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The incidence of stroke during TAVI up to 5 % (minimum ). Stroke risk reduction during TAVI is a critical requirement that can be a deterrent against this wonderful Intervention.

Many devices are being considered

  1. EmbolX (Edwards life science)
  2. Emrella
  3. Sentinel (Claret medical)
  4. TriGaurd (Keystone)

1-s2.0-S1050173818300112-gr2

 

TriGaurd 3just got the approval from CE and appear promising. (REFLECT trial) It is inserted through the transfemoral route , deflects embolic material to descending aorta since it covers all the three branches of Arch.What happens to these deflected particles? Any bodys guess.

So , in my understanding it converts potential brain embolisation to peripheral microemboli , wh

This image has an empty alt attribute; its file name is triguard-3tavi-tavr.jpg

A nice descriptive animation .https://player.vimeo.com/video/232995629

While, these innovative aortic arch filters reduce the risk of periprocedural embolic stroke, please mind, TAVR patients continue to be at significant risk for stroke over a long period. This is due to other late causes like TAVR leaflet thrombosis, atrial fibrillation, arch atheromas, and bleeding due antiplatelet agents.

Reference

1.WienekeVlastra, JeroenVendrik,  Karel T.Koch et al Cerebral protection devices during transcatheter aortic valve implantation  Trends in Cardiovascular Medicine  Volume 28, Issue 6, August 2018, Pages 412-418

2.(REFLECT trial) 

 

           Practice of cardiology is simple as long we don’t dwell deep into coronary physiology.

One of my patients asked, why he was told his total occlusion in LAD appears safer now, which was subtotal a few months ago.I told him, it is indeed true. It is the fear of subtotal disease that’s prone to a fresh coronary event. In total occlusion, chances of that happening are less or nil.

 

How can you say 100% block is safe?  Is that always true?

No, it’s not always true. He was surprised when I said it is not 100 %, even 90% lesion can be safe if it’s not causing significant angina and responding to OMT. Of course, It is the morphology and stability of the lesion that will dictate* the outcome in the subtotal occlusion. If the lesion is stable, FFR is good >.8 (TMT is poor man’s FFR equivalent )  you can leave it as it is. Doing OCT /Virtual histology /NIR spectroscopy to define the vulnerability of plaque is neither practical nor desirable (Extreme academics is injurious to health) 

So it is not the degree of the block that’s going to matter, but the effects of that block on distal circulation that will decide the rules of the myocardial revascularisation game. But unfortunately, both you, (the patients) we (the cardiologist) are finding it so difficult to come to terms with this basic truth in spite of multiple guidelines. 

 

Meanwhile, CTO however makes it much easier to make a decision. One need not bother the content of CTO unless you plan an Intervention. I guess there is no FFR for CTO. Are we aware of any studies that have quantified antegrade flow across a 10% patent LAD and compare it with the Collateral flow in LAD in 100% CTO?

We have long glorified a concept of the open artery hypothesis. (Mainly in Post STEMI though) No one has dared to test and compare a hypothesis that a closed artery might still score over the open in at least some of the subsets of stable CAD. Such a study can never be ethically forbidden after all its a well-observed truth in the real world. 

Reference 

Trials on CTO  revascularisation DECISION CT (Not useful )   EURO-CTO  (May be useful) 

 

 

 

EURO CTO https://academic.oup.com/eurheartj/advance-article-abstract/doi/10.1093/eurheartj/ehy220/4990878?redirectedFrom=fulltext

Can you guess how many drugs a busy physician on an average writes in their prescription in his office ?

Three ? , Five , Six ,  . . . . Nine,? There is no specific study available for this non-academic query. I have got stunned to see a maximum of 18 drugs in one prescription. So, it should be anything between  1 to 18. May be a mean around 6 or so (Make your own guesstimate)

There is strong evidence to suggest writing a drug prescription has become a (un)conditioned habit-forming act. My professor* used to say generally 2 to 3 drugs are sufficient for most of the common illnesses we encounter (Only in extraordinary situation one may need to go beyond this )

One evidence less estimate though a random observation  among  the physicians suggested the bottom half of any long list of drug prescription is redundant and it doesn’t really address the specific problem the patient is suffering. Meanwhile ,the concept of poly-pill is making drug compliance easier in many cardiovascular and diabetic diseases.

*William Osler

Final message

Number of drugs human body can handle simultaneously without any harm is  often an ignored chapter in the Principles of clinical pharmacology and therapeutics.

