Systolic Heart Failure

1. Systolic Heart Failure

2. Types of Heart Failure Systolic heart failure - failure of contraction Diastolic heart failure- failure of relaxation This lecture concentrates on systolic heart failure

3. Staging system of Heart Failure A - patients at risk, but no structural or functional defects, (CAD,HTN, DM, metabolic syndrome, obesity) B - pts with structural heart disease but do not manifest symptoms of heart failure (LV enlargement or dysfunction, LVH, valvular heart disease)

4. Staging system of Heart Failure C - pts with prior or current symptoms that can be controlled with standard medications D - pts with severe disease, frequent hospitalizations, often requiring advanced therapies

5. NYHA Functional Classification Class I - pts with disease but no symptoms that limit activity Class II - pts with slight limitations of physical activity related to symptoms of HF (dyspnea, fatigue) Class III - pts with marked limitations of physical activity, but no symptoms at rest Class IV- pts cannot carry out any physical activity without limitation and may have symptoms even at rest

6. Systolic Heart Failure �Backward� failure theory Decreased contractility results in increased LV diastolic pressure causing fluid build up in the pulmonary vasculature. Symptoms include dyspnea, orthopnea, abdominal fullness, leg swelling Signs include JVD, gallops(S3), MR/TR murmurs, rales, peripheral edema

7. Systolic Heart Failure �Forward� failure theory Inadequate cardiac output at rest or with exercise stress results in decreased perfusion to vital organs Symptoms include fatigue, weakness, dizziness, poor mentation, anorexia, nausea Signs include pallor, cold extremities, tachycardia, hypotension

8. Initial insult (AMI etc) causes changes in neurohormonal profile and direct myocyte changes Causes myocyte hypertrophy and impairs myocyte function End result is chamber remodeling which causes progression in ventricular dysfunction and HF

9. Key Neurohormonal Mediators Bad Players Norepinephrine Angiotensin II Aldosterone Endothelin Vasopressin Tumor necrosis factor Good Players Natriuretic peptides Nitric oxide prostacyclin

10. Bad players stimulate hypertrophy, cause remodeling, fibrosis, apoptosis and contraction abnormalities This leads to vasoconstriction, sodium and fluid retention

11. Good players are antihypertrophic, antiproliferative and vasodilatory They result in reverse remodeling and encourage diuresis

13. Etiologies: CAD (65%) Idiopathic dilated cardiomyopathy Alcoholic/toxin-induced cardiomyopathy Infectious/Inflammatory process Familial dilated cardiomyopathy Peripartum cardiomyopathy Stress-induced cardiomyopathy Endocrine/Nutritional causes Iron overload cardiomyopathy Tachycardia mediated cardiomyopathy

14. Etiologies CAD Most common cause (65%) Reversible Revascularization can markedly improve outcomes

15. Etiologies Idiopathic dilated cardiomyopathy Diagnosed when all other causes have been excluded

16. Etiologies Alcohol/toxin induced cardiomyopathy Alcoholic CM prevalence is estimated at 20% of all DCM Alcohol has a direct acute and chronic toxic effects on the myocardium (> 7 drinks/day for >5 years) Cocaine and other catecholaminergic drugs Chemotherapeutic drugs (anthracyclines)

17. Etiologies Infectious/Inflammatory Coxsackie B(#1) HIV, mycoplasma, HCV, Lyme Chagas disease, endemic in South and Central America Lupus, scleroderma, RA, Kawasaki, Churg-Strauss and others

18. Etiologies Familial dilated cardiomyopathy at least 20-30% of all DCM Can be autosomal dominant or recessive, X-linked, or mitochondrial Associated with myscular dystrophies

19. Etiologies Peripartum cardiomyopathy Development of clincal HF in the last month of pregnancy or the first 5 months after peripartum Half of all women normalize within 6 months and have a good prognosis NO ACE/ARB if pregnant or breast feeding

20. Etiologies Stress-induced cardiomyopathy Other names include tako-tsubo, apical ballooning, or broken heart syndrome Reversible cause of acute systolic dysfunction resembles a large anterior wall MI Associated with emotional, surgical, or dramatic stresses and catecholamine surge Improves over days to weeks, usually with complete resolution of LV function

