Primary Prevention Of Coronary Disease Research Articles

Hormone replacement therapy and cardio-vascular disease

The results of large randomized trials such as the Women's Health Initiative (WHI), Heart and Estrogen / Progestin Replacement Study (HERS) or Estrogen Replacement and Atherosclerosis Study (ERAS) as well as the Million Women Study (MWS) which does not meet criteria RCT, concerning, among others the impact of HRT on breast cancer risk, thromboembolism, or the aging processes in the central nervous system caused the recent big confusion in the medical community , causing distrust about the safety and advisability of HRT in menopausal women. The paper presents an overview of the available, current literature on HRT. It was found that HRT should not be used in both primary and secondary prevention of coronary heart disease Great expectations was associated with an earlier initiation of therapy, before the advent of atherosclerosis - but there is currently no conclusive data about its role in the primary prevention of coronary disease. Oral HRT increases the risk of thromboembolic events - that is why you should prefer the form of a transdermal. HRT may increase the risk of ischemic stroke (but early initiation of therapy does not increase the risk of stroke) and should not be used in the primary prevention of stroke.

Coronary Disease Deaths: From Birth Cohorts to Prevention

Cardiovascular diseases remain the number one cause of death in most of the western world. However, mortality from coronary disease nonetheless started to decline in several countries including the United States and part of western Europe 4 decades ago, and this decline has continued until the present time. Conceptually, the decline in coronary disease mortality could reflect a decrease in the incidence of coronary disease with fewer new cases occurring, or a decline in its case fatality, or a combination thereof. Progress in the primary prevention of coronary disease would decrease incidence while improvement in medical care and secondary prevention would increase survival. Hence, describing temporal trends in different populations and examining their causes is important and can help to design interventions, deploy prevention strategies, and advocate for policy changes. Despite the importance of this endeavor, quantifying the role of each of the aforementioned components in coronary mortality decline remains a difficult task and the determinants of the decline are still incompletely understood. This matter is further complicated by the fact that the respective contribution of potential determinants likely evolved over time and across countries. Within this context, studies of trends according to person, place, and time have the potential to shed some light on this subject. The article by Ocana-Riola et al reports an in-depth analysis of temporal trends in mortality from ischemic heart disease in southern Spain, aiming at separating age, birth cohort, and period effects. In epidemiology, age effect can be defined as a change in the outcome rate according to age, irrespective of birth cohort and calendar time; cohort effect can be defined as a change in the outcome rate according to year of birth, irrespective of age and calendar time; and period effect can be defined as a change in the outcome rate affecting an entire population at some point in time, irrespective of age and birth cohort. The study pertains to 145 539 deaths from ischemic heart disease that occurred in Andalusia between 1981 and 2008 among individuals aged between 30 and 84 years. For age effect, as expected, mortality from ischemic heart disease increased substantially with age for both men and women. Concerning birth cohort effect, the risk of

Early Increase in Autoantibodies Against Human Oxidized Low-Density Lipoprotein in Hypertensive Patients After Blood Pressure Control

Oxidized lipoproteins and antioxidized low-density lipoprotein (anti-oxLDL) antibodies (Abs) have been detected in plasma in response to blood pressure (BP) elevation, suggesting the participation of the adaptive immune system. Therefore, treatment of hypertension may act on the immune response by decreasing oxidation stimuli. However, this issue has not been addressed. Thus, we have here analyzed anti-oxLDL Abs in untreated (naive) hypertensive patients shortly after initiation of antihypertensive therapeutic regimens. Titers of anti-oxLDL Abs were measured in subjects with recently diagnosed hypertension on stage 1 (n = 94), in primary prevention of coronary disease, with no other risk factors, and naive of antihypertensive medication at entry. Subjects were randomly assigned to receive perindopril, hydrochlorothiazide (HCTZ), or indapamide (INDA) for 12 weeks, with additional perindopril if necessary to achieve BP control. Abs against copper-oxidized LDL were measured by enzyme-linked immunosorbent assay. Twelve-week antihypertensive treatment reduced both office-based and 24-h ambulatory BP measurements (P < 0.0005). The decrease in BP was accompanied by reduction in thiobarbituric acid-reactive substances (TBARS) (P < 0.05), increase in anti-oxLDL Ab titers (P < 0.005), and improvement in flow-mediated dilation (FMD) (P < 0.0005), independently of treatment. Although BP was reduced, we observed favorable changes in anti-oxLDL titers and FMD. We observed that anti-oxLDL Ab titers increase after antihypertensive therapy in primary prevention when achieving BP targets. Our results are in agreement with the concept that propensity to oxidation is increased by essential hypertension and anti-oxLDL Abs may be protective and potential biomarkers for the follow-up of hypertension treatment.

