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VBWG Improving Outcomes in Heart Failure: New Insights From Vascular Biology.

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Presentation on theme: "VBWG Improving Outcomes in Heart Failure: New Insights From Vascular Biology."— Presentation transcript:

1 VBWG Improving Outcomes in Heart Failure: New Insights From Vascular Biology

2 VBWG Heart Failure: A Public Health Concern

3 VBWG Lloyd-Jones DM et al. Circulation. 2002;106:3068-72. 0 5 10 15 20 25 Attained age (years) Cumulative risk (%) Men 40 20% Lifetime risk for HF after age 40 Women Framingham Heart Study 50 60708090 0 5 10 15 20 25 0 Lifetime risk for HF for given index age is cumulative through age 94 years 4050 60708090

4 VBWG Hypertension is the No. 1 risk factor for HF 20 40 60 0 HTN Population- attributable risk (%) MIAnginaVHDLVHDiabetes Hazard ratioM2.16.31.42.52.21.8 W3.36.01.72.12.83.7 MenWomen Levy D at al. JAMA. 1996;275:1557-62. VHD = valvular heart disease Framingham Heart Study

5 VBWG Diabetes: A frequent comorbidity with HF Bell DSH. Diabetes Care. 2003;26:2433-41. Bertoni AG et al. Diabetes Care. 2004;27:699-703. Adams KF et al. Am Heart J. 2005;149:209-16. Framingham data show  HF in diabetic adults age 45 to 74 years – 2x  in men; 5x  in women Medicare sample of diabetic adults age ≥65 years (1994–1999): – HF prevalence in 1994: 22.4% – Annual HF incidence: 7.9% – Similar incidence by sex and race – Significant ↑ with age and diabetes-related comorbidities National registry of >100,000 patients hospitalized with HF (mean age 72.4 years) – 44% had diabetes

6 VBWG Diabetes is the No. 1 risk factor for HF in women with coronary disease Bibbins-Domingo K Jr et al. Circulation.2004;110:1424-30. Adjusted hazard ratio Diabetes Atrial fibrillation Myocardial infarction >1 event Creatinine clearance <40 Current smoking BMI >35 Left bundle branch block LV hypertrophy Systolic BP ≥140 3.1 2.9 2.5 2.3 2.1 1.9 1.6 1.5 00.511.522.533.5 HERS study

7 VBWG Increasing risk for HF in women with CHD: Impact of diabetes, renal insufficiency, obesity Bibbons-Domingo K et al. Circulation.2004;110:1424-30. CrCl (ml/min) = creatinine clearance HERS study; 2391 women with CHD and no HF at baseline 0 2 4 6 8 10 12 14 CHDCHD + DMCHD + DM + BMI >36 CHD + DM + CrCl <42.8 1.2 2.8 7.0 12.8 Annual HF incidence (%)

8 VBWG Heart Failure Pathophysiology

9 VBWG Important pathophysiologic mechanisms in HF (1) Coronary arteries Obstruction Inflammation Modified from Jessup M, Brozena S. N Engl J Med. 2003;348:2007-18. Cardiac abnormalities Myocardium or myocyte Myocardial relaxation Abnormal excitation- contraction coupling  -Adrenergic desensitization Hypertrophy Necrosis Fibrosis Apoptosis FunctionalStructural Left ventricular chamber Remodeling – Dilation – Increased sphericity – Aneurysmal dilatation or wall thinning – Concentric hypertrophy Mitral regurgitation Intermittent ischemia or hibernating myocardium Induced arterial and ventricular arrhythmias Altered ventricular interaction

10 VBWG Important pathophysiologic mechanisms in HF (2) RAAS SNS (norepinephrine) Vasodilators (bradykinin, nitric oxide, prostaglandins) Natriuretic peptides Cytokines (endothelin, tumor necrosis factor, interleukins) Vasopressin Matrix metalloproteinases Jessup M, Brozena S. N Engl J Med. 2003;348:2007-18. Biologically active tissue and circulating substances

11 VBWG Important pathophysiologic mechanisms in HF (3) Jessup M, Brozena S. N Engl J Med. 2003;348:2007-18. Genetics, ethnicity, sex Age Use of alcohol, tobacco, toxic drugs Coexisting conditions Hypertension Diabetes Renal disease Coronary artery disease Anemia Obesity Sleep apnea Depression Patient factors

12 VBWG Neurohormonal model of HF Ventricular remodeling Neurohormonal activation – RAAS, SNS Increased cytokine expression Immune and inflammatory changes Altered fibrinolysis Oxidative stress Apoptosis Altered gene expression Energy starvation Injury to myocytes and extracellular matrix Electrical, vascular, renal, pulmonary muscle, and other effects Heart failure McMurray J, Pfeffer MA. Circulation. 2002;105:2099-106.

