Patients with acute heart failure (AHF) require urgent in‐hospital treatment for relief of symptoms. The main reason for hospitalization is congestion, rather than low cardiac output. Although ...congestion is associated with a poor prognosis, many patients are discharged with persistent signs and symptoms of congestion and/or a high left ventricular filling pressure. Available data suggest that a pre‐discharge clinical assessment of congestion is often not performed, and even when it is performed, it is not done systematically because no method to assess congestion prior to discharge has been validated. Grading congestion would be helpful for initiating and following response to therapy. We have reviewed a variety of strategies to assess congestion which should be considered in the care of patients admitted with HF. We propose a combination of available measurements of congestion. Key elements in the measurement of congestion include bedside assessment, laboratory analysis, and dynamic manoeuvres. These strategies expand by suggesting a routine assessment of congestion and a pre‐discharge scoring system. A point system is used to quantify the degree of congestion. This score offers a new instrument to direct both current and investigational therapies designed to optimize volume status during and after hospitalization. In conclusion, this document reviews the available methods of evaluating congestion, provides suggestions on how to properly perform these measurements, and proposes a method to quantify the amount of congestion present.
Aims
Acute heart failure (AHF) has a poor prognosis. We evaluated 3- and 12-month mortality in different clinical classes of AHF patients from 30 European countries who were included in the EuroHeart ...Failure Survey (EHFS) II.
Methods and results
Follow-up data were available for 2981 AHF patients, of these 62% had a history of chronic HF. One-year mortality after discharge was lower in patients with de novo AHF when compared with acutely decompensated chronic HF (ADCHF), 16.4 vs. 23.2% (P < 0.001). Cardiogenic shock conferred the highest cumulative 1-year mortality (52.9%) as a result of in-hospital mortality of 39.3%. Long-term prognosis in decompensated AHF was also dismal. Hypertensive HF was associated with the lowest mortality (13.7% at 1 year). Age, prior myocardial infarction, creatinine level, and low plasma sodium were independently associated with mortality during the whole follow-up period. Diabetes, anaemia, and history of chronic HF were associated with worse and hypertension with better long-term survival. History of cerebrovascular disease was associated with worse short-term outcome.
Conclusion
Early and late mortality differ between de novo AHF and ADCHF and between clinical classes of AHF. EHFS II identifies clinical risk markers and demonstrates the importance of a thorough characterization of AHF populations according to history and clinical presentation.
Acute heart failure (AHF) is a major cause of hospitalizations. Severe dyspnea, pulmonary congestion and low cardiac output with peripheral vasoconstriction and renal hypoperfusion is a main form of ...clinical presentation. Most patients with acute worsening have a pre-existing decompensated chronic heart failure (ADCHF), but AHF may also occur as a first manifestation of a previously unknown heart disease. Myocardial ischemia, cardiac arrhythmias, non-compliance with medication and infections are frequent precipitating factors. Management of AHF depends on the underlying heart disease and cause of decompensation. In patients with ADCHF vasodilators and iv diuretics are first-line drugs for rapid reduction of dyspnea and congestion. In patients with signs of low cardiac output and oliguria, inotropic agents are also often administered to prevent further deterioration. Beta-adrenergic agents and phosphodiesterase inhibitors correct the hemodynamic disturbance, but may also induce arrhythmias and worsen myocardial ischemia. Inotropic therapy therefore remains controversial. A novel class of drugs, the calcium sensitizers, represent a new therapeutic option. Levosimendan was shown to improve myocardial contractility without increasing oxygen requirements and to produce peripheral and coronary vasodilation. Its therapeutic effects and tolerance have been tested in several trials. The present review focuses on the clinical pharmacology and therapeutic utility of levosimendan in patients with ADCHF.
Aims
Acute heart failure (HF) is a common but ill‐defined clinical entity. We describe patients hospitalised with acute HF in regard of clinical presentation, mortality, and risk factors for an ...unfavourable outcome.
Methods and results
We conducted a prospective study including 312 consecutive patients from two European centers hospitalised with acute HF, defined as new onset or worsening of symptoms and signs of HF within 7 days. The mean age was 73 years and 56% were men. Twenty‐eight percent had de‐novo acute HF and 72% a decompensation of chronic HF. Coronary heart disease (CHD) was the most frequent underlying heart disease, elevated blood pressure >150 mmHg and acute ischemia being the most important triggers. Four percent of the patients had cardiogenic shock, 13% presented with pulmonary edema. LV‐EF was <35%, 35−50% and >50% in 35%, 32% and 33% of the patients, respectively. ICU‐treatment was necessary in 39% of the patients. Thirty‐day mortality (11%) was increased in the presence of shock or elevated troponin T levels. Twelve‐month all‐cause mortality (29%) increased in the presence of shock, left ventricular dysfunction, renal insufficiency, CHD, and age.
