5.4 Echocardiographic features of dilated cardiomyopathy

Contractile dysfunction and impaired left ventricular ejection fraction are hallmarks of dilated cardiomyopathy. Dilatation of the ventricle is a compensatory mechanism to maintain an adequate stroke volume. Aside from the above mentioned features, patients with dilated cardiomyopathy may have several other abnormalities.

5.4.1 Contractile dysfunction

By definition, the ejection fraction is below 55%. Typically the ventricle is globally hypocontractile. However, there may be certain variations in the degree of regional dysfunction. Such differences may be partly explained by the geometry of the heart, myocardial mechanics, or regional variations in myocardial damage (i.e. myocarditis). Contractility is quite commonly better in the posterolateral region. Such variations in contractility make it difficult to distinguish between ischemic and dilated cardiomyopathy.

Video Platform Video Management Video Solutions Video Player Severely enlarged and hypocontractile left ventricle in dilated cardiomyopathy. Contraction is also dyssynchronous

In subtle and incipient forms of dilated cardiomyopathy, contractile dysfunction may be limited to the longitudinal component (see myocardial mechanics). As the disease progresses, other deformation parameters as well as torsion and diastolic untwisting will be affected.

Assessment of left ventricular function should include visual estimation of ejection fraction and, whenever possible, calculation of ejection fraction (biplane Simpson or 3D methods). Other parameters that may be used are fractional shortening (M-mode), calculation of contractility (dP/dt), or the Tei index.

5.4.2 Dilated left ventricle

The degree of left ventricular dilatation is highly variable and depends on the stage of disease as well as the severity of left ventricular dysfunction. In the acute phase, the ventricle is just mildly dilated or may even be normal in size because compensatory dilatation has not yet developed. Patients with additional volume overload (mitral or aortic regurgitation) tend to have larger ventricles. With progressive dilatation the ventricle assumes a more spherical shape.

Video Platform Video Management Video Solutions Video Player Spherical geometry of the left ventricle in a patient with a severely dilated left ventricle. Note that septal motion is biphasic (dyssynchrony).

5.4.3 Thin myocardial wall

The left ventricular wall in typical dilated cardiomyopathy is rather thin. However, as the left ventricle is enlarged, the total left ventricular mass may be increased.

The thickness of the septum may be increased in patients with left ventricular hypertrophy who develop dilated cardiomyopathy.

5.4.4 Dyssynchrony

When individual myocardial segments contract at different points in time, the condition is referred to as an abnormal contraction pattern or left ventricular dyssynchrony. Dyssynchrony may not be limited to the ventricle (intraventricular dyssynchrony), but may also occur between the right and left ventricle (interventricular dyssynchrony). In this case, blood is ejected from the left ventricle (aortic flow) much later than it is from the right ventricle (pulmonary flow). There is overwhelming evidence for the damaging effects of dyssynchrony on the heart. Dyssynchronous contraction is inefficient in respect of hemodynamics as well as "energy expenditure". It results in further deterioration of cardiac function. Detection and assessment of dyssynchrony in patients with heart failure is very important because these patients may benefit to a great degree from cardiac resynchronization therapy (CRT).

Specific pacemakers with placement of an additional lead into the coronary sinus permit cardiac resynchronization (CRT) in patients with dyssynchrony.

This section will provide a basic overview of dyssynchrony while Chapter 23 (Echocardiography and Resynchronization Therapy) will address specific indications for cardiac resynchronization therapy, the role of echocardiography in selecting patients, and how to optimize settings in CRT systems.

Dyssynchrony is caused by delayed electrical conduction. This may occur in various situations:

• bundle branch block
• right ventricular (or single chamber) pacing or
• during ectopic ventricular beats.

5.4.4.1 Dyssynchrony and bundle branch block

By far the most common cause of dyssynchrony is complete left bundle branch block.

Dyssynchrony occurs less frequently in right than in left bundle branch block.

Left bundle branch block is a common finding in patients with dilated cardiomyopathy. It is present in approximately one third of patients. The likelihood of developing a left bundle branch block increases with the severity of left ventricular dysfunction. More than one half of patients with severely reduced left ventricular function have a left bundle branch block.

The wider the QRS complex, the more frequent and severe is dyssynchrony.

There are several ways to detect dyssynchrony on the echocardiogram. Experienced investigators can detect abnormal contraction patterns simply by observing the motion of the left ventricle on the two-dimensional image. On a four-chamber view the ventricle will show a "hula hoop" or rocking motion.

Video Platform Video Management Video Solutions Video Player Dilated cardiomyopathy in a patient with a very wide (180 ms) left bundle branch block (LBBB) and distinct dyssynchrony. The ventricle shows rocking motion.

The motion of the septum is often biphasic and will demonstrate rapid early systolic inward motion. This is followed by contraction of the lateral wall. A second inward motion of the septum may be observed very late in systole. This may also be observed on a short-axis view of the ventricle.

Not all patients with dyssynchrony have the same contraction pattern.

The delay between contraction of the septum and the posterolateral wall (SPWMD) is also seen in the M-mode.

Video Platform Video Management Video Solutions Video Player M-mode tracing showing dyssynchrony between the septum and the posterolateral wall (septal to posterior wall motion delay = SPWMD). The inward motion of the septum occurs long before that of the posterolateral wall

A very simple way of assessing dyssynchrony is to measure electromechanical delay: one measures the delay between the onset of the QRS complex and the start of the LVOT signal on a PW spectral Doppler tracing. Significant dyssynchrony is present when the interval is longer than 140 ms.

Several other echo modalities permit detection and quantification of dyssynchrony (see table).

Modalities Tissue Doppler imaging (PW) Contraction delay between different segments; index of dyssynchrony Tissue Doppler imaging (M-mode) Timing of events Speckle-tracking echocardiography Time to peak regional strain PW Doppler measurements of dyssynchrony Electromechanical delay (intraventricular delay)
Interventricular delay
Timing of diastole Three-dimensional echocardiography Contraction delay between different segments; dyssynchrony index M-mode Septal to posterolateral wall motion delay

The application of these techniques will be discussed in Chapter 23: Echocardiography and resynchronization therapy.