Definition, clinical presentation and management of HEART FAILURE

a short summery on definition, clinical presentation and management of HEART FAILURE

1. Sura M, MD Internist & Cardiologist Assistant Professor Of Internal Medicine HU-CMHS CVS Lecture Series For Medical Students Lectures HF RF & VHD Pericardial Diseases IE, IHD, HTN

2. HEART FAILURE Sura M, MD Internist & Cardiologist Ass. Professor of Medicine HU-CMHS Dece 15, 2023

3. Definition (Previous definition) A complex clinical syndrome that results from structural or functional impairment of ventricular filling or ejection of blood. Which in turn leads to the cardinal clinical symptoms of dyspnea and fatigue( may limit exercise tolerance) and signs of HF, namely edema and rales . A clinical syndrome characterized by dyspnea, fatigue and fluid retention.

4. Definition of Heart Failure: Definitions of HF vary widely in the Medical Literature

5. HF Vs CHF 6

6. Classification of HF The main terminology used to describe HF is historical and is based on measurement of the LVEF(Left Ventricular Ejection Fraction) Differentiation of patients with HF based on LVEF is important due to: Underlying etiologies Demographics Co-morbidities and Response to therapies 7

7. Terminologies/ Classification: LVEF HF with a reduced EF (HFrEF) LVEF ≤ 40% Formerly called systolic failure Commonly presented with LV chamber dilatation HF with mildly reduced EF ( HFmrEF ) LVEF 41-49% Formerly called HF with “mid range” HF with a preserved EF ( HFpEF ) LVEF ≥ 50% Formerly called diastolic failure Diagnosis is challenging Accounts ~ 50% of HF 8

8. 4. HF with improved EF ( HFimpEF ) HF with improved EF ( HFimpEF ): HF with a baseline LVEF ≤40%, a ≥10 point increase from baseline LVEF, and a second measurement of LVEF >40%. 9

9. Terminologies: Time course of HF Asymptomatic LV dysfunction (ALVD) A patient who has never exhibited the typical symptoms and/or signs of HF and with a reduced LVEF(≤40%) 10

10. 2. Chronic HF: Patients who have had HF for some time are often said to have ‘Chronic HF’ Stable: A treated patient with symptoms and signs that have remained generally unchanged for at least 1 month is said to be ‘stable Decompensated: If chronic stable HF deteriorates Compensated 11

11. 3. Acute HF New onset/ de novo (20%) Decompensated Transient: recurrent or episodic It can be With a de novo presentation of HF With worsening of previously chronic stable HF 12

12. Acute Heart Failure Syndromes AHF can be defined as the new onset or recurrence of symptoms and signs of HF requiring urgent or emergent therapy and resulting in unscheduled care or hospitalization. ( Braunwalds 12e. 2022 pp946) Nomenclature: Acute heart failure syndromes Acute heart failure Acute( ly ) decompensated heart failure Acute decompensation of chronic heart failure 13

13. NYHA Functional Classification of HF Class I – Asymptomatic No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. Class II – Mild symptom Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF. (i.e. carrying heavy packages, long distance walking, climbing 2 flights of stairs ). 14

14. NYHA Class Class III – Moderate symptoms Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF(i.e. Getting dressed, short distance walking, climbing one flight of stairs) Class IV – Severe symptoms Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest 15

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16. ACCF/AHA Stages of HF Stage A: At Risk for HF Patients who are at high risk for developing HF but do not have structural heart disease or symptoms of HF (e.g., patients with diabetes mellitus or hypertension). Stage B: Pre HF Patients who have structural heart disease but do not have symptoms of HF (e.g., patients with a previous MI and asymptomatic LV dysfunction). 17

17. AHA/ACC Stage Stage C: HF Patients who have Structural heart disease with prior or current symptoms of HF (e.g ., patients with a previous MI with dyspnea and fatigue) Stage D: Advanced HF Patients with refractory HF requiring special interventions ( e.g., patients with refractory HF who are awaiting cardiac transplantation). 18