Planning primary prevention of coronary disease

Effective prevention of the current annual $400 billion losses from atherosclerosis and cardiovascular disease (CVD) will require preventing primary causes rather than just decreasing signs and symptoms (risk factors) produced by those causes. All CVD risk factors predict a likelihood of CVD, but not all are causes of CVD. As a result, reducing some health risk assessment biomarkers may not appreciably reduce CVD and death. Careful review of molecular events connecting diets to death identifies two modifiable food imbalances that cause major chronic diseases in Americans. They are 1) imbalance between ingestion and expenditure of food energy, and 2) imbalance between omega-3 and omega-6 essential fatty acid levels in ingested foods. Health insurers could reduce costs and revolutionize preventive health care by monitoring omega-3 and omega-6 proportions in blood fatty acids and by using personalized interactive food choice software to adjust food intakes to fit individual preferences.

Abstract: P628 PRO-INFLAMMATORY EFFECTS OF APOLIPOPROTEIN CIII ON MONOCYTIC CELLS

This study was aimed to examine cholesteryl ester transfer protein (CETP), apolipoprotein AI and CIII gene polymorphisms, and to verify whether these genetic determinants are associated with the prevalence of myocardial infarction (MI) or type 2 diabetes. The TaqIB restriction fragment length polymorphism (RFLP) in intron I of the CETP gene, the MspI in the third intron of the APOAI gene, and also SstI in the 3′ untranslated region of the APOCIII gene were determined using standard methods. The prevalence of these polymorphisms was compared between diabetic (n = 119), and non-diabetic (n = 100) middle-aged individuals of both sexes. We found a higher prevalence of the B2B2 genotype of the CETP gene among diabetics than that observed in non-diabetics (P < 0.05), and a lower prevalence of this genotype among patients with previous MI (P < 0.02). The MspI polymorphisms of the APOAI gene showed that M1++ genotype was found mainly in diabetic patients (P < 0.04). Conversely, the SstI polymorphism of APOCIII gene was not significantly associated with either MI or diabetes. Therefore, among these genetic polymorphisms, TaqIB of CETP and MspI of apolipoprotein AI appeared to help significantly to identify diabetic individuals. In particular, the former may have an additional role in the primary prevention of coronary disease.

Severity of Myocardial Infarction

Cardiovascular disease constitutes a burden of epidemic proportion,1 and understanding its determinants is essential to designing effective interventions. Doing so requires the ability to track disease burden at the population level. In the United States, without national registries, community surveillance is the method of choice.2 Community surveillance studies are mostly retrospective by design, rely on diagnostic codes for case finding, and require a defined population in which events can be consistently and reliably captured and validated with standardized approaches. Applied to cardiovascular disease, community surveillance measures its burden in communities by tracking the incidence of events, their severity, and their mortality, thereby enabling the appraisal of the components of cardiovascular diseases in a given population.2 Because of the aforementioned methodological requirements, few surveillance studies exist in the United States. They include the Atherosclerosis Risk in Communities (ARIC) Study,3 the Minnesota Heart Survey,4 the Olmsted County Study,5 and the Worcester Heart Attack Study.6 The data from these studies indicate that, although deaths from coronary disease have declined, the incidence of myocardial infarction in the United States has remained mostly stable. Thus, the decline in mortality can be envisioned as reflecting an improvement in survival, which may be mediated by a declining severity of myocardial infarction. Article p 503 The article by Myerson et al7 in this issue of Circulation specifically addresses this important and understudied issue in ARIC between 1987 and 2002. They examined a large, multiracial population and relied on several indicators, including the composite Predicting Risk of Death in Cardiac Disease Tool (PREDICT) score to conclude that the severity of infarction declined over time. Indeed, the proportion of infarctions with major ECG abnormalities, ST-segment elevation, and Q waves decreased, as did biomarker values and the proportion of persons presenting with shock. …

