Bd1e Management Of Heart Failure
Upcoming SlideShare
Loading in...5
×

Like this? Share it with your network

Share
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
No Downloads

Views

Total Views
2,504
On Slideshare
2,504
From Embeds
0
Number of Embeds
0

Actions

Shares
Downloads
121
Comments
0
Likes
1

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide
  • FIGURE 25–6 Stages of heart failure and treatment options for systolic heart failure. Patients with stage A heart failure are at high risk for heart failure but do not have structural heart disease or symptoms of heart failure. This group includes patients with hypertension, diabetes, coronary artery disease, previous exposure to cardiotoxic drugs, or a family hisotry of cardiomyopathy. Patients with stage B heart failure have structural heart disease but have no symptoms of heart failure. This group includes patients with left ventricular hypertrophy, previous myocardial infarction, left ventricular systolic dysfunction, or valvular heart disease, all of whom would be considered to have New York Heart Association (NYHA) class I symptoms. Patients with stage C heart failure have known structural heart disease and current or previous symptoms of heart failure. Their symptoms may be classified as NYHA class I, II, III, or IV. Patients with stage D heart fialure have refractory symptoms of heart failure at rest despite maximal medical therapy, are hospitalized, and require specialized interventions or hospice care. All such patients would be considered to have NYHA class IV symptoms. ACE = angiotensin-converting enzyme; ARB = angiotensin receptor blocker; VAD = ventricular assist device. (Reprinted from Jessup M, Brozena S: Heart failure. N Eng J Med 348:2007-2018, 2003) .
  • FIGURE 25–17 Treatment algorithm for patients with chronic heart failure (HF) with a reduced ejection fraction (EF). After the clinical diagnosis of HF is made, it is important to treat the fluid retention that the patient experienced before starting an angiotensin-converting enzyme (ACE) inhibitor (or an angiotensin receptor blocker (ARB) if the patient is ACE intolerant). Beta blockers should be started after the fluid retention has been treated and/or the ACE inhibitor has been uptitrated. If the patient remains symptomatic, an ARB, aldosterone antagonist, or digoxin can be added as triple therapy. The fixed-dose combination of hydralazine–isosorbide dinitrate should be added to an ACE inhibitor and beta blocker in African American patients with New York Heart Association (NYHA) Class II, II, or IV HF. Device therapy should be considered in addition to pharmacological therapy for appropriate patients. CRT = cardiac resynchronization therapy; ICD = implantable cardioverter-defibrillator. (From Mann DL: Heart failure and cor pulmonale. In Kasper DL, Braunwald E, Fauci AS, et al (eds): Harrison’s Principles of Internal Medicine. 17th ed. New York, McGraw-Hill, 2007 [in press].)
  • TABLE 25–5 Pharmacological and Device Therapy in Patients with Chronic Heart Failure (HF). (Modified from Swedberg K, Cleland J, Dargie H, et al: Guidelines for the diagnosis and treatment of chronic heart failure: Executive summary (update 2005): The Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology. Eur Heart J 26:1115, 2005.)
  • TABLE 25–9 Drugs for the Prevention and Treatment for Chronic Heart Failure. (Modified from Mann DL: Heart failure and cor pulmonale. In Kasper DL, Braunwald E, Fauci AS, et al (eds): Harrison’s Principles of Internal Medicine. 17th ed. New York, McGraw-Hill, 2007 (in press).)
  • TABLE 25–10 Mortality Rates in Placebo-Controlled Trials of Patients with Chronic Heart Failure (EF <40%), with Acute Myocardial Infarction, or at Risk for Heart Failure. (Modified from Bristow MR, Linas S, Port DI: Drugs in the treatment of heart failure. In Zipes DP, Libby P, Bonow RO, Braunwald E (eds): Braunwald’s Heart Disease. 7th ed. Philadelphia, Elsevier, 2004, pp 569-601.)
  • TABLE 23-7 Crude, Annualized Mortality Rates in Renin-Angiotensin-Aldosterone System Inhibitor Placebo-Controlled Trials Conducted in Chronic Heart Failure (HF) from Systolic Dysfunction, Left Ventricular (LV) Dysfunction after Myocardial Infarction, or in Patients Without LV Dysfunction at Risk for HF
  • TABLE 23-8 Properties of Widely Used Angiotensin-Converting Enzyme Inhibitors
  • Candesartan in ACE-I intolerant patients Another study, Val-HeFT looked at valsartan in HF and found: The primary outcomes of the Val-HeFT study was all-cause mortality, and combined all-cause mortality plus morbidity, which included hospitalization for heart failure, cardiac arrest with resuscitation, or need for intravenous support for worsening heart failure. 30 After 2 years of follow up, analysis of the data showed no effect of valsartan on all-cause mortality. However, there was a statistically significant risk reduction of 0.87 (95% confidence interval 0.79, 0.96) in the combined outcome of all-cause morbidity and mortality, or a 13% decline ( P = 0.009).
