Henry Viiis Succession Acts - Free Essay Example

Sample details Pages: 5 Words: 1624 Downloads: 2 Date added: 2017/09/18 Category Advertising Essay Type Argumentative essay Did you like this example? 148. 216 Document Exercise, Assignment 1. Student ID # 99245875 THE FIRST SUCCESSION ACT, 1534. The Act of Succession 1534 is a statute issued by the English Parliament under the reign of King Henry VIII, which confirmed the annulment of Henry’s marriage to Queen Katherine and validated Henry’s marriage to Anne Boleyn. Also, through this Act the line of succession moved to the children of his marriage to Anne, or any future marriages, effectively removing Mary, Henry’s only surviving child from his marriage to Katherine of Aragon, as heir. Furthermore, the Act contained a clause that subjects must swear an oath recognising the terms of the Act, any refusal would be held as a treasonable offence. A predominant pre-occupation of Henry during his reign was to establish a clear line of succession for the Tudor dynasty. When his marriage to Catherine of Aragon failed to produce a male heir, Henry became convinced this was punishment under devine law for mar rying his dead brother’s wife (Lotherington, p. 71). He petitioned the Pope for an annulment of the marriage, however the Pope was under the influence of Charles V of Spain, Katherine of Aragon’s nephew, and ultimately refused Henry an annulment (Robinson, 2010). Henry also had ambitions to marry his mistress Anne Boleyn. There followed numerous Acts of Parliament instigated by Henry and his close advisors; beginning with the Act in Restraint of Appeals, which stated that ‘no appeals were to be made from England to Rome in any matters concerning wills, marriages, or payments to the Church; cases were to go no further than the Archbishop’ (Lotherington, p. 4), that paved the way for a break from the papacy enabling Henry to fulfil his personal ambitions. The main claim in relation to grounds for annulment of Henry’s marriage to Katherine was that it was incestuous, therefore illegal, as Katherine had previously been married to Henry’s broth er Arthur, despite Katherine’s solemn claim that her marriage to Arthur had never been consummated (Fraser, pp. 139-40). With the backing of Thomas Cranmer; a key figure in Henry’s reformation policies, (Cranmer had replaced Wolsey as Arch Bishop of Canterbury in 1533 after Wolsey’s failure to obtain for Henry an annulment from the Pope (Lotherington, p. 2). ) Katherine’s claims were disregarded, ‘being before lawful wife to Prince Arthur your elder brother, which by him was carnally known’ (Act of Succession, 1934), thereby allowing Parliament to deem the marriage ‘against the laws of Almighty God’, therefore annulled. The Act goes on to declare the marriage of Henry VIII and Anne Boleyn (secretly married by Thomas Cranmer in January 1533, as Anne was pregnant and Henry was desperate for the child to be legitimate (Fraser, p. 187)), valid. The validation of this marriage on Cranmer’s ‘grounds of judgement’ is said in the Act to be confirmed also by ‘the whole clergy of this realm in both the Convocations, and by both the universities thereof, as by the Universities of Bologna, Padua, Paris, Orleans’ (Levine, 1973). Here again Cranmer’s role in the annulment is significant. It was at the suggestion of Cranmer, before his elevation to Arch-bishop (and possibly partly as a result of), that Henry ‘gather enough support to persuade the Pope of the justice of his cause royal agents were sent to universities across Europe to win backing for the King’s cause’(Lotherington, p. 79). While the support garnered may have been ineffective in persuading the Pope, it is almost certainly used as a persuasion tool to back the validation of the annulment to Katherine; and marriage to Anne. Henry’s ambition to secure a Tudor line of succession aligns in the Act with his marriage to Queen Anne. Accordingly the order of succession went ‘first to the King’s sons by Queen Anne and their heirs, second to the King’s sons by future wives and their heirs, third to Princess Elizabeth. ’ (Levine, 1973). Glaringly obvious in this order of seniority is the absence of Lady Mary, Henry’s only surviving child from his marriage to Katherine. Due to the annulment Mary, the previous rightful heir is omitted from of the line of succession leaving Princess Elizabeth, child of Henry and Anne, heir presumptive. Also contained in Henry’s First Succession Act was a clause whereby all subjects must take an oath swearing to the contents of the Act, refusal would be an act of treason. It also became a treasonable offence to speak, act or write; against the King, against his marriage to Anne, against his heirs by this act (Levine, 1973). Through this clause Henry has laid a pre-emptive strike against anyone who might challenge the legitimacy of his marriage and heirs. Significantly, this highlights Henry’s use of Parliament to ensure his personal ambitions were carried out and demonstrates the shift in subordination of canon law to statute law during Henry’s reign. THE SECOND SUCCESSION ACT, 1536. The Second Succession Act of 1536 (repealing the First Act of Succession, 1534), following the conviction and execution of Anne Boleyn for adultery and treason, cites Parliamentary legitimization of Henry’s marriage to Jane Seymour and the line of succession passing to the lawful issue from this marriage. The Act declared both Henry’s marriage, to Katherine; and to Anne, to be void and also illegitimized the issue from each marriage, this being Mary and Elizabeth. This Act effectively left Henry VIII with no legitimate heir until the birth of Edward in 1537. The Act cites Parliamentary validation for Henry’s next choice of wife, Jane Seymour with praise for her ‘convenient years and pureness of flesh and blood’ (Williams, 1967). This highlights th e unprecedented power of Parliament and King in relation to what had been previously Church matters. In comparison to the First Act, where Henry’s marriage to Queen Anne is ‘solmenized’ by Cranmer, who held the highest church position in England as the Arch Bishop of Canterbury; in the Second Act, Henry’s marriage to Queen Jane is solemnized according to the laws of Holy Church, which by now meant the Church of England; which Henry established and claimed himself to be head of after the Act of Supremacy in 1534 (Lotherington, p. 85). Significantly this highlights the complete break with Rome and the shift in power from papal authority to the unprecedented power of the King, as head of state and church. In the Act, Parliament acknowledges Henry’s perceived ‘intolerable perils’ that he has had to endure through his ‘unlawful’ marriage to Katherine, with the inclusion now also of his ‘unlawful’ marriage to A nne. Significant in the Second Act in regards to Henry’s previous marriage to Katherine, is the comparison of wording with the First Act, in which Parliament deems the marriage to be ‘void and annulled’ (Levine, 1973); in the Second Act Parliament deems the marriage as ‘void and annihilate (Williams, 1967)’. The wording in the First Act acknowledges that a marriage did exist but was revoked due to the lawlessness of the union, the Second Act uses the word ‘annihilate’ implying that the marriage never existed, thereby lending weight to the credibility of the exclusion of Mary as a rightful heir. Again Henry’s pre-occupation with producing a male heir to succeed the throne and ensure a strong stable line of succession is evident in this Act. Albeit the birth of Elizabeth, Henry’s marriage to Anne failed o produce the desired male heir and Henry became disillusioned with Anne’s ability to do so (Fraser, p. 232). The timely execution of Anne Boleyn in 1536 allowed Henry to disentangle himself from his marriage to Anne without a drawn out legal struggle as there had been with Katherine. The only problem that needed to be addressed with regards to this marriage, it seems, was to declare it void, to be able to justify the displacement of Elizabeth as rightful heir and ensure succession to a male heir from his next union, that to Jane Seymour. Hence the inclusion in the Act that any children from either previous marriage ‘.. shall be taken reputed and accepted to be illegitimate and utterly foreclosed excluded and barred to claim challenge or demand any inheritance as lawful heir or heirs to your highness by lineal descent’ (Williams, 1967) in reference to both Mary and Elizabeth. This enforcement by Parliament declaring both Mary and Elizabeth bastards effectively left the King without an heir apparent. However, provision is given in the Act ‘that all issue, hereafter to be had and procreate between your highness and your queen Jane, shall be your lawful children and heirs’ (Williams, 1967), this in conjunction with the repealing of the First Succession Act, established that the next in line of succession would be ‘the first son of your body between your highness and your said lawful wife queen Jane begotten’(Williams, 1967). Henry’s ambitions were realised with the birth of Edward, his son by Queen Jane, in 1537. Significantly, the strategies used by Henry to secure a male heir, of which both the First Succession Act 1534 and Second Succession Act 1536 were part, instigated widespread radical changes in the role of church, state and monarch in England that became known as the ‘Henrician Reformation’ (anon). Ultimately, and perhaps unwittingly of Henry, due to his personal obsession with a male heir, these changes can be questioned as fast-tracking the revolutionary Protestant Reformation in England. BIBLIOGR APHY Levine, First Succession Act, 1534. From 25. Henry VIII cap. 22; Stat Realm iii. 471-4, 1973, pp. 151-53. (provided Course Material), 1973. Lotherington, J. (ed), The Tudor Years, London: Hoddler and Stoughton, 2nd ed. , 2003. Fraser, A. , The Wives of Henry VIII, New York: Alfred A Knopf, Inc. , 1992. Robinson, B. , An Overview of the Reformation, retrieved 25 June 2010 from https://www. bbc. co. uk/history/british/tudors/reformation_overview_0 Williams, The Second Succession Act, 1536. St. 28 Hen. VIII, c. 7 (Stat Realm, III, 655)1967, pp. 452-53. (provided Course Material), 1967. Don’t waste time! Our writers will create an original "Henry Viiis Succession Acts" essay for you Create order

The Effects Of Parenting On The Development Of Self...

