A Practical Approach to Transesophageal Echocardiography Chapter 2 Flashcards
What is the normal LV wall thickness in men vs women? How do you measure it?
Normal values (reference range) for both posterior (inferolateral) wall and septal wall thickness: Men 0.6 to 1.0 cm; women 0.6 to 0.9 cm.
Measurements of LV wall thickness are typically made in the transgastric (TG) mid short-axis (SAX) view (excluding the papillary muscles, Fig. 3.1). Measurements can be made from 2D or M-mode recordings, although 2D is the preferred method, since M-mode measurements are subject to inaccuracies caused by nonperpendicular placement of the M-mode cursor (1). Usually, both septal wall thickness at end diastole (SWTd) and posterior wall thickness at end diastole (PWTd) are reported. Septal wall thickness is measured from the right septal surface to the left septal surface, whereas posterior wall thickness is measured from epicardial surface to endocardial surface (being careful not to include pericardial tissue). Wall thickness increases with age, even in normal populations
How do you calculate Relative Wall Thickness?
Relative wall thickness (RWT) is often used in patients with LV hypertrophy. In TEE the measurements are again made in a TG SAX and may be calculated from either of the two formulae given below. RWT is expressed as a decimal and used to describe LV hypertrophy and remodeling.
Relative wall thickness (RWT) mm = (2 × PWTd)/LVIDd or (PWTd + SWTd)/LVIDd
Normal values: Men 0.24 to 0.42 cm; women 0.22 to 0.42 cm (1,2).
In these two formulae, LVIDd refers to the minor-axis diameter measurement (LV cavity, see below). A regional wall thickness equal to or greater than 0.42 denotes concentric hypertrophy (wall thickness is increased in the presence of a normal internal diameter) and an RWT less than 0.42 denotes eccentric hypertrophy (dilated LV). The distinction between the two forms of hypertrophy is of prognostic interest, as concentric hypertrophy is associated with a higher incidence of cardiovascular events than eccentric hypertrophy.
How do you measure LV diameter?
Linear measurements of chamber size are defined by a minor- (short-) axis diameter and a major- (long-) axis diameter (Fig. 3.2).
The minor-axis diameter measurement is made at, or immediately below, the level of the mitral valve tips and perpendicular to the long-axis diameter (1). That means it should be measured in the midesophageal (ME) two-chamber view or TG two-chamber view at the level of the papillary muscles, rather than in the TG SAX view which is created at the level of the papillary muscle bodies.
The major-axis diameter (LV length) is typically made in the ME two- or four-chamber view since the apex is not well seen in the TG two-chamber view. The measurement is made from the midpoint of a line connecting the two opposite points of the mitral annulus to the endocardium at the apex. The longer of the two lengths acquired from the ME two- and four-chamber views, is the recommended measurement to use.
Normal values (mean) for minor-axis diameter (LVID) (1):
In diastole : men 50.2 ± 4.1 mm and women 45.0 ± 3.6 mm
In systole : men 32.4 ± 3.7 mm and women 28.2 ± 3.3 mm
In general, a minor-axis diameter greater than 5.4 cm during diastole is considered enlarged.
Normal value for fractional shortening in men vs. women?
LV systolic function estimates based on linear measurements are known as endocardial fractional shortening,
Endocardial fractional shortening (%) = {(LVIDd − LVIDs)/LVIDd} × 100
Normal values: men 25% to 43%, women 27% to 45
How do you measure LV fractional area change?
Area measurements offer some improvements in accuracy over linear dimensions, as more of the LV is represented in the measurement. LV systolic function estimates based on area measurements are known as fractional area change (FCA).
Fractional area change (FAC) (%) = {(LVAd − LVAs)/LVAd} × 100
Normal values: >35%
The area of the LV cavity is measured at end-systole (LVAs) and at end diastole (LVAd) and used to calculate FAC (Fig. 3.11). Most commonly these measurements are made from the TG mid SAX view of the LV, but when this view is suboptimal, long-axis views can be substituted. The endocardium is manually traced around the LV cavity ignoring the papillary muscles. Fractional area change is essentially the measurement which is mentally made when a clinician “eyeballs” the left ventricular ejection fraction (LVEF).
A TG SAX view is acquired and a mental estimate of FAC is made. If the apex is normal, 15% is added; if akinetic, zero is added; and if dyskinetic, 15% is subtracted. If there is hypokinesia of the apex, a value of 5% to 10% is added.
How to measure dP/dT? Normal value?
The rate of rise in left ventricular pressure (dP/dT) has been demonstrated to be well correlated with systolic function. The greater the contractile force exerted, the greater the rise in ventricular pressure. Previously this could only be measured invasively with LV catheterization; however continuous-wave Doppler (CWD) determination of the velocity of a mitral regurgitant (MR) jet allows calculation of instantaneous pressure gradients between the left ventricle and the left atrium.
Left atrial pressure variations in early systole can be considered to be negligible; therefore, the rising segment of the MR velocity curve should essentially reflect LV pressure increase only.
If the rate of rise in ventricular pressure is reduced because of poor LV function, the rate of increase of the MR jet velocity will also be low.
