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Archive for the ‘cardiology -Therapeutics’ Category

Confronting Sgarbossa criteria from chennai !

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Arrhythmias, tagged , , , , on April 16, 2011| 1 Comment »

Left bundle branch block (LBBB)   has a curious but important relationship with  STEMI . LBBB inflicts a dramatic change in qrs morphology   with  a diagonally  opposite   polarity of ventricular activation . This masks    the initial qrs vector  and  makes it a difficult task  to diagnose acute MI in this setting. The ST segment which is of primary importance  in STEMI is   lifted  up due to altered repolarization .

LBBB can be associated  with  STEMI in the following ways

  • Acute necrotic LBBB  with massive myocardial damage – Impending shock
  • Chronic LBBB with acute STEMI
  • Transient ischemic LBBB during STEMI
  • Rate dependent  LBBB (Usually tachycardic  ,  rarely bradycardic  )
  • STEMI in pacemaker rhythms

While every one of the above can be experienced ,  the most common diagnostic conundrum  occurs ,  when a patient   comes with acute  chest pain and LBBB . There has been many criterias  suggested to diagnose STEMI in the presence  of LBBB.

The criteria  proposed  by Sgarbosa  (A  GUSTO   off shoot )  in 1996  caught our imagination .One prime reason for this is ,  it came from the prestigious NEJM and Duke university combine. Suddenly this became the de- facto standard to diagnose  STEMI 

In the  past 15  years  ,  our experience in one of largest coronary  care units in India , we have   found this criteria   to have  little utility value  in STEMI and LBBB  . Most of the time  a correct diagnosis was made  by   simple clinical guessing .

Next to  clinical assessment, we found cardiac enzymes (Troponin and CPK ) were reliable in diagnosing  STEMI with LBBB.

Surprisingly ,echocardiography  was as unreliable as ECG .( The paradoxical  septal motion invariably confuses the already  confused  cardiology fellow who usually does the emergency echo  !) 

Even as our  CCU documentation was  far from satisfactory  , now this article from Mayo exactly reflect  our observation.

Sorry   Sgarbosa . . . the criteria was  based  on  sound observation and a  good  electrical principle  . . . still LBBB is able to beat   it convincingly ! ( Very low sensitivity !)

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Cardiologists beware . . .Bicycle rides threaten angioplasty procedures !

Posted in cardiac drugs, Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology-Land mark studies, tagged , , , on April 14, 2011| Leave a Comment »

What do you advice a patient with single vessel  CAD  with milder forms of angina or no angina ?

Medical management ?  May be you are right . But most of us do not  follow this  correct advice.  Why ?  We have a inherent bias against  medical management  . Cath labs exude  unmatched glamor and  attraction in various forms  to both cardiologists and their patients.   Now , here is a   surprise  finding  , unpalatable though , for many of  us !  Simple jogging or bicycling can have equal if not  more relief  than even a angioplasty . This study which came in 2004  was made sure , not to  gain a prominent place in cardiology literature.

http://circ.ahajournals.org/cgi/content/full/109/11/1371?linkType=FULL&resid=109/11/1371&journalCode=circulationaha

Let me pedal faster . . . cardiologists are after me !

The circulation article

How does exercise help in reversing CAD  ?

We know the prerequisite for plaque formation is the endothelial  injury along with lipid accumulation. Further ,  high local adrenergic(vasomotor) tone ,   growth factors and inflammatory activity would accelerate the plaque formation.

Regular exercise  has been  convincingly  shown to improve  the endothelial function. It  restores  the optimal adrenegric tone in the coronary micro circulation so the blood flow is brisk and pro-coagulant  activity is reduced .

It is easy to accept  the fact ,   exercise  can  prevent   progression of plaque   . . .A question that lingers in many including  many  cardiologists is this   . . .How  is it possible   for exercise to  regress well  established plaques ?

When   exercise  can   dissolve  huge  fat loaded  abdominal  tummy  in matter of weeks ,   there need not be any doubt  about the efficacy  of   exercise  in regressing   minute  lipid laden  coronary tummies (also called as plaques) .

(Of course , the  above statement  is supported by  documented  angiographic evidence  as well !)  Read below and  also the AVERT study .

Final message

Attention  all CAD patients ,  empower yourself , you  can become your own  cardiologist . You can perform angioplasties with bicycle  at zero  cost ,  of course  you have to pay for the bicycle !