Primary prevention of coronary disease. Observations on the results of an American intervention study

Drug Prescribing for Patients with Chronic Kidney Disease in General Practice: a Cross-Sectional Study

Relationship between gene polymorphisms and prevalence of myocardial infarction among diabetic and non-diabetic subjects

This study was aimed to examine cholesteryl ester transfer protein (CETP), apolipoprotein AI and CIII gene polymorphisms, and to verify whether these genetic determinants are associated with the prevalence of myocardial infarction (MI) or type 2 diabetes. The TaqIB restriction fragment length polymorphism (RFLP) in intron I of the CETP gene, the MspI in the third intron of the APOAI gene, and also SstI in the 3′ untranslated region of the APOCIII gene were determined using standard methods. The prevalence of these polymorphisms was compared between diabetic ( n = 119), and non-diabetic ( n = 100) middle-aged individuals of both sexes. We found a higher prevalence of the B2B2 genotype of the CETP gene among diabetics than that observed in non-diabetics ( P < 0.05), and a lower prevalence of this genotype among patients with previous MI ( P < 0.02). The MspI polymorphisms of the APOAI gene showed that M1++ genotype was found mainly in diabetic patients ( P < 0.04). Conversely, the SstI polymorphism of APOCIII gene was not significantly associated with either MI or diabetes. Therefore, among these genetic polymorphisms, TaqIB of CETP and MspI of apolipoprotein AI appeared to help significantly to identify diabetic individuals. In particular, the former may have an additional role in the primary prevention of coronary disease.

The choice of hormone replacement therapy or statin therapy in the treatment of hyperlipidemic postmenopausal women.

(a) Statins: the major measurable effect of these drugs is to reduce total and LDL cholesterol. In RCT trials, the Scandanavian Simvastatin Survival Study (4S), the Cholesterol and Recurrent Event (CARE) and Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID), approximately 20% of subjects were female, in whom CHD events, but not CHD or total mortality were reduced. (b) HRT: there is data available from a single RCT of continuous combined premarin and medroxyprogesterone acetate (MPA) against placebo, The Heart Estrogen Replacement Study (HERS). A study of 2763 women and mean duration of 4.1 years. This study was neutral, with no reduction in CHD events or mortality. There were more events in the first year, and fewer in years 3-5. Other studies of HRT have been observational and positive for HRT. The effects of treatment on lipoproteins with statins, HRT and combination of statin and HRT have been investigated. In secondary prevention for hyperlipidemic women to achieve cholesterol <5, low density lipoprotein (LDL)<3 mmol/l statins will be first choice, possibly with HRT additionally for its other benefits on cardiovascular risk factors.

Use HRT for primary prevention of coronary disease?

Use HRT for primary prevention of coronary disease?

Check-up in cardiologic view

The concept of the primary prevention of coronary disease is certainly widely accepted today and supports check-up visits of apparently healthy persons. The goals of check-up's viewed by the cardiologist are the detection of coronary risk factors and the identification of asymptomatic patients with coronary disease to initial preventive measures. In some instances, a personal health problem forces the patient to a check-up visit. The major coronary risk factors of heredity, cigarette-smoking, hypercholesteremia, hypertension can be detected by taking the history, performing a physical examination and a blood-sampling for cholesterol. Additional investigations such as an ECG or an exercise-test are only indicated in symptomatic patients or in persons at high coronary risk.

