dilated cardiomyopathy

what are the causes of dcm

idiopathic

genetic

infections

toxins(alcohol, chemo)

ischemic heart disease

what are the clincial symptoms of dcm?

fatigue

dyspnea

heart failure symptoms(fluid build up, swelling)

what are 8 different echo findings we will see if a patient has DCM?

LV abnormalities

LA enlargement

RV involvement

MV and TV abnormalities

Diastolic Dysfunction

Pulmonary Hypertension

Spontaneous Echo Contrast & Thrombus formation

GLS

what kind of LV abnormalities will we see and why?

LV dilation- increased LVED and LVES dimensions

Globally reduced systolic function- decreased EF <40%

thinned myocardium- due to chamber enlargement

increased LV volumes - higher edv and esv

reduced myocardial contractility- generalized hypokinesis (weak contractions)

why do we have LA enlargement and what might the patient also have?

due to chronic volume overload with possible afib

what would we see if the DCM is severe enough to affect the RV?

rv dilation

reduced rv systolic function

how do we assess rv systolic function

tapse

what kind of MV abnormalities will we see and why?

functional MR due to annular dilation and papillary muscle displacement

decreased mitral valve leaflet coaptation where the leaflets dont close properly

what kind of TV abnormalities will we see and why?

functional TR which is secondary to RV enlargement and annular dilation

****describe what we would see when there is diastolic dysfunction in dcm

decreased E/A ratio later stages - impaired relaxation due to worsening heart failure

increased E/A ratio early stages- restrictive filling pattern due to increased LV filling pressures

Prolonged IVRT

Pulmonary Hypertension

elevated PAP (doppler of TR velocity (>2.8m/s)

why do we have a prolonged IVRT?

since the ventricle relaxes more slowly, it takes less time for the pressure in the LV to fall before the MV opens

why does pulmonary hypertension happen in a patient with DCM?

as pressures rise in LV and LA (from added volume) the pressure backs up into the pulmonary veins, lungs and pulmonary arteries

why would we see spontaneous echo contrast?

"smoke - like " swirling in LV due to low cardiac output and stagnant blood flow

why would LV apical thrombus be common in severe cases?

its seen in the LV apex with contrast echo because blood is moving much more slowly

how would the GLS show in DCM

reduced GLS >-10% to -15% which indicates early myocardial dysfunction even before EF decreases

how do we assess GLS

"bullseye" pattern on strain imaging - shows diffuse hypokinesis