This article “hypes up” the importance of physical activity in the management of CAD. But , it has to be  combined with optimal anti anginal drugs, good lipid control , blood pressure and diabetes  control  if present  , stress reduction  and good  sleep  to keep the CAD and cardiologists  at bay !

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A curious phenomenon called dual acute coronary syndrome !

Posted in Cardiology - Clinical, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Coronary artery disese, tagged , , , , on April 14, 2011| Leave a Comment »

We know  acute coronary syndrome  presents* with  either  STEMI or NSTEMI. (*It actually doesn’t present , it is our understanding and interpretation ).  Bifurcating  ACS into two is more by convention and convenience .Does  the intra-coronary  plaque  dynamics  really  permit us to divide ACS in to two distinct ECG  entities ?

Are we oversimplifying it ?  Probably yes.

The following paper was presented in the cardiological society annual scientific session in New Delhi few years ago (2006)

It generated an intense debate  , finally the chair person  reluctantly concluded such events are  possible. . .

but need more proof   . What is your take on this issue ?

DUAL   ACUTE   CORONARY SYNDROME

S.Venkatesan ,G.Gnanavelu,V.Jaganathan,

Department of cardiology . Madras Medical College. Chennai

Acute coronary syndrome (ACS)  is  classified into  STEMI  and NSTEMI and has gained universal acceptance. The classification was done by   clinical & electro physiological   findings    with   some   pathological basis. The   classification   came into vogue primarily to simplify the decision making process of thrombolysis. ( STEMI –Thrombolysis eligible .NSTEMI  Thrombolysis ineligible.) The limitation of this classification is well   exposed   as   we   now know,    STEMI can evolve into NSTEMI and NSTEMI can evolve into STEMI .   Identifying the culprit artery in ACS is   not straight forward especially in NSTEMI. Adding further complexity   is   the newer   observations that diffuse vessel inflammation,  and  multiple active plaques(MAP) are responsible for many of the episodes of  ACS.

In this scenario   there   could be two are more pathological processes   one   resulting   in  a total occlusion   and other sub total occlusion resulting in both patterns of ACS simultaneously .(STEMI & NSTEMI  Dual ACS)

We   describe two  patients  who had   presented to our CCU  . Both had STEMI one in  lateral  other in anterior wall . They   were thrombolysed   as per  criteria. Both patients had gross ST depression (>4mm)  elsewhere. In one patient it  corresponded  to the reciprocal  leads .The outcome of  thrombolysis  was turbulent .Both patients worsened and one developed  recurrent VT . Paradoxically the ST elevation   regressed   indicating a successful   thrombolysis  in the STEMI  territory  even as the ST depression  was worsening in the other leads. Angiogram   revealed   multivessel CAD with   recannalised  LAD  lesion with eccentric , thrombus containing  lesion in RCA/LCX. One patient expired and other was referred for revascularisation.

We   believe   both of our   patients  experienced  Dual ACS.

When to suspect dual ACS ?

Dual ACS is likely , when  STEMI is associated with ST depression  in at least 5mm in any two leads  or   when there is disproportionate  reciprocal ST depression ( > 2mm of primary). The reason for the poor outcome could be due to a therapeutic conflict between   STEMI & NSTEMI as the former  is  thrombolysis friendly while the later is not . Role of   thrombolysis in  such situations were ACS wanders between STEMI & NSTEMI is not defined. Another possibility is the concept of reciprocal ST elevation,   where in the index event  could be NSTEMI and STEMI is a secondary response  and  thrombolysis is apparently  contraindicated.

We conclude that in patients with ACS,   two or more   plaques can simultaneously get  activated  and  present  as a combination  of STEMI / NSTEMI   in the same  patient  in two different coronary arteries.(Dual ACS) .We suggest   that in every  patient who present with  STEMI  a possibility of   dual ACS  is to specifically considered,  as  thrombolysis could be disastrous  and  instead  they  should  reach   the  cath  lab directly.  .

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A big set back for low molecular weight heparin . . . but a huge step forward for our patients !

Posted in cardiac drugs, cardiology -Therapeutics, tagged , , on April 7, 2011| Leave a Comment »

The economics of  parenteral  anti-coagulation  took a paradigm shift more than a decade ago.  That was the arrival of low molecular weight heparin in the early 1990s.  The conventional regular heparin ( so called  unpurified /unfractionated )  was ridiculed   over the years. Lobbying   for LMWH was so strong  no one could  dare – stop this pseudo academic onslaught  flying high  with series of powerful articles  in major journals .

