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The effect of lamivudine therapy in hepatic decompensation during acute exacerbation of chronic hepatitis B.

BACKGROUND/AIMS: Severe acute exacerbation (AE) of chronic hepatitis B (CHB) can lead to hepatic decompensation and death. The aim of this study was to investigate the effect of lamivudine therapy in hepatic decompensation during such AEs. METHODS: In a 10-month period, a total of 60 consecutive AE patients with jaundice and prolonged prothrombin time over 3s were treated with lamivudine 150 mg daily. As a historical control, another 31 CHB patients with AE resulting in hepatic decompensation hospitalized in an immediate past 6-month period were enrolled for comparison. RESULTS: Patients in both groups were comparable in clinical and biochemical features. After a median treatment period of 6 weeks (range 1-48 weeks), all of the 25 patients with pretherapy bilirubin level < 20 mg/dl in the treatment group survived, while five (25%) of 20 patients in the control group died (P=0.013; odds ratios, 2.667; 95% confidence interval, 1.787-3.979). However, the mortality rate was similar in patients with pretherapy bilirubin level > or =20 mg/dl in both groups. CONCLUSIONS: These results suggest that lamivudine may prevent fatality in CHB patients with hepatic decompensation if therapy starts early enough or before serum bilirubin level rise over 20 mg/dl, but helps little if serum level already risen over that level.

Adult↗

[Bilateral corneal endothelial decompensation after postsepticemia coma].

We report a case of unexplained bilateral corneal endothelial decompensation after a coma. A 71-year-old man with no medical history presented with bilateral endothelial decompensation that required penetrating keratoplasty of the left eye combined with cataract surgery. This coma was caused by septicemia originally due to staphylococcus infection following catheter placement in preparation for a CT scan. Visual acuity of the left eye was 20/400 and 20/100 in the right eye when the patient awoke from the coma. After examination, we noted only stromal thickening and Descemet membrane folds causing corneal edema predominating OS. The rest of the exam was normal. Six months after surgery, visual acuity improved to 20/25. The most probable physiopathological mechanism of this decompensation is an iatrogenic complication from drugs administered during the patient's stay in intensive care (oxacillin), but we cannot rule out direct aggression of a bacterium or its toxin or the decompensation of a preexisting pathology.

Aged↗

Increase of resting levels of superoxide anion in the whole blood of patients with decompensated liver cirrhosis.

The aim of this study is to investigate the relationship between the resting level of superoxide anion (O2.) and liver cirrhosis (LC). The resting levels of superoxide anion in the whole blood of healthy controls and patients with compensated or decompensated LC were measured, by an ultra-sensitive chemiluminescence (CL) analyzer and lucigenin amplification. The assay system can be performed in the absence of leukocyte isolation and stimulant administration. The results showed that the blood CL levels of compensated cirrhotic patients (381.0 +/- 201.5 counts/10 s, mean +/- SD, n = 24) were similar to that of healthy controls (467.9 +/- 299.5 counts/10 s, n = 24). However, the blood CL levels of decompensated cirrhotic patients (2083.5 +/- 1462.4 counts/10 s, n = 24) were significantly greater than that of healthy controls and patients with compensated LC (both p < .001, Student's t-test). The correlation analysis revealed that the blood CL levels in cirrhotic patients were significantly correlated with serum concentrations of albumin (r = -0.65, p < .001) and total bilirubin (r = +0.42, p < .005). However, there was no significant correlation between the blood CL levels and serum levels of transaminases (GOT and GPT). These results suggest that blood levels of superoxide of decompensated cirrhotic patients were greater than those of healthy controls or compensated cirrhotic patients. Moreover, the increase of blood levels of superoxide in decompensated cirrhotic patients is related to the impairment of liver function but not to the inflammation.

Acridines↗

Time course of respiratory decompensation in chronic obstructive pulmonary disease: a prospective, double-blind study of peak flow changes prior to emergency department visits.

