Acute Congestive Heart Failure Patients Research Articles

Prognostic effect of a vasopressin V2 receptor antagonist in acute congestive heart failure patients with hypoperfusion, the wet-cold pattern.

This study investigated whether the oral vasopressin V2 receptor antagonist tolvaptan has beneficial effects on mortality in real-world congestive heart failure (CHF) patients with hypoperfusion (i.e. the wet-cold pattern), from the viewpoint of cardiorenal syndrome. Data on 5511 consecutive CHF patients were extracted from the Tokyo CCU Network data registry. Congestion and hypoperfusion were defined by Nohria-Stevenson clinical profiles at the time of hospitalization. Propensity scores for tolvaptan use were calculated for each patient and used to assemble two matched cohorts of patients receiving tolvaptan or not in the CHF with and without hypoperfusion groups. Of the entire study cohort, 1073 patients (19%) had CHF with hypoperfusion (i.e. the wet-cold pattern). In-hospital mortality was significantly higher for CHF patients with than without hypoperfusion (log-rank, P < 0.001). The rate of tolvaptan use did not differ significantly between CHF patients with and without hypoperfusion (15% vs. 14%, respectively; P = 0.7848). In the propensity-matched CHF with hypoperfusion cohort, there was a significant association between the use of tolvaptan and a reduction in in-hospital mortality (log-rank, P = 0.0052). Conversely, in the matched CHF without hypoperfusion cohort, tolvaptan use was not associated with in-hospital mortality (log-rank, P = 0.4417). There was a significant association between the use of tolvaptan and a reduction in in-hospital mortality in CHF patients with, but not without, hypoperfusion. These findings hint at possible individualized therapies for patients with CHF.

Complement and contact system activation in acute congestive heart failure patients.

Recent experimental data indicate a pathogenic role of complement activation in congestive heart failure (CHF). The aim of this study was to evaluate contact and complement systems activation in patients hospitalized for an acute episode of CHF. Forty-two of 80 consecutive patients admitted at our hospital with confirmed diagnosis of acute CHF were enrolled. They underwent blood sampling within 24 h from admission (T0) and at clinical stability (T1). Patients were stratified for ejection fraction (EF) based on echocardiographic test. We measured plasma levels of C3, C4, sC5b-9 and cleaved high molecular weight kininogen (contact activation marker). At T1, C3 levels increased significantly compared to T0 (97±2 versus 104±3% of total pooled plasma, P < 0·01). Classifying patients according to EF, only patients with preserved EF presented a significant increase of C3 from T0 to T1 (99±3 versus 108±4%, P=0·03). When the sample was stratified according to clinical outcome, C3 (98±3 versus 104±4%, P=0·03) and sC5b-9 levels (204±10 versus 230±11 ng/ml, P=0·03) were increased in patients who had positive outcome after hospitalization. CHF patients with preserved EF and positive outcome after hospitalization showed higher levels of sC5b-9 in the T1 period compared with T0 (211±14 versus 243±14 ng/ml, P=0·04). Our results suggest that the complement system reacts differently if CHF occurs with preserved or reduced EF. This finding is interesting if we consider the difference in epidemiology, pathogenesis and possible therapeutic approaches of these two clinical entities.

The NF-kB regulates the SHP-1 expression in monocytes in congestive heart failure.

It has been shown that functional recovery of patients with acute congestive heart failure (ACHF) after treatment with conventional drugs (CD) is mediated by suppression of inflammation in peripheral blood mononuclear cells. Here, we analyzed gene expression profiles of monocytes from symptomatic ACHF patients (NYHA Class III-IV) before and after pharmacological treatment with CD. The treatment was associated with selective down-regulation of "TNFR signaling" and pro-inflammatory mediators CCL5, MIP-1α receptor, CD14, ITGAM, and significant up-regulation of "TNFR signaling" as evidenced by increase in anti-inflammatory factors including NF-kBIA, TNFAIP3 and SHP-1. In monocyte TNF-alpha-stimulated there is a down-regulation of the phosphatase SHP-1 which induces a significant activation of TAK-1/IKK/NF-kB signaling. These findings suggest that the therapeutic impact of CD treatment in symptomatic ACHF includes negative regulation of the NF-kB signaling in monocytes and the improvement of the SHP-1 activity.