The major plus point  claimed for LMWH was   the convenience of administration  without any monitoring .

This convenience masked  some of the vital  truths  about these drugs

  • First and foremost ,  LMWH never proved it’s cost  effectiveness  and worthiness in a convincing manner.
  • Acute administration  by IV route was rarely practiced globally  which was used in all major trials.
  • The onset of action with subcutaneous route  always lagged behind in real ACS.
  • It would  seem ,  the  greatest advantage claimed by LMWH ( of not requiring monitoring  ) is the biggest suspect ,  as we would not know , whether the drug really reaches the peak action or not.

If  raw economics  brought these futile drug to the fore front  ,  the  only  possible way to stop this  redundant  drug was again by the  same  economics ! This , exactly  is happening  now . Suddenly , many  research  papers  are coming out   claiming  the superiority of good old heparin  over LMWH .

Thanks to recession , new  global health polices and politics .

This week’s NEJM restores  at- least some of the   stolen credit  to the regular  heparin after 10

long years !


http://www.nejm.org/doi/full/10.1056/NEJMoa1014475?query=TOC

Assumptions and bias

The above observation by the author  can be labeled as an  extreme form of bias against a wonder drug called LMWH.

It may be  argued  not all LMWH can be considered equal .Will the  outcome from the above trial  results be extrapolated to  enoxaparine  as well  ?What  is your gut feeling ? Gut is many times right than  hyped up RCTS !

In a large tertiary  hospital  where we work  , we have  never switched to the LMWH   in the  bygone  decade (  Both in critical care unit and post op unit )  .We have to withstand   a big  hue and cry and  were   even  humiliated for using regular heparin in our ICU . Now  . . . we  stand fully vindicated !

There are many such falsehoods  that  need to be  corrected in the medical literature. Sooner it happens , better for the humans  of  this planet . We should be glad  . . .things are moving in that direction.

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What is the role of “routine” oxygen in the coronary care unit during acute STEMI ?

Posted in cardiac drugs, Cardiology - Clinical, cardiology -Therapeutics, Uncategorized, tagged , on April 7, 2011| Leave a Comment »

Oxygen has an ubiquitous place in any  critical care unit. If some body is labeled as  critically ill , it becomes mandatory  for a tube to  be inserted per nasal. It is more of a conditioned  reflex and  sort of a socio- medical necessity .The futility of oxygen administration in critically ill is most evident in the management of STEMI.

Inconvenient  questions

  1. Does the oxygen  we  supply ,  ever reach the disputed  site   myocardium             (From  the port of entry . . . namely the nose  )
  2. Does it improve  the myocardial salvage ?

There is generally no hypoxia associated with STEMI . Even if it is there , the  ischemic myocyte can not be oxygenated by increasing the systemic saturation as the problem is with the   delivery of oxygen due to defective supply.

What does the guidelines say regarding o2  ?

Read  yourself    http://circ.ahajournals.org/cgi/content/full/110/5/588

Final message

Routine oxygen administration  is  required  to create  the intensive care ambiance .

Oxygen administration  by default has no scientific role.

However,   it is generally not harmful . As long  a drug is  not harming the patients , inappropriate  therapy is   forgiven by modern medicine.

When  is oxygen really indicated in STEMI ?

  • Significant persistent  Hypoxia
  • Associated LVF
  • Any arrhythmia
  • COPD

Forbidden discussions  in academic forums

Oxygen  administration has  become  mandatory to generate revenue  for the cash starved  corporates .It  is a standard practice to charge these patients on hourly  basis  of o2 usage  in many hospitals.

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A deadly cardiovascular complication of noise pollution !

Posted in Cardiology - Clinical, cardiology -Therapeutics, myocardial disease, Uncategorized, tagged , , , , , , , on April 6, 2011| Leave a Comment »

An  unwanted , unexpected , unpleasant sound  is  often referred to as  noise

Human ears , are  not meant to  hear  only the  pleasant  sound . We live in a noisy world. It is believed every cell in the body has ( Auditory ?) sense  receptors. But , the noise is perceived  only at brain .It is  incidental our ears  are located  right beside the brain , adjacent to  parieto  -temporal cortex . The auditory nerve  has   its  nucleus  located dangerously close to vasomotor centers of  brain stem .

