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Archive for November, 2008

                                            The science of medicine has evolved over 2000 years since the stone age days.It has  currently reached  a glorious era with  cutting edge  scientifc  technology .Today  one can map the entire human genetic blue print and intervene in the  disease  even before they manifest .One can   keep dying people alive for years with multi organ transplantation. Modern medicine has taught us  how human sufferings can be prevented and life can be prolonged (with or without purpose !)

The term conservative management  conveys two different

meanings for medical professionals.

conservativ-3

For other group of physicians

 

conservative-4

                         

                             Ever since the days of  application of leech over the  head for treating migraine and a crude knife abdominotomy for emergency exit of babies from  pregnant mothers in distress  , healer’s   mind has always  perceived “something  has to be done  urgently when some body suffers”  this sort of  reaction is probably  inherited  and is related to  the primitive flight or fight response .

This may be true in  some of the emergencies but it is untrue in many of the non emergencies.

                                          Unfortunately ,  our mind  finds it difficult   to differentiate  between these  situations . With constant exposure to dramatic medical breakthroughs , modern day physician is made to believe   “Some thing  is always  better than nothing  when illness strikes. Human body is a wonderful machine which has it’s own service station ! in the form autoregulation  and the meticulous  homeostatic mechanisms. Only if the disease process overwhelms,  it needs intervention.( Typical example:In the routine viral fever , you don’t adminster Acyclovir or other antiviral  for all of them !

                                        The problem with early aggressive approach is,  it fails to give an oppurtunity  for the body’s natural defence forces  to respond. Further , we will  never ever know how the administered treatment is going to fare vis a viz the natural response.( With due respects to RCTs).   While the field of medicine   has  so much  evolved , our thought process,  especially  the  aspect of clinical  reasoning  has always been lagging behind .It is now considered  as inferior or even unscientific  treatment  if  some one follows a conservative approach to a problem even if  it  provides   same outcome of that of an invasive or aggressive approach ( The classical example is PCI for chronic stable angina The COURAGE study).

The other major issue is the hazards of unwarrnted  invesitigations , drugs and procedures

Classical example:No one knows how much morbidity or mortality the routine Swan ganz catheter  caused when it was rampantly used for over two decades to monitor central venous pressure .It is estimated  that in modern medicine  there are at least  few  drugs or devices  in each speciality waiting  for the same fate  as that of  the swan ganz catheter.

No body knows when it will be exposed .Our EBM will take it’s own time . . .Till that time humanity need to suffer.

This thinking is not new  The concept  “First do no harm is over 2000 years old”

hippocrates-primum-non-nocere

Questions in search of answers

 Does law of conservation of energy applicable to human body and medicine  ? 

 Can we defy death with modern medicine ?

Final message

  • Conservative management is still  a great medical concept  in many situations  and one should not allow it to die  by the whims and fancies of the modern scientific forces.
  • Whatever you do on the patent’s body  do it ,  only if it is going to helpful for him /her. If you are unsure  Whether a given  treatment  is going to help or not ask this question to an expert .
  • The widely prevailing  dogma  of aggression is always better than  non aggression  has absolutely no evidence.
  • So approach a clinical issue disease by disease ,  individual by individual.
  • Now , in this era  high tech  medicine  ,  It is lot more tougher to choose a conservative path as the pressure to do more and more  looms  larger ! It is easier to follow the crowd  than a path of your own .
  • Always remember it needs a  stronger  mind to  act according to our conscience !

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                    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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                                        Angina pectoris , classically occur on exertion and gets relieved on rest .This is called typical chronic stable angina as described by Heberden (CSA ) .  Unstable angina(UA), the term originally described by Noble O Fowler in early 1970s. ( Also being referred as  intermediate coronary syndrome , preinfarction angina etc).The definition for unstable angina has evolved  over the years  and currently  refers to .

 1.All new onset angina of any degree* Some include severe angina only ! New onset angina of very mild degree on exertion could be the onset of the first episode of  stable  angina. 

 2.Rest angina of more than >30 mts not relieved by taking sublingual nitroglycerine.

 3.All Post MI angina

 4.Any angina in patients who have been stented by PCI.

How to recognise a patient  who is shifting from  stable angina to  UA ? 
UA is  to be suspected when  a patient develops. 
5.More frequent episodes than usual
6.Angina occurring at lesser level of exertion than before 
7.Angina radiating to new site ( Example : Chest pain radiating  to jaw rather than to the usual left arm or vice versa)

Why the first episode of angina is given a special status and often considered critica ?

