3. LV Systolic Performance and Pathology Flashcards
What is a normal LV Ejection Fraction?
55% for both men and women
What are the pros and cons of linear measurements of LV function?
Pro:
Lowest interobserver variability
Accurate
Con:
Least accurate representation of LV function where there are regional abnormalities
Linear measurements of LV function - Types?
- Endocardial fractional shortening
- LV wall thickness
- Relative wall thickness
Endocardial fraction shortening
- Type of linear measurement to assess LV function
- Using M-mode of transgastric short-axis of LV just above papillary muscles
= (LVIDd-LVIDs)/LVIDd x 100
Normal men: 25-43%
Normal women: 27-45%
LVIDd=LV internal diameter, diastole
LVIDs=LV internal diameter, systole
Left ventricular wall thickness
- Type of linear measurement to assess LV function
- Using transgastric short-axis of LV
- Measure both septal wall and inferior wall at END DIASTOLE
Septal Wall: right septal surface to left septal surface
Inferior Wall: Epicardial surface to endocardial surface
Normal men: 0.6-1.0cm
Normal women: 0.6-0.9cm
Relative Wall Thickness
- Type of linear measurement to assess LV function
- Using M-mode of transgastric short-axis of LV just above papillary muscles at END DIASTOLE
- Apply to patients with LV hypertrophy
= (2 x PWTd)/LVIDd or (PWTd+SWTd)/LVIDd
Normal men: 0.24-0.42cm
Normal women: 0.22-0.42cm
> 0.42cm = concentric hypertrophy
(wall thickness increased, normal internal diameter)
<0.42cm = eccentric hypertrophy
(dilated internal ventricle)
LVIDd = LV internal diameter diastolic PWTd = posterior wall thickness, end diastole IWTd = inferior wall thickness, end diastole
Planimetric Evaluation of LV - Types?
- Fractional area change
Fractional Area of Change
- Only planimetric eval of LV function
- Uses transgastric short-axis at level of papillary muscles, or long-axis
= (LVAd-LVAs)/LVAd x 100
Normal men: 56-62%
Normal women: 59-65%
LVAd = LV area, end diastole LVAs = LV area, end systole
Volume Evaluation fo LV - Types?
- Volumetric equations from linear measurements
2. Volumetric equations using planimetric measurements
What LV volume increased risk of morbidity and mortality?
> 70mL
Normal men: 22-58mL
Normal women: 19-49mL
Cubed Formula
- Used to assess LV function with volumes from linear measurements
- Relies on assumption of LV being symmetrical and elliptical
- Overestimates size of dilated ventricles since they tend to dilate primarily along the short axis (which is then cubed)
LV Volume (ml) = LVIDminor ^3
LVIDminor = septal to lateral wall (4 chamber or TG) or anterior to posterior (2 chamber)
- Measured at level of mitral chord
Volumetric Equations using planimetric equations, Types?
- Single plane ellipsoid
- Biplane ellipsoid
- Hemisphere-cylinder or bullet
- Modified Simpson’s (disks)
Single plane ellipsoid for LV volume
- Relies on assumption of LV being symmetrical
- Measurements obtained in 4 chamber or 2 chamber
LV Volume (mL)= 8 x [(LVAlax)^2/3piLVIDmj]
LVAlax = LV area from 2 or 4 chamber LVIDmj = LV internal diameter major, end diastole
Biplane ellipsoid for LV volume
- Relies on assumption of LV being symmetrical
- Incorporates LVIDmj and LVAlax (both aquired from 2 or 4 chamber) and LVIDmin and LVAsax (obtained from TG short-axis above papillary muscles)
= (piLVIDmj/6) x (4LVAsax/piLVIDmin) x (4LVAlax/pi* LVIDmj)
Bullet Formula for LV volume
- Preferred method to use if difficulty seeing the endocardial border of the apex
LV Volume (mL) = 5/6 x LVAsax x LVIDmj
LVAsax obtained in TG short-axis
LVIDmj obtained in 2 or 4 chamber
Modified Simpson’s rule for LV volume
- LV described as a series of 20 disks
- Underestimates significantly if endocardial border of the apex if difficult to see or with foreshortening
- Should use x-plane and use both 4 and 2 chamber views
LV Mass from Linear Measurements
- Myocardial volume x density of myocardial tissue
- Myocardial volume determined by subtracting LV cavity volume from total LV volume
- LV mass/BSA preferred
- Increased LV mass stronger predictor of mortality than low EF
= 0.8 x [1.04 x {(LVIDmj + PWT +SWT)^3 - (LVIDmj)^3}] +0.6
LV Mass
Normal men: 88-244g
Normal women: 67-162g
LV mass/BSA
Normal men: 49-115 g/m^2
Normal women: 43-95 g/m^2
LV Mass from Planimetric Measurements
- Either bullet or ellipsoid methods are used with tracing of both endocardial and epicardial surfaces with subtraction of the two
- Proprietary formula
Rate of Ventricular Pressure Rise - dP/dT
- dP/dT correlates with systolic function
How to:
- MR jet obtained with CWD
- Cursor placed on MR profile at 1 m/s and then at 3 m/s
- Time interval between those two velocities recorded
- Pressure differential over this period of time = 32mmHg by Bernoulli
= 4(3^2)-4(1^2) = 32
dP/dT = 32mmHg/time recorded (s)
Normal > 1000 mmHg/s
What is the gold standard of LV volume?