Primary prevention of coronary disease in diabetes; Limitations of the methods used to estimate CHD risk

Primary prevention of coronary disease in diabetes; Limitations of the methods used to estimate CHD risk

Primary prevention of coronary disease

In 1995, the latest year for which statistics are available, heart disease, cancer, and stroke continued to be the three leading causes of death in the United States. Notably, however, a wealth of experience has confirmed that hygienic interventions such as diet, exercise, weight loss, and smoking cessation can reduce the toll from heart disease while also reducing the morbidity and mortality associated with stroke and cancer. This chapter will describe the rationale for the primary prevention of coronary heart disease (CHD), review the basic concepts involved in cholesterol screening and update the reader regarding key preventive measures, such as diet, exercise, and smoking cessation. Also highlighted will be recent clinical trial results suggesting the benefits of lipid-lowering drugs in “high-risk” individuals who have not experienced a coronary event. These findings represent an exciting advance that emphasizes the value of preventive efforts in curbing CHD.

Treating hyperlipidemia for the primary prevention of coronary disease. Are higher dosages of lovastatin cost-effective?

To compare the average and marginal life-time cost-effectiveness of increasing dosages of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, such as lovastatin, for the primary prevention of coronary heart disease (CHD). We estimated the lifelong costs and benefits of the modification of lipid levels achieved with lovastatin based on published studies and a validated CHD prevention computer model. Patients were middle-aged men and women without CHD, with mean total serum cholesterol levels of 6.67, 7.84, and 9.90 mmol/L (258, 303, and 383 mg/dL), and high-density lipoprotein cholesterol levels of 1.19 mmol/L (46 mg/dL), as described in clinical trials. We estimated the cost per year of life saved for dosages of lovastatin ranging from 20 to 80 mg/d that reduced the total cholesterol level between 17% and 34%, and increased high-density lipoprotein cholesterol level between 4% and 13%. After discounting benefits and costs by 5% annually, the average cost-effectiveness of lovastatin, 20 mg/d, ranged from $11,040 to $52,463 for men and women. The marginal cost-effectiveness of 40 mg/d vs 20 mg/d remained in this range ($25,711 to $60,778) only for persons with baseline total cholesterol levels of 7.84 mmol/L (303 mg/dL) or higher. However, the marginal cost-effectiveness of lovastatin, 80 mg/d vs 40 mg/d, was prohibitively expensive ($99,233 to $716,433 per year of life saved) for men and women, irrespective of the baseline total cholesterol level. Assuming that $50,000 per year of life saved is an acceptable cost-effectiveness ratio, treatment with lovastatin at a dosage of 20 mg/d is cost-effective for middle-aged men and women with baseline total cholesterol levels of 6.67 mmol/L (258 mg/dL) or higher. At current drug prices, treatment with 40 mg/d is also cost-effective for total cholesterol levels of 7.84 mmol/L (303 mg/dL) or higher. However, treatment with 80 mg/d is not cost-effective for primary prevention of CHD.

Targeting lipid-lowering drug therapy for primary prevention of coronary disease: an updated Sheffield table

The Scandinavian Simvastatin Survival Study (4S) 1 Scandinavian Simvastatin Survival Study Group Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994; 344: 1383-1389 Summary PubMed Scopus (11230) Google Scholar and West of Scotland Coronary Prevention Study (WOSCOPS) 2 Shepherd J Cobbe SM Ford I et al. for the West of Scotland Coronary Prevention Study Group Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med. 1995; 333: 1301-1307 Crossref PubMed Scopus (7448) Google Scholar showed that the benefit of treatment with inhibitors of hydroxymethyl-glutaryl-coA-reductase (statins) in preventing major coronary heart disease (CHD) events substantially outweighs any harm when serum cholesterol averages 5·5 mmol/L or higher1 and when the risk of CHD events (myocardial infarction or coronary death) is 1·5% per year or higher. 2 Shepherd J Cobbe SM Ford I et al. for the West of Scotland Coronary Prevention Study Group Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med. 1995; 333: 1301-1307 Crossref PubMed Scopus (7448) Google Scholar The accepted priority for statin treatment is secondary prevention in patients who already have coronary disease or other clinically overt atherosclerotic disease and serum cholesterol of 5·5 mmol/L, or higher, since these patients have a high risk of CHD events (3-6% per year). 3 Haq IU, Ramsay LE, Pickin DM, Yeo WW, Jackson PR. Payne JN. Lipid-lowering for prevention of coronary heart disease: what policy now? Clin Sci (in press). Google Scholar , 4 Haq IU Jackson PR Yeo WW Ramsay LE Sheffield risk and treatment table for cholesterol lowering for primary prevention of coronary heart disease. Lancet. 1995; 346: 1467-1471 Summary PubMed Google Scholar We have estimated that 4·8% of the UK population aged 35-69 years may be candidates for secondary prevention. 3 Haq IU, Ramsay LE, Pickin DM, Yeo WW, Jackson PR. Payne JN. Lipid-lowering for prevention of coronary heart disease: what policy now? Clin Sci (in press). Google Scholar