The Effects of Parenting on the Development of Self-Regulation in Children Pamela Whitaker 999998221 University of Toronto Introduction to Development (PSY210H1-S) The Effects of Parenting on the Development of Self-Regulation in Children Effective regulation of emotions has been viewed as a developmental achievement that serves as an essential requirement for numerous other developmental tasks. Specifically, because powerful emotions have the potential to disorganize or disrupt multiple psychological processes, modulation of their experience and expression has been considered crucial for basic state regulation, behavioural exploration, cognitive processing, and social competence (Sheppes Gross,†¦show more content†¦Family demographics, parenting style, level of control, and warmth and responsiveness demonstrated by parents proves to have a lasting effect on the child’s self-regulation as they develop. Positive aspects of the previously mentioned variables are positively correlated with successful self-regulation skills in children. Self-regulation creates a foundation for school readiness, successful peer relationships, and the growth of self-understandings, which includes one’s self-concept, self-esteem, and moral development. Family Demographics and Parenting Style A child’s development occurs foremost through the reciprocal interactions with the family unit. Parents usually establish the foundation for good self-regulation by providing an environment that is warm, nurturing, and encourages trust. Piotrowski, Lapierre, and Linebarger (2012) focus their research on understanding the correlates of self-regulatory abilities among children. The study was aimed at evaluating various demographic and parenting variables in order to isolate the correlates of self-regulation. Demographic variables of interest in relation to child self-regulation in the study included factors such as child age, family income, and parenting style. Demographic variables are important to consider because children,

Cardiovascular Diseases Free Essays

string(121) " of plaque will increase as the result of high level of cholesterol, type LDL, so called â€Å"bad cholesterol† in blood\." Cardiovascular disease Introduction Heart disease is No. 1 killer disease worldwide. It causes 12 million deaths annually. We will write a custom essay sample on Cardiovascular Diseases or any similar topic only for you Order Now Thanks to the rising health awareness and government programmes this number significantly reduce during last 30 years. Coronary heart disease and cardiovascular disease Cardiovascular diseases are diseases of the heart (cardiac muscle ) or blood vessels (vasculature). Cardiovascular disease (CVD) means all the diseases of the heart and circulation (blood vessels disease) including coronary heart disease (angina and heart attack) and stroke, as well as coronary and periphery blood vessels disease (problems with circulation). Diseases from this group are the biggest killer in Europe and USA, but developing and non-develop countries too. The final and most tragic consequence of different types of heart disease is heart attack with tragic consequences. Heart diseases are caused by atherosclerosis, a disease of arterial blood vessels resulted from atheroma i. . plaques accumulated (forming; sticking) on artery walls which makes the blood vessels nonelastic and narrowed and leads to decreased blood flow. For the atherosclerosis doctors very often use alternative name chronic cardiovascular disease. The opposite group acute heart disease made group of diseases which are dangerous for patients lives. Acute heart diseases include conditions or illnesses wh ich usually have a rapid onset of symptoms and may resolve within days with or without treatment. A condition or illness that is sudden or severe. On the other hand a condition or illness that arises slowly over days or weeks and may or may not resolve with treatment made a group of chronic heart disease. Both of them are caused by atheroma and the most known are next: a) Acute heart disease Heart attack is caused by lack of O2 in heart muscle cells. Very often it is caused by rupture of â€Å"hard plaques† patches which result in blood clots and partially or completely block blood flow and cause a heart attack. When a fiber cap becomes thin, these â€Å"hard plaques† can suddenly rupture, spilling their contents, resulting in blood clots that partially or completely block blood flow and cause a heart attack http://www. authorstream. com/Presentation/nitin-35423-heart-diseases-science-technology-ppt-powerpoint/ Cholesterol glossary. http://www. mybwmc. org/library/28/000225 Stroke Stroke is death of brain cells caused by obstructed blood flow to parts of the brain. Since the level of LDL cholesterol is main cause of narrowed of blood vessels, it is necessary control it. If not treated properly, high LDL cholesterol can cause a stroke. Cholesterol glossary. http://www. mybwmc. org/library/28/000225 b) Coronary heart disease Heart disease (coronary heart disease), When the plaque build up in th conorary arteries heart does not get sufficient blood, the condition is called coronary artery disease or coronary heart disease. Atherosclerosis is a disease of arterial blood vessels in which plaques form on artery walls. This is a consequence of different substances circulating in the bloodstream (inflammatory cells, proteins, cholesterol and calcium) sticking inside the vessel walls. Plaque patches influence on narrowing blood flow in the artery. ttp://www. bodybuilding. com/fun/gastelu5. htm Peripheral artery disease (reduced blood flow in the limbs, usually the legs Coronary plaque Coronary plaque is a term which use in practice as a synonym for atheroma or atherosclerosis. Patches of atheroma are formed from substances that circulate in the bloodstream. They consist of lipid, or fat, cores covered by collagen fiber cap s which are sticking to the inside of the vessel walls. Over time plaque or patch of atheroma increases making an artery narrower and the blood flow through the artery is reducing. We can see the changes in blood vessels caused by plaque in the Figure 1. Figure 1 Artery with the patches of atheroma – plaque Preventing Cardiovascular Diseases. Patient. co. uk. emis www. patient. co. uk/health/Preventing-Cardiovascular-Diseases. htm (March 13, 2013) http://medicineworld. org/blogs/heart/blog/permalinks/Jan-2006/coronary-plaque-detection-by-molecular-imaging. html (March 13, 2013) Mature plaques typically consist of two main components: soft, lipid-rich atheromatous â€Å"gruel† and hard, collagen-rich sclerotic tissue. Lipid-rich and soft plaques are more dangerous than collagen-rich and hard plaques because they are more unstable and rupture-prone and highly thrombogenic after disruption. Researchers have found that many people who have heart attacks do not have arteries narrowed by plaque. Many heart attacks are now known to be caused by soft or vulnerable plaques, located on an inflamed part of an artery. This plaque can burst, leading to the formation of a blood clot that can cause a heart attack. The 2009 issue of â€Å"The American Journal Pathology† edited explanation of those relations discovered by Olga Ovchinnikova and er colleagues. They found that inflammation results in the formation of soft (vulnerable) plaque which is filled with different cell types that promote blood clotting. This leads to a reduction of mature collagen, resulting in thinner caps that are more likely to rupture, even in the cases when total level of plaque isn’t extremely high. The authors advocate d ifferent viewpoints about relations between the plaque level and structure, i. e. its influence on heart attack. The first group claims that described types of blockages cause only about 30 percent of heart attacks. On the other hand, some sources state that more than two-thirds of acute coronary events result from rupture of coronary plaques. However problems that plaque creates are extremely dangerous for people’s life and it is very important to prevent and monitor its appearance and changes. Graphs of vulnerable plaque and rupture of plaque which causes a heart attack is presented below. Figure 2 Vulnerable atherosclerotic plaques. Vulnerable atherosclerotic