Dr.S.Venkatesan MD

Group clashes in pulmonary hypertension

November 7, 2024 by dr s venkatesan

PH is an important clinical cardio-pulmonary entity , which we confront day to day. Though the prevalence of PH in a community is just 1 % (25 times less than systemic hypertension) it deserves a special place as the diagnosis is more complex and outcome is often adverse.

The defining criteria , the classification, and grading of PH has always been a difficult and dynamic academic task .Right from WHO’s 1974 definition, we have 7 global symposiums , last one happened few months ago, in July 2024 in Barcelona.

We have made rapid strides in all aspects of PH right from molecular , genetic , imaging and therpeutics. Still, there is one important issue that has been overlooked for quiet some long. The concept of fitting PH in 5 groups based on etiology, though appear to simplify things, there is a significant flaw.

The overlaps in etiology

1.The group 1 contains the famous , (now obsolete entity of primary pulmonary hypertension) Idiopathic PH , meaning that we don’t know the cause of it or we have excluded all known causes. Meanwhile, group 5 also has set of conditions of PH of unknown or unclear etiology. So, a IPH of group one can migrate to either group 4 or group 5 or vice versa.

2.PH due to congenital heart disease can be in both Group 1 and 3

3.If you take PH due to some of the connective tissue order, I am sure, it can fall into any of the 5 groups

Suggestions for the next PH working group

It is desirable that the next working group should acknowledge existence of inter and intra group overlaps of PH in a more clear manner. Either we should take away the groupism or the current definition of group 5 need to be more elaborate . It says multi-factorial. Instead we can try to find what are the groups it is likely to have an overlap. Should we need another a sixth group ? GO-PH (Group overlapping PH)

There can also be a place for combined etiological-hemodyanmic classification . (Example : Group 1 .Pre capillary .Group 1 Intra-capillary as in PVOD) . CTEPH though essentially is a precap PH, the risk factors of CTEPH and HFpEF can be shared one, making it combined pre and post cap PH a distinct possibility. )

Final message

While the problem of groupism in PH exists, the issue of highest importance in PH is something different. This is more philosophical . We need to be very clear what we mean by Idiopathic. As physicians, we must realize how relative this terminology is . What is idiopathic in your hospital, (However big you are) may turn out to be a missed case of mixed connective tissue disorder or silent CTEPH detected only by V/Q scan or a dual energy CT or a rare case of PVOD by judiciously reading a pulmonary angiogram in a dedicated PH center.

*Also we must recall, statistically up to 80% of PH is due to left heart (This HFpEF stuff has jacked this incidence still more ) and lung disease. Our efforts and resources should be used judiciously for optimal diagnosis and management of common conditions first.

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Posted in Uncategorized | Tagged classification of ph, esc acc aha guidlines for pulmonary hypertension, etiology of ph, group 5 pulmonary hypertension, group 6 pulmonary hypertension, HFpEF, itra capillary ph, paris, post, primary pulmonary hypertension, pulmonary hypertension, pulmonary hypertension symposium barcelona, pulmonary vascular ressitance, pvod, pvr, Vienna, wood units in ph |

Principles of practice medicine is an art or science?

November 2, 2024 by dr s venkatesan

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Why cardiologists are not guilty, with a fundamental Issue in STEMI management ?

November 1, 2024 by dr s venkatesan

Time window for intervention with thrombolysis in STEMI starts from onset of chest pain, but when it comes to primary PCI, a different time window takes the center stage, pushing the former to the background. In primary PCI, the distorted time window starts right from the patient arrival at the door of (either the ER ) or cath lab, and many times, endlessly extend beyond the prescribed time.

Why this dichotomy ?

No guideline bothers to reiterate , that if the S2D time is prolonged, D2B need to be correspondingly short or ultrashort. How can we have uniform standard of 90-120 minutes D2B in all STEMI cases ? Why the cardiology community is silent on this crucial time mis-management error ?

Answer

I think the answer should be one of the following .

1.It is intentional .

2.Ignorance

3.To favor the perceived superiority pPCI .

Only time will answer.

Curiously, none of the globally accepted standard guidelines seem to realize that, they have not given sufficient weightage to this aspect of coronary time window , while gathering the evidence.(Most papers on pPCI never mention about S2B times vis a vis with IRA TIMI flows)

Final message.

No amount of guidelines will lead us to proper pathway of coronary care ,unless we are ready to course- correct and eliminate basic errors. Of course, If we are knowingly straying from the right path, there is no escape for our patients from science.