18. Patient generally progress from one stage to the next unless disease progression is slowed The stages are progressive and inviolate ; once a patient moves to a higher stage , regression to an earlier stage of HF is rarely observed but with GDMT and risk Factor management, HF remission is likely 19

19. Comparison 20

20. Epidemiology of HF Worldwide > 26 million people are affected by HF Developed countries 2% of adult population, ↑ with age – 10% in > 65yo Lower in women than in men but the prevalence is equal because of their longer life expectancy 21

21. Epidemiology The overall prevalence of HF is thought to be increasing In part because current therapies for cardiac disorders, such as MI, VHD, and arrhythmias , are allowing patients to survive longer 22

22. Epidemiology Admissions for HF has tripled during the last three decades. It will continue to grow: Aging of the population, Greatly improved survival after MI Availability of effective therapy for prevention of sudden death. 23

23. Epidemiology In the emerging nations very little is known about prevalence or risk of developing HF due to lack of population-based studies 24

24. In Ethiopia 25

25. Etiology HF may result from disorders of the pericardium, myocardium, endocardium, heart valves, or great vessels or from certain metabolic abnormalities. Any conditions that leads to alteration of LV structure and function can lead to heart failure. 26

26. Underlying cause of HF In developed countries, CAD is the leading cause of HF in men and women accounting for 60–75% of HF 75% contributed by HTN including most patients with CAD In 20–30% of the cases of HFrEF the exact etiologic basis is not known These patients are referred to as having nonischemic , dilated, or idiopathic cardiomyopathy 27

27. Developing countries Rheumatic heart disease remains a major cause of HF in Africa and Asia , especially in the young Hypertension is an important cause of HF in the African and African-American populations. Chagas ' disease is still a major cause of HF in South America 28

28. Socioeconomic shift of developing country: CAD is becoming emerging disease in developing countries 29

29. Etiology of HFrEF (LVEF≤40%) 30 Coronary Artery Disease Myocardial infarction Myocardial ischemia Chronic Pressure Overload Hypertension Obstructive valvular disease Chronic volume overload Regurgitant valvular disease Intracardiac (left-to-right) shunting Extracardiac shunting

30. Etiology(HFrEF) Nonischemic dilated cardiomyopathy Familial/genetic disorders Infiltrative disorders Toxic/drug-induced damage Metabolic disorder Viral Chagas ’ disease Disorders of rate and rhythm Chronic Bradyarrhythmias Chronic Tachyarrhythmias 31

31. Etiology Chronic lung disease Cor pulmonale Pulmonary vascular disorders 32

32. Etiology of HFpEF (LVEF>40-50%) Pathologic hypertrophy Primary (hypertrophic cardiomyopathies) Secondary (hypertension) Aging Endomyocardial disorders Restrictive cardiomyopathy Infiltrative disorders (amyloidosis, sarcoidosis ) Storage diseases (hemochromatosis) Fibrosis 33

33. High-Output States Metabolic disorders Thyrotoxicosis Nutritional disorders (Beriberi) Excessive blood flow requirements Systemic arteriovenous shunting Chronic anemia 34

34. Causes for both HF r EF and HF p EF CAD Hypertension Obstructive Valvular disease Infiltrative disorders Metabolic disorder 35

35. Summary: Causes of HF CAD Hypertension Cardiomyopathies Valvular Heart Disease Congenital Heart Disease Pericardial Diseases Metabolic/Infiltrative disorders Arrhythmias 36

36. Dietary Indiscretion: Excess Salt and Alcohol Intake Myocardial Ischemia/Infarction Arrhythmias: Tachyarrhythmia Or Bradyarrhythmia Discontinuation Of HF Therapy Infection: Endocarditis, Pneumonia, Pyelonephritis, Sepsis Rheumatic Recurrence Myocarditis Anemia Thyrotoxicosis Pregnancy Precipitating Factors