.

When  excess noise enters our ears it vibrates  the brain stem as well . Noise travels in the nervous system as electrical  impulse , so it is natural  for  to expect a  spill over to the  nearby  adrenergic  centers  .

A sudden explosion or a thunder will skip a few heart beats is it not ?  Similarly , when   we experience  pleasant  sound /  melody**   it  soothes   the nerves ,  this forms the basis of musical  therapy.

So  it is logical to conclude   , when the  nice  music  has a capacity to heal ,  unwanted  noise  is expected   to injure  our biological system.

** A rock fan under the influence of  drug  may feel a every nonsense  as melody . . . is a different  story !

It is observed strokes and MI are more common in urban areas congested  with traffic chaos. Here is an article from European  Heart  journal   with  solid evidence on this topic.

Excess noise   could  result in  cerebral  or coronary arterial  spasm ,  thrombotic  occlusion or even a hemorrhage ?*

  • Noise  induced adrenergic trigger and spasm of blood vessel
  • Adrenergic  surge  and resultant hypertension

Associated  Phenomenon along with noise

  • Anger
  • Anxiety
  • Fear (A noise associated with a  missile attack  in the  war zone )
  • Relative  hypoxia , Air pollution in noisy  environment .

*A distinction must be made between   chronic noise  pollution  vs  Acute noise intoxication.

For  those who want  more depth in this  topic , I  was surprised to find  this  exclusive journal  that documents noise and human health .

Final message

Excessive noise  can have a detrimental effect in the nervous system . Since  cardiovascular system  is also under    neurological command  it  is  expected to  share the ill effects.

A comforting news for healthy men and women  . Noise per se  can not be termed  as a  coronary  risk factor . It can  (at worst ) be a  trigger  for an event  in individuals who have other major risk factors.

 

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New criteria required to define LV dilatation !

Posted in Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , , , , on April 4, 2011| Leave a Comment »

Human heart is a compact elastic organ .  We know elasticity is lost when it is stretched beyond a point.This is what happens in dilated  cardiomyopathy .When the heart muscle fibers stretch  too long from the baseline  it loses its ability to contract and relax   efficiently.In fact  , after a cut of point even if it comes the original length the elastic fibers are fractured and suffer from irreversible damage.

Among  the systolic vs diastolic dimension it is the diastolic dimension that becomes important in defining dilatation.

When do you say a ventricle is dilated?

  1. When the EDD (End diastolic dimension) > 60mm
  2. EDD > 56mm
  3. EDD > 10 % from baseline
  4. EDD > 25 %  from baseline

Any of the above can be right.

The normal human ventricle measures  between 35 to 55mm in diastole .

Currently accepted  definition for enlargement of heart is EDD  of 56 mm and above. Some believe  in a more strict criteria of 60mm.

Consider the following situation

A man with 35mm EDD   can increase 20mm ( ie 60 % )  from of his baseline  and still be  labeled as  normal LV  dimension ! . If the above patient  is  destined to develop dilated cardiomyopathy    his  heart  would  begin  its  final  journey  slowly but   surely ( from 35 mm  ! ) . So ,  according to current criteria  we can diagnose  DCM only after it travels the half way towards hell .   What a way to define DCM  ! Be cautious LV dimensions can fool  you  . . .

If the EF is low and symptoms develop early ,  one may recognise  the above  entity ( at least erroneously !) as non dilated cardiomyopathy or RCM.

If  the patient is relatively asymptomatic and   if we   overlook  the  baseline  LV parameters ,  we are likely  to miss  most of the early  DCMs

Final message

We need to stress the importance of baseline LV dimension in defining DCM  . It is proposed  from this  site ,  an increase of 25 %   and above from baseline  can be   included as an   additional  criteria  for  LV dilatation . This  could  help us understand   the early muscle dynamics in DCM.

Un-Answered questions

  1. How to diagnose  early DCM ?
  2. When does the EF begins to decline in DCM ?
  3. What is the relation between EDD and EF %?
  4. Is HF with preserved LV function ( previously called diastolic dysfunction ) is the earliest point in the natural history of  DCM
  5. Is there a overlap  between non dilated cardiomyopathy , RCM and early phase of DCM ?

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Sino-Junctional rhythm : When a restless pacemaker goes for a walk down the lane !