Conclusions
This prospective study shows that despite modern treatment, morbidity and mortality of patients hospitalised with acute HF remain high.
The aim of this work was to compare hepatocellular toxicity and pharmacological activity of amiodarone (2-n-butyl-3-3,5 diiodo-4-diethylaminoethoxybenzoyl-benzofuran; B2-O-Et-N-diethyl) and of eight ...amiodarone derivatives. Three amiodarone metabolites were studied, namely, mono-N-desethylamiodarone (B2-O-Et-NH-ethyl), di-N-desethylamiodarone (B2-O-Et-NH(2)), and (2-butyl-benzofuran-3-yl)-(4-hydroxy-3,5-diiodophenyl)-methanone (B2) carrying an ethanol side chain (2-butylbenzofuran-3-yl)-4-(2-hydroxyethoxy)-3,5-diiodophenyl-methanone; B2-O-Et-OH. In addition, five amiodarone analogs were investigated, namely, N-dimethylamiodarone (B2-O-Et-N-dimethyl), N-dipropylamiodarone (B2-O-Et-N-dipropyl), B2-O-carrying an acetate side chain 4-(2-butyl-benzofuran-3-carbonyl)-2,6-diiodophenyl-acetic acid; B2-O-acetate, B2-O-Et carrying an propionamide side chain (B2-O-Et-propionamide), and B2-O carrying an ethyl side chain (2-butylbenzofuran-3-yl)-(4-ethoxy-3,5-diiodophenyl)-methanone; B2-O-Et. A concentration-dependent increase in lactate dehydrogenase leakage from HepG2 cells and isolated rat hepatocytes was observed in the presence of amiodarone and of most analogs, confirming their hepatocellular toxicity. Using freshly isolated rat liver mitochondria, amiodarone and most analogs showed a dose-dependent toxicity on the respiratory chain and on beta-oxidation, significantly reducing the respiratory control ratio and oxidation of palmitate, respectively. The reactive oxygen species concentration in hepatocytes increased time-dependently, and apoptotic/necrotic cell populations were identified using flow cytometry and annexin V/propidium iodide staining. The effect of the three least toxic amiodarone analogs on the human ether-a-go-go-related gene (hERG) channel was compared with amiodarone. Amiodarone, B2-O-acetate, and B2-O-Et-N-dipropyl (each 10 microM) significantly reduced the hERG tail current amplitude, whereas 10 microM B2-O-Et displayed no detectable effect on hERG outward potassium currents. In conclusion, three amiodarone analogs (B2-O-Et-N-dipropyl, B2-O-acetate, and B2-O-Et) showed a lower hepatocellular toxicity profile than amiodarone, and two of these analogs (B2-O-Et-N-dipropyl and B2-O-acetate) retained hERG channel interaction capacity, suggesting that amiodarone analogs with class III antiarrhythmic activity and lower hepatic toxicity could be developed.
Abstract Objective To identify factors associated with short term mortality in hospitalised patients with heart failure. Background Hospitalisation is frequent in patients with heart failure and is ...associated with a high mortality. Methods The Euro Heart Failure survey collected data from patients with suspected heart failure. We searched this data for predictors of short term mortality. Results Of 10,701 patients, 1404 (13%) died within 12 weeks of admission. On univariate analysis, increasing age, hyponatraemia, renal impairment, hyperkalaemia, anaemia, severe mitral regurgitation, severe LV systolic dysfunction(LVSD), increasing QRS and female sex carried adverse prognosis. ACEI, beta-blockers, nitrates, anti-thrombotic and lipid lowering drugs were associated with a better prognosis. On multivariable analysis the following provided independent prognostic information: increasing age (OR per SD = 1.5, 95% CI 1.4–1.6), severe LVSD (1.8, 1.5–2.1), serum creatinine (1.2, 1.2–1.3), sodium (0.9, 0.8–0.9), Hb (0.9, 0.8–0.9) and treatment with ACEI (0.5, 0.5–0.6), beta-blockers (0.7, 0.6–0.8), statins (0.6, 0.5–0.7), calcium channel blockers (0.7, 0.6–0.8), warfarin (0.5, 0.4–0.6), heparin (1.7, 1.4–1.9), anti-platelet drugs (0.6, 0.5–0.6) and need for inotropes (5.5, 4.6–6.6). A simple risk score (range 0–11) identified cohorts with a 12 week mortality ranging from 2% to 44%. Conclusions Simple and readily available clinical variables and a risk score based on medical history and routine tests that all patients admitted with heart failure have, can identify patients with good, intermediate and high short term mortality.