Post- amble

How is this possible in this cutting edge scientific era.?

*The problem with hyper Intelligence is, that any amount of scientific evidence can be created to show, what we are doing is right.

What could be a lesson we can learn here ?

If symptom to lysis time is less than 50% of Symptom to balloon time , probably,every such patient should enter “pharmaco- Invasive or pharmaco only” strategy according to the prevailing CAG anatomy.

Counterpoint

D2B is under you control. S2B is not in your control*, so simply don’t bother about the former. The other possible argument for ignoring symptom to balloon time ,is late lysis doesn’t work that effectively, hence the only option is PCI however delayed it is. But, in the process, we forget , most times we are the ones who created this deadly delay and master the art of loosing the golden hour in STEMI , that is backed up with flawless RCTs.

*Is S2B is really not in out control ? Yes , it is true, until we replace S2B to S2R (R-Revascularisation) time. This is unlikely to happen as long as we strongly believe balloons have the exclusive capacity to revascularize the IRA.

Reference

S2D -Symptom to door time

S2B-Symptom to balloon time

D2B– Door to balloon time

S2R*-Newly proposed . Symptom to revascularisation time (any modality)

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Posted in Uncategorized | Tagged d2b to stb time, symptom 2 balloon s2b time, time window in lysis vs primary pci, time windows in acs stemi |

25th Anniversary of a landmark study in coronary revascularization

October 30, 2024 by dr s venkatesan

This study was released in NEJM without much fanfare at the fag end of the last century, (rather the millennium) in 1999. Dr. Bertram Pitt and his team scripted this from the Department of Medicine, University of Michigan School of Medicine, Ann Arbor, USA. One can’t expect even in your dreams a study like this would be be done in the future.

This study tested PTCA vs with a single lipid lowering drug in terms of plaque regression. This conclusion is explicitly illustrated here, and the dramatically dissociated Kaplan and Myers would tell the whole story.

Can you name this trial that can withstand any period of time?

One clue : We do prescribe this drug every day and it beats angioplasty. Some of you may have got it right. Yes, It is the AVERT study: Atorvastatin versus revascularization treatment.(Ref 1) that dare to compare PTCA with a humble statin one to one, and we found the winner long long ago. This study also defined the bench mark for dosage of high intensity Atrovastatin at 80mg/per day.

Final message

I am sure, many of the current generation cardiologists may not know about this study and the conclusion might amuse them as well . The truth is , It deserves a 25-year anniversary celebration. Wishes and congratulations to Dr. Bertram Pitt.

Reference

Pitt B, Waters D, Brown WV, van Boven AJ, Schwartz L, Title LM, Eisenberg D, Shurzinske L, McCormick LS. Aggressive lipid-lowering therapy compared with angioplasty in stable coronary artery disease. Atorvastatin versus Revascularization Treatment Investigators. N Engl J Med. 1999 Jul 8;341(2):70-6. doi: 10.1056/NEJM199907083410202. PMID: 10395630.

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Posted in Uncategorized | Tagged acc esc scai guidelines, atorvastatin vs ptca, avert study, courage trial, Dr Bertram Pitt, ISCHEMIA trial, medicaltherapy vs ptca, orbita, stable angina, statins, university of michigan |

What is the mechanism of LBBB in DCM ? How does left bundle branch pacing correct it ?

October 26, 2024 by dr s venkatesan

Here is an attempt for a brief answer that starts with query.

1.The mechanism of LBBB in DCM is

1.Discrete proximal LBBB

2.Diffuse distal LBBB

3. Myocardial LBBB (It is just a LBBB morphology in ECG, due to delayed conduction and not a true LBBB )

4. It is always a combination of any of the above three components.

Answer :Either 3 or 4 should be the answer I think .It need to be reminded, the etiology of cardiomyopathy plays a crucial role in determining the cause of LBBB. In ischemic DCM, it could be localized necrosis and scarring . In infiltrative disease like sarcoid or Amyloid it is patchy destruction of conduction system. In idiopathic or genetic DCM, it could be a defect in various forms of structural or functional Inopathy.

2.Does LBBB gets corrected by left bundle branch pacing ?

No, it doesn’t correct it in all . This fact, by itself tell us what could be the true mechanism of LBBB in dilated cardiomyopathy. In selected patients with discrete proximal LBBB the strength of the pacemaker stimuli might breakthrough the block. Though the concept longitudinal splitting of left bundle and the proximal pre-destined left bundle fibre disease is attractive, mind you, bulk of LBBBs are diffuse. LBB pacing can’t work in majority of these patients.

