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Archive for the ‘Hypertension’ Category

Next to the atmospheric pressure, the most curious pressure to understand is stored within the human circulatory system. Yes, it is the “blood pressure” fondly referred to as BP by both physicians and patients. (When worried men & women visit us and say, that they are suffering from BP, please make it a point to clarify, BP is a sign of existence of life, rather than a dreaded pathology ) 

Why should blood have pressure?

BP is lateral pressure exerted by flowing blood on the vessel wall (or is it the propelling pressure head ? It is to be noted, cuff pressure doesn’t measure this !) BP is generated by the heart in systole and sustained by the vascular system in both systole and diastole. BP is measured as mmHg. It can also be expressed as PSI(Pounds /sq Inch)  or Pascals or ATMs. If you allow me to spoil with some physics. Pressure is force per unit area ie Newton/m². So, pressure is essentially a force. Force is mass times the acceleration. Mass is weight independent of gravity, while the acceleration of blood is essentially the force of gravity added to the velocity of blood flow. If you think gravitational waves and planetary positions might influence the mass of blood (and hence the BP)  you may not be insane. (Environmental & astrological influence of BP and cardiovascular events need not a be mythology) (Oomman A,  J Indian Med Assoc. 2003 )     (Robert D Brook Cardiac clinic 2017)

How is it regulated?

Physics uttered at the bedside is sure to appear as nonsense for practicing physicians. Forget It. BP is not only a continuous variable, the neural, hormonal, cardiac control mechanisms are also in a dynamic flux. What we need to bother is, how to sustain a mean BP of around 90 mmHg within the human circulation, with robust autoregulation. (For the fellows in cardiology, it is a dangerously simplified teaching & belief  that cardiac stroke volume determines systolic BP and PVR determines diastolic BP) In fact, It is the systolic pressure that confers the energy required for diastolic BP. Regulation of BP is all about large vessel stiffness,  neuro-humoral tone of small vessels, water and sodium metabolism. This makes the kidney a central organ for long-term control of BP. It must also be emphasized BP is regulated in a regional and organ-specific manner. (Ex -The cuff brachial artery pressure may tell little about what is happening at the glomerular perfusion pressure )

Who are the guardians of BP?

Though general Physicians , Neurologists, Nephrologists even Endocrinologsts  have more geograhcial rights  cardiologists have largely taken siege over the entity of SHT because the heart happens to be a glamorous victim organ. We are witnessing an almost intoxicating number of cardiovascular trials on hypertension, right from Framingham’s days of 1970s to just released BP LLTC in 2021, trying to bring down cardiovascular risk. Based on the accrued evidence, the guardians of human  BP in various global institutions bring out strategies to reduce the risk of vascular injury. Have we succeeded in this  Intravascular number game.? I think we are. At what cost?

Two repeatedly asked two trivial questions 

  1. What is normal BP  &  When to start treatment?
  2. How much lower is best for our body?

Probably, we have got an answer for the first question from this Impactful publication. 

 

I think this study is trying to tell us, there is no normality for blood pressure in terms of risk reduction in cardiovascular disease. (Please recall, one JNC -Joint national committee  was dissolved after  including a controversial term pre-hypertension in healthy public  few years back) What will be the implication for this study? Its core conclusion is about 5 mmHg BP reduction across any subset of adult population will reduce CVD risk considerably. I am sure this study is so intense and powerful it will take at least a decade for its conclusion to fade away. So, can we make these funny conclusions? Hereafter we need not measure BP before starting treatment. Just administer drugs to any live adult who has blood & pressure. (J or U curve need a big debate later)

Mind you, sustained  5mmhg reduction* can be brought by any of the following habits. A salt moderated fruit-rich diet, reasonable physical activity, good sleep, a stroll in the park, yoga, a deep breath, having a pet, watching a movie in a quiet evening, having a loving  family, and so on so forth (Of course, 5mg Amlodipine, 40 mg of Telmisartan, or a  paradise device can do the same, with an add on pride)

*There is a big catch in this landmark paper. Read the title again. The important take-home point is that this 5mmhg lowering should strictly come by pharmacological means, not by any other means. (Correct me if I am not correct)

Final message 

We got the final answer from this marvelously done meta-analysis for the toughest question in cardiology. Hereafter  It’s going to be a celebration time for mankind, who struggle in a hypertensive world.

Post-ample

True, sustained high BP is a major risk factor for stroke, heart failure, and CVD. However, it is also true BP can’t* do much damage to the coronary artery without the help from its naughty cousins DM & dyslipidemia. All three parameters must be optimized in unison. May I propose a rough rule? It may be called DFL index for the collective CVD target.  Diastolic BP, fasting blood sugar and LDL all should converge around a unitless number of 70 to 80. 

*HT is a powerful risk factor for stroke and HFpEF. 

Reference

https://www.thelancet.com/action/showPdf?pii=S0140-6736%2821%2900590-0

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We know LVH and SHT go together . Mind you , this is not an Intimate relationship.

Widespread utilisation  of echocardiography  has revealed  , definite  LVH occurs only in about 20% (A guess !) of  HT . (Do you know in the Famingham study the incidence of LVH  after 12 year follow up was a paltry 3 % .Will you agree with that ? Mind you , It was in 1969 when Echo was not there )

What determines LVH ?  The clear answer is elusive. It is easy to escape  from the issue by calling it  multi factorial !

Why don’t you try this question .

My guess would be ,  magnitude ( or  even duration of HT !)  is  less important than genetic predisposition  or  associated diabetes ,  renal involvement.Our analysis from  hypertension clinic reveals LVH is many fold common in secondary HT  when compared to primary HT !

I often used to provoke the students by saying if the LVH is gross in HT it can not be primary , 9/10 times  ! Invariably  we find some  other  association or reason for the HT !

Link to related topic in this site

Why-lvh-does-not-occur-in-all-patients-with-systemic-hypertension ?

How-diabetes-modifies-lvh-due-to-hypertension ?

incidence of lV left ventricular hypertrophy framingham study

Next  . . .

How does LVH regress with treatment ?

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Systemic hypertension (SHT )  is the commonest  clinical entity encountered in cardiology consultations . 95 % of  HT is considered primary. The remaining 5 %  form the most important class of HT (Secondary to renal parenchymal, vascular , endocrine,  etc)

How  intelligent is this traditional classification of HT  ?

The incidence of primary and secondary  HT varies depending  upon the level of investigation we do . One of my  regular patient  who gets to me for  HT .He  is 42 year old man  works in financial institution  with lots of work stress and he was marginally obese as well .  He was investigated for all known cause of secondary HT and every parameter  was found to be normal and was being treated as   primary HT.

When he was about to leave my clinic he  bowled  this google !

Doctor , why do  you call  mine as  primary HT   ?  . . . When you yourself  say  my stress and weight is responsible for  high blood pressure ?

Primary vs secondary HT

Valid question is it not !  . .  . I told him   “somehow”  ,   we have not  been taught   in medical schools  , to consider stress  of life  as a factor  responsible for  developing secondary  HT !

Final message

Strange  definitions in medicine continue .  Not every one with high stress  levels develop HT  .There  are  some unknown factors operating  .Till we know that we  will keep calling them as primary HT .

( Who  knows the  man  who raised this question  may   show up  with adrenal hyperplasia  or a renal parenchymal dysfunction 5  years down the lane !)

We live by perceived  knowledge  on a moment to moment basis  ! . Ignorance  tries  to lock the doors of knowledge .

But we  continue to open new doors . That is the  only  purpose of medical research !

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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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