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Archive for January, 2017

Knowledge can be a dangerous asset sometimes . A modern day cardiologist reassured a patient  who had an unusual dyspnea after a muti-vessel stenting for a not so complex lesions following an anterior MI.The doctor  was not mystified when the patient uttered this complaint. In fact he was so cool , reassured the patient since he was taking  Ticagrelor ,and it’s well recognised to cause dyspnea in some patients.

Few days later patient  called  again and informed that the  dyspnea is getting more intense  and ultimately he was rushed to hospital only to diagnose  subacute stent occlusion and a fresh ACS.

What do you learn from this story ?

Caution , extreme caution is required when dealing with symptoms following PCI and especially dyspnea.

A brief review about  Ticagrelor dyspnea conundrum

  • Ticagrelor  ,a reversible P2Y12 blocker  has a peculiar side effect of dyspnea (Which happens to be a cardinal symptom of heart disease as well )
  • Its reported by up to 30 % of patients who receive it.
  • It can be either exertional  or even at rest.
  • It seems to be dose dependent
  • Onset within 24 hrs , upto 1 week.
  • Pulmonary function not affected.
  • Cardiac function thought to be unaffected.(No correlation with LVEDP though)

Mechanism of dyspnea with Ticagrelor (Presumed)

  • Its direct cortical effect due  sensory neurone  P2Y12 blockadae.
  • Due to Adenosine

Remedy 

  • Reassurance(Possible in few , but risky unless absolutely confident)
  • Encourage Tea intake (Theophylline might nullify if its Adenoisine induced .
  • Discontinuation is  the specific option (up to 10%)

Final message.

Dyspnea is a  unique side effect of Ticagrelor. Unexplained dyspnea is a delicately dangerous symptom in a post MI patient as it may directly imply a silent ischemia induced LV contractile dysfunction and acute raise in LVEDP.

Don’t ever take it easy and attribute all episodes of  dyspnea to Tiacagrelor .If you are really not convinced consider switching the patient to a different anti-platelet drug. Its simply not worth for both patient and physician to spend anxious moments.

Reference 

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This paper was presented as a poster (Not good enough for  oral ! ) in the just concluded CSI 2016  (Cardiological society of India ) Annual conference at Kochi, India.

dr-venkatesan-e-poster

What constitutes successful  Primary PCI ?   A proposal to include “ LV dysfunction”  as an  essential  criteria !

A  series of breakthrough technologies  in drugs , devices, techniques has revolutionised the management of STEMI in modern times.This  includes various formats of heparin , antiplatelet agents thrombolytics  and coronary interventions.Of all these, primary PCI is considered to be the greatest thing to happen in STEMI care.

The success of primary PCI is currently defined as diameter stenosis less than 30% and TIMI 3 flow on final angiography without procedural complication. True success of reperfusion essentially lies  in the salvage of myocardium and in the prevention of LV dysfunction. In real world scenario we often find a paradox , ie Inspite of  successful pPCI by current definition a subset of patients suffer from significant  LV dysfunction. Surprisingly, LV dysfunction has  never been included in the definition of successful primary PCI .

success-of-primary-pci

In this context we did a reversed cohort  study  of patients with significant LV dysfunction (<40%) following primary PCI to find out possible factors contributing to LV dysfunction.10 patients who had LV dysfunction inspite of successful primary PCI were the subjects of the study. Patients with late PCI  beyond 12  hours were excluded .Echocardioraphy had been done at discharge and 2 weeks after the procedure to assess LV function.

TIMI  3  flow  has been  documented in all  patients at the time of primary PCI.6 patients had undergone pPCI within 6 hours.4 had it by 12 hours. 7 patients had a smooth , fast  pPCI as described by standard protocol.Of these,  2 patients had LV dysfunction inspite of TIMI 3 flow established early.7 patients 3 had complex angioplasty with no reflow managed subsequently.One had deferred stenting after 4 days for IRA.Non IRA lesion were also  tackled in two.

We also confirmed  there is no linear no correlation  between TIMI flow and  subsequent LV function .This becomes vital as time and again we are seeing PCI reports with successful TIMI 3 flow only to find  weeks later  thinned scarred ventricle. Time to reperfuse with anticipated and unanticipated procedural delay  was also  a critical  factor.

However, its clear the  incidence of significant LV dysfunction inspite of  timely, and apparently smooth  PCI is real .Why this happens is beyond the current reasoning. A scientific basis for  individual myocardial sensitivity to ischemic time is yet to be found. (Dynamic host dependent time window ?)

Meanwhile , It seems prudent , we should awake to a harsh reality of practicing coronary care  with a seemingly incomplete criteria for success of pPCI . Its proposed,  an  acceptable levels of  “LV dysfunction at discharge ” (It could be > 50 %) as an essential criteria  to define the success of pPCI  .Custodians of STEMI care should  immediately rectify this glaring omission. This will dramatically impact the current  outcome analysis of STEMI and help Improve the quality of care.

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