DILATED CARDIOMYOPATHY
There are multiple etiologies for dilated cardiomyopathy that fall into the general categories of ischemic and nonischemic (as given in the classificstion below this video)
Classification of Cardiomyopathy and Diseases Resulting in Acute or Chronic Left Ventricular Dysfunction
Dilated cardiomyopathy
Idiopathic cardiomyopathy
Familial cardiomyopathy
Noncompacted myocardium
Postpartum cardiomyopathy
Hemachromatosis
Infectious
Postviral myocarditis
Human immunodeficiency virus related
Legionella infection
Sepsis (gram negative)
Toxic cardiomyopathy
Adriamycin
Alcohol
Carbon monoxide poisoning
Other chemotherapy
High-output cardiomyopathy
Tachycardia-mediated cardiomyopathy
Thyrotoxicosis
Nutritional (beriberi, thiamine deficiency)
Peripheral left-to-right shunt lesions
Anemia
Hypertrophic cardiomyopathy
Asymmetric septal hypertrophy (idiopathic hypertrophic cardiomyopathy)
Obstructive vs. nonobstructive
Concentric hypertrophic cardiomyopathy
Isolated apical hypertrophic cardiomyopathy
Atypical hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Idiopathic
Infiltrative
Amyloidosis
Glycogen storage diseases
Hemachromatosis
Post-radiation therapy
Endocardial fibroelastosis
Other
Friedreich ataxia
Muscular dystrophies
Clinically, cardiomyopathies share a constellation of symptoms that can be present to varying degrees, including congestive heart failure, low-output state, fatigue, dyspnea, arrhythmias, and sudden cardiac death. Echocardiography serves as a definitive tool for establishing the presence and type of cardiomyopathy, may provide information regarding the specific etiology, and can be used to accurately track the physiologic abnormalities associated with the cardiomyopathy. The American College of Cardiology/American Heart Association guidelines for management of congestive heart failure consider echocardiography a Class I diagnostic test, implying that it is generally indicated and useful in all patients with congestive heart failure and suspected cardiomyopathy. Additionally, echocardiography and Doppler imaging can provide valuable prognostic information and serve as a guide to success of therapy.
Although the primary diagnostic features of dilated cardiomyopathy are left ventricular dilation and systolic dysfunction, other secondary features are nearly ubiquitous and substantially contribute to the development of symptoms. These include diastolic dysfunction with chronic elevation of left atrial pressure, secondary mitral regurgitation, and secondary pulmonary hypertension. The primary and secondary abnormalities seen in dilated cardiomyopathy are:
Echocardiographic Abnormalities in Cardiomyopathy
Left ventricular dilation
Increasing sphericity of left ventricular geometry
Apical and lateral displacement of papillary muscles
Functional mitral regurgitation
Left ventricular thrombus
Left atrial dilation
Atrial fibrillation
Left atrial thrombosis/stasis of blood
Pulmonary hypertension
Tricuspid regurgitation
Right ventricular dilation
The most common clinical presentation of dilated cardiomyopathy is congestive heart failure symptoms with shortness of breath and exercise intolerance. Depending on severity and duration, patients with dilated cardiomyopathy can present with New York Heart Association Class I to IV symptoms.
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The echocardiographic features of dilated cardiomyopathy parallel the primary and secondary findings were stated above. Left ventricular dilation is ubiquitous and a requisite component for establishing the diagnosis.
The degree of dilation can be mild or substantial with left ventricular internal dimensions of as large as 8.0 cm occasionally being encountered. The distribution of systolic dysfunction within the left ventricular walls is dependent on whether the cardiomyopathy has an ischemic etiology.
Classically, if an ischemic etiology is present, there will be greater regional variation in systolic dysfunction than if the process is nonischemic. It should be emphasized, however, that in documented nonischemic cardiomyopathy, there will be regional variation in the degree of systolic dysfunction, typically with the proximal portions of the inferoposterior and posterior lateral walls having preserved function when compared with other left ventricular segments.
As a consequence of dilation and systolic dysfunction, the left ventricle takes on a more spherical geometry that further contributes to the deterioration of left ventricular systolic function because the spherical geometry interferes with the contractile efficiency of the myocardial fibers.
Normally, the long axis dimension of the left ventricle exceeds the minor axis dimension (diameter) with a ratio of 1.6:1 or greater. With progressive dilation, the minor axis increases disproportionally, and the ratio of long to minor axis decreases.
Typically, a ratio (sphericity index) of less than 1.5:1 implies marked pathologic remodeling. The increasing spherical geometry results in apical and lateral displacement of the papillary muscles.
This has the result of effectively reducing the length of the mitral apparatus as compared with the anulus and results in secondary functional mitral regurgitation
Once the diagnosis has been established, it is clinically useful to quantify the degree of systolic dysfunction. Parameters that have diagnostic and prognostic importance include any of the linear- or area-based measurements of left ventricular size from which the derived parameters of fractional shortening and fractional area change can be calculated.
Additionally, the left ventricular cavity volume can be determined from several methods (the Simpson rule is the most often used) from which the stroke volume and ejection fraction can be calculated.
Other parameters of systolic function can be derived from Doppler echocardiography.
Of all the different modalities, those that have the most diagnostic and prognostic relevance include end-diastolic and systolic volumes and ejection fraction
There are several M-mode findings that provide diagnostic information in patients with systolic dysfunction. The first of these is the E-point to septal separation (EPSS) defined as the distance (in millimeters) from the anterior septal endocardium to the maximal early opening point (E-point) of the mitral valve.
Because the internal dimension of the left ventricle is proportional to diastolic left ventricular volume and the maximal excursion of the mitral valve in diastole is proportional to the mitral stroke volume, the ratio of the two dimensions will
be proportional to the ejection fraction.
As such, limited mitral valve opening (manifested by a greater distance between the E-point and the septum) is an indirect indicator of a reduced ejection fraction. The normal EPSS is 6 mm, with progressively larger EPPS representing a lower ejection fraction