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Posts Tagged ‘nejm’

                                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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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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Which is  the most important factor that determines thrombolysis failure in STEMI  ?

  1. Thrombus load .
  2. Drug efficiency
  3. Time delay
  4. Presence of a mechanical lesion
  5. Hemodynamic instability

Answer : 3 .(Though all 5 factors operate )

Failed thrmbolysis occur in about 40-50% after streptokinase and slightly less with TPA   and TNK-TPA . Delayed arrival and late thrombolysis are  most common cause of failed thrombolysis. As the time flies , the  myocardium gets damaged and the intra coronary  thrombus gets organised .Both these processes make delayed thrombolysis a futile exercise.

               Not all STEMI patients have large thrombus burden. There need to be a critical load of thrombus for thrombolytic to be effective

Some may have a major mechanical lesion in the form of plaque fissure, prolapse and it simply blocks the coronary artery mechanically like a boulder on the road  . The poor  streptokinse  or the rich Tenekteplace !  nothing can move this boulder .The only option here is emergency PCI .

How will you know when the patient  arrives in ER with STEMI whether his/ her coronary artery is blocked with soft thrombus or hard mechanical boulder ?

It is impossible to know.That’s why primary PCI has a huge advantage.  But still thrombolysis is useful as some amount of thrombus will be there in all patients with STEMI.Lysing this will provide at least a  trickle of  blood flow that will jeep the myocardium viable and enable us to take for early PCI.

Final message

The commonest cause for thrombolytic failure is the time of administration and the degree of underlying mechanical lesion  . So  it does not make sense  to blame  streptokinase always !

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                                     Hypertension is considered a major cardiovascular risk factor.Hypertension  can have multiple physiological and pathological effects on heart . The common response to  raised arterial pressure is the hypertrophy of the left ventricle ( LVH). This can increase the risk of heart failure in few ( Mainly diastolic failure)  It is a leading cause for stroke  and   less often a  coronary event.

What links Hypertension and  coronary artery disease

                                           Coronary artery disease is almost synonymous with atherosclerosis. There is no separate entity called hypertensive coronary artery disease. But HT can accelerate the process of atherosclerosis. It is widely understood, hypertension can cause  physical endothelial damage and functional impairment of endothelial function.The physical damage ie enothelial disruption , or erosion is a very uncommon phenomenon . So currently  there is sufficient clinical experience  HT is considered dangerous for coronary artery only if it is with the  company of diabetes and hyperlipidemia. (This will seem controversial as it is against the findings of iconic Framingham trial!)

What the medical community refers to hypertension , may not be really so inside  for the coronary arteries.

                                             The relationship between brachial cuff blood pressure and the intra coronary pressure has very little linear relationship. So one should recognise it is the intra coronary hypertension that has a immediate impact on the coronary events. Now only , we are beginning to understand the complexities  of the relationship between HT and CAD. If we analyse a series of individuals HT per se is not a very serious risk factor for CAD* , but it is a number one risk factor for stroke. 

Why HT in isolation  often result in stroke , rather than a MI ?

While HT  is notoriously common to result  intracerebral hemorrhage, the same HT  would not cause  intramyocardial bleeds . Why ?

What is protecting the myocardium against this complication ?

                                      The exact mechanism  is not clear.Acute surges of blood pressure can increase the risk of stroke many times  but  rarely precipitate  a coronary event(  But may cause a LVF) . The reasons could be the coronary endothelial shearing stress is less than the cerebral blood vessels.Both cerebral and coronary circulation has  auto regulatory mechanism . The coronary auto regulation is more robust in that it does not allow  intra coronary pressures to reach critical levels .There is no clinically relevant intra myocardial hemorrhage reported  even during malignant hypertension.

*But a  high intra coronary pressure can sometimes  result in spontaneous coronary dissection and plaque fissure .Lipid mediated injury is vey much facilitated in a high pressure environment.

Has Controlling blood pressure  to optimal levels  , reduced the overall CAD morbidity and mortality ?

                    The answer is yes, ( But not an emphatic yes ! ) Some studies had been equivocal. It is very difficult to say , how much benefit is attributable to BP reduction  per se  and   how much is attributable to indirect effect on atherosclerosis prevention.

