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How to select a wrong patient for PCI, in stable multi vessel CAD ?

December 12, 2025 by dr s venkatesan

Revascularization in chronic CAD is be primarily based on

A. Angina & its severity

B. Inducible Ischemia by stress test

C. Coronary anatomy & FFR/IFR based.

D.Total Plaque burden , plaque morphology & Vulnerability

E.As per the cardiologist’s wish

F As per patient’s wish or their Insurance limits

Trying to Answer

*Revascularization means, first we should document, there is significantly reduced baseline myocardial blood flow to the distal myocardium (which would mean near total block).

*Then, we must realize ischemia and angina are two different things. Ischemia can exist without angina; similarly, angina can occur without an obstructive epicardial lesion, that is due to demand or microvascular disease.

*It is also vital to understand that PCI or CABG is meant mainly for symptom relief. PCI is just a lesion-specific temporary fix. Note that symptom means angina; dyspnea relief after revascularization, either by PCI or CABG, is an exception, not a rule.

*Plaque burden and its vulnerability are major determinants of long-term survival. In multivessel CAD, we can’t attend to all by PCI.

*It is also a fact that , while PCI can successfully fix an eccentric vulnerable plaque, it can very easily destabilize a non-vulnerable plaque if the metals are not maintained properly.

*It is wise to understand medical management , which by stabilizing and regressing a plaque, is technically a medical revascularization process . I am sure no cardiologist would be ready to accept this (Request them to go through AVERT study : Atorvastatin beats PTCA) So, the correct decision to revascularize is based on the presence of significant symptoms of angina that are refractory to a trial of anti-anginal drugs.

Reference

Few are worth mentioning* (As RCTs seem to fight with each other)

*There are dozens of guidelines and hundreds of RCTs, and meta-analyses that have addressed this question. I am afraid none have answered it clearly or we are not able to follow it, as the conclusions colludes with our wish. Not being able to find an answer to research question despite large systematic studies, implies, RCTs may not be the real solution in many clinical queries.

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Hardware update : Ringer coronary perfusion catheter for perforation management.

December 10, 2025 by dr s venkatesan

Coronary arterial perforation continues to be challenging task . There are multiple options to arrest the perforation as listed below.

Image source Ref : 1

Still, we don’t have a quick balloon occlusion strategy that maintains antegrade flow. Here is a new innovation, a circumferentially inflating balloon (like an airbag or a parachute from the catheter) that can maintain the antegrade flow. This may be vital in salvaging or preventing a myocardial infarction. This balloon catheter is named the Ringer balloon, manufactured by Teleflex. ( _K_andzari DE, Alqarqaz M, Nicholson. et al J Soc Cardiovasc Angiogr Interv.2025 Jul 22;4(7):103575. doi: 10.1016/j.jscai.2025. )

Source : Teleflex website

Reference

1.Perforation-management ,A review article Molly Silkowski, Anbukarasi Maran, -An assessment of balloon tamponade, Ringer balloon, covered stents, coils, and thrombin.

2.Link to the Teleflex website

3.Link to a video lecture on Ringer balloon

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AI clinical consults : Beware of machine hallucinations, that could become a permanent medical record of your patients.

December 6, 2025 by dr s venkatesan

It is predicted, (or already happening ) atleast 30 % of clinical consults happen with AI assistsnce or with completely with machines.

The Initial work up is suggested by the AI bots, even in ER rooms. They may be right in 80% of times. But, who is it to filter and grab those remaining 20%. No one , except a astutely learnt clinician. Unfortunately, there is no super AI to do this job.

Final message

This is the beginning of, a new exciting & dangerous era, for the medical profession. If we are not vigilant or loose our common sense, these bots will soon reach their next destination, ie patient’s bed side.

Reference

BMJ in its current Issue address these  aspects of increasing AI usage in the clinical consults

1. Clinical competencies for using generative AI in patient care BMJ 2025; 391 doi: https://doi.org/10.1136/bmj-2025-085324 

https://doi.org/10.1136/bmj-2025-085324

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Guilty lessons in cardiology : Learn to Ignore significant LV dysfunction, following a successful primary PCI

December 4, 2025 by dr s venkatesan

Interventional cardiology’s flag-bearing procedure primary PCI stands tall and is being projected to be the greatest thing to happen for the human heart during the critical times of STEMI. The aim is to do a fast PCI to salvage the myocardium. Unfortunately ,It has become a strange habit, (endorsed by even learned cardiology forums) to define the success of primary PCI based on the restoration of TIMI 3 flow in the IRA, and not on the amount of myocardium salvaged .

What is more worrisome is, the fact, that almost every experienced cardiologist knows, crystal clear, that there is a pitiful relationship between TIMI flows at the epicardial artery and subsequent LV function. Of course, it might improve as time goes on. Still, it is unacceptable to define success of pPCI prematurely. some times, as early as the patient is wheeled out of cath lab.

