David S. Roffman, PharmD, BCPS/AQ Cardiology Professor Pharmacy Practice and Science
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Transcript of David S. Roffman, PharmD, BCPS/AQ Cardiology Professor Pharmacy Practice and Science
Management of Acute Decompensated Heart Failure
Washington Metropolitan Society of Health-System Pharmacists
September 28, 2013Rockville Maryland
David S. Roffman, PharmD, BCPS/AQ CardiologyProfessor
Pharmacy Practice and ScienceSchool of Pharmacy
University of Maryland
Financial Disclosures for David S. Financial Disclosures for David S. Roffman, PharmDRoffman, PharmD
Nothing to discloseNothing to disclose
Learning Objectives
At the completion of the lecture, the participants will be able to:
1. Describe the typical presentation of acute decompensated heart failure (ADHF)2. List the therapeutic objectives associated with pharmacologic therapy for ADHF3. State the indications, adverse effects, and monitoring parameters for the use of inotropes, vasodilators, pressors, and loop diuretics in the treatment of ADHF
4. Describe emerging pharmacotherapeutic options for ADHF
2013 ACCF/AHA Guideline for the Management of Heart Failure
A Report of the American College of Cardiology A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Foundation/American Heart Association Task Force on
Practice GuidelinesPractice Guidelines
Heart Failure GuidelinesHeart Failure Guidelines
http://circ.ahajournals.org/content/early/2013/06/03/CIR.0b013e31829e8776.citation
Class IClass I Benefit >>> RiskBenefit >>> Risk
Procedure/ Procedure/ Treatment Treatment SHOULD SHOULD be be performed/ performed/ administeredadministered
Class IIaClass IIa Benefit >> RiskBenefit >> RiskAdditional studies Additional studies with focused with focused objectives neededobjectives needed
IT IS REASONABLE IT IS REASONABLE to perform to perform procedure/administeprocedure/administer treatmentr treatment
Class IIbClass IIb Benefit ≥ RiskBenefit ≥ RiskAdditional studies Additional studies with broad objectives with broad objectives needed; Additional needed; Additional registry data would registry data would be helpfulbe helpful
Procedure/Treatment Procedure/Treatment MAY BE MAY BE CONSIDERED CONSIDERED
Class IIIClass III Risk ≥ BenefitRisk ≥ BenefitNo additional studies No additional studies neededneeded
Procedure/Treatment Procedure/Treatment shouldshould NOT NOT be be performed/administeperformed/administeredred SINCE IT IS SINCE IT IS NOT HELPFUL AND NOT HELPFUL AND MAY BE HARMFULMAY BE HARMFUL
Level A:Level A: Data derived from multiple randomized clinical trials or meta-analyses Data derived from multiple randomized clinical trials or meta-analyses
Multiple populations evaluatedMultiple populations evaluated
Level B:Level B: Data derived from a single randomized trial or nonrandomized studies Data derived from a single randomized trial or nonrandomized studies
Limited populations evaluatedLimited populations evaluated
Level C:Level C: Only consensus of experts opinion, case studies, or standard of care Only consensus of experts opinion, case studies, or standard of care
Very limited populations evaluatedVery limited populations evaluated
Applying Classification of Recommendations and Level of Evidence
Level of Evidence:
Definitions of HFrEF and HFpEF
http://circ.ahajournals.org/content/early/2013/06/03/CIR.0b013e31829e8776.citation
Clinical Profiles of Hospitalized HF Patients
Volume overloadVolume overload– pulmonary/systemic vascular pulmonary/systemic vascular
congestioncongestion– precipitated by acute BP increaseprecipitated by acute BP increase
Profound depression of COProfound depression of CO– hypotensionhypotension– renal insufficiencyrenal insufficiency– shock syndromeshock syndrome
Signs/symptoms of bothSigns/symptoms of both
The diagnosis of heart failure is primarily based on signs and symptoms derived from a thorough history and physical exam. Clinicians should determine the following:
a. adequacy of systemic perfusion;b. volume status;c. the contribution of precipitating factors and/or co-morbidities d. if the heart failure is new onset or an exacerbation of chronic disease; ande. whether it is associated with preserved, normal, or reduced ejection fraction.
Chest radiographs, echocardiogram, and echocardiography are key tests in this assessment.
