Dr.S.Venkatesan MD

ST segment depression is the classical response to stress during  excercise stress testing. (EST)Not all types of ST segment are  pathological.The ST segment should depress  atleast 1 mm below the  isoelectric segment and it should be depressed for 80msec from the  J point.

It must  satisfy   two criteria .

1. The quantum of ST depression should be >   1mm at 80msec from  J point.
2. Slope of ST segment

Always pathological slopes

• Horizontal
• Down sloping

Most often pathological

• Slow up sloping

Non pathological slope

• Rapid up sloping with ST depression
• Rapid Up sloping  depression of  only the J point( The classical  normal physiological response to excercise )

Horizontal or down sloping ST segment is easily recognised .When there is  junctional ST depression with a ST segment that is  climbing upwards , it is some times difficult to interpret.

How do you measure the slope of ST segment ?

We don’t have the trouble of measuring it as the computer does this job automatically. But a cardiology fellow  need to know how it is measured !

A slow upsloping ST segment( <1.5mv.sec )can be a significant marker of ischemia.This is especially true in established CAD or individuals at high risk . For  so slow up sloping a .5mm allowance is given to filter out false positive (ie to improve sensitivity) . So for slow up sloping ST segment , to be reported as positive it should depress atleast 1.5mm or some times  2mm.

Available evidence suggest a rapidly upsloping ST segment (> 1.5mv /Sec)  is a non ischemic response irrespective of the quantum of ST  depression  at 80msec. However ,  a rapidly upsloping ST  is rarely depressed beyond 2mm .( This is because , the geometric hyperbolic curve  of ST segment does not allow a situation of  3mm ST depression at 80msec with rapid upsloping )

What is the  angiographic correlation of  slow upsloping ST segment depression?

Few studies are availbale  to address the issue. It is believed  slow up sloping  of  ST depression is often associated with CAD but it is very rare to find a critical and proximally located CAD.Left main disease is almost never manifest with slow upsloping ST depression.

What is the significance of slow upsloping  ST in clinical situations like unstable angina ?

It is rare for cardiologist to diagnose or “even look for” slow or  rapid up sloping ECGs in coronary care units. But , a  patient with stable  CAD ,  sinus tachycardia ,  angina can exactly mimic a stress test  situation .

Some of the low risk UA , mainly secondary UA due to increase demand situations manifest with slow upsloping ST depression , while classical thrombotic occlusions produce the typical horizontal or downsloping ST segment depression.

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It is often said life is a cycle , time machine rolls without rest and reach  the same  point  again and again . This is  applicable for the  knowledge cycle as well .

We  live a life ,  which is infact a  “fraction of a time”(<100years) when we consider the evolution of life in our planet for over 4 million years.

Man has survived and succumbed to various natural and  self inflicted diseases &  disasters. Currently,  in this  brief phase of life  , CAD is the major epidemic , that confronts  modern  man.It determines the ultimate  life expectancy . The fact that ,  CAD is a new age  disease   and  it was  not  this rampant ,   in our ancestors  is well known .The disease has evolved with man’s pursuit for knowledge and wealth.

A simple example of how the management of CAD over 50 years will  help assess the importance of  “Time in medical therapeutics”

• 1960s: Life style modification and Medical therapy  is  the standard of care in all stable chronic  CAD The fact is medical and lifestyle management remained the only choice in this period as   other options were not available. (Absence of choice was  a blessing as we subsequently realised  ! read further )
• The medical  world started looking for options to manage CAD.
• 1970s : CABG was  a major innovation for limiting angina .
• 1980s: Plain balloon angioplasty a revolution in the management of CAD.
• 1990s: Stent scaffolding of    the coronaries  was  a great add on .Stent  was too  dangerous  for routine use  was to be used only in bail out situations
• Mid 1990s : Stents  reduced restenosis. Stents are  the greatest revolution for CAD management.Avoiding stent in a PCI  is unethical , stents  should be liberally used. Every PCI should be followed by stent.
• Stents have potential complication so a good luminal dilatation with stent like result (SLR)  was  preferred so that we can avoid stent related complications.
• 2000s: Simple  bare metal stents are not enough .It also has significant restenosis.
• 2002: BMS are too notorius for restenosis and may be dangerous to use
• 2004 : Drug eluting stents are god’s gift to mankind.It eliminates restenosis by 100% .
• 2006:  Drug eluting stents not only eliminates restenosis it eliminates many patients suddenly by subacute stent thrombosis
• 2007 : The drug is not  the culprit in DES it is the non bio erodable polymer that causes stent thrombosis. Polymer free DES  or   biodegradable stent , for temporary scaffolding  of the coronary artery  (Poly lactic acid )  are likely to  be the standard of care .
• All stents  are  potentially dangerous for the simple reason any metal within the coronary artery  has a potential for acute occlusion.In chronic CAD it is not at all necessary to open the occluded coronary arteries , unless  CAD is severely symptomatic in spite of best  medical therapy.
• 2007: Medical management is superior to PCI  in most of the situations in chronic CAD  .(COURAGE study ) .Avoid PCI whenever possible.
• 2009 :The fundamental principle of CAD management  remain unaltered. Life style modification,  regular  exercise ,  risk factor reduction, optimal doses of anti anginal drug, statins and aspirin  is the time tested recipe for effective management of CAD .

