Acute Heart Failure Syndromes
2005; Lippincott Williams & Wilkins; Volume: 112; Issue: 25 Linguagem: Inglês
10.1161/circulationaha.105.590091
ISSN1524-4539
AutoresMihai Gheorghiade, Faı̈ez Zannad, George Sopko, Liviu Klein, Ileana L. Piña, Marvin A. Konstam, Barry M. Massie, Edmond Roland, Shari Targum, Sean P. Collins, Gerasimos Filippatos, Luigi Tavazzi,
Tópico(s)Mechanical Circulatory Support Devices
ResumoHomeCirculationVol. 112, No. 25Acute Heart Failure Syndromes Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessReview ArticlePDF/EPUBAcute Heart Failure SyndromesCurrent State and Framework for Future Research Mihai Gheorghiade, MD, Faiez Zannad, MD, PhD, George Sopko, MD, MPH, Liviu Klein, MD, MS, Ileana L. Piña, MD, Marvin A. Konstam, MD, Barry M. Massie, MD, Edmond Roland, MD, Shari Targum, MD, Sean P. Collins, MD, Gerasimos Filippatos, MD, Luigi Tavazzi, MD and Mihai GheorghiadeMihai Gheorghiade From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). , Faiez ZannadFaiez Zannad From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). , George SopkoGeorge Sopko From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). , Liviu KleinLiviu Klein From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). , Ileana L. PiñaIleana L. Piña From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). , Marvin A. KonstamMarvin A. Konstam From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). , Barry M. MassieBarry M. Massie From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). , Edmond RolandEdmond Roland From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). , Shari TargumShari Targum From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). , Sean P. CollinsSean P. Collins From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). , Gerasimos FilippatosGerasimos Filippatos From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). , Luigi TavazziLuigi Tavazzi From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). and From the Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Ill (M.G., L.K.); INSERM-CHU Nancy, Dommartin-lès-Toul, France (F.Z.); the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.); University Hospital of Cleveland, Cleveland, Ohio (I.L.P.); New England Medical Center, Boston, Mass (M.A.K.); Veterans Affairs Medical Center, San Francisco, Calif (B.M.); Agence Française de Securité Sanitaire Produits de Santé, Paris, France (E.R.); Food and Drug Administration, Rockville, Md (S.T.); University of Cincinnati, Cincinnati, Ohio (S.P.C.); University of Athens Hospital Attikon, Athens, Greece (G.F.); and IRCCS Policlinico San Matteo, Pavia, Italy (L.T.). and for the International Working Group on Acute Heart Failure Syndromes Originally published20 Dec 2005https://doi.org/10.1161/CIRCULATIONAHA.105.590091Circulation. 2005;112:3958–3968Acute heart failure syndromes (AHFS) poses unique diagnostic and management challenges. This syndrome has recently received attention from researchers, clinicians, regulatory agencies, and the pharmaceutical industry. However, there is no consensus on its definition, epidemiology, pathophysiology, appropriate therapeutic options, and directions for future research.This document is the result of the First and Second International Workshop on Acute Heart Failure Syndrome that took place in May 2004 and April 2005. At these workshops, a selected group of physician scientists, epidemiologists, clinicians, regulatory and governmental funding agencies, and industry representatives from North and South America and Europe convened to develop a platform for future investigative approaches and management of AHFS. Subsequently, emergency physicians, who play a pivotal role in the early management of AHFS, contributed to this document.DefinitionAHFS is defined as gradual or rapid change in heart failure (HF) signs and symptoms resulting in a need for urgent therapy. These symptoms are primarily the result of severe pulmonary congestion due to elevated left ventricular (LV) filling pressures (with or without low cardiac output). AHFS can occur in patients with preserved or reduced ejection fraction (EF). Concurrent cardiovascular conditions such as coronary heart disease (CHD), hypertension, valvular heart disease, atrial arrhythmias, and/or noncardiac conditions (including renal dysfunction, diabetes, anemia) are often present and may precipitate or contribute to the