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Diastolic dysfunction is a common clinical cardiac problem which has no specific therapy.It can occur either in isolation or in combination with systolic dysfunction.The later may  be more common.

Isolated diastolic dysfunction

  • Hypertensive heart disease.
  • Aortic valvular stenosis
  • Restrictive cardiomyopathy
  • Early stages of CAD
  • Pericardial disorders
  • Idiopathic stiff ventricles

In association with systolic dysfunction

  • Dilated cardiomyopathy (20%)
  • In any form of cardiac failure some degree of diastolic dysfunction is noted .

General principles of management

Even though there is no specific drugs to tackle diastolic dysfunction the following measures may have significant impact.

  1. Correct the underlying problem.(HT/CAD etc)
  2. Reduce the basal  heart rate .At lower heart rates as diastole is prolonged , the stiff muscles has  extra time to relax and stretch itself  longer.
  3. Regular isotonic exercise  preconditions the muscle  for smooth contraction  relaxation .
  4. Optimise diuretics (Excessive diuretics has an  adverse effect on the  diastolic pressure profile across the AV valves)
  5. Avoiding positive inotropic agents like digoxin .This will not be possible in combined dysfunction.
  6. ACE inhibitors, ARBs, Aldosterone have some benefits as they could prevent tissue proliferation in the cardiac interstitium
  7. Milrinone (The non digoxin positive inotrpic)show some promise

What are the  treatments in the horizon ?

Antifibrotic drugs   ,Antiproliferative drugs

Collagen breakers ,

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We know human heart contracts and relaxes in an active manner .Systole happens when calcium is pumped from the cytoplasm into the actin myosin complex and diastole occur when the calcium is  returnded back into the sarcoplasmic reticulam .The rate of calcium reuptake  is detemined by the  molecules calmodulin ,  phospholamban and it’s functional status .

When the heart fails acutely , as in asystolic cardiac arrest , does it fail in systole or diastole ?

The seemingly simple question can never be answered dogmatically.

Pathological studies of post moretm specimens suggest contraction band necrosis is a feature of systolic cardiac arrest .We are not yet sure  yet . . . How a heart will appear when it stops in diastole .In fact , if a heart gets struck in systole it means systole has actually  occured  and  because it fails to relax  it  assumes a  stone like contracture  state .

While  the  molecular basis  are pretty much confusing  , what is clear is we do get number of clinical situations where a acute diastolic dysfunction may occur.

Flash pulmonary edema

The mechanism in the former could be sudden afterload mediated mechanical stunning while in the later ischemia mediated acute contractile and diastolic dysfunction.

In both situations there is severe pulmonary venous HT and class 4 pulmonary edema. The credance to concept  of acute diastolic dysfunction came to light , when  we noticed many of  these patient with acute LVF had preserved EF %   and absence of MR to explain acute pulmonary edema .

*Coronary vasospasm–induced acute diastolic dysfunction in a patient with Raynaud’s phenomenon http://www.springerlink.com/content/g1774g34544q2482/

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The most common ECG dilemmas one encounters is to differentiate between the ST segment depression and T wave inversion due to LVH from that of primary ischemia.

Very often  , the entity is misdiagnosed . The implication can be serious , and adding further complexity is exercise stress testing is alos prone for errors in these group of patients as false negative or positive results are very common due to basline  ST/T changes.So it needs a CAG to confirm or rule out CAD in many .

Still the clinical acumen with the help of ECG can help us to a great extent !

A rough and approximate way to identify primary ischemia is given below.

Though these  humble ECG features may not be specific to diagnose CAD . One  need to remember even a normal coronary angiogram is  not synonymous with normal coronary arteries !

Read this blog on limitations of CAG .

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STEMI is the most common cardiac emergency . It  removes  more human lives out of this planet than any other illness. Fortunately  modern medicine has an answer to this deadly disease  . Of course ,  we are far  . . . far away  from conquering it. Only  if a  patient with STEMI reach the hospital  one   can   make a significant  impact on it.

This , unfortunately does not happen in about 30 % of  patients . They  never reach the   hospital . It does not imply all those   who do not reach hospital die . Current  understanding is that the incidence of  out of hospital  STEMI  deaths have been overestimated. The classical teaching of  50% die before reaching the hospital is based on data from old community observations  when the awareness , transport, modalities were grossly inadequate.

Now most of the  patients has access to emergency  care  like  911 /108 etc .

