Evolving Nature of a Complex Bifurcation PCI

By Dr. Salman Arain

85 year old man admitted with CP in setting of HTN. Had has symptoms for a few months. ECG showed ST depression and the EF was 45%. The referring sent him for CABG but the (chief) surgeon was hesitant because the patient is a Jehovah’s witness (can not receive blood), low platelets (85k), and high Cr (1.9)

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What is your ABC analysis? As a reminder:
A – angiographic analysis,
B – bifurcation strategy,
C – calcium modulation,
D – device (MCS) selection if any, and
E – execution strategy?

Ok, so the resolution of our case…

These were my thoughts going into the case…

A. Functional last conduit because the RCA is critical. The entire body of the LM is involved. Heavy calcium is an understatement.

B. Medina 1,1,1 – both arteries need to be addressed. Our plan was to perform DK crush.

C. Rota and/or IVL. ‘Relative’ disadvantages to both – Rota will require me to remove the wire from one of the branches. IVL will prolong LM occlusion (= ischemic) time.

D. Definitely Impella supported.

E. Plan – perform RHC for reserve, insert Impella, wire both LAD and LCX, PTCA LM into LAD, IVUS then decide on rota strategy, finish with DK crush. Stage RCA.

We started by doing a RHC. The PA pressures were not too bad (48) and the PA sat was reassuring 58%. We opted for dual access.

We resolved that issue with a TurnPike LP microcatheter. You can drive the MC by torquing it. We knew we were going to fix the LAD with rota so I did a 1.5 mm angioplasty to allow the LAD to breathe while we did IVUS.

With the LAD and LCX fixed, the LM is more manageable now. We opted to finish the T-stent and use IVUS to see if further optimization was needed.Our bifurcation plan rapidly evolved during the case. It was DK crush before the case, mini crush after I put the proximal LCX stent in, and ended up being a T-stent because of how well the stent had landed at the ostium.

You can see the patient is becoming restless. I think that it was likely from leg ischemia related to the Impella sheath.

Also, the guide had softened and came out. Note the stent deformation on account of the calcium module at the ostium. There is a recoil after high-pressure NC ballooning.

Here is the CFA after Impella removal. We did not use single access because I wanted to use a 7 French guide without any of the drama. A 7 French sheath is often quite snug in the Impella insertion sheath. The double access also allowed us to ensure that the bleeding at the Impella insertion site had completely stopped before the patient left the Cath Lab. This was on on account of his inability to receive blood being a Jehovah’s witness.

The patient did very well. He was up and about the next day. He did have a mild bump in his creatinine, but we kept him for a few days.

I plan to perform an PET in four weeks and then decide if he needs the RCA fixed. Again, he is an 85 year old who has been doing quite well until now.

The End. 🙏🏼

I am going to share a series of still frames that shows the changing morphology of the LM lumen. This is baseline.

Here is the balloon inflation. Note the upward displacement of the nodules.

This is after our aggressive POT. Note the smoother upper curvature.

Failure to Treat Hypertension

Close Case Study

Presentation and physician action

A young man came to his internal medicine physician over several years for various symptom-focused visits. On the majority of these visits the patient’s blood pressure readings were elevated. Two months after his last exam, the patient died suddenly at home. He was 31 years of age. The cause of death was determined to be a complete occlusion of the left anterior descending artery (LAD).

Autopsy findings were inconsistent with hypertensive coronary artery disease, as there was no heart enlargement, dilation of the left ventricle, pitting of the kidney surfaces, or dilation of the aorta. The pathologist did not see any evidence of end-stage organ damage caused by untreated hypertension. The pathologist concluded that the cause of death was from atherosclerotic plaque becoming disrupted and traveling to the LAD, causing occlusion and a fatal arrhythmia.

Both the pathologist and consulting cardiologist agreed this heart attack could not have been prevented since the patient did not suffer from hypertension-induced coronary artery disease.

 The defendant, while providing reasonable episodic care, did not address the patient’s elevated blood pressure. The physician says he instructed the patient to watch his diet, but this was not documented in the records. The physician did not order any lab work or evaluations addressing the hypertension.

Allegations

The patient’s family filed a lawsuit against the physician for failure to diagnose and treat hypertension. It was further alleged that the physician failed to order proper evaluations and lab work and failed to provide the patient with precautions and advice on lifestyle changes. The plaintiffs argued that had the physician treated the patient’s hypertension, it would have prevented the sudden heart attack and death.