The aim of this study was to look at changes in peak expiratory flow rates (PEFR) prior to emergency department visits for decompensated chronic obstructive pulmonary disease (COPD). It was designed as a prospective, double-blind study at the Albuquerque Veterans Affairs Medical Center. Twelve patients with an irreversible component of airflow obstruction on pulmonary function tests were assessed. At entry, all subjects were instructed in the use of a mini-Wright peak flow meter with electronic data storage. They then entered a 6-month monitoring phase in which they recorded PEFR twice daily, before and after bronchodilators. The meter displays were disabled so that the patients and their physicians were blinded to all values. Medical care was provided in the customary manner. Patients were considered to have respiratory decompensation if they required treatment for airflow obstruction in the Emergency Department (ED) and no other causes of dyspnea could be identified. Simple linear regression was used to model changes in PEFR over time. The 12 subjects had 22 episodes of respiratory decompensation during 1741 patient-days of observation. Two episodes could not be analysed because of missing values. Ten episodes in seven subjects were characterized by a significant linear decline in at least one peak flow parameter prior to presentation. The mean rates of change for the four daily parameters varied from 0.22% to 0.27% predicted per day (or 1.19 to 1.44 1 min-1 day-1). The average decrement in these parameters ranged from 30.0 to 33.8 1 min-1 (or 18.6%-25.9% of their baseline values). No temporal trends were found for the 10 episodes occurring in the other five subjects. We concluded that respiratory decompensation is characterized by a gradual decline in PEFR in about half of cases. Future studies should be done to elucidate the mechanisms of respiratory distress in the other cases.

Bronchodilator Agents↗

Serial measure of cardiac troponin T levels for prediction of clinical events in decompensated heart failure.

BACKGROUND: This study determined whether serial determinations of cardiac troponin T (cTnT) in decompensated heart failure (HF) are predictive of clinical events (death, need for readmission for new episode of HF decompensation, or both) during 1 year of follow-up. METHODS AND RESULTS: Sixty-two patients with decompensated HF were enrolled in this cohort. The first measurement of cTnT (cTnT1) was from a blood sample drawn within 4 days of hospital admission; the second measurement (cTnT2) was on blood obtained 7 days later. Forty-nine clinical events (16 deaths, 10 readmissions, 23 combined readmission and deaths) occurred during the follow-up. The independent predictors of clinical events were: cTnT1>.020 ng/mL (P<.050), cTnT2>.020 ng/mL (P<.050), and serum sodium<135 mEq/L (P<.050). Based on levels of cTnT1 and cTnT2>.020 ng/mL (+) or </=0.020 ng/mL(-), patients were divided into 2 groups: group 1 (cTnT1-, cTnT2- or cTnT1+, cTnT2-), group 2 (cTnT1-, cTnT2+ or cTnT1+, cTnT2+). Group 2 patients had higher rates of death (45.0% versus 71.4%, P<.050), hospital readmission (35.0% versus 61.9%, P<.050), and clinical events (55.0% versus 90.5%, P<.010) than group 1 patients. CONCLUSIONS: Persistently increased cTnT levels (>.020 ng/mL) are predictive of higher rates of death and hospital readmission for decompensated HF.

Adult↗

Determinants of early mortality in patients with decompensated chronic hepatitis B treated with antiviral therapy.

BACKGROUND & AIMS: Chronic hepatitis B is a leading cause of death worldwide. To identify patients who might require urgent liver transplantation despite antiviral therapy, we investigated the determinants of early mortality in a large cohort of patients with decompensated chronic hepatitis B treated with lamivudine. METHODS: One hundred fifty-four North American patients with decompensated chronic hepatitis B received lamivudine for a median of 16 months. Univariate and multivariate Cox regression modeling was used to develop a model of 6-month mortality. RESULTS: A biphasic survival pattern was observed, with most deaths occurring within the first 6 months of treatment (25 of 32, 78%) because of complications of liver failure. The estimated actuarial 3-year survival of patients who survived at least 6 months was 88% on continued treatment. In multivariate modeling, elevated pretreatment serum bilirubin and creatinine levels as well as the presence of detectable hepatitis B virus (HBV) DNA (by the bDNA assay) pretreatment were significantly associated with 6-month mortality. An equation approximating the probability of early mortality was developed from these variables. CONCLUSIONS: Our data demonstrate a distinct alteration in the slope of the survival curve after 6 months of lamivudine treatment for decompensated chronic hepatitis B. An equation consisting of 3 widely available pretreatment laboratory parameters was developed that can be used to predict the likelihood of early death in patients receiving lamivudine for decompensated chronic hepatitis B. These observations may help identify patients who can be stabilized with suppressive antiviral therapy vs. those who require urgent liver transplantation.

Adult↗

A rapid test for B-type natriuretic peptide correlates with falling wedge pressures in patients treated for decompensated heart failure: a pilot study.

