cardiomyopathy 2
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CARDIOMYOPATHY
Athena Poppas, MD
Associate Professor of Medicine,
Brown Medical School
Director, Echocardiography Laboratory
Rhode Island Hospital
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Cardiomyopathies
Definition: diseases of heart muscle
1980 WHO: unknown causes
Not clinically relevant
1995 WHO: diseases of themyocardium associated with cardiac
dysfunction pathophysiology each with multiple etiologies
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Cardiomyopathy
WHO Classificationanatomy & physiology of the LV
1. Dilated
Enlarged
Systolic dysfunction
2. Hypertrophic Thickened
Diastolic dysfunction
3. Restrictive
Diastolic dysfunction
4. Arrhythmogenic RV dysplasia Fibrofatty replacement
5. Unclassified
Fibroelastosis
LV noncompaction
Circ 93:841, 1996
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CM: Specific Etiologies
Ischemic
Valvular
Hypertensive Inflammatory
Metabolic
Inherited Toxic reactions
Peripartum
Ischemic: thinned, scarred tissue
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Dilated Cardiomyopathy
Dilation andimpaired contraction of ventricles:
Reducedsystolic 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 cases3X more prevalent among males and African-Americans
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DCM: Etiology
Ischemic
Valvular
Hypertensive
Familial
Idiopathic
Inflammatory
Infectious
Viralpicornovirus, Cox B, CMV, HIVRicketsial - Lyme Disease
Parasitic - Chagas Disease, Toxoplasmosis
Non-infectious
Collagen Vascular Disease (SLE, RA)
Peripartum
ToxicAlcohol, Anthracyclins (adriamycin), Cocaine
Metabolic
Endocrinethyroid dz, pheochromocytoma, DM, acromegaly,
Nutritional
Thiamine, selenium, carnitine
Neuromuscular (Duchenes Muscular Dystrophy--x-linked)
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Prognosis depends on Etiology
1230 pts. referred for unexplained CM. Felker GM. NEJM 2000;342:1077
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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
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DCM: toxic
Alcoholic cardiomyopathy
Chronic use
Reversible with abstinence Mechanism?:
Myocyte cell death and fibrosis
Directly inhibits: mitochondrial oxidative phosphorylation
Fatty acid oxidation
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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
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DCM: PeripartumDiagnostic 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.
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PPCM: Prognosis
Death from CM: 91-97 245 CM deaths in US, 0.88/100,000 live births,
70% peripartum
Increased risk with:
Maternal ageAA 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 ES relationship
Lampert MB. AJOG.1997.176.189.
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Dilated Cardiomyopathy
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MECHANISMS IN HEART FAILURE
Hemodynamic Derangement
Clinical Heart Failure
Arrhythmia
Neurohormones
Cytokines
Oxidative stress
Ischemic injury
Myocardial disease
GeneticsAltered molecular expression
Ultrastructural changes
Myocyte hypertrophy
Myocyte contractiledysfunction
Apoptosis
Fibroblast proliferation
Collagen deposition
Ventricular remodeling
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Pathophysiology
Initial Compensation for impaired myocyte contractility:
Frank-Starling mechanism
Neurohumoral activation
intravascular volume
Eventual decompensation
ventricular remodeling
myocyte death/apoptosisvalvular regurgitation
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Pathophysiology: Starling Curve
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Pathophysiology: Neurohumoral
Adrenergic nervoussystem
Renin-angiotensin-aldosterone axis
Vasopressin
Natriuretic peptides
Endothelin
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Reduced Response to Adrenergic Stimulation
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Renin-Angiotensin-Aldosterone Pathways
Angiotensinogen
Angiotensin-I
Angiotensin-II
Renin
ACE
AT-1 Receptor
Chymase
Bradykinindegradation
ACE-inhibitor
Angiotensinreceptor
blocker
Aldosterone
Spironolactone
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Angiotensin-II Effects
Vasoconstriction
Aldosterone
production Myocyte hypertrophy
Fibroblast proliferation
Collagen deposition
Apoptosis
Pro-thrombotic
Pro-oxidant Adrenergic stimulation
Endothelial dysfunction
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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)
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Ventricular
Remodeling in HeartFailure
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Ventricular Remodeling following MI
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Extracellular Stimuli of Myocyte
Hypertrophy
Type Examples
Mechanical Stretch
Vasoactive peptides Angiotensin-II
Endothelin-1
adrenergic agonists Norepinephrine
Peptide growth factors Fibroblast GF
Insulin-like GF
Cytokines TNF-
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Clinical Findings
Biventricular Congestive Heart Failure
-Low forward Cardiac Output-fatigue, lightheadedness, hypotension
-Pulmonary Congestion-Dyspnea,-orthopnea, & PND
-Systemic Congestion
-Edema-Ascites
-Weight gain
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Physical Exam
Decreased C.O.