21. Etiologies Endocrine/Nutritional causes Rare Hypothyroidism/thyrotoxicosis Diabetes/obesity (risks, stage A) Acromegaly and GH deficiency Pheochromocytoma Thiamine (wet beriberi - high output form) Carnitine, selenium

22. Etiologies Iron overload cardiomyopathy Can be primary (hereditary) or secondary Hereditary hemochromatosis is common in Northern Europeans and results in iron deposition in the heart, joints, liver, skin (bronze diabetes) Gold standard for diagnosis is liver biopsy

23. Etiologies Tachycardia mediated cardiomyopathy Often difficult to discern whether tachycardia is primary force driving the cardiomyopathy or secondary phenomenon Treatment of heart rate improves and can normalize LV function Pharmacologic, cardioversion, or ablation

24. Clinical Evaluation History Symptoms and functional class Angina Arrhythmias Alcohol history Past medical history (chemo etc) Evaluate volume status

25. Clinical Evaluation Physical Volume status Hemodynamics Murmurs Vitals with orthostatics

26. Clinical Evaluation Laboratory Chemistries Renal function CBC with dif LFT TSH HbA1c Lipids BNP

27. Clinical Evaluation Studies CXR ECG (Holter) Echocardiogram

28. Clinical Evaluation Rule out CAD since it is the most common cause and is reversible Patients should have angiography if the have angina or known ischemia, or if they have a high likelihood of CAD

29. Clinical Evaluation Endomyocardial biopsy is not part of a routine evaluation It is only useful if the results will influence therapy, such as in the following conditions Sarcoidosis, amyloidosis Hypereosinophillic syndrome Fulminant myocarditis Giant cell myocarditis Drug toxicities

30. Management Any patient who presents with first either the first episode of heart failure or with acute decompensation of previously stable heart failure they should be evaluated for the cause of their deterioration

31. Clinical Evaluation Drugs to avoid in heart failure NSAIDs Most antiarrhythmics Most calcium channel blockers (felodipine, amlodipine are likely safe) thiazolidinediones

32. Management Drugs in Heart Failure Diuretics loop diuuretics are preferred over thiazides if renal function is impaired

33. Management Drugs in Heart Failure ACE inhibitors ACE inhibitiors, start at low dose and titrate slowly following creatinine and potassium levels ACE inhibitors are first line, but ARB may be used instead if history of cough or angioedema Evidence is soft for addition of ARB to ACE

34. Management Drugs in Heart Failure Beta blockers carvedilol, metoprolol, succinate and bisoprolol) Start low and titrate slowly Relative contraindications include reactive airway disease, aymptomatic bradycardia, SM with recurrent hypoglycemia, resting limb ischemia

35. Management Drugs in Heart Failure Aldosterone antagonists Cautious use in patients with Creat >1.5 or K >5 Closely follow K and Cr Avoid K and salt substitutes Patients must urgently address dehydration secondary to the risk of renal failure Limited study populations NYHA III-IV Post-MI with reduced EF and symptoms or DM

36. Management Drugs in Heart Failure Digoxin Symptomatic improvement with reduced hospitalizations in patients with mild to moderate heart failure Less effective in women than men Optimal target level is 0.6 - 0.9, above which there is an increase in mortality Drug interactions: amiodarone

37. Management Drugs in Heart Failure Nitrate-Hydralazine Inferior to ACE/ARB but should be used for patients who are intolerant of these drugs Should be used in addition to ACE-I and beta blockers in African-American patients who have persistent NYHA class II-IV symptoms

38. Management Drugs in Heart Failure Warfarin may be sued in patients with low ejection fraction and Atrial fibillation Intracardiac thrombus Previous thromboembolism Prophylactic use is controversial

39. Management Drugs in Heart Failure Aspirin if the patient has ischemic cardiomyopathy or atherosclerotic vascular disease If the patient has non-ischemic cardiomyopathy do not use aspirin

40. Management Non-pharmacologic treatment Nutritional counseling regarding sodium restriction, fluid restriction and alcohol Daily weight and symptom assessment with an understanding of how to take action if there is a change Regular physical activity Education on the importance of compliance

41. Device Therapy ICD Half of pts with HF die suddenly from arrhythmias Implantation of and internal cardioverter defibrillator may improve survival in centain subsets of patients

