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What determines LVH in systemic hypertension ?

Posted in Cardiology -Mechnisms of disease, Cardiology -unresolved questions, Clinical cardiology, Hypertension, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , on October 28, 2013| Leave a Comment »

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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2013 ESC hypertension guidelines : A final attempt to infuse common sense !

Posted in cardiology -Therapeutics, Cardiology hypertension, Uncategorized, tagged , , , , , , , on July 31, 2013| Leave a Comment »

Hypertension is  probably the most   important clinical entity for physicians
for decades .With the advent of modern interventional cardiology management of HT with  drugs have become a  less glamarous job for us. Still , the quantum of the problem and it’s impact on the  risk of CAD and progression   remain a major issue.
There many  different bodies periodically coughing  up guidelines  to manage HT.
  1. JNC from USA
  2. British Hypertension society from UK
  3. European society of cardiology
  4. World hypertension league
  5. Finally WHO guidelines* ( It is not a regular exercise ,WHO releases it  as and when it feels like !)

The stakes are high for the drug industry .Anti hypertensive drugs are the  major source of revenue  to them . Any dip in per capita consumption will have direct impact on their health ! ( WHO bothers about public health ? )

The so called scientific  guidelines,  are generally made balancing patients health vis a vis drug companies health .I have found more often than not it was tilted towards the industry .

The fact that there are multiple guideline with varying impact factors makes sure the confusion among the global physician intact . This is one of the aims of the pharma companies as they influence heavily  when to initiate the treatment ,  and what we are  supposed to prescribe.
Some of the guideline are notorious for insinuations . One example was about the definition of pre hypertension  few years ago .It has since been removed  from the literature after a critical debate .

* One may wonder why I’m focusing always  on non scientific  issues more than academics .(I some how feel non scientific factors are going to impact our health more than any other factor in the coming  generations  )

Now is the beginning of a balance .

European society of cardiology 2013 guidelines for hypertension
Among these guidelines  I would  think  ESC is close to reality and fairness.
Even    it was carrying dubious advices till recently .Now they have come out with new one in 2013.Most changes are  welcome.
  1. It is essentially about cleansing the contaminated guidelines
  2. Removing unnecessary medications
  3. Unified definition.
  4. More efforts to identify true secondary HT
The salient  points
There are  18 point update in the ESC 2013 . All of them are great . Essentially they are about the basics we have been  taught as we learnt in our final year MBBS. (The rest of our life we have to unlearn  the junk we have accrued over the years  from various CMEs )
I can modify it and  short list
  1. Do not start too early .Have universal definition (Now 140mmhg)
  2. Respect non drug treatment ,( However attractive the  gold tipped pen the  representative leaves  in your consulting suit !)
  3. Avoid using multiple drugs
  4. Never miss a secondary HT .( If  diastolic BP> 110mmh almost always a renal component would be there .Remember Conn syndrome (Primary aldosteronism )  is 10 times more common than much hyped pheochromocytoma ! Just do K+ levels to detect this )
  5. In CAD patients never treat HT in isolation .( Measure blood pressure with sugar and  lipid 120 /70 mg of LDL )
ESC 2013 is a commendable Initiative . It has  tried to remove most errors of the past .obviously  the pharma industry will be unhappy as it will definitely bring down  total drug consumption the  population.
Final message
HT  is an important target  for prevention and management of CAD
Thanks to the much maligned pharma industry  .
We have good drugs.Use it judiciously . Try to reduce the number of drugs .
If possible make them drug free.
If a patients taking   beta  blocker for associated  cardiac condition do not add another anti HT drug . (Recall  from your distant memory , beta blocker is a anti HT drug too !)
Simply follow common sense . (* If you think you  lack  it  ,  get  it from your learnt patients .Many  of them have in plenty . I often do that . One  question they keep asking  “Should I take this drug  life long doctor ?”  is a definite common sense booster!  )

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The most important article on hypertension ever to be published :Loose cuff hypertension !

Posted in Cardiology - Clinical, Cardiology hypertension, Uncategorized, tagged , , , , , , , , , on November 13, 2010| Leave a Comment »

Blood pressure  measurement ,   probably  is the commonest investigation done  in our patients  in  the entire field of medicine . It is such a common thing ,  both physicians  and patients  fail to perceive  it as  an investigation . (It indeed is !)