Posted in cardiac drugs, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology-Arrhythmias, tagged , , , , , , , , , , on April 3, 2011| Leave a Comment »

SA node is  the ultimate   power  center  of heart located in the junction of SVC and right atrium .In normal physiology  it fires  at a rate of  60 -90 /minute   that  dictates  the  ventricular rate  .

SA node is a linear  spindle shaped structure with a length of  1.5cm . The P cells with unique mitochodria  are  responsible for pace making activity  . The ion responsible for pacemaker current is mainly  calcium  with the initial 25 % push given  by  sodium current as well .  These cells are predominately under vagal control.Even though  pace making activity  is normally restricted to the SA node  , the vagal innervation is such that  the pacemaker  has a  potential to shifts it’s activity  both functionally  geographically.

In fact , there is constant flux of pacemaker activity  with  the entire length of SA node.The  cranial   aspect  SA node has more fire  power than its caudal tip . It is possible Sinus tachycardia  and sinus  bradycardia could represent  minor changes in the firing focus in its cranio-caudal axis.Further the P cells of  sinus node can spill all over the atria and even up to AV node.

What is wandering  atrial pacemaker ?

This entity is poorly defined  in literature.  With pace making cells scattered all around  there is no surprise to note dynamic pacemaker  shifts  even in healthy people. This is  especially common in young athletes.

Wandering can occur

  • Within SA node ( Shift of focus of p cell firing .No visible changes in ECG )
  • Within SA node and atria
  • Between SA node and AV node. (Sino-Junctional rhythm )

Effect on ECG

  • Baseline bradycardia.
  • Changing P wave morphology
  • Change in PR intervals
  • Intermittent absent (Rather concealed  )  P wave if  is also possible
  • RR interval can also show minor variation.

Image Modifed from http://www.eheart.org

Clinical significance of  Wandering pacemaker(WAP )

  • A Benign condition generally has no clinical significance.
  • It is often an expression of  high vagal tone.
  • Usually transient.
  • Can be unmasked by beta or calcium blockers.
  • Severe forms of wandering  pace maker can be a marker of sinus node dysfunction  and  would need  further evaluation
  • In  the coronary care units it is  associated  with infero-posterior MI when the vagal fibers are  insulted.

Differential diagnosis .

  • Some times it  need to  be differentiated form ectopic atrial rhythm /Low atrial/Coronary sinus rhythm etc .
  • Sinus  slowing  followed by a  functional escape and  reemergence of sinus beat   can be a termed as a form of wandering  pacemaker

Final message

WAP : This attractive and  descriptive ECG entity  is   largely insignificant in clinical cardiology .

It should not be confused with more dangerous cardiac arrhythmia  like sinus pauses and arrest .

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In diabetic nephropathy . . . Is there a proteinuria equivalent in heart ?

Posted in Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), myocardial disease, Uncategorized, tagged , , , , , on April 1, 2011| Leave a Comment »

Diabetes is a systemic disease affecting  almost every cell  that metabolises  glucose .What begins  as  a minor  functional impairment  ,   worsens gradually and ultimately   end up in severe  structural changes.The basement membrane of  cells  face  the brunt of the attack .  (In the strict sense every cell has a basement  but it is well  developed only in kidneys ) . We also  know , diabetes  is able to inflict universal damage by targeting the vascular endothelial cells.

In the kidneys DM makes the  glomerulus  more porous causing protein leak*  and ultimately damages the tubules and end up in CRF. In the retina it excretes the  proteinaceous  material into the vital layers  and result in  retinopathy and progressive visual loss.

* Micro/Macro albuminuria

In fact , there is  a very close link between eyes  and the kidneys  Nephrologists   hesitate to make a diagnosis  of diabetic nephropathy without ocular  changes. The peripheral vascular disease and diabetic foot are  another expression of this microvascular  dysfunction.

What is the impact on cardiac micro-circulation ?

Whenever significant diabetic nephropathy is present there must be a significant cardiac micro- angiopathy as well.This is now  a fact than an assumption. We are not recognizing it rather  ! (If only we have a cardiac  creatinine we can easily identify diabetic myocardial protein leak !)

When kidneys lose protein , cardiac capillaries  lose proteins to interstitial   space  and result  in progressive  fibrotic reaction . We know  extravasaation   of high osmolar  proteins   can play havoc  in cardiac interstitium  !