Let us mind the length of our prescriptions and ensure less harm to our beloved patients.

Related material

This was my old presentation made about polypharmacy in CHF :Perils and pearls

PDF format of the presentation

 

 

  

Psychological factors both depression and anxiety do confer a significant risk for CAD. However, a distinction must be made between risk factors and triggers. It is highly likely, depression has more consistent correlation with chronic CAD than anxiety. 

Primary anxiety per-se is of less of a risk factor for chronic CAD, while it can still be a trigger for cardiac events. (when it occurs over heightened baseline risk) Primary depression increases the CAD risk many fold by slowing the system making it sedentary and promote endothelial dysfunction, which is the key promotor of atherogenic CAD.

It is also noted, anxiety is less associated with obesity (when compared to depression). Further,catecholamine fluctuations that are so common in anxiety states may act like an exercise equivalent ( It’s my quirky hypothesis to be tested by future generations)

Emotions have a complex equation with neuro cardiac axis .Sudden emotional deaths due to possible arrhythmias or stress cardio-mypathies are important areas for research.

Sharing my presentation in one of the Annual physiologists conference held at Chennai in 2016.

Topic: Emotional Triggers in ACS 

 

Click here fro PDF version of the presentation

 

 

No one would have Imagined a generally Innocuous entity called Diabetes will emerge into a  “single disease sub-speciality” in medicine”. Thanks to the global authorities  & pharma Industry for making this speciality a formidable one. The link between diabetes and cardiology is so strong, now with pharmacological strategies looking for overlapping Indications.

 

Let me share a presentation in one of the cardiology meet in 2017 at Thiruvananthpuram.TAN CSI meet , India.

 

Click here for a  PDF version 

The days are gone when anti-diabetic drugs were alleged to increase CVD mortality. New generation anti-diabetic drugs (SGLT-2 Inhibitors) are coming up that actively dictate and demand us to use it for reducing CVD risk.

(Am I crazy, to look ahead for stand-alone Indication for SGLT Inhibitors for cardiac failure in non-diabetic as well, as a powerful osmotic diuretic !)

Its almost like playing a billiards game in absolute blindness.

It is not an unusual scenerio, to see the balloon catheter delicately bending at IAS puncture site , dodging and deflecting with random jerks as it tries to steal a entry in a few diastolic milliseconds time window when the fish mouthed mitral valve opens in sub square cm areas of MVO trembling in fast atrial fibrillation.

Agree ?

Gathered some tips to cross a difficult mitral valve during PTMC.

This is a PPT presentation taken from archive (Made in 2012)

Please pardon , it lacks audio.

PDF version : Prof SV PTMC mitral valve crossing

Final message

Often times Its noted we tend to struggle more at the mitral valve crossing than at IAS puncture during PTMC. Experience prevails over Image assistance. Assessment of LA size , IAS plane , and sub valvular disease seem to be critical. Probably the secret of success which I found out was , smart guys never hesitate to repeat IAS puncture site for optimal trajectory .Over the wire technique is not forbidden.

Unfortunately, TTE guidance is of little use to cross the mitral valve. Co-registration of fluro/3D TEE is promising , but most cardiologist continue to rely on their experience.

This always Intrigues me ! why we have abandoned retrograde crossing through the Aortic valve that avoids the dreaded IAS puncture. (Refer Dr V.K.Bahl AIIMS Newdelhi in a large series from Greece : Retrograde PTMC J Am Coll Cardiol 1998;32:1009–16)

I don’t know whether you have seen this before. Surely , I haven’t seen a presentation such as this one.

Place: Annual scientific meet ASE 2013. Minneapolis

Presentor:Dr.Partho Sengupta, Mount Sinai hospital, New york.

Its a 3D presentation in “space” without a screen by Holography.

The stunning 15 minutes lecture take us into the myocardial architecture, with speckles , flow vortex echocardiography and fluid kinetic energy mapping.

Don’t miss, a dramatic live teleporting of ASE president on to the stage. 

 

Can you Imagine , where does this technology take us to the future ?

Patients may reach doctor’s offices by holographic teleport for a medical examination or vice versa. Yes, it’s all going to happen someday.

 

 

 

 

Coronary collateral circulation is one of the major determinants of symptoms and outcomes in chronic CAD. But, we generally shrug off the value of coronary collateral circulation in acute coronary syndrome. The fact is, it has a myocardial mitigating effect following sudden total occlusion.