Hypertension during ACS

                            High blood pressure during an episode of unstable angina or STEMI can increase the myocardial oxygen demand and worsen the ischemia. It requires optimal control with nitroglycerine ( Preferably ) or beta blocker and ACE inhibitors.Even though HT is commonly associated  with ACS,  one can not be sure the ACS is preciptated by HT. Many times the sympathetic surge during an ACS keeps the blood pressure high.It is a common experience the blood pressure suddenly dropping to normal or hypotensive levels once the pain and anxiety is controlled.

Hypertension during thrombolysis

                           High blood pressure is a relative contraindication for thrombolysis.It need to be emphasised here, It is the  the fear of stroke that make  it contraindicated .The heart can tolerate  thrombolytic agents delivered at high BP .In fact logically ,  hemodynamically and also  practically it is obseved , thrombolytic agents administered at relatively high blood pressure (140-160 systolic) has better thrombolysis than a patient who is lysed at 100mmhg.

                       The coronary pressure head which contain the thrombolytic agent (streptokinase and others ) need to have pressure jet effect on the thrombus.So the  mean coronary perfusion pressure becomes  a critical determinant of success of thrombolysis.

                            It is a paradox of sorts , very high blood pressures are a relative contraindication for thrombolysis and at the same time normal pressure patients fare less well to thrombolysis.

 Final  message

                        Hypertension continues to be a major cardiovascular risk factor.It has direct and indirect effects on the heart.Generally HT is more of a risk factor for stroke than CAD.A slightly high BP ( Just around the  upper limits of normal or just above it ) has a hemodynamic advantage during thrombolysis.(Class C evidence )

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What is herd behavior ?

It is a behavioral pattern where in animals and humans in large numbers , tend to behave in the same way at the same time without application of mind .


Herd behavior in human societies

Herd behaviour describes how individuals in a group can act together without planned direction. The term pertains to the behaviour of animals in herds, flocks, and schools, and to human conduct during activities such as stock market bubbles and crashes, street demonstrations, sporting events, episodes of mob violence and even everyday decision making, judgement and opinion forming. This is very much applicable to medical profession also.(Ref:Wikipedia)

Herd behaviour in animals and human how they are different ?

“surprise ! surprise ! There is  very little difference  noted , according to Hamilton”

A group of animals fleeing a predator shows the nature of herd behavior. In the often cited article “Geometry For The Selfish Herd,” evolutionary biologist W. D. Hamilton said each individual group member reduces the danger to itself by moving as close as possible to the center of the fleeing group. Thus the herd appears to act as a unit in moving together, but its function emerges from the uncoordinated behavior of self-seeking individuals.

Among humans for example when panicked individuals confined to a room with two equal and equidistant exits, a majority will favor one exit while the minority will favor the other.

Medical professionals as a herd


The practicing habits of  medical professionals  move , symmetrically as a herd . When a top journal or a opinion leader utters something every one tend to move in that direction .

If a herd leader says a particular treatment is great, every one will say yes . If he says nay every one will say nay !

No one will really question the direction they move ? Unless the correction occurs from within the herd. No external forces usually are effective.Herding is also benefitial many times as rapid propogation of scientific facts needs such behavior ,but it needs constant scrutiny.

 

Herd behavior example 1 : The most  typical example is the drug prescribing pattern of anti hypertensive agents over the past half century.The movement  from diuretics to beta blocker , from beta blockers to calcium blockers and to ACE inhibitor and again to diuretic  , then to ARBs and currently shying strongly away from beta blockers, in between  have a brief encounter with alpha blockers and finally  back to diuretics.

If a  particular physician by his insight , had clinged onto  diuretics ( Away from the herd ) for over three decades he is a real exemption , although branded old timed  and unscientific , he has been the most scientific medical professional indeed !

Herd mentality example 2 : Every one says so !  so it must be true ! Hormone replacement therapy good or bad goes with the leader of the herd . 

Herd mentality example 3: Very few cardiologists will be ready to agree the fact that , simple digoxin and diuretic ,ACEI, beta blocker,  administration could be as effective as  the costly cardiac resynchronisation therapy in atleast some of patients with wide QRS cardiac failure ( As we know up to 30 %  wide QRS CHF population do not respond to CRT) 

Defying Herd mentality resulted in major break throughs in medicine

               When every one was  saying beta blocker was harmful in CHF one person from Briton defied it ( Wagenstein, and now beta blockers are the mainstay in the management of CHF! )

There are hundreds of treatment modalities popularised by such herd behavior

Who is the watch dog  , whether science is moving in the correct direction ?