pathophysiology of this syndrome.1–3Public Health IssuesHF hospitalizations have risen steadily, with >1 million in 2004 in the United States4; a similar number has been reported in Europe. In the United States, it is estimated that these hospitalizations account for >75% of the 46 billion dollars spent each year on the care of HF patients.4 Although much has been accomplished in the management of chronic HF, the absence of evidence-based clinical practice guidelines for AHFS is striking in comparison to the progress made in the treatment of acute myocardial infarction (MI) (Table 1). TABLE 1. Similarities and Differences Between Acute MI and AHFS Resulting in Hospitalization in the United StatesAcute MIAHFSACC/AHA indicates American College of Cardiology/American Heart Association.Incidence1 million per year1 million per yearMortality PrehospitalizationHigh? In-hospital3–4%3–4% After discharge (60–90 d)2%10%Myocardial injuryYesLikelyPathophysiological target(s)Clearly defined (coronary thrombosis)UncertainClinical benefits of interventions in published clinical trialsBeneficialMinimal/no benefit or deleterious compared with placeboACC/AHA recommendationsLevel ANoneThe underlying cause of HF hospitalizations has been viewed traditionally as merely a problem of volume overload and/or low cardiac output, usually precipitated by dietary indiscretion and/or medication nonadherence. These hospitalizations were an expected part of the chronic HF continuum. The failure to consider AHFS as a separate entity with distinct epidemiology and pathophysiology may have contributed to the slow progress of its recognition and management. The lack of agreement within the HF community (including regulatory agencies) regarding prognosis and the appropriate goals of therapy (eg, symptom relief versus prevention of repeated hospitalizations and improvement in survival) has also delayed advances in AHFS management. The first randomized placebo-controlled AHFS trials were published as late as 2002.5,6 None of the placebo-controlled AHFS studies conducted to date has shown either a consistent improvement of in-hospital or postdischarge survival or a decrease in readmissions.EpidemiologyUntil recently, the clinical characteristics, management patterns, and outcomes of patients hospitalized with AHFS have been poorly defined, being generated from small clinical trials and retrospective analyses of medical records or administrative databases. Data from almost 200 000 patients hospitalized for HF from the Euro-HF survey, the Acute Decompensated Heart Failure National Registry (ADHERE), and the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) in the United States provided much-needed information on the epidemiology of AHFS1–3,7 (Table 2). TABLE 2. Epidemiology of AHFSADHERE (n=110 000)Euro-HF (n=11 000)OPTIMIZE-HF (n=48 612)COPD indicates chronic obstructive pulmonary disease; IV, intravenous; and ICD/CRT, implanted cardioverter/defibrillator/cardiac resynchronization therapy.Important demographic characteristics Mean age, y757173 Women, %524752Known heart failure, %756587Preserved EF, %405449Medical history, % CHD576850 Hypertension725371 Diabetes442742 Atrial fibrillation314331 Renal insufficiency301730 COPD31…28Serum sodium 120 ms), %30……Clinical profile at presentation Mean systolic blood pressure, mm Hg145133142 Systolic blood pressure >140 mm Hg, %502948 Dyspnea at rest, %344044 Dyspnea on exertion, %893561 Rales, %67…64 Jugular venous distension, %……28 Peripheral edema, %662065Outpatient medication use before hospitalization, % Diuretics708766 ACE inhibitors406240 Angiotensin receptor blockers12512 β-Blockers483753 Digoxin283623 Aldosterone antagonists…217 Hydralazine……3 Nitrates263222In-hospital management, % IV diuretics708766 IV nesiritide8…11 IV inotropes10…9 Pulmonary artery catheter placement5…4 Coronary angiography10…9 Revascularization242 ICD/CRT placed……2Outcomes HF symptoms at discharge, % Unchanged/worse<1… 2 kg weight loss at discharge, %50…50 Median length of stay, d484 In-hospital mortality, %474 60–90 days postdischarge mortality, %…6.59 60–90 days readmissions, %…2430Clinical ClassificationAHFS encompasses at least 3 clinical distinct entities: (1) Worsening chronic HF associated with reduced or preserved LVEF (70% of all admissions); (2) de novo HF (eg, after a large MI; sudden increase in blood pressure superimposed on a noncompliant LV) (25% of all admissions); and (3) advanced HF (ie, refractory to therapy) with severe LV systolic dysfunction, associated with a continually worsening low-output state (5% of all admissions).Although it may be difficult to apply this classification at the time of hospital presentation, this becomes important for in-hospital and postdischarge management.Clinical Profile at PresentationData from large registries show that AHFS manifestation may vary with 1 or several distinct clinical conditions1–3,7,8 (Table 3). TABLE 3. Clinical Presentations of AHFSClinical PresentationIncidence*Signs and SymptomsCharacteristics* Of all AHFS admissions.