37. Precipitating Factors Initiation Of Medications Calcium Antagonists (Verapamil, Diltiazem )   Nonsteroidal Anti-inflammatory Drugs (NSAIDS )  Antiarrhythmic Agents [All Class I Agents, Sotalol (Class III)] Anti-TNF Antibodies Worsening Hypertension Acute Valvular Insufficiency Stress (Emotional, Physical, Environmental, Excess Fluid) Pulmonary Embolism 38

38. Pathogenesis of HF HF is a progressive disorder that is initiated after an index event ( sudden or insidious ) from: Damages the heart muscle, with a resultant loss of functioning cardiac myocytes or Disrupts the ability of the myocardium to generate force, thereby preventing the heart from contracting normally Regardless of the nature of the inciting all produce a decline in pumping capacity of the heart 39

39. Pathogenesis A decline in pumping activity of the heart leads to tissue hypoperfusion – activates a compensatory mechanisms (SNS, RAAS, and cytokine systems) Initially, these mechanisms are beneficial and adaptive , sustaining heart rate, blood pressure, and cardiac output, and thus maintaining organ perfusion These improves the pumping capacity of the heart , and in most instances the patient remain asymptomatic or minimally symptomatic for few years 40

40. In the short term the compensatory mechanisms able to restore CV function to normal – patient remains asymptomatic With time sustained activation of the compensatory mechanisms leads to sec damage – worsening LV remodeling and subsequent decompensation

41. The sustained activation of these compensatory mechanisms leads to a series of EOD within the myocardium  R emodeling (secondary damage) 42

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43. ` Definition- it refers to the changes in LV mass, volume, and shape and the composition of the heart that occur after cardiac injury and/or abnormal hemodynamic loading conditions 44

44. Changes that occur LV remodeling Include: LV dilatation LV Thinning Increased in LV end diastolic volume Decrease in Stroke volume Mitral valve Incompetence 45

45. HF with preserved EF: Pathogenesis Understanding of the mechanisms that contribute to the development of HF with a preserved EF is still evolving. Diastolic dysfunction was thought to be the only mechanism responsible for the development of HF with a preserved EF Diastolic dysfunction can occur alone or in combination with systolic dysfunction in patients with HF. 46

46. Additional extracardiac mechanisms may be important, such as increased vascular stiffness and impaired renal function. 47

47. Clinical Manifestations The cardinal symptoms of HF are fatigue and shortness of breath. Cause of breathlessness is multifactorial Pulmonary congestion due to LVF Accumulation of interstitial and intra alveolar fluid, stimulating juxta capillary J receptors, causing Rapid Shallow breathing Decreased pulmonary compliance Increased airway resistance Respiratory fatigue and Anemia 48

48. Orthopnea Dyspnea in recumbent position Occurs due to redistribution of fluid from splanchnic circulation and lower extremities Causes increase in pulmonary capillary pressure. Nocturnal cough is usually associated with this symptom Relieved by sitting upright . This symptom is more common in patients with co morbid obesity or ascites 49

49. Paroxysmal Nocturnal Dyspnea- Definition – it refers to acute episode of shortness of breath and coughing that generally occur at night and awaken patient from sleep usually 1 – 3 hours after recline. Associated with coughing or wheeze Mechanism – increased pressure in bronchial arteries leading to airway compression (+) interstitial pulmonary edema = increased airway resistance. Orthopnea symptoms resolve after upright posture, but coughing and wheezing may persist even after upright posture 50

50. Cardiac asthma Is closely related to PND Characterized by wheezing secondary to bronchospasm , and must be differentiated from primary asthma and pulmonary causes of wheezing. 51

51. Trepopnea Dyspnea may occur specifically in recumbency on the left side Self-protecting mechanism to augment cardiac output and to attenuate the imbalance of cardiac autonomic nervous activity. It results from disease of one lung, one major bronchus, or chronic congestive heart failure. 52

52. Bendopnea Shortness of breath when bending forward E.g. When putting on their shoes or socks Elevated right ventricular and left ventricular filling pressures. Novel Symptom of Advanced Heart Failure 53

