Posts Tagged ‘reciprocal st depression’

ST segment depression is a fairly common observation in anterior precardial leads. It   is  due to

  1.  Pure electrical phenomenon (Referred to as reciprocal changes)*
  2.  Additional  ischemia in LAD territory
  3.  It could imply  the IRA  is  a critically occluded  LCX and STEMI is actually an   infero -posterior STEMI
  4.  Simply  indicate a  multi vessel disease.
  5. Many times  reciprocal changes may simply indicate extensive nature of the  index  inferior MI.

How to differentiate reciprocal ischemia from true  remote ischemia ?*

  • Logically true ischemia patients  should suffer from double dose of angina (Infarct pain plus ischemic). Most of these patients will present in a   scenario of  post infarct persistent  angina . Patients with   pure electrical reciprocal  changes are relatively  quiet and  severe distress is uncommon.
  • In true ischemia  , both patterns are  not temporally related  in time. If its a  pure electrical phenomenon they should be linked in time .
  • Disproportionate ST segment depression  (ST elevation  in inferior lead  is  2 mm  while ST depression in v1,v2, v3 is >  3 mm )
  • Persistence of ST depression even after thrombolysis  or PCI to IRA.
  • Worsening with thrombolysis would suggest ST depression in V1V2 and v3  is indeed an  episode of  true NSTEMI  of LAD , where thrombolysis is contraindicated. (Also  read  – A  related article  dual acute coronary syndrome in this site )
  • Echocardiogram will give us a clue .One can  detect ischemic the wall motion defect in the segment in dispute .(Reciprocals do not show WMA )
  • Coronary angiogram   would provide   definite  answer to the speculations in most  . Still , it may   require a FFR  to confirm ischemia in the contra lateral artery.

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Is reciprocal ST  segment changes  occur  only in STEMI ? Can it occur in UA/NSTEMI ?   


                      Even   after   100 years of electro cardiology   the electrophysiological mechanism of ST elevation in STEMI  and ST depression in Unstable  angina is   still in the hypothetical stages. One popular theory   says that the   current of injury   as we see   as  ST  segment elevation  in surface ECG  is  actually   an illusion. It’s   apparently due to   constant negative current    pushing down the   rest of ECG segments. Ironically   the concept   of  reciprocal ST depression in patients who have  ST elevation is well debated  for over 3 decades and  is considered  a  settled issue. It   probably   represents , a  purely electrical phenomenon where the  tail end  of the  lead   picks up the opposite vector. Even   as   conflicts   continue to confront the basic electro physiological   concepts management    strategies   of   acute coronary syndromes is witnessing   great strides.
                                     We   hypothesized   if   ST depression occurs as response to ST elevation it’s logic to expect strong ST depressive forces should  possibly elevate The ST segments in the reciprocal leads .
In fact  we have seen this phenomenon in three distinct  clinical situations. 
1) ST   elevation   in posterior leads: Patients who present   with isolated   ST depression in V1,  V2 , V3  and  ST elevation in posterior chest leads V7, V8 .These patients were initially thought to have isolated posterior MI. But later the cardiac enzymes were found to be normal   indicating no myocardial necrosis   echo evaluation revealed wall motion defects in anterior segments rather than in posterior segments. CAG revealed critical   LAD disease .  This we believe a pure reciprocal ST elevation in the posterior leads to  a  ST depressive forces in anterior leads.
 2) Inferior  ST   elevation   with ST depression   in   V4- V6 : Few  patients who present with  infero    lateral STEMI   later  do not  evolve into  Q  MI but as a NSTEMI .The initial ST elevation  was found  be transient and  disappeared  much earlier,  while the  ST depression  lateral leads persisted.
 3) ST elevation in AVR   in high risk unstable angina :As   already reported in the literature,  we have seen  ST  elevation in AVR  in patients with  high risk unstable angina. This was   more often observed when there is > 3mm ST depression in V4-V6. The AVR  ST elevation  possibly   represents   the  reciprocal  vector.
                                            ST elevation in certain   specific leads in   some of the patients with ACS,   could   be   a pure reciprocal   electrical phenomenon   to   dominant ST depressive forces in Opposite leads .  And hence   ST elevation in the surface ECG during early hours of ACS   should be interpreted more cautiously. The   sanctity   assocociated with ST segment   elevation   could  be  opened   for debate. 
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