Read this land mark article  how medical research can be distorted by such learned behavior  and how scientific research should not be done .

Click on the image .

 This post is not intended to hurt anyone . It  reflects , human beings are not  fully evolved  yet , in the onging  process of evolutionary biology.

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                                          CRT , cardiac resynchronisation therapy  is being  projected  as a revolutionary treatment for cardiac failure , where a failing heart is rewired electrically through multiple leads and make it contract  more effectively.The success rate of CRT was highly variable.The basic question here  is,  there should be a  significant  documentation of desynchronisation  prior to CRT , for resynchronisation to be effective. Further , the sites of  myocardial  stimulation ( Coronary sinus/LV epicardial) , dose of electricity and the sequence of stimulation and the  electrical delay  are very  critical. Achieving this into perfection  is not a simple job and is  real rocket science ! ( If we can achieve 5 % of what  the normal purkinje network do within the LV we can term it a huge success.) Let us hope we catch up with nature . Finally , it is ironical  the sites of LV pacing ,  electrophysiologists  select currently  is infact not selected by them but pre selected by the patients coronary venous anatomy ! .So as on date ,  one can imagine how scientific this treatment could be !

                                         Initially it was adviced for patients with only wide qrs later for even normal qrs patients.When people started using it indiscriminately  insurance companies started to rethink and thus came the   RETHINQ study in NEJM  and brought a full stop to CRT in normal qrs CHF.

How to identify who will benefit from  the costly CRT  ?

It is a million dollar question. So millions of dollars were spent to identify the correct tool to identify the true responders to CRT.Echo cardiography with sophisticated methods tissue doppler, tissue tracking and , 3 D echo ,velocity vector imaging were done .These methods are not only costly but also time consuming and  hugely expertise driven.

Does all this  efforts with  advanced echo techniques worthwhile ?

This simple question was addressed in PROSPECT study in circulation

Click to read the article

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                                Acute coronary syndrome (ACS) is currently classified as STEMI and NSTEMI.This classification came into vogue  primarily to  triage patients for thrombolysis eligibility , as ST elevation is the  only criteria for thrombolysis.The  earlier term  non q MI  is largely used  to denote the  present day NSTEMI. In the past q  MI was referring to transmural MI non q MI  to non transmural  pathologically.(Of course , now we know  the relationship between q waves and transmurality is not good )

So when can we still use term non q MI ?

These terminologies of STEMI and NSTEMI are made on admission  at the emergency room.  ACS being a dynamic entity these  patients can  have rapidly changing  ST shifts , from depression to elevation and vice versa. Fresh T wave changes can also occur .Q waves  may or may not develop ,  depending upon the damage sustained to the myocardium and the efficacy of thrombolysis / PCI. So it should be emphasised here STEMI,  NSTEMI ,  q  MI ,  non q MI are the  descriptions of the  same group of patients in different time frames. The common mode of  evolution  of  STEMI  is  to q MI and NSTEMI  into non q MI. Cross overs can occur.

 

 

 The problem here is NSTEMI getting converted into STEMI  is quiet common and has no nomenclature issues . But  when   STEMI down grades  into NSTEMI  there is apparent  nomenclature incompatibility .This category of  patients have  no other labelling option other than “A STEMI evolving into non q MI”. Because one can’t label  STEMI  evolving into NSTEMI as  many of  them  will  have a residual ST elevation as well.

What is the final message ?

The term non q MI is still relevant and is used at discharge , in a patient with STEMI when he or she evolves without a q wave .In the setting of unstable angina , NSTEMI has largely replaced  the term  non q MI either on admission or at discharge.

Before I close

                 The important point to remember here  is NSTEMI getting converted into STEMI  is an adverse outcome and  in fact, it is  a complication and the patient should get an immediate  thrombolysis or PCI , while a STEMI getting converted into non Q MI is generally a  major therapeutic success.( Effective salvaging and preventing q waves )

//

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                Human civilisation has met so many challenges.Man kind has enjoyed the benefits of modern medicine for over a century.Now comes the new threat.Threat from within.The onslaught of marketing force has contaminated the medical science .

              It is widely  recognised  commerce is masquereading as science , from stem cell research to futile and costly  drugs, and  questionable  devices and procedures . 

How is the medical  community responding to this  issue ? 

Silence  is the response !  Why silent ? Are we the part of the problem ?  Occasional articles in the  Annals of medicine, Lancet, BMJ, or JAMA talk about these issues and nothing happens next .

