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Heart Failure

Heart Failure. Final common pathway for many cardiovascular diseases whose natural history results in symptomatic or asymptomatic left ventricular dysfunction Cardinal manifestations of heart failure include dyspnea, fatigue and fluid retention

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Heart Failure

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  1. Heart Failure • Final common pathway for many cardiovascular diseases whose natural history results in symptomatic or asymptomatic left ventricular dysfunction • Cardinal manifestations of heart failure include dyspnea, fatigue and fluid retention • Risk of death is 5-10% annually in patients with mild symptoms and increases to as high as 30-40% annually in patients with advanced disease

  2. Main causes • Coronary artery disease • Hypertension • Valvular heart disease • Cardiomyopathy • Cor pulmonale

  3. Compensatory changes in heart failure • Activation of SNS • Activation of RAS • Increased heart rate • Release of ADH • Release of atrial natriuretic peptide • Chamber enlargement • Myocardial hypertrophy

  4. NYHA Classification of heart failure • Class I: No limitation of physical activity • Class II: Slight limitation of physical activity • Class III: Marked limitation of physical activity • Class IV: Unable to carry out physical activity without discomfort

  5. New classification of heart failure • Stage A: Asymptomatic with no heart damage but have risk factors for heart failure • Stage B: Asymptomatic but have signs of structural heart damage • Stage C: Have symptoms and heart damage • Stage D: Endstage disease ACC/AHA guidelines, 2001

  6. Types of heart failure • Diastolic dysfunction or diastolic heart failure • Systolic dysfunction or systolic heart failure

  7. Factors aggravating heart failure • Myocardial ischemia or infarct • Dietary sodium excess • Excess fluid intake • Medication noncompliance • Arrhythmias • Intercurrent illness (eg infection) • Conditions associated with increased metabolic demand (eg pregnancy, thyrotoxicosis, excessive physical activity) • Administration of drug with negative inotropic properties or fluid retaining properties (e. NSAIDs, corticosteroids) • Alcohol

  8. Goals of treatment • To improve symptoms and quality of life • To decrease likelihood of disease progression • To reduce the risk of death and need for hospitalisation

  9. Approach to the Patient with Heart Failure Assessment of LV function (echocardiogram, radionuclide ventriculogram) EF < 40% Assessment ofvolume status Signs and symptoms of fluid retention No signs and symptoms offluid retention Diuretic(titrate to euvolemic state) ACE Inhibitor Digoxin b-blocker

  10. Effects of SNS Activation in Heart Failure • Dysfunction/death of cardiac myocytes • Provokes myocardial ischemia • Provokes arrhythmias • Impairs cardiac performance These effects are mediated via stimulation of b and a1 receptors Am J Hypertens 1998; 11: 23S-37S

  11. Carvedilol in Heart Failure • Effective receptor-blockade approach to heart failure • Negative inotropic effect counteracted by vasodilation • Provides anti-proliferative, anti-arrhythmic activity and inhibition of apoptosis • Prevents renin secretion Drugs of Today 1998; 34 (Suppl B): 1-23.

  12. US Multicenter Program Placebo Carvedilol % Risk (n=398) (n=696) Reduction All-cause 31 22 65%mortality (7.8%) (3.2%) Death due to progressive 13 5 heart failure (3.3%) (0.7%) Sudden death 15 12 (3.8%) (1.7%) Risk of hospitalization for 78 78 27%cardiovascular reasons (19.6%) (14.1%) Combined risk of 98 110 38%mortality & hospitalization (25%) (16%) NEJM 1996; 334:1349-1355

  13. ANZ Multicentre Heart Failure Trial Placebo Carvedilol % Risk (n=208) (n=207) Reduction All-cause 26 20 24%mortality (12.5%) (10%) Risk of hospitalization for 84 64 28%cardiovascular reasons (40%) (31%) Combined risk of 97 74 29%mortality & hospitalization (47%) (36%) Lancet 1997; 349: 375-380.