Legal implications

The patient came to the physician nine times over an 8-year period for various symptoms. During this time the patient never described any chest pain or dyspnea that would have increased the suspicion of heart disease in such a young patient. However, high blood pressure is a risk factor for heart disease, and the patient’s initial blood pressure reading was 164/110 mm Hg. Although the blood pressure read­ings fluctuated, consultants felt the patient had stage 1 hypertension.

Though most consultants agreed stage 1 hypertension does not require immediate medication, they were critical of the physician’s inaction (not taking repeat read­ings, considering family history of hypertension, documenting in the medical chart discussions of hypertension counseling, conducting lab studies for lipid profiles and other tests).

Most defense consultants agreed that it was a judgment call to treat this young man for borderline hypertension, and the lack of hypertension treatment had no bearing on the sudden MI. However, they all stated that the patient should have been more closely monitored with regular blood pressure checks, diagnostic labs, and counseled on modi­fying diet and lifestyle.

Making this case more difficult to defend was the physician’s admission at deposition that he was not clear on the standard of care in treating hypertension.

Disposition

This case was settled on behalf of the internal medicine physician.

Risk management considerations

Incomplete documentation often hinders the defense of lawsuits. Each patient encoun­ter should include the chief complaint, examination findings and prior diagnostic tests results (if applicable), assessment, clinical impression or diagnosis, and the plan of care. Not only did this physician not support his clinical impression of the patient’s blood pres­sure, the only acknowledgement of the blood pressure readings was a circle around the numbers.

Completed histories are the basis for patient information. It is not unusual to have a pa­tient complete a questionnaire before the appointment as this helps expedite the patient visit; however, reviewing the form and completing areas left blank may provide additional insight. By initialing and dating each page, a physician can provide verification that the information was reviewed.

Some consultants believed that, given the patient’s family history of hypertension, medi­cations should have been started immediately. Most consultants agreed that education on dietary and lifestyle changes was more important the first year. Unfortunately, the patient’s chart supported the plaintiffs’ view that the physician failed to advise the patient of his cardiovascular and hypertension risk factors.

Physicians can make themselves more defensible by obtaining a complete his­tory, documenting each patient encounter, and documenting any education provided to the patient. This assists both the patient in making informed choices and the physician, should the patient allege failure to diagnose and treat.

Search Engines for Researchers

Google is so powerful that it “hides” other search systems from us. We just don’t know the existence of most of them.

Meanwhile, there are still a huge number of excellent searchers in the world who specialize in books, science, other smart information.

Keep a list of sites you never heard of.

http://www.refseek.com – Academic Resource Search. More than a billion sources: encyclopedia, monographies, magazines.

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https://link.springer.com – access to more than 10 million scientific documents: books, articles, research protocols.

http://www.bioline.org.br is a library of scientific bioscience journals published in developing countries.

http://repec.org – volunteers from 102 countries have collected almost 4 million publications on economics and related science.

http://www.science.gov is an American state search engine on 2200+ scientific sites. More than 200 million articles are indexed.

http://www.base-search.net is one of the most powerful researches on academic studies texts. More than 100 million scientific documents, 70% of them are free.

The Gordian Knot

Using Contrast To Cut The Gordian Knot! A Complicated CTO Intervention

By Dr. Salman Arain

This is the complete angio. The patient is 57 years old with CCS 3 angina. He had bypass surgery 13 years ago. His EF is 35 to 40%.

Viability Study

So, the question for our Cardio experts:

1) What do you recommend? PCI, re-do CABG, EECP or OMT alone?
2) If you choose PCI, which vessel would you go after first?
3) And what CTO strategy would you use? Retrograde PCI may or may not be the best answer here.
4) What do you know about the coronary sinus reducer, and would you consider that?

Tricky. The problem with the LCX is that the caps are all ambiguous and there are several bifurcations.

The LAD CTO is long but at least there is a well defined cap and a relatively straight course. Unfortunately the LAD septals supply the PDA which itself is occluded proximally and does not connect to the PLBs.

The RCA is the trickiest of all three. One thing to keep in mind is that the patient is post CABG – so any perforations would be more difficult to treat.

Ok, here is how it all played out. First a few thoughts about choosing the vessel to intervene upon.

The LAD has the most favorable anatomy but needs to be fixed least urgently. The proximal 1/3 is patent and the mid segment has a graft.