Hence, it is largely a desired assumption ,that LBB pacing could correct the LBBB and restore the defective synchronization . It is true pacing near the bundle branches carry better chance of synchronous contraction, provided distal circuits are perfect. (Which is more often, not the case) Unfortunately, while technology allow us to replace a defective valve or even transplant a entire heart. we can’t replace a defective ventricular electrical circuit board with a brand new printed Purkinje network in lieu of the diseased one. At best, we can try to stimulate the heart it two or three sites . (Mind you, the natural Purkinje network runs for few kilo-meters of indicate wiring)

Is LBB area pacing or CSP a real Innovation ?

May be yes. But, until the the mechanism of LBBB in a given patient with cardiac failure is completely understood , we can’t choose a right mode of pacing and re-synchronisation modality. Unfortunately ,there appears to be a herd mentality, gradually creeping in many of us, to jump over from traditional RV /RA pacing to the bundle branch area pacing , as an alternative to CRT or even regular bradycardia pacing.

There is less compelling academic reasons to change, than we think. There are lot of, ‘if and buts” in this Innovation.

It is worth-while to wait, watch and think before we adopt this modality for mass consumption in heart failure with wide qrs complex.

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Posted in Uncategorized | Tagged acc aha hrd criteria for cardaic pacing, av vv synchrony, cardiac resynchronization therapy, crt vs lbbb area pacing, ddd pacing bi ventricular pacing, esc guidelines for pacing, his bundlepacing, lbbb area, lbbb pacing, qrs cosmetology, rv back up lead |

An Inspirational journey in the Annals of Medical Science

October 24, 2024 by dr s venkatesan

This book is dedicated to all those amazing scientists of the past & present who laid the foundation of modern medicine with their selfless hard work. Footprints of their legacy can be felt in everything we do in our daily clinical practice.

Hope, at least few of the readers get inspired by this book. It is available in both print and kindle versions. Let me state, with all honesty, this book is written with zero commercial interest. ( I guess , publishers somehow read my mind .The agreement clearly says the author can get only about 25 % the sale value of a book. That’s fine. May be it will help running this website.

Surprised to find the book in this month’s best seller in Medical history category . I don’t know how is this possible ? as the total number copies sold are still less than 100, since published !

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Root cause analysis of inappropriate Interventions in cardiology : The culprit is sitting pretty in front of us !

October 17, 2024 by dr s venkatesan

Some two decades ago, we, the cardiology community started writing guidelines, recommendations, protocols, whatever you call it, in managing specific clinical problems in cardiology. In this model, there is a class of recommendation supported by different level of evidence. This concept looked perfectly scientific, futuristic, and grew so well .It has been considered the de facto standard of practice.(Still it is) A few years ago, these guidelines were made more attractive and user-friendly by color-coding these guidelines.as green, yellow, orange, and red, akin to traffic signals.

In the same decades, as we glorified these guidelines, the rate of inappropriate intervention parallelly raised. Every global forum talk about reducing unnecessary treatments, and improving the cost-effectiveness. It is explicitly clear the purpose of these glorified guidelines in the last 20 years were spectacularly defeated.

When we think for few moments, who or what could be the culprit ? , one can realize easily the same guidelines turned out to be the culprits, by giving a room and liberty to cardiologists to drive through cath lab, crossing the yellow and orange signals . In my perception, very few cardiologists thinks 2B is a relative contraindication. and 2A is just a shot of chance. Why then ?, they should get a prime place in the recommendation chart. How many of us realize, these complex guidelines (? inadvertently) acts as a “temptation amplifier” to many ,energetic skilled, go get it, cardiologists.

A reality check

Many of my colleagues find no wrong in doing other than class 1 Indication . They justify it by saying they offer the benefit of doubt (or as off label usage) to their patients. No one talks about harm that comes out of same doubting. Right now, when we analyzed( mostly reliable personal info sharing) up to 50-75% procedures in cath lab are done by physicians who cross either orange, yellow, or even red signals. Fortunately or unfortunately , there is no officers on cath lab highways to give a ticket or to capture evidence. Only our conscience remain the CCTV.

A 10 second animated solution to a vexing ethical dysfunction in cardiology

Final message

What shall be done to improve the appropriateness of the treatment Interventions ?

There is a simple solution is readily available, but I am sure it is never going to happen .

