Risk scoriilg is an instrument to assess both the relative risk as well as the absolute risk of developing Cardio-vascular disease and moltality in an individual. As told earlier, co-existence oC multiple lisk factol-s magnifies the risk of CAD in an exponenlial manner. This has given rise to the concept of co~llprehensive Cardio-vascular risk or total risk score, quantil'ying an individual's overall rislc of developing CVD because of the confluence of risk factors. In risk scoring the weightage given to different risk factors are summed up to get the final score which in turn indicates the probability of the disease. There are different methods of risk scoring - some use mathematical model, some usc charts and some use computer programmes. The risk factor variables used in calculation also differ among the various methods. However all of them give some idea about the rclativePreventive Cardiology al~d the absolute risk and help in taking a decision about the preventive nleasclres and drug treatment.
Relative risk is the ratio of the likelihood of CAD developing in persons with and without a given risk factpr or at a given intensity of a risk factor. Absolute iisk is the probability of developing CAD in a finite period, e.g., within the next ten years. In a sense, relative risk reflects the rate at which a person is accruing absolute risk. Serunl cholesterol data provide a good exainple of the difference between relative and absolute risk. A young person with a high serum cholesterol level carries a low absolute risk for CAD but has a high relative risk compared with.another yourlg with a low serum cholesterol level. The 11y percholesteroleinic young adult is unlikely to develop CAD in the next ten years, but his or her chances of having premature CAD in the long-tern~ (e.g. before age 65) are high.
Long-term follow-up data from Flamingham confirnl this concept: cholesterol levels measured in young adulthood are inversely associated with life expectancy.Results from other studies also support the concept that a high relative risk in young adulthood is transformed into a high absolute iisk in the long run. The goal fer reducing elevated serum cholesterol in young adults thus is to retard atherogenesis throliglaout life, not to prevent myocardial infarction in the next decade. This aiin justifies efforts to detect elevated serum cholesterol in young aduits advising lifestyle anodificntion. There is a misconception on the part of some investigators t.hat absolute risk for CAD can be allnost fully reversed by therapy initiated after atherosclerosis has become aggressive cl~oles~erol-1oweri~1g ad~arnced. Certailsly redaction of serum cholesterol levels in patients with advanced atherosclerc~tic disease does substantially reduce morbidity and mortality froan CAD but the persistently high rate of coronary events even in those patients who receive cholesterol-lowering dnigs reveals that risk cannot be fuilly reversed.
Risk scoling is essential for planning the line of management of a patient. The Framinghain risk scoring was the first such method - which took six va~iables to predict the 10 and 20 year risk of CAD. Framinghain risk scorcs furnish two ways to estimate relative ~isk. One compares a given individual's esti~natecl risk with the absolute risk of an individual at low risk, i.e., a person who is largely without risk factors. The other compares a given individual's estimated risk with the risk of an average person of the sanae age and sex. The latter ratio is coininonly used,although it tends to underestimate the preventable coinponent of coronary risk. A better way to assess the full potential for risk reduction, when introduced relatively early in life, is to compare estimated absolute risk with truly low risk. Total excess risk for an individual patient can be estimated by subtracting that person's absolute risk from the absolute risk of a person of the same age and sex who is at low iisk.
Absolute iisk assessment charts are now included with many guidelines to enable clinicians (and their patients) rapidly to measure a patient's absolute risk of coronary heart disease or Cardio-vascular disease. The current Joint British chat and New Zealand chart are similar in concept, both having been strongly influenced by the 1994 Joint European societies' charts. Both incorporate the same age categories and risk factors, with blood pressure and the total cholesterol: high density lipoprotein cholesterolratio presented as co~atinuous vaiiables. While the New Zealand chat assesses five year risk of all Cardio-vascular disease in eight discrete categories, the Joint British chart assesses ten year risk of coronaiy heart disease in three risk bands. As well as iisk, the IVew Zealand charts enable one to estimate the five year benefit of treatment, expressed as events prevented per I00 patients treated and as the number of patients needing treatment (NNT) for five years to prevent one event. The Sheffield tables, which were specifically designedto target lipid lowering therapy to patients at high absolute risk, simplify treatment decisioils by using a truncated risk factor set and by enabling estimation of risk above specified treatment cut off 1evel.s. Eloodpressure levels are dichotomised,and only the most recent version of the tabies include high density lipoprotein cholesterol. Like the Joint British charts, the Sheffield tables estimate the ten year risk of coronary heart disease.
All the risk charts mentioned above used risk prediction equations dcrived from the Framingham heart study. The Framingham risk score is widely used but it has certain limitations. Framingham equations can predict coronary lisk with reasonable accuracy in white men and women in the Europe and USA. However,little is known about the charts' predictive validity in high risk groups such as South Asians, Polynesians, or African Americans. One must understand that the ethnic variations in the risk factor effect will int-luence the calculated risk in different ethnic groups. For the Indians, the cut-off point for cholesterol level,weight, waist hip ratio generally underestimate the risk of CAD and the threshold need to be lowered for risk estimation.