plaques. A. Atherosclerosis in a chronic disease that leads to plaque rupture and vascular occlusion. B. Cross-section of a lethal coronary plaque rupture. Adapted from Heistad D. Unstable coronary-artery plaques. N Engl J Med. 2003. Atherosclerosis Modeling In-vitro. http://www. remedi. uzh. ch/research/disease. html Figure 3 Plaque Rupture and Heart attack http://hon. nucleusinc. com/generateexhibit. php? ID=30468A=1027 Factors influencing plaque growth and stability Based on everything mentioned above and medical experience the conclusion about relations between heart attack and other cardiovascular disease and the level of plaque increasing are found. The higher the level of plaque the higher risk of heart disease will be. The level of plaque will increase as the result of high level of cholesterol, type LDL, so called â€Å"bad cholesterol† in blood. You read "Cardiovascular Diseases" in category "Essay examples" When the level of LDL is normal, blood can pass in and out of the blood vessels without problems, but if it significantly increase particles of the blood will accumulate and sooner or later provoke trigger (cause) heart attack. Other very important factors influencing plaque level increasing are high blood pressure and cigarette smoking. Both factors accelerate the plaque formation changing (damaging) artery walls and even more, helping cholesterol forming. Medical experience proved that plaque composition and vulnerability (hard or soft plaque) is more responsible for the conversion of a stable disease to a life-threatening condition than the plaque size. Except the plaque vulnerability the risk of plaque disruption is are consequence of rupture triggers (extrinsic forces). Soft plaque – lipid-rich one is more dangerous because of its instability and higher probability for rupture. Even (IAKO) Although â€Å"hard plaque† that one having higher level of calcium influence on the blood vessels walls and their â€Å"hardness† experience show that heart attacks are mostly caused by soft plaque disruption. Figure 4 Plaque rupture and its consequences in the form of heart diseases http://www. nature. com/nrg/journal/v7/n3/fig_tab/nrg1805_F2. html Risk factors of coronary heart disease Risk factors influencing cardiovascular disease we can group based on their stability into the three groups: a) Modifiable risk factors In this group hypertension is the most dangerous risk factor for heart attacks, but even more for stroke. It is forming as the result of abnormal blood lipid levels which means high total cholesterol, high levels of triglycerides and high levels of low-density lipoprotein or low levels of high-density lipoprotein (HDL). Smoking, physical inactivity, Type 2 diabetes, and a diet full with saturated fats are risk factors strongly influencing the heart disease. All of them are treatable and patients (individuals) belonging into the different types of risk customers’ groups should avoid practice them. b) Non-modifiable risk factors The factors from this group mostly are constant, like the case in gender or family history. Others are changing when time is passing, like age and lifestyle and personal habits. Older people have more chance to get heart attack and the man, especially those having â€Å"bad medical history†. Ration between man and woman are changing when women past the menopause. After that the level of risk is similar as the men’s one. As I’ve presented there is direct correlation between cardiovascular disease and condition and health of blood vessels, more precisely of developing atheroma, means level and structure of plaque in vessels. On the other development of plaque and its level is directly influenced by level of cholesterol and some other elements which are connected with individual person and his/her life and genetic predispositions. As with the other diseases everybody has some risk of developing atheroma, but some risk factors increase the risk level for several categories. Those risk factors include: fn 12 †¢Fixed risk factors – factors that person cannot change: oA strong family history which means close relatives who developed heart disease or a stroke before they were 55 (for males) or 65 (for female). Severe baldness in men at the top of the head. oAn early menopause in women. oAge. Older people have more risk to develop atheroma. oEthnic group. Medical data show that people from different ethnic group have different risk for heart diseases. †¢Treatable or partly treatable risk factors include different health problems caused basically by the same causes as the: oHypertension (high bl ood pressure). oHigh cholesterol blood level. oHigh triglyceride (fat) blood level. oDiabetes. oKidney diseases causing diminished kidney function. All factors from this group have to be controlled and monitor. Any kind of their complication probably will trigger more serious problems such as heart attack or stroke. †¢Lifestyle risk factors that can be prevented or changed. Actually these factors PRETHODE precede to those belonging to the second group. Except the genetic factors way of life and daily habits are the more responsible for different kind of heart diseases. Those factors are: oSmoking (Smoking cigarette increase blood pressure, decrease HDL; damages arteries and blood cells and increases heart attacks. Passive smoking is also a risk factor for cardiovascular disease ) oLack of physical activity. Obesity (People who are overweight (10-30% more than their normal body weight) have 2 to 6 times the risk of developing heart disease. ) oAn unhealthy diet and eating too much salt. oExcess alcohol. Looking on those three groups one can easily conclude that people with â€Å"bad predisposition† having high fixed risk factors have to think about their lifestyle risk factors ev en more, in order to try to decrease the second group of factors (treatable or partly treatable risk factors). On the other hand some of risks are more dangerous than the others; for example smoking increases risk for heart disease more than obesity. And of course combination of two or more risk factors increases significantly the level of risks; older man (or woman) who smokes, without physical activity and with bad eating habits has more chance to get some of previously explained disease than the one who have â€Å"just one of bad habits†. The more risk factors someone has the greater is the likelihood that he/she will develop cardiovascular disease, unless taking action to modify his/her risk factors and working to prevent them compromising his/her heart health. That doesn’t mean that people with â€Å"good genes† can be irresponsible and ZANEMARITI risk factors from other groups. With or without genetic predisposition modern life significantly increases a risk of heart disease for everybody. Hormones impact on lipids and other risk factors Different numbers of man and women died from heart attack initiated a lot of research about hormones’ influence on the risk factor and heart disease development. Number of men died from the heart attack outnumbered the number of women in pre-menopause period, but in the post-menopause data show completely opposite situation. A percentage of women in post-menopause having heart disease and dying from heart attack increase dramatically and now outnumbered the men. The main reasons for those changes are connected to the level of hormones and their influence on level and structure of cholesterol and consequently on risk factors and heart disease. As mentioned before total cholesterol actually is made of two different types of cholesterol: LDL – low density lipoprotein (LDL), so called bad cholesterol and high density lipoprotein (HDL). High levels of LDL cholesterol lead to atherosclerosis increasing the risk of heart attack and ischemic stroke. HDL cholesterol reduces the risk of cardiovascular disease as it carries cholesterol away from the blood stream. http://www. walgreens. com/marketing/library/careguides/careguide. jsp? docid=000225=28=High%20Cholesterol Estrogen, a female hormone, raises HDL cholesterol levels, partially explaining the lower risk of cardiovascular disease seen in premenopausal women. But after menopause (natural or surgical) when a level of estrogen significantly decreases total cholesterol rises, low density