Tachycardia
BP and pulse pressurecool extremities (vasoconstriction)
Pulsus Alternans (end-stage)
Pulmonary venous congestion:
ralespleural effusions
Cardiac:
laterally displaced PMI
S3 (acutely)
mitral regurgitation murmurSystemic congestion
JVDhepatosplenomegaly
ascites
peripheral edema
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Diagnostic Studies
CXR-enlarged cardiac silhouette,
vascular redistribution interstitial edema,
pleural effusions
EKGnormal
tachycardia, atrial and ventricular
enlargement, LBBB, RBBB, Q-waves
Blood Tests(ANA,RF, Fe2+, TFTs,ferritin,)
Echocardiography
LV size, wall thickness function
valve dz, pressures
Cardiac Catheterizationhemodynamics
LVEF
angiography
Endomyocardial Biopsy
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Echo in dilated CM
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Influence of EF on Survival inPatients with Heart Failure
Vasan RS et al. J Am Coll Cardiol. 1999;33:1948-55
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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, butsymptoms 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 Fai lure1999;5:357-382
Criteria for NYHA Functional Classification
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Aim of Treatment
Preload reduction
Diuretics
venodilators
Vasodilators
ACEI
Inotropes
Acutely
Chronically
mortality
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Vasodilator Agents in Heart Failure
Drug Mechanism Action Use
Nitroglycerinand long-
acting nitrates*
Direct via nitricoxide
Veno /arterioloar
Hemodynamic;anti-ischemic;
long term
Nitroprusside Direct via nitricoxide
Arteriolar >venodilation
Hemodynamic
Hydralazine* Direct Arteriolar ?long term*
ACEinhibitors#
Reduced A-IIIncr. bradykinin
Veno /arterioloar
Long-term
*Hydralazine and a long-nitrate shown to reduce mortality long-term
# Other actions (aside from vasodilation) likely to be important
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Dobutamine and Milrinone Effects
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Electrical and Mechanical
Ventricular Dyssynchrony Experimentallyinduced LBBB has effect on:
expressionof regional stress kinases
calcium-handling proteins.
Expression of p38-MAPK(a stress kinase) iselevated in the endocardiumof the late-activated region, whereas phospholamban is
decreased. Sarcoplasmatic reticulum Ca2+-ATPaseis
decreased in the region of early activation.
D l t i H d i
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Deleterious HemodynamicEffects of LV Dyssynchrony
Diminished SV & CO due:
Reduced diastolic filling
time1
Weakened contractility 2
Protracted MVregurgitation 2
Post systolic regionalcontraction 3
Atrio-
ventricular
Inter-V
Intra-V
Cazeau, et al. PACE2003; 26[Pt. II]: 137143
1. Grines CL, Circulation1989;79: 845-853
2. Xiao HB, Br Heart J1991;66: 443-447
3. Sgaard P, JACC 2002;40:723730
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CRT: CardiacResynchronization Therapy
1. Improved hemodynamics Increased CO Reduced LV filling
pressures
Reduced sympatheticactivity Increased systolic function
w/o MVO2
2. Reverse LVremodeling/architecture Decreased LVES/ED
volumes Increased LVEF
Circ 02, JACC 02, JACC02, NEJM02
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Risk of Sudden Death c/w EF
Patients withoutLV Dysfunction
(LVEF >35%)
Maggioni AP. GISSI-2 TrialCirculation. 1993;87:312-322.
