Download Free Medical Cardiomyopathy PowerPoint Presentation

Cardiomyopathy PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Cardiomyopathy" by Athena Poppas, MD.

This medical PowerPoint presentation talks about Cardiomyopathy. Cardiomyopathy is a term used to describe diseases of the heart muscle, where the heart muscle becomes weakened or enlarged, making it difficult for the heart to pump blood effectively. There are several types of cardiomyopathy, including:

Dilated cardiomyopathy: The most common type, where the heart muscle becomes stretched and thin, making it difficult for the heart to pump blood effectively.

Hypertrophic cardiomyopathy: A genetic condition where the heart muscle becomes abnormally thick, making it difficult for the heart to relax and fill with blood properly.

Restrictive cardiomyopathy: A rare condition where the heart muscle becomes stiff, making it difficult for the heart to fill with blood properly.

Arrhythmogenic right ventricular cardiomyopathy: A rare condition where the heart muscle in the right ventricle becomes replaced by fatty tissue, leading to abnormal heart rhythms.

Symptoms of cardiomyopathy can include shortness of breath, fatigue, chest pain, and palpitations. Treatment options depend on the type and severity of the condition and may include medications, lifestyle changes, or in some cases, surgery or a heart transplant.

Tags : Cardiomyopathy, Dilated cardiomyopathy, Hypertrophic cardiomyopathy, Restrictive cardiomyopathy, Arrhythmogenic right ventricular cardiomyopathy, cardiology, cardiology PowerPoint presentation

Published on : Mar 17, 2023 | Views : 2449 | Downloads : 1

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

CARDIOMYOPATHY Athena Poppas, MD Associate Professor of Medicine, Brown Medical School Director, Echocardiography Laboratory Rhode Island Hospital
Slide 2-

Cardiomyopathies Definition: diseases of heart muscle 1980 WHO: unknown causes Not clinically relevant 1995 WHO: “diseases of the myocardium associated with cardiac dysfunction “ pathophysiology each with multiple etiologies
Slide 3-

Cardiomyopathy WHO Classification anatomy & physiology of the LV Dilated Enlarged Systolic dysfunction Hypertrophic Thickened Diastolic dysfunction Restrictive Diastolic dysfunction Arrhythmogenic RV dysplasia Fibrofatty replacement Unclassified Fibroelastosis LV noncompaction Circ 93:841, 1996
Slide 4-

CM: Specific Etiologies Ischemic Valvular Hypertensive Inflammatory Metabolic Inherited Toxic reactions Peripartum Ischemic: thinned, scarred tissue
Slide 5-

Dilated Cardiomyopathy Dilation and impaired contraction of ventricles: Reduced systolic function with or without heart failure Characterized by myocyte damage Multiple etiologies with similar resultant pathophysiology Majority of cases are idiopathic incidence of idiopathic dilated CM 5-8/100,000 incidence likely higher due to mild, asymptomatic cases 3X more prevalent among males and African-Americans
Slide 6-

DCM: Etiology Ischemic Valvular Hypertensive Familial Idiopathic Inflammatory Infectious Viral – picornovirus, Cox B, CMV, HIV Ricketsial - Lyme Disease Parasitic - Chagas’ Disease, Toxoplasmosis Non-infectious Collagen Vascular Disease (SLE, RA) Peripartum Toxic Alcohol, Anthracyclins (adriamycin), Cocaine Metabolic Endocrine –thyroid dz, pheochromocytoma, DM, acromegaly, Nutritional Thiamine, selenium, carnitine Neuromuscular (Duchene’s Muscular Dystrophy--x-linked)
Slide 7-

Prognosis depends on Etiology 1230 pts. referred for unexplained CM. Felker GM. NEJM 2000;342:1077
Slide 8-

DCM: Infectious Acute viral myocarditis Coxasackie B or echovirus Self-limited infection in young people Mechanism?: Myocyte cell death and fibrosis Immune mediated injury BUT: No change with immunosuppressive drugs
Slide 9-

DCM: toxic Alcoholic cardiomyopathy Chronic use Reversible with abstinence Mechanism?: Myocyte cell death and fibrosis Directly inhibits: mitochondrial oxidative phosphorylation Fatty acid oxidation
Slide 10-