  • Candesartan added to background therapy (ACE-I and BB) – resulted in statistically significant reduction in CV mortality and HF hospitalization
  • TABLE 23-9 Properties of Widely Used Angiotensin Receptor Blockers
  • TABLE 23-10 Biological Responses Mediated by Adrenergic Receptors in the Human Heart
  • FIGURE 23-6 Schematic representation of selected components of the cardiac myocyte beta 1 - and beta 2 -adrenergic receptor pathways. The beta 1 -adrenergic receptor is illustrated with direct coupling through G αs to voltage-sensitive Ca 2+ channels as well as to Ca 2+ channels by cyclic adenosine monophosphate (cAMP-dependent protein kinase A (PKA) phosphorylation. AC = adenylyl cyclase; AR = adrenergic receptor; ATP = adenosine triphosphate; CAMK = calmodulin-activated kinase; PDE = phosphodiesterase; PHLMBN = phospholamban; SR = sarcoplasmic reticulum.
  • TABLE 23-11 Adrenergic Receptor Blocking Affinities of Beta-Blocking Agents in Human Receptors
  • TABLE 23-13 Beta Blocker Trials Conducted in Chronic Heart Failure, with 12-Month Mortality Rates Taken from Survival Curves When Data Not Directly Available in Published Material
  • TABLE 25–10 Mortality Rates in Placebo-Controlled Trials of Patients with Chronic Heart Failure (EF <40%), with Acute Myocardial Infarction, or at Risk for Heart Failure. (Modified from Bristow MR, Linas S, Port DI: Drugs in the treatment of heart failure. In Zipes DP, Libby P, Bonow RO, Braunwald E (eds): Braunwald’s Heart Disease. 7th ed. Philadelphia, Elsevier, 2004, pp 569-601.)
  • TABLE 23-12 Starting and Target Doses for Beta Blockers
  • Slide 27 The results of the MERIT-HF study indicate that treatment with TOPROL-XL added to standard heart failure therapy reduces the risk of mortality and morbidity. 1,2 The combined endpoints of all-cause mortality plus all-cause hospitalization and of mortality plus heart failure hospitalization showed consistent effects in the overall study population and the subgroups, including women and the US population. However, in the US subgroup and women, overall mortality and cardiovascular mortality appeared less affected. Analyses of female and US patients were carried out because they each represented about 25% of the overall population. 2 Slide and Notes References 1. MERIT-HF Study Group. Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL randomised intervention trial in congestive heart failure (MERIT-HF). Lancet . 1999:353:2001-2007. 2. TOPROL-XL Prescribing Information. AstraZeneca. Wayne, PA. 27
  • FIGURE 25–16 Kaplan-Meier analysis of the probability of survival in patients in the placebo and beta blocker groups in the MERIT-HF (top), CIBIS II (middle), and COPERNICUS (bottom) trials. CHF = chronic heart failure; CI = confidence interval; RR = relative risk. (Data from The Cardiac Insufficiency Bisoprolol Study II [CIBIS II]: A randomised trial. Lancet 353:9, 1999; Effect of metoprolol in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure [MERIT-HF]. Lancet 353:2001, 1999; and Packer M, Coats AJ, Fowler MB, et al; Carvedilol Prospective Randomized Cumulative Survival Study [COPERNICUS] Group: Effect of carvedilol on survival in severe chronic heart failure. N Engl J Med 344:1651, 2001.)
  • TABLE 25–8 Diuretics for Treating Fluid Retention in Chronic Heart Failure*. (Modified from Hunt SA, Abraham WT, Chin MH, JL, et al: ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 112:e154, 2005.)
  • FIGURE 25–9 Sites of action of diuretics in the kidney. AVP = arginine vasopressin.
  • TABLE 25–9 Drugs for the Prevention and Treatment for Chronic Heart Failure. (Modified from Mann DL: Heart failure and cor pulmonale. In Kasper DL, Braunwald E, Fauci AS, et al (eds): Harrison’s Principles of Internal Medicine. 17th ed. New York, McGraw-Hill, 2007 (in press).)
