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Cardiology Review: Heart Failure and Valve Disease March 17, 2016 Dr. Sharon Chih Assistant Professor Medicine University of Ottawa Heart Institute Outline • Heart Failure – Causes – Clinical features – Management • Approach to valve disease – Mitral stenosis and regurgitation – Aortic stenosis and regurgitation Definition: Heart Failure • Condition where the heart cannot pump an adequate supply of blood at normal filling pressures to meet the metabolic needs of the body • Clinically – Reduced cardiac output – Congestion – Impaired quality of life – Reduced life expectancy Distinguish from cardiomyopathy • Pathologic abnormality of myocardium resulting in abnormal myocardial structure - cardiac dilatation and hypertrophy • All patients with cardiomyopathy do not have HF Classification of Heart Failure Causes • Multiple ways to consider classification: – Etiologic – Systolic vs. Diastolic – Right vs. Left General Causes of HF 1. 2. 3. 4. Ischemic heart disease Valvular disease Hypertension Dilated cardiomyopathy • • • • • • 5. 6. Idiopathic Myocarditis / pericarditis Arrhythmias Thyroid disease Pregnancy Toxins (alcohol, chemotherapy) Hypertrophic cardiomyopathy Restrictive cardiomyopathy • • • Amyloid Sarcoidosis hemochromatosis Mechanisms and Causes of HF Impaired Contractility Myocardial infarction Transient ischemia Chronic volume overload MR/AR Dilated cardiomyopathy Increased Afterload AS Uncontrolled HTN Systolic Dysfunction Left Sided HF Diastolic Dysfunction Obstruction of LV filling MS Pericardial constriction or tamponade Impaired ventricular relaxation LVH Hypertrophic cardiomyopathy Restrictive cardiomyopathy Transient ischemia Mechanisms and Causes of HF Cardiac Causes Left sided HF Pulmonary stenosis Right ventricular infarction Right Sided HF Pulmonary Vascular Disease Pulmonary embolism Pulmonary HTN Right ventricular infarction Parenchymal pulmonary disease COPD Interstitial lung disease Chronic infections Adult respiratory distress syndrome Diagnosis of HF • • • • Constellation of symptoms and signs CXR Echocardiogram Serum BNP testing Symptoms and Signs of HF Increased filling pressures Congestion Poor Cardiac Output Poor Perfusion Assessing Perfusion • Symptoms – Fatigue – Confusion – Dyspnea • Signs – – – – – – Hypotension Tachycardia Cool extremities Altered mental status Rising creatinine Liver enzyme abnormalities Congestion • Left-Sided – Symptoms • Dyspnea • Orthopnea • Paroxysmal nocturnal dyspnea – 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 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) 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 • 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) 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 doughnutshaped 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 cuffing Alveolar edema Kerley B The Role of the Echo in HF Diagnosis • Essential screening tool for all patients suspected with HF – – – – – Systolic and diastolic performance Regional wall motion abnormalities Valvular disease Pericardial disease Pulmonary hypertension Natriuretic Peptides Schlendorf et al. Curr Treat Options Cardiovasc Med Natriuretic Peptides - Diagnosis SO YOUR PATIENT HAS HEART FAILURE… WHAT NOW? The clinical course of heart failure with associated types and intensities of available therapies Larry A. Allen et al. Circulation. 2012;125:1928-1952 Copyright © American Heart Association, Inc. All rights reserved. Functional Classification ACC/AHA STAGES OF HEART FAILURE STAGE A •High risk for developing HF (diabetes, CKD, HTN) •No structural disorder of the heart STAGE B •Structural disorder of the heart (e.g.. Previous MI) •Not yet developed symptoms of HF STAGE C •Past or current symptoms of HF •Symptoms associated with underlying structural heart disease STAGE D •End stage disease •Requires specialized treatment strategies NYHA FUNCTIONAL CLASS CLASS I •No symptoms and no limitations in physical activity •No shortness of breath when walking, climbing stairs etc. CLASS II •Mild symptoms and slight limitation during ordinary physical activity CLASS III •Marked limitation in activity due to symptoms (fatigue, shortness of breath) with less than ordinary activity (e.g.. Short distances or ADL’s) INCREASING SEVERITY OF HEART FAILURE CLASS IV •Severe limitation, may experience symptoms at rest Goals of Therapy 1. 2. 3. 4. 