13 VBWG Diabetes pathogenesis accelerates HF Kirpichnikov D et al. J Card Fail. 2003;9:333-44. Activation of protein kinase C Hyperglycemia Heart failure Decreased intracellular calcium removal Activated RAAS Activated sympathoadrenal system Cardiac fibrosis Cardiomyocyte death Decreased myocardial contractile strength Diastolic dysfunction Systolic dysfunction Diabetes

14 VBWG RAAS in CV continuum: Pivotal role of AT 1 receptors in the failing heart Adapted from Wassmann S, Nickenig G. Eur Heart J Suppl. 2004;6(suppl H):H3-9. Renin ACE B 1 /B 2 receptor AT 1 receptor Angiotensinogen Angiotensin I Angiotensin II AT 2 receptor NO Vasodilation Growth inhibition Apoptosis Degradation Bradykinin/Kinins Reactive oxygen species Pro-inflammatory process Vasoconstriction Cellular growth/proliferation Apoptosis Neurohormonal activation ? Clinical significance

15 VBWG Primary targets of treatment in HF Jessup M, Brozena S. N Engl J Med. 2003;348:2007-18.

16 VBWG Angiotensin receptor blockade in the CVD continuum Atherosclerosis Myocardial infarction Endothelial dysfunction  ARB Coronary heart disease Plaque rupture  ARB Risk factors Dilation/ Remodeling Heart failure End-stage heart failure   ARB Hypertension Hyperlipidemia Diabetes  ARB Wassmann S, Nickenig G. Eur Heart J Suppl. 2004;6(suppl H):H3-9.  ARB

17 VBWG Clinical Trial Update

18 VBWG Survival studies of  -blockade in HF 0.50.01.0 II-IV III/IV* III/IV CIBIS-II Bisoprolol MERIT-HF Metoprolol succinate CR/XL All pooled Relative risk and 95% CI Patients (N) Favors  -blocker Total mortality Placebo/  -blocker NYHA class EF mean COPERNICUS Carvedilol 2647 3991 2289 8927 28% 20% CIBIS-II Investigators. Lancet. 1999;353:9-13. MERIT-HF Study Group. Lancet. 1999;353:2001-7. Packer M et al. N Engl J Med. 2001;344:1651-8. 228/156 217/145 190/130 635/431 P 0.0001 0.00009 0.00013 *not recorded in COPERNICUS, but placebo mortality indicates III/IV

19 VBWG MERIT-HF: Metoprolol succinate CR/XL lowers risk of hospitalization with/without diabetes Placebo (n = 490) Metoprolol succinate CR/XL (n = 495) Total # hospitaliz/ patient-yrs (%) 50 26 25 15 –53% P = 0.0087 –44% P = 0.0039 25 9 10 30 50 70 –37% P = 0.0026 –35% P = 0.0002 All randomized NYHA III/IV, EF <25% DiabetesNo diabetes DiabetesNo diabetes Deedwania PC et al. Am Heart J. 2005;149:159-67. 16 13

20 VBWG MERIT-HF: Benefit of  -blockade with/without diabetes 145 50 14 95 31 200 72 20 128 40 Relative risk (95% CI) All patients randomized Diabetes Diabetes, severe HF No diabetes No diabetes, severe HF All patients randomized Diabetes Diabetes, severe HF No diabetes No diabetes, severe HF* 0.01.0 Favors metoprolol succinate CR/XL Favors placebo All-cause mortality Hospitalization for CHF Metoprolol succinate CR/XL Deedwania PC et al. Am Heart J. 2005;149:159-67. 217 61 24 156 48 294 108 40 186 64 Placebo Events (n) *Severe HF = NYHA class III/IV, EF<0.25

21 VBWG Pooled HF trials: Effect of  -blockade on survival in diabetic patients 312 2335 2647 985 3006 3991 Relative risk (95% CI) Diabetes No diabetes All All 3 studies 0.01.0 CIBIS II MERIT-HF Total (n) randomized Deedwania PC et al. Am Heart J. 2005;149:159-67. 1.8 33/27 195/129 228/156 61/50 156/95 217/145 635/431 Deaths (n) Placebo/  -blockade 589 1700 2289 COPERNICUS 190/130 Diabetes No diabetes All Diabetes No diabetes All 1886 7041 8927 Diabetes No diabetes All