OBJECTIVES: To determine if changes in B-type natriuretic peptide (BNP) levels can accurately reflect acute changes in pulmonary capillary wedge pressure during treatment of decompensated heart failure. BACKGROUND: Tailored therapy of decompensated congestive heart failure with hemodynamic monitoring is controversial. Other than the expense and complications of Swan-Ganz catheters, its use in titration of drug therapy has no conclusive end point. Because BNP reflects both elevated left ventricular pressure and neurohormonal modulation and has a short half-life, we hypothesized that levels of BNP would decline in association with falling wedge pressures. Final BNP levels would perhaps signify a new set point of neuromodulation. METHODS AND RESULTS: Twenty patients with decompensated New York Heart Association (NYHA) class III-IV congestive heart failure (CHF) undergoing tailored therapy were studied. BNP levels were drawn every 2 to 4 hours for the first 24 hours (active treatment phase) and then every 4 hours for the next 24 to 48 hours (stabilization period). Hemodynamic data was recorded simultaneously. In 15 patients whose wedge pressure responded to treatment in the first 24 hours, there was a significant drop in BNP levels (55%) versus nonresponders (8%). There was a significant correlation between percent change in wedge pressure from baseline per hour and the percent change of BNP from baseline per hour (r = 0.79, P <.05). When the wedge pressure was kept at a stable, low level during the stabilization phase, BNP levels continued to fall another 37% (937 +/- 140 pg/mL at 24 hours to 605 +/- 128 pg/mL). Patients who died (n = 4) had higher final BNP levels (1,078 +/- 123 pg/mL v 701 +/- 107 pg/mL). CONCLUSIONS: The data suggest that rapid testing of BNP may be an effective way to improve the in-hospital management of patients admitted with decompensated CHF. Although BNP levels will not obviate the need for invasive hemodynamic monitoring, it may be a useful adjunct in tailoring therapy to these patients.

Aged↗

Effect of nesiritide (B-type natriuretic peptide) and dobutamine on ventricular arrhythmias in the treatment of patients with acutely decompensated congestive heart failure: the PRECEDENT study.

BACKGROUND: Dobutamine is commonly used as a means of treating decompensated congestive heart failure (CHF). Although typically effective at improving short-term hemodynamics and symptomatology, the frequent occurrence of arrhythmias and tachycardia is undesirable. In this randomized, multicenter trial, we compared the safety and clinical effectiveness of the cardiac hormone nesiritide (human B-type natriuretic peptide) with dobutamine in hospitalized patients with decompensated CHF. METHODS: The study population consisted of 255 patients who were randomized to 1 of 2 doses of intravenous nesiritide (0.015 or 0.03 microg/kg/min) or dobutamine (> or =5 microg/kg/min) and stratified by means of an earlier history of ventricular tachycardia. Patients were also assessed with 24 hour Holter recordings immediately before and during study drug therapy and by means of signs and symptoms of CHF. RESULTS: Dobutamine significantly increased the mean (1) number of ventricular tachycardia events per 24 hours by 48 +/- 205 (P =.001), (2) repetitive ventricular beats per hour by 15 +/- 53 (P =.001), (3) premature ventricular beats per hour by 69 +/- 214 (P =.006), and (4) heart rate by 5.1 +/- 7.7 beats per minute (P <.001). These end points were significantly decreased or unchanged in the nesiritide groups. Nesiritide did not increase heart rate, despite a greater reduction of blood pressure. Both drugs were similarly effective means of improving signs and symptoms of CHF. CONCLUSIONS: Dobutamine is associated with substantial proarrhythmic and chronotropic effects in patients with decompensated CHF, whereas nesiritide actually reduces ventricular ectopy or has a neutral effect. Compared with dobutamine, nesiritide may be a safer, short-term treatment for patients with decompensated CHF.

Aged↗

Increased liver decompensation risk with atypical hepatitis C virus antibody levels.