The Hospitalized Patient
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It is recommended that the following common potential precipitating factors for acute HF be identified as recognition of these comorbidities, is critical to guide therapy:
• acute coronary syndromes/coronary ischemia• severe hypertension• atrial and ventricular arrhythmias• infections• pulmonary emboli• renal failure• medical or dietary noncompliance
The Hospitalized Patient
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Concentrations of BNP or NT-proBNP should be measured in patients being evaluated for dyspnea in which the contribution of HF is not known. Final diagnosis requires interpreting these results in the context of all available clinical data and ought not to be considered a stand-alone test.
The Hospitalized Patient
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Acute coronary syndrome precipitating HF hospitalization should be promptly identified by electrocardiogram and cardiac troponin testing, and treated, as appropriate to the overall condition and prognosis of the patient.
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Patients Being Evaluated for Dyspnea
Therapeutic Objectives for Acute Decompensated Heart
Failure Improve survival?Improve survival? Resolve pulmonary vascular Resolve pulmonary vascular
congestioncongestion Preserve end organ performancePreserve end organ performance Achieve previous baseline heart failure Achieve previous baseline heart failure
status (NYHA Classification)status (NYHA Classification) Reduce the risk of rehospitalizationReduce the risk of rehospitalization
Recommended Therapies for Hospitalized HF Patients
http://circ.ahajournals.org/content/early/2013/06/03/CIR.0b013e31829e8776.citation
Recommended Therapies for Hospitalized HF Patients
http://circ.ahajournals.org/content/early/2013/06/03/CIR.0b013e31829e8776.citation
Patients admitted with HF and with evidence of significant fluid overload should be treated with intravenous loop diuretics. Therapy should begin in the emergency department or outpatient clinic without delay, as early intervention may be associated with better outcomes for patients hospitalized with decompensated HF (Level of Evidence: B).
If patients are already receiving loop diuretic therapy, the initial intravenous dose should equal or exceed their chronic oral daily dose. Urine output and signs and symptoms of congestion should be serially assessed, and diuretic dose should be titrated accordingly to relieve symptoms and to reduce extracellular fluid volume excess. (Level of Evidence: C).
The Hospitalized Patient Treatment With Intravenous Loop Diuretics
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The Hospitalized Patient
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Intensifying the Diuretic Regimen
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When diuresis is inadequate to relieve congestion, as evidence by clinical evaluation, the diuretic regimen should be intensified using either:
a. higher doses of loop diuretics;b. addition of a second diuretic (such
as metolazone, spironolactone or intravenous chlorthiazide) or
c. Continuous infusion of a loop diuretic.
Ultrafiltration is reasonable for patients with refractory congestion not responding to medical therapy.
The Hospitalized Patient
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Ultrafiltration and Intravenous Inoptropic Drugs
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Effect of HF treatment should be monitored with careful measurement of fluid intake and output; vital signs; body weight, determined at the same time each day; clinical signs (supine and standing) and symptoms of systemic perfusion and congestion. Daily serum electrolytes, urea nitrogen, and creatinine concentrations should be measured during the use of intravenous diuretics or active titration of HF medications.
The Hospitalized Patient
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Monitoring and Measuring Fluid Intake and Output
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Diuretic Strategies in Patients with Acute Decompensated
Heart Failure
A. A. Bolus dosing more effectiveB. Continuous infusion more effectiveC. Higher dose more effective than lower doseD. Both B and C are correct
Diuretic Strategies in Patients with Acute Decompensated
Heart Failure
In a prospective, double-blind, randomized trial, we assigned 308 patients with acute decompensated heart failure to receive furosemide administered intravenously by means of either a bolus every 12 hours or continuous infusion and at either a low dose (equivalent to the patient’s previous oral dose) or a high dose (2.5 times the previous oral dose). The protocol allowed specified dose adjustments after 48 hours. The co-primary end points were patients’ global assessment of symptoms, quantified as the area under the curve (AUC) of the score on a visual-analogue scale over the course of 72 hours, and the change in the serum creatinine level from baseline to 72 hours.
