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Posts Tagged ‘Chronic stable cad’

Yes, it is a triple vessel disease, with one tight lesion and at least two other significant lesions. One of them appears diffuse as well. 

Representative Image: Source courtesy DOI: 10.14740/cr548w LicenseCC BY-NC 4.0

“What to do next?. Is he symptomatic?  Yes. Definitely has significant angina” but LV function is normal.

“Ok then. If you are daring enough, ask this question”.

Which lesion is causing angina?

No easy answer at all. Try looking for some clues right from history, ECG, stress ECHO, meticulous assessment of individual lesions. Realize, even sophisticated imaging like SPECT, PET functional MR, may not help much either.

Oftentimes, we need to use the lean resources of collective common sense and clinical acumen. 

  • If it is post ACS status,  consider residual ischemia in the culprit artery is the cause for angina.
  • Second, consider the tightest lesion as angina-related.
  • Or the complex, eccentric, thrombotic lesion is responsible.
  • Next, consider LAD as default lesion as  angina related artery (Statistically right 75%, prognostically perfect decision) 
  • Watch for ECG changes during chest pain (ST depression usually don’t localize, but experience tell us V5 /V6 ST depression is more likely to be LAD ischemia )
  • Echo wall motion defect either during rest or (more usefully) in stress can really help. (It needs some effort to look for Wall motion mapping with coronary lesion subtending segment)
  • What about balloon inflation test during PTCA ? . Prompt angina when a lesion is occluded may give a direct clue.

Want to get more confused?

  • Ask your colleagues for an opinion either online or offline.
  • Do FFR/QFR/IFR  and OCT and look for intracoronary pressure-flow data and plaque burden. We are entitled to get excited about fibrous cap thickness, and hunt for vulnerable lesions and decide thereupon.  

Finally some easy options. 

Which lesion is causing angina? Never entertain that troubling question at all. (Need not  squeeze your coronary intellect you know ) 

Consider every lesion as important 

  • Get ready to stent all three or more lesions.(Many times forbidden though !)
  • (or) More convenient, refer to CABG. (Surgeons will welcome for sure )

Final message

Which lesion is causing angina? is indeed an important query one should raise. This paves way for selective focussed PCI in deserving lesions alone. However, when dealing with complex lesions subsets. the most pragmatic way as of today is to educate the patient and include them in the decision-making process (Never forget to offer medical management as a permanent option, especially if there is no critical LAD disease, and say thanks to  ISCHEMIA/COURAGE/ BARI 2D.)

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Why ISCHEMIA trial conclusions often make us nervous?

Because, we know we can’t follow the lessons from it with true intent, as many of us are near slaves to Invisible Interventional forces in some form or other.

I would think, ISCHEMIA trial in one sense was a wasted effort. We always knew OMT is superior to any sort of PCI in stable CAD  (Backed up with COURAGE /BARI 2D/and of course the deadly exposure by ORBITA )

Anyway, we did ISCHEMIA for the sake of deniers, with huge public funding to prove the truth as truth.

Still, I am sure ISCHEMIA will be looked down, by most elite Intervenionlists. For the rest, it becomes a tough fight with their conscience. 

A recent review on European cardiology review 

Final message 

I don’t know, how many more trials would be required to tell us the same story all over again. Hope we grow enough COURAGE to follow the ISCHEMIA lessons. Let us (try to ) make a full stop on this issue.

 

 

 

 

 

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