Acute heart failure (AHF) with preserved left ventricular ejection fraction (PLVEF) represents a significant part of AHF syndromes featuring particular characteristics. We sought to determine the ...clinical profile and predictors of in-hospital mortality in patients with AHF and PLVEF in the Acute Heart Failure Global Survey of Standard Treatment (ALARM-HF). This survey is an international observational study of 4,953 patients admitted for AHF in 9 countries (6 European countries, Mexico, and Australia) from October 2006 to March 2007. Patients with PLVEF were defined by an LVEF ≥45%. Of the total cohort, 25% of patients had PLVEF. In-hospital mortality was significantly lower in this subgroup (7% vs 11% in patients with decreased LVEF, p = 0.013). Candidate variables included demographics, baseline clinical findings, and treatment. Multivariate logistic regression analysis showed that the variables independently associated with in-hospital mortality included systolic blood pressure at admission (p <0.001), serum sodium (p = 0.041), positive troponin result (p = 0.023), serum creatinine >2 mg/dl (p = 0.042), history of peripheral vascular disease and anemia (p = 0.004 and p = 0.015, respectively), secondary (hospitalization for other reason) versus primary AHF diagnosis (p = 0.043), and previous treatment with diuretics (p = 0.023) and angiotensin-converting enzyme inhibitors (p = 0.021). In conclusion, patients with AHF and PLVEF have lower in-hospital mortality than those with decreased LVEF. Low systolic blood pressure, low serum sodium, renal dysfunction, positive markers of myocardial injury, presence of co-morbidities such as peripheral vascular disease and anemia, secondary versus primary AHF diagnosis, and absence of treatment with diuretics and angiotensin-converting enzyme inhibitors at admission may identify high-risk patients with AHF and PLVEF.
Abstract Misplacement of electrodes can change the morphology of an electrocardiogram (ECG) in clinical important ways. To assess the frequency of these errors in different clinical settings, we ...collected ECGs routinely performed at the cardiology outpatient clinic and the intensive care unit. Lead misplacement was suspected when one of the following morphological changes occurred: QRS axis between 180° and −90°, positive P wave in lead aVR, negative P waves in lead I and/or II, very low (<0.1 mV) amplitude in an isolated peripheral lead, or abnormal R progression in the precordial leads. We analyzed 838 ECGs and identified 37 ECGs suspicious for electrode misplacement, from which 7 were confirmed. The frequency of ECG artifacts due to switched electrodes was 0.4% (3/739) at the outpatient clinic and 4.0% (4/99) at the intensive care unit ( P = .005). In conclusion, errors in ECG performance do occur with an increasing frequency in an acute medical care setting.
Specific criteria have been established to define the occurrence of myocardial infarction (MI) and stroke in cardiovascular clinical trials, but there is not a consistent definition for heart ...failure. Heart failure events appear to occur at a rate that is similar to stroke and MI in trials of hypertension, hyperlipidaemia, diabetes, and coronary heart disease, yet a consistent approach to defining heart failure events has not yet been realized. The wide range of definitions used in clinical trials makes it difficult to interpret new data in the context of existing literature. This inconsistency has led to challenges in determining the incidence of heart failure in cardiovascular studies and the effects of interventions on these endpoints. This paper examines issues related to defining heart failure events in cardiovascular clinical trials and presents a definition to formally address this issue.
Aims To explore drug exposure, frequency of adverse drug reactions (ADRs), types of ADRs, predisposing risk factors and ADR‐related excess hospital stay in medical inpatients.
Methods Structured data ...regarding patient characteristics, ‘events’ (symptoms, laboratory results), diagnoses (ICD10) and drug therapy were collected using a computer‐supported data entry system and an interface for data retrieval from electronic patient records. ADR data were collected by ‘event monitoring’ to minimize possible bias by the drug monitor. The causality of each event was assessed in relation to disease(s) and drug therapy.
Results The analysis included 4331 (100%) hospitalizations. The median observation period was 8 days. The median number of different drugs administered per patient and day was 6 and varied between 4 (Q1 ) and 9 (Q3 ) different drugs in 50% of all hospital days. In 41% of all hospitalizations at least one disease‐unrelated event could be possibly attributed to drug therapy. Clinically relevant ADRs occurred in 11% of all hospitalizations. In 3.3% of all hospitalizations ADRs were the cause of hospital admission. The incidence of possibly ADR‐related deaths was 1.4. Factors predisposing for clinically relevant ADRs were female gender and polypharmacy. ADR‐related excess hospital stay accounted for 8.6% of hospital days.
Conclusions These data demonstrate the feasibility of the developed ‘event monitoring’ system for quantitative analysis of ADRs in medical inpatients. With increasing numbers of recorded patients the pharmacoepidemiological database provides a valuable tool to study specific questions regarding drug efficacy and safety in hospitalized patients.
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