
4 AJTCCM VOL. 30 NO. 1 2024
ORIGINAL RESEARCH: ARTICLES
injury, contribute to these conditions.
Secondary DCM occurs as a result of any
myocardial insult that causes LV failure
and subsequent ventricular enlargement.
Secondary causes include alcohol abuse,
ischaemic heart disease, hypertension,
infectious myocarditis (e.g. viral, parasitic
or bacterial), drug-induced myocarditis
(e.g. anthracyclines, cyclophosphamide,
heavy metals), peripartum cardiomyopathy,
metabolic, endocrine or haematological
disorders, infiltrative diseases such as
sarcoidosis, and collagen vascular diseases.[4,6]
A diagnosis of primary or idiopathic DCM is
established only aer the exclusion of known
secondary causes. We included patients
with suspected or conrmed DCM in our
study only aer comprehensive exclusion of
secondary causes.
e primary investigations used for DCM
evaluation are echocardiography and CMR.
Transthoracic echocardiography is generally
the initial diagnostic modality employed.
It is able to detect chamber dynamics,
valvular motion, and gross morphological
and functional anomalies. However,
several factors, such as the experience of
the operator, a smaller field of view and
unfavourable patient body characteristics,
limit its imaging capability. Transoesophageal
echocardiography is not limited by a
restricted field of view, but is an invasive
technique.[7] Also, neither echocardiographic
technique enables tissue characterisation of
the myocardium.
CMR is a valuable technique for the
diagnosis and prognosis of patients with
DCM. It provides high spatial and temporal
resolution, enhanced so-tissue contrast, and
improved cardiac tissue characterisation.
CMR has therefore been established as
an essential non-invasive tool for the
comprehensive evaluation of patients with
DCM.[8]
Findings at CMR include global
enlargement of the LV or both ventricles
and systolic dysfunction (decreased ejection
fraction <40%). e ventricular enlargement
is usually uniform with normal wall
thickness. e EDV (≥140 mL) and ESV are
elevated.[9,10] In our study, all the patients had
variable degrees of cardiomegaly; 85% had
systolic dysfunction with a reduced LVEF
and elevated LV EDV.
Wall motion abnormalities are also
seen in DCM, generally in the form of
global hypokinesis. Valvular dysfunction
is frequently evident as a result of chamber
expansion and annular strain. Ventricular
thrombus may be a problem in patients with
DCM because of diminished wall mobility.
[10] In our study, 95% of the patients had
contractile dysfunction. Valvular dysfunction
was seen in 85% of the patients. None of the
patients had an intracardiac thrombus or clot.
CMR makes it possible to differentiate
between ischaemic cardiomyopathy and
idiopathic DCM. DCM shows either no
abnormal enhancement[11] or curvilinear mid-
myocardial or subepicardial LGE, unrelated to
A B
C D
Fig. 1. A 55-year-old woman with primary dilated cardiomyopathy. (A) Two-chamber cine two-
dimensional steady-state free precession and (B) morphological T2-weighted black blood four-
chamber long-axis images acquired at 3-Tesla show a markedly dilated le ventricle. e calculated
le ventricular end-diastolic volume was 256 mL. e patient had severely decreased le ventricular
systolic function (le ventricular ejection fraction 19%). (A) also shows mild pericardial eusion.
Late-enhancement short-axis (C) and four-chamber long-axis (D) images show abnormal mid-
myocardial late gadolinium enhancement in the interventricular septum (arrows).
A B
Fig. 2. A 40-year-old man with primary dilated cardiomyopathy. (A) Le ventricular outow tract
steady-state free precession and (B) four-chamber long-axis steady-state free precession images
acquired at 3-Tesla show a markedly dilated le ventricle (le ventricular end-diastolic volume
339 mL). e patient was clinically symptomatic and had severely decreased le ventricular
systolic function (le ventricular ejection fraction 26.5%). No abnormal delayed enhancement
was seen with gadolinium administration.