Knowledge of serum markers of liver decompensation would facilitate care of patients with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections. HCV load and anti-c33c and anti-NS5 levels did not distinguish 28 HCV- and HIV-positive predecompensation patients from 28 matched control patients, whereas more patients than controls had high anti-c100(p) and low anti-c22(p). In multivariate analysis, decompensation was associated with high anti-c100(p) titer (>/=1:4050; odds ratio [OR], 3. 4; 95% confidence interval [CI], 1.1-11.5) and low anti-c22(p) (<1:36,450; OR, 3.0; 95% CI, 1.0-10.2) and with antibody band strength at 1:50 dilution (anti-c100[p] OR, 7.0; 95% CI, 1. 7-48.9; anti-c22[p] OR, 7.1; 95% CI, 1.7-49.2). With high anti-c100(p) or low anti-c22(p), sensitivity for decompensation was 86%-96% and specificity was 21%-36%; with both markers, sensitivity was 29%-32% and specificity was 93%-96%. Although the mechanisms for these associations are unknown, if these findings are verified in other populations, anti-c100(p) and anti-c22(p) might be valuable surrogate markers for liver decompensation risk.

Case-Control Studies↗

Incidence of and factors associated with hepatocellular carcinoma among hepatitis C virus and human immunodeficiency virus coinfected patients with decompensated cirrhosis.

We compared the incidence of and factors associated with hepatocellular carcinoma (HCC) among hepatitis C virus (HCV)-monoinfected subjects and human immunodeficiency virus (HIV)/HCV-coinfected individuals, both with decompensated cirrhosis. In a retrospective study, a cohort of 180 individuals with HIV coinfection and 1037 HCV-monoinfected patients with decompensated HCV-related cirrhosis from eight centres in Spain were analyzed. HCC was found in 234 (23%) HCV-monoinfected subjects and in four (2%) HIV-coinfected subjects (p<0.001). At the time of the first hepatic decompensation, 188 (17%) and 4 (2%) (p<0.001) patients in the former and in the latter group, respectively, showed HCC. Fifty-four (11%) patients without HCC at baseline developed such a disease during follow-up. There were no incident cases among the HIV-coinfected population. The density of incidence (95% IC) of HCC in HIV/HCV-coinfected and HCV-monoinfected patients was 0 (0-1.70) and 3.31 (2.70-4.64) cases per 100 person-years (p<0.001), respectively. Lack of HIV infection [adjusted odds risk (AOR) (95% IC)=16.7 (3.9-71.1)] and high alanine aminotransferase levels [AOR (95% IC)=2.5 (1.1-5)] were the only two independent predictors of the emergence of HCC. In the group of patients in whom the date of HCV infection could be estimated, the time elapsed until HCC diagnosis was shorter among HIV-coinfected subjects. The incidence of HCC in patients with HCV-related cirrhosis after the first hepatic decompensation is lower in HIV-coinfected patients. This is probably due to the fact that HIV infection shortens the survival of HCV-coinfected patients with end-stage liver disease to such an extent that HCC not had a chance to emerge.

Aged↗

Prevention and management of corneal decompensation.

While the chances of corneal decompensation following lens implantation are low, they are greater than in nonimplant cataract surgery and increase with the passage of time postoperatively. All the factors leading to corneal decompensation are not known, but available evidence suggests the most significant is trauma at the time of surgery. The likelihood of corneal decompensation can be limited by careful patient selection and surgical techniques and by appropriate management of postoperative complications. In the event of irreversible corneal decompensation, penetrating keratoplasty, with or without removal of the implant lens, offers a substantial chance of visual rehabilitation.

Age Factors↗

The effect of the Milwaukee brace on spinal decompensation in idiopathic scoliosis.

Decompensation of the spine was evaluated in 22 patients with idiopathic thoracolumbar or lumbar scoliosis, both prior to and following treatment in a Milwaukee brace. Curves ranged from 25 degrees to 47 degrees and were followed for an average of three and a half years beyond skeletal maturity. The average time in brace was 47 months. Initial decompensation was unrelated to a patient's age, skeletal maturity, curve location, or curve magnitude. At follow-up, there was no predictable improvement in decompensation despite compliant brace treatment. Changes in decompensation did not correlate with length of brace wear, initial magnitude or changes in curve magnitude, or skeletal age at which treatment was begun.

Braces↗

Management of flatback and related kyphotic decompensation syndromes.

