Left Ventricular Dilation and Systolic Functional Impairment

The principal hallmark of DCM is left ventricular cavity dilation , although enlargement of other cardiac chambers also often occurs. Left ventricular cavity enlargement is usually quantified by measuring increased LV end-diastolic and end-systolic dimensions and volumes. Although the myocardial walls may be either of normal thickness or thinned, the total left ventricular mass is increased due to the overall increase in LV size. Furthermore, measures of LV systolic function such as fractional shortening, ejection fraction, stroke volume, and cardiac output are typically reduced ( Fig. 22.1 ).

Apical four-chamber views from two patients with dilated cardiomyopathy.

(A) End-diastolic (upper panel) and end-systolic (lower panel) frames from a patient with dilated cardiomyopathy (DCM) and New York Heart Association (NYHA) functional class IV, referred for left ventricular assist device (LVAD) implantation. The biplane left ventricle (LV) end-diastolic and end-systolic volume indices are measured at 147 and 126 mL/m ² , respectively, indicating severe LV dilation. The calculated stroke volume is reduced at 48 mL, and the ejection fraction by the Simpson’s biplane method is 14%. Both atria are also severely enlarged: the left atrial volume is 76 mL/m ² (indexed to body surface area [BSA]), and the right atrial volume is 64 mL/m ² . See Video 22.1 (left panel) for the corresponding moving images. (B) End-diastolic (upper panel) and end-systolic (lower panel) frames from a patient with DCM and NYHA class II, presenting in regular heart failure clinic follow-up. The biplane end-diastolic and end-systolic volume indices are measured at 121 and 90 mL/m ² , respectively, also indicating a severely dilated LV. The calculated stroke volume, however, is preserved at 68 mL, while the ejection fraction by Simpson’s biplane method is 26%. In this patient, there was only mild to moderate left atrial (LA) enlargement: the left atrial volume is 34 mL/m ² , and the right atrial volume indexed to BSA is 12.6 mL/m ² . See corresponding Video 22.1 (right panel) . (A and B) Although there is severe LV dilation and severe LVEF reduction in both these examples, the calculated stroke volume of the patient in (B) is virtually normal, as opposed to the patient in (A). In addition to a preserved stroke volume, there is only initial LA dilation in the patient in (B), suggestive of potentially lower LV filling pressures and accounting for a better functional class. See further text for additional figures comparing these two patients.

It should be emphasized that, although the stroke volume is reduced in most cases, LV cavity dilation may initially serve to compensate by restoring stroke volume (measured on echocardiography as the difference between the LV end-diastolic and end-systolic volume). Namely, a larger ventricle can eject much more volume than a smaller one, even with the same amount of contraction (i.e., segmental deformation) ( Fig. 22.2 ). Hence, the final cardiac output may be initially preserved despite impairment in ejection fraction (measured as the stroke volume divided by LV end-diastolic volume). Restoration of stroke volume by ventricular dilatation is an integral part of the process of LV remodeling in the adaptation to changes in contractility and loading conditions. Thus, (1) in DCM, although inherent myocardial dysfunction and diminished myocardial contractility is the primary defect, ventricular dilation may enable the generation of the same amount of stroke volume with less deformation, and (2) in volume overload states (e.g., valvular regurgitation, such as functional mitral regurgitation), an increased amount of stroke volume is required and may be generated (with the same amount of contractility) by an LV that dilates to adapt (see Fig. 22.2 ). Indeed, preservation of stroke volume (as well as an increase in heart rate) to maintain overall cardiac output may explain why the severity of symptoms can remain relatively low despite notably impaired left ventricular ejection fraction (LVEF), despite the fact that the latter correlates strongly with prognosis. Conversely, symptoms of congestive heart failure are more directly related to elevated LV filling pressures (see below). Fig. 22.1 and Video 22.1 provide an example of two patients with severely dilated left ventricles and severely reduced LVEF but different LV stroke volumes, atrial sizes, and functional class.

Relation of ventricular size, stroke volume, and deformation.

Ventricular size is expressed as end-diastolic volume (ED volume), and deformation is expressed as strain.

From Bijnens B, Cikes M, Butakoff C, Sitges M, Crispi F. Myocardial motion and deformation: what does it tell us and how does it relate to function? Fetal Diagn Ther . 2012;32[1–2]:5–16, with permission from S. Karger AG, Basel.

Based on the described principles of remodeling, the left ventricular shape changes with disease progression from the typical elongated shape to a more globular one. A simple measurement that can quantify this is the sphericity index , defined as the ratio of the LV length and width ( Fig. 22.3 ). A normal sphericity index is greater than 1.6; in DCM, this is generally reduced , implying pathologic remodeling with notable cavity dilation (see also Fig. 20.5 in Chapter 20 ).

The sphericity index as a measure of left ventricle cavity dilation and globular remodeling.

