http://WWW.HEARTDIABETESCARE.COM
SAMIKSHAHEARTCARE 57698d5b9ec66b0b6cfb5b6b False 536 1
OK
background image not found
Found Update results for
'population'
5
BEST CARDIOLOGY HOSPITALS IN BANGALORE Cardiac failure Cardiac failure is an increasingly common condition affecting about 1% of the population but much higher proportions of older people. It is responsible for an increasing number of hospital admissions. The various aetiologies have been discussed above, but the most common cause is now ischaemic heart disease rather than hypertensive heart disease. This reflects the improved modern management of hypertension in the population. The definition of heart failure has always included reference to the inability of the heart to meet the metabolic needs of the body. The earliest concepts of heart failure were of inadequate cardiac pump function and associated salt and water retention. Treatment was aimed at improving cardiac contractility and removing salt and water from the body. In the 1970s the concept of after-load reduction was introduced. This was based partly on the realisation that vasoconstriction was part of the problem. This has led to the modern neuro-hormonal concept of heart failure. It is clear that many of the features of cardiac failure are a result of stimulation of the renin-angiotensin-aldosterone system and sympathetic stimulation. These responses of the body to the fall in cardiac output temporarily increase cardiac performance and blood pressure by increasing vascular volumes, cardiac contractility and systemic resistance. In the medium and longer term these responses are maladaptive. They increase cardiac work and left ventricular volumes and lead to myocardial fibrosis with further loss of myocytes. Most recently it has become clear that heart failure is also an inflammatory condition, with evidence of cytokine activation. Work is underway to establish a role for treatment of this part of the condition. Current drug treatment has been successful in blocking many of the maladaptive aspects of neuro-hormonal stimulation. Many of these treatments have become established after benefits have been ascertained in large randomised controlled trials. These trials have also led to the abandoning of certain drugs (often those that increase cardiac performance) that were shown to have a detrimental effect on survival (e.g. Milrinone). The principles of treatment of heart failure are as follows: 1 Remove the exacerbating factors. 2 Relieve fluid retention. 3 Improve left ventricular function and reduce cardiac work; improve prognosis. 4 Protect against the adverse effects of drug treatment. 5 Assess for further management (e.g. revascularisation, transplant). 6 Manage complications (e.g. arrhythmias). 7 Protect high-risk patients from sudden death.
HEART SPECIALISTS IN HEBBALABANGALORE Case-based learning: cardiovascular risk assessment Mr RF is 60 years old and presents for a check-up because he is concerned he may be at risk of heart disease. Objectives for the group to understand How should this type of request be managed What can be done to assess an individual’s future cardiac risk, and what can be done to improve the prognosis for those at increased risk Epidemiology and population health The presenter should ask the group to consider the concept of risk factors for cardiovascular disease and the differences between population risk factors and those for an individual. How did the concept of risk factors arise Presenting symptoms and clinical examination What questions should be asked of Mr RF to begin the risk factor assessment 1 Is there a history of ischaemic heart disease or symptoms of heart disease 2 Has his cholesterol level been checked in the past What was itHas it been treated with diet or drugs, or both Has the level improved 3 Is he a diabetic, or has he had an abnormal blood sugar measurement 4 Is there a history of high blood pressure Has this been treated If so, how 5 Is there a history of heart disease in the familIf so, who has been affected and at what age 6 Does he smoke? How many cigarettes a day If he has ceased smoking, when did he stop 7 Does he exercise regularly 8 Have any cardiac investigations been performed before What were the results 9 Is there a history of peripheral arterial disease (claudication) or erectile dysfunction The group should appreciate that considerable information about risk can be obtained by asking simple questions. What physical examination should be performed
