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Archive for the ‘cardiology- coronary care’ Category

                                            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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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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                                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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Non ST elevation Myocardial infarction  (NSTEMI) is a major mode of presentation of acute coronary syndrome.

Patients present with clinical unstable angina and  elevated cardiac enzymes or troponin.

ECG features can be any of the following.

1.ST depression (70-80%)

2.T wave inversion(10-20%)

3.Both ST depression and T wave inversion

4Post MI NSTEMI  -ECG changes variable ( Ironically ,even a residual  ST elevation may be present)

5.Normal ECG.

                                     Bulk of the NSTEMI belong to ST depression group.NSTEMI with purely T wave inversion is less common but occurs mainly in perioperative settings, pre existing CAD.NSTEMI with normal ECG is very rare  but can occur.

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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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During acute  ischemia the most immediate requirement for the heart is

A.Blood

B.Oxygen

C.Glucose

D.High energy ATPs

E.Free fatty acid

Answer : A  will be considered  by most , as  correct answer .  A can provide B to E . But it is also a fact heart can survive without  A.  

Myocardium requires energy first  ! it does not in fact bother about from where it is coming at the time of crises.It may be right if you restore the coronary blood flow all other components (B-E) are made available to the heart .

The heart can survive off  the coronary circulation with only chemical support during cardiac surgery and also a during  heart transplantation  explanted  donor heart survives on a ice box during transit and till it is transplanted into the recipient heart

But ironically we spend much of our energy and efforts in restoring blood flow.One need to spare a thought about the quality of blood also . This is especially important  in the setting of ischmia  where a  metabolic centric approach will add further benefit.

Energy based approach to ischemia : Is it relevent ?

Heart is a fascinating  mechano biological organ  pumping   millions of  gallons of blood  .Fuel for this is self generated  on a continuous basis  from the circulation blood .So  the key to human survival is the coronary blood flow that supplies the fuel and nutrients to the heart. When this key supply line is under threat  during  acute coronary syndrome cardiologist have  the only option of restoring the compromised blood supply by any means . But during chronic ischemia there is  no  urgency. There has always been an option of enriching the  blood with energisers like ATPs,  glucose,  hemoglobin etc .Providing energy support to the failing heart has never captured the imagination of cardiac physicians until recently.Still most are skeptical about  the concept of biochemical ischemia.

Click to download full PPT presentation

Metabolic manipulation of  CAD( Will be available shortly)

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                             Glucose is the molecule of life   ,burnt every second inside the body at the energy store house called mitochondria. Heart , the most active organ in the body  gets  bulk  of it’s energy supply  from fatty acids,  glucose and a little from keto acids. Under anerobic conditions this energy substrates shifts towards glucose .

                             We are  rarely inclined to think  that heart  can ever suffer from hypoglycemia ! But hypoglycemia can have distinct direct and indirect effects on heart.  In fact indirect effects due to activation of adrenergic activation is more obvious.An episode of hypoglycemia can precipitate an arrhythmia . Glucose potassium insulin infusion

 

 

 

Final message

Hypoglycemia , can be a trigger of ACS .This aspect is poorly recognised and studied.

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