† Its incidence may be related to the definition used (clinical vs radiographic).1. Elevated systolic blood pressure>50%Usually develop abruptlyPredominantly pulmonary (radiographic/clinical) rather than systemic congestion due to rapid fluid redistribution from systemic to pulmonary circulation; many patients have preserved EF2. Normal systolic blood pressure>40%Develop gradually (days or weeks) and are associated with significant systemic congestionDespite high ventricular filling pressure, radiographic pulmonary congestion may be minimal because of pulmonary vasculature/lymphatics adaptation due to chronic elevated left atrial pressures3. Low systolic blood pressure (<90 mm Hg)<8%Usually have a low cardiac output with signs of organ hypoperfusionMany of those patients have advanced or end-stage HF4. Cardiogenic shock<1%Rapid onsetPrimarily complicating acute MI, fulminant myocarditis5A. Pulmonary edema<3%†Rapid or gradual onsetClinical: severe dyspnea, tachypnea, tachycardia, and hypoxemia, requiring immediate airway interventionRadiographic: present in up to 80% of patients; often not associated with clinical pulmonary edema5B. "Flash" pulmonary edema?Abrupt onsetPrecipitated by severe systemic hypertension. Uncorrected, respiratory failure and death ensue. Patients are easily treated with vasodilators and diuretics. After blood pressure normalization and reinstitution of routine medications, patients can be discharged within 24 h6. Isolated right HF?Rapid or gradual onsetNot well characterized; there are no epidemiological data (eg, acute cor pulmonale, right ventricular infarct)7. Acute coronary syndromes (&25% of acute coronary syndromes patients have signs/symptoms of HF)?Rapid or gradual onsetMany such patients may have signs and symptoms of HF that resolve after initial therapy or resolution of ischemia8. Post-cardiac surgery HF?Rapid or gradual onsetOccurring in patients with or without previous ventricular dysfunction, often related to worsening diastolic function and volume overload immediately after surgery.In-Hospital Clinical ProfileAfter the initial management, AHFS patients can be divided into 2 groups: (1) Those continuing to improve and needing optimization of long-term therapies according to published guidelines and (2) those having recurrent symptoms requiring "rescue therapy," defined as unplanned or urgent intervention.Pathophysiological Targets for Therapy and ResearchTraditionally, the primary therapeutic goals for acute HF exacerbation were reduction in pulmonary capillary wedge pressure (PCWP) and/or increase in cardiac output. However, other therapeutic targets may include blood pressure control, myocardial protection, neurohormonal modulation, and preservation of renal function.HemodynamicsHigh LV Filling PressureIncrease in LV filling pressure (cardiopulmonary congestion) is the main reason for AHFS admission and readmission.1–3 Cardiopulmonary congestion leads to further neurohormonal activation,9 subendocardial ischemia,10 and progressive mitral and/or tricuspid regurgitation due to altered ventricular geometry. In addition, high right atrial pressures lead to myocardial edema accompanied by a decreased diastolic function and contractility.11 Although the exact triggers of congestion are not known, excess salt intake, renal dysfunction, neurohormonal and cytokine activation, and medications may contribute to fluid retention.Decreased Cardiac OutputDespite the fact that a decreased cardiac output may be present in AHFS, increasing the cardiac output during hospitalization does not appear to predict outcomes.12Elevated Blood PressureA significant and relatively abrupt increase in systemic blood pressure occurs in AHFS that may be related to a surge in neurohormonal and cytokine