  14. Effect of carvedilol on progressionof congestive heart failure All randomized patients Endpoint Placebo Carvedilol (n=134) (n=232) Primary endpoint 28 (21%) 25 (11%)* Death due to CHF 4 (3%) 0 (0%) Hospitalization due to worsening CHF 8 (6%) 9 (4%) Increase in CHF medication 16 (12%) 16 (7%) * Placebo vs. carvedilol, p = 0.008 Drugs of Today 1998; 34 (Suppl B): 1-23.

  15. COPERNICUS: Effect on Mortality 35% Mortality (%) 22nd Congress of European Society of Cardiology, August 2000

  16. COPERNICUS: Mortality reduction inspecial patient groups with carvedilol EF < 15%, hospitalised3 or more times during prior year for worsening heart failure EF<20%, hospitalised for heart failure in year prior to study entry Mortality reduction (%) 22nd Congress of European Society of Cardiology, August 2000

  17. Carvedilol vs. Metoprolol Change in LVEF (%) from baseline Circulation 2000; 102: 546-551

  18. Dosage guidelines for Carvedilol in heart failure • Patient selection • Stable on background medications (diuretics, digoxin and/or ACE inhibitors) • Not in a fluid-overload state • Not hypotensive 2 weeks 3.125 mgbid Doubled every2 weeks Max dose 25 mg bid (<85 kg); 50 mg bid (>85 kg) • Before dose increase • Evaluate for • Worsening heart failure • Vasodilation • Bradycardia • After each new dose initiation • Observe for signs of dizziness or light headedness for one hour

  19. Management of Complications Transient worsening of heart failure (e.g. increasing dyspnea, decreasing exercise capacity) • Increase dose of diuretic and/or ACE inhibitor • If necessary, reduce carvedilol dose and/or prolong titration interval • Search for other possible causes (e.g. thyroid malfunction, infection, non-compliant drug intake, excessive liquid intake, etc.) Vasodilatory Symptoms (dizziness, light headedness, symptomatic hypotension) • Decrease diuretic dose and, if necessary, ACE inhibitor dose • If the cessation of both is not successful, reduce carvedilol dose and/or prolong titration interval

  20. Management of Complications (Contd.) Bradycardia (Pulse rate below 55 beats/min) • Check and eventually reduce digitalis dose • If necessary, reduce carvedilol dose and/or prolong titration interval • Withdraw carvedilol only in the event that hemodynamics are affected Symptoms of Bronchial obstruction • Search for other possible causes (e.g., concurrent infection, subacute pulmonary edema) • Reduce dose of, or withdraw, carvedilol only after possible causes for symptoms have been ruled out

  21. The role of angiotensin II in the progression of heart failure Coronary artery disease Cardiomyopathy Cardiac overload Left ventricular dysfunction  Arterial blood pressure Renin release ­ Angiotensin II Aldosterone release Inotropy and hypertrophy of Na+ and water retention Vasoconstriction vascular and cardiac cells ¯ Peripheral organ blood flow Cardiac remodelling Left ventricular ¯ ¯ Skeletal muscle Renal dilation & hypertrophy blood flow blood flow Pump failure Exercise intolerance Oedema

  22. ACE Inhibitors: physiologic benefits Arteriovenous Vasodilatation •  pulmonary arterial diastolic pressure •  pulmonary capillary wedge pressure •  left ventricular end-diastolic pressure •  systemic vascular resistance •  systemic blood pressure •  maximal oxygen uptake (MVO2)

  23. ACE Inhibitors: physiologic benefits •  LV function and cardiac output •  renal, coronary, cerebral blood flow • No change in heart rate or myocardial contractility • no neurohormonal activation • resultant diuresis and natriuresis

  24. ACE Inhibitors: clinical benefits • Increases exercise capacity • improves functional class • attenuation of LV remodeling post MI • decrease in the progression of chronic HF • decreased hospitalization • enhanced quality of life • improved survival