What does the evidence say ?

The incidence of moderate or severe LV dysfunction even after a timely pPCI is still significant. The average incidence hovers around 36% .It would mean , atleast one third of patients who undergo pPCI leave the hospital with significant myocardial damage, but the cath lab report would say proudly , it is a successful pPCI without any untoward events. (Mind you, in the strict sense, even treated no-reflow should come under partial failure of pPCI, which again constitutes another 20%) Ref : Papapostolou S, et al, A Long-term clinical outcomes of transient and persistent no-reflow following percutaneous coronary intervention (PCI): a multicentre Australian registry. EuroIntervention. 2018 Jun 20;14(2):185-193.

Comparative studies that looked into LV function following pPCI

Study (Year, Location)Sample SizeLV Dysfunction DefinitionIncidence (%)Key Predictors
Khaled et al. (2022, Saudi Arabia)2863LVEF ≤30% (early, <24h echo)36%Anterior STEMI, high troponin, renal impairment, multi-vessel disease
Liu et al. (2023, China)186LVEF decline (long-term, 4y)54 %High peak troponin I, anterior STEMI, prior MI, low baseline LVEF
Kim et al. (2018, Korea)1736LVEF ≤40% (3-12m echo)14%Baseline LVEF ≤40%, renal insufficiency, high peak CK/CKMB
Parodi et al. (2007, Italy)500<40% (Variable)27-60% range citedAnterior MI, large infarct size
HORIZONS-AMI (2011)Large RCTHeart failure post-PCI5-9%Thrombus burden, delayed reperfusion

​Note a curious point : The HORIZONS-AMI had a very low incidence of LV dysfunction totally a disconnected with the reality

Final message

It is a height of deceit, when some of us are still canvasing patients, emphasizing , that  it has 95% success, hiding behind the TIMI 3 flow at IRA. Still waiting for the day of reckoning (Read my 2016 presentation in CSI Kochi conference) when the ACC/ESC/SCAI , will ultimately redefine the definition of successful pPCI to include a cut off of post-procedure EF of at least 50%.

Let us not stop with that, we have to mitigate the LV dysfunction with all our might. This implies early preventive and protective measures to maintsin  the microvascular integrity , which is responsible for this epicardial-myocardial dissociation.

Reference

  1. Khaled S, Shalaby G. Severe left ventricular dysfunction earlier after acute myocardial infarction treated with primary percutaneous coronary intervention: predictors and in-hospital outcome. A Middle Eastern tertiary center experience. J Saudi Heart Assoc. 2022;34(4):257-63. https://doi.org/10.37616/2212-5043.1325sha257-263.pdf​j-saudi-heart​
  2. Liu C, Guo M, Cui Y, Wu M, Chen H. Incidence and predictors of left ventricular function change following ST-segment elevation myocardial infarction. Front Cardiovasc Med. 2023;10:1079647. https://doi.org/10.3389/fcvm.2023.1079647pmc.ncbi.nlm.nih+1​
  3. Kim DH, Park CB, Jin ES, Hwang HJ, Sohn IS, Cho JM, Kim CJ. Predictors of decreased left ventricular function subsequent to follow-up echocardiography after percutaneous coronary intervention following acute ST-elevation myocardial infarction. Exp Ther Med. 2018;15(5):4089-96. https://doi.org/10.3892/etm.2018.5962spandidos-publications+1​
  4. Parodi G, Memisha G, Carrabba N, Signorini U, Migliorini A, Cerisano G, Bolognese L. Prevalence, predictors, time course, and long-term clinical implications of left ventricular functional recovery after mechanical reperfusion for acute myocardial infarction. Am J Cardiol. 2007;100(12):1718-22. https://doi.org/10.1016/j.amjcard.2007.07.022pubmed.ncbi.nlm.nih​
  5. Kelly DJ, Gershlick T, Witzenbichler B, Guagliumi G, Fahy M, Dangas G, Lansky AJ, Mehran R, Stone GW; HORIZONS-AMI Trial Investigators. Incidence and predictors of heart failure following percutaneous coronary intervention in ST-segment elevation myocardial infarction: the HORIZONS-AMI trial. Am Heart J. 2011;162(4):663-70. https://doi.org/10.1016/j.ahj.2011.07.032pubmed.ncbi.nlm.nih+1​

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Hippocratic oath : A Patient version

December 4, 2025 by dr s venkatesan

While patient rights has been extensively discussed and debated , there is some concern especially in country like India, where violence against medical professionals has increased to prohibitive levels. This is mainly attributed to low levels of tolerance and high expectations from the doctors and hospitals.

