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001-es BibID:	BIBFORM076735
Első szerző:	Bouchez, Stefan
Cím:	Levosimendan in Acute and Advanced Heart Failure: an Expert Perspective on Posology and Therapeutic Application / S. Bouchez, F. Fedele, G. Giannakoulas, F. Gustafsson, Veli-Pekka Harjola, K. Karason, M. Kivikko, D. von Lewinski, F. Oliva, Z. Papp, J. Parissis, Piero Pollesello, G. Pölzl, C. Tschöpe
Dátum:	2018
ISSN:	0920-3206
Megjegyzések:	Levosimendan, a calcium sensitizer and potassium channel-opener, is widely appreciated by many specialist heart failure practitioners for its effects on systemic and pulmonary hemodynamics and for the relief of symptoms of acute heart failure. The drug's impact on mortality in large randomized controlled trials has been inconsistent or inconclusive but, in contrast to conventional inotropes, there have been no indications of worsened survival and some signals of improved heart failure-related quality of life. For this reason, levosimendan has been proposed as a safer inodilator option than traditional agents in settings, such as advanced heart failure. Positive effects of levosimendan on renal function have also been described. At the HEART FAILURE 2018 congress of the Heart Failure Association of the European Society of Cardiology, safe and effective use levosimendan in acute and advanced heart failure was examined in a series of expert tutorials. The proceedings of those tutorials are summarized in this review, with special reference to advanced heart failure and heart failure with concomitant renal dysfunction. Meta-analysis of clinical trials data is supportive of a renal-protective effect of levosimendan, while physiological observations suggest that this effect is exerted at least in part via organ-specific effects that may include selective vasodilation of glomerular afferent arterioles and increased renal blood flow, with no compromise of renal oxygenation. These lines of evidence require further investigation and their clinical significance needs to be evaluated in specifically designed prospective trials.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Inodilators Inotropes Acute heart failure Advanced heart failure Levosimendan Renal function
Megjelenés:	Cardiovascular Drugs And Therapy. - 32 : 6 (2018), p. 617-624. -
További szerzők:	Fedele, Francesco Giannakoulas, George Gustafsson, Finn Harjola, Veli-Pekka Karason, Kristian Kivikko, Matti von Lewinski, Dirk Oliva, Fabrizio Papp Zoltán (1965-) (kardiológus, élettanász) Parissis, John Pollesello, Piero Pölzl, Gerhard Tschöpe, Carsten
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001-es BibID:	BIBFORM010418
Első szerző:	Brugts, J. J.
Cím:	The rationale and design of the PERindopril GENEtic association study (PERGENE) : a pharmacogenetic analysis of angiotensin-converting enzyme inhibitor therapy in patients with stable coronary artery disease / Brugts, J. J., de Maat, M. P., Boersma, E., Witteman, J. C., van Duijn, C., Uitterlinden, A. G., Bertrand, M., Remme, W., Fox, K., Ferrari, R., Danser, A. H., Simoons, M. L., The EUROPA-PERGENE Investigators
Dátum:	2009
ISSN:	0920-3206 (Print)
Megjegyzések:	Angiotensin-converting enzyme (ACE) inhibitors reduce clinical symptoms and improve outcome in patients with hypertension, heart failure, and stable coronary artery disease (CAD) and are among the most frequently used drugs in these patient groups. For hypertension, treatment is guided by the level of blood pressure. In the secondary prevention setting, there are no means of guiding therapy. Prior attempts to target ACE-inhibitors to those patients that are most likely to benefit have not been successful, mainly due to the consistency in the treatment effect in clinical subgroups. Still, for prolonged prophylactic treatment with ACE-inhibitors it would be best to target treatment to only those patients most likely to benefit, which would considerably lower the number needed to treat and increase cost-effectiveness. A new approach for such "tailored-therapy" may be to integrate information on the genetic variation between patients. Until now, pharmacogenetic research of the efficacy of ACE-inhibitor therapy in CAD patients is still in a preliminary stage. METHODS: The PERindopril GENEtic association study (PERGENE) is a substudy of the EUROPA trial, a randomized double-blind placebo-controlled multicentre clinical trial which demonstrated a beneficial effect of the ACE-inhibitor perindopril in reducing cardiovascular morbidity and mortality in 12.218 patients with stable coronary artery disease (mean follow-up 4.2 years). Blood tubes were received from patients at the beginning of the EUROPA trial and buffy coats were stored at -40 degrees C at the central core laboratory. Candidate genes were selected in the renin-angiotensin-system and bradykinin pathways. Polymorphisms were selected based on haplotype tagging principles using the HapMap genome project, Seattle and other up-to-date genetic database platforms to comprehensively cover all common genetic variation within the genes. Selection also took into consideration the functionality of SNP's, location within the gene (promoter) and existing relevant literature. The main outcome measure of PERGENE is the effect of genetic factors on the treatment benefit with ACE-inhibitors. The size of this pharmacogenetic substudy allows detection with a statistical power of 98% to detect a difference in hazard ratios (treatment effect) of 20% between genotypes with minor allele frequency of 0.20 (two-sided alpha 0.05). CONCLUSION: The PERGENE study is a large cardiovascular pharmacogenetic study aimed to assess the feasibility of pharmacogenetic profiling of the treatment effect of ACE-inhibitor use with the perspective to individualize treatment in patients with stable coronary artery disease.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Angiotensin-Converting Enzyme Inhibitors Cardiovascular Diseases control Coronary Artery Disease Double-Blind Method Female Follow-Up Studies Humans Male Perindopril Pharmacogenetics Polymorphism, Single Nucleotide Randomized Controlled Trials as Topic Research Design
Megjelenés:	Cardiovascular Drugs and Therapy. - 23 : 2 (2009), p. 171-181. -
További szerzők:	de Maat, M. P. Boersma, E. Witteman, J. C. Duijn, C., van Uitterlinden, A. G. Bertrand, M. Remme, W. Fox, K. Ferrari, Roberto Danser, A. H. Simoons, M. L. Édes István (1952-) (kardiológus) The EUROPA-PERGENE Investigators
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001-es BibID:	BIBFORM010153
Első szerző:	Harangi Mariann (belgyógyász, endokrinológus)
Cím:	Benefits and difficulties in measuring HDL subfractions and human paraoxonase-1 activity during statin treatment / Harangi Mariann, Seres Ildikó, Harangi János, Paragh György
Dátum:	2009
ISSN:	0920-3206 (Print)
Megjegyzések:	Dyslipidaemia including decreased high density lipoprotein cholesterol concentration is one of several factors that have been implicated in increased cardiovascular risk. Since their introduction in the 1980s, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have emerged as the one of the best-selling class of medications to date, with numerous trials demonstrating powerful efficacy in preventing cardiovascular diseases. Although statins have been shown to modestly raise or not alter HDL-cholesterol, their effect on HDL subfractions and on HDL-associated enzymes including human paraoxonase- 1 (PON1) has not yet been fully explored. This review summarizes the currently availabe data on the effect of statins on HDL subfractions and on PON1 activity with a particular emphasis on the clinical relevance of these effects. Moreover, methodological problems of HDL subfraction and PON1 activity determinations are also discussed.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Cardiovascular Drugs and Therapy. - 23 : 6 (2009), p. 501-510. -
További szerzők:	Seres Ildikó (1954-) (biokémikus) Harangi János (1950-) (biokémikus, kromatográfus) Paragh György (1953-) (belgyógyász)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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