53. Cheyne -Stokes respiration Referred to as periodic respiration/cyclic respiration Cheyne -Stokes respiration is present in 40% of patients with advanced Associated with low cardiac output. Generally is indicative of an adverse prognosis 54

54. Cheyne -Stokes respiration is caused by an increased sensitivity of the respiratory center to arterial Pco 2 and a lengthy circulatory time. There is an apneic phase, during which arterial Po 2 falls and arterial Pco 2 rises 55

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57. Other symptoms  like – Anorexia – Nausea – Early satiety – Abdominal pain – Abdominal fullness – Congestive hepatomegaly – RUQ pain Confusion , disorientation, sleep disturbances, Nocturia 58

58. Physical examination Patient will present with laboured breathing in an acute LVF. He/she may not be able to finish the sentence due to shortness of breath. He / she may have difficulty to talk due to shortness of breath. Blood pressure may be normal or high in early HF , may decrease consequently and is usually low. 59

59. Low pulse pressure (reduced stroke volume) Sinus tachycardia (increased sympathetic activity) cool peripheries, cyanosis of tips of fingers and nail bed. 60

60. Jugular Venous Pressure Jugular venous pressure – – Indicates right atrial pressure – It is measured in terms of (cm of H2O) – Normal < 8 cm of H2O – Method – measure highest point of JVP vertically from sternal angle and add 5 cm of H2O – Positive Abdomino - Jugular reflux 61

61. Respiratory system – Bilateral rales / crepitations may be present as a result of transudate of fluid from intravascular space to intraalveolar space. – May be accompanied by expiratory wheeze ( cardiac asthma). Pleural effusion may/may not be present. 62

62. Pleural effusions occur most commonly with biventricular failure. Although pleural effusions are often bilateral in HF, when they are unilateral , they occur more frequently in the right pleural space 63

63. Cardiovascular system – Apical impulse may shift inferiorly / laterally . – Sustained apical impulse is felt in severe LVH. – S3 gallop ( protodiastolic gallop) can be heard. – Left parasternal impulse in cases if severe RVH – S4 gallop is usually present in diastolic dysfunction. – MR or TR may be present additionally. 64

64. Abdomen – Hepatomegaly is present ( tender / pulsatile) – Pulsations in liver indicate tricuspid regurgitation – Ascites , Jaundice , raised liver enzymes – Peripheral edema can be pre tibial or pre sacral edema 65

65. Cardiac Cachexia Cachexia in HF can be diagnosed and defined as involuntary non-edematous weight loss ≥6% of total body weight within the previous 6–12 mo It may occur in 5–15% of patients with HF, especially those with HFrEF Cachexia augurs a poor overall prognosis . 66

66. Possible causes of cachexia Cause for cachexia is multifactorial Elevation of Basal Metabolic Rate Elevated circulating cytokines like TNF Congestion of intestinal veins Reduced anabolic drive, prolonged immobilization and physical deconditioning, All together characterized by catabolic/anabolic imbalance 67

67. Diagnosis of HF 68

68. The diagnosis of HF is relatively straightforward when the patient presents with classic signs and symptoms of HF; However, the signs and symptoms of HF are neither specific nor sensitive. 69

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71. Framingham criteria 72

72. WORK UP AHA/ACC class I recommendation for Diagnostic testing CBC, FBS and A1C, electrolytes, LFT, RFT, lipid profile, TSH, Iron Studies CXR 12 lead EKG Echocardiography 73

73. Electrocardiogram (ECG) Cardiac rhythm/rate[ AF,Bradyarrhythmia,Tachyarrhythmia .. ] Chamber size: LVH Evidence of Ischemia: Prior MI{ Presence or absence of Q wave } Acute MI{ST segment elevation} QRS duration: to ascertain whether the patient may benefit from resynchronization therapy Electrolyte imbalance A normal ECG virtually excludes LV systolic dysfunction 74

