Cardiology Review: Heart Failure and Valve Disease March 30, 2009

1. Cardiology Review:Heart Failure and Valve DiseaseMarch 30, 2009 Dr. Lisa Mielniczuk Assistant Professor Medicine University of Ottawa Heart Institute

2. Outline Heart Failure Causes Symptoms Treatments Approach to valve disease Aortic stenosis and regurgitation Mitral stenosis and regurgitation

4. HF Prevalence in Canada -HF is a growing problem across North America, including Canada � the overall prevalence of HF is estimated at 1%, but clearly regional variation exists -highest prevalences in regions where CAD also high � southern ONT and Quebec, new brunswick and manitoba. -HF is a growing problem across North America, including Canada � the overall prevalence of HF is estimated at 1%, but clearly regional variation exists -highest prevalences in regions where CAD also high � southern ONT and Quebec, new brunswick and manitoba.

5. Majority of HF Patients Treated by GPs/FPs -fanily doctors take a leading role in the care of HF � across Canada the majority of patients admitted with HF are looked after by GP (data from CIHI from 99-2000 demonstrating MRP in hospital. Younger patients, men and those living in urban areas are more likely to be cared for by specialist. -fanily doctors take a leading role in the care of HF � across Canada the majority of patients admitted with HF are looked after by GP (data from CIHI from 99-2000 demonstrating MRP in hospital. Younger patients, men and those living in urban areas are more likely to be cared for by specialist.

6. Why Heart Failure?

7. Definition Condition where the heart cannot pump an adequate supply of blood at normal filling pressures to meet the metabolic needs of the body Clinically Ventricular dysfunction Reduced exercise capacity Impaired quality of life Shortened life expectancy

8. Cardiomyopathy Characterized by ventricular Dilatation Hypertrophy Frank Starling: CO = SV x HR Laplace: Tension = Press x rad/ 2 x thick -indpt of the cause of the damage there are several responses to injury for the heart � the most common is dilatation of a chamber and hypertrophy. (fibrosis can occur � but more specifically in myocardial infarcts) -hypertrophy � refers to increase muscle cell mass to to cellular hypertrohpy � implies that the weight of the heart is increased � usually reflects an increased afterload or preload -dilatation � refers to increase in size of the chamber � due to increased pre load or volume overload-indpt of the cause of the damage there are several responses to injury for the heart � the most common is dilatation of a chamber and hypertrophy. (fibrosis can occur � but more specifically in myocardial infarcts) -hypertrophy � refers to increase muscle cell mass to to cellular hypertrohpy � implies that the weight of the heart is increased � usually reflects an increased afterload or preload -dilatation � refers to increase in size of the chamber � due to increased pre load or volume overload

9. -enlargement of all 4 chambers, heart assumes a more spherical shape-enlargement of all 4 chambers, heart assumes a more spherical shape

11. Gross Pathologic Findings Enlargement of all 4 chambers Normal valves with regurgitation Enlargement and distortion of the subvalvular apparatus Intracavitary thrombi

12. Heart Failure -in a normal heart, cardiac output increases as a function of preload. Decreased LV contractility is characertized by a heart that is shifted downward. Point a is normal person at rest. Point B is the same person after developing systolic dysfunction. , stroke volume has fallen (decreased LV emptying) and the LVEDV has increased. This increase in EDV is compensatory (on the ascending part of the curve) because it will increase SV for the next beat. BUT further augmentation in LV filling in the heart puts patients on C � where SV is not increased but symptoms of pulmonary congestion develop-in a normal heart, cardiac output increases as a function of preload. Decreased LV contractility is characertized by a heart that is shifted downward. Point a is normal person at rest. Point B is the same person after developing systolic dysfunction. , stroke volume has fallen (decreased LV emptying) and the LVEDV has increased. This increase in EDV is compensatory (on the ascending part of the curve) because it will increase SV for the next beat. BUT further augmentation in LV filling in the heart puts patients on C � where SV is not increased but symptoms of pulmonary congestion develop

13. Classification of Cardiomyopathy Multiple ways to consider classification: Etiologic Systolic vs. Diastolic Right vs. Left Pathologic

14. General Causes of HF Coronary artery disease Myocardial infarction Valve disease Idiopathic cardiomyopathy Hypertension Myocarditis / pericarditis Arrhythmias Thyroid disease Pregnancy Toxins (alchohol, chemotherapy)