  • FIGURE 23-5 Changes from baseline in pulmonary capillary wedge pressure in patients in decompensated heart failure treated with placebo, nitroglycerin, or nesiritide. (From Publication Committee for the VMAC Investigators: Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure. A randomized controlled trial. JAMA 287:1531, 2002.)
  • TABLE 25–7 Possible Precipitating Factors for Acute Decompensation in Patients with Chronic Heart Failure (HF). (From Mann DL: Heart failure and cor pulmonale. In Kasper DL, Braunwald E., Fauci AS, et al (eds): Harrison’s Principles of Internal Medicine. 17th ed. New York, McGraw-Hill, 2007 (in press).)

Transcript

  • 1. Management of Chronic Heart Failure DR.SAMEER AMBAR DEPT OF CARDIOLOGY JNMC BELGAUM, INDIA [email_address]
  • 2.  
  • 3.  
  • 4.
    • Asses the functional class
    • BP <130/80 mm of Hg
    • Good glycaemic control
    • LIPIDS LDL < 100 (IHD) <70 (DM)
    • Avoid smoking, alcohol
    • Sodium restriction <2gms /day
    • Fluid restriction ,2 Litres/day
  • 5.  
  • 6.  
  • 7. ACEI MECHANISM OF ACTION VASOCONSTRICTION VASODILATATION Kininogen Kallikrein Inactive Fragments Angiotensinogen Angiotensin I RENIN Kininase II Inhibitor ALDOSTERONE SYMPATHETIC VASOPRESSIN PROSTAGLANDINS tPA ANGIOTENSIN II BRADYKININ A.C.E.
  • 8.  
  • 9.  
  • 10.
    • SAVE ( NEJM 1992 327:669-677)
    • 2231 pts EF<40%, 3-16d post MI , without sx of heart failure ,
    • Up to 50 mg Captopril tid for 42 mo
    • AIRE (Lancet 1993:342:821)
    • 2006 patients 3-10 days post MI with any evidence of post infarct clinical HF,
    • Up to 5 mg Ramipril bid for 15 mos
    • TRACE (NEJM 1995; 333: 1670-1676)
    • 1749 pts 3-7 days post MI with EF<=35%, with or without symptomatic HF
    • trandolapril for 24-50 mos
    ACEI IN POST MI HF
  • 11.
    • Mortality
    • SAVE: 25% (placebo) vs 20% (captopril) - 19% RRR
    • AIRE: 23% (placebo) vs 17% (ramipril) - 27% RRR
    • TRACE: 42.3% (placebo) vs 34.7% (trandolapril)- 24% RRR
  • 12.  
  • 13.  
  • 14. ARBs Clinical Study:
    • 1.Elite-II. Study:
    • Enrolled Target: CHF P’t
    • Drug: losartan v.s. captopril
    • Primary Endpoint:CHF Improvement
    • Result: losartan is not better than captopril
    • 2.Va-HeFT Study:
    • Enrolled Target: CHF P’t
    • Drug: valsartan + Usual Group v.s. Usual Group
    • Primary Endpoint: CHF Event-Free Probability
    • Result: Reduce M/M by 13.3%
  • 15. Granger CB, et al. Lancet . 2003;362:772-776. CHARM-Alternative Number at risk Candesartan 1,013 929 831 434 122 Placebo 1,015 887 798 427 126 0 1 2 3 Years 0 10 20 30 40 50 Placebo Candesartan HR 0.77 (95% CI 0.67-0.89), P =.0004 Adjusted HR 0.70, P <.0001 3.5 406 (40.0%) 334 (33.0%) Proportion With CV Death or CHF Hospitalization (%) Primary outcome of CV death or CHF hospitalization
  • 16. 55% on BB
  • 17.  
  • 18. When to use Angiotensin receptor blockers
    • 1. There has been no definite mortality or morbility advantage of ARBs over ACE inhibitors demonstrated
    • 2. Consider ARB in patient who is ACE inhibitor eligible if the patient is intolerant of ACE inhibitors because of cough, renal insufficiency, or hyperkalemia
  • 19. When to use Angiotensin receptor blockers
    • 3. In the patient who is apparently ACE inhibitor intolerant, rule out other causes of presumed side effect:
    • a. Cough-evaluate for pulmonary edema
    • b. Hyperkalemia-concurrent potassium supplementation, potassium-sparing diuretic use
    • c. renal insufficiency-evaluate for prerenal azotemia, NSAID use
    • 4. The incidence of cough and hyperkalemia is lower with ARBs versus ACE inhibitors
    • There does not appear to be a significant difference in incidence of renal insufficiency
  • 20.  