Felker GM, Lee KL, Bull DA, et.al., N Engl J Med 2011;364:797-805
Felker GM, Lee KL, Bull DA, et.al., N Engl J Med 2011;364:797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
Felker GM, Lee KL, Bull DA, et.al., N Engl J Med 2011;364:797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
Felker GM, Lee KL, Bull DA, et.al., N Engl J Med 2011;364:797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
Felker GM, Lee KL, Bull DA, et.al., N Engl J Med 2011;364:797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
Felker GM, Lee KL, Bull DA, et.al., N Engl J Med 2011;364:797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
Fluid and Sodium Restriction in Acute Decompensated Heart
Failure
Fluid and sodium restriction in Fluid and sodium restriction in ADHF patients improves weight loss ADHF patients improves weight loss and clinicaal stability in and clinicaal stability in hospitalized ADHF patientshospitalized ADHF patients
– A. TrueA. True– B. FalseB. False
Aggressive Fluid and Sodium Restrictionin Acute Decompensated Heart Failure
A Randomized Clinical Trial
To compare the effects of a fluid-restricted To compare the effects of a fluid-restricted (maximum fluid intake, 800 mL/d) and sodium (maximum fluid intake, 800 mL/d) and sodium restricted (maximum dietary intake, 800 mg/d) restricted (maximum dietary intake, 800 mg/d) diet (intervention group [IG]) vs. a diet with no diet (intervention group [IG]) vs. a diet with no such restrictions (control group [CG]) on weight such restrictions (control group [CG]) on weight loss and clinical stability during a 3-day period loss and clinical stability during a 3-day period in patients hospitalized with ADHFin patients hospitalized with ADHF
JAMA Intern Med. 2013;173(12):1058-1064
Aggressive Fluid and Sodium Restrictionin Acute Decompensated Heart Failure
A Randomized Clinical Trial
JAMA Intern Med. 2013;173(12):1058-1064
Aggressive Fluid and Sodium Restrictionin Acute Decompensated Heart Failure
A Randomized Clinical Trial
JAMA Intern Med. 2013;173(12):1058-1064
Aggressive Fluid and Sodium Restrictionin Acute Decompensated Heart Failure
A Randomized Clinical Trial
JAMA Intern Med. 2013;173(12):1058-1064
The Hospitalized Patient
In all patients hospitalized with HF, both with preserved and low ejection fraction, transition should be made from intravenous to oral diuretic therapy with careful attention to oral diuretic dosing and monitoring of electrolytes. With all medication changes, the patient should be monitored for supine and upright hypotension and worsening renal function and HF signs/symptoms.
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Invasive hemodynamic monitoring should be performed to guide therapy in patients who are in respiratory distress or with clinical evidence of impaired perfusion in whom the adequacy or excess of intracardiac filling pressures cannot be determined from clinical assessment.
In patients with clinical evidence of hypotension associated with hypoperfusion and obvious evidence of elevated cardiac filling pressures (e.g., elevated jugular venous pressure; elevated pulmonary artery wedge pressure), intravenous inotropic or vasopressor drugs should be administered to maintain systemic perfusion and preserve end-organ performance while more definitive therapy is considered.
The Hospitalized Patient
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Preserving End-Organ Performance
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Intravenous Inotropic Agents Used in ADHF
http://circ.ahajournals.org/content/early/2013/06/03/CIR.0b013e31829e8776.citation
Inotropic Support in Acute Heart Failure
In the presence of significant In the presence of significant hypotension, dopamine may enhance hypotension, dopamine may enhance both blood pressure and peripheral both blood pressure and peripheral organ perfusion.organ perfusion.
Dopamine, in pressor doses (greater Dopamine, in pressor doses (greater than 5 mcg/kg/min), increases than 5 mcg/kg/min), increases myocardial oxygen demand and myocardial oxygen demand and potentially limits augmentation of potentially limits augmentation of peripheral perfusion via peripheral peripheral perfusion via peripheral vasoconstrictionvasoconstriction
Issues with Intravenous Inotropes
Initial choice of therapyInitial choice of therapy WeaningWeaning Patient related variablesPatient related variables Differences in efficacyDifferences in efficacy Adverse effect profileAdverse effect profile Survival dataSurvival data ““Long-term” infusionsLong-term” infusions
Invasive hemodynamic monitoring can be useful for carefully selected patients with acute HF who have persistent symptoms despite empiric adjustment of standard therapies, and
a. whose fluid status, perfusion, or systemic orpulmonary vascular resistances are uncertain;b. whose systolic pressure remains low, pr is associated with symptoms, despite initialtherapy;c. whose renal function is worsening with therapy;d. who require parenteral vasoactive agents; ore. who may need consideration for advanced device therapy or transplantation.
The Hospitalized Patient
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Routine use of invasive hemodynamic monitoring in normotensive patients with acute decompensated HF and congestion with symptomatic response to diuretics and vasodilators is not recommended.
Use of parenteral inotropes in normotensive patients with acute decompensated HF without evidence of decreased organ perfusion is not recommended.
