| 1. |
- Johansson, Peter, et al.
(författare)
-
Association Between Prehospital Delay and Subsequent Clinical Course in Patients With/Hospitalized for Heart Failure
- 2012
-
Ingår i: Journal of Cardiac Failure. - : Elsevier. - 1071-9164 .- 1532-8414. ; 18:3, s. 202-207
-
Tidskriftsartikel (refereegranskat)abstract
- Background: The clinical consequences of prehospital delay in heart failure (HF) patients are unknown. This study explores the relationship between prehospital delay of HF patients and length of hospital stay, plasma values of brain natriuretic peptides (BNP) as well as the association of delay with all-cause mortality, readmission for HF, or all-cause readmissions during short-(60 days) and long-term (18 months) follow-up. less thanbrgreater than less thanbrgreater thanMethods: Data from 1023 hospitalized HF patients mean aged 71 years from the Coordinating study evaluating Outcomes of Advising and Counselling in HF study were analyzed. less thanbrgreater than less thanbrgreater thanResults: Patients who delayed less than 1 day had significantly shorter stay in hospital (10 days vs. 11 days, P = 0.033). They also had significantly (P = 0.004) lower median plasma values of BNP (377 pg/mL) at discharge compared to patients who delayed andgt;24 hours (492 pg/mL). Delay was not related to all-cause mortality and/or readmissions for HF. less thanbrgreater than less thanbrgreater thanConclusion: Although patients with a prehospital delay less than 1 day were more symptomatic on admission, they had a shorter hospital stay as well as lower plasma values of BNP at discharge. Delay was not associated hospital readmissions or mortality after discharge.
|
|
| 2. |
- Ghali, Jalal K, et al.
(författare)
-
The influence of renal function on clinical outcome and response to beta-blockade in systolic heart failure: insights from Metoprolol CR/XL Randomized Intervention Trial in Chronic HF (MERIT-HF).
- 2009
-
Ingår i: Journal of cardiac failure. - : Elsevier BV. - 1532-8414 .- 1071-9164. ; 15:4, s. 310-8
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Limited information is available on the risk and impact of renal dysfunction on the response to beta-blockade and mode of death in systolic heart failure (HF). METHODS AND RESULTS: Renal function was estimated with glomerular filtration rate (eGFR) using the simplified Modification of Diet in Renal Disease (MDRD) equation. Patients from the Metoprolol CR/XL Controlled Randomized Intervention Trial in Chronic HF (MERIT-HF) were divided into 3 renal function subgroups (MDRD formula): eGFR(MDRD) > 60 (n = 2496), eGFR(MDRD) 45 to 60 (n = 976), and eGFR(MDRD) < 45 mL/min per 1.73 m(2) body surface area (n = 493). Hazard ratio (HR) was estimated with Cox proportional hazards models adjusted for prespecified risk factors. Placebo patients with eGFR < 45 had significantly higher risk than those with eGFR > 60: HR for all-cause mortality, 1.90 (95% confidence interval [CI], 1.28 to 2.81) comparing placebo patients with eGFR < 45 and eGFR > 60, and for the combined end point of all-cause mortality/hospitalization for worsening HF (time to first event): HR, 1.91 (95% CI, 1.44 to 2.53). No significant increase in risk with deceased renal function was observed for those randomized to metoprolol controlled release (CR)/extended release (XL) due to a highly significant decrease in risk on metoprolol CR/XL in those with eGFR < 45. For total mortality, metoprolol CR/XL vs placebo: HR, 0.41 (95% CI. 0.25 to 0.68; P < .001) in those with eGFR < 45 compared with HR, 0.71 (95% CI, 0.54 to 0.95; P < .021) for those with eGFR > 60; corresponding data for the combined end point was HR, 0.44 (95% CI, 0.31 to 0.63; P < .0001) and HR, 0.75 (0.62 to 0.92; P = .005, respectively; P = .095 for interaction by treatment for total mortality; P = .011 for combined end point). Metoprolol CR/XL was well tolerated in all 3 renal function subgroups. CONCLUSIONS: Renal function as estimated by eGFR was a powerful predictor of death and hospitalizations from worsening HF. Metoprolol CR/XL was at least as effective in reducing death and hospitalizations for worsening HF in patients with eGFR < 45 as in those with eGFR > 60.
|
|
| 3. |
- Johansson, Peter, et al.
