| 91. |
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| 92. |
- Wilhelmsen, Lars, 1932, et al.
(författare)
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Risk of coronary events by baseline factors during 28 years follow-up and three periods in a random population sample of men
- 2004
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Ingår i: J Intern Med. - 0954-6820. ; 256:4, s. 298-307
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: To investigate the predictive value of risk factors for coronary events measured in midlife during three separate periods over a follow-up period extending through 28 years. METHODS: A total of 7437 men aged 47-55 years and free of myocardial infarction at baseline were examined. Risk of coronary events (nonfatal myocardial infarction and coronary deaths) was analysed for the entire period and for 0-15, 16-21 and 22-28 years' follow-up, using age-adjusted and multiple Cox regression analyses. RESULTS: Age, diabetes, elevated blood pressure and serum cholesterol were all independently associated with increased risk of coronary events for the entire 28 years as well as for each of the periods. A family history of coronary events amongst fathers, mothers and siblings was independently significant for the entire follow-up period, and the risk did not decline with extended follow-up. Effort-related chest pain was a strong and independent risk factor for the first 21 years but not thereafter. The importance of smoking decreased over time and was not significantly associated with outcome during the last period. Stress was also significant for the entire 28 years, but in selected periods only up to 21 years. Body mass index, low physical activity and low social class were inconsistently or not at all related to outcome in multiple analyses.
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| 93. |
- Wilhelmsen, Lars, 1932, et al.
(författare)
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Saving lives, money and resources: drug and CABG/PCI use after myocardial infarction in a Swedish record-linkage study
- 2010
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Ingår i: European Journal of Health Economics. - : Springer Science and Business Media LLC. - 1618-7598 .- 1618-7601 .- 1439-6637. ; 11:2, s. 177-184
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Tidskriftsartikel (refereegranskat)abstract
- Drug costs are increasing despite the introduction of cheaper generic drugs. The aim of the present study was to analyse the entire costs of hospital care, out-patient care, and the cost of drugs for 16 months following a myocardial infarction (MI) to see to what extent drug costs contribute to the overall costs of care. Diagnoses and costs for care as well as mortality data obtained from the Vastra Gotaland Region, Sweden, and drug costs from the Swedish Board of Health and Welfare, were merged in a computer file. Patients registered from 1 July 2005 to 30 June 2006 were followed from 28 days after an MI, with follow-up until 31 October 2006. Of 4,725 patients, 711 died before the start of the study and 721 during follow-up. Higher age [hazard ratio (HR, 95%CI) = 1.06 (1.05-1.07)], previous MI [HR = 1.31 (1.13-1.53)] and diabetes mellitus [HR = 1.34 (1.13-1.58)] were associated with increased mortality, which decreased with coronary interventions: CABG/PCI [HR = 0.19 (0.14-0.27)]. In a multivariable analysis, mortality was lower for patients taking simvastatin [HR = 0.62 (0.50-0.76)] and clopidogrel [HR = 0.58 (0.46-0.74)]. Costs for out-patient care accounted for 25% and drugs for 5% of total costs. If patients not treated with simvastatin or clopidogrel had received these drugs, an additional 154-306 lives might have been saved. Drug costs would be higher, but total costs lower. Thus, even expensive drugs may reduce overall costs.
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| 94. |
- Wilhelmsen, Lars, 1932, et al.
(författare)
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Secular changes in cardiovascular risk factors and attack rate of myocardial infarction among men aged 50 in Gothenburg, Sweden. Accurate prediction using risk models
- 2008
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Ingår i: Journal of Internal Medicine. - : Wiley. - 1365-2796 .- 0954-6820. ; 263:6, s. 636-43
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: Coronary risk factor changes were related to attack rate of acute myocardial infarction (AMI). METHODS AND RESULTS: Cross-sectional population samples of 50-year-old men were examined every 10th year from 1963 to 2003. Attack rates of AMI were recorded from 1975 to 2004. Prevalence of smoking decreased from 56% in 1963 to 22% in 2003. Leisure time physical activity decreased (n.s.), while psychological stress remained the same. Diabetes prevalence increased from 3.6% to 6.6%. Body mass index (BMI) increased from 24.8 to 26.4 kg m(-2). Blood pressures decreased from 138.2/90.6 to 134.7/84.9 mmHg (P = 0.00001). Serum total cholesterol decreased from 6.42 to 5.50 mmol L(-1) (P = 0.0001), but serum triglycerides increased from 1.26 to 1.71 mmol L(-1) (P = 0.0001). The multivariable risk according to total cholesterol, blood pressure and smoking for AMI decreased from the set value 1.0 in 1963 to 0.418. From 1975-1979 to 2000-2004 attack rates for AMI for the age groups 35-44, 45-54 and 55-64 declined to 45%, 46% and 45%, respectively. The 28-day case fatality declined from 30%, 38% and 46% to 12%, 16% and 20%. CONCLUSION: The more than 50% decline in attack rate of AMI during 30 years was comparable with the decline in risk factors.