143 Emergency Medical Services Initiation of Non-Invasive Positive Pressure Ventilation in Urban Acute Congestive Heart Failure Patients

143 Emergency Medical Services Initiation of Non-Invasive Positive Pressure Ventilation in Urban Acute Congestive Heart Failure Patients

Red cell distribution width predicts short- and long-term outcomes of acute congestive heart failure more effectively than hemoglobin.

The present study compared short- and long-term prognostic values of red blood cell distribution width (RDW) with those of hemoglobin (Hgb) among patients with acute congestive heart failure (CHF) in a cardiac care unit. The cross-sectional study examined data from 521 patients with acute CHF who were admitted to a cardiac care unit and followed up for 24 months (median). Mean Hgb levels in patients who succumbed (DIH) or remained alive (AIH) were 11.0±1.8 and 11.8±2.6 g/l (P>0.05), respectively. Median values of RDW were 16.2% and 14.4%, respectively (P<0.0001). During the 24-month follow-up, mean levels of Hgb in groups with and without endpoints were 11.4±2.5 and 12.5±2.4 g/dl (P<0.0001), respectively. Median RDW values were 14.9 and 13.8%, respectively (P<0.0001). Logistic regression analysis showed that in-hospital mortality was significantly associated with RDW (P=0.044), New York Heart Association (NYHA) functional class IV (P=0.0037), estimated glomerular filtration rate (eGFR) (P=0.042) and C-reactive protein (P=0.0044), but not with Hgb (P=0.10). The multivariate Cox proportional hazard model selected RDW [hazard ratio (HR), 2.19; P<0.0001], left ventricular ejection fraction (HR 0.81, P=0.0016), age (10-year increase; HR 1.19, P=0.0017) and NYHA functional classes III/IV (HR 1.52, P=0.0029) as independent predictors of long-term outcomes after adjustment, but not Hgb (HR 1.01, P=0.86). Higher RDW values in acute CHF patients at admission were associated with worse short- and long-term outcomes and RDW values were more prognostically relevant than Hgb levels.

Respiratory sound energy and its distribution patterns following clinical improvement of congestive heart failure: a pilot study.

BackgroundAlthough congestive heart failure (CHF) patients typically present with abnormal auscultatory findings on lung examination, respiratory sounds are not normally subjected to additional analysis. The aim of this pilot study was to examine respiratory sound patterns of CHF patients using acoustic-based imaging technology. Lung vibration energy was examined during acute exacerbation and after clinical improvement.MethodsRespiratory sounds throughout the respiratory cycle were captured using an acoustic-based imaging technique. Twenty-three consecutive CHF patients were imaged at the time of presentation to the emergency department and after clinical improvement. Digital images were created (a larger image represents more homogeneously distributed vibration energy of respiratory sound). Geographical area of the images and respiratory sound patterns were quantitatively analyzed. Data from the CHF patients were also compared to healthy volunteers.ResultsThe median (interquartile range) geographical areas of the vibration energy image of acute CHF patients without and with radiographically evident pulmonary edema were 66.9 (9.0) and 64.1(9.0) kilo-pixels, respectively (p < 0.05). After clinical improvement, the geographical area of the vibration energy image of CHF patients without and with radiographically evident pulmonary edema were increased by 18 ± 15% (p < 0.05) and 25 ± 16% (p < 0.05), respectively.ConclusionsWith clinical improvement of acute CHF exacerbations, there was more homogenous distribution of lung vibration energy, as demonstrated by the increased geographical area of the vibration energy image.

