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Archive for the ‘Cardiology-Coronary artery disese’ Category

What is the Ideal time window for rescue PCI ?

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Coronary artery disese, tagged , , , on March 31, 2013| Leave a Comment »

Answer :

In cardiogenic shock it is A . In all others it is probably  C.

While D may be  considered as  an  essential target criteria  for completing the  rescue PCI

Read also

Why-we-often-follow-a-reckless-time-window-for-rescue-angioplasty ?

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I am damn sure this MCQ will trouble you !

Posted in cardiology -Therapeutics, Cardiology hypertension, cardiology- coronary care, Cardiology-Coronary artery disese, tagged , , , , on March 31, 2013| Leave a Comment »

Answer

The tie is between “B” and “D ”

We know in hypertensive hearts LV primarily fails in diastole . Lungs get congested due to raised LVEDP .Here is a catch . . .  if diastole is  terribly dysfunctional  how can be systole be near  normal  ? (After all  . . . systole is not a  distant cousin of diastole !)

How is  that  high blood pressure maintained in spite of LV failure* ?

Is it due to  well-preserved  EF and cardiac Index ?  or Is it due to extreme levels of peripheral sympathetic activity mediated by catecholamine surge triggered by LVF.

We have attempted to measure  LVEF in patients with flash pulmonary edema and acute severe hypertension .It was a real messy echocardiography . We could not conclude much but one thing is  clear in acute hypertensive  LVF   the LV was vigorously contracting in , probably making the option D  more correct .

* The other way of  reasoning is    . . .  it is because  of high blood pressure the LVF  has occurred . LV contractility has no contribution in maintaining the high BP ( Not in line with  the age  old concept of LV contractility  a major determinant of systolic blood pressure !)

(Having said that  . . . we also see patients with severe LV dysfunction with  severely  stunned , ventricles in association with hypertension and LVF . In fact many of the reversible DCMs are due to sudden surge in blood pressure )

Other mechansims of LVF and lung congestion is

  • Extreme tachycardia and shortening of diastole
  • Mitral regurgitation
  • Assocaited  CAD unmasked by sudden raaise  in heart rate .

Postamble

If  this article has confused  you a little  , It has achieved  one of it’s  objective .  !  I expect more  from   young cardiology fellows to address the issue !

Reference

This NEJM article   authored by Sanjay  Gandhi  has almost answered the hemodynamics of acute LVF and HT .

mechanism of acute lvf in hypertension flash pulmonary edema lvedp in ht nejm 2005 sanjay gandhi

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Extreme anxiety due to new onset “Normal ECG”

Posted in cardiology -ECG, Cardiology -unresolved questions, Cardiology-Arrhythmias, Cardiology-Coronary artery disese, tagged , , , on February 28, 2013| 4 Comments »

We know  new onset LBBB  creates considerable anxiety . We  experienced a  reverse situation recently . A 72 year old  man who is known to have chronic LBBB  for over  5 years came  to CCU with vague  chest  discomfort .

His   ECG  was  perfectly normal . . . every one  was  curious !

My ECG always looked like this doctor  !  Now you say it has normalised and you say it concerns you  ! I am really worried  doctor  !

What does it mean doctor ?

Cardiologist : I do not know . Any sudden change in rhythm even if it is from abnormal to normal is to be given importance .

Patient : Is  the  going bad ?

Cardiologist :  I do not know

Patient : Should I  get admitted ?

Cardiologist : I think so  but you need to undergo few blood tests and repeat an ECG .

Patient : Oh  what ?  you  are not sure either !  Are you not an expert in heart  disease doctor ?

Cardiologist : I think I am . I wish I have an answer to  your question .

Follow up

This patient was admitted in intermediate care ward and observed for 12 hours .

His enzymes and Troponin were negative . Echo showed normal LV function .

He was discharged later and adviced  a stress test .

What is the the mechanism of normal ECG  here ?

Intermittent LBBB due to rate dependency is common .But this  man  had persistent chronic LBBB for > 5 years which got normalized .That mystified us !

Can transient ischemia of left bundle  accelerate  the conduction ?