lipoprotein (LDL) cholesterol rises, and high density lipoprotein (HDL) cholesterol does not change or decreases slightly. This is the reason why negative hormones’ effect after menopause increasing more than proportionally. Some authors argue that even influence of estrogen on LDL and HDL level is proved it is yet unclear whether increase in risk is caused, at least partially, by increased level of androgen (the other of hormones belong to steroid as estrogen too), which is characteristics of menopause too. This sexual dimorphism means a lower incidence in atherosclerotic diseases in premenopausal women, which subsequently rises in postmenopausal women to eventually equal that of men. These observations point towards estrogen and progesterone playing a lifetime protective role against CAD in women. As exogenous estrogen and estrogen plus progesterone preparations produce significant reductions in low-density lipoprotein (LDL) cholesterol levels and significant increases in high-density lipoprotein (HDL) cholesterol, this should in theory lower the risk of CAD. UKLOPITI U ONO GORE Among estrogen’s positive effects on the heart are: †¢Reducing the LDL (â€Å"bad†) cholesterol in the blood. †¢Increasing the HDL (â€Å"good†) cholesterol in the blood. †¢Helping to keep blood vessels open. †¢Lowering blood pressure at night. †¢Reducing blood viscosity (how sticky the blood is), a property that may cause blood clots which could result in a heart attack or stroke. Estrogen’s effects on clotting are complicated, however, since there also is an increased risk for thromboembolism (a blood clot that blocks a vessel) in women taking estrogen. Possibly enhancing fibrinolysis, which is the body’s natural process for breaking down blood clots. Read more: http://ehealthmd. com/content/what-are-benefits-hrt#ixzz2NbWR3MxY http://ehealthmd. com/content/what-are-benefits-hrt#axzz2NbW1GJJN Nutrition guidelines As presented before three different groups of risk factor exist. Some of them people can cha nge but the other are fixed, non-changeable because they caused by genetic heritage ( ) influences. Controllable factors are connected to the lifestyle of person. Lifestyle changes can prevent or slow the development of coronary plaque and heart disease. In order to prevent a disease development one have to keep track of his/her blood pressure and cholesterol levels. Choosing a heart-healthy diet is vital in controlling weight, which helps keep blood pressure and cholesterol levels down. Foods high in cholesterol and saturated fat should be avoided, and quitting smoking is imperative. Regular exercise and an increased overall activity level contribute to heart health and help reduce stress. The risk of cardiovascular disease is possible to reduce following recommendation for lifestyle changing: Cessation of smoking and avoidance of second-hand smoke. Nutrition should ensure a healthy diet wiht total diet no more than 8% of saturated + trans fatty acids of total energy intake. All people, especially ones with high risk factors should lower alcohol consumption As the prevention physical activities are recommended – at least 30 minutes of moderate intensity physical activity per day or three days week (i. e. 150 mins/week minimum). Currently practiced measures to prevent cardiovascular disease include: †¢A low-fat, high-fiber diet including whole grains and plenty of fresh fruit and vegetables (at least five portions a day)[29][30] †¢Tobacco cessation and avoidance of second-hand smoke;[29] †¢Limit alcohol consumption to the recommended daily limits;[29] consumption of 1-2 standard alcoholic drinks per day may reduce risk by 30%[31][32] However excessive alcohol intake increases the risk of cardiovascular disease. [33] †¢Lower blood pressures, if elevated, through the use of antihypertensive medications[citation needed]; †¢Decrease body fat (BMI) if overweight or obese;[34] Increase daily activity to 30 minutes of vigorous exercise per day at least five times per week;[29] †¢Decrease psychosocial stress. [35] Stress however plays a relatively minor role in hypertension. [36] Specific relaxation therapies are not supported by the evidence. [37] Routine counselling of adults to advis e them to improve their diet and increase their physical activity has not been found to significantly alter behaviour, and thus is not recommended. [38] http://www. news-medical. net/health/What-is-Cardiovascular-Disease. aspx http://www. barnesandnoble. om/w/prevent-halt-and-reverse-heart-disease-joseph-piscatella/1100260037 Primary and secondary prevention of heart disease It is necessary start with prevention from heart disease as early as possible. Changes in the number of people killed by heart attack in developed countries show that prevention and awareness about this group of disease help to http://circ. ahajournals. org/content/123/20/2274/F2. expansion. html health plans must continue to drive cardiovascular care further along the continuum toward primary prevention of cardiovascular disease (CVD). CVD risk factors should be managed not only after a coronary event has occurred, but also before the onset of such and event. Ideally, health lifestyles should be promoted with all patients so that risk factors for CVD never develop. In this way, CVD care can be moved from the inpatient setting to the outpatient setting. Sidney C. Smith Jr, MD. Focus on Cardiovascular Disease; A Word About the Quality of Care in Cardiovascular Disease. Director, Center for Cardiovascular Science and Medicine University of North Carolina at Chapel Hill. http://www. qualityprofiles. rg/leadership_series/cardiovascular_disease/cardiovascular_introduction. asp Key priorities for implementation Primary prevention of CVD †¢For the primary prevention of CVD in primary care, a systematic strategy should be used to identify people aged 40–74 who are likely to be at high risk †¢People should be prioritised on the basis of an estimate of their CVD risk before a full formal risk assessment. Thei r CVD risk should be estimated using CVD risk factors already recorded in primary care electronic medical records †¢Risk equations should be used to assess CVD risk People should be offered information about their absolute risk of CVD and about the absolute benefits and harms of an intervention over a 10-year period. This information should be in a form that: opresents individualised risk and benefit scenarios opresents the absolute risk of events numerically ouses appropriate diagrams and text (See www. npci. org. uk) †¢Before offering lipid modification therapy for primary prevention, all other modifiable CVD risk factors should be considered and their management optimised if possible. Baseline blood tests and clinical assessment should be performed, and comorbidities and secondary causes of dyslipidaemia should be treated. Assessment should include: osmoking status oalcohol consumption oblood pressure (see ‘Hypertension’, NICE clinical guideline 34) obody mass index or other measure of obesity (see ‘Obesity’, NICE clinical guideline 43) ofasting total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides (if fasting levels are not already available) ofasting blood glucose orenal function oliver function (transaminases) thyroid-stimulating hormone (TSH) if dyslipidaemia is present †¢Statin therapy is recommended as part of the management strategy for the primary prevention of CVD for adults who have a 20% or greater 10-year risk of developing CVD. This level of risk should be estimated using an appropriate risk calculator, or by clinical assessment for people for whom an appropriate risk calculator is not available or approp riate (for example, older people, people with diabetes or people in high-risk ethnic groups) †¢Treatment for the primary prevention of CVD should be initiated with simvastatin 40 mg. If there are potential drug interactions, or simvastatin 40 mg is contraindicated, a lower dose or alternative preparation such as pravastatin may be chosen. Secondary prevention of CVD †¢For secondary prevention, lipid modification therapy should be offered and should not be delayed by management of modifiable risk factors. Blood tests and clinical assessment should be performed, and comorbidities and secondary causes of dyslipidaemia should be