15. Dilated Cardiomyopathy CAD is the most common cause of systolic dysfunction What are the other non-ischemic causes of a dilated cardiomyopathy? Idiopathic (50%) Familial Substance abuse Myocarditis Infiltrative disease Peripartum HIV Chemotherapy Electrolyte imbalance Nutritional: thiamine,scurvy

16. Mechanisms and Causes of HF

17. Mechanisms and Causes of HF

19. Functional Classification The ACC defined 4 stages of heart failure in the last consensus guidelines. (ref:ACC/AHA 2005 Chronic Heart Failure Guideline Update, Journal of the American College of Caridiol, 2005;46:1116-1143 ) This highlights the point that we should think of HF in those who are at risk (stage A and B) even before they have developed symptomatic HF. The NYHA functional classification is a well-accepted definition of exercise capacity in the setting of HF. The ACC defined 4 stages of heart failure in the last consensus guidelines. (ref:ACC/AHA 2005 Chronic Heart Failure Guideline Update, Journal of the American College of Caridiol, 2005;46:1116-1143 ) This highlights the point that we should think of HF in those who are at risk (stage A and B) even before they have developed symptomatic HF. The NYHA functional classification is a well-accepted definition of exercise capacity in the setting of HF.

20. Stages of Heart Failure

21. Diagnosis of HF Constellation of symptoms and signs CXR Alternative Methods Invasive hemodynamic studies Echocardiogram Serum BNP testing

22. Symptoms and Signs of HF

23. Evaluating the JVP Consensus: <2 cm above the sternal angle considred normal and >4cm ASA is abnormal http://cal.fmc.flinders.edu.au/gemp/ClinicalSkills/clinskil/year1/cardio/cardio04.htm 

24. Congestion Left-Sided Symptoms Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Fatigue Signs S3 gallop Displaced apex MR Pulmonary rales Loud P2 Right-Sided Symptoms Peripheral edema Abdominal bloating Nausea Anorexia Signs Elevated JVP Hepatomegaly Ascites Edema

25. Assessing Perfusion Symptoms Fatigue Confusion Dyspnea sweating Signs Hypotension Tachycardia Cool extremities Altered mental status Rising creatinine Liver enzyme abnormalities

26. Pulmonary Edema General Considerations Increase in the fluid in the lung Generally, divided into cardiogenic and non-cardiogenic categories. Pathophysiology Fluid first accumulates in and around the capillaries in the interlobular septa (typically at a wedge pressure of about 15 mm Hg) Further accumulation occurs in the interstitial tissues of the lungs Finally, with increasing fluid, the alveoli fill with edema fluid (typically wedge pressure is 25 mm Hg or more)

27. Cardiogenic vs. Noncardiogenic pulmonary edema Cardiogenic pulmonary edema Heart failure Coronary artery disease with left ventricular failure. Cardiac arrhythmias Fluid overload -- for example, kidney failure. Cardiomyopathy Obstructing valvular lesions -- for example Myocarditis and infectious endocarditis Non-cardiogenic pulmonary edema -- due to changes in capillary permeability Smoke inhalation. Head trauma Overwhelming sepsis. Hypovolemia shock Acute lung re-expansion High altitude pulmonary edema Disseminated intravascular coagulopathy (DIC) Near-drowning Overwhelming aspiration Acute Respiratory Distress Syndrome (ARDS) Re-expansion By drainage of a large pleural effusion with thoracentesis Of the lung collapsed by a large pneumothoraxRe-expansion By drainage of a large pleural effusion with thoracentesis Of the lung collapsed by a large pneumothorax

28. CXR Findings of Pulmonary Edema cardiogenic pulmonary edema Kerley B lines (septal lines) Seen at the lung bases, usually no more than 1 mm thick and 1 cm long, perpendicular to the pleural surface Pleural effusions Usually bilateral, frequently the right side being larger than the left If unilateral, more often on the right Fluid in the fissures Thickening of the major or minor fissure Peribronchial cuffing Visualization of small doughnut-shaped rings representing fluid in thickened bronchial walls Non-cardiogenic pulmonary edema Bilateral, peripheral air space disease with air bronchograms or central bat-wing pattern Kerley B lines and pleural effusions are uncommon Typically occurs 48 hours or more after the initial insult Stabilizes at around five days and may take weeks to completely clear On CT Gravity-dependent consolidation or ground glass opacification Air bronchograms are common Collectively, the above four findings comprise pulmonary interstitial edema The heart may or may not be enlarged When the fluid� enters the alveoli themselves, the airspace disease is typically diffuse, and there are no air bronchograms \ -cuffing � is fluid in the bronchial wall � looks like donuts Correlates with LAP � Normal (5-10) Cephalizatioin 10-15, kerly b 15-20, pulmonary interstital edema 20-25, alveloar edema >25 Collectively, the above four findings comprise pulmonary interstitial edema The heart may or may not be enlarged When the fluid� enters the alveoli themselves, the airspace disease is typically diffuse, and there are no air bronchograms \ -cuffing � is fluid in the bronchial wall � looks like donuts Correlates with LAP � Normal (5-10) Cephalizatioin 10-15, kerly b 15-20, pulmonary interstital edema 20-25, alveloar edema >25