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How to predict success in CTO : The Japanese CTO score sheet !

Posted in Cardiology -Interventional -PCI, Cardiology-Coronary artery disese, cath lab tips and tricks, cto chronic total occlusion, PCI PTCA Hardware, tagged , , on February 28, 2013| Leave a Comment »

Japanese are the pioneers in CTO reopening .(I understand they do less   CABG surgeries  for  religious reasons ) CTO is the ultimate test for cardiologist patience .  it may  take  hours to open up a CTO (or even to abandon it .)  Here is a  success prediction tool from Japan .

cto score success in chronic total occlusion

j cto score sheet

Source courtesy  : JACC: Cardiovascular Interventions Volume 4, Issue 2, February 2011

Reference

http://www.sciencedirect.com/science/article/pii/S193687981000912X

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CTO : The most important factor that determines the successful PCI ?

Posted in cardiology- coronary care, Cardiology-Coronary artery disese, cath lab tips and tricks, cto chronic total occlusion, Hardware techniques tips, tagged , , , , , , on February 27, 2013| Leave a Comment »

chronic total occlusion cto tips and tricks

Answer :

While each one of the above factor appears very much important  morphology of the lesion is the  clear winner  ( Which includes , the content of the lesion , hardness , micro channels , thickness of the proximal and distal caps, the length and   tortuosity   of the CTO     ( which is invisible ) the collateral status will ultimately determine the success)

It is becoming increasingly clear  cardiologist expertise is getting less and  less important .

Finally ,  it must  be told to our  younger generation of cardiologists , crossing a  CTO and deploying a stent  is not synonymous with success .It should result in long term sustained distal flow and make a significant impact on the patients symptoms (If at all any !) and survival.

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One more cause for Q waves without Infarct !

Posted in cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Coronary artery disese, tagged , on January 31, 2013| Leave a Comment »

We know q waves are not synonymous with Infarct . It just represents electrical activity going away from the electrode.This is why it can occur  even in physiologically in many leads.

Non  infarct Q wave can be recorded with

  • LVH
  • Fibrosis
  • Fluid/Air in beneath  the recording lead
  • Thick chest wall/pericardium (More often Poor  R wave )

rv cavity potential in inferior leads mimicking inferior mi q in

When a chamber enlarges (Any chamber )  it is  brought near the chest wall the electrode may pick up the intra cavity potential that is recorded as q waves .

(The q wave in V5-V6 in severe volume overload of LV may represent LV cavity potential )

Similarly qR complex in severe RV  enlargement  in V1 represent RA cavity potential.Right ventricle is anatomically a difficult chamber to understand. It is located anterior below the sternum  the inferior and posterior aspect of the RV  is facing the diapharagmatic  surface

copd ra rv enlargement mimic inferior mi q waves in 2 3 avf differential diagnosis

In huge RV enlargement , RV cavity potential or( even RA )  can be picked up by limb leads . While cavity potential is well picked up by unipolar pre-cadial leads , it is uncommon for limb lead  record  intracavitory  potential. However  this patient , who was diagnosed  as inferior MI by a  resident ,  turned out to be a clear case of severe  pulmonary hypertension due to  COPD .

Final  message

One  more differential diagnosis for  inferior MI in ECG  exists. A grossly dilated RA, RV due to COPD  with  severe  pulmonary hypertension.

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Stunning images of left main in routine echocardiography !

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, cardiology-Anatomy, Cardiology-Coronary artery disese, Echo library and gallery, echocardiography, great illustrations in cardiology, tagged , , , on January 23, 2013| Leave a Comment »

If only  . . . we get  an  image like this , echo can help rule out most  left main disease with conviction .

Have a close look  at it ! One can get a good image of  coronary ostia in short axis view . But , here it is well visualized  in long axis .

left main

I tried to put color flow within left  main .

left main color flow

What about pulsed  Doppler across left main ?

After all it needs 2mm sample volume and this left main was near 4.5mm . So keep trying !

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“Inferior MI” by ECG . . . “Anterior MI” by echocardiography . How common is that ?

Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Cardiology -unresolved questions, cardiology-Anatomy, Cardiology-Coronary artery disese, Clinical cardiology, echocardiography, tagged , , , , , , , , , , , , , on January 14, 2013| Leave a Comment »

Surprises are hall-marks of medical science . The cardiologists do  get  it ,   in enough doses   from  echo  labs  on a regular basis !   . One such thing is  the total ECG-ECHO myocardial  territorial  mismatch following  a STEMI .  Human myocardial segments are divided by cardiologists  by 17 segments by echocardiogram . Long before  echo came into vogue ,  electro-cardiologists  divided the  heart electrically into three zones to  localise MI . (Anterior , inferior and  the  poorly defined entity  lateral walls* ) .Inferior and posterior  segments are  almost used interchangeably. So , when we have 17  echo  segments to be fit into these three electrical category !   were  bound to have  some overlap . The issues of fitting in septal segments is really complex as septum  is a three dimensionally engulfs all three electrical surface of the heart .

* By the way , anatomists  never agreed about existence of walls in heart.They simply said  , heart has smooth  surfaces that blends with one another.  We cardiologist have  built imaginary walls and struggling to come out it !

We will   try to answer the question that’s been asked here .  “Inferior MI”  by ECG   . . . “Anterior MI”  by  echocardiography . How common is that ?

Possible causes for this wrong call

Technical errors  in  acquiring echo  imaging plane  or  it’s interpretation is the commonest . Many  times  ,  obliquely obtained long axis view  wrongly and strongly  suggests  a septal  MI  instead of   inferior posterior MI. This is  because  in  apical 4  chamber view  bulk of   septum  (Basal and mid third )  lies   in the  infero-posterior region .

wall motion defect

Perhaps ,  misunderstanding this  septal  geography is  the  commonest cause for  erroneously  calling inferior MI as anterior  in echocardiography . (A simple clue is the presence of MR . (It  fixes the infarct in infero-posterior zone with 90% accuracy )

Rotation  and  posture of heart

Alignment of the septum to the rest of the chambers  can influence  , how three inferior leads is going to look  at the septum (There can be  considerable errors  -Electrical myopia ? as these leads are located distantly )  . The plane of the septum is such that  in horizontal hearts  septal electrical activity  will be directed infero posteriorly inscribing a q waves in inferior leads rather than anterior leads . One can expect such ECG /Echo discrepancy in the following subset as well

  • Post CABG patients (Any pericardiotomy will make the septal motion  erratic )
  • Obese persons
  • COPD

There are three  more  situations  ,  which   mystified me   with  definite  ECG/ECHO  mismatch

  1. LVH and STEMI  is always an engima . Counter clockwise rotation when accopany  LVH  that masks anterior MI  electrically . It  however inscribes a   q wave in inferior leads.
  2.  In dominant LCX lesions  ( with at-least  one  major OM    )  and  left main bifurcation  STEMIs  ,  combination of  anterior and inferior  wall motion defects are  quiet common . When a such  a  MI evolves ( with or without  revascularization )   regeneration of R wave can be  time shifted . Septal R wave may appear  much earlier and inferior R may follow or vice versa . .Further,  anterior MI  may  evolve as  Non q MI  making it  ECG blind ,   still  echo may pick up the WMA . So there can be important  ECG-ECHO mismatch in myocardial segmental geography .
  3. Further , WMA  need not  always be an  infarct  .Any new episode of ischemia  can result in WMA . Hence a patient  with inferior Q waves  in ECG may experience anterior wall motion defect meagerly  due to fresh episode of   ischemia (This we should not attribute  to  old anterior  MI. It is also possible intra-myocardial conduction delays can elicit remote wall motion defects.

Final message

By general rule  , ECG  correlates  well  with  ECHO  for localising myocardial segments   . At times ,  it  can  really be tricky , and we  get into above situation  in echo labs.

While ,  it is common to observe  ECGs  to mimic  inferior MI  at the first look  and  subsequently echo  revealing  anterior  infarct ,  the reverse is also very much possible .

The  mechanisms are varied and technical  issues are for more frequent than true clinical discrepancy .The issue has important management implications.