treated. Assessment should include: osmoking status oalcohol consumption oblood pressure (see ‘Hypertension’, NICE clinical guideline 34) obody mass index or other measure of obesity (see ‘Obesity’, NICE clinical guideline 43) ofasting total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides (if fasting levels are not already available) ofasting blood glucose orenal function oliver function (transaminases) othyroid-stimulating hormone (TSH) if dyslipidaemia is present. Statin therapy is recommended for adults with clinical evidence of CVD †¢People with acute coronary syndrome should be treated with a higher intensity statin. Any decision to offer a higher intensity statin should take into account the patient’s informed preference, comorbidities, multiple drug therapy, and the benefits and risks of treatment †¢Treatment for the secondary prevention of CVD should be initiated with simvastatin 40 mg. If there are potential drug interactions , or simvastatin 40 mg is contraindicated, a lower dose or alternative preparation such as pravastatin ay be chosen †¢In people taking statins for secondary prevention, consider increasing to simvastatin 80 mg or a drug of similar efficacy and acquisition cost if a total cholesterol of less than 4 mmol/litre or an LDL cholesterol of less than 2 mmol/litre is not attained. Any decision to offer a higher intensity statin should take into account informed preference, comorbidities, multiple drug therapy, and the benefit and risks of treatment http://www. eguidelines. co. uk/eguidelinesmain/guidelines/summaries/cardiovascular/nice_lipid_modification. php How to lower the risk of cardiovascular disease The risk of cardiovascular disease is possible to reduce following recommendation for lifestyle changing: Cessation of smoking and avoidance of second-hand smoke. Nutrition should ensure a healthy diet wiht total diet no more than 8% of saturated + trans fatty acids of total energy intake. All people, especially ones with high risk factors should lower alcohol consumption As the prevention physical activities are recommended – at least 30 minutes of moderate intensity physical activity per day or three days week (i. . 150 mins/week minimum). Cessation of smoking The aim of this measure is complete cessation of smoking and avoidance of second-hand smoke. Patient and their families need to stop smoking. Those who are unable to quit may need professional help in form of counselling, behavioral therapy and even pharmacological therapy. Nicotine replacement therapy (NRT) is the first line choice of medication. Nutrition The aim of thi s measure is to ensure a healthy diet. Total diet should have no more than 8% (of total energy intake) of saturated + trans fatty acids. All patients are advised to take approximately 1g Eicosapentaenoic acid (EPA) and Docosahexaenoic acid (DHA) and more than 2g Alpha Linolenic Acid (ALA) daily. Diet should have vegetables, fruits and legumes, grain-based foods, moderate amounts of lean meats, poultry, fish and reduced fat dairy products. EPA and DHA can be obtained from oily fish and marine n-3 (fish oil) capsule supplements. Alcohol consumption All patients should be advised to lower alcohol consumption. Men should drink no more than 2 standard drinks per day and women no more than 1 standard drink per day. Physical activity The aim of this measure is to raise physical activity and exercise to the recommended goal of at least 30 minutes of moderate intensity physical activity on most, if not all, days of the week (i. e. 150 mins/week minimum). Maintaining a healthy body weight The aim should be to achieve a waist measure of less than or equal to 94 cm in men and less than or equal to 80 cm in women. The body mass index (BMI) should be maintained at 18. 5–24. 9 kg/m2 Lowering blood cholesterol The aim of therapy should be to maintain blood cholesterol at: †¢Low density lipoprotein (LDL) at – less than 2. mmol/L †¢HDL – more than 1. 0 mmol/L †¢Triglyceride (TG) less than 1. 5 mmol/L The blood cholesterol can be maintained with the use of pharmacotherapy. Statins are commonly used lipid lowering drugs. Those with diabetes and atherosclerosis need stringent blood cholesterol control as well. Other lipid lowering drugs include fibrates like gemfibrosil, clofibrates etc, Eze timiber and niacin. Lowering blood pressure High blood pressure is one of the important risk factors for cardiovascular disease. Those with coronary heart disease, diabetes, kidney disease or stroke need tight blood pressure control. The aim should be a blood pressure of less than 130/80 mm of Hg. Diabetes and blood sugar control Those diagnosed with diabetes need stringent blood sugar control to prevent cardiovascular damage. HbA1c levels should be maintained at less than 7%. Other drugs to lower risk of cardiovascular disease Other drugs used to lower risk of cardiovascular diseases include: †¢Antiplatelet agents – this includes Aspirin and Clopidogrel. These drugs when given to patients with risk of heart attacks may prevent such attacks and events. †¢ACE inhibitors like Enalapril, Captopril, Lsinopril and How to cite Cardiovascular Diseases, Essay examples Cardiovascular Diseases Free Essays string(121) " of plaque will increase as the result of high level of cholesterol, type LDL, so called â€Å"bad cholesterol† in blood\." Cardiovascular disease Introduction Heart disease is No. 1 killer disease worldwide. It causes 12 million deaths annually. We will write a custom essay sample on Cardiovascular Diseases or any similar topic only for you Order Now Thanks to the rising health awareness and government programmes this number significantly reduce during last 30 years. Coronary heart disease and cardiovascular disease Cardiovascular diseases are diseases of the heart (cardiac muscle ) or blood vessels (vasculature). Cardiovascular disease (CVD) means all the diseases of the heart and circulation (blood vessels disease) including coronary heart disease (angina and heart attack) and stroke, as well as coronary and periphery blood vessels disease (problems with circulation). Diseases from this group are the biggest killer in Europe and USA, but developing and non-develop countries too. The final and most tragic consequence of different types of heart disease is heart attack with tragic consequences. Heart diseases are caused by atherosclerosis, a disease of arterial blood vessels resulted from atheroma i. . plaques accumulated (forming; sticking) on artery walls which makes the blood vessels nonelastic and narrowed and leads to decreased blood flow. For the atherosclerosis doctors very often use alternative name chronic cardiovascular disease. The opposite group acute heart disease made group of diseases which are dangerous for patients lives. Acute heart diseases include conditions or illnesses wh ich usually have a rapid onset of symptoms and may resolve within days with or without treatment. A condition or illness that is sudden or severe. On the other hand a condition or illness that arises slowly over days or weeks and may or may not resolve with treatment made a group of chronic heart disease. Both of them are caused by atheroma and the most known are next: a) Acute heart disease Heart attack is caused by lack of O2 in heart muscle cells. Very often it is caused by rupture of â€Å"hard plaques† patches which result in blood clots and partially or completely block blood flow and cause a heart attack. When a fiber cap becomes thin, these â€Å"hard plaques† can suddenly rupture, spilling their contents, resulting in blood clots that partially or completely block blood flow and cause a heart attack http://www. authorstream. com/Presentation/nitin-35423-heart-diseases-science-technology-ppt-powerpoint/ Cholesterol glossary. http://www. mybwmc. org/library/28/000225 Stroke Stroke is death of brain cells caused by obstructed blood flow to parts of the brain. Since the level of LDL cholesterol is main cause of narrowed of blood vessels, it is necessary control it. If not treated properly, high LDL cholesterol can cause a stroke. Cholesterol glossary. http://www. mybwmc. org/library/28/000225 b) Coronary heart disease Heart disease (coronary heart disease), When the plaque build up in th conorary arteries heart does not get sufficient blood, the