Even though BP is  considered as a  clinical sign , measuring it requires a device called sphygmomanometer  . The BP apparatus has to be properly calibrated  with the mercury  , the tubing, the bladder  , inflation balloon  etc   need to be perfect.

The following fallacies are noted in the measurement of  blood pressure . Some of them are rampant* !

Patient

  • Posture of recording
  • Anxiety -White coat /Gender

Device

  • Cuff width/Length
  • Arm circumference

Ocular errors

It is surprising , such an important tool has a scale of 2mm markings which is prone for parallax errors of light with  mercury column undulating .

Physician factors*

  • Hasty cuff syndrome , Rapid deflation .
  • Absent minded recording – Failure to note phase 4 to phase 5  due to inattention
  • Failure to hear phase 4 muffling  (Aging  medico  -Auditory insufficiency !)

It is  not at all  surprising  to note,   two BP readings rarely match ,  even if it is recorded by the same person with  same machine at the same time !

There are many  articles that describe in detail  ,  how to record blood pressure properly. But this article from  a relatively unknown  journal   from Purdue university  ,  tells  us  most   scientifically  , what  has been taken for granted  by the medical  community for so long  .

Loose cuff  hypertension (Link to the journal of  Cardiovascular engineering )

How much  stiffness  is to be applied in  the arm for optimal pressure recording ?

What is the incidence of hypertension due to  loose cuff  ?

Final message

The BP apparatus ,  though appears  as  an   innocuous   machine ,   the readings  that emerge  from it  determines ,  how millions of our fellow human beings are going to be labeled  ! ( High pressured  humans ,  slaves to  anti hypertensive  drug marketeers    for  rest of their  life ) .

So , realise  how important  it is , to measure  the blood pressure properly    !  Never be casual . . . with  this  machine .

Experience has taught us ,  while  it is very easy to name an  individual  wrongly as hypertensive  , it  often needs  Herculean  efforts  to remove this medical tag from their neck . The reasonings  are  many .( Academic , non academic and patient factors included )

Finally , in this funny planet  it is  a personal observation ( Or is it  an imagination ?)    some  men and women   tend to  enjoy  ,   being  referred to  as  high pressured !   Loose cuff  or tight cuff   ,  it simply do not bother them  !

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Why LVH does not occur in all patients with systemic hypertension ? ?

Posted in Cardiology -Mechnisms of disease, Hypertension, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , on September 7, 2009| Leave a Comment »

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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What determines left ventricular hypertrophy in patients with hypertension ?

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , on December 9, 2008| Leave a Comment »

                                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.

lvh-4

                              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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What is intracoronary and intracerebral hypertension ?

Posted in Cardiology - Clinical, cardiology -Therapeutics, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , on November 14, 2008| Leave a Comment »

                    circulatory                                                                            A normally  functioning  circulatory system is vital for our survival . We have about 6000 ml of  blood, circulating  all over the  body in an  approximate time of 15-20 seconds.The pressure at which this blood moves across the body is called the blood pressure . Hypertension  or simply , high blood pressure is an undesirable  hemodynamic disturbance  in human circulatory system.Systemic hypertension is the most common type of hypertension. The blood pressure is primarily  dependent  on the status of the blood vessel(vascular resistance)  and cardiac contractility. This regulation is under  many neural and hormonal factors.Further  the blood pressure varies depending  upon the blood vessel calibre, and the local milieu.There is a progressive drop in blood pressure from major arteries to the small arteries .The pressure drop is maximum  across the arterioles to reach the venules .The venous circulation has the lowest pressure, it ends up at right atrium with a mean pressure of 0- 5mmhg.

Importance of regional variation of blood pressure.

It should be realised  ,  each organ has it’s own regulated blood pressure.The brain  perfuses by the  intracerebral pressure .The lungs decide how much should be the pulmonary arterial pressure.The kidney not only controls it’s own pressure but also  has a major regulatory role in  systemic pressure by rennin angiotensin system.The examples are numerous, portal system has it’s unique pressure controlling hepatic hemodynamics. The  retinal blood vessels regulate  intra ocular pressure. While the human  circulatory system has a wide variation of blood pressure  across the breadth and length of vascular system,  it is ironical a single snap shot BP with a brachial cuff is used  to define the normality and if it is normal every thing is thought to be  hunky dory !