Cholesterol Policy and the Primary Prevention of Coronary Disease: Reflections on Clinical and Population Strategies

Despite billions of dollars spent on targeted and population-wide strategies aimed at reducing human consumption of saturated fat and cholesterol, aspects of the diet-heart connection remain a source of debate. At least part of the uncertainty arises from a growing appreciation that the relationship between dietary habits, serum lipids, and atherosclerosis is more complex than was previously thought. While we wait for answers from clinical and basic research, what is to be done? This review examines evidence about clinical policies and population strategies for the primary prevention of coronary disease, with specific reference to diet and dyslipidemias. It also summarizes some current policies and offers conclusions about broad directions for further policy development.

Risk factors for coronary disease and stroke in men and women

Summary We studied the influence of gender on the relations between cholesterol and coronary mortality, and between diastolic blood pressure and stroke mortality. Men (n = 7137) and women (n = 8262) aged 45-64 years from Renfrew and Paisley in the west of Scotland were first examined in 1972-76, and then followed for 17 years. Coronary and stroke mortality were calculated as deaths per thousand patient-years, and adjusted for the effects of competing risk factors. Plasma cholesterol was positively related to coronary mortality in both sexes. Absolute risk of coronary death was however, so much less in women that a woman with high cholesterol (>7. 2 mmol/l) was at lower risk than a man with low cholesterol (< 5.0 mmol/l). Diastolic blood pressure was positively related to stroke mortality in both sexes, but here the absolute risks were similar in each sex. Stroke mortality was highest in hypertensive men and women who smoked and had hyperlipidaemia. Although for primary prevention of stroke by treatment of hypertension, similar management could be used in men and women, primary prevention of coronary disease by lipid-lowering may well require different policies for the two sexes, corresponding to their different absolute risk and potential for benefit.

Cholesterol Policy and the Primary Prevention of Coronary Disease: Reflections on Clinical and Population Strategies

Cholesterol Policy and the Primary Prevention of Coronary Disease: Reflections on Clinical and Population Strategies

Sheffield risk and treatment table for cholesterol lowering for primary prevention of coronary heart disease.

When used for the secondary prevention of coronary heart disease, treatment with an inhibitor of hydroxymethylglutaryl-coenzyme-A reductase results in worthwhile benefit that clearly exceeds any risk in patients whose risk of coronary death is 1.5% or more per year. This evidence can be extrapolated logically to primary prevention of coronary disease provided that treatment is targeted at those with similar or higher risk. We present a table that refines previously proposed methods of risk prediction. The table identifies subjects who have the specified degree of coronary risk; shows the serum cholesterol concentration that confers that degree or risk in the individual; and identifies subjects who will not have this degree of risk, irrespective of their cholesterol concentration. It is simple enough for use in ordinary practice. The table highlights the predominant effect of age on coronary risk; a person who is free of vascular disease and younger than 52 years is unlikely to have the specified degree of risk. Even in older people (60-70 years) several risk factors are generally required to attain this degree of risk. Some people are candidates for lipid- lowering drug treatment with serum cholesterol as low as 5.5 mmol/L, whereas others with cholesterol as high as 9.0 mmol/L are not. Although cholesterol lowering is a powerful method for preventing coronary events in people at high risk, cholesterol measurement by itself is not a good way to identify those with high coronary risk. The method can be adapted readily to target a different level of coronary risk as new evidence on the benefit and risk of treatment becomes available.

Aspirin for primary prevention of coronary disease.

Aspirin for primary prevention of coronary disease.