Angina is the  clinical expression of   myocardial ischemia.The course of  the  first  episode of angina , can not be predicted.It could be a the beginning of a chronic disease process, or it could be a progressive coronary occlusion as in unstable angina /NSTMEI , or the onset of even a STEMI.
In contrast a patient with chronic stable angina  has a predictable chest pain , at a particular level of exertion, radiation to same site, same character, and the patient knows for sure the pain  would promptly dissappear  when he takes rest or nitroglycerine  tablets.

What is the underlying pathology in UA ?  

Generally it is very rare for  a stable plaque to produce a  serious episode of unstable angina .It  requires  an unstable plaque* to  precipitate an unstable angina !
Unstable plaque refers to any plaque which is eroded, fissured, ruptured or  hanging  eccentrically ,  with
an active thrombus.

What is the significance of post PCI angina?

It is an irony, any angina following PCI is to be considered unstable as sudden occlusion of stent is quiet common.This is a paradox of sorts as one would wonder in a patient  with CSA who undergoes PCI with stenting  of left anterior descending coronary artery  (LAD)  all his subsequent episodes of angina  will be labelled as UA  even if a stable angina occur in his other coronary artery.And these patients would go for early invasive approach and potentially inappropriate interventions even if they are at low risk !

Is all angina at rest can be termed as unstable angina ?

No, but many times ,  rather most of the times  cardiologist believe all rest angina to be unstable.

What are the situations where stable angina can occur at rest?

An episode of angina during mental stress, or post prandial* state are very common in patients with CSA. This gets relieved after the stress. Some times  patients with CSA during episodes of fever may get angina at rest .These are considered variants of stable angina.
Post prandial angina , may be considered by some as unstable

How often a diagnostic confusion occur between CSA and UA ?

Generally, this issue is rarely addressed in cardiology literature , for the  simple reason it is never considered an  issue at all !
According to Canadian cardiovascular society grade 4 stable angina  is almost similar to unstable angina , as it denotes angina occurs with minimal effort or even at rest. In fact CCSC grade 4 should be termed as UA.

Can ECG be useful to identify stable angina from unstable angina ?

                                    ECG will some times  come to our rescue when one is confused between stable and unstable angina even though resting ST depression can occur in both stable and unstable angina . Statistically , if ST depression is noted during an episode of angina it is more likely to be UA rather than CSA. . Apart  from ECG , Troponin T or I levels may be elevated in some of the patients with unstable angina. Rarely stable angina can also show elevated troponin.

In patients with systemic hypertension and LVH or cardiomyopathy resting ST depression may not indicate UA 

So differentiation between, stable and unstable angina even though appear simple and  straight forward, it requires a diligent appraisal of history , physical examination (Aortic stenosis /HCM  may cause stable angina)  and ECG, enzyme evaluation.

Final message

In any coronary care unit ,  admissions with initial diagnosis of  ACS/UA/NSTEMI , subsequently turn out to be simple stable coronary artery disese . This error happens because the chest pain  or ECG changes  are aggravated by non cardiac factors like a mental stress or a post operative stress  or fever etc.
There could  be another school of thought, that is to err on the side of  safety, and manage all  rest angina as UA  .But the hazards of unwarranted therapy might exceed the risks of leaving these patients alone.
In this context ,there is a need for a new definition for unstable angina .
One ideal version could be . . .
  • Any angina , of any degree  which is caused  mainly by the supply side defect (By a acute thrombotic /disruptive plaque   occluding the  coronary lumen  with a imminent danger of myocardial infarction is to termed as real UA.
  •  All post MI and post PCI angina are unstable angina
  •  Rest angina which occurs due to increased demand situations need not be  labelled  as unstable angina for the simple reason  there is neither an active plaque nor a  fresh thrombus likely  in these patients. They rarely develop  recurrent angina or MI . The mechanism of angina at rest here is most often due to a tachycardia and resultant increase in MVO2 .(myocardial oxygen consumption) .Currently they are called as secondary unstable angina.In fact , anti thrombotic drugs are misused in these situations as they satisfy the criteria of UA/NSTEMI.

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          During CABG arterial grafts are always preferred over venous grafts , for the simple reason the grafted vessel has to carry arterial blood and not the venous blood. Saphenous veins are tuned to carry venous blood at low pressure.The mean coronary arterial pressure is around 40mmhg and this will damage the saphenous venous endothelium more quickly. The reocculsion rate at 10 years for venous grafts  can reach  60%.