 

 

It is widely acknowledged now , aging of humanity  is nothing but aging of our vascular system

                                    So we should have new parameters to assess individual organ’s vascular health as well as the currently popular systemic vascular health.The single important factor that determine coronary endothelial damage is the intra coronary pressure.It is never taken into account in any of the cardivascular mortality studies. This is the prime reason for  the widely prevalent conflict in the cardiology literature , namely : Controlling systemic  blood pressure has poor correlation with  cardiovascular outcome. Many of the so called normotensive individuals  have serious hemodynamic injury in their  coronary arteries.This was made apparent in the  ASCOT LLA  study , in which patients with  near normal blood pressure also benefited from statin therapy , implying  endothelial damage could occur at any level of systemic blood pressure.

What is the normal intracoronary pressure  ? When do you diagnose intracoonary hypertension?

The normal intracoronary pressure is around 40mmhg . Intra coronary hypertension as a clinical entity  is yet to be  recognised . There is no defintion available for intracoronary HT  , intracerebral hypertension as well. 

It’s still a  long way to  go , for the cardiology and neurology  community to assess non invasively  intracoronary pressures and  intra cerebral arterial pressure to prevent  coronary events ant strokes.

Final message

Simple risk prediction using brachial cuff blood pressure is a grossly unscientific method (Sorry, i really mean it ) to assess one’s vascular health.There has been  few attempts like vascular endothelial health assessment by fore arm blood  flow , central aortic pressure (Instead of brachial cuff pressure) as an  index for risk predictment and  assessment for hypertension is suggested.

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Systemic hypertension: The untold story !

Posted in Cardiology - Clinical, Cardiology-Land mark studies, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , on November 3, 2008| Leave a Comment »

 

Is it true , once a patient is labelled as a hypertensive he remains  hypertensive life long ? Is it possible to withdraw antihypertensive drugs  permanently ?

  • Systemic  hypertension is the most common clinical entity and it forms the bulk of the physician consultations world over.
  • The anti hypertensive drugs are  one of the most commonly  prescribed medication  by the medical professionals .
  •  It is estimated , the major chunk of  revenue to pharma industry is contributed by antihypertensive  drugs.
  •  SHT , is being maintained  as a  major , global cardiovascular risk factor , by  periodically refixing the target blood pressure  to lower levels  by various committees.
  • The terminology of pre hypertension for blood pressure between 120-140 was hugely controversial    and some societies refused  to accept this entity.

Is there a case for withdrawal of anti hypertensive agents  among our patients ?

Yes , in fact there is a strong case for it.

While on the one hand there is a sustained effort ( By whom !)  to increase the drug usage , very early in the course of hypertension , there is also a silent progress in our knowledge ,  regarding withdrawl of anti hypertensive agents in all those undeserving patients .

It is estimated 42% *of the so called hypertensives especially elderly can be successfully weaned of anti hypertensive drugs with out any adverse effect.( Mark R Nelson BMJ. 2002 October 12; 325(7368): 815.)

What are the situations where we can successfully with draw anti hypertensive drugs?

  • The most common group of patients  are the ones, where  the anti hypertensive drugs are  started prematurely , with out giving an option for non drug life style  approach.These patients and their physicians continue to believe , anti HT drugs are sacred and essential !
  • There is another  major group of patients who have had a temporary  elevation of BP due to a stressful environment.These patients  get drugs permanently for a temporary problem . These patients need  to be reassessed.
  • Some of the elderly  patients,  with the onset of  age  related autonomic dysfunction ,these  drugs are poorly tolerated and  even have  disastrous effects .In this population  it is desirable , to wean off the anti HT drugs  and switched over to life style  medication whenever possible.

Final message

Essential or primary hypertension is not a permanent  disease, in bulk of our population. It reflects the  state of  the  blood pressure on a day to day basis  and is a continuous variable. All patients who have been labelled as hypertensives( Either by us or others) should be constantly reviewed  and considered for withdrawal of the drugs if possible.

* Note this rule does not apply in all secondary hypertensions, during  emergencies, uncontrolled hyper tension with co existing CAD /diabetes /dyslipidemias etc .

Please refer to these forgotten Landmark articles

Does Withdrawl of Anti hypertensive Medication 

Increase the Risk of Cardiovascular Events?

