Archive for July, 2021

A 75-year-old male post CABG with severe LV dysfunction and ICD and dual-chamber pacer in situ presented with NSTEMI.

An angiogram revealed something, and he got this form of treatment. ? What is it?

Image and case courtesy Patel R, Ghadiam H, Patel P, et al. (April 05, 2020) Angina Leading to Metal in the Heart: An Interesting Case of Saphenous Vein Graft Coiling. Cureus 12(4): e7546. doi:10.7759/cureus.7546

Features of SVG venous graft aneurysm

Graft aneurysm what are the risks?

  • Thrombosis
  • Recurrent ACS
  • Rupture 


  • Vascular plug
  • Multiple coils  (Does coil occlusion offer a permanent cure?  I can’t think so )
  • Covered stent
  • None. No Intervention Just OAC & observe, follow up can be a good option and can beat all above three in many patients.


1.Ramirez FD, Hibbert B, Simard T, Pourdjabbar A, Wilson KR, Hibbert R, Kazmi M, Hawken S, Ruel M, Labinaz M, et al. Natural history and management of aortocoronary saphenous vein graft aneurysms: a systematic review of published cases. Circulation 2012;126:2248–2256.CrossrefMedlineGoogle Schola

2.Dieter RS, Patel AK, Yandow D, Pacanowski JP Jr, Bhattacharya A, Gimelli G, Kosolcharoen P, Russell D. Conservative vs. invasive treatment of aortocoronary saphenous vein graft aneurysms: treatment algorithm based upon a large series. Cardiovasc Surg 2003;11:507–513.CrossrefMedlineGoogle Scholar

3.Nolke L, McGovern E, Wood AE: Saphenous vein graft aneurysms; the true, false and ugly!. Interact Cardiovasc Thorac Surg. 2004, 3:631-633. 10.1016/j.icvts.2004.07.011

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TAVR is a game-changing structural interventional procedure that delivers an Aortic valve percutaneously. With hardware and expertise constantly Improving, excellent outcomes are common. However, this video clip reminds us, nothing can be taken for granted in any Intervention. (Sharing a Twitter feed Courtesy Raffaele Piccolo)

Why did this complication happen? Hardware, technique, or a fragile Aorta?  or just bad time  The fatal perforation seems to have occurred near the distal arch, with no visible signs of porcelain Aorta or gothic aortic arch. What could have been done? Could an ultra-fast deployment of a covered stent with ECMO support possible? Extremely difficult task.

Further reading 

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Evidence-based medicine (EBM) is being projected as a scientific God’s secret specialty. Physicians who don’t follow EBM are considered unfit non-professionals. Presumably, in pursuit of truth, all those glamorous official bodies in cardiology bring out umpteen number of protocols, guidelines, advisories, and recommendations.

The blueprint for EBM

We have the famous 3 levels of recommendation backed up by different levels of evidence. Many of us trust these as the jury’s final verdict for most illnesses in cardiology. I would like to bring one particular issue about this hugely popular model of EBM. It is about one specific class of Indication referred to as 2b. The other day, there was an intense argument for an ICD in a young HCM patient and CRT in DCM based on this 2b stuff. Kindly request all of you to pause for a moment and introspect. We can realize, class 2b plays a mischievous game in EBM with the English language “may and may not”. It tries to push subconsciously an interventional bias from equipoise, in spite of lack of good evidence and clear divergence of opinion and a possible trend towards harm.

Further, there is widespread reluctance in many cardiac workgroups to refer class 3 recommendations as an absolute (or at least relative contraindication) It was strange to note one of my colleagues argued that,  class 3 is also a fair recommendation, to accept or reject is in our domain. I was initially shocked to hear that but had to agree with him ultimately as we realized a significant chunk of interventions we do, like delayed PCI > 24 hrs, CTOs, and chronic stable belongs to the proud class 3 recommendation. The debate came to a funny end when a senior cardiologist confessed somehow class 3 seemed to be a lesser evil than even class 2B.

Final message

For the sake of our patients, we need to bring an urgent reform in the EBM. Let us merge class 2b with class 3 and put it in a single basket and keep it out of reach to all tempting stakeholders. We shall display only class 1 in our therapeutic showcase.


(*Dynamic recommendations is the norm in science, as we accumulate evidence with time.. Agreed, let us do this silently in research labs. Don’t bring it to practical guidelines. No, can’t agree. Freedom to indulge with an experimental modality in a no-option patient must always be there as we are able to give the benefit of doubt to these helpless patients. This is a valid argument but we must not forget even in dire situations  good option need not be a compulsive action, it can be in action as well)



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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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“Third wave? what is that”

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Basic science lessons are promptly forgotten by the time we reach the final year of medical school. How about recalling them decades into clinical practice ? The mechanism of systemic edema revolves around the interplay between hydrostatic pressure, colloid pressure, interstitial pressure. However, In the pulmonary circuit, it gets a little more complex. Acute pulmonary edema begins to occur at around 18mmhg  PCWP. What is special about this number 18? Nothing great. The lung begins to ooze when the LVEDP/LA mean pressure exceeds the colloid osmotic pressure, (that keeps fluid in situ) within the pulmonary capillaries, which is about 18mmhg. Interstitial fluid begins to collect as the basal rales go onto develop frank alveolar edema at 25mmhg. Of course, chronic situations like mitral stenosis both lymphatic reserve and thickened interstitial fibrotic process keep threshold still higher) 

To simplify, whatever be the mechanism on the left heart, during acute pulmonary edema for the lungs to get flooded, we need a well-functioning right ventricle. If only the RV has enough wisdom*, it should take the cue and slow down and help the LV out by reducing its preload. (RV’s afterload is LV’s preload right )

We know, the lungs are protected from congestion in a number of chronic right ventricular diseases, pericardial disorders, severe PH. This happens in RV infarction. This lung-protective effect might explain the heterogeneous nature of outcome in RVMI (bad to excellent) 

Final message

We know, the commonest cause of pulmonary edema is due to acute LVF. Now add one more mechanism in the genesis/and or maintenance of pulmonary edema. Vigorously contracting, RV is equally culpable. 

Here is an Important paper that discusses the key role of RV in the precipitation of acute pulmonary edema.

Some more questions relevant to this topic

1.What is the effect of RV dysfunction on paroxysmal nocturnal dyspnea & orthopnea? 

2.Explain class 3 Forrester’s hemodynamic grading of acute MI. (Why PCWP goes down in grade 3 compared to grade 2?)


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