Fibrinogen-to-Albumin Ratio in Patients with Acute Heart Failure.

The fibrinogen-to-albumin ratio (FAR) in the acute phase of acute heart failure (AHF) has seldom been evaluated.A total of 1,402 hospitalized AHF patients were analyzed. We calculated FAR using the following formula: plasma fibrinogen (g/L) /serum albumin (g/L) × 1,000. Patients were divided into 3 groups according to FAR value quartiles (low-FAR [Q1, FAR ≤ 564, n = 352], middle-FAR [Q2/Q3, 565 ≤ FAR ≤ 1,071, n = 700], and high-FAR [Q4, FAR ≥ 1,072, n = 350]). The median (interquartile range) FAR value was 855 (710-1,103). A multivariate logistic regression model showed that C-reactive protein (per 1 mg/dL increase; odds ratio [OR]: 1.307, 95% CI: 1.250-1.3366, P < 0.001), ischemic heart disease etiology (OR: 1.691, 95%CI: 1.227-2.331, P = 0.001), and diabetes mellitus (DM; OR: 1.624, 95%CI: 1.188-2.220, P = 0.002) were independently associated with high FAR values. Kaplan-Meier curve analysis showed that prognosis of all-cause mortality within 730 days was significantly poorer (P = 0.033) in the high-FAR group than in the other 2 groups. Conversely, in the low-albumin group, the prognosis of all-cause mortality was significantly poorer (P = 0.006) in the low-FAR group than in the other groups. A Cox regression model revealed that in the low-albumin group, a low FAR value was an independent predictor of 730-day mortality (hazard ratio [HR]: 0.503, 95% CI: 0.287-0.881, P = 0.016) and HF events (HR: 0.444, 95%CI 0.276-0.712, P = 0.001).Elevated FAR was associated with inflammation, DM, and ischemic etiology, and with adverse outcomes in the whole AHF group, whereas low FAR was independently associated with adverse outcomes in the low-albumin group.

Organ dysfunction, injury, and failure in cardiogenic shock.

BACKGROUND: Cardiogenic shock (CS) is caused by primary cardiac dysfunction and induced by various and heterogeneous diseases (e.g., acute impairment of cardiac performance, or acute or chronic impairment of cardiac performance). MAIN BODY: Although a low cardiac index is a common finding in patients with CS, the ventricular preload, pulmonary capillary wedge pressure, central venous pressure, and systemic vascular resistance might vary between patients. Organ dysfunction has traditionally been attributed to the hypoperfusion of the organ due to either progressive impairment of the cardiac output or intravascular volume depletion secondary to CS. However, research attention has recently shifted from this cardiac output ("forward failure") to venous congestion ("backward failure") as the most important hemodynamic determinant. Both hypoperfusion and/or venous congestion by CS could lead to injury, impairment, and failure of target organs (i.e., heart, lungs, kidney, liver, intestines, brain); these effects are associated with an increased mortality rate. Treatment strategies for the prevention, reduction, and reversal of organ injury are warranted to improve morbidity in these patients. The present review summarizes recent data regarding organ dysfunction, injury, and failure. CONCLUSIONS: Early identification and treatment of organ dysfunction, along with hemodynamic stabilization, are key components of the management of patients with CS.

Trends in Sudden Death Following Admission for Acute Heart Failure.

Few studies on sudden death (SD) after admission for acute heart failure (AHF) have been published. A total of 1,664 patients with AHF were enrolled in this study, and 1,261 patients who were successfully followed up during the first year after admission were analyzed. The primary end point was SD, which was defined as out-of-hospital cardiac arrest. The median follow-up period from admission was 1,008 days (range 408 to 2,132). In total, 505 patients (40.0%) died: 341 (67.5%) died of cardiovascular causes and 55 (10.9%) died of other causes. Of the 505 who died, 80 (15.8%) experienced SD. The proportion of SDs increased in the later phases of follow-up (0 to 1 year, 10.3%; 1 to 2 years, 18.0%; 2 to 5 years, 18.8%; ≥5 years, 28.2%; p <0.001). A multivariate logistic regression model showed that younger age was independently associated with SD (60 to 69 years: odds ratio 2.249, 95% confidence interval 1.060 to 4.722; <60 years: odds ratio 3.863, 95% confidence interval 1.676 to 8.905). Kaplan-Meier curves showed that the incidence of cardiovascular death was highest during the acute phase, whereas the incidence of SD increased gradually over the entire follow-up period. In conclusion, the incidence of SD was surprisingly high in patients with AHF, accounting for 16% of long-term mortality. The proportion of SDs increased during the very late follow-up phases.