Right bundle branch block and long‐term mortality in patients with acute congestive heart failure

Risk stratification in acute congestive heart failure (ACHF) is poorly defined. The aim of the present study was to assess the impact of right bundle brunch block (RBBB) on long-term mortality in patients presenting with ACHF. The initial 12-lead electrocardiogram was analysed for RBBB in 192 consecutive patients presenting with ACHF to the emergency department. The primary endpoint was all-cause mortality during 720-day follow-up. This study included an elderly cohort (mean age 74 years) of ACHF patients. RBBB was present in 27 patients (14%). Age, sex, B-type natriuretic peptide levels and initial management were similar in patients with RBBB when compared with patients without RBBB. However, patients with RBBB more often had pulmonary comorbidity. A total of 84 patients died during follow-up. Kaplan-Meier analysis revealed that mortality at 720 days was significantly higher in patients with RBBB when compared with patients without RBBB (63% vs. 39%, P = 0.004). In Cox proportional hazard analysis, RBBB was associated with a two-fold increase in mortality (hazard ratio 2.18, 95% CI 1.26-3.66; P = 0.003). This association persisted after adjustment for age and comorbidity. RBBB is a powerful predictor of mortality in patients with ACHF. Early identification of this high-risk group may help to offer tailored treatment in order to improve outcome.

Interleukin-6, tissue factor and von Willebrand factor in acute decompensated heart failure: relationship to treatment and prognosis.

Arterial thrombotic and thromboembolic complications are increased in congestive heart failure (CHF), and are a particular problem in acute decompensated heart failure, which carries a poor prognosis. As interleukin-6 (IL-6) has been shown to induce the potent procoagulant tissue factor (TF) in experimental models, we hypothesized that the pro-inflammatory IL-6 may be one mechanism contributing to thrombosis in heart failure, mediated via endothelial expression of TF on activated/damaged cells [indicated by plasma von Willebrand factor (vWF)]. Seventy-seven patients (67% men, New York Heart Association class III-IV, 87%) with acute CHF were recruited, and were compared with 53 chronic stable CHF patients in sinus rhythm (66% men, New York Heart Association class III-IV, 2%) and 37 healthy controls (68% men). Acute CHF patients in sinus rhythm had elevated baseline levels of IL-6 (P < 0.0001), TF (P = 0.041) and vWF (P < 0.0001) (all measured by enzyme-linked immunosorbent assay) compared with both chronic CHF and healthy control groups. A correlation exists in acute CHF between baseline TF and IL-6 (Spearman r = 0.64, P < 0.0001). After 3 months treatment, with control or alleviation of heart failure symptoms in 40 patients, there was a fall in levels of IL-6 (P < 0.0001) and vWF (P < 0.0001), but levels still remained significantly higher than healthy controls. Patients who died at 6 months follow-up also had higher baseline levels of IL-6 (P = 0.008), TF (P = 0.037) and vWF (P = 0.039) when compared with those who remained alive. Elevated IL-6 may contribute to the thrombotic and thromboembolic complications in acute heart failure, in a process mediated via increased TF and vWF. Improvement of symptoms and plasma markers after treatment of acute CHF and prediction of prognosis by the markers may be useful in the clinical setting.

Low urinary 6-sulfatoxymelatonin levels in patients with severe congestive heart failure.

To assess urinary 6-sulfatoxymelatonin excretion in patients admitted to the hospital because of congestive heart failure (CHF). Urinary 6-sulfatoxymelatonin was measured by a specific radioimmunoassay in 33 hospitalized patients with CHF and in 146 healthy ambulatory volunteers. Individuals with hepatic or renal failure were excluded from the sample. Data were analyzed by the Mann-Whitney test and regression analysis. 6-Sulfatoxymelatonin levels were significantly lower in CHF patients than controls (median 2.6 vs 6.02 microg, p < 0.0001). This decrease was observed regardless of beta-adrenergic blocker or benzodiazepine medication. A significant decrease in 6-sulfatoxymelatonin excretion occurred with age. There were no significant differences in urinary 6-sulfatoxymelatonin levels between chronic and acute CHF patients. The results suggest that circulating melatonin levels are low in patients with CHF. Such a decrease may precede aggravation of heart failure.

Acute Congestive Heart Failure and Tumor Necrosis Factor Alpha.