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| 95. |
- Wilhelmsen, Lars, 1932, et al.
(författare)
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SLCO1B1 variants and statin-induced myopathy--a genomewide study.
- 2008
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Ingår i: The New England journal of medicine. - 1533-4406. ; 359:8, s. 789-99
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Lowering low-density lipoprotein cholesterol with statin therapy results in substantial reductions in cardiovascular events, and larger reductions in cholesterol may produce larger benefits. In rare cases, myopathy occurs in association with statin therapy, especially when the statins are administered at higher doses and with certain other medications. METHODS: We carried out a genomewide association study using approximately 300,000 markers (and additional fine-mapping) in 85 subjects with definite or incipient myopathy and 90 controls, all of whom were taking 80 mg of simvastatin daily as part of a trial involving 12,000 participants. Replication was tested in a trial of 40 mg of simvastatin daily involving 20,000 participants. RESULTS: The genomewide scan yielded a single strong association of myopathy with the rs4363657 single-nucleotide polymorphism (SNP) located within SLCO1B1 on chromosome 12 (P=4x10(-9)). SLCO1B1 encodes the organic anion-transporting polypeptide OATP1B1, which has been shown to regulate the hepatic uptake of statins. The noncoding rs4363657 SNP was in nearly complete linkage disequilibrium with the nonsynonymous rs4149056 SNP (r(2)=0.97), which has been linked to statin metabolism. The prevalence of the rs4149056 C allele in the population was 15%. The odds ratio for myopathy was 4.5 (95% confidence interval [CI], 2.6 to 7.7) per copy of the C allele, and 16.9 (95% CI, 4.7 to 61.1) in CC as compared with TT homozygotes. More than 60% of these myopathy cases could be attributed to the C variant. The association of rs4149056 with myopathy was replicated in the trial of 40 mg of simvastatin daily, which also showed an association between rs4149056 and the cholesterol-lowering effects of simvastatin. No SNPs in any other region were clearly associated with myopathy. CONCLUSIONS: We have identified common variants in SLCO1B1 that are strongly associated with an increased risk of statin-induced myopathy. Genotyping these variants may help to achieve the benefits of statin therapy more safely and effectively. (Current Controlled Trials number, ISRCTN74348595.)
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| 96. |
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| 97. |
- Yusuf, Salim, et al.
(författare)
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Telmisartan, ramipril, or both in patients at high risk for vascular events.
- 2008
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Ingår i: The New England journal of medicine. - 1533-4406. ; 358:15, s. 1547-59
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: In patients who have vascular disease or high-risk diabetes without heart failure, angiotensin-converting-enzyme (ACE) inhibitors reduce mortality and morbidity from cardiovascular causes, but the role of angiotensin-receptor blockers (ARBs) in such patients is unknown. We compared the ACE inhibitor ramipril, the ARB telmisartan, and the combination of the two drugs in patients with vascular disease or high-risk diabetes. METHODS: After a 3-week, single-blind run-in period, patients underwent double-blind randomization, with 8576 assigned to receive 10 mg of ramipril per day, 8542 assigned to receive 80 mg of telmisartan per day, and 8502 assigned to receive both drugs (combination therapy). The primary composite outcome was death from cardiovascular causes, myocardial infarction, stroke, or hospitalization for heart failure. RESULTS: Mean blood pressure was lower in both the telmisartan group (a 0.9/0.6 mm Hg greater reduction) and the combination-therapy group (a 2.4/1.4 mm Hg greater reduction) than in the ramipril group. At a median follow-up of 56 months, the primary outcome had occurred in 1412 patients in the ramipril group (16.5%), as compared with 1423 patients in the telmisartan group (16.7%; relative risk, 1.01; 95% confidence interval [CI], 0.94 to 1.09). As compared with the ramipril group, the telmisartan group had lower rates of cough (1.1% vs. 4.2%, P<0.001) and angioedema (0.1% vs. 0.3%, P=0.01) and a higher rate of hypotensive symptoms (2.6% vs. 1.7%, P<0.001); the rate of syncope was the same in the two groups (0.2%). In the combination-therapy group, the primary outcome occurred in 1386 patients (16.3%; relative risk, 0.99; 95% CI, 0.92 to 1.07); as compared with the ramipril group, there was an increased risk of hypotensive symptoms (4.8% vs. 1.7%, P<0.001), syncope (0.3% vs. 0.2%, P=0.03), and renal dysfunction (13.5% vs. 10.2%, P<0.001). CONCLUSIONS: Telmisartan was equivalent to ramipril in patients with vascular disease or high-risk diabetes and was associated with less angioedema. The combination of the two drugs was associated with more adverse events without an increase in benefit. (ClinicalTrials.gov number, NCT00153101 [ClinicalTrials.gov].).