22 VBWG GEMINI: Design Bakris GL et al. JAMA. 2004;292:2227-36. Objective:Compare effects of  -blockers with different pharmacologic properties on glycemic and metabolic control in patients with diabetes and hypertension receiving RAAS blockade Participants:1235 patients Randomized to treatment: Carvedilol 6.25 mg to 25 mg bid (n = 498) or Metoprolol tartrate 50 mg to 200 mg bid (n = 737) Follow-up:35 weeks Glycemic Effects in diabetes Mellitus: carvedilol-metoprolol comparison IN hypertensIves study

23 VBWG Bakris GL et al. JAMA. 2004;292:2227-36. Metoprolol tartrate Carvedilol % (SD)P P HbA 1c 0.15 (0.04)<0.001 0.02 (0.04)0.65 Insulin sensitivity –2.00.48 –9.10.004 GEMINI: Change in HbA 1c and insulin sensitivity Endpoint (mean  )

24 VBWG RESOLVD substudy: Effect of metoprolol succinate CR/XL on glucose and insulin Demers C et al. Canadian Cardiovascular Congress; 2004. Calgary. 247 patients with heart failure Mean LVEF 28% 18% female 26% with diabetes At 17 weeks, patients taking enalapril  candesartan were randomized to – Metoprolol succinate CR/XL ≤200 mg/d* (n = 130) or – Placebo (n = 117) Blood samples analyzed at 17 weeks and after 43 weeks *Phase 2 regimen Randomized Evaluation of Strategies fOr Left Ventricular Dysfunction

25 VBWG RESOLVD substudy: No effect on glucose and insulin with metoprolol succinate CR/XL Glucose ( mmol/L) Insulin ( mmol/L) Glucose (mmol/L) Insulin (mmol/L) Metoprolol succinate CR/XL 8.261078.31 † 108 † Placebo8.281168.38139 Demers C et al. Canadian Cardiovascular Congress; 2004. Calgary. 17 weeks*43 weeks *Phase 2: Start metoprolol succinate CR/XL † P = NS vs placebo

26 VBWG Implications for  -blockade in diabetes and HF HF is a frequent, often fatal complication of diabetes  -Blockers are safe and well tolerated by patients with HF and diabetes  -Blockade benefits diabetic patients by decreasing hospitalizations for HF and improving survival It is time to remove existing barriers for use of  -blockers in patients with HF and diabetes Deedwania PC et al. Am Heart J. 2005;149:159-67.

27 VBWG MERIT-HF: Mortality benefit of  -blockade in the elderly All-cause mortality 0 5 10 20 15 369121518 Placebo P = 0.0008 Months Risk reduction 37% 0 Deedwania PC et al. Eur Heart J. 2004;25:1300-9. Metoprolol succinate CR/XL % Patients 2 4 6 369121518 Placebo Metoprolol succinate CR/XL P = 0.0005 Months 0 0 % Patients 0 3 6 12 9 369 1518 Placebo P = 0.0032 Months Risk reduction 43% 0 Sudden death HF mortality Metoprolol succinate CR/XL N = 1982 age ≥65 years % Patients Risk reduction 61%

28 VBWG Meta-analysis:  -Blockade improves survival in elderly HF patients Dulin BR et al. Am J Cardiol.2005;95:896-8. COPERNICUS Carvedilol (U.S.) CIBIS-II MERIT-HF Overall BEST Placebo better –1110  -blocker better Risk ratio (95% CI) 0.75 (0.58–0.98) 0.45 (0.24–0.86) 0.70 (0.49–0.99) 0.70 (0.52–0.95) 0.76 (0.64–0.90) 0.91 (0.78–1.05) P = 0.002 Hazard ratio

29 VBWG SENIORS: Design 2128 patients with HF or LVEF ≤35% ≥70 years of age (mean, 76 years) Randomly assigned to − Nebivolol titrated to 10 mg once daily over 16-week maximum (n = 1067) − Placebo (n = 1061) Primary outcome: Composite of all-cause mortality or CV hospital admission (time to first event) Follow-up: median 21 months Flather MD et al. Eur Heart J. 2005;26:215-25. Study of the Effects of Nebivolol Intervention on Outcomes and Rehospitalization in Seniors with heart failure