  25. Asymptomatic Patients Enalapril SOLVD Prevention Trial EF<35%  HF progression,  hospitalization Captopril SAVE, GISSI-3, ISIS-4Post MI, EF <40%  overall mortality,  re-infarction  hospitalization,  HF progression

  26. Symptomatic Patients Hydralazine + Isosorbide dinitrate VHeFT-I mortality, improved functional class as compared with use of digoxin and diureticsVHeFT-II proved less effective than enalapril

  27. Dosage of ACE inhibitors: ATLAS study Low-dose High-dose (2.5-5 mg) (32.5-35mg) Cardiovascular 44.9% 42.5% mortality All-cause mortality + hospitalisation for 83.8% 79.7% cardiovascular reason All-cause mortality + hospitalisation for 60.4% 55.1% heart failure Circulation 1999;100:2312-18

  28. AIRE AIRE Study demonstrated efficacy of ramipril on mortality and morbidity in CHF post-MI NYHA class I-III patients • 2006 patients enrolled in a double-blind,randomized, placebo-controlled study • 27% reduction in the risk of death • 23% decrease in progression to severe / resistant heart failure Lancet. 1993; 342:821-828

  29. Guidelines to ACE Inhibitor Therapy • Contraindications • Renal artery stenosis • Renal insufficiency (relative) • Hyperkalemia • Arterial hypotension • Cough • Angioedema • Alternatives • Hydralazine + ISDN, AT-II inhibitor

  30. Guidelines to ACE Inhibitor Therapy • All patients with symptomatic heart failure and those in functional class I with significantly reduced left ventricular function should be treated with an ACE inhibitor, unless contraindicated or not tolerated • ACE inhibitors should be continued indefinitely • It is important to titrate to the dosage regimen used in the clinical trials … in the absence of symptoms or adverse effects on end-organ perfusion • In very severe heart failure, hydralazine and nitrates added to ACE inhibitor therapy can further improve cardiac output

  31. ACE Inhibitor Therapyin Heart Failure Patients(Ejection Fraction < 0.40) Systolic Blood Pressure <100 mmHg (or elevated creatinine) 100-139 mmHg (or recent intense diuresis) >140 mmHg Lowest Dose,Short-Acting Usual Starting Dose, Long-or Short-Acting Intermediate Dose, Long- or Short-Acting Follow-Up Every 1-2 Weeks Stable BP and Creatinine Level Symptomatic Low BP or Rising Creatinine Level Stop ACE Inhibitor Therapy Residual Excess Fluid? Increase ACE Inhibitor Dose; Follow-Up Every 1-2 Weeks Y N Stop Diuretic and ACE Inhibitor Therapy Refer to specialist Target Dose Resume ACE Inhibitor Titration Return to Baseline BP and Creatinine Level ? N Y

  32. Diuretics • Indicated in patients with symptoms of heart failure who have evidence of fluid retention • Enhance response to other drugs in heart failure such as beta-blockers and ACE inhibitors • Therapy initiated with low doses followed by increments in dosage until urine output increases and weight decreases by 0.5-1kg daily

  33. Digoxin • Enhances LV function, normalizes baroreceptor-mediated reflexes and increases cardiac output at rest and during exercise • Recommended to improve clinical status of patients with heart failure due to LV dysfunction and should be used in conjunction with diuretics, ACE inhibitors and beta-blockers • Also recommended in patients with heart failure who have atrial fibrillation • Digoxin initiated and maintained at a dose of 0.25 mg daily • Adverse effects include cardiac arrhythmias, GI symptoms and neurological complaints (eg. visual disturbances, confusion)

  34. Summary of drug treatment for CHF Asymptomatic Mild to moderate Moderate LV dysfunction CHF to severe CHF ACE inhibitor Digoxin Digoxin Beta blocker Diuretics Diuretics ACE inhibitor ACE inhibitor Beta blocker Beta blocker Spironolactone

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