Patients with
LV Dysfunction
(LVEF < 35%)
No PVBs
1-10 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
A ti h th i d ICD
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Anti-arrhythmic drugs, ICDplacebo and Death
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What are the two characteristicfindings in DCM?
H t i H t hi
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Hypertensive HypertrophicCardiomyopathy
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Women and Hypertension
Prevalence of HTN in Women from NHANES-III. Burt VL. Hypertension 95
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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
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Zile MR. Circ;105:1387
Echo Doppler Parameters
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Diastolic Dysfunction
Kawaguchi M. Circ 2003.107:714
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Zile MR. Circ;105:1387
Isolated Diastolic HF
Isolated Systolic HF
Systolic & Diastolic HF
What is the difference
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What is the differencebetween systolic and
diastolic LV dysfunction?
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Hypertrophic Cardiomyopathy
Left ventricular hypertrophy not due to pressure overloadHypertrpohy 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%)
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Etiology
Familial in ~ 55% of cases with autosomal dominant transmission
Mutations in one of 4 genes encoding proteins of cardiac sarcomereaccount for majority of familial cases
-MHCcardiac troponin T
myosin binding protein C-tropomyosin
Remainder are
spontaneous
mutations.
H t hi C di th
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Hypertrophic Cardiomyopathy
H t hi C di th
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Hypertrophic Cardiomyopathy
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Hypertrophiccardiomyopathy
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Apical HypertrophicCardiomopathy
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Pathophysiology
HCM ith tfl b t ti
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HCM with outflow obstructionDynamic LVOT obstruction (may not be present at rest)
SAM (systolic anterior motion of mitral valve)
LVOT Obstruction LVOT gradientwall 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 diastolicdysfunction than to outflow tract obstruction
Syncope: LVOT obstruction (failure to increase CO during exercise
or after vasodilatory stress) or arrhythmia.
h l
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Physical Exam
Bisferiens pulse (spike and dome)S4 gallop
Crescendo/Descrescendo systolic ejection murmur
HOCM vs. Valvular AS Intensity of murmurHOCM AS
Valsalva (preload, afterload) Squatting ( preload, afterload) Standing (preload, afterload)
Holosystolic apical blowing murmur of mitral regurgitation
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Diagnostic Studies
EKG NSR
LVH
septal Q waves
2D-Echocardiography LVH; septum >1.4x free wall
LVOT gradient by Doppler
Systolic anterior motion ofthe mitral valeregurgitation
Cardiac Catheterization LVOT gradient and pullback
provocative maneuvers
Brockenbrough phenHCM-ASH using contrast
Cardiac Catheterization
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Cardiac Catheterization
LV pullback
Brockenbrough-Braunwald Signfailure of aortic pulse pressure to rise post PVC
Provocative maneuvers:Valsalva
amyl nitrate inhalation
Atrial Fibrillation
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Atrial FibrillationAcute 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 blockersDigitalis is relatively contra-indicated- positive inotrope
DC Cardioversion
No p wave P wave present
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TreatmentFor symptomatic benefit
-blockers mvO2 gradient (exercise)
arrythmias
Calcium Channel blockersAnti-arrhythmics
afib
amiodorone
Disopyramide
AICD for sudden death
antibiotic prophylaxis for endocarditis
No therapy has been shown to improve mortality
HCM: Surgical Treatment
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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 replacement5 year symptomatic benefit in ~ 70% of patients
Dual Camber (DDD pacemaker) pacing
decreases LVOT gradient (by~25%)
randomized trials have shown little longterm benefitpossible favorable morphologic changes
ETOH septal ablation
AICD to prevent sudden death
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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 nosymptoms 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.
