Introduction:
LVH is one of the commonest pathologies that is dealt in the day to day cardiology setup.
LVH which on ECHO appears just as thickened myocardium either symmetrical or asymmetrical.
MRI plays a vital role in deciphering the various causes of these LVH,
quantification of fibrosis if any,
along with LV morphometry.
MRI has a major role in prognostication and follow up.
Background:
LVH refers to an increase in LV mass,
is a pathophysiological condition which occurs due to primary and secondary extrinsic factors (hypertension,
valvular heart diseases and in athletes).
Physiological adaptation to chronically increased volume/pressure load results in LV remodeling.
There are other coexisting factors which contribute to disease progression and sudden cardiac death (refer figure 1). The presence of LVH is an independent risk factor for sudden cardiac death [1].
Therefore,
insights into the clinical presentation and diagnosis are essential for early diagnosis and management.
Causes of LVH (refer figure 2):
· Intrinsic/Primary: Hypertrophic cardiomyopathy (HCM)
· Extrinsic/Acquired:
a) Pressure overload: Hypertension (HTN),
subvalvular aortic stenosis (SAS),
aortic valvular stenosis,
Supravalvular aortic stenosis,
coarctation of aorta.
b) Volume overload: Aortic valvular regurgitation.
c) Infiltrative myocardial disease: Cardiac Amyloidosis,
Sarcoidosis,
Anderson Fabry’s disease,
Danons disease,
Iron overload cardiomyopathy,
Myocarditis,
Cardiac tumors.
· Exercise related: Athlete's Heart.
Pathophysiology:
Genetic and non-genetic factors influence hemodynamic and non-hemodynamic risk factors resulting in stimulation of protein synthesis and resulting in LVH.
1.
Hemodynamic risk factor:
Increase in pressure overload/afterload is the most important mechanical factor for increased stress on LV wall which stimulates myocardial collagen and fibroblasts,
remodeling of gap junctions,
ion channel and cytoskeleton resulting in structural changes (LV remodeling with fibrosis).
This is also reflected in coronary arteries reducing the flow reserve (refer figure 3).
2.
Non-Hemodynamic risk factor:
Main physiological response for fibrosis is linked to Renin angiotensin aldosterone system(RAAS) and increased cardiac sympathetic nervous system transmission (noradrenaline) (refer figure 4) [2].
Primary LVH (HCM) occurs due to myocyte and myofibrillar herringbone pattern disarray,
hyperchromasia,
interstitial fibrosis,
dysplasia of arteries [3].
LV remodeling results in three end results on LV myocardium (refer to figure 5):
Evaluation of LVH:
· Imaging modalities - refer to figure 6.
· Cardiac MRI protocol – refer to figure 7.
LVH APPROACH:
LVH - Imaging Definitions [4]
1.Thickening of the LV wall >12 mm (Measured at end-diastole on 3 chamber view).
2. Increased LV Mass normalized to body surface area (>113g/m2 in males and >95 g/m2 in females).