There has been multiple Incidents where doctors are attacked, even when a life is lost due an incurable disease in spite of well administered treatment . Many patients are unable to differentiate the natural history of illness , any death is looked upon as medical negligence. In this context, there is a call for patient education and teaching them responsibilities and make them understand the complexity and uncertainty in the science of biology, and also accept the reality of inadvertent errors in judgment and execution in medical practice. 

A curious solution is suggested .Yes , its called Hippocratic Oath : Patient version .The father of medicine would have never thought , a day would come , when patients might, try to prevail over the Doctors .Readers may decide about the political correctness , utility and practicality of such an oath.

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SCAD : No dissection is spontaneous

December 2, 2025 by dr s venkatesan

“Nothing moves without an external physical force”

SCAD is a popular entity among cardiologists in angiographically sub-categorizing of ACS, especially in women. The entity is indeed important to recognize, as the otherwise omnipresent PCI, is contraindicated in SCAD.

Meanwhile, we can’t take every suspicious-looking dissecting flap as SCAD in women. The word spontaneous in SCAD, could often convey a potentially erroneous meaning, for the simple reason, plaque ruptures and fissures that triggers dissections of varying lengths can be spontaneous as well.

By the way, any tips to differentiate SCAD from spontaneous plaque ruptures and fissures ?

OCT in SCAD : A SCAD caused by an intimal tear (arrow) resulting in expansion of a false lumen and an intramural hematoma (plus sign). B SCAD caused by de novo injury and bleed inside vessel wall resulting in the false lumen with intramural hematoma (plus sign) Source Shah, T et al  Curr Cardiol Rep 24, 529–540 (2022). https://doi.org/10.1007/s11886-022-01676-7

Final message

Nothing moves with out a force either from witjin or external . In both SCAD or plaque rupture , an emotional or hemodynamic stress is responsible.

The above list to differentiate SCAD from plaque fissure is big, but few are actually useful. Sometimes, the confirmation comes from the direct feel and the haptics of the lesion and the level of difficulty in crossing the lesion.

Caution : However, in explict clinical situations, as in a young pregnant women with ACS,  who has a long spiral dissection , never diagnose anything other than SCAD.

Post-amble: * I wonder, how did the cardiology literature accumulated so much OCT data in SCAD, it should have been very risky procedure  in those friable vessels. If PCI is contraindicated , OCT comes very close to it.

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What is the realistic definition for “fact vs fake” news

November 18, 2025 by dr s venkatesan

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Does IVS hypertrophy occur in Pulmonary hypertension ?

November 18, 2025 by dr s venkatesan

Interventricular septum, is the common shared wall between LV and RV . For various biological and hemodynamic reasons , this sharing never follows the law of equity.. It has a bias toward the bigger brother LV. Still, it never lets the RV down in contributing to RV function.

Let us see, how the IVS behaves when it comes to responding, to RV pressure overload .It is clear ,from what we know so far, IVS behavior rarely follows a pattern. We know it resists the pressure and transforms to a D shape. Does the D shaped LV really trigger an increased IVS thickness ?

IVS hypertrophy in RVH : A mixed mystery pheonmenon

In pulmonary hypertension (PHT) or any right ventricular hypertrophy (RVH), the interventricular septum (IVS) does not hypertrophy primarily due to its unique hemodynamic positioning, as IVS is anatomically and functionally linked with left ventricular (LV) mechanics. Unlike LV, the chronic RV pressure overload which is required for septal myocyte growth is rarely sustained because RV tends to dilate as well, in the process interrupting hypertrophy.

RVH occurs with elevated pulmonary artery pressures , but the pressure distibution is uneven. It is more on RV free wall and outflow tract rather than the septum. The pressure distribution concentrated at the RV free wall (infundibulum and body) .Also, the trabeculae sparing effect on IVS from direct overload .

RV free wall hypertrophy defined as thickness exceeding 5 mm on echo in subcostal view in end diastole, ideally on inspiratory phase when it is maximally filled. ( MRI is a still more reliable index of RVH severity) correlating well with RV function and prognosis.

Final message

IVS rarely hypertrophies in RVH in most pathological RV pressure overload conditions. This is due to the complex shape of the RV as well as the non-uniform pressure distribution of RV intracavitary pressure. Unlike LVH, there is no strict concentric RVH. RV free wall hypertrophy is the best index for accurate identification and quantification of RVH.

A note of caution

Congenital heart diseases like isolated valvular PS, TOF can cause severe IVS hypertrophy. Similarly some Inherited or acquired infiltrative diseases can cause disproportionate RVH .We should be cautious , not to mis-classify IVS hypertrophy as LV pathology in these situations.

