of traditional high-fat, high-sugar foods and lack of physical activity.

2. Research has shown that individuals in the Western region of Saudi Arabia have a higher prevalence of obesity, which is a major risk factor for atherosclerosis.

3. In addition to lifestyle factors, genetic predisposition plays a significant role in the development of atherosclerosis in the Western region of Saudi Arabia.

4. Studies have indicated that the Western region of Saudi Arabia has a higher prevalence of hypertension, which is another important risk factor....

1. The prevalence of diabetes in the Western region of Saudi Arabia significantly contributes to the high incidence of atherosclerosis, as evidenced by regional health surveys and clinical studies.

2. Dietary habits, particularly the high intake of trans fats and sugars, are a major risk factor for atherosclerosis in this region, supported by dietary analysis and epidemiological data.

3. Genetic predispositions unique to the population in the Western region of Saudi Arabia play a critical role in the development of atherosclerosis, as indicated by genetic research and family history studies.

4. The sedentary lifestyle prevalent among the urban population in the Western region....

Atherosclerosis is a chronic inflammatory disease that affects the walls of arteries, including the coronary arteries that supply the heart muscle with oxygen and nutrients. When atherosclerosis occurs in the coronary arteries, it can lead to the development of coronary artery disease, a condition characterized by the narrowing or blockage of these blood vessels, limiting blood flow to the heart. As a result, the heart may not receive enough oxygen, leading to symptoms such as chest pain (angina) or even a heart attack. Coronary atherosclerosis is a major cause of sudden cardiac death, a devastating event that occurs when the....