The Hospitalized Patient
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Parenteral Inotropes
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Vasodilator Support in Acute Heart Failure
Nitroglycerin, nitroprusside, and Nitroglycerin, nitroprusside, and nesiritide, have been demonstrated nesiritide, have been demonstrated to improve symptoms and to improve symptoms and hemodynamics in acute heart hemodynamics in acute heart failure.failure.
Vasodilator Support in Acute Heart Failure
Nitroprusside infusions (initial Nitroprusside infusions (initial dose 0.1 mcg/kg/min) improve dose 0.1 mcg/kg/min) improve symptoms of pulmonary symptoms of pulmonary congestion, and signs of congestion, and signs of peripheral perfusion.peripheral perfusion.
Titration of infusion rate is initailly Titration of infusion rate is initailly based on invasive hemodynamic based on invasive hemodynamic monitoring.monitoring.
Vasodilator Support in Acute Heart Failure
Nitroprusside patient variables:Nitroprusside patient variables:– Chronic liver diseaseChronic liver disease– Renal insufficiencyRenal insufficiency– Blood pressureBlood pressure– Malnourished patientsMalnourished patients
Vasodilator Support in Acute Heart Failure
Nitroprusside toxicities:Nitroprusside toxicities:– Cyanide intoxication: metabolic Cyanide intoxication: metabolic
acidosisacidosis– Thiocyanate toxicity: Hyper-reflexia, Thiocyanate toxicity: Hyper-reflexia,
seizures, altered mental status. seizures, altered mental status. Serum concentration assay availableSerum concentration assay available
Vasodilator Support in Acute Heart Failure
Nitroglycerin infusion may be Nitroglycerin infusion may be preferred in patients an active or preferred in patients an active or recent history of ischemia.recent history of ischemia.
Nitroglycerin is a less potent Nitroglycerin is a less potent arteriolar dilator than arteriolar dilator than nitroprussidenitroprusside
Vasodilator Support in Acute Heart Failure
Nesiritide is a brain naturetic peptide (BNP) Nesiritide is a brain naturetic peptide (BNP) which has significant vasodilator effects.which has significant vasodilator effects.
Dosing regimen, 0.2 mcg/kg bolus followed Dosing regimen, 0.2 mcg/kg bolus followed by 0.01 mcg/kg/min continuous infusionby 0.01 mcg/kg/min continuous infusion
Reduces LV filling pressure, variable effect on Reduces LV filling pressure, variable effect on CO, urine output, sodium excretionCO, urine output, sodium excretion
Better than diuretics for dyspneaBetter than diuretics for dyspnea Longer t ½ than nitroglycerin or Longer t ½ than nitroglycerin or
nitroprussidenitroprusside Adverse renal outcomesAdverse renal outcomes
History of New Treatments in ADHF
1988: Milrinone approved based 1988: Milrinone approved based on small hemodynamic studieson small hemodynamic studies
2000: Levosimendan approved in 2000: Levosimendan approved in Sweden then 40 countriesSweden then 40 countries
2001: Nesiritide based on 489 2001: Nesiritide based on 489 patient VMAC trialpatient VMAC trial
Research on Drugs for Acute Heart Failure
PubMed search for “heart failure” (19,154)/”randomized controlled trials”(2176)/”acute disease”(61) for novel, intravenous treatments for acute heart failure
Search results: Levosimendan, nesiritide, rolofylline, tezosentan
Levosimendan (REVIVE I and II)
700 patients, placebo controlled700 patients, placebo controlled Primary endpoint: Clinical Primary endpoint: Clinical
composite based on patient composite based on patient global assessment during first 5 global assessment during first 5 days of treatment (positive)days of treatment (positive)
Increased ventricular/atrial Increased ventricular/atrial arrhythmias, symptomatic arrhythmias, symptomatic hypotension, early mortalityhypotension, early mortality
JCHF. 2013;1(2):103-111. doi:10.1016/j.jchf.2012.12.004
Levosimendan vs. Dobutamine (SURVIVE)
1327 patients1327 patients Primary endpoint: All cause Primary endpoint: All cause
mortality at 180 days not mortality at 180 days not achievedachieved
No secondary endpoints achievedNo secondary endpoints achieved Decreased BNPDecreased BNP
JAMA. 2007 May 2;297(17):1883-91
Nesiritide (ASCEND-HF)
Placebo controlled post approval Placebo controlled post approval trialtrial
Prespecified primary endpoint Prespecified primary endpoint (dyspnea relief) not met(dyspnea relief) not met
No beneficial effect on hospital No beneficial effect on hospital readmisiion, all-cause mortality, readmisiion, all-cause mortality, worsening renal functionworsening renal function
N Engl J Med 2011;365:32-43
Rolofylline (Protect)
2033 patients2033 patients Failed to meet primary clinical Failed to meet primary clinical
composite endpointcomposite endpoint No reduction in hospital No reduction in hospital
readmissionsreadmissions Complicated by seizures and Complicated by seizures and
strokestrokeN Engl J Med 2010; 363:1419-28
Tezosentan (VERITAS)
1448 patients1448 patients No improvement in dyspneaNo improvement in dyspnea No improvement in worsening No improvement in worsening
heart failure or death at 7 daysheart failure or death at 7 days No improvement in renal function, No improvement in renal function,
hospital readmission or mortalityhospital readmission or mortality
JAMA 2007;298:2009-19
Medications should be reconciled in every patient and adjusted as appropriate on admission to and discharge from the hospital.