5. Identify and Treat the Underlying Cause Eliminate the acute precipitant Manage HF symptoms Slow progression of LV disease Improve long-term survival 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 Progression of underlying disease Heart Failure Management Guidelines • CCS 2014 focused update: CJC 2015;31:3-16 • ACCF/AHA 2013: JACC 2013;62:e147-239 • ESC 2012: EHJ 2012;33:1787-1847 • ACCF/AHA/HRS focused device update: JACC 2012;60:1297-1313 • HFSA 2010: Journal of Cardiac Failure 2010;16:475-539 • NHF/CSANZ 2011 update: MJA 2011;194:405-9 Overview of Chronic HF Management 1. Nonpharmacologic 2. Pharmacologic 3. Surgery 4. Devices 5. Heart transplantation Nonpharmacologic 1. 2. 3. 4. 5. 6. 7. 8. Physical exercise Diet • Na restriction <1500 mg/d • Fluid restriction: 1-1.5 L/d • Low saturated fat, high fibre Smoking cessation Abstain from alcohol Vaccinations • Pneumococcal, influenza Avoid medications that may exacerbate HF • NSAIDS, thiazolidinediones, non-dihydropyridine Ca channel blockers, tyrosine kinase inhibitors, clozapine, TCA Screen for depression/anxiety Education • Indications/adverse effects of medications • Symptoms to monitor • Management of fluid retention • Regular contact with GP/Cardiologist Pharmacologic 1. Prognostic • ACEI/ARB • Beta-blockers • Mineralcorticoid receptor antagonists • Hydralazine/Nitrates • ARNI 2. Reduce hospitalisations/Improve symptoms • Ivabradine • Digoxin 3. Other • Iron • Antithrombotics BB ACE I sprionolactone diuretics ACEI/ARB/Nitrates+Hydralazine • ACEI for symptomatic and asymptomatic patients EF ≤40% Class I Recommendation, Level of Evidence A • ACEI intolerance • Cough, angioedema: ARBs Class I Recommendation, Level of Evidence A • Renal failure/↑K+: hydralazine/nitrate Class IIb Recommendation, Evidence C • Hydralazine/isosorbide dinitrate recommended in addition to BB/ACEI for symptomatic HF • African Americans: Class I Recommendation, Level of Evidence B • Non African Americans: Class IIa Recommendation, Level of Evidence B A-HEFT Taylor et al. NEJM, 2004 •N = 1050 AA, NYHA III-IV •ACEI + BB •Hydralazine 37.5-75 mg tds ISDN 20-40 mg tds •RRR 43% (NNT = 25) SOLVD Exner et al. NEJM, 2001 •Enalapril vs. placebo •Hospitalisations higher in blacks •Significant benefit with enalapril in whites but not blacks Beta-Blockers • BB for symptomatic and asymptomatic patients EF ≤40% Class I Recommendation, Level of Evidence A • Use BB shown to be effective in trials • Carvedilol 3.125 – 25 mg bd • Metoprolol succinate 12.5 – 200 mg od • Bisoprolol 1.25 – 10 mg od • Nebivolol 1.25 – 10 mg od • DO NOT use when patient is WET or in SHOCK • Wait till acute episode has resolved then initiate • Start low and go slow - titrate q 2 weeks • Try NOT to stop…unless WET or in SHOCK • Reduce dosage if necessary. Avoid abrupt discontinuation • Reinstate gradually before discharge Mineralcorticoid Receptor Antagonists TRIAL RALES Pitt et al. NEJM 1999;341:709 EPHESUS Pitt et al. NEJM 2003;348:1309 EMPHASIS – HF Zannad et al. NEJM 2011;364:11 MRA N Spironolactone 1663 25-50 mg od NYHA LVEF RRR Mortality NNT III-IV ≤35% 30% 9 Eplerenone 25-50 mg od 6632 2wk post MI + HF or DM ≤40% 15% 44 Eplerenone 25–50 mg od 2737 ≤30%* 24% 33 II *<35% if QRS >130 ms) • MRA for NYHA II-IV patients EF ≤35% despite ACEI/BB Class I Recommendation, Level of Evidence A • Not recommended if Creatinine <220, K < 5.0 mmol/L • Monitor creatinine and potassium 1 wk, 4 wk, 3 mnths What does the MCC want? • How will you make the diagnosis? – Keep it on your differential of acute/chronic dyspnea – Look for the signs and symptoms of heart failure – Recognize the underlying causes of HF – Echo/ chest xray / labs What does the MCC Want? • How will you treat? – Acutely: diuretics, identify and remove precipitant – Chronically: beta blocker, ACEI etc. • When to refer to a specialist? – Persistent or severe symptoms – Poor treatment response – Uncertain diagnosis Valvular Disease Heart Sounds: A Review Heart Sounds Mitral Stenosis • Restriction and narrowing of mitral valve • Impairment of left ventricular filling 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 MS - Pathophysiology • LA pressure increases – Increased pulmonary pressures • LA dilatation – Atrial fibrillation • Stagnation of blood in LA – thromboembolism 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 MS - Examination 1. Loud S1 – From calcification of mitral valve 2. Opening snap – Sudden tensing of chordae and