Relative risk is the ratio of the likelihood of CAD developing in persons with and without a given risk factpr or at a given intensity of a risk factor. Absolute iisk is the probability of developing CAD in a finite period, e.g., within the next ten years. In a sense, relative risk reflects the rate at which a person is accruing absolute risk. Serunl cholesterol data provide a good exainple of the difference between relative and absolute risk. A young person with a high serum cholesterol level carries a low absolute risk for CAD but has a high relative risk compared with.another yourlg with a low serum cholesterol level. The 11y percholesteroleinic young adult is unlikely to develop CAD in the next ten years, but his or her chances of having premature CAD in the long-tern~ (e.g. before age 65) are high.
Long-term follow-up data from Flamingham confirnl this concept: cholesterol levels measured in young adulthood are inversely associated with life expectancy.Results from other studies also support the concept that a high relative risk in young adulthood is transformed into a high absolute iisk in the long run. The goal fer reducing elevated serum cholesterol in young adults thus is to retard atherogenesis throliglaout life, not to prevent myocardial infarction in the next decade. This aiin justifies efforts to detect elevated serum cholesterol in young aduits advising lifestyle anodificntion. There is a misconception on the part of some investigators t.hat absolute risk for CAD can be allnost fully reversed by therapy initiated after atherosclerosis has become aggressive cl~oles~erol-1oweri~1g ad~arnced. Certailsly redaction of serum cholesterol levels in patients with advanced atherosclerc~tic disease does substantially reduce morbidity and mortality froan CAD but the persistently high rate of coronary events even in those patients who receive cholesterol-lowering dnigs reveals that risk cannot be fuilly reversed.
Risk scoling is essential for planning the line of management of a patient. The Framinghain risk scoring was the first such method - which took six va~iables to predict the 10 and 20 year risk of CAD. Framinghain risk scorcs furnish two ways to estimate relative ~isk. One compares a given individual's esti~natecl risk with the absolute risk of an individual at low risk, i.e., a person who is largely without risk factors. The other compares a given individual's estimated risk with the risk of an average person of the sanae age and sex. The latter ratio is coininonly used,although it tends to underestimate the preventable coinponent of coronary risk. A better way to assess the full potential for risk reduction, when introduced relatively early in life, is to compare estimated absolute risk with truly low risk. Total excess risk for an individual patient can be estimated by subtracting that person's absolute risk from the absolute risk of a person of the same age and sex who is at low iisk.
Absolute iisk assessment charts are now included with many guidelines to enable clinicians (and their patients) rapidly to measure a patient's absolute risk of coronary heart disease or Cardio-vascular disease. The current Joint British chat and New Zealand chart are similar in concept, both having been strongly influenced by the 1994 Joint European societies' charts. Both incorporate the same age categories and risk factors, with blood pressure and the total cholesterol: high density lipoprotein cholesterolratio presented as co~atinuous vaiiables. While the New Zealand chat assesses five year risk of all Cardio-vascular disease in eight discrete categories, the Joint British chart assesses ten year risk of coronaiy heart disease in three risk bands. As well as iisk, the IVew Zealand charts enable one to estimate the five year benefit of treatment, expressed as events prevented per I00 patients treated and as the number of patients needing treatment (NNT) for five years to prevent one event. The Sheffield tables, which were specifically designedto target lipid lowering therapy to patients at high absolute risk, simplify treatment decisioils by using a truncated risk factor set and by enabling estimation of risk above specified treatment cut off 1evel.s. Eloodpressure levels are dichotomised,and only the most recent version of the tabies include high density lipoprotein cholesterol. Like the Joint British charts, the Sheffield tables estimate the ten year risk of coronary heart disease.
All the risk charts mentioned above used risk prediction equations dcrived from the Framingham heart study. The Framingham risk score is widely used but it has certain limitations. Framingham equations can predict coronary lisk with reasonable accuracy in white men and women in the Europe and USA. However,little is known about the charts' predictive validity in high risk groups such as South Asians, Polynesians, or African Americans. One must understand that the ethnic variations in the risk factor effect will int-luence the calculated risk in different ethnic groups. For the Indians, the cut-off point for cholesterol level,weight, waist hip ratio generally underestimate the risk of CAD and the threshold need to be lowered for risk estimation.