condition is called coronary artery disease or coronary heart disease. Atherosclerosis is a disease of arterial blood vessels in which plaques form on artery walls. This is a consequence of different substances circulating in the bloodstream (inflammatory cells, proteins, cholesterol and calcium) sticking inside the vessel walls. Plaque patches influence on narrowing blood flow in the artery. ttp://www. bodybuilding. com/fun/gastelu5. htm Peripheral artery disease (reduced blood flow in the limbs, usually the legs Coronary plaque Coronary plaque is a term which use in practice as a synonym for atheroma or atherosclerosis. Patches of atheroma are formed from substances that circulate in the bloodstream. They consist of lipid, or fat, cores covered by collagen fiber cap s which are sticking to the inside of the vessel walls. Over time plaque or patch of atheroma increases making an artery narrower and the blood flow through the artery is reducing. We can see the changes in blood vessels caused by plaque in the Figure 1. Figure 1 Artery with the patches of atheroma – plaque Preventing Cardiovascular Diseases. Patient. co. uk. emis www. patient. co. uk/health/Preventing-Cardiovascular-Diseases. htm (March 13, 2013) http://medicineworld. org/blogs/heart/blog/permalinks/Jan-2006/coronary-plaque-detection-by-molecular-imaging. html (March 13, 2013) Mature plaques typically consist of two main components: soft, lipid-rich atheromatous â€Å"gruel† and hard, collagen-rich sclerotic tissue. Lipid-rich and soft plaques are more dangerous than collagen-rich and hard plaques because they are more unstable and rupture-prone and highly thrombogenic after disruption. Researchers have found that many people who have heart attacks do not have arteries narrowed by plaque. Many heart attacks are now known to be caused by soft or vulnerable plaques, located on an inflamed part of an artery. This plaque can burst, leading to the formation of a blood clot that can cause a heart attack. The 2009 issue of â€Å"The American Journal Pathology† edited explanation of those relations discovered by Olga Ovchinnikova and er colleagues. They found that inflammation results in the formation of soft (vulnerable) plaque which is filled with different cell types that promote blood clotting. This leads to a reduction of mature collagen, resulting in thinner caps that are more likely to rupture, even in the cases when total level of plaque isn’t extremely high. The authors advocate d ifferent viewpoints about relations between the plaque level and structure, i. e. its influence on heart attack. The first group claims that described types of blockages cause only about 30 percent of heart attacks. On the other hand, some sources state that more than two-thirds of acute coronary events result from rupture of coronary plaques. However problems that plaque creates are extremely dangerous for people’s life and it is very important to prevent and monitor its appearance and changes. Graphs of vulnerable plaque and rupture of plaque which causes a heart attack is presented below. Figure 2 Vulnerable atherosclerotic plaques. Vulnerable atherosclerotic plaques. A. Atherosclerosis in a chronic disease that leads to plaque rupture and vascular occlusion. B. Cross-section of a lethal coronary plaque rupture. Adapted from Heistad D. Unstable coronary-artery plaques. N Engl J Med. 2003. Atherosclerosis Modeling In-vitro. http://www. remedi. uzh. ch/research/disease. html Figure 3 Plaque Rupture and Heart attack http://hon. nucleusinc. com/generateexhibit. php? ID=30468A=1027 Factors influencing plaque growth and stability Based on everything mentioned above and medical experience the conclusion about relations between heart attack and other cardiovascular disease and the level of plaque increasing are found. The higher the level of plaque the higher risk of heart disease will be. The level of plaque will increase as the result of high level of cholesterol, type LDL, so called â€Å"bad cholesterol† in blood. You read "Cardiovascular Diseases" in category "Papers" When the level of LDL is normal, blood can pass in and out of the blood vessels without problems, but if it significantly increase particles of the blood will accumulate and sooner or later provoke trigger (cause) heart attack. Other very important factors influencing plaque level increasing are high blood pressure and cigarette smoking. Both factors accelerate the plaque formation changing (damaging) artery walls and even more, helping cholesterol forming. Medical experience proved that plaque composition and vulnerability (hard or soft plaque) is more responsible for the conversion of a stable disease to a life-threatening condition than the plaque size. Except the plaque vulnerability the risk of plaque disruption is are consequence of rupture triggers (extrinsic forces). Soft plaque – lipid-rich one is more dangerous because of its instability and higher probability for rupture. Even (IAKO) Although â€Å"hard plaque† that one having higher level of calcium influence on the blood vessels walls and their â€Å"hardness† experience show that heart attacks are mostly caused by soft plaque disruption. Figure 4 Plaque rupture and its consequences in the form of heart diseases http://www. nature. com/nrg/journal/v7/n3/fig_tab/nrg1805_F2. html Risk factors of coronary heart disease Risk factors influencing cardiovascular disease we can group based on their stability into the three groups: a) Modifiable risk factors In this group hypertension is the most dangerous risk factor for heart attacks, but even more for stroke. It is forming as the result of abnormal blood lipid levels which means high total cholesterol, high levels of triglycerides and high levels of low-density lipoprotein or low levels of high-density lipoprotein (HDL). Smoking, physical inactivity, Type 2 diabetes, and a diet full with saturated fats are risk factors strongly influencing the heart disease. All of them are treatable and patients (individuals) belonging into the different types of risk customers’ groups should avoid practice them. b) Non-modifiable risk factors The factors from this group mostly are constant, like the case in gender or family history. Others are changing when time is passing, like age and lifestyle and personal habits. Older people have more chance to get heart attack and the man, especially those having â€Å"bad medical history†. Ration between man and woman are changing when women past the menopause. After that the level of risk is similar as the men’s one. As I’ve presented there is direct correlation between cardiovascular disease and condition and health of blood vessels, more precisely of developing atheroma, means level and structure of plaque in vessels. On the other development of plaque and its level is directly influenced by level of cholesterol and some other elements which are connected with individual person and his/her life and genetic predispositions. As with the other diseases everybody has some risk of developing atheroma, but some risk factors increase the risk level for several categories. Those risk factors include: fn 12 †¢Fixed risk factors – factors that person cannot change: oA strong family history which means close relatives who developed heart disease or a stroke before they were 55 (for males) or 65 (for female). Severe baldness in men at the top of the head. oAn early menopause in women. oAge. Older people have more risk to develop atheroma. oEthnic group. Medical data show that people from different ethnic group have different risk for heart diseases. †¢Treatable or partly treatable risk factors include different health problems caused basically by the same causes as the: oHypertension (high bl ood pressure). oHigh cholesterol blood level. oHigh triglyceride (fat) blood level. oDiabetes. oKidney diseases causing diminished kidney function. All factors from this group have to be controlled and monitor. Any kind of their complication probably will trigger more serious problems such as heart attack or stroke. †¢Lifestyle risk factors that can be prevented or changed. Actually these factors PRETHODE precede to those belonging to the second group. Except the genetic factors way of life and daily habits are the more responsible for different kind of