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| 98. |
- Zannad, Faiez, et al.
(författare)
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Prevention of cardiovascular disease guided by total risk estimations - challenges and opportunities for practical implementation: highlights of a CardioVascular Clinical Trialists (CVCT) Workshop of the ESC Working Group on CardioVascular Pharmacology and Drug Therapy.
- 2012
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Ingår i: European Journal of Preventive Cardiology. - : Oxford University Press (OUP). - 2047-4873 .- 2047-4881. ; 19:6, s. 1454-1464
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Forskningsöversikt (refereegranskat)abstract
- This paper presents a summary of the potential practical and economic barriers to implementation of primary prevention of cardiovascular disease guided by total cardiovascular risk estimations in the general population. It also reviews various possible solutions to overcome these barriers. The report is based on discussion among experts in the area at a special CardioVascular Clinical Trialists workshop organized by the European Society of Cardiology Working Group on Cardiovascular Pharmacology and Drug Therapy that took place in September 2009. It includes a review of the evidence in favour of the 'treat-to-target' paradigm, as well as potential difficulties with this approach, including the multiple pathological processes present in high-risk patients that may not be adequately addressed by this strategy. The risk-guided therapy approach requires careful definitions of cardiovascular risk and consideration of clinical endpoints as well as the differences between trial and 'real-world' populations. Cost-effectiveness presents another issue in scenarios of finite healthcare resources, as does the difficulty of documenting guideline uptake and effectiveness in the primary care setting, where early modification of risk factors may be more beneficial than later attempts to manage established disease. The key to guideline implementation is to improve the quality of risk assessment and demonstrate the association between risk factors, intervention, and reduced event rates. In the future, this may be made possible by means of automated data entry and various other measures. In conclusion, opportunities exist to increase guideline implementation in the primary care setting, with potential benefits for both the general population and healthcare resources.
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| 99. |
- Zannad, Faiez, et al.
(författare)
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Risk stratification in cardiovascular disease primary prevention - scoring systems, novel markers, and imaging techniques
- 2012
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Ingår i: Fundamental and Clinical Pharmacology. - : Wiley. - 0767-3981 .- 1472-8206. ; 26:2, s. 163-174
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Forskningsöversikt (refereegranskat)abstract
- The aim of this paper is to review and discuss current methods of risk stratification for cardiovascular disease (CVD) prevention, emerging biomarkers, and imaging techniques, and their relative merits and limitations. This report is based on discussions that took place among experts in the area during a special CardioVascular Clinical Trialists workshop organized by the European Society of Cardiology Working Group on Cardiovascular Pharmacology and Drug Therapy in September 2009. Classical risk factors such as blood pressure and low-density lipoprotein cholesterol levels remain the cornerstone of risk estimation in primary prevention but their use as a guide to management is limited by several factors: (i) thresholds for drug treatment vary with the available evidence for cost-effectiveness and benefit-to-risk ratios; (ii) assessment may be imprecise; (iii) residual risk may remain, even with effective control of dyslipidemia and hypertension. Novel measures include C-reactive protein, lipoprotein-associated phospholipase A 2, genetic markers, and markers of subclinical organ damage, for which there are varying levels of evidence. High-resolution ultrasound and magnetic resonance imaging to assess carotid atherosclerotic lesions have potential but require further validation, standardization, and proof of clinical usefulness in the general population. In conclusion, classical risk scoring systems are available and inexpensive but have a number of limitations. Novel risk markers and imaging techniques may have a place in drug development and clinical trial design. However, their additional value above and beyond classical risk factors has yet to be determined for risk-guided therapy in CVD prevention. © 2012 The Authors Fundamental and Clinical Pharmacology © 2012 Société Française de Pharmacologie et de Thérapeutique.
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