  • 21. Beta blockade in Heart failure
    • Beta receptor levels in heart failure
      • Normal Heart B1 80 : B2 20
      • Severe Heart Failure B1 60 : B2 40
        • B1 receptors to selectively down-regulate secondary to high levels of catecholamine
        • B2 agonists retain full inotropic activity mediated through a B2 population that is not significantly decreased
  • 22.  
  • 23. Effect of Sympathetic Activation in Heart Failure
    • CNS Sympathetic Outflow
    • Sympathetic activity to
    • kidneys & blood vessels
    Activation of RAS Vasoconstriction Sodium retention Disease Progression
    • Cardiac sympathetic Activity
    • 1
    • Receptors
    • 2
    • Receptors
    • 1
    • Receptors
    Myocyte death Increased arrhythmias
  • 24.  
  • 25. Benefit Of Beta Blockers
    • Improve symptoms and clinical status
    • Increase LV ejection fraction
    • Little effect on exercise tolerance
    • Reduce frequency of hospitalizations for heart failure
    • Decrease mortality
  • 26. Action
    • Time dependant improvement in LV remodelling
    • Reduce cetecholamine myocyte toxicity
    • Improved B1 signaling
    • Antiapoptosis
    • antiarrthymic
    • RAAS inhibition
  • 27. Sympathetic Activation B1 Receptors B2 Receptors A1 Receptors Cardiotoxicity Carvedilol Metoprolol Propranolol
  • 28.  
  • 29.  
  • 30.  
  • 31.  
  • 32. Clinical Trials
    • Prospective Randomized Evaluation of Carvedilol on Symptoms and Exercise (PRECISE)
      • 278 patients with chronic stable symptomatic heart failure EF<35% despite diuretics and ACE
      • Carvedilol group was associated with greater improvement in NYHA Class
      • 39% reduction in combined risk of death/hospitalization for any reason
      • 46% reduction in risk of hospitalization for cardiovascular reason
    Circulation 1996;94:2793-2799
  • 33. Clinical Trials
    • Merit-HF Trial( metaprolol randomised interventional trial in CHF)
      • 3991 patients with an ischemic or nonischemic cardiomyopathy (NYHA Class II or III) randomized to either Metoprolol XL up to 200mg/day or placebo.
      • Metoprolol XL was associated with a 35% reduction in mortality
    Amer J Cardiol 1997;80:54J-58J
  • 34. MERIT-HF METOPROL-XL: Mortality and Morbidity MERIT-HF Study Group. Lancet. 1999;353:2001-2007
  • 35.
    • NYHA III/IV
    • EF <0.25
    Post-MI Patients with Severe Heart Failure (n= 384) Jánosi A et al, Am Heart J 2003;146:721-8 MERIT-HF
  • 36. Total Mortality Months of follow-up Per cent 20 15 10 5 0 Placebo Metoprolol CR/XL p = 0.0004 Risk reduction = 40% 0 3 6 9 12 15 18 Jánosi A et al, Am Heart J 2003;146:721-8 MERIT-HF Post-MI Patients
  • 37. Per cent 12 9 6 3 0 Risk reduction = 50% Sudden Death Placebo Metoprolol CR/XL p = 0.0004 0 3 6 9 12 15 18 Jánosi A et al, Am Heart J 2003;146:721-8 MERIT-HF Post-MI Patients Months of follow-up
  • 38. Per cent 5 4 3 1 0 Risk reduction = 49% Death from Worsening Heart Failure Placebo Metoprolol CR/XL p = 0.021 2 0 3 6 9 12 15 18 Jánosi A et al, Am Heart J 2003;146:721-8 MERIT-HF Post-MI Patients Months of follow-up
  • 39. Total Number of Hospitalizations Heart failure p=0.006 -32% All-cause ns -8% CV cause p=0.037 -17% MERIT-HF Post-MI Patients Jánosi A et al, Am Heart J 2003;146:721-8
  • 40. Post-MI severe CHF Total mortality Cardiac death/nonfatal MI History of revasc. (PTCA or CABG) 40% 45% Risk reduction Events Plac/Beta 122/74 44/24 37/26 132/74 46/22 42/27 All Post-MI patients Post-MI severe CHF All Post-MI patients Relative risk and 95% CI 0.0 1.0 History of revasc. (PTCA or CABG) Jánosi A et al, Am Heart J 2003;146:721-8 MERIT-HF Post-MI Patients
  • 41. Effect of metoprolol and placebo treatment on survival and hospitalization risk in class III and IV HF MERIT-HF Goldstein S et al. J Am Coll Cardiol 2001; 38(4):932-8 Endpoint Metoprolol (N) Placebo (N) Risk reduction (%) p value Total mortality 45 72 39% 0.0086 CV mortality 40 70 44% 0.0028 Sudden death 22 39 45% 0.024 Death from worsening HF 13 28 55% 0.015 Total hospitalizations 273 363 27% 0.0037 Total hospitalizations due to worsening HF 105 187 45% <0.0001
  • 42. Comparison of findings in subanalysis and entire MERIT-HF cohort MERIT-HF Goldstein S et al. J Am Coll Cardiol 2001; 38(4):932-8 Endpoint Reductions in entire MERIT-HF cohort Reductions in class III and IV MERIT-HF subset Total mortality -34% -39% Sudden death -41% -45% Death due to worsening HF -49% -55%
  • 43.