30. Goals of Therapy Identify and Treat the Underlying Cause Eliminate the acute precipitant Manage HF symptoms Modulate the neurohormonal response Improve long-term survival -treating underlying cause may be difficult � can require surgical valve or coronary repair, treatement HTN, cessation of alcohol -modulating the neurohormonal response � to help prevent adverse ventricular remodeling in oder to slow progression of LV dysfunction-treating underlying cause may be difficult � can require surgical valve or coronary repair, treatement HTN, cessation of alcohol -modulating the neurohormonal response � to help prevent adverse ventricular remodeling in oder to slow progression of LV dysfunction

31. Precipitants of HF Increased metabolic demands Fever, anemia, infection, tachycardia, hyperthyroidism, pregnancy Increased circulating volume Excessive salt or fluid in diet Renal failure Increased afterload Hypertension PE Impaired contractility Negative inotropes Ischemia Failure to take medications

32. Pharmacotherapy

33. Management Strategy

34. Beta Blockers The MERIT-HF trial randomized 3991 patients with NYHA class II to IV heart failure who were treated with digoxin, angiotensin converting enzyme inhibitors, and digoxin to metoprolol CR/XL or placebo. Kaplan-Meier curves show a significant reduction in total mortality at 12 months with metoprolol (7.2 versus 11 percent for placebo, p = 0.006). Data from The MERIT-HF Study Group, Lancet 1999; 353:2001 In the MERIT-HF trial of 3991 patients metoprolol CR/XL reduced the number of patients requiring hospitalization for any reason by 18 percent compared to placebo (p = 0.004), the number admitted for a cardiovascular cause by 25 percent (p<0.001), and the number admitted for worsening heart failure by 35 percent (p<0.001) (panel A). There was an equivalent reduction in the number of hospital days (panel B). Data from Hjalmarson, A, Goldstein, S, Fagerberg, B, et al. JAMA 2000; 283:1245. The MERIT-HF trial randomized 3991 patients with NYHA class II to IV heart failure who were treated with digoxin, angiotensin converting enzyme inhibitors, and digoxin to metoprolol CR/XL or placebo. Kaplan-Meier curves show a significant reduction in total mortality at 12 months with metoprolol (7.2 versus 11 percent for placebo, p = 0.006). Data from The MERIT-HF Study Group, Lancet 1999; 353:2001 In the MERIT-HF trial of 3991 patients metoprolol CR/XL reduced the number of patients requiring hospitalization for any reason by 18 percent compared to placebo (p = 0.004), the number admitted for a cardiovascular cause by 25 percent (p<0.001), and the number admitted for worsening heart failure by 35 percent (p<0.001) (panel A). There was an equivalent reduction in the number of hospital days (panel B). Data from Hjalmarson, A, Goldstein, S, Fagerberg, B, et al. JAMA 2000; 283:1245.

