Dr.S.Venkatesan MD

Which is most important component in any medical research paper ?

September 11, 2021 by dr s venkatesan

There are about 30000 scientific journals and two million papers every year. Of which 5000 are in medicine (Ref : World university news) 

Now, take a deep breath and answer this query. What do you think is the most important aspect of any scientific or medical research in the current era ?

Final message

With due respect to all researchers, What do you think is the most important aspect of any scientific or medical research?  This query is very much relevant today. All components are equally important is an easy way out. But, that’s not the pathway that will take us to the truth.

Postamble  

Having answered the above question, no way, we can escape from this question –“Which could be the least important component “?

I guess you got it right. In the current scenario, my choice is striking and is sandwiched in the middle of the 7 responses..

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Posted in Ethics in Medicine, evidence based cardiology, Medcal research | Tagged duplicate medical research, ebm, evidence based medicine, finger criteria, how to do medical research, how to right a scientific paper, junk research, medical education, medical research ethics, rct randomised control trial, research methodology, student t test |

D-Cube syndrome : DES-Dengue-DAPT

September 9, 2021 by dr s venkatesan

Background

A 52-year-old diabetic woman who had undergone recent PCI with a DES developed a febrile illness which was diagnosed as Dengue fever. She has been taking DAPT (Dual antiplatelet) meticulously to maintain her stent. Now, her platelet count has dropped from 1.5 and subsequently to 1 lakh. She is asking now, whether to stop DAPT or not? What is the risk of stent occlusion if she stops? 

The D³ cube syndrome 

Infectious diseases rarely bother a cardiologist (maybe a few IE,  myocarditis, etc). Now, a unique situation is emerging.

*Dengue affects 50-100 million people worldwide every year and one billion are at risk. CAD affects 5 % of the population that amounts to  350 million. As we fight CAD, 2 million coronary stents are implanted annually and at least one-third of them may be on DAPT at any time.

When a  global population is at risk of an infection that targets human platelets and another chunk of the same population in whom platelets are targeted with drugs, what is the Incident risk of overlap between these two groups? 

 

If you look at these two maps, I think we will not hesitate to call both Dengue and DES a global epidemic affecting the platelet function. The top one depicts the world stent market and the bottom Dengue prone countries

 

Mechanism of thrombocytopenia in dengue

The mechanism of thrombocytopenia in dengue is not clear. Both production at the marrow level and destruction in the periphery is attributed. The antibody-mediated NS (nonstructural protein) is the original antigenic sin  (Click to know more)

Chiao-Hsuan Chao PLoS Pathog. 2019 Apr; 15(4): e1007625. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6497319/

Meanwhile, DAPT paralyzes the platelet by blocking  P2Y12 and COX. It is obvious Dengue virus amplifies the antiplatelet action and increases the bleeding risk at any point during the illness.M

Risky period

Bleeding periods is highly unpredictable. The late recovery phase seems to be critical for hemorrhagic risk.it can go up to  2 to 3 weeks or even a month. (When we don’t have data, only experience becomes data. )

How to manage Antiplatelet agents in post PCI patients with dengue? 

While we have guidelines to stop DAPT during the need for emergency surgeries, the same can not be adopted in Dengue.(Curiously, we can stop DAPT without much fear, after all, dengue antigenic responses take up the role of antiplatelet agent )

Presario from Brasil proposed a practical suggestion.Pesaro AE  (Dengue: cardiac manifestations and implications in antithrombotic treatment. Arq Bras Cardiol. 2007 Aug;89(2):e12-5)

 

Wishnu Aditya et all Proceedings of Singapore Healthcare 2019 reports a mini case series 

Switching to other drugs like eptifibatide or NSAIDs is not an option. 

Post dengue prolonged platelet dysfunction

Though the platelet count returns to normal soon after recovery, long-term platelet defects are also reported. This has implications in resumption of DAPT. Surprisingly, dengue recovery phase thrombocytosis also happens for some unknown reason. Ref: Rebound thrombocytosis causing MI following dengue fever? (Roy A, et al  Indian Heart J. 2007 Jan-Feb;59(1):94)

Final message

When both Dengue &  post PCI epidemics are trying to match in numbers, I guess D³ syndrome (Dengue-DES-DAPT)  would soon become a significant clinical issue. 

Now going back to the title question, Should I stop DAPT or not? 