STUDY DESIGN: The authors, in this retrospective study, examined a group of patients with flatback syndrome and a related kyphotic decompensation syndrome. Results of nonrealignment treatment as well as revision surgery with sagittal realignment were reviewed. OBJECTIVES: To determine effectiveness of physical therapy and limited surgical (instrumentation removal) as well as major realignment surgical treatment in the sagittally malaligned spine. SUMMARY OF BACKGROUND DATA: Flatback is a sagittal plane deformity associated with distraction instrumentation for scoliosis correction. Kyphotic decompensation syndrome involves malaligned fusions from the sacrum for disease other than scoliosis. Several studies describe surgical realignment for flatback involving instrumentation systems no longer commonly applied. Guidelines for a systematic approach to flatback and kyphotic decompensation syndromes are lacking. METHODS: Forty-eight patients with flatback and kyphotic decompensation syndromes were reviewed. Treatment groups were defined by treatment approach and level of previous fusion. Effectiveness of treatment was reviewed in terms of radiographic sagittal alignment and self-reported pain. RESULTS: Twenty patients were treated without realignment revision surgery. Twenty-eight patients were treated with anterior and posterior osteotomies and realignment with instrumentation. For patients originally fused to the sacrum, realignment averaged 12 cm. Pain was reduced from 7 to 3 (10-point scale). In patients fused to L4 or L5, realignment averaged 7 cm. Pain was reduced from 6 to 2. Magnetic resonance imaging revealed viable caudal discs in four patients who were consequently spared extension of fusion to the sacrum. CONCLUSIONS: Treatment without realignment surgery demonstrated long-term success in 27% of cases. The latter all had two intact discs below the previous fusion and sagittal malalignment less than 4 cm. Realignment surgery effectively reduced pain in patients failing a conservative approach.

Adolescent↗

Differential regulation of ET(A) and ET(B) in the renal tissue of rats with compensated and decompensated heart failure.

Endothelin-1 (ET-1) exerts its biological actions through two receptor subtypes: endothelin-A (ETA) receptor and endothelin-B (ETB) receptor. We demonstrated previously that ET-1 induces systemic and renal cortical vasoconstriction via ETA whereas ETB mediates medullary vasodilation. Congestive heart failure (CHF) is characterized by increased vascular resistance and impaired renal hemodynamic and excretory function. While the pathophysiological effects of ET-1 in CHF are well established, the status of ETA and ETB in the kidney is poorly characterized. The present study examined the immunostaining and localization of ETA and ETB in the renal cortex and medulla of rats with experimental CHF induced by aorto-caval fistula. Rats with CHF were further subdivided, based on their daily urinary sodium excretion, into rats with compensated (urinary sodium excretion > 1200 microEq/day) and decompensated CHF (urinary sodium excretion < 200 microEq/day). ETA is predominantly localized to the cortex mainly in the peritubular capillaries, and is upregulated in rats with compensated and decompensated CHF compared with sham controls. In contrast, ETB is preferentially expressed in the outer and inner medulla, mainly in the vasa recta, the thick ascending limb of Henle's loop and the collecting duct. While compensated CHF is associated with upregulation of ETB in the collecting duct and vasa recta, decompensated CHF is accompanied with enhanced ETB abundance in the vasa recta and remarkable downregulation of this receptor subtype in the collecting duct. The findings suggest that upregulation of ETA may lead to a decrease in cortical blood flow while upregulation of ETB in the vasa recta probably contributes to the preservation of medullary blood flow. Furthermore, downregulation of ETB in the collecting duct, only in rats with decompensated CHF, could contribute to sodium retention in that subgroup.

Animals↗

Nesiritide for pulmonary arterial hypertension with decompensated cor pulmonale.

Pulmonary arterial hypertension complicated by decompensated cor pulmonale is a challenging clinical problem with few effective therapeutic options. B-type natriuretic peptide is a pluripotent hormone that promotes diuresis and natriuresis, vasodilates systemic and pulmonary vessels, and reduces circulating levels of endothelin and aldosterone. It may represent a possible therapeutic strategy for decompensated cor pulmonale in the same manner that it is used to treat decompensated left heart failure. The authors report their experience with B-type natriuretic peptide as adjunctive therapy for pulmonary arterial hypertension complicated by decompensated cor pulmonale. A detailed case report is presented followed by the evaluation of a series of 11 cases occurring in eight patients from December 2002 through April 2004.

Adult↗

Probability of liver cancer and survival in HCV-related or alcoholic-decompensated cirrhosis. A study of 377 patients.