DCM: inherited Familial cardiomyopathy 30% of ‘idiopathic’ Inheritance patterns Autosommal dom/rec, x-linked, mitochondrial Associated phenotypes: Skeletal muscle abn, neurologic, auditory Mechanism: Abnormalities in: Energy production Contractile force generation Specific genes coding for: Myosin, actin, dystophin…
Slide 11-

DCM: Peripartum Diagnostic Criteria 1 mo pre, 5 mos post Echo: LV dysfunction LVEF < 45% LVEDD > 2.7 cm/m2 Epidemiology/Etiology 1:4000 women JAMA 2000;283:1183 Proposed mechanisms: Inflammatory Cytokines: TNFa, IL6, Fas/AP01 JACC 2000 35(3):701.
Slide 12-

PPCM: Prognosis Death from CM: ’91-97 245 CM deaths in US, 0.88/100,000 live births, 70% peripartum Increased risk with: Maternal age AA 6.4x greater Whitehead SJ. ObGyn2003;102:1326. Risk of recurrent pregnancy Retrospective survey : 44 women (16 vs 28) Reduced EF, CHF 44% vs 21%, mortality 0 vs. 19% Elkyam U. NEJM.2001;344:1567. DSE:contractile reserve reduced in patients 7 women: change in Vcfc σES relationship Lampert MB. AJOG.1997.176.189.
Slide 13-

Dilated Cardiomyopathy
Slide 14-

MECHANISMS IN HEART FAILURE Hemodynamic Derangement Clinical Heart Failure Arrhythmia Neurohormones Cytokines Oxidative stress Ischemic injury Myocardial disease Genetics Altered molecular expression Ultrastructural changes Myocyte hypertrophy Myocyte contractile dysfunction Apoptosis Fibroblast proliferation Collagen deposition Ventricular remodeling
Slide 15-

Pathophysiology Initial Compensation for impaired myocyte contractility: Frank-Starling mechanism Neurohumoral activation  intravascular volume Eventual decompensation ventricular remodeling myocyte death/apoptosis valvular regurgitation
Slide 16-

Pathophysiology: Starling Curve
Slide 17-

Pathophysiology: Neurohumoral Adrenergic nervous system Renin-angiotensin-aldosterone axis Vasopressin Natriuretic peptides Endothelin
Slide 18-

Reduced Response to Adrenergic Stimulation
Slide 19-

Renin-Angiotensin-Aldosterone Pathways Angiotensinogen Angiotensin-I Angiotensin-II Renin ACE AT-1 Receptor Chymase Bradykinin degradation ACE-inhibitor Angiotensin receptor blocker Aldosterone Spironolactone
Slide 20-

Angiotensin-II Effects Vasoconstriction Aldosterone production Myocyte hypertrophy Fibroblast proliferation Collagen deposition Apoptosis Pro-thrombotic Pro-oxidant Adrenergic stimulation Endothelial dysfunction
Slide 21-

The Kidney in Heart Failure Reduced renal blood flow Reduced glomerular filtration rate Increased renin production Increased tubular sodium reabsorption Increased free water retention (vasopressin)
Slide 22-

Ventricular Remodeling in Heart Failure
Slide 23-

ppt slide no 23 content not found
Slide 24-

Extracellular Stimuli of Myocyte Hypertrophy
Slide 25-

Clinical Findings Biventricular Congestive Heart Failure -Low forward Cardiac Output -fatigue, lightheadedness, hypotension -Pulmonary Congestion -Dyspnea, -orthopnea, & PND -Systemic Congestion -Edema -Ascites -Weight gain
Slide 26-

Physical Exam Decreased C.O. Tachycardia  BP and pulse pressure cool extremities (vasoconstriction) Pulsus Alternans (end-stage) Pulmonary venous congestion: rales pleural effusions Cardiac: laterally displaced PMI S3 (acutely) mitral regurgitation murmur Systemic congestion  JVD hepatosplenomegaly ascites peripheral edema
Slide 27-

Diagnostic Studies CXR -enlarged cardiac silhouette, vascular redistribution interstitial edema, pleural effusions EKG –normal tachycardia, atrial and ventricular enlargement, LBBB, RBBB, Q-waves Blood Tests (ANA,RF, Fe2+, TFT’s,ferritin,) Echocardiography LV size, wall thickness function valve dz, pressures Cardiac Catheterization hemodynamics LVEF angiography Endomyocardial Biopsy
Slide 28-

Echo in dilated CM
Slide 29-

Influence of EF on Survival in Patients with Heart Failure Vasan RS et al. J Am Coll Cardiol. 1999;33:1948-55
Slide 30-