42. Device Therapy Cardiac resynchronization therapy Used for patients with a conduction delay, meaning the walls of the ventricle contract at different times Allows contraction of the ventricle to be more efficient because it forces all walls of the heart to contract at the same time

43. Management Device Therapy ICD EF < 30-35% History of inducible arrhythmia, sudden cardiac death BiVentricular pacemaker QRS >120 EF< 35% NYHA III-IV

44. Guidelines Chronic stable Heart Failure Therapy Stage A: Treat all underlying disorders, such as HTN, DM, lipids, thyroid dysfunction and CAD Modify all social factors, such as alcohol, diet, smoking Consider starting ACE-I if patient has diabetes, CAD or HTN

45. Guidelines Chronic stable Heart Failure Therapy Stage B: All therapies listed under stage A Utilize beta blocker and ACE-I in all patients with a history of AMI or any patient with reduced EF Evaluate patients for valvular heart disease and recommend surgery for any hemodynamically significant valvular disorders Consider ICD for patients after AMI with EF < 30%

46. Guidelines Chronic Stable Heart Failure Therapy Stage C: All therapies listed under stages A and B Aldosterone antagonists should be started in patients with NYHA III-IV and a reduced EF Institute diuretics and salt/fluid restriction Consider the addition of hydralazine/imdur in African-American patients, may also be used in place of ACE-I in patients unable to take ACE-I Consider digoxin in patients with symptoms and EF<30% ICD if EF<30-35% CRT if EF<35%, NYHA III-IV, QRS>120

47. Guidelines Refractory Heart Failure Stage D All therapies listed under stages A, B and C Refer eligible patients for transplant/heart failure center Consider LVAD for destination therapy Consider Swan placement to guide therapy End-of-life care should be discussed, including option of deactivating ICD

48. Management Acute Decompensated Heart Failure Patients need to be evaulated regarding congestion(wet versus dry) and for adequate perfusion (cold versus warm) Most patients are wet and warm, others may be in shock and are wet and cold

49. Management Acute Decompensated Heart Failure Wet and warm treatment Diuresis vasodilators

50. Management Acute Decompensated Heart Failure Wet and warm treatment Diuresis inotropes vasodilators

51. Management ADHF: Vasolilators Nitroprusside Arterioral and venodilator, avoid in ischemic patients Nitroglycerin Primarily venodilator, best if ischemie cause of HF Nesiritide Allows for diuresis and improved relaxation, concerns for mortailiuty and dosing

52. Management ADHF: inotropes Milrinone/Dobutamine Limited role Use with low output state with marginal blood pressure despite adequate filling pressure Risk of tachyarrhythmias and hypotension

53. Management ADHF Device therapy LVAD(left ventricular assist device), device connected to the left ventricle to mechanically pump blood and rest the heart Ventricular reconstruction surgery Heart transplant

54. LVAD

55. Case 1 55 year old male presents with mild dyspnea on exertion. He denies angina or dizziness. There is no significant past medical history. He drinks 2-3 glasses of wine per week On physical exam BP 134/70, HR 125. There is no JVD. Lungs are clear. Heart is tachycardic with irregular rhythm. Routine labs are normal. EKG shows AF. Echo demonstrates global hypokinesis with ejection fraction of 35%

56. What is the patients NYHA functional class I II III IV

57. What is the patients heart failure stage A B C D

58. What do you recommend for this patient Admit to hospital for IV diuresis Encourage him to stop drinking alcohol and re-evaluate in 6 months Admit to hospital for endomyocardial biopsy Start a medication to slow heart rate

59. 71 yo male with known reduced EF presents to ER with worsening dyspnea and new orthopnea. BP is 150/80, he has elevated JVP, bibasilar rales and lower extremity edema. EKG shows ischemic changes with ST segment depression. Which drug is most useful in addition to diuretics Nitroglycerin Milrinone Dobutamine diltiazem

60. 68 yo male with EF 35% presents to clinic. His is asymptomatic on furosemide 20mg daily. He is on no other medications. Which is the next best step Increase furosemide to 40mg Add nitrate/hydralazine combination Add high dose atenolol Add low dose lisinopril and low dose carvedilol Make no changes

61. Which of the following patients is a good candidate for ARB therapy 45 yo with K> 6.0 on lisinopril 65 yo with HF but on no medications 56 yo with occasional nocturnal cough on lisinopril None of the above