BACKGROUND: Although chronic alcohol intake and chronic hepatitis C may progress to cirrhosis and hepatocellular carcinoma (HCC), few data are available about survival and probability of developing HCC in decompensated cirrhosis of both aetiologies. METHODS: This study identified factors related with probability of developing HCC and survival in a cohort of 377 consecutive patients with decompensated HCV-related cirrhosis (200 cases) or alcoholic cirrhosis (177 cases) without known HCC, hospitalized for their first hepatic decompensation, as well as to evaluate differences between both aetiologies. Patients were followed for a mean period of 39 +/- 2 months. RESULTS: During follow-up, 42 patients (11.1%) developed HCC (16.5% vs 5.1%) in groups HCV and alcohol, respectively; p = 0.0008), and 131 patients (34.7%) died (42% vs 26.6% in groups HCV and alcohol, respectively; p = 0.002). Age and HCV-cirrhosis were independently related to HCC development, while baseline age and Child-Turcotte-Pugh score were independently correlated with survival. CONCLUSION: Survival in decompensated HCV-related or alcoholic cirrhosis is influenced by age and baseline Child-Turcotte-Pugh score, without differences in cirrhosis aetiology. The risk of developing HCC is greater in HCV-related cirrhosis than in alcoholic cirrhosis.

Age Distribution↗

Clinical and hemodynamic effects of nesiritide (B-type natriuretic peptide) in patients with decompensated heart failure receiving beta blockers.

The use of beta blockers in congestive heart failure presents a therapeutic challenge for patients with acute episodes of decompensation. Such patients may be less responsive to positive inotropic agents, whereas the beneficial effects of nesiritide, which are not dependent on the beta-adrenergic receptor signal-transduction pathway, may be preserved. This analysis of the Vasodilation in the Management of Acute CHF trial evaluated the safety and efficacy of nesiritide in decompensated congestive heart failure patients receiving beta blockers. The Vasodilation in the Management of Acute CHF trial was a multicenter, randomized, controlled evaluation of nesiritide in 489 hospitalized patients with decompensated congestive heart failure. One hundred twenty-three patients were on chronic beta-blocker therapy at enrollment (31 randomized to placebo, 50 to nesiritide, and 42 to nitroglycerin). Primary end points included pulmonary capillary wedge pressure and dyspnea evaluation at 3 hours. Patients receiving nesiritide, but not IV nitroglycerin, had significantly reduced pulmonary capillary wedge pressure vs. placebo at 3 hours regardless of beta-blocker use. The use of beta blockers did not alter the beneficial effects of nesiritide on systemic blood pressure, heart rate, or dyspnea evaluation. In nesiritide-treated subjects, safety profiles were similar regardless of beta-blocker use. Thus, the clinical and hemodynamic benefits and safety of nesiritide are preserved in decompensated congestive heart failure patients receiving chronic beta blockade.

Adrenergic beta-Antagonists↗

Accuracy of tissue Doppler echocardiography in the emergency diagnosis of decompensated heart failure with preserved left ventricular systolic function: comparison with B-type natriuretic peptide measurement.

BACKGROUND: Tissue Doppler echocardiography provides a reliable noninvasive estimation of left ventricular (LV) filling pressures irrespective of LV ejection fraction. However, the diagnostic accuracy of E/Ea ratio has not been adequately determined in patients with suspected heart failure (HF) with preserved LV systolic function in the acute care setting. OBJECTIVE: To investigate the accuracy of E/Ea ratio in the emergency diagnosis of decompensated HF with preserved LV systolic function. METHODS: Seventy patients with a LV ejection fraction >or=45%, 32 with decompensated HF (77 +/- 12 years of age), and 38 with noncardiac cause of acute dyspnea (74 +/- 12) were enrolled. B-type natriuretic peptide (BNP) was measured on admission; lateral, septal and average E/Ea ratios were calculated within 24 hours. RESULTS: Using receiver-operating characteristic curves to evaluate diagnostic performance, BNP (AUC of 0.875, P < 0.0001) and E/Ea ratios (AUC of 0.90-0.92, P < 0.0001) provided similar accuracy for predicting decompensated HF. Optimal cutoffs were 146 pg/ml for BNP (sensitivity and specificity of 90.6% and 76.3%), 9.8 for lateral E/Ea (83.3% and 88.9%), 12.7 for septal E/Ea (76.7% and 91.4%), and 11.5 for average E/Ea ratio (80% and 94.3%). On multivariate logistic regression analysis, average E/Ea ratio yielded independent additional information to a model based on the clinical judgment and BNP level according to the standard cutoff of 100 pg/ml. CONCLUSIONS: Tissue Doppler echocardiography is accurate for predicting decompensated HF with preserved LV systolic function and may be used as a diagnostic complement to inconclusive BNP level in this setting.

Acute Disease↗