It is  the era of coronary care in the streets . The concept is  , If the patient is not reaching the hospital , let the coronary care reach the patient ! In spite of all these there  are  major “time pockets” which stand between the patient and his /her  ailing heart .

There has been  lot of  analysis of the  various components  of  delay in  STEMI. Of course  ,this is directly dependent upon the  economic and health  status of a country .  For example   in country like  Sweden emergency cardiac services  can reach the  patient  within 10 mts ,  while a person suffering from an MI in a remote Indian village can reach the hospital only after  most of the  myocardium undergoes complete necrosis !

Even in urban areas  where there is  excellent emergency  services  are available the following factors have a great role  in determining  the  time window  and outcome .

  1. Symptom   recognition by self
  2. Early Reactions -(Example : Spouse response time )
  3. Calling for help -Role of Close relatives and family members.
  4. Transport delays ( vehicle personal/public/Traffic jams )
  5. Hospital entry /ER woos . . .
  6. Door to ECG time
  7. ECG interpretation time
  8. Reperfusion decision time
  9. Door to Needle ( Hospital door ? CCU door ?)
  10. Door to Balloon (Cath lab door ?)

Among the above  10  time pockets can you guess which  has the greatest potential to make a deep impact on the outcome of STEMI ?

Yes , you are right The first two !Patient misinterpretation of symptoms is the key obstacle for effective care of STEMI .What drives a patient from home or office to a hospital .It is the symptom .If it is  severe  there is acceleration of every aspect of patient  transport to the hospital .The spouse response time is also critical.The problem with STEMI is many times it can occur less dramatically so the patient is likely to miss it!So cognitive response to symptom becomes vital .An intelligent patient or spouse shortens this time window .

Whether to call emergency service or use personal transport ?

This is some times difficult decision especially in country like India. One has to make a rapid assessment , what is the chances of getting   a 911/108  services within 15 mts. Developed countries have improved upon ER response time. The issue here is the  destination of the patient should be a place where there is a facility  to manage a primary VF . In short the ultimate aim of STEMI management in the early hours  is to narrow the physical distance between the patient and a defibrillator . This requires availability of  health care personnel , equipment , simple physical  presence of medical  personnel is not sufficient .They should be able to recognise  the VF and shock  when needed . Next come the method of reperfusion . Shifting to a tertiary hospital for primary PCI or to the nearest hospital for thrombolysis is a separate issue that needs elaborate discussion.

Where should the victim go ?

  • To  the  tertiary care hospital
  • A nearest nursing home
  • His  family physician
  • Nearest General practitioner

The answer is not a simple one . There  will always be a  trade off between optimal STEMI care and  the common  panic reaction  &  false alarm  and  wastage of ER resources .

Since the first  hour is very crucial  , the outcome  depends lot  on the patient response pattern .Health education and awareness become vital .Emergency medcation , self adminstred aspirin may be an answer in the future.

What ails emergency cardiac care in our country ?

Every citizen of a country should be made aware of the nearest   cardiac medical  facility  ie  . Coronary care unit (CCUs)  . It is an  unfortuante fact , many of our country people have it  in their finger tips  , the  movie house that is showing the current hit & restaurant that  serves best cuisine , have zero knowledge about the  nearest  coronary care unit in their  vicinity . Many  lives have been lost because of this ignorance  . More important than this  , is lives are lost   on transit to many ill-equipped ambulances and some times even  hospitals .

In the modern era  STEMI patient should not  die  due to an  electrical death (Venticular fibrillation)  within a ambulance or a hospital .An ambulance that do not have a defibrillator is not an ambulance at all .It is a sorry state of affairs  some hospitals do have such ambulances .

There are  numerous instances of patients dying in the ER due to poor response time of para medics  in defibrillating a VF.  It should be made a cognisable offence* to allow a patient die for lack of  proper defibrillation within the hospital premises

There has also been instances of good intentional deaths , as a patient is shifted for a better place for  catheter  reperfusion strategies  . If these centres are located  in the other end of   city ,  the door ( In fact it is  the   second door  to balloon time )  to balloon time is directly related to the degree of traffic jam ! and has a great potential to accelerate the death of myocardium and some time the patient as well

*Deaths due to pump failure , cardiogenic shock is an allowed mode of death in STEMI as the natural history demands it ! Some body has to die for the sake of statistics

How to recognise the ACS early : Read  the link elsewhere in my blog.


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For  all those youngsters , who are into the mystery world of medical research  , please begin your journey with this great book.  The greatness lies in it’s  simplicity in expression & search of truth !