    • 40% reduction in Total Mortality
    • 50% reduction in Sudden Death
    • 32% reduction in number of hospitalizations for Worsening Heart Failure
    Jánosi A et al, Am Heart J 2003;146:721-8 MERIT-HF Post-MI Patients Mortality/Hospitalizations Summary
  • 44.  
  • 45.
    • Enrolled 2289 patients with severe HF (LVEF <25%)
    • Randomized to carvedilol in a target dose of 25 mg bid for up to
    • 29 months
    Carvedilol Prospective Randomized Cumulative Survival Trial (COPERNICUS) 35% reduction in the risk of all-cause mortality among patients with severe congestive heart failure (CHF) treated with carvedilol compared to placebo
  • 46. COPERNICUS: Effect of carvedilol on the combined risk of morbidity and mortality Death or hospitalization for HF 0.000004 p value Endpoint COPERNICUS and CAPRICORN 0.00004 31% Death or hospitalization for a CV reason 0.76 Death or hospitalization for any reason Relative risk reduction 24% 0.00002 Odds ratio 27% 0.73 0.69
  • 47. Beta Blockers Post MI LV dysfunction
    • CAPRICORN( carvedilol post infarct survival control in LVD)
      • 1959 pts post MI LVEF<40%
      • Randomized to carvedilol or placebo
      • Results:
        • Lower all cause mortality (12% vs. 15%)
        • Lower non-fatal MI
    Lancet 2001; 357: 1385–90
  • 48. CAPRICORN All-Cause Mortality 0 0.5 1 1.5 2 2.5 Carvedilol n=975 Placebo n=984 Years Proportion Event-free
    • 23%
    • (2%, 40%)
    Risk reduction 0 0.90 0.70 0.60 0.80 The CAPRICORN Investigators. Lancet . 2001;357:1385-1390. Mortality Rates: Placebo 15%; Carvedilol 12% Carvedilol Post-Infarct Survival Control in LV Dysfunction 1.00
  • 49. Clinical Use Of Beta Blockers
    • Recommended for patients with NYHA class II-IV
    • General contraindications:
      • Decompensated heart failure
      • Severe claudication
      • Bronchospasm
      • Advanced heart block
      • Use with caution if patient requires inotropes for support of circulatory function
  • 50. Beta-Blockade
    • Cardiac Output
    • Renal
    • Blood Flow
    Sodium Retention Worsening Heart Failure
  • 51. Considerations in selecting a beta-blocker
    • Patients should be clinically stable and euvolemic before initiating beta-blocker therapy
    • Start at low doses and titrate upward gradually (doubling every 2-4 weeks)
    • Patients may experience an initial exacerbation of heart failure symptoms because of transient worsening of cardiac output
  • 52. Clinical Use Cont . . .
    • Clinical response may not be seen until 2 to 3 months after initiation of therapy
    • Abrupt withdrawal can lead to dramatic deterioration
    • Patient education paramount
  • 53. Outcome in Post-MI Patients with Heart Failure CAPRICORN and MERIT-HF 1 Time to first event CAPRICORN All-cause mortality All-cause mortality/CV hosp. 1 MERIT-HF 23% 8% Risk reduction p- value p=0.03 Plac/Beta 151/116 122/74 40% p=0.0004 CAPRICORN MERIT-HF 367/340 326/258 ns 22% p=0.002 The CAPRICORN Investigators, Lancet 2001;357:1385-90 Jánosi A et al, Am Heart J 2003;146:721-8 Relative risk and 95% CI 0.0 1.0 Metoprolol CR/XL  1 Metoprolol CR/XL  1 Carvedilol  1  2 (  1 ) Carvedilol  1  2 (  1 )
  • 54. LVEF: Change From Baseline Within Treatment-arm Comparison * P < 0.05; ** P < 0.01; *** P < 0.001 Enalapril Carvedilol & Enalapril Carvedilol -1 0 1 2 3 4 5  LVEF (%) *** *** *** *** *** ** * M6 M12 M18 M6 M18 M12 M6 M12 M18
  • 55. Diuretics
  • 56.  
