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- Böhm, Michael, et al.
(författare)
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Heart rate at baseline influences the effect of ivabradine on cardiovascular outcomes in chronic heart failure: analysis from the SHIFT study
- 2013
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Ingår i: Clinical research in cardiology : official journal of the German Cardiac Society. - : Springer Science and Business Media LLC. - 1861-0692. ; 102:1, s. 11-22
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: We analysed the effect of ivabradine on outcomes in heart failure (HF) patients on recommended background therapies with heart rates >/=75 bpm and <75 bpm in the SHIFT trial. A cut-off value of >/=75 bpm was chosen by the EMEA for approval for the use of ivabradine in chronic heart failure. METHODS: The SHIFT population was divided by baseline heart rate >/=75 or <75 bpm. The effect of ivabradine was analysed for primary composite endpoint (cardiovascular death or HF hospitalization) and other endpoints. RESULTS: In the >/=75 bpm group, ivabradine reduced primary endpoint (HR 0.76, 95 % CI 0.68-0.85, P < 0.0001), all-cause mortality (HR 0.83, 95 % CI, 0.72-0.96, P = 0.0109), cardiovascular mortality (HR 0.83, 95 % CI, (0.71-0.97, P = 0.0166), HF death (HR 0.61, 95 % CI, 0.46-0.81, P < 0.0006), and HF hospitalization (HR 0.70, 95 % CI, 0.61-0.80, P < 0.0001). Risk reduction depended on heart rate after 28 days, with the best protection for heart rates <60 bpm or reductions >10 bpm. None of the endpoints was significantly reduced in the <75 bpm group, though there were trends for risk reductions in HF death and hospitalization for heart rate <60 bpm and reductions >10 bpm. Ivabradine was tolerated similarly in both groups. CONCLUSION: The effect of ivabradine on outcomes is greater in patients with heart rate >/=75 bpm with heart rates achieved <60 bpm or heart rate reductions >10 bpm predicting best risk reduction. Our findings emphasize the importance of identification of high-risk HF patients by high heart rates and their treatment with heart rate-lowering drugs such as ivabradine.
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- Komajda, Michel, et al.
(författare)
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Relations between professional medical associations and the health-care industry, concerning scientific communication and continuing medical education: a Policy Statement from the European Society of Cardiology.
- 2012
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Ingår i: European Heart Journal. - : Oxford University Press. - 0195-668X .- 1522-9645. ; 33:5, s. 666-674
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Tidskriftsartikel (refereegranskat)abstract
- Physicians have an ethical duty to keep up-to-date with current knowledge. Professional medical associations such as the European Society of Cardiology (ESC) support these obligations. In Europe, the costs of continuing medical education (CME) are insufficiently supported from governments and employers; however, medical associations have been criticized for accepting alternative financial support from industry. Medical education and training in research include learning how to assess the quality and reliability of any information. There is some risk of bias in any form of scientific communication including intellectual, professional, and financial and it is essential that in particular, the latter must be acknowledged by full disclosure. It is essential that there is strong collaboration between basic and clinical researchers from academic institutions on the one hand, with engineers and scientists from the research divisions of device and pharmaceutical companies on the other. This is vital so that new diagnostic methods and treatments are developed. Promotion of advances by industry may accelerate their implementation into clinical practice. Universities now frequently exhort their academic staff to protect their intellectual property or commercialize their research. Thus, it is not commercial activity or links per se that have become the target for criticism but the perceived influence of commercial enterprises on clinical decision-making or on messages conveyed by professional medical organizations. This document offers the perspective of the ESC on the current debate, and it recommends how to minimize bias in scientific communications and CME and how to ensure proper ethical standards and transparency in relations between the medical profession and industry.
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- McAlister, Finlay A, et al.
(författare)
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Renal dysfunction in patients with heart failure with preserved versus reduced ejection fraction: impact of the new Chronic Kidney Disease-Epidemiology Collaboration Group formula.
- 2012
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Ingår i: Circulation. Heart failure. - 1941-3297. ; 5:3, s. 309-14
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Tidskriftsartikel (refereegranskat)abstract
- Prior studies in heart failure (HF) have used the Modification of Diet in Renal Disease (MDRD) equation to calculate estimated glomerular filtration rate (eGFR). The Chronic Kidney Disease-Epidemiology Collaboration Group (CKD-EPI) equation provides a more-accurate eGFR than the MDRD when compared against the radionuclide gold standard. The prevalence and prognostic import of renal dysfunction in HF if the CKD-EPI equation is used rather than the MDRD is uncertain.We used individual patient data from 25 prospective studies to stratify patients with HF by eGFR using the CKD-EPI and the MDRD equations and examined survival across eGFR strata. In 20 754 patients (15 962 with HF with reduced ejection fraction [HF-REF] and 4792 with HF with preserved ejection fraction [HF-PEF]; mean age, 68 years; deaths per 1000 patient-years, 151; 95% CI, 146-155), 10 589 (51%) and 11 422 (55%) had an eGFR <60 mL/min using the MDRD and CKD-EPI equations, respectively. Use of the CKD-EPI equation resulted in 3760 (18%) patients being reclassified into different eGFR risk strata; 3089 (82%) were placed in a lower eGFR category and exhibited higher all-cause mortality rates (net reclassification improvement with CKD-EPI, 3.7%; 95% CI, 1.5%-5.9%). Reduced eGFR was a stronger predictor of all-cause mortality in HF-REF than in HF-PEF.Use of the CKD-EPI rather than the MDRD equation to calculate eGFR leads to higher estimates of renal dysfunction in HF and a more-accurate categorization of mortality risk. Renal function is more closely related to outcomes in HF-REF than in HF-PEF.
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- Villard, Eric, et al.
(författare)
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A genome-wide association study identifies two loci associated with heart failure due to dilated cardiomyopathy
- 2011
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Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 32:9, s. 1065-1076
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Tidskriftsartikel (refereegranskat)abstract
- Aims: Dilated cardiomyopathy (DCM) is a major cause of heart failure with a high familial recurrence risk. So far, the genetics of DCM remains largely unresolved. We conducted the first genome-wide association study (GWAS) to identify loci contributing to sporadic DCM.Methods and results: One thousand one hundred and seventy-nine DCM patients and 1108 controls contributed to the discovery phase. Pools of DNA stratified on disease status, population, age, and gender were constituted and used for testing association of DCM with 517 382 single nucleotide polymorphisms (SNPs). Three DCM-associated SNPs were confirmed by individual genotyping (P < 5.0 10−7), and two of them, rs10927875 and rs2234962, were replicated in independent samples (1165 DCM patients and 1302 controls), with P-values of 0.002 and 0.009, respectively. rs10927875 maps to a region on chromosome 1p36.13 which encompasses several genes among which HSPB7 has been formerly suggested to be implicated in DCM. The second identified locus involves rs2234962, a non-synonymous SNP (c.T757C, p. C151R) located within the sequence of BAG3 on chromosome 10q26. To assess whether coding mutations of BAG3 might cause monogenic forms of the disease, we sequenced BAG3 exons in 168 independent index cases diagnosed with familial DCM and identified four truncating and two missense mutations. Each mutation was heterozygous, present in all genotyped relatives affected by the disease and absent in a control group of 347 healthy individuals, strongly suggesting that these mutations are causing the disease.Conclusion: This GWAS identified two loci involved in sporadic DCM, one of them probably implicates BAG3. Our results show that rare mutations in BAG3 contribute to monogenic forms of the disease, while common variant(s) in the same gene are implicated in sporadic DCM.
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