The Hospitalized Patient
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In patients with reduced ejection fraction experiencing a symptomatic exacerbation of HF requiring hospitalization during chronic maintenance treatment with oral therapies known to improve outcomes, particularly ACE inhibitors or ARBs and beta-blocker therapy, it is recommended that these therapies be continued in most patients in the absence of hemodynamic instability or contraindications.
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Reconciling and Adjusting Medications
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Serelaxin
Recombinant human relaxin-2 (peptide that regulates maternal adaptations to pregnancy)
Increased arterial compliance, cardiac output, renal blood flow.
Suggested benefit on dyspnea and post-discharge clinical outcomes in patients admitted with evidence of congestion, normal to elevated blood pressure, mild to moderate renal dysfunction.
Serelaxin (RELAX-AHF)
Prospective, randomized, double-blind, Prospective, randomized, double-blind, placebo-controlled, parallel group trial placebo-controlled, parallel group trial 1161 patients comparing serelaxin to 1161 patients comparing serelaxin to placebo.placebo.
The RELAX-AHF trial tested the hypothesis that serelaxin-treated patients would have greater dyspnea relief compared with patients treated with standard care and placebo
Lancet 2013; 381: 29–39
Serelaxin (RELAX-AHF)Inclusion Criteria
Acute heart failure within past 16 hours, Acute heart failure within past 16 hours, Dyspnea at rest or minimal exertionDyspnea at rest or minimal exertion
Pulmonary congestion on CXRPulmonary congestion on CXR BNP BNP >> 350 ng/L, NT-proBNP > 1400
ng/L GFR 30 – 75 ml/min/1.73 m2
Systolic BP > 125 mm Hg Treated with > 40 mg iv furosemide
Lancet 2013; 381: 29–39
Serelaxin
June 2013: FDA grants serelaxin “breakthrough-June 2013: FDA grants serelaxin “breakthrough-therapy” designation based on RELAX-HF Trialtherapy” designation based on RELAX-HF Trial
Breakthrough designation therapy reserved for Breakthrough designation therapy reserved for the development or review of drugs seen as the development or review of drugs seen as poteentiaal game changers for serious and life-poteentiaal game changers for serious and life-threatening conditions that have preliminary threatening conditions that have preliminary evidence in at least one clinically significant evidence in at least one clinically significant endpoint over other available therapiesendpoint over other available therapies
Other Investigational Drugs for AHF
TRV027– Β-arrestin-biased AT1R ligand, competitively inhibits G-protein
signaling– Reduces MAP, increases cardiac contractility, maintains stroke
volume, preserves GFR– Anti-apoptotic effect
Ularitide– Synthetic foem of urodilatin (naturetic peptide produced by
kidneys)– Binds to specific naturetic peptide receptors, imcreasing
intracellular cyclic GMP– Relaxes smooth muscle cells, vasodilation and increased renal
blood flow– Ongoing TRUE-AHF study: Symptoms, HF improvement, and
death
Other Investigational Drugs for AHF
Omecamtiv mecarbil– Selective cardiac myosin activator– ATOMIC-AHF was a randomized, double-blind, placebo-controlled Phase ATOMIC-AHF was a randomized, double-blind, placebo-controlled Phase
II clinical trial that enrolled 613 patients hospitalized with acute heart II clinical trial that enrolled 613 patients hospitalized with acute heart failure (AHF) treated for 48 hours with an intravenous formulation of failure (AHF) treated for 48 hours with an intravenous formulation of omecamtiv mecarbil or placebo and designed to evaluate the safety, omecamtiv mecarbil or placebo and designed to evaluate the safety, pharmacokinetics, pharmacodynamics, and potential efficacy of pharmacokinetics, pharmacodynamics, and potential efficacy of omecamtiv mecarbil in patients with AHFomecamtiv mecarbil in patients with AHF
– The primary efficacy endpoint of dyspnea symptom response was not The primary efficacy endpoint of dyspnea symptom response was not met; favorable trends between the dose and plasma concentration of met; favorable trends between the dose and plasma concentration of omecamtiv mecarbil and dyspnea response. The incidence of worsening omecamtiv mecarbil and dyspnea response. The incidence of worsening heart failure within seven days of initiating treatment appeared lower in heart failure within seven days of initiating treatment appeared lower in each of the cohorts on omecamtiv mecarbil. Rates of adverse events each of the cohorts on omecamtiv mecarbil. Rates of adverse events (AEs), serious AEs, adjudicated deaths and hospitalizations were similar (AEs), serious AEs, adjudicated deaths and hospitalizations were similar between omecamtiv mecarbil and placebo groups. Omecamtiv mecarbil between omecamtiv mecarbil and placebo groups. Omecamtiv mecarbil was not associated with an increased incidence of tachyarrhythmias nor was not associated with an increased incidence of tachyarrhythmias nor were heart rate or blood pressure adversely affected.were heart rate or blood pressure adversely affected.