74. Chest X-ray(CXR) Cardiomegaly Identify non cardiac causes of the patient’s symptoms Acute HF have evidence of pulmonary hypertension, interstitial edema, and/or pulmonary edema, The majority of patients with chronic HF do not. The absence of these findings in patients with chronic HF reflects the increased capacity of the lymphatics to remove interstitial and/or pulmonary fluid The negative predictive value of chest radiography is too low to definitively exclude HF 75

75. Pulmonary edema Cephalization Prominent upper lobe vasculature (indicating pulmonary venous hypertension) are the most prominent “ Butter fly” Pattern: Classic chest radiograph appearance Kerley B lines Thin horizontal linear opacities extending to the pleural surface caused by accumulation of fluid in the interstitial space Pleural effusions and/or fluid in the right minor fissure also be seen. 76

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77. Echocardiography Assessment of LV systolic function (LVEF) Assessment of LV Diastolic function Chamber size : Ventricular Dilatation/hypertrophy Atrial dilatation Valve abnormalities Wall motion Abnormality Regional WMA: IHD Global decreased WMA: DCMP Assessment of right ventricular function and pulmonary arterial pressure 78

78. Biomarkers: Natriuretic Peptides The most commonly measured natriuretic peptides are B-type (i.e., brain) natriuretic peptide (BNP) N-terminal pro–B type natriuretic peptide (NT- proBNP ) It is amino-terminal cleavage pro-peptide equivalent of BNP Released from cardiomyocytes in response to stretch from failing heart 79

79. Importance Diagnosis of HF , especially in setting of clinical uncertainty Establishing prognosis or disease severity in chronic HF Can be useful to achieve optimal dosing of GDMT 80

80. High negative predictive value BNP <100 pg /mL rules out HF in patients presenting with dyspnea in the acute care setting BNP > 400 or 500 pg /mL confirms HF in patients with dyspnea 81

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82. Pitfalls: BNP…NT Pro BNP Increase with age and renal impairment, More elevated in women Can be elevated in right HF from any cause BNP levels may increase in patients taking ARNIs Levels can be falsely low in obese patients 83

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85. Goal of treatment Goals of HF therapy Improve symptoms and quality of life Prevent disease progression Prolong survival 86

86. For patients with LV systolic dysfunction but remain asymptomatic (class I ) the goal should be to slow disease progression by blocking neurohormonal systems that lead to cardiac remodeling For patients who have developed symptoms (class II–IV), the primary goal should be to alleviate fluid retention, lessen disability, and reduce the risk of further disease progression and death. 87

87. Principles of Management General Measures Treat Congestive state/symptomatic treatment Prevent cardiac Remodeling/Treat underlying cause 88

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89. Management of HFrEF General Measures Identify and correct the cause of LVD, if possible Comorbid illness- eg HTN, dyslipidemia, DM Look and address precipitating factors Limited/avoid alcohol Abstain smoking Immunization (pneumococcus and influenza) Prophylaxis (rheumatic, endocarditis) 90

90. General: Physical activity and exercise training Routine modest isotonic exercise (walking/riding a stationary-bicycle, selected pts with NYHA class I to III HF Avoid the exercise training in those with HFrEF: Who have had a major CV event or procedure within the past 6 wks ; In patients receiving cardiac devices that limit the ability to achieve target HRs ; In pts with significant arrhythmia or ischemia 91

91. Exercise training should be considered when symptoms have stabilized and patient is euvolemic Regular daily physical activity that does not induce symptoms, for all patients with stable HF symptoms and impaired LV systolic function; to prevent muscle deconditioning 92

92. Exercise benefit Reduction in mortality Hospital Admissions ↓ Health-related quality of life ↑ 93

93. Diet Dietary Na restriction (2 to 3 g daily) is recommended in all patients with HF Further restriction (<2 g daily) may be considered in moderate to severe HF Caloric supplementation for cardiac cachexia 94