                                                    Left internal mammary artery (LIMA) is the most commonly used arterial graft. This is usually anastamosed with LAD. The lumen of LAD &  LIMA are more or less equal and they match well in character also !

The other advantage  of  LIMA graft  is ,   blood    tends to  flow  both during systole and diastole in a smooth fashion.. Since the venous graft which  hangs from the root of aorta , the  ostium  of venous graft lacks the  hemodynamic benefits of   coronary sinus . (We know the coroanry sinus acts like a  reservoir for  the smooth release of  blood flow into coronary arteries.)

Finally ,  the most important feature of LIMA is

  It is a live graft

LIMA’s proximal origin from subclavian is left intact, so LIMA acts as a live vessel with it’s  vasa vasorum intact ,  which means the endothlium derived relaxing factor (EDRF-Nitric oxide) secretion is not interrupted.This makes the LIMA  an excellent graft , self protected against reocclusion.One may call it a drug eluting graft !

 What is the patency rate for LIMA ?

LIMA patency rates at 10 years is nearly 90 %  .But the graft patency depends on many factors , like diabetes, age, gender, surgical technique ,(Now , beating heart CABG is very popular , where the LIMA patency is said to be slightly lower than conventional CABG) Sequential LIMA grafts, free LIMA graft ( Which  loses the advantage of being  a live graft) have relatively lower patency rates.

What are the other arteries used in CABG ?

Other arteries that could be used are radial artery, right internal mammary artery, and gastro epiploic artery.The patency rates of all these arteries far less than LIMA .

cabg-2

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                                Coronary artery  by pass graft surgery has become the most common cardiac surgery done world over ever since it was first introduced by Favalaro in 1969.The common indications  are, triple vessel disease and left main disease in any of the following situationsE.

Elective CABG(Non emergent)

1.Chronic stable angina

Either emergent or elective

1.Unstable angina

Emergency CABG*

1.Acute myocardial infarction.-Cardiogenic shock

2.Failed thrombolysis

3.Failed primary PCI

4.Complications during routine PCI(Cath lab crashes !  etc)

5.As an associate procedure after a  mechanical complication during MI (Septal rupture, Acute MR etc)

*In emergency situations even a single vessel disease would require a  CABG

Hybrid CABG

Combining CABG and PCI in the same patient is followed in very few centres .(Example LAD graft and RCA angioplasty)This is done in patients who have co morbid conditions who can not tolerate prolonged surgical times.Further there can be situations  one lesion is very ideal for PCI  while for other grafting is the only solution.

Controversial CABG

1.CABG as a primary revascularisation  in STEMI*

(Rarely done now , almost obsolete , primary PCI has almost replaced it  . . . but it is still  useful if performed within 6 hours of MI )

2.Incidentally detected CAD*  following routine coronary angiogram.

( *CABG for incidentally detected asymptomatic CAD is  increasing in many parts of world )

Inappropriate CABG

         If it’s triple vessel disese it must be CABG -CASS study (1980s)

                       Coronary artery surgery study (CASS) still has considerable influence among the  cardiology  community in the decision making process  for CABG , even though it is many decades old .There has been a phenomenal development in both medical as well as interventional techniques since  CASS . (Thrombolysis, Statins, ACEI, PCI  DES to name a few) .

                     When CASS study was done many decades ago,it was believed triple vessel disese constitute a  homogeneous population and  carry  the same clinical significance . For example a 90% proximal LAD , 50% RCA and 50% OM technically qualify for a CABG and unfortunately , some of them are  subjected to it even in  2008 !  Now we clearly know, it is not the number of diseased vessels  that is important, but it’s location, severity , LV function, presence or absence of diabetes . Finally , the presence of revascularisation eligible myocardium must be documented in all post MI patients . (Technically referred to viable & ischemic myocardium ).              

              Currently , with the  PCI  & medical management has grown so much, CABG should be reserved only for, critical triple vessel disese , with at least one proximally located lesion (Mostly  LAD  or Left main ), especially in diabetic individuals.

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                                This is a  hemodynamic concept paper by Libanoff in 1968 published in circulation.This paper elegantly proved that  the rate of fall of pressure across the mitral valve will predict the mitral valve orifice.     This key paper formed the foundation on which  Liv hatle developed the echocardiographic pressure half time .This pressure half time derived mitral orifice area ( 220/PHT) is key parameter world over for assessing  severity of mitral stenosis non invasively .

Click on the link get this article .This article is available free fulltext from circualtion web site

pressure-half-time

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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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