Of course ,  coronary angiogram will pin point the   anatomy , still  it also has  strong limitations in localizing myocardial segments (to which it supplies ) especially with multi-vessel  CAD and  collateral dependent circulation .

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Top 5 conditions that closely mimic and often mistaken for STEMI !

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology- coronary care, Cardiology-Coronary artery disese, Infrequently asked questions in cardiology (iFAQs), STEMI-Primary PCI, tagged , , , , , , on November 11, 2012| 4 Comments »

Top 5 conditions that closely mimic and often mistaken for STEMI !

  1. Early repolarisation syndrome
  2. Left bundle branch block(LBBB)/ Left ventricular hypertrophy(LVH)
  3. Hyperkalemia
  4. Pericarditis
  5. Brugada syndrome

ERS

The repolarisation is due to  K + efflux . The  K channel porosity  is subjected to high degree of genetic  variations .If the repolarisation starts even by 10 milli- second earlier,  it would have early take off from descending  limb of R wave  and  the J point  ST segment appear elevated.

  • Common  in young  males . Especially in vago-tonic persons with relative baseline bradycardia
  • The ST elevation in ERS is often global .
  • Concavity is upwards .
  • ST elevation can be dynamic ( Further  confusing the picture ! )
  • On EST it  is expected to the  touch the baseline .
  • Benign entity in most . ( False alarm of STEMI is the major risk !)
  • There is some evidence ERS may confer a risk  of  primary VF ,  if they  experience a true STEMI  (Michel Haïssaguerre 2008  NEJM )

* STEMI in ERS :  The issue becomes too delicate ,  if  a  patient with ERS  develops  a true ACS .   ERS being a common ECG pattern in general population , it is not wise to label  every  chest pain in  ERS patient as benign . Suspicious  ones demand observation in step down units , at least !

LBBB

 “Any patient with  LBBB & chest pain . . . suspect  MI”  .

Unfortunately,  this rule is  too reverently followed by  physician community.  In fact ,  ACC/AHA guidelines  reinforced this behavior ,  as it  added a key word  in  their STEMI guidelines   “New onset”  or   “presumably new onset ”  LBBB is  an  indication for PCI/Thrombolysis    .( Physician presumption is a too delicate thread  to hang  our concepts !   )

               Every LBBB is new onset unless you have  a  documented proof otherwise  . . .   it seems to suggest !

Probably , this  is the reason many of the LBBBs are thrombolysed when they present to ER in an acute fashion . Of course , we can apply criteria of  Sgarbossa  to differentiate !  however flimsy it may appear . It  help us to exclude few benign LBBBs. Still ,  Sgarbossa will  struggle to  differentiate  an acute STEMI  in Chronic LBBB  from an  acute LBBB in  old AWMI .

Simply put . . . even old MIs  are at risk of  acute intervention if they have LBBB  and vague chest pain !

How to overcome this ?  Always rely on clinical  features  . If  STEMI is causing the LBBB ,  it  should be a large extensive one and you can not  expect the patient to be  comfortable .(Logic  would suggest necrosis of  large  parts of IVS is necessary to cause LBBB ) Chronic  LBBBs  are relatively comfortable  .

Of course , there  is one another  issue to comprehend  ie  transient ischemic LBBB .We do not know the true incidence  and long-term significance of this entity . Here , LBBB is  not due to necrosis of  the bundle but due to ischemia . (Almost impossible to differentiate it from  rate dependent LBBB  with  aberrancy  )

Role of enzymes and Echocardiogram in LBBB  and suspected STEMI .

You can always ask  for   Troponin  T / CPK MB .(They are helpful only  if 3 hours have elapsed , can we afford to wait ? ) . LBBB  due to STEMI  will  purge  a large quantum of cardiac enzymes from the infarcted zone . (So a marginal elevation is not going to help!)