Proteins are the particles of life   . . . but in wrong places  it can  transform into deadly  molecules  in a fraction of time !

Hence ,  the cardiac protein leak in diabetes can cause  any of the following clinico -pathologic entities.

  • A mild left ventricular  hypertrophy .
  • Increase global  cardiac  mass (Similar to bulky kidneys  seen in early diabetic nephropathy )
  • Simple diastolic dysfunction.
  • Severe restrictive features
  • NDCM (Non dilated cardiomyopathy )
  • Finally a DCM  like  transformation

How to recognize cardiac protein leak ?

  • Clinically it presents either as  angina or early heart failure symptoms ( not both usually ) .Diastolic dysfunction  in echo,  positive stress test , patchy thallium uptake abnormality  often with  features  of   syndrome X  is also recognised.
  • Many of the low flow or slow flow phenomenon  in coronary angiograms  might reflect micro-circulatory dysfunction .
  • This is recognised by prolonged TIMI frame counts  and  prolonged  coronary sinus filling and emptying time .

What about macro-vascular  complications  in diabetes ?  How is it different from micro-vascular complications ?

Though we expect a direct  link between  micro and macro  vascular complication ,   the later  appears  to a  patho-genetically  independent  process . This will be addressed later.

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V for . . . ventricular tachycardia

Posted in cardiac drugs, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Arrhythmias, tagged , , on March 31, 2011| 1 Comment »

Read with caution . This  may either injure or cure your patient !

Click on the ECG to view what happend !

 

How does  verapamil  terminate a  VT  ?

Physicians  often  debate  vigorously before   labeling  a cardiac arrhythmia as ventricular , atrial junctional  , abberant or not etc etc .  But  for  an arrhythmia   it matters little  from what  chamber it is going to to originate . After all ,  any cell in the heart if excited can generate an arrhythmia .  The ion channel abnormality and the influx and efflux of ions  that determines how a drug is going to terminate an arrhythmia.

In fact , way back  in 1989 the Sicilian Gambit stressed this concept when classifying anti-arrhythmic drugs .This classification taught us  , even though there is a  huge list of  clinical cardiac arrhythmias  , from the therapeutic point of view there are only a handful of receptors  (scattered  all around ) to target  !

When we look at this angle , we realise  , many of  ventricular action potentials  have  important slow  calcium currents  similarly  junctional action  potentials do have some  sodium currents.  Calcium current  is present in every  myocardial cell  more so in the vicinity of AV junction.  Further , at times of ischemic or hemodyanmic stress these ion channels  may  take a different avatar altogether.Slow sodium channels and fast calcium channels etc !  (A wild imagination or is it a fact ?) Other important targets are potassium channels

Heart is a complex structure both macro and microscopically  .  In the three dimensional  histopathologic   interface between atrium  and ventricle (Especially in the  basal areas , outflow tracts  , around the AV grooves ) there  are  lot of sharing  and overlap of  different morphology  of cells . A high septal VT can behave  exactly like an SVT  which  includes the  tendency to get terminated by calcium channel blockers.

Amiodarone is a most popular  drug for VT termination ? Are we clear about the mechanism of it’s  action in terminating VT ?

It is  more of a perception and belief  that  class 3 action   may be   responsible for termination of VT by Amiodarone . In reality it is very difficult   to prove this point.  As Amiodarone  has all the  4 classes  action that includes beta and calcium blocking properties.. In fact ,  now  there is evidence  to  suggest   beta or calcium blocking action  may be more important in terminating  VT when  it is administered  IV  . (While  the class 3 action predominates in long term oral therapy )

A verapamil sensitive   VT may  successfully  be terminated by  Amiodarone  not by its  unique  action  instead it   may simply represent  its  calcium blocking  property.

Final message

Many  of the  VTs terminated by Amiodarone   could  also be verapamil sensitive . Since verapamil is never tried first we will never ever know the incidence of such phenomenon that gives pseudo credit  to Amiodarone

It may not be big crime to try injection verapamil in some of  the  stable ventricular tachycardias( As my fellow did ) especially  when we we know there is an entity called verapamil sensitive VT !


Q for the readers :

How many deaths are reported in cardiology  literature  regarding    fatality  following   verapamil  in   VT ?

I am trying to find  the answer the  data is very hard to come by !

Critical comments welcome.

 

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