stenotic leaflets on valve opening 3. Diastolic murmur – Low frequency – Severity relates to duration MS - Diagnosis • ECG – LAE, RVH – Atrial fibrillation • CXR – LAE, pulmonary vascular redistribution – Prominent pulmonary arteries • Echo – Thickened MV – LAE MS - Treatment • Percutaneous balloon valvuloplasty – Minimally calcified – No significant MR – No thrombus • Surgical repair • Diuretics for vascular congestion • Decrease HR if AF • Anticoagulation Mitral Regurgitation • Structural abnormality of mitral valve apparatus resulting in leaking of blood back to LA during systole MR - Causes MITRAL ANNULUS •Annular calcification (MAC) LEAFLETS •Rheumatic disease •Endocarditis •Myxomatous disease (MVP) CHORDAE TENDINAE •Rupture •endocarditis PAPILLARY MUSCLE •Dysfunction (MI or ischemia) LEFT VENTRICLE •Cavity dilatation MR - Pathophysiology • Portion of the LV stroke volume ejected into LA – Forward CO is less than total LV CO • • • • ↑ LA volume ↓ forward CO ↑ Volume in LV subsequently Severity of MR depends on: – – – – SVR opposing LV blood flow LA compliance Duration of regurgitation Size of orifice during regurgitation MR – Clinical Presentation • Chronic – Fatigue – If LV contractile dysfunction – heart failure • Acute – Pulmonary edema – hypotension MR - Examination 1. Murmur – Pansystolic murmur heard at apex 2. S3 – Reflects increased volume returning to LV in early diastole 3. LV displacement – If LV enlargement present MR - Diagnosis • CXR – Pulmonary edema if acute – Left atrial and ventricular dilatation • Echo – Identifies structural cause of MR – LV /LA size and function MR - Treatment • Acute MR – Reduce the resistance to forward flow (Vasodilators) – Relieve pulmonary edema (Diuretics) • Chronic – Operative repair once symptoms develop or LV starts to dilate Aortic Stenosis • Thickened and restricted opening of aortic valve • Obstruction to LV outflow Normal Tricuspid Aortic Valve Aortic Stenosis Normal Tricuspid Aortic Valve Senile Degenerative / Calcific Aortic Valve Aortic Stenosis Normal Tricuspid Aortic Valve Congenital Bicuspid Aortic Valve Aortic Stenosis Normal Tricuspid Aortic Valve Rheumatic Aortic Valve Aortic Stenosis Causes: • Valvular – Congenital, acquired calcific, rheumatic • Subvalvular – Hypertrophic cardiomyopathy • Supravalvular – Coarctation, congenital AS - Pathophysiology • Blood flow across the AV is impeded • Once AVA ↓ 50%: – Significant LV pressure needed to drive blood into aorta – Results in LV hypertrophy – ↓ LV compliance (Stiffer LV) => Increased end diastolic pressure 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 Symptom Median survival Angina 5 yrs Syncope 3 years HF 2 years AS -Exam 1. Carotid pulse – Weakend (parvus) and delayed (tardus) due to LV obstruction 2. Murmur – Late peaking systolic ejection murmur 3. S4 – Atrial contraction into stiff LV 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 Aortic Regurgitation AR - Causes • Abnormalities of valve leaflets – Congenital (bicuspid valves) – Endocarditis – Rheumatic • Dilatation of aortic root – Aortic aneursym – Aortic dissection – Syphilis 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 AR – Clinical Manifestations • SOB on exertion • Fatigue • Decreased exercise tolerance AR - Examination • Murmur – Blowing diastolic along LSB • Widened pulse pressure Name Description Bisferins Double impulse Corrigans Marked distention and collapse deMusset Head bobbing Duroziez To and fro murmur Hill Greater popliteal SBP Muller Uvula pulsations Quincke Nail bed pulsation Traube Pistol shot femoral art 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 What does the MCC want? • What is your ddx of a patient with a systolic murmur? – Systolic ejection: aortic stenosis (pulmonary stenosis) – Pansystolic: mitral regurgitation or tricuspid regurgitation (VSD) What does the MCC Want? • How do I know if it is pathologic? – Severity (loud, new) – Other signs of heart dysfunction – Concomitant HF, arrhythmia, ischemia etc. • What do I do about it? – Echo, ECG, labs – Refer to specialist – Treat HF if an issue – Endocarditis prophylaxis What does the MCC Want? • What is the ddx of a diastolic murmur? – Aortic regurgitation – Mitral stenosis – (tricuspid stenosis) • How do I know if it is pathologic? – Chances are it is • What do I do about it? – Echo, chest xray, labs – Treat HF – refer 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 or LV dysfunction