Download this 1 MB  marvel  ,  free from  http://www.jameslindlibrary.com  in less than a minute

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Heart rate and human survival has an inverse relationship. This is in fact true for  all mammals.The tortoise which has a heart rate of  6/mt lives for over 200 years. The rat which has heart rate of 500 dies does not even  celebrate it’s first birth day ! Human beings with an average heart rate of 70 lives for 70 years. 

There is a belief  human heart is programmed to beat for certain trilion beats in it’s life time .It is possible ,  with evidence mounting this belief  could  indeed be true .

People with low heart rate simply outlive the ones with  fast heart rate ! Is this due to simple fact they conserve their heart rate .Each human has a reserve of few trillion heart beats for usage in his or her life time .So if this is true what does regular vigorous  exercise do to our longevity ! These are pure fantasy questions that need to be answered !

The truth may be regular excercise even though raises the heart rate to high levels it keeps our vagal tone high and maintain the basl heart rate low and there by conserving both heart rate and myocardial oxygen consumption.The other evidence for heart rate being vital in prolonging life is the proven benefits of beta blockers in patients with decompensated  heart.

Read the excellent issue dedicated to the  importance of heart rate for human survival especially in relation to cardiovascular disease .

From the  publishers of dialogues in cardiology .This knowledge sharing comes free of cost

Courtesy of  Servier

http://www.dialogues-cvm.org/pdf/19/DCVM19_05.pdf

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Atherosclerosis   remains the number one cause for all vascular disease of human beings. It probably  kills more  patients than all other causes put together .

Modern medicine has never conquered the disease. How  the vascular system ages and why some develop premature atherosclerosis remains largely speculative. While it is true , we have identified some major risk factor for development and progression of the atherosclerosis  , patients with out any of those risk factors do develop severe atherosclerosis !So researchers sought to look for some other risk factors . There lies the difficulty  and irony .

We always tend to the research with the affected population .When we know millions of people with the so called risk factors live comfortably , there lies an opportunity  to  analyse why they are protected against the onslaught of atherosclerosis .It is always convenient to blame it or bless it on the genetic predisposition .But we need to look beyond that .Of course  . every genetic expression has to  manifest phenotypically .

While the search for all those hidden secrets has to continue , we should also realize in pursuit of breakthrough we some times waste our energy in false targets  for too many decades !

The reality as on today is ,  there is no reliable  &  undisputed drug available to arrest atherosclerosis  (Some would love to call statin so . . . )

While  our basic science colleagues struggle  in molecular  factories and biological models in pursuit of answer against  atherosclerosis , our elite  cardiac physicians   carry on with the cosmetic touches over this   progressive disease  in  sophisticated cath labs.

Let us hope  man prevails over nature . . .

A cartoon , Just for laughs . . .

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Diabetes is the scourge of mankind .( Womankind too ! In fact it affect women more than men !) When we say DM  & Cardiovascular disease we mean the type 2 maturity onset DM  .Even a lay person  can  recognise  the strong  link between DM and increased cardiovascular mortality .

While logic would make the same lay person believe , that  proper  control of diabetes will eliminate  CVD risk that was acquired . Alas . . . how foolish science can be

The problem in medicine is 1 + 2 is  3  only if it’s counted antegradely   , 2 + 1 is rarely three !

Unfortunately even many of the medical professionals  do not realise this fact and keep the  logic  above reality and continue to believe in what they believe .

When we find,   a  disease process that tend to  continue even after the  offender ( Here incresed blood sugar ) is removed  then there is questionable relationship between the offender and the victim .

This is what we have learnt in over 50 years of diabetic research . Now we have so much controversy and confusion.The savior of diabetes insulin itself may be the offender (ACCORD Trial ) Or is it insulin like growth factor , or circulating peptides ( named and unnamed )

So the debate and research  goes in an unknown  and uncharted direction  . . . The drug companies periodically need some studies to bond the link between DM and CVD to keep the per capita consumption of antidiabetic drugs .

And the only fact remains  true is a good life style with physical activity  with peaceful pursuit of life  will keep the diabetes at bay . . .

So till that time we reach the reality ,  there is no other option  but to experience articles which add on to the  confusion rather than clarity .Read the latest metanalysis  about the link between DM & CVD  . . . and  I can assure you the confusion is  guaranteed

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)60697-8/abstract#

Expect soon another trial , that contradicts the above trials conclusion  .

Title talk

So now  you can answer  the title question : Why we struggle to prove the beneficial effect of strict diabetic control on cardiovascular events ?