DIABETIC CLINICS IN DODDABALLAPUR ROAD BAMNGALORE Low-density lipoproteins Sixty to seventy per cent of total cholesterol is transported as LDL, and total cholesterol measurements usually reflect LDL levels. In both males and females, coronary heart disease risk is proportional to LDL and total cholesterol. As seen above, LDL supplies cholesterol to peripheral tissues. High concentrations of LDL in the serum accelerate atheroma by interacting with damaged endothelium. Oxidation of LDL accelerates this process. A total cholesterol of 5.5 mmol/L, or LDL of 3.5 mmol/L, is usually considered the upper limit of normal but even these levels seem to be responsible for an increased population risk of atheroma. Populations with lower average levels than these have less coronary disease. Lower levels are beneficial for patients with established coronary disease or multiple risk factors. It is not yet clear whether the lowering of total cholesterol to less than 4.0 (LDL 2.0) provides further benefit or whether a target level is indeed the correct approach. Trials of more aggressive cholesterol lowering are underway.14 Although a reduced HDL level (< 1) is associated with increased risk, there is no evidence as yet that raising HDL has beneficial effects. An elevation of triglyceride levels (> 1.7) is also considered a marker of increased risk, but there is no evidence to what level they should be reduced. Exogenous
DIABETIC CLINICS IN DODDABALLAPUR ROAD BAMNGALORE Low-density lipoproteins Sixty to seventy per cent of total cholesterol is transported as LDL, and total cholesterol measurements usually reflect LDL levels. In both males and females, coronary heart disease risk is proportional to LDL and total cholesterol. As seen above, LDL supplies cholesterol to peripheral tissues. High concentrations of LDL in the serum accelerate atheroma by interacting with damaged endothelium. Oxidation of LDL accelerates this process. A total cholesterol of 5.5 mmol/L, or LDL of 3.5 mmol/L, is usually considered the upper limit of normal but even these levels seem to be responsible for an increased population risk of atheroma. Populations with lower average levels than these have less coronary disease. Lower levels are beneficial for patients with established coronary disease or multiple risk factors. It is not yet clear whether the lowering of total cholesterol to less than 4.0 (LDL 2.0) provides further benefit or whether a target level is indeed the correct approach. Trials of more aggressive cholesterol lowering are underway.14 Although a reduced HDL level (< 1) is associated with increased risk, there is no evidence as yet that raising HDL has beneficial effects. An elevation of triglyceride levels (> 1.7) is also considered a marker of increased risk, but there is no evidence to what level they should be reduced. Exogenous
Diabetologists in Sahakara Nagar, Bangalore • Low-density lipoproteins Sixty to seventy per cent of total cholesterol is transported as LDL, and total cholesterol measurements usually reflect LDL levels. In both males and females, coronary heart disease risk is proportional to LDL and total cholesterol. As seen above, LDL supplies cholesterol to peripheral tissues. High concentrations of LDL in the serum accelerate atheroma by interacting with damaged endothelium. Oxidation of LDL accelerates this process. A total cholesterol of 5.5 mmol/L, or LDL of 3.5 mmol/L, is usually considered the upper limit of normal but even these levels seem to be responsible for an increased population risk of atheroma. Populations with lower average levels than these have less coronary disease. Lower levels are beneficial for patients with established coronary disease or multiple risk factors. It is not yet clear whether the lowering of total cholesterol to less than 4.0 (LDL 2.0) provides further benefit or whether a target level is indeed the correct approach. Trials of more aggressive cholesterol lowering are underway.14 Although a reduced HDL level (< 1) is associated with increased risk, there is no evidence as yet that raising HDL has beneficial effects. An elevation of triglyceride levels (> 1.7) is also considered a marker of increased risk, but there is no evidence to what level they should be reduced. Exogenous Endogenous Chylom. (TG & Chol.) LDL receptor tissues HDL and FFA Endogenous chol. Endothelium (Lipoprotein lipase) Endothelium (Lipoprotein lipase) FFA FFA LDL IDL LIVER Plasma LCAT VLDL Monog. Chylomic. remnant (Chol.) Intestinal cell Carries 3/4 of total chol. Dietary TG
1
false