heart diseases. Those factors are: oSmoking (Smoking cigarette increase blood pressure, decrease HDL; damages arteries and blood cells and increases heart attacks. Passive smoking is also a risk factor for cardiovascular disease ) oLack of physical activity. Obesity (People who are overweight (10-30% more than their normal body weight) have 2 to 6 times the risk of developing heart disease. ) oAn unhealthy diet and eating too much salt. oExcess alcohol. Looking on those three groups one can easily conclude that people with â€Å"bad predisposition† having high fixed risk factors have to think about their lifestyle risk factors ev en more, in order to try to decrease the second group of factors (treatable or partly treatable risk factors). On the other hand some of risks are more dangerous than the others; for example smoking increases risk for heart disease more than obesity. And of course combination of two or more risk factors increases significantly the level of risks; older man (or woman) who smokes, without physical activity and with bad eating habits has more chance to get some of previously explained disease than the one who have â€Å"just one of bad habits†. The more risk factors someone has the greater is the likelihood that he/she will develop cardiovascular disease, unless taking action to modify his/her risk factors and working to prevent them compromising his/her heart health. That doesn’t mean that people with â€Å"good genes† can be irresponsible and ZANEMARITI risk factors from other groups. With or without genetic predisposition modern life significantly increases a risk of heart disease for everybody. Hormones impact on lipids and other risk factors Different numbers of man and women died from heart attack initiated a lot of research about hormones’ influence on the risk factor and heart disease development. Number of men died from the heart attack outnumbered the number of women in pre-menopause period, but in the post-menopause data show completely opposite situation. A percentage of women in post-menopause having heart disease and dying from heart attack increase dramatically and now outnumbered the men. The main reasons for those changes are connected to the level of hormones and their influence on level and structure of cholesterol and consequently on risk factors and heart disease. As mentioned before total cholesterol actually is made of two different types of cholesterol: LDL – low density lipoprotein (LDL), so called bad cholesterol and high density lipoprotein (HDL). High levels of LDL cholesterol lead to atherosclerosis increasing the risk of heart attack and ischemic stroke. HDL cholesterol reduces the risk of cardiovascular disease as it carries cholesterol away from the blood stream. http://www. walgreens. com/marketing/library/careguides/careguide. jsp? docid=000225=28=High%20Cholesterol Estrogen, a female hormone, raises HDL cholesterol levels, partially explaining the lower risk of cardiovascular disease seen in premenopausal women. But after menopause (natural or surgical) when a level of estrogen significantly decreases total cholesterol rises, low density lipoprotein (LDL) cholesterol rises, and high density lipoprotein (HDL) cholesterol does not change or decreases slightly. This is the reason why negative hormones’ effect after menopause increasing more than proportionally. Some authors argue that even influence of estrogen on LDL and HDL level is proved it is yet unclear whether increase in risk is caused, at least partially, by increased level of androgen (the other of hormones belong to steroid as estrogen too), which is characteristics of menopause too. This sexual dimorphism means a lower incidence in atherosclerotic diseases in premenopausal women, which subsequently rises in postmenopausal women to eventually equal that of men. These observations point towards estrogen and progesterone playing a lifetime protective role against CAD in women. As exogenous estrogen and estrogen plus progesterone preparations produce significant reductions in low-density lipoprotein (LDL) cholesterol levels and significant increases in high-density lipoprotein (HDL) cholesterol, this should in theory lower the risk of CAD. UKLOPITI U ONO GORE Among estrogen’s positive effects on the heart are: †¢Reducing the LDL (â€Å"bad†) cholesterol in the blood. †¢Increasing the HDL (â€Å"good†) cholesterol in the blood. †¢Helping to keep blood vessels open. †¢Lowering blood pressure at night. †¢Reducing blood viscosity (how sticky the blood is), a property that may cause blood clots which could result in a heart attack or stroke. Estrogen’s effects on clotting are complicated, however, since there also is an increased risk for thromboembolism (a blood clot that blocks a vessel) in women taking estrogen. Possibly enhancing fibrinolysis, which is the body’s natural process for breaking down blood clots. Read more: http://ehealthmd. com/content/what-are-benefits-hrt#ixzz2NbWR3MxY http://ehealthmd. com/content/what-are-benefits-hrt#axzz2NbW1GJJN Nutrition guidelines As presented before three different groups of risk factor exist. Some of them people can cha nge but the other are fixed, non-changeable because they caused by genetic heritage ( ) influences. Controllable factors are connected to the lifestyle of person. Lifestyle changes can prevent or slow the development of coronary plaque and heart disease. In order to prevent a disease development one have to keep track of his/her blood pressure and cholesterol levels. Choosing a heart-healthy diet is vital in controlling weight, which helps keep blood pressure and cholesterol levels down. Foods high in cholesterol and saturated fat should be avoided, and quitting smoking is imperative. Regular exercise and an increased overall activity level contribute to heart health and help reduce stress. The risk of cardiovascular disease is possible to reduce following recommendation for lifestyle changing: Cessation of smoking and avoidance of second-hand smoke. Nutrition should ensure a healthy diet wiht total diet no more than 8% of saturated + trans fatty acids of total energy intake. All people, especially ones with high risk factors should lower alcohol consumption As the prevention physical activities are recommended – at least 30 minutes of moderate intensity physical activity per day or three days week (i. e. 150 mins/week minimum). Currently practiced measures to prevent cardiovascular disease include: †¢A low-fat, high-fiber diet including whole grains and plenty of fresh fruit and vegetables (at least five portions a day)[29][30] †¢Tobacco cessation and avoidance of second-hand smoke;[29] †¢Limit alcohol consumption to the recommended daily limits;[29] consumption of 1-2 standard alcoholic drinks per day may reduce risk by 30%[31][32] However excessive alcohol intake increases the risk of cardiovascular disease. [33] †¢Lower blood pressures, if elevated, through the use of antihypertensive medications[citation needed]; †¢Decrease body fat (BMI) if overweight or obese;[34] Increase daily activity to 30 minutes of vigorous exercise per day at least five times per week;[29] †¢Decrease psychosocial stress. [35] Stress however plays a relatively minor role in hypertension. [36] Specific relaxation therapies are not supported by the evidence. [37] Routine counselling of adults to advis e them to improve their diet and increase their physical activity has not been found to significantly alter behaviour, and thus is not recommended. [38] http://www. news-medical. net/health/What-is-Cardiovascular-Disease. aspx http://www. barnesandnoble. om/w/prevent-halt-and-reverse-heart-disease-joseph-piscatella/1100260037 Primary and secondary prevention of heart disease It is necessary start with prevention from heart disease as early as possible. Changes in the number of people killed by heart attack in developed countries show that prevention and awareness about this group of disease help to http://circ. ahajournals. org/content/123/20/2274/F2. expansion. html health plans must continue to drive cardiovascular care further along the continuum toward primary prevention of cardiovascular disease (CVD). CVD risk factors should be managed not only after a coronary event has occurred, but also before the onset of such and