When does it appear? We did a small analysis (PDF version)

We found it is noted in 25% of patients. With reference time of appearance,  6% had it within 12hrs and in few, it was noted as early as 6 hrs. One caveat is,  we may not know whether its preexisting collateral due to chronic multivessel CAD. I am sorry to note this study did not address the outcome analysis. We however documented patients with good collaterals had negligible wall motion defect and near-normal function post PCI. Some of you can pursue research in this area. 

Potential role of collaterals in ACS

  1. It limits the infarct size
  2. Keep the myocardium alive and give us time to intervene
  3. Can converts a potential Q-MI to non-Q MI
  4. Possibly prevent primary VT/VF and hence dreaded sudden death in early STEMI
  5. Prevent early adverse remodeling of the left ventricle.

When these points appeared just my assumptions, Dr. Ali Aldujeli, (Lithuanian University of Health Sciences, Kaunas) in his presentation, at TCT 2020 confirms many of them are  Indeed true

Final message

I agree, in the era of instant gratification with primary PCI,  relying on coronary collaterals may appear a lesser professional virtue. Still, we may need to respect nature. Many times it bails us out.

Current update 2020

Alsanjari, O., Chouari, T., Williams, T.,  Angiographically visible coronary artery collateral circulation improves prognosis in patients presenting with acute ST segment‐elevation myocardial infarction. Catheterization and Cardiovascular Interventions.  Volume96, IssueSeptember 1, 2020 Pages 528-533

 

 

Superficially, tissue hypoxia might look similar to Ischemia but differs in one important aspect. Though the hypoxic myocardium is short of oxygen, the respiratory excreta from cells ie Co2, lactic acid, and free radicles are promptly cleared and flushed as blood flow is normal. Hence, generally acute  Ischemia of tissues is more cell threatening than regional hypoxia at any organ level. 

How do you classify hypoxia? we need to go to physiology classes again.

There are 4 types. Ischemic -Hypoxia, systemic hypoxia, Anemic hypoxia, Histo-toxic hypoxia.A good reference to read (Ošt’ádal B., Kolář F. (1999) Myocardial Hypoxia and Ischemia. In: Cardiac Ischemia: From Injury to Protection. Basic Science for the Cardiologist, vol 4. Springer, Boston, MA.)

The question we want to address here is the effect of systemic hypoxia on LV function.

We encounter this in different settings.

Chronic hypoxia  :In COPD, there can be slow adaptation, still there will be some definite impairment of myocardial function.(Which may not be important in normal times but will tell at times of other stress ) Many studies have documented COPD to compromise LV function. In fact, DCM has a link with some severe forms of COPD (Personal observation, will try to get the evidence )

In acute hypoxia(Non-Ischemic) it causes organ dysfunction.(Acute pulmonary embolism, and sepsis.) We see this often in IMCU with ventilated patients with  multisytem defects a poorly contractile ventricles. Some of us used to report this entity with a empirical term global hypokinesia due to hypoxia. The effect of systemic hypoxia on cardiac metabolism is complex as the heart has a unique ability to survive with ketones in anaerobic metabolism at least for a few hours to days.

It is truly fascinating to note, how the human donor heart makes a stunning statement (to the coronary blood flow obsessed cardiologists) when it is shipped in ice bags with exclusive support of metabolic juices without a single drop of blood and come alive in the recipients without any damage. Is it not a wholesome proof? , for temporary survival, the heart just require ATPs and high energy bonds, not blood in the real sense. 

Here is a 1962 paper that analyzed how the heart is able to survive hypoxia. Walter F. BallingerII and Heinz Vollenweider Anaerobic  Metabolism of Heart   Circulation Research. 1962;11:681–685

How to study the effect of chronic hypoxia on LV function? 

We may lack animal models but Ironically we have perfect human hearts to study the effect of hypoxia on the myocardium. They are cyanotic congenital heart disease.  Here is one of the rare reports based on only two patients that address this issue. The authors (Neeraj Awasthy et al) to be appreciated for this pertinent observation.I think we need to look further. Even in TGA, the urgency to perform an arterial switch within a month or so is not only hemodynamic regression in LV  mass facing pulmonary circuit but also early hypoxic injury to LV  myocardium.

One more area of research
 
The corona pandemic gives us an opportunity to study the behavior of heart with extreme hypoxia all around.The presumed 5 % Incidence of global LV dysfunction with COVID pneumonia is hypoxia-related or viral myocarditis we are not clear yet.

Reference