(författare)
-
Depression and the delay between symptom onset and hospitalization in heart failure patients.
- 2011
-
Ingår i: European Journal of Heart Failure. - : Wiley. - 1388-9842 .- 1879-0844. ; 13:2, s. 214-219
-
Tidskriftsartikel (refereegranskat)abstract
- AIMS: Heart failure (HF) patients frequently suffer from episodes of deterioration and may need medical treatment. An adequate reaction from the patient is needed to decrease the delay between the onset of deterioration and consulting a medical professional (i.e. consulting behaviour). The aim of the present study was to evaluate whether depressive symptoms are associated with the duration of the delay between the onset of symptoms of worsening HF and hospitalization, and to examine how consulting behaviour correlates to depressive symptoms and delay in HF patients. METHODS AND RESULTS: Data on the time between the onset of symptoms of worsening HF and hospitalization, depressive symptoms, and self-care behaviour were collected in 958 HF patients (37% female; age 71 ± 11 years; New York Heart Association functional class II-IV), using validated questionnaires. The median delay time of the total sample was 72 h (ranging from 0 to 243 days). Patients with depressive symptoms delayed longer compared with those without depressive symptoms (120 vs. 54 h, P= 0.001). Patients with depressive symptoms had a 1.5 times higher risk for a delay of ≥72 h, independent of demographic and clinical variables (P= 0.008). Consulting behaviour did not correlate with depressive symptoms but was weakly associated with delay (r= -0.07, P= 0.03). CONCLUSIONS: Heart failure patients with depressive symptoms have a significantly longer delay between HF deterioration and hospital admission. Interventions designed to improve the consulting behaviour in HF patients with depressive symptoms may have a limited effect on delay. Further research is needed to obtain more insight into the mechanisms underlying the relationship between delay and depression.
|
|
| 4. |
- Johansson, Peter, et al.
(författare)
-
Depressive symptoms and inflammation in patients hospitalized for heart failure
- 2011
-
Ingår i: American Heart Journal. - : Elsevier Science B.V., Amsterdam. - 0002-8703 .- 1097-6744. ; 161:6, s. 1053-1059
-
Tidskriftsartikel (refereegranskat)abstract
- Background Depressive symptoms in patients with heart failure (HF) are common and might be associated with inflammation. No studies have examined both the cross-sectional and prospective association between inflammation and depressive symptoms in patients with HF with adequate correction for disease severity. The aim of this study was to describe if the cytokines interleukin-6 (IL-6) and C-reactive protein (CRP) are associated with depressive symptoms in hospitalized HF patients. Methods Data from 517 patients hospitalized for HF from the COACH study were analyzed on inflammation markers (IL-6 and CRP) and depressive symptoms (Center for Epidemiological Studies Depression-Scale). Results Heart failure patients with depressive symptoms (n = 208, 40%) had significantly higher plasma values of IL-6 (median 12.8 pg/mL vs median 11.0 pg/mL, P = .018) and CRP (median 2.4 mg/mL vs median 2.1 mg/mL, P = .03) compared with the nondepressed patients. Structural equation modelling showed that the factor inflammation (including IL-6 and CRP) was associated with depressive symptoms (beta = 0.18, P less than .05) when left ventricular ejection fraction and plasma values brain natriuretic peptides were included in the model. A small negative (beta = -0.18, P less than .05) effect was found between inflammation at baseline and the change in depressive symptoms during the 18 months of follow-up. Conclusions Higher levels of inflammatory markers are independently associated with depressive symptoms in HF patients, even after correcting for disease severity. There is no clear relationship between inflammation at baseline and depressive symptoms during the 18 months of follow-up.
|
|