  • 57. Diuretics
  • 58.  
  • 59. RALES(randomised aldactone evaluation study)
    • 1663 patients Class 3-4 CHF, LVEF<35% on ACE-inhibitor/diuretic/dig
    • randomized to 25 mg spironolactone vs. placebo
    • issues:
      • only 10% of patients on beta blockers
    NEJM 1999:341:709-17
  • 60. RALES
    • Results: 46% mortality placebo vs 35% spironolactone (30% RRR)
    • adverse effects:
      • 10% of pts in spironolactone group developed gynecomastia.
      • -serious hyperkalemia (K>6) 14% vs 10% (not statist sig)
  • 61. EPHESUS(eplerenone post AMI HF efficacy and survival study)
    • 6642 patients:
    • a) 3-14 days post MI ,
    • b) EF<40,
    • c) CHF (rales, pulm venous congestion seen on CXR, 3rd heart sound) OR Diabetes
    • randomized to 25 mg eplerenone titrated up to 50 mg po qd
    NEJM 2003;348:1309-21
  • 62.
    • Results:
      • One year mortality: 15% risk reduction (11.8% vs 13.6%)
      • CV death or cardiovascular hospitalizations (26% vs 30.0%)
    • (75% of patients on beta blockers)
    • adverse effects:
      • serious hyperkalemia (K>6) Epler- 5.5% vs plac- 3.9% (p=.002)
      • serious hypokalemia (K<3.5) Epler- 8.4% plac- 13.1% (p<.001)
      • gynecomastia- 0.5% vs 0.6%
    EPHESUS
  • 63. Criteria for treatment with spironolactone
    • New York heart Association class 3-4
    • Left ventricular ejection fraction <35%
    • Serum creatinine <2.5 mg/dL
    • Serum potassium <5 mmol/L
    • Baseline treatment with ACE inhibitor (or other vasodilator if ACE inhibitor intolerance), loop diuretic, and digoxin as indicated
  • 64. Digoxin
    • Digoxin has a significant role in improving symptoms and rehospitalization rate
    • No impact on the total and cardiovascular mortality
    • Usually used only in severe CHF or in patients who remain symptomatic with optimal treatment
    • Digoxin is useful in CHF with atrial fibrillation
  • 65. Digoxin
    • DIG trial
    • 6800 pts EF <45%
    • 0.25 mg/day
    • 22% reduction in hospitalisation
    • No mortlity benefit
    • 28% RRR of death in post hoc analysis
  • 66.  
  • 67. Nesiritide
    • Identical to human BNP
    • Causing vasodilation and decrease LV filling pressure
    • Decrease pulmonary capillary wedge pressure
    • Improves patients’ symptoms
    • Improvement in hemodynamics VMAC trial 5.8 mm of hg decrease on PCW
  • 68. Nesiritide
    • 2 mcg/kg bolus infusion 0.01-0.03 mcg/kg/min for 3 hrs
    • Improved safety profile compared with dobutamine with fewer arrhythmias and better outcomes
    • It should not be used in patients who are overdiuresed, hypotensive, or present with other signs of inadequate perfusion - Worsening of renal failure (45%)
  • 69.  
  • 70. Inotropes
    • Inotropes: direct adrenergic agonists, phosphodiesterase inhibitors, and dopaminergic agonists
    • Inotropes improve short term hemodynamics, they do not improve and in several cases may worsen long-term survival
    • Oral inotropic agents have resulted in excess mortality in patients with HF
  • 71. Amiodarone
    • Antiarrhythmic effect
    • Low dose amiodarone was safe and significantly reduced 2-year mortality (33.5% vs 41.4%, p=0.02)
    • in patients with moderate to severe HF (GESICA trial)
    • Another trial did not demonstrate mortality benefit, either all-cause or sudden death
  • 72. Anticoagulation
    • LVEF < 30%
    • LV thrombus
    • Atrial fibrillation
    • INR 2-3
  • 73.  
  • 74. Thank you