30 VBWG SENIORS: Primary and secondary outcomes 100 90 80 70 60 50 100 90 80 70 60 50 06121824300612182430 HR 0.86 (0.74–0.99) P = 0.039 Time (months) All-cause mortality or CV hospital admission (primary outcome) Nebivolol Time (months) All-cause mortality (main secondary outcome) HR 0.88 (0.71–1.08) P = 0.214 Nebivolol 332 (31.1%) Placebo 375 (35.3%) Placebo Event- free survival (%) 169 (15.8%) 192 (18.1%) Flather MD et al. Eur Heart J. 2005;26:215-25. No. of events: Nebivolol Placebo HR = hazard ratio

31 VBWG SENIORS: Clinical relevance Confirms data indicating  -blockade benefits elderly HF patients Extends evidence for benefit of  -blockade to a broad range of elderly patients (age >70 years) with HF, including those with mild or preserved LV function As in previous large trials, both all-cause mortality and CV hospital admissions show a similar and consistent effect with  -blockade Flather MD et al. Eur Heart J. 2005;26:215-25.

32 VBWG Benefit of  -blockade on mortality in urban patients with HF N = 551; 62% African American, 20% White, 15% Hispanic NYHA class III/IV HF: No  -blocker group 60%;  -blocker group 45% 0 10 20 P < 0.001 06 No  -blockers  -blockers Months 12 Death at 1 year (%) No  -blocker132115100  -blocker239229212 Estep JD et al. Am Heart J. 2004;148:958-63. 17% 4%

33 VBWG Not all  -blockers are the same AtenololTenormin  1 selective YesNot FDA- approved for HF BisoprololZebeta  1 selective N/ANot FDA- approved for HF Metoprolol tartrate Lopressor or generic  1 selective YesNot FDA- approved for HF Metoprolol succinate CR/XL TOPROL-XL  1 selective No200 mg qd CarvedilolCoregNon-selective (  1,  1,  2 ) No25 mg bid † LabetalolNormodyneNon-selective (  1,  1,  2 ) YesNot FDA- approved for HF Generic name Brand name* Properties AB-rated generic equiv available Dose for HF *  see prescribing information † COPERNICUS; other trials 50 mg bid for >75 kg

34 VBWG Metoprolol tartrate vs metoprolol succinate CR/XL: Significant pharmacokinetic differences Andersson B et al. J Card Fail. 2001;7:311-7. Metoprolol tartrate 50 mg x 3 142208 300 200 100 0 Metoprolol succinate CR/XL 100 mg Metoprolol succinate CR/XL 200 mg Metoprolol tartrate 50 mg Time (h) Metoprolol succinate CR/XL 200 mg x 1 Metoprolol succinate CR/XL 100 mg x 1 Three-way crossover in patients with HF; N = 15 Plasma concentration (mmol/L)

35 VBWG Effect of metoprolol succinate CR/XL vs atenolol on exercise heart rate/SBP over 24 h Blomqvist I et al. Eur J Clin Pharmacol. 1988;33(suppl):S19-24. N = 10 healthy men Systolic BPExercise heart rate Time (hours) Mean exercise SBP (mm Hg) 190 180 170 160 150 0 02812244 160 140 120 100 0 0281224 Time (hours) 4 Mean exercise heart rate (bpm) Placebo Atenolol 50 mg Metoprolol succinate CR/XL 100 mg Placebo Atenolol 50 mg Metoprolol succinate CR/XL 100 mg

36 VBWG Recommended ACEI doses do not completely halt Ang II formation in HF 42 HF patients on 40 mg long-acting ACEI (fosinopril, lisinopril, enalapril) or captopril 150 mg Jorde UP et al. Circulation. 2000;101:844-6. *P < 0.05 vs after valsartan † P < 0.05 vs 10 ng/kg Ang I 20 0  Radial artery systolic pressure (mm Hg) 25 15 10 5 0 100 20010 † † Angiotensin I (ng/Kg) ACEI + valsartan ACEI * *

37 VBWG CHARM Program: 3 Component trials comparing candesartan with placebo Target dose, candesartan 32 mg Overall trial: All-cause death Primary outcome: CV death or CHF hospitalization Median follow-up, 37 months CHARM- Alternative CHARM- Added CHARM- Preserved n = 2028 LVEF ≤40% ACE inhibitor intolerant n = 3023 LVEF >40% ACE inhibitor treated/not treated n = 2548 LVEF ≤40% ACE inhibitor treated Pfeffer MA et al. Lancet. 2003;362:759-66. Granger CB et al. Lancet. 2003;362:772-6. McMurray JJV et al. Lancet. 2003;362:767-71. Yusuf S et al. Lancet. 2003;362:777-81.

