Left ventricular hypertrophy (LVH) is one of the most common structural heart disease.Systemic hypertension, aortic valve disease are responsible for the bulk of the cases .Some of the LVH occur due to cardiomyopathy (HCM/Non HCM variants).Athlete’s heart is a physiological response to exercise and it is largely a normal entity.
How many patients with SHT develop LVH ?
It is surprising to note , not every patient with SHT develop LVH .In fact estimates suggest only about 30-40% of chronic hypertensive individuals develop SHT .
What are the determinants of LVH in SHT ?
- Magnitude of systolic pressure
- Magnitude of diastolic pressure
- Pulse pressure
- Duration of SHT
- Age
- Gender
- Body weight/Obesity
- Effect of treatment
While any of the above factors may operate in determining LVH
none of the above are important than this
“Genetic susceptibility ”
The myosin isoforms are determined by the genes .The re expression of fetal isoforms in adults is responsible for LVH in many .This is determined by the genetic homogeneity
LVH in renal disease
Secondary hypertension due to renal dysfunction is a major determinant of LVH. This is espcially true if the pateints are dialysis dependent.The mechanism are not clear .
Diabetes and SHT : LVH friendly forces
When diabetes alone and SHT alone is less likely to result in LVH the combination of these two entities greatly increase the likely hood of LVH.DM induced microangitis amplifies the after load effect of HT and result in early LVH.Further this LVH is different from pure forms of hypertensive LVH in that the interstitium goes for hypertrophy and in some cases neovascualrisation. In hypertensive LVH it is predominately myocyte hypertrophy with little interstitial proliferation. this has important therapeutic implication as any drug which reduce the blood pressure can regress pure myocytic hypertrophy, while in diabetic LVH regression is difficult to achieve .
Lipid levels inversely related to LVH ?
There is no consistent relation between lipids and LVH .Occasional reports suggest a negative correlation.
Which LVH is associated with diastolic dysfunction ?
It is a well known fact , LVH has major effect on LV diastolic function.But it is also a fact only some forms of LVH develop this. Now it is clear only if the interstitial hypertrophy occur diastolic dysfunction is manifested. Even as the as the hypertrophied myocyte continue to relax the interstitium do not have molecular mechanisms to relax .Hence, as discussed earlier , diabetic hypertensive patient often develop diastolic dysfunction .
Final message
LVH is not a simple expression of raised after load.It has major non hemodynamic determinants which if identified , could have important therapeutic implication.
Coming soon . . .
Can coronary artery disease induce LVH in the absence of SHT or DM ?
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