So the CAD  therapeutic  journey  found  it’s  true  destination  ,  where it started in 1960s.

Final message

Every new option of therapy must be tested  against every past option .There are other reverse cycles  in cardiology  that includes the  role of diuretics  in SHT , beta blockers in CHF etc. It is ironical , we are in the era  of rediscovering common sense with sophisticated research methodology .What our ancestors know centuries ago , is perceived to be great scientific breakthroughs . It takes  a  pan continental , triple  blinded  randomised trial   to prove physical activity is good  for the heart .(INTERHEART , MONICA  studies etc) .

Medical profession is bound to experience hard times in the decades to come ,  unless we  look back in time and “constantly scrutinize”  the so called  scientific breakthroughs and  look  for genuine treasures for a great future !

Common sense protects more humans than modern science and  it comes free of cost  too . . .

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Opening the chronically occluded coronary(CTO)  artery  gives the ultimate sense of  achievement and satisfaction for the cardiologist.  Of course , the patient may  or may not share the same feeling  . . . ! There are simple  and  complex CTOs . Some CTOs are opened in few minutes ,  some fail even after  hours of manipulation . For successful CTO opening  both  hardware and technique  are equally important.

Now we understand , acquiring expertise   with one or two guidewires  and mastering  them  is the key to success. Frequent changing of guidewires and other hardware  has increased the complication.

Definition of success in CTO

Unfortunately cardiologists  have varied perception on this vital issue . Most believe opening a CTO is synonymous with success . Some perceive  even crossing a  CTO with a guidewire is  a partial  success ! Real success lies in providing  sustained  opening  and restoring flow till  the  micro circulatory level. Advancing the distal blood flow for a short distance at a low velocity   can not be termed a success . It must be ensured  all  the  branches of    opened coronary artery must be perfused . This is a tricky issue as we can only  guess the number  of branches it had , before getting occluded.

The other most important  factor in determining the success of CTO  opening is the status of distal microcirculation . A dead myocardium does not welcome  the blood flow ! .It simply rejects it and this results in lower grades of TIMI flow. This factor is  mainly responsible for the negative clinical  outcome of   major PCI trials( TOAT, COURAGE)

The newer devices are helping us to  achieve our goal .

• Retrograde approach through collaterals
• Sub initmal tracking of CTOs
• Japanese have pioneered the CTO interventions

http://www.abbottvascular.com/av_dotcom/url/content/en_US/10.10.270.10:10/general_content/Abtdiv_General_Content_0000182.htm

http://www.flowcardia.com/index1.html

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ECG is the summated  recording  of individual  myocyte electrical activity from the body surface .The single cell action potential  represent the classical description of ionic  flows within and outside the cardiac myocyte. ECG is nothing but the electrical recording of systematic flow of ionic currents. When one looks at qrs complex  we should  mentally see the  Na ions getting in  .When  the ST/QT segment begins the calcium  enters ( Some chloride also )  and K + begins to leave cells .As we look at the sharp or blunted  T waves we are actually looking at potassium channel activity.

The phase 0 is  the rapid inflow of sodium ions into the cell. Contrary to this  , during the repolarisation of myocytes  the   efflux of potassium from the cells occur more slowly .This  , along with slow calcium influx create   the sustained dome of action potential .The phase 3  begins with a rapid efflux of k+   which corresponds to inscription of T waves.Phase 4 occurs in diastolic depolariation .

Note : *Na exit from cells occur very fast  ( Which is not mentioned in the diagram  .This again is an  important event  . Pharmacologically Na channel manipulation  is  often  done .All class 1 anti arrhythmic drugs block  this channel.