MRI
Tissue Doppler Imaging (TDI) - General
- Low-pass filters are used to screen out high velocity movement (blood) and focus on low velocity of tissues
- Opposite of usual doppler use
- Myocardial motion is low velocity, high amplitude (blood is high velocity, low amplitude)
- Optimize frame rate with narrow image sector
- Angle of interrogation is critical. Tissue must be parallel to beam or TDI will be underestimated.
TDI - Waveform
Systole = negative deflection (tissue moving away from probe)
- BiPhasic during isovolumic contraction
- Initially downward deflection is early myocardial activation at base of the heart which pulls annulus toward apex (occurs with MV closure)
- Upward deflection due to displacement of annulus upward due to contraction of apex
- Monophasic during ejection
- Annulus moves down as LV completely contracts and ejects
TDI - Normal Values
Systolic velocity
Normal: > 7.5cm/s
LV Failure: <3cm/s
** Peak velocities
Color Tissue Doppler (Curved M Mode)
Markers are placed at various points along ventricular wall and provides velocities against time
- Produces mean velocities (lower than regular TDI numbers)
Red = Movement toward probe Blue = Movement away from probe
Pros vs TDI
- Utilizes spatial info and can assess regional and global LV function
- Can identify post-systolic shortening
Pros vs 2D echo
- Endocardial borders are not needed to be seen, so dropout in walls that lie parallel to beam not a limitation
** Uses TDI technology so angle of interrogation remains critical
Strain and Strain Rate
Strain = segmental myocardial deformation (shape/length change)
Strain Rate = rate of myocardial deformation change
- Extrapolation of TDI technology
- Strain and SR are NOT direct measures of contractility because deformation can be affected by preload, after load, myocardial stiffness.
Blue (positive) = myocardial lengthening
Red (negative) = myocardial shortening
Akinetic = green
In 4 chamber: systole = red, diastole = blue
In TG SAX: systole = blue, diastole = red
b/c in SAX myocardium thickens in systole
Pro v TDI:
- Is not fooled by tethering, like TDI
- Better determining infarcted v non-infarcted tissue
Speckle Tracking
Uses 2D Gray images to calculate strain
- Unique acoustic marker configurations (speckles) are identified and their movement and direction are tracked to create velocity vectors
Pros v Traditional strain:
- Speckle tracking doesn’t rely on TDI technology, so angle of interrogation does not introduce error
- Any wall that can be visualized can be interrogated
LV Ventricle Synchrony
- As LV fails, areas of LV begin to contract at slightly different times
- Either due to conduction system issues, or mechanical (scarring that prohibits proper electrical conduction)
- Typically inferior or lateral walls will be delayed
- Can be performed with M-mode or TDI
Abnormal
Septal to posterior wall delay > 130ms
Septal to lateral wall delay >65ms
* These patients benefit from cardiac resynchronization
What are the types of cardiomyopathy?
- Primary
- disease confined to the heart (genetic, nongenetic, acquired) - Secondary
- generalized process involving heart and other organs
Types of Primary Cardiomyopathy
- Genetic
- Hypertrophic cardiomyopathy (HCM)
- Noncompaction of the left ventricle - Mixed (Genetic and Nongenetic)
- Dilated cardiomyopathy (DCM)
- Primary restrictive cardiomyopathy - Acquired
- Myocarditis
- Tako-Tsubo (apical ballooning) cardiomyopathy
- Peripartum cardiomyopathy
Types of genetic cardiomyopathies
- Hypertrophic cardiomyopathy
2. Noncompaction of the left ventricle
Hypertrophic Cardiomyopathy
- Primary genetic cardiomyopathy - autosomal dominant
- Heterogenous group characterized by hypertrophied, NONDILATED LV that is NOT secondary to HTN or AS
- Subtypes
1) Concentric
2) Septal (diffuse vs asymmetric septal hypertrophy)
3) Apical - Preserved systolic function
- LV dyssynchrony common
- Dynamic LVOT obstruction common
Dynamic LVOT obstruction and SAM
- Obstruction results from SAM of mitral valve causing coaptation with bulging septum
- Physiologic theories of SAM
1) LVOT obstruction produces Venturi effect on mitral valve
2) Abnormal papillary muscle orientation from LV remodeling
3) Abnormal elongated anterior mitral leaflet
Echo findings of SAM
- AML-septal contact during systole
- Posterolaterally directed MR jet during mid-systole (poss into diastole)
- Turbulent LVOT flow
- Late systolic peaking velocity (dagger) on CW of LVOT
- Systolic notching on M-mode tracing of aortic valve (early aortic valve closure)
Non-compaction of left ventricle
- Congenital cardiomyopathy
- Characterized by deep sinusoids between enlarged trabeculae
- Result of arrested embryogenesis of LV