Continuation of Outpatient ACE/ARB Therapy
Blood pressureBlood pressure Renal functionRenal function Volume dependencyVolume dependency Substitution of Substitution of
hydralazine/nitrateshydralazine/nitrates
The Hospitalized PatientIn patients hospitalized with HF with reduced ejection fraction not treated with oral therapies known to improve outcomes, particularly ACE inhibitors or ARBs and beta-blocker therapy, initiation of these therapies is recommended in stable patients prior to hospital discharge.
Initiation of beta-blocker therapy is recommended after optimization of volume status and successful discontinuation of intravenous diuretics, vasodilators, and inotropic agents. Beta-blocker therapy should be initiated at a low dose and only in stable patients. Particular caution should be used when initiating beta-blockers in patients who have required inotropes during their hospital course.
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In patients with evidence of severely symptomatic fluid overload in the absence of systemic hypotension, vasodilators such as intravenous nitroglycerin, nitroprusside or neseritide can be beneficial when added to diuretics and/or in those who do not respond to diuretics alone.
The Hospitalized Patient Severe Symptomatic Fluid Overload
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The Hospitalized Patient
Comprehensive written discharge instructions for all patients with a hospitalization for HF and their caregivers is strongly recommended, with special emphasis on the following 6 aspects of care: diet, discharge medications, with a special focus on adherence, persistence, and uptitration to recommended doses of ACE inhibitor/ARB and beta-blocker medication, activity level, follow-up appointments, weight monitoring, and what to do if HF symptoms worsen.
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Reconciling and Adjusting Medications
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Recommendations for Hospital Discharge
http://circ.ahajournals.org/content/early/2013/06/03/CIR.0b013e31829e8776.citation
Improvement of Guideline Beta-Blocker Improvement of Guideline Beta-Blocker Prescribing in Heart Failure: A Cluster-Prescribing in Heart Failure: A Cluster-
Randomized Pragmatic Trial of a Pharmacy Randomized Pragmatic Trial of a Pharmacy InterventionIntervention
We conducted a pragmatic cluster-randomized trial, where facilities (n 5 12) with patients (n 5 220) were the clusters. Eligible patients had a beta-blocker prescription that was not guideline concordant. Level 1 intervention included information to a pharmacist on facility guideline concordance. Level 2 also provided a list of patients not meeting guideline goals. Intervention and follow-up periods were each 6 months. Achievement of full concordance with recommendations was low (4%e5%) in both groups, primarily due to lack of tolerability. However, compared with level 1, the level 2 intervention was associated with 1.9-fold greater odds of improvement in prescribing (95% confidence interval [CI] 1.1e3.2). Level 2 patients also had greater odds of a higher dose (1.9, 95% CI 1.1e3.3). The intervention was aided by the patient lists provided, the electronic medical record system, and staff support..
Journal of Cardiac Failure Vol. 19 No. 8 2013
Acute Decompensated Heart Failure
Few well controlled trialsFew well controlled trials Little data to demonstrate Little data to demonstrate
improved morbidity/mortalityimproved morbidity/mortality Need for newer, more effective, Need for newer, more effective,
lower ADR-inducing agentslower ADR-inducing agents