35. Beta Blockers and Functional Class In the SOLVD-prevention trial of 4223 patients with mostly asymptomatic left ventricular (LV) dysfunction, those receiving a beta blocker and enalapril had a significantly lower all cause mortality compared to those receiving beta blocker or enalapril alone (relative risk 0.7); this was due to a significant reduction in death from arrhythmia or pump failure. Data from Exner, DV, Dries, DL, Waclawiw, MA, et al. J Am Coll Cardiol 1999; 33:916. Kaplan-Meier analysis of survival in patients with chronic heart failure (HF) who were maintained on digoxin, diuretics, and an angiotensin converting enzyme inhibitor and then treated with carvedilol or placebo. Therapy with carvedilol was associated with a significant improvement in survival (p<0.001). Data from Packer, M, Bristow, MR, Cohn, JN, et al for the US Carvedilol Heart Failure Study Group, N Engl J Med 1996; 334:1349. In the COPERNICUS trial of 2289 patients with class IV heart failure and a left ventricular ejection fraction carvedilol significantly reduced the risk of death by 38 percent compared to placebo (P = 0.0001). The drug also reduced the combined end point of death and hospitalization by 24 percent (P< 0.001). Data from Packer, M, Coats, AJ, Fowler, MB, et al. N Engl J Med 2001; 344:1651. In the SOLVD-prevention trial of 4223 patients with mostly asymptomatic left ventricular (LV) dysfunction, those receiving a beta blocker and enalapril had a significantly lower all cause mortality compared to those receiving beta blocker or enalapril alone (relative risk 0.7); this was due to a significant reduction in death from arrhythmia or pump failure. Data from Exner, DV, Dries, DL, Waclawiw, MA, et al. J Am Coll Cardiol 1999; 33:916. Kaplan-Meier analysis of survival in patients with chronic heart failure (HF) who were maintained on digoxin, diuretics, and an angiotensin converting enzyme inhibitor and then treated with carvedilol or placebo. Therapy with carvedilol was associated with a significant improvement in survival (p<0.001). Data from Packer, M, Bristow, MR, Cohn, JN, et al for the US Carvedilol Heart Failure Study Group, N Engl J Med 1996; 334:1349. In the COPERNICUS trial of 2289 patients with class IV heart failure and a left ventricular ejection fraction carvedilol significantly reduced the risk of death by 38 percent compared to placebo (P = 0.0001). The drug also reduced the combined end point of death and hospitalization by 24 percent (P< 0.001). Data from Packer, M, Coats, AJ, Fowler, MB, et al. N Engl J Med 2001; 344:1651.

36. ACE Inhibitors and Survival Decreased mortality in patients with advanced NYHA class III or IV heart failure after treatment with enalapril compared to placebo (p = 0.003). Data -from The CONSENSUS Trial Study Group, N Engl J Med 1987; 316:1429. -consensus one of the first RCT for ACE I � very sick population � look at placebo mortality rateDecreased mortality in patients with advanced NYHA class III or IV heart failure after treatment with enalapril compared to placebo (p = 0.003). Data -from The CONSENSUS Trial Study Group, N Engl J Med 1987; 316:1429. -consensus one of the first RCT for ACE I � very sick population � look at placebo mortality rate

37. ACE Inhibitors and Heart Failure A meta-analysis of five trials involving 12,763 patients with left ventricular dysfunction who were followed for 35 months found that therapy with an angiotensin converting enzyme (ACE) inhibitor significantly reduced mortality (23 versus 26.8 percent, odds ratio 0.80, p<0.0001). There is continuing divergence in the mortality curves during the follow-up that exceeds four years. Data from Flather, MD, Yusuf, S, Kober, L, et al. Lancet 2000; 355:1575 - -curves separate beyond one yearA meta-analysis of five trials involving 12,763 patients with left ventricular dysfunction who were followed for 35 months found that therapy with an angiotensin converting enzyme (ACE) inhibitor significantly reduced mortality (23 versus 26.8 percent, odds ratio 0.80, p<0.0001). There is continuing divergence in the mortality curves during the follow-up that exceeds four years. Data from Flather, MD, Yusuf, S, Kober, L, et al. Lancet 2000; 355:1575 - -curves separate beyond one year

39. Valvular Disease

40. Mitral Stenosis Restriction and narrowing of mitral valve Impairment of left ventricular filling

41. Mitral Stenosis - Causes Rheumatic Fever (>90% cases) 50% patients will have known history Average 20 years prior to clinical symptoms Congenital stenosis of MV Extensive calcification endocarditis

42. MS - Pathophysiology LA pressure increases Increased pulmonary pressures LA dilatation Atrial fibrillation Stagnation of blood in LA thromboembolism

43. MS - Clinical Presentation Natural history variable 10 year survival (symptoms) 50-60% Early onset Dyspnea and reduced exercise capacity Advanced SOB at rest Pulmonary congestion (orthopnea, PND etc) Pulmonary HTN (RHF) Hoarseness from laryngeal nerve compression -natural history depends on the extent of symptoms, mean survival 3 years once pulmonary HTN develops -the more severe the MS the more symptoms � related to high atrial and pulmonary venous pressures -early on � once exercise and shorten DFP � more symptoms-natural history depends on the extent of symptoms, mean survival 3 years once pulmonary HTN develops -the more severe the MS the more symptoms � related to high atrial and pulmonary venous pressures -early on � once exercise and shorten DFP � more symptoms