Click below  to read one such article from the recent issue of Annals !

 

 

Let us hope the world financial crisis currently we are witnessing , would be good for human health as all futile market driven  , enforced medical expenditure goes bust !

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 Rescue thrombolysis in acute   myocardial   Infarction  

 *Venkatesan sangareddi ,Madras medical college,Chennai.India

 

 

   Back ground  Failed thrombolysisin acute myocardial infarction occurs in 30-40% of patients. The incidence of progressive pathological remodelling and cardiac failure is high in these patients. The approach to the patient with failed thrombolysis is generally considered to be catheter based and the outcome is not clear. Bleeding can be troublesome in patients, taken for interventional procedures in the immediate post thrombolytic state. The option of repeat thrombolysis has not been studied widely and is not popular among cardiologists.

Methods:We present our experience with six patients (Age 42-56, M-6, F-0) who were thrombolysed for failed first thrombolysis. All had anterior MI and had received either urokinse or streptokinase (between four to nine hours) after the onset of chest pain. All of them had persistent ST elevation, angina not responsive to maximal doses of IV NTG and beta blockers. The initial thrombolysis was deemed to have failed. Repeat thrombolysis with streptokinase (15 lakhs) was given between 16 and 24 th hour. The clinical outcome following the second thrombolysis was rewarding. It relieved the angina, ST segment elevation came down by 50% and coronary angiogram done at 2-4 weeks showed complete IRA patency in four out of six patients. The factors responsible for failed thrombolysis is complex and multifactorial. A logical explanation from the fundamentals of clinical pharmacology would suggest that a common cause of failure of any drug is due to a inadequate first dose.

Conclusion :We conclude that repeat (Rescue) thrombolysis can be an effective medical intervention for failed thrombolysis in AMI.

Personal perspective                  

                             Repeat  thrombolysis for failed ( initial ) thrombolysis  is still   considered  a  fantasy treatment  by most of the cardiologists !  The utility and efficacy of this modality of  treatment (Rescue thrombolyis ) , will never be known to humanity , as planning  such a  study , in a large population  would  promptly be  called unethical by the modern day cardiologists.

                     While a cathlab based cardiologist  take on the lesion head on with multiple attempts  , it is an irony , poor  thrombolytic agents are given only one shot  and if failed in the first attempt,  it is doomed to be a  failure for ever.Currently,  the incidence of  failed thromolysis could be up to a whooping 50 %  .There has not been much scientific initiative  to enhance the efficacy of these drugs.

                            Common sense and logic would suggest it  is the  inadequate first dose ,  improper delivery , pharmacokinetics is   the major cause of failure of action of  a drug in clinical therapeutics.

If the first  dose is not working ,  always think about another  incremental dose if found safe to administer.

Can we increase the dose of thrombolytic agents  as we like ? Will it not increase the bleeding risk to dangerous levels ?

This is a clinical trial  question.

  • In patients with prosthetic valve thrombosis and acute pulmonary embolism we have safety data of administering of  1 lakh units for an hour for up to 48 hours.

Can  the same regimen be tried in STEMI if the initial thrombolysis has  failed  and emergency intervention is not possible  ?

Logic would say yes . Unfortunately we can’t go with logic alone in medicine .We need scientific data ( with or without logic ! ).But now ,  as we realise common sense is also a integral part of therapeutics  It is called as level 3 evidence / expert consensus by AHA/ACC .

Applying  mind , to all relevant issues ,  continuous streptokinase infusion 1 lakh/hour for 24-48 hours in patients with failed thrombolysis can indeed be an option,  especially when the patient is sinking and  no immediate catheter based intervention  possible .This study question is open to all researchers , and may be tested in a scientific setting if feasible.

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Answer: Do  coronary angiogram  for all patients  who had suffered from an acute myocardial infarction* ( Forget about all those mulitpage ACC/AHA  guidelines !).

For an  interventional cardiologist ,  it is often  considered a crime to  follow a conservative  approach !

*Caution This one line guideline is not based on scientific fact  but reality based . Ideally one should identify  high risk subsets among the patients who had an AMI .Patients who had complications during the MI get immediate CAG. Others need  a focused LV function asessment ,  pre discharge  sub maximal excercise stress test or perfusion studies .But this concept has been  virtually replaced by pre discharge coronary angiogram for all ,  in many  of the centres in the world.

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