“Like any walk of life a hidden culprits are easy to catch, but it is so difficult if is seen right in front of you”

Let ACC, ESC, SCAI, HRS, & CSI all sit together and debate to get rid of all those confusing and contaminating clutter in the guidelines, and retain only the class 1 and possibly Class 2A .

Counterpoint

Guidelines are written with a clear application of mind ,taking into account of available evidence and growing science, Hence indications are dynamic. Class 2B can become Class 1 , While even a Class 1 can become a Class 3. So we have to take a chance and live with it. May be some truth in it. But the issue is beyond this . We know, as of now there is no true restrictions in spite of the guidelines. It is a secret truth a huge number of late PCIs, CTOs, Mitra clips, LAA devices, AF ablations are performed under the Orange -red border zone.

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What is new in Heart failure management ? Ultrasonic cardiac re-synchronization : The WiSE -CRT device

October 12, 2024 by dr s venkatesan

Cardiac resynchronization (CRT ) as a modality for severe or refractory cardiac failure patients with wide QRS complex, is practiced for nearly two decades. It works on the principle of aggregating mechanically wasted and disorganized myocardial contractile force into a coherent forward pushing activity. This is done by stimulating the heart at strategic points by inserting wires. In the process, CRT improves the ejection fraction and possibly reduce mitral regurgitation.

Still, the optimal benefit of CRT concept has been difficult to extract from this device. The primary reason is, the LV epicardial lead pacing site was pre-selected by the coronary sinus anatomy. This has made the whole concept of RV-LV synchronization a futile exercise in many. No surprise, non, poor responders or even adverse responders were as high as true responders.

What is new in CRT ?

While one group of electrical scientists is trying hard to create evidence that conduction system pacing (CSP) is equivalent to CRT, that is devoid of procedural complexity of CRT. We now have one more technology, on the verge of approval by the FDA . This uses tiny leadless endocardial electrodes in well-selected sites within the chamber of LV .

free from scars. This can be done with aid of with intracardiac echo imaging. This electrode is stimulated by self-generated electricity from an external ultrasonic waves transmitted from the surface of the heart.

This weeks JAMA has reported an encouraging results with this device .The study documented reduction in end systolic volume by 16% and the ejection fraction as well. (Red 1)

What about totally leadless CRT ?

Yes it’s in the offing. Micra device which is lead less RV pacing system is being combined with WiSE CRT, making a totally leadless CRT a possibility. .

A patient chest X-ray showing both Micra and WiSE-CRT systems. Green: Micra leadless pacemaker; blue: WiSE-CRT system LV endocardial electrode; and red: WiSE-CRT system subcutaneous battery and ultrasound generator. CRT, cardiac resynchronization therapy. (Carabelli A, Jabeur M, Jacon P, Rinaldi CA, European experience with a first totally leadless cardiac resynchronization therapy pacemaker system. Europace. 2021 May 21;23(5):740-747. )

Final message

WiSE CRT uses some revolutionary technology and it is a welcome addition in few eligible patients. However, advanced heart failure therapy never means it can be achieved only by state-of-the-art technology. Cardiac failure management remains basically disciplined medical management and a holistic approach to improve the quality of life. Only few lucky patients end up getting heart transplantation, the ultimate treatment.

One of my patients said he reduced his weight corresponding to his reduction in ejection fraction and he now walks double the distance than before. The answer is that simple; you can use a 100k device and try to walk 30 meters extra or use the free option.

Reference

1.Singh JP, Rinaldi CA, Sanders P, et al. Leadless Ultrasound-Based Cardiac Resynchronization System in Heart Failure. JAMA Cardiol. 2024;9(10):871–879. doi:10.1001/jamacardio.2024.2050

2.Okabe T, Hummel JD, Bank AJ, Niazi IK, McGrew FA, Kindsvater S, Oza SR, Scherschel JA, Walsh MN, Singh JP. Leadless left ventricular stimulation with WiSE-CRT System – Initial experience and results from phase I of SOLVE-CRT Study (nonrandomized, roll-in phase). Heart Rhythm. 2022 Jan;19(1):22-29. doi: 10.1016/j.hrthm.2021.06.1195. Epub 2021 Jul 29. PMID: 34332966.

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Posted in Uncategorized | Tagged cardaic resynchronization therapy, coronary sinus anatomy and crt, crt d vs crt p, crt vs cp, epeicardial lead lv, good reponders in crt, non responders in crt, ultrasonic cardiac resynchronization, wise crt device |

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