To perform a dP/dT measurement (Fig. 3.13), the MR jet is interrogated with CWD. The cursor is placed on the MR velocity profile at 1 m/s and then at 3 m/s and the time interval between the two points is determined (10). Using the simplified Bernoulli equation, the pressure differential is [4(3)2] – [4(1)2] or 32 mm Hg.
dP/dT is therefore 32 mm Hg divided by the time interval in seconds.
Normal values exceed 1,000 mm Hg/s.
Manifestations of HOCM?
Clinical diagnosis is made by the 2DE finding of LV wall thickening with a small LV cavity in a patient without other causes for LV hypertrophy.
There are several phenotypic expressions that are recognized with the hypertrophy being concentric, limited to the septum or to the apex of the LV.
HCM limited to the septum, which may be either diffuse hypertrophy throughout the septum or only in the basal or mid-wall regions, has also been known as asymmetric septal hypertrophy (ASH), hypertrophic obstructive cardiomyopathy (HOCM), or idiopathic hypertrophic subaortic stenosis (IHSS).
Asymmetry is expressed by a septal wall to free wall (posterior wall) thickness ratio greater than 1.4.
Although systolic function is usually preserved in HCM until late in the disease, LV dyssynchrony is common in all forms.
HOCM and LVOT obstruction?
Many HCM patients have the propensity to develop dynamic obstruction of the left ventricular outflow tract (LVOT) either under resting or provoked conditions. This LVOT obstruction is also associated with systolic anterior motion (SAM) of the MV in which the anterior mitral leaflet (AML) coapts with the bulging septum during systole (Fig. 3.27; Video 3.6).
Several theories have been proposed to explain SAM, such as the LVOT dynamic obstruction creates a Venturi effect causing coaptation of the AML with the septum; abnormally oriented papillary muscles secondary to LV remodeling; an abnormal AML which is elongated with an increased surface area facilitating coaptation with the septum.
Echocardiographic findings of SAM in HCM include AML septal contact during systole, posterolaterally directed mid-systolic MR associated with SAM (Video 3.6) which can persist into diastole, a turbulent color flow Doppler pattern in the LVOT, a late systolic peaking velocity profile on continuous-wave interrogation of the LVOT (Fig. 3.28), and systolic “notching” on the M-mode tracing of the aortic valve (premature closure of the aortic valve).
Noncompaction of the left ventricle manifestations
LV noncompaction (LVNC) is an uncommon and recently recognized cardiac disease with sporadic or familial occurrence. LVNC has a heterogeneous clinical presentation and is difficult to diagnose. It may present in isolation or in association with cardiovascular abnormalities. It’s true incidence and prevalence are therefore not precisely known
LVNC involves predominantly the apex of the LV with deep sinusoids between enlarged trabeculae caused by arrested embryogenesis of the LV. A cross-section of the apex of the LV resembles the appearance of a natural sponge. Noncompaction of the LV may be an isolated finding or may be associated with other congenital heart anomalies such as complex cyanotic congenital heart disease. Noncompaction of the LV results in systolic dysfunction and heart failure although arrhythmias and sudden death are also frequent clinical presentations. Thrombi may form within the sinusoids and being in continuity with the LV cavity may produce embolic events.
Diagnosis?
Left ventricular outflow tract (LVOT) obstruction demonstrating typical late systolic peaking (“dagger-shaped”) gradient across the LVOT as the cross-sectional area becomes progressively smaller during systole. Note the high gradients generated.
Diagnosis?
Left ventricular inferior wall aneurysm.
First video: Transgastric (TG) two-chamber view.
Second video: TG basal short-axis view (SAX).
LV Pseudoaneurysm vs aneurysm?
The ability to distinguish a true aneurysm from a pseudoaneurysm is critical because pseudoaneurysms have a high incidence of spontaneous rupture and therefore require surgical correction. A pseudoaneurysm represents a chronic ventricular rupture contained by pericardium. Therefore, a pseudoaneurysm is a saccular structure that communicates directly with the pericardial space.
Two-Dimensional Characteristics
A pseudoaneurysm is characterized by a narrow orifice (neck) arising from the ventricular chamber; the ratio of the size of the orifice to the maximal aneurysmal diameter is less than 0.5 (Fig. 3.39; Video 3.14). The size of the small neck rarely exceeds half the maximal parallel internal diameter of the aneurysmal sac (46). The LV cavity size decreases in systole while the false aneurysm gradually expands.
Quantitative Doppler Characteristics
Doppler echocardiography has proved useful in diagnostically difficult cases and demonstrates bidirectional flow of blood between the pseudoaneurysm and the LV. Color flow Doppler echocardiography usually demonstrates mosaic jets exiting the LV in systole and entering the pseudoaneurysm cavity. In diastole, this mosaic pattern occurs within the LV, confirming the turbulent ebb and flow of blood to and from the pseudoaneurysm. One may also see a profound variation in maximal Doppler flow velocity throughout the respiratory cycle, with inspiration causing a significant increase in the maximal flow velocity (46).
Associated Findings
Spontaneous echo contrast and thrombus within the pseudoaneurysm cavity are frequent findings.