The LCX has an ambiguous cap and several branches that need to be rescued. It is important not only because of its own distribution, but because it is the best retrograde conduit to the RCA via the PLB.

RCA is the trickiest because it requires a combined antegrade and retrograde approach. Also, the PDA is occluded and is cut off from the large PLB system. So an occluded bifurcation somewhere!

Thus, we decided to go after the LCX – it was the one that would give us the greatest advantage in addressing the RCA.

Here are some dual injection angios to better show you the connections.

There are several ways to tackle a CTO – some antegrade and some retrograde. We have focused on and specialized in contrast modulation of plaque. This requires puncturing the proximal cap and then using micro injections of contrast. The technique is also called a modified Carlino injection after Mauro Carlino who described

Here is the setup for the LCX intervention by means of CAP (aka Carlino). Notice the ambiguous cap.

This is not the typical cloud. It is tubular which means we must be extra plaque

So we used a Gaia 2 to redirect our MC and repeat the contrast injection. Now we see the vessel architecture – as well as re-entry!

This is just the injection clip. The typical result is seen towards the LCX. There contrast mediated STAR into the OM2!

So we wired the LCX first, then treated the bifurcation, and used a dual lumen catheter to wire the OM2.

We used IVUS to confirm that we were not going to jail off the side branch with our stent. We used JSBT!

And here is the final angio. You can see that we are nicely set up for a retrograde intervention on the RCA in a few weeks.

And now you have the complete name for the case: Using Contrast To Cut The Gordian Knot! A Complicated CTO Intervention

Afterword. I think this case highlights how far coronary PCI has come – as a specialty. In my fellowship, this talk of dissecting and injecting contrast and going epicardial would have been blasphemous. And now it is routine in selected centers of course.

The upshot is that CABG is no longer the end of the road. The end of the road is the end of the road – and that is not in sight for coronary PCI!!!

Dr. Zaka Khan wrote: Regarding Coronary sinus reducer – This was original developed by Neovasc . A Canadian startup. There main two products for Cosira and Tiara. Cosira was designed for controlled occlusion of CS to improve symptoms of refractory Angina . It does improve at least 1 CCS class. Would work only in cases of refractory angina and evidence of reversible ischemia. It increases coronary microvasculature flow.
Tiara was supposed to be Transseptal Mitral valve replacement system without need for apical approach.
Company got into litigation with Edward’s and then few guys at UPEN. Material used for Tiara was manufactured by Boston Sci and hence they jumped into the mix. Cosira system was bought into by Shockwave medical.
Tiara is still somewhere and the fight goes on.
Many investors lost money because of legal battles. Would have been a big hit like TAVR .

Questions by Dr. Afaq Motiwala answered by Dr. Arain:

) Does the micro catheter injection into the cap create more extensive dissection (if you are extra plaque) and make it harder to get into true lumen? Yes and no. That is where we have honed our technique. It’s all a matter of understanding the contrast cloud.

2) How did the ivus help you with side branch? It helped confirm that I was in true lumen and that the side branch was not jailed behind plaque.

3) Where did you place your balloon for jsbt? Balloon from OM2 to top branch and stent in the main body of the OM2

4)The small branch you preserved with a wire, does it have some contained hematoma? Any need to tamponade it or it’s inconsequential? It does, but the flow was good without a dissection in multiple views. So OK to follow clinically. These are very small branches.

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It was important to preserve the OM2 trifurcation. You can see the size of it in the cranial view. The top branch fills OM1 and the bottom two supply the PLB. I plan to fix both eventually.

Dr. Amin H. Karim wrote: The cath diagram took me back to pre-EMR days when we routinely made these after watching the cine on Trajano. They were very reflective of the coronary anatomy as well as recording one’s personal notes. 30 years later when we look at these in the patient’s chart it gives a good idea of the pre-intervention anatomy. Computer diagrams are no match and I feel sorry for your younger colleagues when they pull their patient records decades later, they will be looking at a computer cartoon that is a far cry from the real anatomy. Both Michael DeBakey and Denton Cooley gave a lot of importance to the cath diagram on patients referred for surgery and both would hang them on the old x-ray box in the OR as a reference! Dr. DeBakey would meticulously put his pencil notes on the diagram and file them on each patient. He would also draw the grafts on another copy and send them to the referral cardiologist. He would pull the file out when patient came in years later for redo