• Never easy to answer this question. It is a fine balance between the risk of bleeding vs the risk of stent thrombosis.No amount of algorithm and guideline may clarify it.
• On any given day, the risk of bleeding in vital spots is more dangerous than thrombus.
• It is wise to withhold antiplatelet drugs in all febrile illnesses when the platelet count is actively falling below 1 lakh. It may not be quixotic thinking to expect dengue viremia to help the DES with its DAPT equivalent action ! in the intervening period.

Reference

1. Ehelepola NDB, Athurupana Bowatte , Dissanayake  Continuation of Dual Antiplatelet Therapy in a Patient with a Coronary Artery Stent with Dengue Hemorrhagic Fever: A Clinical Conundrum.The American Journal of Tropical Medicine and Hygiene, 01 Jan 2020, 102(1):17-19  

2.Wishnu Aditya et all Proceedings of Singapore Healthcare 2019

 

Further queries

What about Heparin, Oral anticoagulation (OAC), usage in suspected Dengue?

Go back to basics. Heparin and OAC don’t affect platelet function. It is 100 % safe to continue.

Really? do you think so? No, coagulation physiology is not that simple. Thrombin and antithrombin interactions happen right on the platelet surface. Any antithrombin drugs do have some antiplatelet action as well. Extreme caution is required again. Withhold them unless absolutely indicated.

 

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Posted in anti platelet drug | Tagged antiplatelet drugs in dengue, clopidogrel prasugrel ticagrelol in dengue fever, dapt in dengue fever, therapeutic issues in dengue and cad, warfarin heparin in dengue |

How did all those calcium entered my father’s coronary artery doctor ?

September 3, 2021 by dr s venkatesan

“It was severe double vessel disease &  turned out to be a complex angioplasty in LAD ” 

Why doctor? what happened?

It was a hard lesion, there was plenty of calcium deposits. It was not clearly visible in the angiogram. I had to do IVUS. Curiously, the calcium was clustered in all the three planes of the vessel ( intima the media and adventitia) and they projected into the lumen blocking the path.

Image collage representation purpose

Thank you, doctor,  how did you manage to remove it,?

It was a real struggle. I had to break the calcium shell before deploying the stent. (What we refer to as lesion preparation). I thought Initially I can displace it with high-pressure balloon inflation, I went up to 40 ATM pressure,  finally needed a  rotational ablation with a burr.  ( IVL -Intravascular ultrasound was an option, but may not have helped either because of heavy Intimal load, Angiosculpts, and the cutting balloons (Wolverines) we don’t have)  

Was it a risky procedure?

Yes, of course, see the sharp burr rotating 150 thousand resolution per second hugging the coronary artery without damaging it

By the way, why did he accumulate so much calcium inside doctor? Can it be due to his daily calcium supplement doctor?

Oh – my ? that is important new Info. I think that wasn’t noted in the case file. Tell me more, How long did he take it? 

I think he is taking it for long years. He is rather obsessed with it, consumes lots of calcium in his diet as well. He was also taking vitamin D as it once went down to 15 ng/ml. He needed to strengthen his bone which was porotic in the Dexa scan. Was that a problem now? But his serum calcium was always normal, Then, from where does, this calcium enter my dad’s coronary artery doctor?

I am sorry I  don’t know the answer so far. Now, your dad seems to teach me a lesson. It has to enter from the bloodstream or happen de nova due to degeneration. Calcium along with phosphate is a tightly regulated metabolism.They are closely linked to diet, bone, renal and endocrine glands function. We don’t understand how there can be a no-relationship between blood calcium and coronary arterial calcium. Again plaque calcium and serum calcium may or may not correlate. Understand our knowledge base with which we treat you. 

That’s ok doctor. But do you think,  should he stop calcium & vitamin D tablets from now on?  

Hmm, you keep asking tough questions. I will be a fool if I asked you to continue right!

Please go through this article from Jhon Hopkins and decide ( & MESA study 10 year follow on calcium supplement Ref 2)

Final message

The human body is a wonderful machine. Calcium is a life-sustaining ion present in each of the 75 trillion cells we have. We are programmed to handle all elements except in a fraction when true pathology strikes. Never try to outsmart our natural homeostasis with unnecessary and unsolicited chemicals. Indiscriminate calcium supplements are definitely an unfriendly guest for the coronary artery.

Now, Is it just a coincidence?  the new epidemic of coronary microcalcification detected by CT scans(What is your Agatston’s score buddy ?) is matching with a steady increase in per capita consumption of calcium and vitamin D tablets.