Unfortunately,  LBBB  can induce wall motion defect in septum that may awkwardly simulate an ischemic wall motion. Even experts have erred in this . One clue  is,  the motion defects  can  not  extend   into anterior wall . It  is confined to septum ,the second clue  is a little delayed  post QRS  thickening of IVS (Septal beaking sign will vouch  for benign LBBB with fair degree of success  )

LVH

  • LVH can mimic a STEMI due to secondary ST/T changes . (Secondary to tall R wave )
  • LVH with incomplete LBBB  – A very common association that can further elevate ST segment in v1 to v3 .
  • Left ventricular hypertrophy  mimics old MI as poor R wave progression in V1 to  V3.
  • Contrary to our belief even Inferior  leads can  show q waves due to  inferior  septal hypertrophy.

Hyperkalemia.

With aging population and rampant  acute and chronic renal disorders it is becoming  a daily affair to get calls from medical units for ECG changes .We know  the rapidity of  efflux  potassium is responsible for ventricular re-polarisation .Phase 2, and 3 are K + exit zones. This is the same phase ST segment and T wave are inscribed.In hyperkalemia  K + accumulates inside the cell and keep  ST/T  segment  elevated .T wave also  becomes tall . It can mimic  both as hyper acute  STEMI .

Read a related article (Dialyisable current of Injury )

Pericarditis

  • ST elevation is not confined to an arterial territory
  • Can be global .(Regional ST elevation  does not exclude pericarditis)
  • ST elevation is concave upwards as in ERS

Link to Read regional pericarditis
Brugada syndrome

Brugada syndrome  is  an ECG -Clinical complex in which ST elevation in pre-cardial leads is associated with  ventricular arrhythmia. The defect lies in sodium channel . It reflects  a mis -match between RV and LV epicardial repolarisation forces .It keeps the RV epi-cardial current afloat and  the pre-cardial leads  facing the RV records ST elevation that  mimics  STEMI. It often  shows  a RBBB pattern and varying patterns of ST morphology  . The  ST segment is  also  subjected to dynamism  , due to change in autonomic tone and myocardial temperature  .(Febrile VTs)

After thoughts

Other close contenders for the top 5 slots

Myocarditis

Acute pulmonary embolism

Dissection of aorta

More

  • Acute stroke (Neurogenic ST elevation )
  • Stress cardiomyopathy (Takot Subo )
  • Acute abdominal conditions mimicking inferior STEMI.
  • Panic attacks /Anxiety states / chronic anti psychotic  medications which are known to elevate ST segments.
  • Contusion chest

(Cocaine hearts / Coronary arterial spasm / LV dyskinetic segments  and  LV aneurysms  were not nominees ! )

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What is the mechanism of dyspnea when it occurs as “Anginal” equivalent ?

Posted in Cardiology - Clinical, Cardiology -unresolved questions, Cardiology-Coronary artery disese, tagged , , on October 31, 2012| Leave a Comment »

Anginal equivalents are distinct  (often vague  ) symptoms that occur in response to myocardial Ischemia , instead of angina. Dyspnea or shortness of breath  is the commonest anginal equivalent . The incidence and exact mechanism  is not clear. Both angina and dyspnea are sensory  events . Both are  perceived  at the level of cortex. Angina occurs when ischemic  muscle  triggers pain signals from the   nerve  twigs engulfing the myocytes membranes  and the vasavasorum.

Dyspnea during myocardial  ischemia  is multi-factorial

  1. Signalling error .( Mismatch between respiratory /Cardiac  receptors  neural traffic)
  2. Cortical perception disorder.
  3. Autonomic neuropathy (Blocks pain signals  but still may carry  myocardial stretch response)
  4. Coronary sinus lactate –  Biochemical /Chemo receptor stimulation
  5. Isolated  Ischemic LV relaxation defects  , and resultant elevation of LVEDP
  6. Ischemic systolic stunning  and secondary  diastolic dysfunction  (elevated PCWP  pulmonary stretch receptors stimulation )
  7. Ischemic MR . Eccentric MR jets and regional and segmental elevation of pulmonary venous pressure has been reported. (Unilateral and segmental pulmonary edema)
  8. It is possible  ,  Ischemic wall motion defect per-se  can induce myocardial stretch and create a feeling of dyspnea.

Out of the above eight factors  which is  most important  ?

The most popular and easy to comprehend   mechanism   is number 5 : Ischemic diastolic dysfunction .

(Fellows will be appreciated if they  know this !   )

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