Long-term Risk Estimation
Many studies have exalnined long-term risks associated with risk factors using traditional epide~niologiciil methods. FI-al-ningham investigalors exalllined lnell and women between 40 to 50 and followed them up to find out their overall survival and CVD free survival a1 85 years and beyond. Factors associated with survival to age 85 included f~lnale gender, lower systolic BP, IOMWI' tot01 cholesterol, better glucose tolerance, no current stnoking and higher level of education attained. In presence of adverse levels of four of these factors in middle age, fewer than 5 per cent of lnen and 15 per cent of women survived to age 85.In another study, men and women with a low risk factor burden (serum cholesterol < 200mg/dl, untreated BP 5 120/80 mmHg, no current stnoking, ~ z o diabetes and no major ECG abnormalities) in middle age had 73-85 per cent lower iislt of' CVD mortality, 40-60 per cent lower total mortality and 6-10 years greater life expectancy.
The Chicago Heart Association Detection Project in Iildustiy have shown that risk factor burden in middle age is associated with quality of life at follow-up in older age. A Finnish study also observed that cholesterol levels in middle agcd men were associated with total mortality and quality of life over 39 years of follow-up.When taken together, all these studies confirm long-term protection with low risk factor burden and substantial long-term risks associated with adverse baseline values of CVD risk factors.
Many studies have exalnined long-term risks associated with risk factors using traditional epide~niologiciil methods. FI-al-ningham investigalors exalllined lnell and women between 40 to 50 and followed them up to find out their overall survival and CVD free survival a1 85 years and beyond. Factors associated with survival to age 85 included f~lnale gender, lower systolic BP, IOMWI' tot01 cholesterol, better glucose tolerance, no current stnoking and higher level of education attained. In presence of adverse levels of four of these factors in middle age, fewer than 5 per cent of lnen and 15 per cent of women survived to age 85.In another study, men and women with a low risk factor burden (serum cholesterol < 200mg/dl, untreated BP 5 120/80 mmHg, no current stnoking, ~ z o diabetes and no major ECG abnormalities) in middle age had 73-85 per cent lower iislt of' CVD mortality, 40-60 per cent lower total mortality and 6-10 years greater life expectancy.
The Chicago Heart Association Detection Project in Iildustiy have shown that risk factor burden in middle age is associated with quality of life at follow-up in older age. A Finnish study also observed that cholesterol levels in middle agcd men were associated with total mortality and quality of life over 39 years of follow-up.When taken together, all these studies confirm long-term protection with low risk factor burden and substantial long-term risks associated with adverse baseline values of CVD risk factors.
Lifetime Risk Estimation
Traditional statistical and epidemiological methods of estimating long-term risks do not accurately reflect population burden of disease. The long-term risk estimation is also problematic because they do not accoullt for competing ri& that hecome increasingly relevant over longer term follow-up. Methods of estimating lifetime risk overcome those difficulties and can provide more accurate risk prediction. Lifetime risk estimation is useful for assessing population burden of a disease, predicting the future burden of the disease and directly comparing absolute lifetime risks between the diseases.
A number of studies have used lifetime risk calculation to examine intluence of risk [actors on the lifetime risk of CAD and CVD. Even taking a single risk factor like total cholesterol level, a Framingham study was able to show disparity between the short-teim and lifetime rislts for CAD. Men at age 50 witli total cholesterol 2401ngldl or higher had a 10 year risk of 15 per cent whereas the lifetime risk was 63 per cent. For women Lhe corresponding figure was 8 per cent and 53 per cent. Using the ATP-111 online risk calculator, a 45 ycar old obese,lion-smoking nondiabetic ~nali with total cl~olesterol of 2001ngId1, HDL cholesterol of 40 mgldl and untreated systolic BP of 135 mmHg has an eslitnatecl hard coronary risk of only 3 per ccnt. However his predicted lifelime risk for CVD is 50 per cent and predicted median survival is abo~tl I0 yeass shorter than a iiian of the same age with optimal risk factors. For a wotnan with samc level of risk factors at age 45, the estimated 10-yeas coronary risk is lcss than 1 per cent, comparcd with a
lifetime risk of nearly 40 per cent. The median survival is also 5 years shorter than of a woman with optimal risk factors.