activation. This presentation relates to an acute increase in afterload in the presence of diastolic rather than systolic dysfunction. In this setting, blood pressure optimization rather than diuresis may be the main therapeutic target.Myocardial Damage/InjurySeveral studies have shown that increased serum troponin levels correlate with poor short- and long-term AHFS prognosis.10 Preliminary research suggests that cellular hypoxia and activation of the renin-angiotensin, adrenergic, cytokine, and nitric oxide systems lead to cell death (apoptosis/necrosis). Should further research establish the presence and magnitude of myocardial injury in AHFS, preventing or limiting it with acute interventions may result in improvement in long-term outcome.Myocardium at RiskViable and noncontractile myocardium is often present in AHFS. Theoretically, the decrease in cardiac contractility that occurs in HF is a compensatory mechanism that lowers energy use by the failing myocardium and thereby improves survival of cardiac myocytes.13In AHFS, high LV diastolic filling pressures, further neurohormonal and cytokine activation, contractility changes, heart rate increase, and/or blood pressure decrease in response to drugs may promote myocardial injury (necrosis or apoptosis), particularly in CHD patients, who often have hibernating myocardium.Coronary PerfusionIn AHFS, coronary perfusion may be diminished because of an increase in LV diastolic pressure coupled with a decrease in blood pressure and/or tachycardia resulting from certain therapeutic interventions (eg, vasodilators or inotropes) and neurohormonal and cytokine activation that facilitate/amplify further endothelial dysfunction. This may be particularly relevant in CHD patients with stunned/hibernating myocardium.14Neurohormonal and Cytokine AbnormalitiesHeightened and/or sustained activation of neurohormones and cytokines deleteriously affects the function and structural integrity of myocytes and vasculature, hemodynamics, coronary perfusion, and renal function.Renal FunctionIn AHFS, renal dysfunction carries a poor prognosis.15,16 A distinction should be made between chronic renal dysfunction resulting from a loss of functioning nephrons and glomerular mass (eg, related to diabetes or hypertension) and "vasomotor nephropathy," defined as transient renal dysfunction related to a afferent/efferent arteriolar perfusion mismatch due to hemodynamic, neurohormonal, and inflammatory factors. This may develop during hospitalization and usually presents with a significant increase in serum urea nitrogen/creatinine ratio in response to diuretic therapy despite continuing presence of fluid overload.9In addition to decreased cardiac output and/or vasodilatation that results in altered renal hemodynamics, further activation of neurohormones (renin-angiotensin-aldosterone system, catecholamines, endothelin, vasopressin) and prostaglandin inhibition contribute to arteriolar glomerular vasoconstriction and urea without creatinine reabsorption in the distal nephron.14 These neurohormonal effects are exacerbated by diuretic-induced neurohormonal activation and possible intravascular volume depletion.Adverse Drug EffectsNon-Potassium-Sparing DiureticsIntravenous loop diuretics may improve symptoms and fluid loss initially but also may contribute to renal function decline. This may be related not only to intravascular volume depletion but also to further neurohormonal activation resulting in a vasomotor nephropathy.11,17 Intravenous loop diuretics may be associated with worse outcomes in AHFS patients.18Inotropic TherapyIntravenous inotropes increase myocardial oxygen consumption, causing myocardial damage in the setting of hibernating myocardium.19 Use of inotropes has consistently been associated with increased mortality.20VasodilatorsExcessive vasodilatation in AHFS may lead to blood pressure decrease, potentially exacerbating myocardial ischemia and renal hypoperfusion.21,22Prognostic FactorsPredictive models for mortality and rehospitalization can aid clinical decision making and patient selection for clinical trials. Several recent clinical trials and observational studies have identified emerging prognostic factors in patients admitted with AHFS8,10,12,16,23–28 (Table 4). TABLE 4. Prognostic Factors in AHFSPrognostic FactorsBUN indicates blood urea nitrogen.Systolic blood pressureHigh admission blood