Left panel, A patient with peripartum cardiomyopathy (a disease that may be of short duration and may remit) with a greater, i.e., more normal, or nonspherical, sphericity index of 2.3. Conversely, the right panel shows a patient with long-standing dilated cardiomyopathy and a low sphericity index of 1.7, suggesting a spherically remodeled left ventricle. (See also Fig. 20.5 .)

Several features of DCM are manifest and quantifiable on m-mode echocardiography (see Chapter 2 ): LV and right ventricular (RV) cavity enlargement, changes in wall thickness and calculated LV mass, as well as reduced segmental wall thickening are classically recognizable on m-mode as signs of LV dilation and poor systolic performance. Poor aortic valve opening with premature closure can be noted in the setting of reduced stroke volume. Due to LV dilatation, the mitral leaflet echoes are often distanced to greater than 1.0 cm of the mitral E-point from the interventricular septum (see Fig. 2.16 ). A characteristic pattern of decreased mitral leaflet opening and an occasional “b-notch” indicative of markedly elevated LV end-diastolic pressure are shown in Fig. 2.15 in Chapter 2 . Impairment in LV systolic function can also be assessed on apical windows by reduced mitral annular planar systolic excursion (MAPSE) ( Fig. 22.4 ). A MAPSE less than 10 mm (usually averaged from 2 to 4 point measurements spaced around the mitral annulus) is indicative of reduced longitudinal LV motion.

Mitral annular planar systolic excursion assessed from mitral annular motion by m-mode echocardiography.

Mitral annular planar systolic excursion (MAPSE) (red mark) , a simple measure of longitudinal left ventricular motion is severely reduced in this patient with dilated cardiomyopathy. The medial (septal) MAPSE is measured on the left panel , and lateral MAPSE is measured in the right panel . The MAPSE measurements are typically averaged, and a value less than 10 mm is considered abnormal.

Similarly to reduced MAPSE, impaired motion of the base of the heart towards the more stationary apex (expressing the longitudinal function of the LV) can be quantified by Doppler Tissue Imaging S’ (systolic) velocity or more advanced parameters of myocardial deformation, such as systolic strain, which is often expressed as global longitudinal strain ( Fig. 22.5 ) or less frequently as systolic strain-rate (see Chapter 6 ), all of which will typically be reduced in DCM.

Global longitudinal strain (GLS) assessed by two-dimensional Speckle Tracking echocardiography.

Global longitudinal strain (GLS) is a more advanced measure of longitudinal left ventricular deformation, which is also severely reduced in this example of a patient with dilated cardiomyopathy (the same patient as Fig. 22.1B ). 4CH , Apical 4-chamber view; ANT , anterior wall; ANT_SEPT , anteroseptal wall; APLAX , apicla long axis view; AVC , aortic valve closure; INF , inferior wall; LAT , laterial wall; POST , posterior wall; SEPT , septum.

Finally, Doppler echocardiography may be used in the hemodynamic assessment of LV systolic function: in addition to volumetric measurements of stroke volume and cardiac output, these calculations can also be performed using the continuity of flow equation (see Chapter 1 ). Multiplication of the cross-sectional area and the time velocity integral of the left ventricular outflow tract (LVOT) will provide the calculation of left ventricular stroke volume ( Fig. 22.6 ), which is typically reduced in advanced DCM. The change of pressure over time (d P /d t ) can be measured when a sufficient mitral regurgitation envelope (recorded by continuous wave Doppler) is present and will also be reduced in most patients with DCM ( Fig. 22.7 ). This noninvasive parameter has shown good correlation with values measured by cardiac catheterization and has been associated with worse prognosis when less than 600 mm Hg/s. For more details on the assessment of LV systolic function, please refer to Chapter 14 .

Doppler-based calculation of left ventricular stroke volume.

According to the continuity of flow equation, the stroke volume is calculated as left ventricular outflow tract cross sectional area (LVOT CSA) × left ventricular outflow tract velocity time integral (LVOT VTI), which in this example (the same patient as Fig. 22.1B) gives a left ventricular (LV) stroke volume of 68 mL ( lower left panel, baseline). As SV decreases with disease progression, the LVOT VTI becomes reduced. Changes in LVOT VTI with heart failure treatment (lower panels) : LVOT VTI measurements in a patient before cardiac resynchronisation therapy (CRT) implantation (lower left panel) , 1 year after CRT implantation (lower middle panel) and 4 years after CRT implantation (lower right panel) . This patient was a responder to resynchronization therapy in whom a clear increase in the LVOT VTI can be seen after CRT device implantation and during further follow-up. Also, note the change in the shape of the LVOT Pulsed wave Doppler trace: the trace is symmetric and triangular with a late peak during the low cardiac output state before CRT; it becomes more asymmetric with an early peak with improved LV function.

The change of pressure over time (d P /d t ) measured from a continuous wave Doppler trace of mitral regurgitation with a very low value in a patient with dilated cardiomyopathy.

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