Apolipoproteins and ischaemic heart disease: implications for screening

Wald, Nicholas; Watt, Hilary; Bailey, Alan; Johnson, Mariana K.; Ledue, Thomas B.; Haddow, James E.

doi:10.1016/s0140-6736(94)90814-1

Cited by 224 publications

(129 citation statements)

References 17 publications

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“…Our study consisted of 21 520 men aged 35-64 years who attended the British United Provident Association (BUPA) Medical Centre between 1975 and 1982; the cohort has been described before (Wald et al, 1994). At the time of the visit, a detailed smoking history was obtained from each man, COHb was measured using whole blood on a CO-Oximiter (Wald et al, 1978) and serum samples were stored at -40°C.…”

Section: Methodsmentioning

confidence: 99%

The dose-response relationship between cigarette consumption, biochemical markers and risk of lung cancer

Law¹,

Morris²,

Watt³

et al. 1997

Br J Cancer

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Summary The relationship between the number of cigarettes smoked per day and the incidence of lung cancer is linear but, from the multistage model of carcinogenesis, it should be quadratic (upwards curving). We investigated this anomaly in a study of 11 403 male never smokers and current smokers in whom carboxyhaemoglobin (COHb) (Day and Brown, 1980). If there are k stages, it can be shown that the incidence of a cancer after time t will be proportional to t1-', and so the plot of the logarithm of age-specific incidence on the logarithm of time will be a straight line with slope k-i. For lung cancer, the incidence increases to the fourth power of age, and hence there are an estimated five stages. Epidemiological observations indicate that smoking affects two of the stages; an early stage because many years elapse between starting smoking and developing an appreciable risk of lung cancer, and a late stage because risk falls rapidly in a person who stops smoking relative to a person who does not (Doll and Peto, 1978;Day and Brown, 1980). If one person smoked twice as many cigarettes per day as another, other factors being equal, the rate of occurrence of both the early stage and the late stage should therefore be approximately doubled in the heavier smoker. As consumption doubles, risk should increase fourfold; the risk of lung cancer should be related to the square of the number of cigarettes smoked per day (the squre or second power as two stages are affected) (Doll and Peto, 1978). Thus, a linear relationship is observed but a quadratic relationship is expected. We report an investigation into this anomaly using two biochemical markers

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Section: Methodsmentioning

confidence: 99%

The dose-response relationship between cigarette consumption, biochemical markers and risk of lung cancer

Law¹,

Morris²,

Watt³

et al. 1997

Br J Cancer

View full text Add to dashboard Cite

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Section: Mayo Clin Proc 1999;74:243-252mentioning

confidence: 99%

“…In fact, conventional "risk factors" fail to predict up to one-third of future deaths due to coronary heart disease. 3,4 Because effective means are available for treating manifest heart disease and for preventing the progression of coronary disease and acute coronary events, accurate identification of persons at risk is essential for efficient and accurate implementation of preventive strategies as part of a case management scenario.Coronary artery calcium is intimately associated with mural atheromatous plaque. [5][6][7][8] The American Heart Association recently reviewed the data validating electron beam computed tomography (EBCT) and its ability to detect and quantify coronary calcification noninvasively.…”

mentioning

confidence: 99%

Electron Beam Computed Tomographic Coronary Calcium Scanning: A Review and Guidelines for Use in Asymptomatic Persons

Rumberger

Brundage²,

Rader

et al. 1999

Mayo Clinic Proceedings

747

449

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“…A combination of elevated LDL-C, elevated triglycerides, and low HDL-C seems to be particularly atherogenic. In addition, high concentrations of Lp(a), a cholesterol-rich lipoprotein with an LDL particle linked to apolipoprotein (a), has been associated with high risk for CAD (24,25). The compelling evidence linking dyslipidemia with CAD and showing benefits of cholesterol reduction or lipid-normalizing strategies led to the recommendation by the American Heart Association that patients with CAD be treated with lipid-lowering agents (26).…”

Section: The Lipid Hypothesis: Lipids and Cvdmentioning

confidence: 99%

Impact of Dyslipidemia in End-Stage Renal Disease

Prichard

2003

Journal of the American Society of Nephrology

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Abstract. Heart disease is a major cause of morbidity and mortality among patients with renal failure. Premature atherosclerotic coronary heart disease is driven by multiple risk factors, including dyslipidemia and oxidative stress. In the nondialysis population, there is overwhelming evidence that treatment of dyslipidemia can significantly improve cardiovascular outcomes. Accumulating data indicate that dialysis patients have atherogenic lipid abnormalities. Although LDL cholesterol (LDL-C) levels in patients who undergo hemodialysis are normal or near normal, increased oxidized LDL-C, triglycerides, and lipoprotein (a) [Lp(a)]; decreased HDL cholesterol (HDL-C); and triglyceride-rich VLDL have been noted. Patients who receive peritoneal dialysis have a more atherogenic lipid profile with increased LDL-C, apolipoprotein B, oxidized LDL-C, triglycerides, and Lp(a) and decreased HDL-C. Furthermore, the LDL particles of peritoneal dialysis patients are small and dense. However, there is a dearth of information regarding the goals, efficacy, and safety of dyslipidemia treatment among dialysis patients. Given the strong evidence of risk reduction and the benefits of lipid-lowering treatment in the nondialysis population, the emerging consensus is that dialysis patients should be treated aggressively for dyslipidemia to an LDL-C goal below 100 mg/dl. Although physicians and patients may be reluctant to add medications because of concerns about polypharmacy, potential decreased compliance, and increased cost, the use of agents such as sevelamer that can serve multiple functions, including phosphate control, lipid lowering (decreased LDL-C and total cholesterol), and anti-inflammatory effects (decreased high-sensitivity C-reactive protein), should be explored and considered for patients who would benefit from such treatment.

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Apolipoproteins and ischaemic heart disease: implications for screening

Cited by 224 publications

References 17 publications

The dose-response relationship between cigarette consumption, biochemical markers and risk of lung cancer

The dose-response relationship between cigarette consumption, biochemical markers and risk of lung cancer

Electron Beam Computed Tomographic Coronary Calcium Scanning: A Review and Guidelines for Use in Asymptomatic Persons

Impact of Dyslipidemia in End-Stage Renal Disease

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