44. MS - Examination Loud S1 From high pressure gradient from LA and LV Opening snap Sudden tensing of chordae and stenotic leaflets on valve opening Diastolic murmur Low frequency Severity relates to duration --

45. MS - Diagnosis ECG LAE, RVH Atrial fibrillation CXR LAE, pulmonary vascular redistribution Prominent pulmonary arteries Echo Thickened MV LAE

46. MS - Treatment Percutaneous balloon valvuloplasty Surgical repair Antibiotics at time of risk Diuretics for vascular congestion Decrease HR if AF anticoagulation

47. Mitral Regurgitation Structural abnormality of mitral valve apparatus resulting in leaking of blood back to LA during systole -normal valve function, requires competent MV such that valve is closed in sytole, coordinated and complex action involving multiple components-normal valve function, requires competent MV such that valve is closed in sytole, coordinated and complex action involving multiple components

48. MR - Causes -causes can be considered by anatomic abnormality-causes can be considered by anatomic abnormality

49. MR - Pathophysiology Portion of the LV stroke volume ejected into LA Forward CO is les than total LV CO Elevation of LA volume Reduction of forward CO Volume related stress on LV Severity depends on: Size of orifice during regurge SVR opposing LV blood flow LA compliance Duration of regurgitation

50. MR � Clinical Presentation Chronic Fatigue If LV contractile dysfunction � heart failure Acute Pulmonary edema hypotension

51. MR - Examination Murmur Pansystolic murmur heard at apex S3 Reflects increased volume returning to LV in early diastole LV displacement If LV enlargement present

52. MR - Diagnosis CXR Pulmonary edema if acute Left atrial and ventricular dilatation Calcification of MV Echo Identifies structural cause of MR LV /LA size and function

53. MR - Treatment Acute MR Vasodilators and diuretics Reduce the resistance to forward flow Relieve pulmonary edema Chronic Operative repair once symptoms develop or LV starts to dilate

54. Aortic Stenosis Thickened and restricted opening of aortic valve Obstruction to LV outflow

55. AS - Causes Age related calcification of valve Rheumatic heart disease Congenital bicuspid AV

56. AS - Pathophysiology Blood flow across the AV is impeded Once AVA reduced by 50%: Significant LV pressure needed to drive blood into aorta Results in LV hypertrophy Reduced LV compliance Increased end diastolic pressure

57. AS � Clinical Presentation Angina Imbalance b/w myocardial oxygen supply and demand Syncope Peripheral vasodilation with inability to augment CO with exercise HF Increased LAP from high LVEDP Contractile dysfunction if longstanding pressure overload -demand increases bc increase muscle mass, and wall stres increases bc increased pressure -supply reduced � b/c of increased LVEDP (gradient of coronary flow � ao pressure � LVEDP -demand increases bc increase muscle mass, and wall stres increases bc increased pressure -supply reduced � b/c of increased LVEDP (gradient of coronary flow � ao pressure � LVEDP

58. AS -Exam Murmur Late peaking systolic ejection murmur Carotid pulse Weakend (parvus) and delayed (tardus) due to LV obstruction S4 Atrial contraction into stiff LV -allows estimate of severity-allows estimate of severity

59. AS - Treatment Only effective treatment for severe symptomatic disease is surgical correction What if asymptomatic? 20% of patients will progress over 20 years if mild disease only Endocarditis prophylaxis

60. Aortic Regurgitation

61. AR - Causes Abnormalities of valve leaflets Congenital (bicuspid valves) Endocarditis Rheumatic Dilatation of aortic root Aortic aneursym Aortic dissection syphilis

62. AR - Pathophysiology Severity of AR Size of regurgitant orifice Pressure gradient across valve in diastole Duration of diastole Acute LV noncompliant LVEDP rises quickly � pulmonary edema Chronic Chronic volume/pressure overload Dilates � well compensated

63. AR � Clinical Manifestations SOB on exertion Fatigue Decreased exercise tolerance

64. AR - Examination Murmur Blowing diastolic along LSB Widened pulse pressure

65. AR - Treatment Asymptomatic disease progresses very slowly Surgery if: Symptoms Impaired LV function Death occurs within 4 years after angina or 2 years after HF

67. Summary Slide Heart Failure Understand causes of systolic and diastolic HF Awareness of the presentation of left vs. right HF Know treatment priniciples Valve Disease Identify the most common causes of 4 common valve lesions Remember clinical presentations Surgery treatment of choice any time symptoms present