- Can be isolated or associated with other congenital heart defects
- Associated problems
1) Decreased LV systolic function and heart failure
2) Sudden death
3) Arrhythmia
4) Thrombus formation in sinusoids with embolic events
Types of Mixed Cardiomyopathies
1) Dilated cardiomyopathy
2) Primary restrictive
Dilated Cardiomyopathy (DCM)
- LV enlargement with normal wall thickness and increased cardiac mass
- Mixed genetic cardiomyopathy, causes:
- Autosomal dominant (1/3)
- Viral infection
- Toxins (Etoh, heavy metal)
- Autoimmune
- Collagen vascular disease
- Pheochromocytoma
- Neuromuscular disease
- Mitochondrial
- Metabolic, endocrine
- Most frequent reason for listing for heart transplantation
- Dilation occurs mostly along SAX and heart becomes more globular
- Associated findings:
- Mitral annulus dilation
- Function MR 2/2 abnormal papillary muscle orientation and mitral leaflet tethering
- Biatrial enlargement
- Apical thrombus
- Diastolic dysfunction
Causes of dilated cardiomyopathy
Mixed genetic cardiomyopathy, causes:
- Autosomal dominant (1/3)
- Viral infection
- Toxins (Etoh, heavy metal)
- Autoimmune
- Collagen vascular disease
- Pheochromocytoma
- Neuromuscular disease
- Mitochondrial
- Metabolic, endocrine
Dilated cardiomyopathy, associated findings
- Mitral annulus dilation
- Function MR 2/2 abnormal papillary muscle orientation and mitral leaflet tethering
- Biatrial enlargement
- Apical thrombus
- Diastolic dysfunction
Primary restrictive cardiomyopathy
- Characterized by:
- Normal or decreased volume of BOTH ventricles
- Biatrial enlargement
- Normal wall thickness and normal valves
- Restrictive diastolic physiology
- Normal systolic function
- Genetic and non-genetic causes
Types of acquired primary cardiomyopathy
- Myocarditis
- Tako-Tsubo (apical ballooning)
- Peripartum
Myocarditis
- Acquired primary cardiomyopathy
- Acute and chronic
- Results in dilated cardiomyopathy and arrhythmias
- Causes:
- Infection
- Drugs, toxins
Tako-Tsubo (apical ballooning) cardiomyopathy
- Rapid onset, related to extreme stress and sympathetic stimulation
- Extensive stunning of mid and apical segments of LV
- Apical half balloons out during systole, while basal half is hypercontractile
Peripartum cardiomyopathy
- Rare cause of severe dilated cardiomyopathy
- 3rd trimester to 5 months post-partum
- 50% -> persistent heart failure, 50% -> full recovery
Constrictive Pericarditis vs Restrictive Cardiomyopathy
Constrictive Pericarditis
- Thickened pericardium
- Normal atrial and LV size
- Normal wall thickness
- Normal myocardium
- Normal systolic function
- Septal movement towards LV during spontaneous inspiration
- Enlarged IVC and hepatic veins
- No MR or TR
- E/A normal or 25% with spontaneous inspiration or mechanical expiration
- Normal decrease ~5%, COPD 10-15%
- IVRT increased with inspiration
- Pulmonary vein flow: S=D during inspiration, D>S with expiration
- Hepatic vein flow: W shaped waved form (large a wave) with decreased diastolic flow with spontaneous expiration
Restrictive cardiomyopathy:
- Normal pericardium
- Enlarged atria
- Small LV size with increased wall thickness
- Granular myocardium
- Reduced systolic function
- No ventricular independence
- Enlarged IVC and hepatic veins
- Usually MR or TR
- E/A > 2.2
- No significant decrease in mitral E wave with spontaneous inspiration
- IVRT does not vary
- Pulmonary vein flow: S<D, no respiratory variation
- Hepatic vein flow: Blunted systolic flow, possibly systolic flow reversal if signifacnt TR
Left Ventricular Hypertrophy, types
- Types:
1) Concentric
2) Eccentric
Concentric LVH
- Parallel replication of sarcomeres without significant chamber enlargement
- Secondary to chronic pressure overload
- Goal = decrease wall stress
- wall stress = (pressure x chamber size)/wall thickness
- Additional LV changes
- Prolonged IVRT
- Reduced compliance -> diastolic dysfunction
- Eventual cardiac function compromise
Eccentric Hypertophy
- Serial replication of sarcomeres with LV chamber enlargement
- Secondary to chronic volume overload
Determine types of hypertrophy, LV mass and Relative wall thickness
Normal: mass 0.42
Concentric hypertrophy: mass increased; RWT >0.42
Eccentric hypertrophy: mass increased; RWT normal
LV True Aneurism
- Frequently 2/2 anterior wall MI
- Form within 90 days of infarct, <5 days portends worse prognosis
Characteristics
- Dilated dyskinetic area with myocardial thinning
- Aneurism neck to maximum aneurism diameter = 0.9-1.0
LV Pseudoaneurism
- chronic ventricular rupture contained by the pericardium
- high incidence of rupture, therefore must be corrected
Characteristics:
- ratio of orifice to max aneurism diameter <0.5
- false aneurism expands in systole while LV contracts
