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Posts Tagged ‘reanl hypertension’

                                Hypertension is the most common clinical  cardiovascular entity.Left ventricular hypertrophy (LVH) is  an important consequence of  HT.In fact, it is considered as a end organ effect or damage. Others being brain, kidney, and peripheral vascular disease.Knowing about LVH is important because it has been linked to increased cardiovascular events.

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                              Though LVH is considered  as a close companion of  HT  it is  surprising  only a minority (15-30%)  show evidence of LVH .Some  experienced clinicians (Level C evidence)  quote even lower < 10 %  .Traditionally LVH was detected by ECG and now it is replaced by echocardiography.

What determines the LVH ?

It will be suprising to note , answer to this question  is  still not  clear .

  • Is it the duration of elevated blood pressure ?
  •  Is it the absolute level of blood pressure ?
  • If so , is it  the systolic BP  , diastolic BP or the mean BP ?
  • Or is it related to the etiology of HT ?
  • There has been no significant correlation between the above parameters

When we don’t know  the answer to a question in medicine , the answer will  generally will be inside the genes !

So in HT also the major determinant of LVH is in the genes that determine the myosin heavy chain  response .

and also ACE gene polymorphism.ACE genes are involved in the expression of growth factors within the myocardium.

An excellent study  on the issue http://www.nature.com/jhh/journal/v17/n3/full/1001523a.html#tbl1

It implicates , gender, age, race etc in the genesis of LVH

Final message

So , the  myocardium does not respond with LVH   in all patients with HT.It happens only in a minority* .Duration of HT can be an important determinant , but  the major factor is  the alteration of genetic switches  within the myocytes How this switches are going to  behave ,  is largely inherited .Regression of LVH is also not uniform again implying lesser role for hemodynamics. (Some studies revealed ACEI have maximum regression  of LVH , later disputed )

*LVH is more consistently seen  in hypertension due to reno vascular  or parenchymal disorders .It is also an observed fact , a  combination of diabetes and HT is more likely to result in  LVH.

The other major issue  that needs explanation in HT/LVH  is   , how much of LVH is due to  myocyte hypertrophy perse  and how much is contributed by interstitial cell hypertrophy(Non myocytic hypertrophy)

This issue will be discussed soon

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Diuretics are the most commonly prescribed anti hypertensive agents.Thiazide diuretics which  was introduced many decades ago ,  lost popularity  in recent years ,  again got a second life after  the publication of ALLHAT trial recently. Now diuretics has become the  the drug of first choice in almost any hypertension unless any specific contraindication.

The most commonly used thaizide is hydrochlorthiazide ,and chlorthalidone.The blood pressure reducing effect is so consistent and smooth , all the currently popular molecules like ACE inhibitors and ARBs come with a combination with thiazide. While every one is clear diuretics are  effective anti hypertensive agent How it does is not clear.

How does a diuretic reduce blood pressure?

A. The exact mechanism is not clear. May not be uniformly effective in all patients  with HT.

B . Salt sensitive HT respond well to diuretics.

C. Volume correction /free water clearance might be a factor

D. Direct effect on vascular smoth muscle documented.The sodium transporter is blocked and  hence   calcium : sodium exchange is prevented .This depletes  intracellular calcium  in vascular smooth muscle cells .Less calcium for actin myosin interaction and hence vasodilatation

E. Thiazides combine well with all other antihypertensive drugs (ACEI, ARB, Beata blockers, calcium blockers)

F. Loop diuretics  like frusemide  can never be  a good antihypertensive agent.

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