The TONE study

Source: The American Journal of Cardiology, Volume 82, Number 12, 15 December 1998 , pp. 1501-1508(8)

http://www.ncbi.nlm.nih.gov/pubmed/9874055

Conclusion of TONE study

The study shows that antihypertensive medication can be safely withdrawn in older persons without clinical evidence of cardiovascular disease who do not have diastolic pressure > or = 150/90 mm Hg at withdrawal, providing that good BP control can be maintained with nonpharmacologic therapy

 

Some of the references for successful withdrawl of antihypertenive drugs

1.Nelson, M; Reid, C; Krum, H; McNeil, J. A systematic review of predictors of maintenance of normotension after withdrawal of antihypertensive drugs. Am J Hypertens. 2001;14:98–105. [PubMed]
2.
Wing, LMH; Reid, CM; Ryan, P; Beilin, LJ; Brown, MA; Jennings, GLR, et al. Second Australian nationalbloodpressure study (ANBP2): Australian comparative outcome trial of ACE inhibitor- and diuretic-based treatment of hypertension in the elderly. Clin Exp Pharmacol Physiol. 1997;19:779–791.
3.
Lee, J. Odds ratio or relative risk for cross-sectional data. Int J Epidemiol. 1994;723:201–203. [PubMed]
4.
Lin, D; Wei, L. The robust inference for the Cox proportional hazards model. J Am Stat Assoc. 1989;84:1074–1079.
5.
Veterans Administration Cooperative Study Group on Antihypertensive Drugs. Return of elevated blood pressure after withdrawal of antihypertensive drugs. Circulation. 1975;51:1107–1113. [PubMed]
6.
Medical Research Council Working Party on the Management of Hypertension. Course of blood pressure in mild hypertensives after withdrawal of long term antihypertensive treatment. BMJ. 1986;293:988–992. [PubMed]
7.
Alderman, MH; Davis, TK; Gerber, LM; Robb, M. Antihypertensive drug therapy withdrawalin a general population. Arch Intern Med. 1986;146:1309–1311. [PubMed]
8.
Blaufox, MD; Langford, HG; Oberman, A; Hawkins, CM; Wassertheil-Smoller, S; Cutter, GR. Effect of dietary change on the return of hypertension after withdrawal of prolonged antihypertensive therapy (DISH). J Hypertension. 1984;2(suppl 3):179–181.
9.
Mitchell, A; Haynes, RB; Adsett, CA; Bellissimo, A; Wilczynski, N. The likelihood of remaining normotensive following antihypertensive drug withdrawal. J Gen Intern Med. 1989;4:221–225. [PubMed]
10.
Myers, MG; Reeves, RA; Oh, PI; Joyner, CD. Overtreatment of hypertension in the community? Am J Hypertens. 1996;9:419–425. [PubMed]
11.
Stamler, R; Stamler, J; Grimm, R; Gosch, F; Dyer, R; Berman, R, et al. Trial of control of hypertension by nutritional means: three year results. J Hypertens. 1984;2(suppl 3):167–170.
12.
Takata, Y; Yoshizumi, T; Ito, Y; Ueno, M; Tsukashima, A; Iwase, M, et al. Comparison of withdrawing antihypertensivetherapy between diuretics and angiotensinconverting enzyme inhibitors in essential hypertensives. Am Heart J. 1992;124:1574–1580. [PubMed]
13.
Whelton, PK; Appel, LJ; Espeland, MA; Applegate, WB; Ettinger, WH; Kostis, JB, et al. Sodium reduction and weight loss in the treatment of hypertension in older persons: a randomised controlled trial of nonpharmacological interventions in the elderly (TONE). JAMA. 1998;279:839–846. [PubMed]
14.
Heart Outcomes Prevention Evaluation Study Investigators. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on death from cardiovascular causes, myocardial infarction, and stroke in high-risk patients. N Engl J Med. 2000;342:145–153. [PubMed]
15.
Howes, L; Krum, H. Withdrawing antihypertensive treatment. Curr Therapeutics. 1988;November:15–20.
16.
Fotherby, MD; Harper, GD; Potter, JF. General practitioners’ management of hypertension in elderly patients. BMJ. 1992;305:750–752. [PubMed]
17.
Jennings, GL; Reid, CM; Sudhir, K; Laufer, E; Korner, PI. Factors influencing the success of withdrawal of antihypertensive drug therapy. Blood Press Suppl. 1995;2:99–107. [PubMed]

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