94. Fluid restriction Fluid restriction generally is unnecessary, but < 2L/d in patients with h ypornatremia and patients whose fluid retention is difficult to control despite high doses of diuretics and Na restriction 95

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96. Heart Failure with Reduced Ejection Fraction ( HFrEF ) Diuretics ACEi (or ARB) ß-blocker ARNI Aldosterone antagonists SGL2i: Dapagliflozin, Empagliflozin Nitrates/Hydralazine SA node Modulator(I f current Inh ): Ivabradine Digoxin Cardiac Myosin Activator: Vericiguat 97

97. Four Core Foundational Medication Classes for HFrEF Beta Blockers Carvedilol, Metoprolol Succinate and Bisoprolol SGL2i Dapagliflozin and Empagliflozin MRAs Spironolactone and Eplerenone RAS-Inhibitors ARNI: Sacubitril/Valsartan ACE- i /ARBs 98

98. Diuretics Loop diuretic ( eg . Furosemide) for congestive symptoms When symptoms clear, use lowest possible dose If volume overload persists, despite optimisation of dose: add a second diuretic ( eg . Metolazone or a Thiazide diuretic) Diuretic Resistance Braking phenomenon- 99

99. Loop diuretics: Furosemide, torsemide , and bumetanide Thiazide diuretics: Hydrochlorthiazide 100

100. Side effects of loop diuretics Hypotension Hypokalemia Ototoxicity 101

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102. Drugs that interfere with the excessive activation of the RAAS and the ANS can relieve ssx of HFrEF by stabilizing and/or reversing cardiac remodeling ACEI/ARBs/ARNI and BBs are the cornerstones 103

103. ACE-Inhibitors ACEI are recommended in patients with HFrEF[EF<40%] And current or prior symptoms, unless Contra indicated to ↓ morbidity and mortality A 23% reduction in mortality and A 35% reduction in the combination endpoint of mortality and hospitalizations 104

104. Inhibiting the enzyme angiotensin I to angiotensin II Inhibit kininase II upregulation of bradykinin ACEIs exert their beneficial effects in HFrEF as a Class Maximum tolerated does is recommended 105

105. ARBs: Angiotensin Receptor Blockers ARBs block the effects of angiotensin II on the angiotensin type 1 receptor For patients who are intolerant of ACE inhibitors because of Cough, Skin rash, and Angioedema 106

106. Hypotension Renal failure Hyperkalemia Nonproductive cough ( 10-20% of patients) Angioedema ( 1% of patients) Adverse Effects : ACE-I

107. Patients intolerant of ACE inhibitors because of hyperkalemia or renal insufficiency are likely to experience the same side effects with ARBs Routine combined use of an ACEI, ARB, and MRA is potentially harmful for pts with HFrEF Continued…

108. Pregnancy Renal artery stenosis with solitary kidney Hyperkalemia >5meq/ml Hypotension Contraindication for ACEi or ARBs

109. Doses 110

110. Indicated for patients with symptomatic or asymptomatic HF and a depressed EF <40% Beta blockers should be initiated in low doses followed by gradual increments in the dose if lower doses have been well tolerated β - Adrenergic Receptor Blockers

111. Patients treated with beta blockers provide a further 35% reduction in mortality on top of the benefit provided by ACEIs alone The titration of beta blockers should proceed no more rapidly than at 2-week intervals It is important to optimize the dose of diuretic before starting therapy with beta blockers 112

112. BB BB should ideally be restricted to—agents tested and proven to improve survival in clinical trials Only 3 BB Carvedilol , Bisoprolol , and Metoprolol succinate 113

113. Bradycardia Exacerbate heart block. Beta blockers are not recommended for patients who have asthma with active bronchospasm Adverse Effects

114. Aldosterone Antagonists/Mineralocorticoid Receptor Antagonists (MRAs) Aldosterone antagonism is associated with a reduction in mortality in all stages of symptomatic NYHA class II to IV HFrEF Spiranolactone : nonselective antagonist Eplerenone : selective antagonist 115