Reference

1.Anderson JJB, Kruszka B, Delaney JAC, et al. Calcium intake from diet and supplements and the risk of coronary artery calcification and its progression among older adults: 10-year follow-up of the Multi-Ethnic Study of Atherosclerosis (MESA). J Am Heart Assoc. 2016;5:e003815.

2.Myung SK, Kim HB, Lee YJ, Choi YJ, Oh SW. Calcium Supplements and Risk of Cardiovascular Disease: A Meta-Analysis of Clinical Trials. Nutrients. 2021 Jan 26;13(2):368. doi: 10.3390/nu13020368. PMID: 33530332; PMCID: PMC7910980

For advanced readers

1. Does calcium stabilise a lesion or destabilize a lesion?

It does both .

2. Is CT calcium score correlate with serum calcium?

Yes, it does.Ref : Sanghoon Shin,  European Heart Journal, Volume 33, Issue 22, November 2012, Pages 2873–2881, https://doi.org/10.1093/eurheartj/ehs152

3. What are the various types of coronary calcium? Which is a more tricky lesion? 

 

 

Image courtesy -Abbot A calcific nodule is the tricky one, as it can be tiny still result in invisible stent malapposition inviting future problems.

 

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Posted in Cardiology -unresolved questions | Tagged calcium supplementation, coronary calcification, intimal medial adventitial calcium, ivl wolverine angiosculpt, opn balloon, orbitel atherectomy, osteoporosis, plaque calcium, rotoablator, serum calcium vs coronary calcium, vitamin d |

This RCA is trying to teach some basic lessons in ACS

August 22, 2021 by dr s venkatesan

Inferior STEMI, and see the first shot in RCA below. The patient was pain-free and hemodynamically stable at the time of the angiogram. (Don’t wonder how this is possible, defying the fundamental rules learned from  animal experiments after acute ligation of the coronary artery)

                

What needs to be done ?

• Go ahead and do a primary PCI as we do in any other  IRA.
• Be watchful, just pass on the wire, feel the lesion, and decide thereupon. Consider intracoronary lysis.
• How about a long stent from proximal to distal RCA?
• Kissing the lesion with DEB in the tightest segment (Not a funny option )

 

 

What was done? How is the patient?

Nothing was done & nothing happened to the patient as well. Just guidewire was crossed and few minutes of balloon touch-up work. Did the patient improve? Can’t say anything because he was fine even with this total occlusion. 

Lessons to be learned 

• The art of leaving a lesion left unattended (rather unstented) in IRA without guilt.
• TIMI zero flow in IRA need not be a death sentence for the distal myocardium, even in STEMI. 
• Sometimes, a simple guidewire crossing can do the same job as a complex angioplasty in an IRA.(For acute salvage TIMI 2 or even TIMI 1 is good enough) Most IRA accidents happen when trying improve upon this in an ectatic vessel.
• Risks of stenting in ectatic /Thrombotic segment is real
• There can be a useful role for  STENTYS self-expanding stents in localized ectasia (Ref 1)
• Long-term OAC (Soon NOACs) is a perfect remedy for protecting this type of coronary. 

* By the way, who are all bothered to know LAD anatomy in this patient.  Is it surprising the  RCA is sending collaterals to the left side in its hour of crisis? Yes. LAD had chronic sub-total lesion as well.

Reference

1.The Role of Self-expanding Stents in Patients with Atypical Coronary Anatomy | ICR Journal https://www.icrjournal.com/articles/role-self-expanding-stents-patients-atypical-coronary-anatomy

 

2.

 

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Posted in Uncategorized | Tagged ectatatic coronary rca, guidewire angioplasty, oac noac for coronary ectasia, plain balloon angioplasty, primary pci |

How to find which lesion is causing angina in multivessel CAD ?

August 20, 2021 by dr s venkatesan

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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Posted in Cardiology - Clinical, Cardiology -Definitions, cardiology- coronary care, Ethics in Medicine, Uncategorized | Tagged ACC AHA ESC Guidelines for multivessel cad, angina related artery ara vs ira, approach to tvd, cabg vs pci vs medical maangement ov cad, Chronic stable cad, courage ISCHEMIA ORBITA BARI 2D trials, IRA vs ARA coronary, triple vessel disease |

How good is late PCI ? in STEMI : A presentation

August 16, 2021 by dr s venkatesan

Late PCI: This is a tricky topic to discuss on any day. A tight walk on the evidence base and a narrow risk-benefit ratio. The problem starts right from the genesis point of the true-time window, to the host-dependent myocyte response to hypoxia. Finally, we have the ubiquitous open artery hypothesis, that can taunt even the best brain in cardiology.  