38 VBWG CHARM Program: Reduction in mortality and morbidity Alternative (LVEF ≤40%; ACEI intolerant) 1.00.80.90.71.2 0.90.70.80.61.21.01.1 Added (LVEF ≤40%; ACEI treated) Preserved (LVEF >40%; ACEI treated/ not treated) Overall CV death or HF hospitalization All-cause mortality Adjusted hazard ratio P heterogeneity = 0.37 Adjusted hazard ratio P heterogeneity = 0.33 Pfeffer MA et al. Lancet. 2003;362:759-66.

39 VBWG CHARM-Overall: CV death and non-CV death—Secondary endpoints 5 10 15 20 25 35 2.03.00.01.03.5 P = 0.45 0 Years % Patients 13% Relative risk reduction (95% CI 4%–22%) P = 0.006 CV death Non-CV death Number at risk Candesartan3803356332712215 761 Placebo3796346431702157 743 Pfeffer MA et al. Lancet. 2003;362:759-66.

40 VBWG CHARM-Overall: Reduction in mortality and nonfatal MI with candesartan Events (n) Placebo/candesartan 344/299 Sudden death HF death CV death Nonfatal MI All deaths 260/209 769/691 148/116 945/886 Nonfatal MI/CV death 868/775 0.50.60.79.08.01.00.5 Risk reduction 15% 22% 12% 23% 9% 21% P 0.036 0.008 0.012 0.032 0.055 0.004 Solomon SD et al. Circulation. 2004;110:2180-83. Demers C et al. Circulation. 2004;110(suppl):Abstract.

41 VBWG CHARM—Low LVEF trials: Risk reductions at 1 and 2 years with candesartan LVEF ≤40% Young JB et al. Circulation. 2004;110:2618-26. 30 33 23 20 50 40 30 20 10 0 CV death/HF hospitalizationAll-cause mortality 1 year 2 years % Reduction P < 0.001 P = 0.001

42 VBWG CHARM Program: Outcomes overview Parameter CHARM Added CHARM Alternative CHARM Preserved CHARM Overall Follow-up (months)41343738 CV deaths (%)23.7 vs 27.3*21.6 vs 24.811.2 vs 11.318.2 vs 20.3* HF hospitalization (%)24.2 vs 28*20.4 vs 28.2*15.9* vs 18.319.9 vs 24.2* Combined endpoint (%)37.9 vs 42.3*33 vs 40*22 vs 24.330.2 vs 34.5* NNT/year to prevent 1 CV death/HF hospitalization854013273 Gleiter CH et al. Cardiovasc Drug Rev. 2004;22:263-84. *statistically significant Candesartan vs placebo

43 VBWG Pfeffer MA et al. Lancet. 2003;362:759-66. Candesartan n/N Placebo n/N Hazard ratio (95% CI)P 163/2715 (6%) 202/2721 (7.4%)0.78 (0.64–0.96)0.02 CHARM-Overall: Reduction in new-onset diabetes n = new-onset diabetes N = total patients

44 VBWG VALIANT: Design 14,800 patients with acute MI + HF/LV dysfunction Receiving conventional therapy Randomly assigned (0.5 days to 10 days after acute MI) – Valsartan 160 mg bid (n = 4909) – Valsartan 80 mg bid + captopril 25 mg tid (n = 4885) – Captopril 50 mg tid (n = 4909) Primary outcome: death from any cause Follow-up: median 24.7 months Pfeffer MA et al. N Engl J Med. 2003;349:1893-906.

45 VBWG VALIANT: Treatments show similar effect on outcome 0.4 0.3 0.2 0.1 0.0 061218243036 0.4 0.3 0.2 0.1 0.0 61218243036 Months Probability of event Death from any causeCombined CV endpoint* 0 CaptoprilValsartan/captoprilValsartan *CV death, reinfarction, or hospitalization for HF Pfeffer MA et al. N Engl J Med. 2003;349:1893-906.