The influence of risk factors on the lifetime risk has been further elaborated in a more recent study. In that study all Framingham participants who were free of atherosclerotic CVD at age 50 were included. Participants were stratified into the following mutually exclusive categories:'Optimal risk factors' (Total cholesterol under I XOmglcll, BP < 120180mmHg, non-smoker, non-diabetic)
'Not-optimal risk faclors' (Total cholesterol 180- 199 mgldl, or BP 120- 1391 80-89 mniHg, non-smoker, iion-diabetic)'Elevated risk factor' (Total cholesterol 200-239nigld1, or BP 140- 159190-99 rnmHg, non-smoke , non-diabetic) Major risk factor' (Total cholesterol > 240 mgldl, BP > 1601100 mmI-Ig, orsmoker, or diabetic)
A total of 3546 men and 4362 women were then followed for a total of 11 1 777 person years. In all, 1757 had one or Inore CVD events, whilc slightly fewer (about 1641) died free of CVD. I11 the lifetime-risk calculation, men and women with 'optimal' risk factor levels at age 50 had a very low risk of developing the disease (5.2 per cent and 8.2 per cent, respectively). With each additioiial risk factor, however, risk of CVD increased dramatically: men and women with two or more major risk factors at age 50 had a 1i.fetime risk of developing CVD of 68.9 per cent for men and 50.2 per cent for women. Median survival was also significantly reduced in people witli two or more risk hlctors at age 50. Diabetes confessed the highest lifelirue risk of ilny single risk factor: 67.1 per cent for tnen and 57.3 per cent for women through age 75 years.Lifetime risk estimation represents o very potentially useS~t1 tool to ider~tiljl palients at risk for CVD. Since absence of eslablislied risk f~~ctors cvcil at age 50 was associated with vely low lifetimc risk fbr CVD ancl markedly longer survival,this should promote efforts at preventing development of risk factors in younger individuals and motivate people to change risky health behaviours and adhere to the recommendations.
Traditional statistical and epidemiological methods of estimating long-term risks do not accurately reflect population burden of disease. The long-term risk estimation is also problematic because they do not accoullt for competing ri& that hecome increasingly relevant over longer term follow-up. Methods of estimating lifetime risk overcome those difficulties and can provide more accurate risk prediction. Lifetime risk estimation is useful for assessing population burden of a disease, predicting the future burden of the disease and directly comparing absolute lifetime risks between the diseases.
A number of studies have used lifetime risk calculation to examine intluence of risk [actors on the lifetime risk of CAD and CVD. Even taking a single risk factor like total cholesterol level, a Framingham study was able to show disparity between the short-teim and lifetime rislts for CAD. Men at age 50 witli total cholesterol 2401ngldl or higher had a 10 year risk of 15 per cent whereas the lifetime risk was 63 per cent. For women Lhe corresponding figure was 8 per cent and 53 per cent. Using the ATP-111 online risk calculator, a 45 ycar old obese,lion-smoking nondiabetic ~nali with total cl~olesterol of 2001ngId1, HDL cholesterol of 40 mgldl and untreated systolic BP of 135 mmHg has an eslitnatecl hard coronary risk of only 3 per ccnt. However his predicted lifelime risk for CVD is 50 per cent and predicted median survival is abo~tl I0 yeass shorter than a iiian of the same age with optimal risk factors. For a wotnan with samc level of risk factors at age 45, the estimated 10-yeas coronary risk is lcss than 1 per cent, comparcd with a
lifetime risk of nearly 40 per cent. The median survival is also 5 years shorter than of a woman with optimal risk factors.
The influence of risk factors on the lifetime risk has been further elaborated in a more recent study. In that study all Framingham participants who were free of atherosclerotic CVD at age 50 were included. Participants were stratified into the following mutually exclusive categories:'Optimal risk factors' (Total cholesterol under I XOmglcll, BP < 120180mmHg, non-smoker, non-diabetic)
'Not-optimal risk faclors' (Total cholesterol 180- 199 mgldl, or BP 120- 1391 80-89 mniHg, non-smoker, iion-diabetic)'Elevated risk factor' (Total cholesterol 200-239nigld1, or BP 140- 159190-99 rnmHg, non-smoke , non-diabetic) Major risk factor' (Total cholesterol > 240 mgldl, BP > 1601100 mmI-Ig, orsmoker, or diabetic)
A total of 3546 men and 4362 women were then followed for a total of 11 1 777 person years. In all, 1757 had one or Inore CVD events, whilc slightly fewer (about 1641) died free of CVD. I11 the lifetime-risk calculation, men and women with 'optimal' risk factor levels at age 50 had a very low risk of developing the disease (5.2 per cent and 8.2 per cent, respectively). With each additioiial risk factor, however, risk of CVD increased dramatically: men and women with two or more major risk factors at age 50 had a 1i.fetime risk of developing CVD of 68.9 per cent for men and 50.2 per cent for women. Median survival was also significantly reduced in people witli two or more risk hlctors at age 50. Diabetes confessed the highest lifelirue risk of ilny single risk factor: 67.1 per cent for tnen and 57.3 per cent for women through age 75 years.Lifetime risk estimation represents o very potentially useS~t1 tool to ider~tiljl palients at risk for CVD. Since absence of eslablislied risk f~~ctors cvcil at age 50 was associated with vely low lifetimc risk fbr CVD ancl markedly longer survival,this should promote efforts at preventing development of risk factors in younger individuals and motivate people to change risky health behaviours and adhere to the recommendations.
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