event. Ideally, health lifestyles should be promoted with all patients so that risk factors for CVD never develop. In this way, CVD care can be moved from the inpatient setting to the outpatient setting. Sidney C. Smith Jr, MD. Focus on Cardiovascular Disease; A Word About the Quality of Care in Cardiovascular Disease. Director, Center for Cardiovascular Science and Medicine University of North Carolina at Chapel Hill. http://www. qualityprofiles. rg/leadership_series/cardiovascular_disease/cardiovascular_introduction. asp Key priorities for implementation Primary prevention of CVD †¢For the primary prevention of CVD in primary care, a systematic strategy should be used to identify people aged 40–74 who are likely to be at high risk †¢People should be prioritised on the basis of an estimate of their CVD risk before a full formal risk assessment. Thei r CVD risk should be estimated using CVD risk factors already recorded in primary care electronic medical records †¢Risk equations should be used to assess CVD risk People should be offered information about their absolute risk of CVD and about the absolute benefits and harms of an intervention over a 10-year period. This information should be in a form that: opresents individualised risk and benefit scenarios opresents the absolute risk of events numerically ouses appropriate diagrams and text (See www. npci. org. uk) †¢Before offering lipid modification therapy for primary prevention, all other modifiable CVD risk factors should be considered and their management optimised if possible. Baseline blood tests and clinical assessment should be performed, and comorbidities and secondary causes of dyslipidaemia should be treated. Assessment should include: osmoking status oalcohol consumption oblood pressure (see ‘Hypertension’, NICE clinical guideline 34) obody mass index or other measure of obesity (see ‘Obesity’, NICE clinical guideline 43) ofasting total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides (if fasting levels are not already available) ofasting blood glucose orenal function oliver function (transaminases) thyroid-stimulating hormone (TSH) if dyslipidaemia is present †¢Statin therapy is recommended as part of the management strategy for the primary prevention of CVD for adults who have a 20% or greater 10-year risk of developing CVD. This level of risk should be estimated using an appropriate risk calculator, or by clinical assessment for people for whom an appropriate risk calculator is not available or approp riate (for example, older people, people with diabetes or people in high-risk ethnic groups) †¢Treatment for the primary prevention of CVD should be initiated with simvastatin 40 mg. If there are potential drug interactions, or simvastatin 40 mg is contraindicated, a lower dose or alternative preparation such as pravastatin may be chosen. Secondary prevention of CVD †¢For secondary prevention, lipid modification therapy should be offered and should not be delayed by management of modifiable risk factors. Blood tests and clinical assessment should be performed, and comorbidities and secondary causes of dyslipidaemia should be treated. Assessment should include: osmoking status oalcohol consumption oblood pressure (see ‘Hypertension’, NICE clinical guideline 34) obody mass index or other measure of obesity (see ‘Obesity’, NICE clinical guideline 43) ofasting total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides (if fasting levels are not already available) ofasting blood glucose orenal function oliver function (transaminases) othyroid-stimulating hormone (TSH) if dyslipidaemia is present. Statin therapy is recommended for adults with clinical evidence of CVD †¢People with acute coronary syndrome should be treated with a higher intensity statin. Any decision to offer a higher intensity statin should take into account the patient’s informed preference, comorbidities, multiple drug therapy, and the benefits and risks of treatment †¢Treatment for the secondary prevention of CVD should be initiated with simvastatin 40 mg. If there are potential drug interactions , or simvastatin 40 mg is contraindicated, a lower dose or alternative preparation such as pravastatin ay be chosen †¢In people taking statins for secondary prevention, consider increasing to simvastatin 80 mg or a drug of similar efficacy and acquisition cost if a total cholesterol of less than 4 mmol/litre or an LDL cholesterol of less than 2 mmol/litre is not attained. Any decision to offer a higher intensity statin should take into account informed preference, comorbidities, multiple drug therapy, and the benefit and risks of treatment http://www. eguidelines. co. uk/eguidelinesmain/guidelines/summaries/cardiovascular/nice_lipid_modification. php How to lower the risk of cardiovascular disease The risk of cardiovascular disease is possible to reduce following recommendation for lifestyle changing: Cessation of smoking and avoidance of second-hand smoke. Nutrition should ensure a healthy diet wiht total diet no more than 8% of saturated + trans fatty acids of total energy intake. All people, especially ones with high risk factors should lower alcohol consumption As the prevention physical activities are recommended – at least 30 minutes of moderate intensity physical activity per day or three days week (i. . 150 mins/week minimum). Cessation of smoking The aim of this measure is complete cessation of smoking and avoidance of second-hand smoke. Patient and their families need to stop smoking. Those who are unable to quit may need professional help in form of counselling, behavioral therapy and even pharmacological therapy. Nicotine replacement therapy (NRT) is the first line choice of medication. Nutrition The aim of thi s measure is to ensure a healthy diet. Total diet should have no more than 8% (of total energy intake) of saturated + trans fatty acids. All patients are advised to take approximately 1g Eicosapentaenoic acid (EPA) and Docosahexaenoic acid (DHA) and more than 2g Alpha Linolenic Acid (ALA) daily. Diet should have vegetables, fruits and legumes, grain-based foods, moderate amounts of lean meats, poultry, fish and reduced fat dairy products. EPA and DHA can be obtained from oily fish and marine n-3 (fish oil) capsule supplements. Alcohol consumption All patients should be advised to lower alcohol consumption. Men should drink no more than 2 standard drinks per day and women no more than 1 standard drink per day. Physical activity The aim of this measure is to raise physical activity and exercise to the recommended goal of at least 30 minutes of moderate intensity physical activity on most, if not all, days of the week (i. e. 150 mins/week minimum). Maintaining a healthy body weight The aim should be to achieve a waist measure of less than or equal to 94 cm in men and less than or equal to 80 cm in women. The body mass index (BMI) should be maintained at 18. 5–24. 9 kg/m2 Lowering blood cholesterol The aim of therapy should be to maintain blood cholesterol at: †¢Low density lipoprotein (LDL) at – less than 2. mmol/L †¢HDL – more than 1. 0 mmol/L †¢Triglyceride (TG) less than 1. 5 mmol/L The blood cholesterol can be maintained with the use of pharmacotherapy. Statins are commonly used lipid lowering drugs. Those with diabetes and atherosclerosis need stringent blood cholesterol control as well. Other lipid lowering drugs include fibrates like gemfibrosil, clofibrates etc, Eze timiber and niacin. Lowering blood pressure High blood pressure is one of the important risk factors for cardiovascular disease. Those with coronary heart disease, diabetes, kidney disease or stroke need tight blood pressure control. The aim should be a blood pressure of less than 130/80 mm of Hg. Diabetes and blood sugar control Those diagnosed with diabetes need stringent blood sugar control to prevent cardiovascular damage. HbA1c levels should be maintained at less than 7%. Other drugs to lower risk of cardiovascular disease Other drugs used to lower risk of cardiovascular diseases include: †¢Antiplatelet agents – this includes Aspirin and Clopidogrel. These drugs when given to patients with risk of heart attacks may prevent such attacks and events. †¢ACE inhibitors like Enalapril, Captopril, Lsinopril and How to cite Cardiovascular Diseases, Papers