115. Mineralocorticoid receptor antagonist (MCRA, MRA) Recommended in symptomatic pts with LVEF ≤ 35%, to reduce morbidity and mortality, unless Contra indicated (Cr ≥ 2.5 mg/dL in Male or ≥ 2.0 mg/ dL in female or eGFR <30 mL/min/1.73m2), and/or K+ ≥ 5m Eq/L Recommended to reduce morbidity and mortality following AMI in pts who have LVEF ≤ 40% who develop symptoms of HF or who have a Hx of DM, unless CI

116. Adverse effects Hyperkalemia Worsening of renal function Gynacomastia : Spiranolactone Close follow up of renal function and serum electrolyte 117

117. ARNI: Angiotensin receptor– Neprilysin inhibitor Classic Drug: Sacubitril -Valsartan Recommended as a replacement for an ACE-I to further reduce the risk of HF hospitalization and death in ambulatory patient with HFrEF Indication: Currently, ARNI is considered as a first-line therapy instead of an ACE-I/ARBs. 118

118. I f -channel inhibitor Classic Drug: Ivabradine Reduce the risk of HF hospitalization or cardiovascular death Indication Symptomatic patients with LVEF ≤35%, In sinus rhythm and a resting heart rate ≥70 bpm Who are unable to tolerate or have contra-indications for a beta-blocker. Patients should also receive an ACE-I (or ARB) and an MRA (or ARB) 119

119. Recommended as part of standard therapy in addition to beta blockers and ACE inhibitors for African Americans with NYHA class II–IV HF Effect due to the beneficial effects of NO on the peripheral circulation Reduce the risk of HF hospitalization and death . Hydralazine and Isosorbide dinitrate

120. Digoxin No Mortality Benefit/ improvement in Quality of Life It Reduces heart failure hospitalizations Indication: Symptomatic despite optimal neurohormonal blockade and adequate volume control Rate control in patient with HF and Atrial fibrillation [ BB>>Digoxin] 121

121. Device Therapy CARDIAC RESYNCHRONIZATION THERAPY [CRT] Indication: Symptomatic patients with HF in sinus rhythm With a QRS duration>149ms and LBBB QRS morphology and With LVEF ≤35% despite OMT in order to improve symptoms and reduce morbidity and mortality . 122

122. Benefit: Improved exercise capacity, Reduction in symptoms, and Evidence of reverse remodeling 123

123. Sudden Cardiac Death Prevention In Heart Failure Implantable Cardioverter - Defibrillator (ICD) Indication NYHA class II or III HF with LVEF≤35% irrespective of etiology Myocardial infarction and optimal medical therapy with residual LVEF ≤30% (even when asymptomatic) Mortality Benefit 124

124. Management of comorbidities Atrial arrhythmia[ Atrial Fibrillation] Carries worse prognosis Rate control, if not ---rhythm control strategy Rhythm control by : pharmacotherapy, percutaneous or surgical technique Recommended anti arrhythmic drugs Amiodarone and dofetilide Others are proarrhythmic 125

125. Anemia in HF: Rx Treat with Intravenous iron using either iron sucrose or carboxymaltose (FCM) Resulted in improvement in functional capacity , symptoms, and QOL(Quality Of Life) Oral iron supplementation does not appear to be effective in treating iron deficiency in HF 126

126. Diabetes in HF Sodium–glucose cotransporter 2 (SGLT2) Empagloflozin / Dapagloflozin Decrease in cardiovascular mortality as well as hospitalizations for heart failure This drug class may represent a viable therapeutic avenue in diabetics with heart failure Thiazolidinediones : worsens heart failure 127

127. Prognosis: Poor prognosis Clinical Symptomatic HF Carries poor prognosis [NYHA Class IV>III>II>I] Cardiac Cachexia Cheyne -stoke respiration SBP <115mmHg Serum creatinine >2.75mg/dl BUN >43mg/dl Increased troponin level 128

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