W ll Thi k d
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Wall Thickness andSudden Death in HCM
Spirito P. N Engl J Med. 2000;342:1778-1785.
0
2
4
6
810
12
14
16
18
20
< 15 16-19 20-24 25-29 > 30
Maximum Left-Ventricular-Wall Thickness (mm)
IncidenceofSudden
Death
(per1,0
00
person/yr)
0
2.6
7.4
11.0
18.2
Prognosis
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Prognosis
Sudden Death 2-4%/year in adults
4-6% in children/adolescentsAICD 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
ischemiapresence of ventricular arrhythmias on Holter (EPS)
EPS
Amiodorone (low dose)
Prophylactic AICD?
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HCM vs Athletes Heart
Endurance training:
Physiologic increase in LV mass
Wall thickness and cavity size
Early HCM vs Athletes heart
DEFINITION: Symmetric,
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Why do patients with HCMdevelop heart failure?
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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
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Amyloid infiltrative CM
Amyloidosis
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Amyloidosis
Primary Amyloidosis
immunoglobulin light chains -- multiple myeloma
Secondary Amyloidosis
deposition of protein other than immunoglobulin
senile
familialchronic inflammatory process
restriction caused by replacement of normal myocardial contractile
elements by infiltrative interstitial deposits
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Amyloidosis
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Amyloid Cardiomyopathy
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Sarcoidosis
Restriction
Conduction System Disease
Ventricular Arrhythmias
(Sudden Cardiac Death)
Endomyocardial Fibrosis
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Endomyocardial Fibrosis
Endemic in parts of Africa, India, South and Central America, Asia
15-25% of cardiac deaths in equatorial Africahypereosinophilic syndrome (Lofflers endocarditis)
Thickening of basal inferior wall
endocardial deposition of thrombus
apical obliteration
mitral regurgitation
80-90% die within 1-2 years
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Pathophysiology of Restriction
Elevated systemic and pulmonary venous pressures
right and left sided congestion
reduced ventricular cavity size with SV and CO
Clinical Findings
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Clinical Findings
Right > Left heart failure
Dyspnea
Orthopnea/PND
Peripheral edema
Ascites/Hepatomegaly
Fatigue/ exercise tolerance
Clinically mimics constrictive Pericarditis
Diagnostic Studies
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Diagnostic Studies
2D-Echo/Doppler-mitral in-flow velocity
rapid early diastolic filling
Catheterization
diastolic pressure equilibrationrestrictive vs constrictive
hemodynamics
Endomyocardial biopsy-definite Dx of restrictive pathology
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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
Constriction vs Restrictive CM
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Constriction vs. Restrictive CM
T t t
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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 CODigoxin (avoid in amyloidosis)
Antiarrhythmics for afib
amiodoronePacemaker for conduction system disease
Anticoagulation for thrombus (esp in atrial appendages)
What is the hemodynamic
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What is the hemodynamicproblem in RCM?
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Arrhythmogenic RV Dysplasia
Myocardium of RV free wall replaced:
Fibrofatty tissue
Regional wall motion/function is reducedVentricular arrhythmias
SCD in young
MRI: RV Dysplasia
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MRI: RV Dysplasia
i
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LV Noncompaction
Diagnostic Criteria
Prominent trabeculations, deep recesses in LVapex
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
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Echo: LV Noncompaction
Cardiomyopathy
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Cardiomyopathy
WHO Classificationanatomy & physiology of the LV1. Dilated
Enlarged
Systolic dysfunction
2. Hypertrophic
Thickened
Diastolic dysfunction
3. Restrictive
Myocardial stiffness
Diastolic dysfunction
4. Arrhythmogenic RV dysplasia Fibrofatty replacement
5. Unclassified
Fibroelastosis