46 VBWG VALIANT: Poorer 1-year outcomes in patients with new-onset or previous diabetes Months Probability of event All-cause mortality Previous vs new diabetes diagnosis Previous vs no diabetes New vs no diabetes diagnosis Aguilar D et al. Circulation. 2004;110:1572-8. 36912 Months Adverse CV events 0.4 0.3 0.2 0.1 0.0 0 36912 0.4 0.3 0.2 0.1 0.0 0 Previous DM No DM New DM Previous DM New DM P = 0.43 P < 0.001 P < 0.005 P < 0.001

47 VBWG Clinical implications of CHARM and VALIANT In HF patients and in patients with acute MI and LV dysfunction, evidence supports – ARBs as alternative to ACEIs (in ACEI–intolerant patients) – Benefit from addition of ARBs to ACEI-based regimens ARBs and ACEIs similarly reduce all-cause mortality and HF hospitalizations in patients with HF or high-risk MI Discharge prescription of ACEI or ARB meets new Medicare/Medicaid quality performance measures for HF/MI with LV dysfunction Lee VC et al. Ann Intern Med. 2004;141:693-704. McClellen MB et al. Ann Intern Med. 2005;142:386-7. ACC/AHA. www.acc.org

48 VBWG Benefit of ARB + ACE inhibitor in HF 0.61.20.8 ARB+ ACEI better 1.0 CHARM (HF) 1.4 ACEI alone better VALIANT (post MI + HF/LV dysfunction) Val-HeFT (HF) 1.20.8 HF hospitalization 1.01.40.6 All-cause mortality ARB+ ACEI better ACEI alone better Voors AA, van Veldhuisen DJ. Int J Cardiol. 2004;97:345-8.

49 VBWG ARBs in LV dysfunction: Before/after CHARM and VALIANT Before CHARM, VALIANT After CHARM, VALIANT ARBs superior to ACEI?No (ELITE II, OPTIMAAL)No ARBs non-inferior to ACEI?? (ELITE II, OPTIMAAL)Yes ARBs additive on top of ACEI?? (Val-HeFT) Yes, HF No, post-MI Combination ARB, ACEI, and  -blocker dangerous? ? (ELITE II, Val-HeFT)No Voors AA, van Veldhuisen DJ. Int J Cardiol. 2004;97:345-8.

50 VBWG Difference in target dosing among ARB trials TrialPatientsStudy drugOutcome CHARM OverallHF LVEF ≤40% LVEF >40% Candesartan 32 mg qd vs Placebo 10%  mortality 13%  CV death 23%  HF hosp ELITE IIHF LVEF ≤40% ≥ 60 years Losartan 50 mg qd vs Captopril 50 mg tid Similar  morbidity/mortality OPTIMAALPost-MI + HFLosartan 50 mg qd vs Captopril 50 mg tid Mortality trend favors captopril No difference in morbidity Val-HeFTHFValsartan 160 mg bid vs Placebo + conventional HF Rx No  mortality 13.2%  morbidity/mortality 28%  HF hosp VALIANTAcute MI + HF/LV dysfunction Valsartan 160 mg bid or Captopril 50 mg tid or Valsartan 80 mg bid + captopril 50 mg tid Similar  mortality/morbidity No added benefit with ACEI+ARB Dickstein K et al. Lancet. 2002;360:752-60. Cohn JN et al. N Engl J Med. 2001;345:1667-75. Pfeffer MA et al. N Engl J Med. 2003;349:1893-906. Pfeffer MA et al. Lancet. 2003;362:759-66. Pitt B et al. Lancet. 2000;355:1582-7.

51 VBWG Impact of RAAS modulation on mortality in HF patients with renal insufficiency Minnesota Heart Survey Odds ratio (95% CI) 0 1 2 3 4 5 6 7 P = 0.65 P = 0.04 P = 0.002 P = 0.17 ≥9060–8930–59<30 Post-discharge mortality ( mean follow-up 15 mo) 64 68 63 48 0 20 40 60 80 ≥9060–8930–59<30 ACEI/ARB Rx at discharge Berger AK et al. Circulation. 2004;110 (suppl III):III-749. No ACEI/ARB at dischargeACEI and/or ARB at discharge GFR (mL/min) % 4926 patients hospitalized with HF

52 VBWG Summary

53 VBWG ACC/AHA stages of systolic HF and treatment options Jessup M, Brozena S. N Engl J Med. 2003;348:2007-18. *In appropriate patients


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