Class 1: No limitation of physical activity. Ordinary physical activity w/o fatigue, palpitation, or dyspnea. Class 2: Slight limitation of physical activity. Comfortable at rest, but symptoms w/ ordinary physical activity Class 3: Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea. Class 4: Unable to carry out any physical activity without discomfort. Symptoms include cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased. J Cardiac Failure 1999;5:357-382 Criteria for NYHA Functional Classification
Slide 31-

Aim of Treatment Preload reduction Diuretics venodilators Vasodilators ACEI Inotropes Acutely Chronically mortality
Slide 32-

Vasodilator Agents in Heart Failure *Hydralazine and a long-nitrate shown to reduce mortality long-term # Other actions (aside from vasodilation) likely to be important
Slide 33-

Dobutamine and Milrinone Effects
Slide 34-

Electrical and Mechanical Ventricular Dyssynchrony Experimentally induced LBBB has effect on: expression of regional stress kinases calcium-handling proteins. Expression of p38-MAPK (a stress kinase) is elevated in the endocardium of the late-activated region, whereas phospholamban is decreased. Sarcoplasmatic reticulum Ca2+-ATPase is decreased in the region of early activation.
Slide 35-

Deleterious Hemodynamic Effects of LV Dyssynchrony Diminished SV & CO due: Reduced diastolic filling time1 Weakened contractility 2 Protracted MV regurgitation 2 Post systolic regional contraction 3 Atrio-ventricular Inter-V Intra-V Cazeau, et al. PACE 2003; 26[Pt. II]: 137–143 1. Grines CL, Circulation 1989;79: 845-853 2. Xiao HB, Br Heart J 1991;66: 443-447 3. Søgaard P, JACC 2002;40:723–730
Slide 36-

CRT: Cardiac Resynchronization Therapy 1. Improved hemodynamics Increased CO Reduced LV filling pressures Reduced sympathetic activity Increased systolic function w/o MVO2 2. Reverse LV remodeling/architecture Decreased LVES/ED volumes Increased LVEF Circ ’02, JACC ’02, JACC ’02, NEJM’02
Slide 37-

Risk of Sudden Death c/w EF Patients withoutLV Dysfunction (LVEF >35%) Maggioni AP. GISSI-2 Trial Circulation. 1993;87:312-322. Patients withLV Dysfunction (LVEF < 35%) No PVBs1-10 PVBs/h> 10 PVBs/h 0.86 A 0.88 0.90 0.92 0.94 0.96 0.98 1.00 0 30 60 90 120 150 180 Days Survival p log-rank 0.002 0.88 0.90 0.92 0.94 0.96 0.98 1.00 0 30 60 90 120 150 180 Days Survival B p log-rank 0.0001 0.86
Slide 38-

Anti-arrhythmic drugs, ICD placebo and Death
Slide 39-

What are the two characteristic findings in DCM?
Slide 40-

Hypertensive Hypertrophic Cardiomyopathy
Slide 41-

Women and Hypertension Prevalence of HTN in Women from NHANES-III. Burt VL. Hypertension ‘95
Slide 42-

Diastolic Dysfunction 40-50% of pts w/ CHF have nml LVEF Vasan JACC ’99 Grossman Circ ‘00 Prevalence: increases with age higher in women Etiology: HTN & LVH Diagnosis: MV& PV Doppler TDI, Color m-mode
Slide 43-

Zile MR. Circ;105:1387 Echo Doppler Parameters
Slide 44-

Diastolic Dysfunction Kawaguchi M. Circ 2003.107:714
Slide 45-

Zile MR. Circ;105:1387 Isolated Diastolic HF Isolated Systolic HF Systolic & Diastolic HF
Slide 46-

What is the difference between systolic and diastolic LV dysfunction?
Slide 47-

Hypertrophic Cardiomyopathy Left ventricular hypertrophy not due to pressure overload Hypertrpohy is variable in both severity and location: -asymmetric septal hypertrophy -symmetric (non-obstructive) -apical hypertrophy Vigorous systolic function, but impaired diastolic function impaired relaxation of ventricles elevated diastolic pressures prevalence as high as 1/500 in general population mortality in selected populations 4-6% (institutional) probably more favorable (1%)
Slide 48-