pressure is associated with lower postdischarge mortalityReadmission rate: 30% at 90 d for both normotensive and hypertensive patientsCHDAssociated with 2-fold increase in postdischarge mortality compared with patients with primary cardiomyopathyIn CHD patients there is an increased postdischarge mortality in response to short-term intravenous milrinone compared with placeboTroponin release30–70% of patients hospitalized with AHFS have detectable plasma levels of cardiac troponinAssociated with a 2-fold increase in postdischarge mortality and a 3-fold increase in rehospitalization rateBUNBUN and BUN/creatinine ratio appear to be better prognostic indicators than creatinineRelatively minor increase in BUN is associated with 2- to 3-fold increase in postdischarge mortalityHyponatremia&25% of patients with AHFS have mild hyponatremiaAssociated with 2- to 3-fold increase in in-hospital and postdischarge mortalityNatriuretic peptidesLevels correlate weakly with elevated LV filling pressuresIncreased levels are associated with higher postdischarge mortality and repeated hospitalizationsPCWPReduction in PCWP during hospitalization, but not an increase in the cardiac output, has been associated with improved postdischarge survivalReduction in PCWP with agents such as milrinone and dobutamine is associated with worse outcomesFunctional capacity6-minute walk test is emerging as an important predictor of postdischarge outcomesOther prognostic factorsLVEF, anemia, diabetes mellitus, new sustained arrhythmias, and nonuse of neurohormonal antagonistsEvaluation Phases of AHFS PatientsThe evaluation of AHFS patients consists of (1) the initial or emergency department (ED) phase; (2) the hospitalization phase; and (3) the predischarge phase (Table 5). The assessments and the management goals differ according to the specific phase. TABLE 5. Evaluation phases in AHFSPhasesGoalsAvailable ToolsBUN indicates blood urea nitrogen; BNP, B-type natriuretic peptide; and NT pro-BNP, N-terminal pro B-type natriuretic peptide.* For example, diet, medication nonadherence, infections, anemia, cardiac arrhythmias, hypertension.Initial or ED phaseEstablish the diagnosisMedical history, signs/symptoms, radiographic findings, biochemical markersDefine the clinical profileBlood pressure, heart rate, signs (pulmonary congestion and/or peripheral edema), ECG, chest x-ray, renal function (BUN and creatinine), electrolytes, troponin, BNP, pulse oximetry, echocardiographyGrading severityNo accepted risk-stratification methods are availableDecide subsequent placementPatient comorbidities, initial response to therapies, workup, social factorsHospitalization phaseMonitor clinical conditionSigns/symptoms, heart rate, ECG, blood pressure (orthostatic changes), body weightMonitor renal functionBUN and creatinine, electrolytesAssess right ventricular and LV filling pressureBlood pressure (orthostatic changes, Valsalva maneuver), echocardiography, impedance cardiography, BNP/NT pro-BNP, pulmonary artery catheterAssess concomitant cardiac and noncardiac conditionsEg, echocardiography, cardiac catheterization, electrophysiological testingAssess myocardial viabilityMRI, stress test, echocardiography, radionuclear studiesDischarge phaseAssess functional capacity6-minute walk test, treadmillEvaluate exacerbating factors*; appropriate corrective strategiesEg, physical therapy, diet control, evaluation for sleep apneaOptimize pharmacological therapyAmerican Heart Association/American College of Cardiology and European Society of Cardiology guidelinesEstablish postdischarge plansInstructions about weight monitoring, medications, smoking cessation, follow-upTreatment of AHFS PatientsThere are 3 phases in the current management of AHFS: The emergency treatment phase, the in-hospital management phase, and the discharge-planning phase. This section briefly addresses the limitations of current therapies and highlights investigational agents.Emergency Treatment PhaseDyspnea and other symptoms and signs of cardiopulmonary congestion are the primary AHFS manifestations and require immediate attention on presentation to the ED or hospital ward. Patients need to be stabilized initially by early administration of diuretics, vasoactive substances, and/or noninvasive ventilation (eg, continuous positive airway pressure [CPAP] or bilevel positive airway press
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