Congestive heart failure is prevalent in the elderly; recurrent hospital admissions for acute deterioration is a major health care problem. We examined tumor necrosis factor alpha levels in 31 congestive heart failure patients who were admitted to the hospital due to acute cardiogenic pulmonary edema. Blood samples were taken within 24 hours of admission and at the time of discharge after recovery. Tumor necrosis factor alpha levels were also measured in 10 stable congestive heart failure outpatients and 16 healthy controls. Tumor necrosis factor alpha level at admission was higher than at time of discharge (4.6Â+/-1.9 vs. 3.4Â+/-1.1 (rg/mL, p is less than 0.02). Mean tumor necrosis factor alpha level of stable congestive heart failure outpatient was 2.6Â+/-0.7 rg/mL healthy controls had significantly lower tumor necrosis factor alpha levels (1.7Â+/-0.7 rg/mL) than congestive heart failure patients (p is less than 0.01). tumor necrosis factor alpha levels were highest among acute congestive heart failure patients. Elevated tumor necrosis factor alpha appears to be related to the exacerbation of congestive heart failure and may be a marker for deterioration. (c) 2000 by CVRR, Inc.

Bi-level positive airway pressure support system use in acute congestive heart failure: preliminary case series.

To describe the use of a noninvasive bi-level positive airway pressure (PAP) support system for ED patients with acute congestive heart failure (CHF). Retrospective case series analysis of ED patients presenting with acute CHF in imminent need of endotracheal intubation (ETI) managed with a bi-level PAP system. The bi-level PAP system was applied at the discretion of the treating emergency physician. Management of the bi-level PAP system, including setting of inspiratory PAP (IPAP) and expiratory PAP (EPAP), weaning, adjunct pharmacologic therapy, and failure of bi-level PAP support, was determined by the treating physician. Only two (9%) of 22 patient presentations necessitated ETI. The mean duration of bi-level PAP therapy was 7.9 hours. The mean maximum IPAP and EPAP settings were 10.8 and 5.8 cm H2O, respectively. Mean intensive care unit length of stay (LOS) was 2.4 days, with a median LOS of only 1 day. There were three deaths in the series; none were attributed to the bi-level PAP system. No technical difficulty with the bi-level PAP system was noted. Noninvasive pressure support ventilation with a bi-level PAP support system may avert ETI in acute CHF patients. This device can be effectively used by ED personnel.

Relationship between plasma atrial natriuretic factor and opioid peptide levels in healthy subjects and in patients with acute congestive heart failure.

We evaluated plasma atrial natriuretic factor (ANF), beta-endorphin, met-enkephalin, dynorphin and noradrenaline levels in 20 healthy subjects and 20 acute congestive heart failure (CHF) patients. In all acute CHF patients plasma values of these hormones were higher than in healthy subjects. The hormonal pattern differed in patients with the more severe acute CHF (group 1) from patients with less severe acute CHF (group 2) (ANF 53.8 +/- 1.0 vs 34.6 +/- 1.5 pg.ml-1, noradrenaline 563.8 +/- 13.4 vs 202.4 +/- 10.6 pg.ml-1, met-enkephalin 41.0 +/- 3.2 vs 17.0 +/- 1.6 fmol.ml-1, dynorphin 46.8 +/- 3.7 vs 25.2 +/- 2.0 fmol.ml-1, P < 0.01; beta-endorphin 50.6 +/- 5.2 vs 41.8 +/- 4.1 fmol.ml-1,ns). Administration of an opioid antagonist (naloxone, 8 mg i.v.) did not modify ANF or noradrenaline concentration in healthy subjects. In group 1 naloxone administration significantly raised ANF (68.0 +/- 1.4 pg.ml-1), noradrenaline (776.6 +/- 18.7 pg.ml-1), blood pressure and heart rate, whereas in group 2 it significantly decreased ANF values (21.9 +/- 0.5 pg.ml-1) and did not modify the other parameters. Our findings suggest that the opioid system affects ANF release in acute CHF. In patients with severe CHF opioid peptides may attenuate ANF secretion reducing noradrenergic stimulation. On the other hand, when CHF is less severe and the sympathetic activity is moderate, opioid peptides may directly stimulate ANF secretion.