Etiology Familial in ~ 55% of cases with autosomal dominant transmission Mutations in one of 4 genes encoding proteins of cardiac sarcomere account for majority of familial cases -MHC cardiac troponin T myosin binding protein C -tropomyosin Remainder are spontaneous mutations.
Slide 49-

Hypertrophic Cardiomyopathy
Slide 50-

Hypertrophic Cardiomyopathy
Slide 51-

Hypertrophic cardiomyopathy
Slide 52-

Apical Hypertrophic Cardiomopathy
Slide 53-

Pathophysiology
Slide 54-

HCM with outflow obstruction Dynamic LVOT obstruction (may not be present at rest) SAM (systolic anterior motion of mitral valve) LVOT Obstruction  LVOT gradient  wall stress  MVO2  ischemia/angina  LVOT gradient:  HR (DFP), preload (LVEDV),  afterload(BP).  LVOT gradient:  BP (Afterload),  LVEDV(preload) Symptoms of dyspnea and angina more related to diastolic dysfunction than to outflow tract obstruction Syncope: LVOT obstruction (failure to increase CO during exercise or after vasodilatory stress) or arrhythmia.
Slide 55-

Physical Exam Bisferiens pulse (“spike and dome”) S4 gallop Crescendo/Descrescendo systolic ejection murmur HOCM vs. Valvular AS Intensity of murmur HOCM AS Valsalva (preload,  afterload)   Squatting ( preload,  afterload)   Standing (preload,  afterload)   Holosystolic apical blowing murmur of mitral regurgitation
Slide 56-

Diagnostic Studies EKG NSR LVH septal Q waves 2D-Echocardiography LVH; septum >1.4x free wall LVOT gradient by Doppler Systolic anterior motion of the mitral valeregurgitation Cardiac Catheterization LVOT gradient and pullback provocative maneuvers Brockenbrough phen HCM-ASH using contrast
Slide 57-

Cardiac Catheterization LV pullback Brockenbrough-Braunwald Sign failure of aortic pulse pressure to rise post PVC Provocative maneuvers: Valsalva amyl nitrate inhalation
Slide 58-

Atrial Fibrillation Acute A. Fib is poorly tolerated -Acute Pulmonary Edema and Shock Chronic a fib - Fatigue, dyspnea and angina Rapid HR - decreased time for diastolic filling and LV relaxation Loss of atrial “Kick” – decreased LV filling - decreased SV and increased outflow tract obstruction Rate slowing with -blockers and Ca2+ channel blockers Digitalis is relatively contra-indicated- positive inotrope DC Cardioversion No p wave P wave present
Slide 59-

Treatment For symptomatic benefit -blockers  mvO2  gradient (exercise) arrythmias Calcium Channel blockers Anti-arrhythmics afib amiodorone Disopyramide AICD for sudden death antibiotic prophylaxis for endocarditis No therapy has been shown to improve mortality
Slide 60-

HCM: Surgical Treatment For severe symptoms with large outflow gradient (>50mmHg) Does not prevent Sudden Cardiac Death Myomyectomy removal of small portion of upper IV septum +/- mitral valve replacement 5 year symptomatic benefit in ~ 70% of patients Dual Camber (DDD pacemaker) pacing decreases LVOT gradient (by~25%) randomized trials have shown little longterm benefit possible favorable morphologic changes ETOH septal ablation AICD to prevent sudden death
Slide 61-

Hypertrophic CM Most common cause of death in young people. The magnitude of left ventricular hypertrophy is directly correlated to the risk of SCD. Young pts with extreme hypertrophy and few or no symptoms are at substantial long-term risk of SCD. . Spirito P. N Engl J Med. 1997;336:775-785. Maron BJ. N Engl J Med. 2000;342:365-373.
Slide 62-

Wall Thickness and Sudden Death in HCM Spirito P. N Engl J Med. 2000;342:1778-1785. Maximum Left-Ventricular-Wall Thickness (mm) Incidence of Sudden Death (per 1,000 person/yr) 0 2.6 7.4 11.0 18.2
Slide 63-

Prognosis Sudden Death 2-4%/year in adults 4-6% in children/adolescents AICD for: survivors of SCD with Vfib episodes of Sustained VT pts with family hx of SCD in young family members High risk mutation (TnT, Arg403Gln) Predictors of adverse prognosis: early age of diagnosis familial form with SCD in 1st degree relative history of syncope ischemia presence of ventricular arrhythmias on Holter (EPS) EPS Amiodorone (low dose) Prophylactic AICD?
Slide 64-