We struggle because  , the beneficial effect is so little or  even may be non existent !

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Looks very much a infarct of  infero posterior territory is it not ?

Have a look at her 2D echo still picture . . .

Are you convinced ?

This women had normal LV systolic and diastolic function with no evidence of constriction.

The explanation for the asymptomatic pericardial thickening is due to a healed  chronic pericarditis .This sort of localised thickening in the posterior aspect is all the more likely following a loculated pericardial effusion.Tuberculosis is a very likely etiology.But this women do not have any markers for tuberculosis.Since she is symptomatic no treatment was offered.She is being followed up.

Discussion .

Q waves are not ” sacred waves” to diagnose myocardial infarction.It simply indicates the  direction of current flow is away from the  recording lead of the ECG .Any thing  electrically inert , that come in the interface between the heart and the recording electrode   can record a q waveWhat are the pathological entities that can produce q waves other than infarct ?

  • Fibrotic myocardium(DCM-Cardiomyopathy)
  • Myocardial Scars
  • Myocyte dis array(LVH, HCM)
  • Air,fluid in pericardium /pleural space
  • Pericardial thickening (As in this patient)
  • Electrical shortcircuits (WPW syndrome)
  • Rarely pure ischemia without necrosis can produce q waves (Electrically stuned myocardium)

Final message

Localised pericardial thickening is  a rare  (?unrecognised) cause for pathological q waves , that may mimic a MI.

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Ventricular tachycardia is the most common wide qrs tachycardia.It is generally taught VT is a  regular wide qrs tachycardia.It indeed appears regular most of the time but in reality it is not.

There are few  situations it shows irregularity . Of course , this irregularity may be due to the associated phenomenon ,  even as the VT focus  fire regularly. But for a physician what is manifested in the given ECG matters.

Frequent capture beats and fusion beats.

We know   AV dissociation is sine qua non of VT. Not withstanding this fact , the sinus impulses always try to enter into the ventricle and looking for the door at AV node to open.Even a fraction of a second is enough for the sinus impulse to sneak through it , the only question is the timing .It should be noted that an  intact VA conduction precludes antegrade AV conduction and fusion and capture beats are rare. So whenever the VA conduction lags behind or sluggish , more capture  beats occur.This obviously make  a VT irregular. This sort of irregular VT can occur in up to 20% .So it is indeed wrong to assume that the  presence of  irregularity one should make a diagnosis of VT.

VT induction phase cycle length fluctuations.

The other reason for VT may be irregular  during the early minutes after the onset of VT. Here the electrical circuit fluctuates till it attains a steady state.

The  VT often takes off  with a turbulent course (Bumpy myocardial boulders due to electrical reactionaries and mechanical scars ) Then the circuit optimises .This happens more so in post MI scar induced VT where the tract can be long and circuitous with considerable delay in conduction. But, once the VT reaches the cruising speed it becomes fairly regular. In ischemia mediated micro reentry or automatic focal VT cycle length variations are less common and they maintain the classic property of the VT namely the regularity.

Drugged VT: The Amiodarone effect.

The effect of class 1 a or 3 drugs on VT is a complex one.Either they revert to SR or it may reduce the VT rate, widen the qrs complex, and make it little irregular.This is especailly common after the cumulative amiodarone effect.

Polymorphic VT

The VT that has polymorphism obviously will be irregular.Torsades is the typical example.

Multifocal ventricular tachycardia(MVT)

Every one is aware of multi focal atrial tachycardia.It is surprising the MVT as an entity is rarely described in literature.Are the ventricles protected against such arrhythmia ? When multifocal VPDs occur very often why it is not transforming into MVT ? It is  possible , once a VT is  initiated it suppresses the other focus like a overdrive pacer  and extinguishes all surrounding electrical activity. But as in parasytolic tachycardia MVT can occur occasionally when  each focus is protected against the other by an entry block.

A VT may switch over from one focus to other.During the time of transition or competition between the two focus if you happen to record a ECG it can be really irregular  and chaotic !

Final message

VT is a regular wide qrs tachycardia  in majority.But this rule is applied only in monomorphic unifocal VTs. Even in monomorphic VTs there are  occasions it may show irregularity due the associated phenomenon.A grossly irregular wide qrs tachycardia always indicate a antidromic AF with accessory pathway.

* Title talks : With due respect to the  experts  ,there is no reason for getting confused .For the  practical working formula VT can be considered as regular tachycardia.

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