It’s obvious  , T wave genesis is greatly influensed by k+ dynamics.A tall t wave indicate high intracellular concentration of k and efflux of K + further slowed down as reduced gradient acrosss the cell membrane.This results in tall t waves.There is  a fairly  good correlation between K+ levels and T wave amplitude.Similarly when there is hypokalemia , there is inversion of T waves with associated  with prolongation of QT interval.

While  T waves are linked to  K +  , the QRS complex is closely linked to Na + concentration , but still sodium levels rarely alter the QRS complex why ?

Hyponatremia is a common electrolytic disorder , especially in elderly and in patients who are over treated with diuretics. Dilutional hyponatremia due to excess free water is a common finding in CHF.While ECG is very helpful  to diagnose hyperkalemia , it is rarely useful in hypo or hypernatremia.

This is  primarily due to two reasons .The Na induced depolarisation is a very fast event  ( Max 80ms) . K+ efflux is a slow event  up to 400 ms . Unlike K +  , Na+  can not prolong the QT interval however low it’s levels are . This is due to the fact Sodium channels have a huge gradient across  the cell even if the serum sodium levels fall. Further,   Na is an extra cellular cation and has little influence  within the myocyte. But , occasionally wide qrs complex or aberrant  conduction , bundle branch defects are observed due to hypo or hypernatremia .The exact mechanism is not known.

Conduction defects and electrolytes

Similarly K+  ions have major effects on SA node and AV node .It can depress them , though reversibly it can have serious consequences. It is very rare for Na+ to have any major effect on conduction tissues. Multiple electrolytic defects with associated acidosis can have variable effect on ECG morphology .Abnormal  calcium and magnesium levels   can have serious effects of cardiac excitabillty.

Note : *Na exit from cells occur very fast   ( Which is not mentioned in the diagram ) .This again is an  important event  . Pharmocologically Na channel manipulation is done with all class 1 anti arrhythmic drugs act on this channel.

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Regional wall motion defect is the sine qua non of STEMI. Whenever there is sudden occlusion of a coronary artery , the segment  it supplies is expected to go in for mechanical dysfunction. This is the fundamental principle of ischemic cascade . But , in NSTEMI ,wall motion defects are not a consistent feature. In fact absence of WMA is much more common than it’s  presence.The concept of ischemic cascade tells us  that chest pain is the last  thing to occur in the series of events following ischemia.

But in reality it seems the myocardium rarely obeys  this rule

The incidence of WMA in unstable angina or NSTEMI could be  at best 25 % . How and why the majority  do not manifest it ?

1. The ischemia has to be extensive to produce WMA.
2. Presence  of even minimal  collateral circulation  could prevent WMA.
3. Sub epicardial or transmural  ischemia are more likely to result in WMA. Isolated subendocardial ischemia could not manifest the WMA as the epicardial band of non ischemic  contractile  myocardial tissue has a  piggyback effect on the ischemic segment and  hence WMA do not manifest.
4. Presence of LVH has an attenuating effect on the WMA.It is  a well realised fact ( Of course ,with very little published evidence !) LVH is a great protector of mechanical dysfunction during ACS.It can even  nullify the  mechanical effects of   STEMI sometimes  . Read my blog advantages of LVH .
5. Some  myocardial segments  which are less exposed to wall stress than others do not manifest WMA. For example, the myocardial segments supplied by the LCX territory are notorious for  being totally silent .
6. WMA equivalents. Some times,  the WMA defect is  very subtle for the eyes , but still good enough to result in  ischemic MR.
7. Electrocardiographically  T wave ischemias rarely produce WMA ,  while  resting ST segment depression > 2mm invariably result in WMA.
8. Some  would  suggest ( Especially the researchers !) WMA  is always there  concealed within as   we are unable to pick it up with  available imaging modalities.Trans thoracic echo has well known   limitations. If we do tissue doppler studies.(TDI) and myocardial strain rate it may show the WMA which is otherwise missed.

*Finally and most importantly  , it need to be emphazised even  few ischemic myocytes can trigger a clinical chest pain while it requires the collective efforts  few million ischemic myocytes  to apply the  “vice like   grip ” on the  myocardial contractility that result in WMA.

Just think about this

The concept of pharmocological stress testing like doutamine stress echo  , relies hugely on the phenomenon of ischemia induced wall motion defect , which is picked up by echocardiography.As we  recognise ,  even  in   real life , true  ACS the incidence of WMA  is very less  , how can ,  it be  logical to expect  pharmocological stressors to give us authentic  information regarding hidden  subclincal CAD.

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