HCM vs Athletes Heart Endurance training: Physiologic increase in LV mass Wall thickness and cavity size Early HCM vs Athlete’s heart DEFINITION: Symmetric, <13mm 947 elite athletes: 16 thickness=13-16mm 15 rowers, EDD=55-63 c/w 728 athletes/22 other NEJM1991;324:295 286 cyclists: 25 thickness 13-15 50% increased EDD w/ 12% reduced LVEF JACC 2004;44:144.
Slide 65-

Why do patients with HCM develop heart failure?
Slide 66-

Restrictive Cardiomyopathy Characterized by: impaired ventricular filling due to an abnormally stiff (rigid) ventricle normal systolic function (early on in disease) intraventricular pressure rises precipitously with small increases in volume Pressure Volume Causes : infiltration of myocardium by abnormal substance fibrosis or scarring of endocardium normal restriction
Slide 67-

Amyloid infiltrative CM
Slide 68-

Amyloidosis Primary Amyloidosis immunoglobulin light chains -- multiple myeloma Secondary Amyloidosis deposition of protein other than immunoglobulin senile familial chronic inflammatory process restriction caused by replacement of normal myocardial contractile elements by infiltrative interstitial deposits
Slide 69-

Amyloidosis
Slide 70-

Amyloid Cardiomyopathy
Slide 71-

Sarcoidosis Restriction Conduction System Disease Ventricular Arrhythmias (Sudden Cardiac Death)
Slide 72-

Endomyocardial Fibrosis Endemic in parts of Africa, India, South and Central America, Asia 15-25% of cardiac deaths in equatorial Africa hypereosinophilic syndrome (Loffler’s endocarditis) Thickening of basal inferior wall endocardial deposition of thrombus apical obliteration mitral regurgitation 80-90% die within 1-2 years
Slide 73-

Pathophysiology of Restriction Elevated systemic and pulmonary venous pressures right and left sided congestion reduced ventricular cavity size with SV and CO
Slide 74-

Clinical Findings Right > Left heart failure Dyspnea Orthopnea/PND Peripheral edema Ascites/Hepatomegaly Fatigue/ exercise tolerance Clinically mimics constrictive Pericarditis
Slide 75-

Diagnostic Studies 2D-Echo/Doppler- mitral in-flow velocity rapid early diastolic filling Catheterization – diastolic pressure equilibration restrictive vs constrictive hemodynamics Endomyocardial biopsy- definite Dx of restrictive pathology
Slide 76-

Cardiac Catheterization Prominent y descent “dip and plateau” rapid atrial emptying rapid ventricular filling then abrupt cessation of blood flow due to non-compliant myocardium
Slide 77-

Constriction vs. Restrictive CM
Slide 78-

Treatment Treat underlying cause r/o constriction which is treatable (restriction poor prognosis) amyloid (melphalan/prednisone/colchicine) Endomyocardial Fibrosis (steroids, cytotoxic drugs, MVR) Hemochromatosis (chelation, phlebotomy) Sarcoidosis (steroids) Diuretics For congestive symptoms, but  LV/RV filling   CO Digoxin (avoid in amyloidosis) Antiarrhythmics for afib amiodorone Pacemaker for conduction system disease Anticoagulation for thrombus (esp in atrial appendages)
Slide 79-

What is the hemodynamic problem in RCM?
Slide 80-

Arrhythmogenic RV Dysplasia Myocardium of RV free wall replaced: Fibrofatty tissue Regional wall motion/function is reduced Ventricular arrhythmias SCD in young
Slide 81-

MRI: RV Dysplasia
Slide 82-

LV Noncompaction Diagnostic Criteria Prominent trabeculations, deep recesses in LV apex Thin compact epicardium, thickened endocardium Stollberger C, JASE ‘04 Other phenotypic findings Prognosis and Treatment Increased risk of CHF, VT/SCD, thrombosis Oechslin EN, JACC ‘00 Hereditary risk Screening of offspring Pregnancy: case report
Slide 83-

Echo: LV Noncompaction
Slide 84-

Cardiomyopathy WHO Classification anatomy & physiology of the LV Dilated Enlarged Systolic dysfunction Hypertrophic Thickened Diastolic dysfunction Restrictive Myocardial stiffness Diastolic dysfunction Arrhythmogenic RV dysplasia Fibrofatty replacement Unclassified Fibroelastosis LV noncompaction