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Persistent use of evidence-based pharmacotherapy in heart failure is associated with improved outcomes.

https://arctichealth.org/en/permalink/ahliterature162325
Source
Circulation. 2007 Aug 14;116(7):737-44
Publication Type
Article
Date
Aug-14-2007
Author
Gunnar H Gislason
Jeppe N Rasmussen
Steen Z Abildstrom
Tina Ken Schramm
Morten Lock Hansen
Pernille Buch
Rikke Sørensen
Fredrik Folke
Niels Gadsbøll
Søren Rasmussen
Lars Køber
Mette Madsen
Christian Torp-Pedersen
Author Affiliation
Department of Cardiology, Gentofte University Hospital, Hellerup, Denmark. gg@heart.dk
Source
Circulation. 2007 Aug 14;116(7):737-44
Date
Aug-14-2007
Language
English
Publication Type
Article
Keywords
Adrenergic beta-Antagonists - administration & dosage - therapeutic use
Adult
Angiotensin II Type 2 Receptor Blockers
Angiotensin-Converting Enzyme Inhibitors - administration & dosage - therapeutic use
Cardiac Output, Low - drug therapy - mortality
Denmark
Drug Prescriptions - statistics & numerical data
Evidence-Based Medicine
Hospital Mortality
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors - administration & dosage - therapeutic use
Patient compliance
Spironolactone - administration & dosage - therapeutic use
Time Factors
Treatment Outcome
Abstract
Undertreatment with recommended pharmacotherapy is a common problem in heart failure and may influence prognosis. We studied initiation and persistence of evidence-based pharmacotherapy in 107,092 patients discharged after first hospitalization for heart failure in Denmark from 1995 to 2004.
Prescriptions of dispensed medication and mortality were identified by an individual-level linkage of nationwide registers. Inclusion was irrespective of left ventricular function. Treatment with renin-angiotensin inhibitors (eg, angiotensin-converting enzyme inhibitors and angiotensin-2 receptor blockers), beta-blockers, spironolactone, and statins was initiated in 43%, 27%, 19%, and 19% of patients, respectively. Patients who did not initiate treatment within 90 days of discharge had a low probability of later treatment initiation. Treatment dosages were in general only 50% of target dosages and were not increased during long-term treatment. Short breaks in therapy were common, but most patients reinitiated treatment. Five years after initiation of treatment, 79% patients were still on renin-angiotensin inhibitors, 65% on beta-blockers, 56% on spironolactone, and 83% on statins. Notably, multiple drug treatment and increased severity of heart failure was associated with persistence of treatment. Nonpersistence with renin-angiotensin inhibitors, beta-blockers, and statins was associated with increased mortality with hazard ratios for death of 1.37 (95% CI, 1.31 to 1.42), 1.25 (95% CI, 1.19 to 1.32), 1.88 (95% CI, 1.67 to 2.12), respectively.
Persistence of treatment was high once medication was started, but treatment dosages were below recommended dosages. Increased severity of heart failure or increased number of concomitant medications did not worsen persistence, but nonpersistence identified a high-risk population of patients who required special attention. A focused effort on early treatment initiation, appropriate dosages, and persistence with the regimen is likely to provide long-term benefit.
Notes
Comment In: Circulation. 2007 Aug 14;116(7):693-517698742
PubMed ID
17646585 View in PubMed
Less detail

Role of kinins in chronic heart failure and in the therapeutic effect of ACE inhibitors in kininogen-deficient rats.

https://arctichealth.org/en/permalink/ahliterature54138
Source
Am J Physiol Heart Circ Physiol. 2000 Feb;278(2):H507-14
Publication Type
Article
Date
Feb-2000
Author
Y H Liu
X P Yang
D. Mehta
M. Bulagannawar
G M Scicli
O A Carretero
Author Affiliation
Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Michigan 48202-2689, USA.
Source
Am J Physiol Heart Circ Physiol. 2000 Feb;278(2):H507-14
Date
Feb-2000
Language
English
Publication Type
Article
Keywords
Angiotensin-Converting Enzyme Inhibitors - therapeutic use
Animals
Cardiac Output, Low - drug therapy - mortality - pathology - physiopathology
Chronic Disease
Heart - drug effects - physiopathology
Hemodynamic Processes - drug effects
Kininogens - blood - deficiency - genetics
Kinins - physiology
Male
Myocardial Infarction - pathology
Myocardium - pathology
Organ Size - drug effects
Rats
Rats, Inbred BN - genetics
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Abstract
Using Brown Norway Katholiek (BNK) rats, which are deficient in kininogen (kinin precursor) due to a mutation in the kininogen gene, we examined the role of endogenous kinins in 1) normal cardiac function; 2) myocardial infarction (MI) caused by coronary artery ligation; 3) cardiac remodeling in the development of heart failure (HF) after MI; and 4) the cardioprotective effect of angiotensin-converting enzyme inhibitors (ACEI) on HF after MI. Two months after MI, rats were randomly treated with vehicle or the ACEI ramipril for 2 mo. Brown Norway rats (BN), which have normal kininogen, were used as controls. Left ventricular (LV) end-diastolic volume (EDV), end-systolic volume (ESV), end-diastolic pressure (EDP), and ejection fraction (EF) as well as myocardial infarct size (IS), interstitial collagen fraction (ICF), cardiomyocyte cross-sectional area (MCA), and oxygen diffusion distance (ODD) were measured. We found that 1) cardiac hemodynamics, function, and histology were the same in sham-ligated BN and BNK rats; 2) IS was similar in BN and BNK; 3) in rats with HF treated with vehicle, the decrease in LVEF and the increase in LVEDV, LVESV, LVEDP, ICF, MCA, and ODD did not differ between BNK and BN; and 4) ACEI increased EF, decreased LVEDV and LVESV, and improved cardiac remodeling in BN-HF rats, and these effects were partially blocked by the bradykinin B(2) receptor antagonist icatibant (HOE-140). In BNK-HF rats, ACEI failed to produce these beneficial cardiac effects. We concluded that in rats, lack of kinins does not influence regulation of normal cardiac function, myocardial infarct size, or development of HF; however, kinins appear to play an important role in the cardioprotective effect of ACEI, since 1) this effect was significantly diminished in kininogen-deficient rats and 2) it was blocked by a B(2) kinin receptor antagonist in BN rats.
PubMed ID
10666082 View in PubMed
Less detail

[Scientific symposium "Treatment and Survival in Cardiac Insufficiency"].

https://arctichealth.org/en/permalink/ahliterature222487
Source
Kardiologiia. 1993;33(12):55-7
Publication Type
Conference/Meeting Material
Date
1993