 

 

 

 

Late-PCI-Download

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Posted in Primary -PCI, Primary PCI |

Ignored concepts in ICU : Protecting RV from ventilator stress

August 13, 2021 by dr s venkatesan

We know the right ventricle is a weak pump compared to LV. This is evident from the triangular pressure-volume loop of RV. RV not only generates less pressure, its thin wall and its direct connectivity to the extrathoracic compartment make it vulnerable to hemodynamic fluctuations whenever Intrathoracic pressure swings.

Note the lowly lying pressure-volume loop of the right ventricle. RV is a too gentle chamber and needs to be handled with extreme care especially when it is failing acutely.

Patients on ventilators are typically exposed to iatrogenic rise and fall in right heart pressure. If continuous airway pressure is kept high it’s directly add on to RV afterload. The second adverse event is through interrupting venous return (preload). 

 Effect of mechanical ventilation on RV

• RV preload is reduced (If they drop too low – they are equivalent to be in “Status Valsalva maneuver” ) 
• RV afterload increases when Inspiratory airway pressure is increased. (
• If RV is grossly dilated it may encroach LV and interfere with its function (Reversed Bernheim effect )
• Many of the unexplained hypotension and reduced cardiac index are due to suboptimal ventilator setting
• Ventilator increases the mean RA pressure, and if there is PFO, it can shunt right to left and aggravate the preexisting systemic hypoxia. 

In some of the situations where RV is already in the fighting mode for survival, imagine its plight when it had to take on the adverse setting of the ventilator as well. This happens in RV infractions. Pulmonary embolism,  dilated cardiomyopathies, Post heart transplant, and in general in many  ARDS patients. Discussing the ventilatory settings and a sound understanding of the prevailing hemodynamics of patients is so important.

Settings need to be optimized (Good to acquire a basic knowledge of from an Intensivist/Anesthetist)

• .Optimal PEEP (Often dynamic but <18cm H2o) 
• Tidal volume 
• Avoid Hypoxic pulmonary vasoconstriction and hypercarbia (<60mmhg)
• RV dysfunction can be an independent indication Proning the patient (Apart from PaO2/Fio2 ratio) 

Final message

It is a paradox, for patients with LV, failure ventilators instantly help as it unloads the left ventricle and relieves pulmonary congestion on the go. The same can’t be said about RV dysfunction. Ventilators interfere with RV  in multiple complex ways. However, simple settings change can improve blood pressure dramatically. Always aim for an RV protective ventilation strategy. Many times It’s in our hands to let the tired RV free, from fighting its friend (or foe).

Reference

A comprehensive resource

1.Disselkamp M, Adkins D, Pandey S, Coz Yataco AO. Physiologic Approach to Mechanical Ventilation in Right Ventricular Failure. Ann Am Thorac Soc. 2018 Mar;15(3):383-389.

2.krishnan 2015 Download

 

3.A. Paternot, X. Repessé, and A. Vieillard-Baron, “Rationale and description of right ventricle-protective ventilation in ARDS,” Respiratory Care, vol. 61, no. 10, pp. 1391–1396, 2016.

 

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Posted in Uncategorized | Tagged impact of mechanical ventilator on rv right ventricle, peep settings for rv failure, post heart transplant ventilatory settings, rv dysfunction in pulmonary, rv function dysfunction, rv infarction, rv pressure volume loop |

Optimal lipid control & Oligonucleotides

August 8, 2021 by dr s venkatesan

Sharing a presentation on lipid control done in 2020. This talks about newer strategies beyond statins.

 

PDF version

lipid-metabolism Download

 

 

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Posted in lipids lipid metabolism, Uncategorized | Tagged dyslipdemia, inclisiran, j curve in ldl, j curve in lipid control, pcsk blockers, ppt on lipid metabolism, siRNA pcsk lipid metabolism, ssss trial simvastatin, statins in primary prevention |

Cardiology Image watch : Its not a stent for sure …then what ?

July 16, 2021 by dr s venkatesan

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 

Management 

• 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.

Reference

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.Crossref, Medline, Google 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.Crossref, Medline, Google 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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Posted in Uncategorized | Tagged coil occlusion of coronary aneurysm, post cabg coronary aneurysm, SVG graft aneurysm |

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