Reference

1.Schneider M, Binder T. Echocardiographic evaluation of the right heart. Wien Klin Wochenschr. 2018 Jul;130(13-14):413-420. doi: 10.1007/s00508-018-1330-3. Epub 2018 Mar 19. PMID: 29556779; PMCID: PMC6061659.

2.Sekine I, Takahashi M, Murata M, Kira Y, Okabe F, Ito T. Pathological analysis of the right ventricular hypertrophy and ventricular interdependence in autopsied hearts with cor pulmonale and pulmonary hypertensive rat hearts. Jpn Circ J. 1989 Oct;53(10):1245-52. doi: 10.1253/jcj.53.1245. PMID: 2533277.

3.Bhattacharya PT, Shams P, Ellison MB. Right Ventricular Hypertrophy. 2024 Mar 16. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan–. PMID: 29763051.

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In HFpEF , which chamber of the heart primarily fails ?

November 14, 2025 by dr s venkatesan

A. Left ventricle

B. Left atrium in isolation

C. Both left ventricle & left atrium

D. Isolated right ventricle failure.

E. It is actually a Bi-Ventricular failure.

Trying to answer

If any one  can answer this question, correctly , he deserves some award. I am yet to find an answer.

HFpEF , by its definition has Normal EF,  diastolic LV failure , LA reservoir dysfunction, combined post and pre cap PHT, with or without RV failure.

Full blown HFpEF has some what curious hemodynmics. Though we expect LA to fail in isolatiin, it is the right ventricle, that over works to tackle the elevated LAP and  PH . Hence, it is likely clinical RV failure would  be more common than LV.

Therorticaly, we can say , HFpEF is typical example of Bi ventricular failure as well, ie LV diastolic ,and RV  systolic failure. If you want to be still more precise, it should be called triple chamber failure (LV,LA & RV)

Final message.

HFpEF continues to be complex clinical  entity, with no single chamber is a primary culprit. It is a multi chamber failure. In fact, the failure initiating chamber may play lesser role than the responding chamber may react disproportionately. Please Note : LA is failure defining chamber. If it can tackle the stiff LV with all its might (compliance and contractility) , no other chamber need to fail.

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Knowing the Heart diseases, with female pre-ponderance

November 13, 2025 by dr s venkatesan

Men are from Mars, women are from Venus. It may not be a fiction.afterall .It runs deep into q-bits and quark particles  of our cells. The well known double X cross chromosome,  epigenetics , along with hormonal interactions with cellular components make many of diseases more female centric.

Most importantly, women who are carrying  a baby , are technically a chimera, and the two-way traffic of genetic materials across the placenta has unexplainable Immune interactions, making autoimmunity almost exclusively a female disorder (SLE, etc.).

Following is the partial list of women-centric heart disease

  • Rheumatic Heart disease: RHD is common in both genders, but it attacks the mitral valve with a strikingly different rate in females, with a ratio of up to 4:1. This difference, however, wanes with aortic valve involvement.
  • Mitral valve prolapse: More common in women, overriding the the fact, there are more tall men , who are likely to have more MVPS
  • Takotsubo (stress) cardiomyopathy: 80-90% casesoccur in women. This is surprising. (Women are known to be great fighters of stress, in all walks of life; they outlive men by 5-10 years in terms of longevity. Still, when it comes to the heart, they seem to be sensitive.)
  • NSTEMI vs STEMI in women (It is rather women are somewhat resistant to STEMI )
  • Sponatneous coronary artery dissection has well known female domnace especailluy in duiring pregnancy (estrogenic vascular elastin fracture , striae gravidourm ?)
  • Coronary microvascular disease: Higher prevalence in women; female rate up to 66%
  • Peripartum cardiomyopathy: Exclusive to women by definition, incidence 1 in 5000 live births
  • Heart failure with preserved ejection fraction (HFpEF): Women represent about 55-60% of cases. Odds are higher for sure. (Is that obesity ?)
  • Primary pulmonary hypertension (Pre -capillary , again hormonal-endothelial interaction ?)
  • Takayasu arteritis (aorto-arteritis): Strikingly high. Female to male ratio approximately 7:1
  • Mitral annular calcification: Female to male ratio roughly 2:1; more severe in women, especially elderly (Aortic annulus , males dominate )
  • In congenital heart disease Atrial septal defect has a female to male ratio approximately 2:1 (To remind TGA is strikingly a male disease)

Missing entities , may be added by readers

Final message

Knowing the gender difference in heart disease may not matter much, if we look at things superficially. Decades down the line, It has a huge potential in preventive cardiology, as the current genome-level interventions and female-specific vaccines might be in the offing.

References

  1. .Gewitz MH, Baltimore RS, Tani LY, Council on Cardiovascular Disease in the Young. Revision of the Jones Criteria for the diagnosis of acute rheumatic fever in the era of Doppler echocardiography: a scientific statement from the American Heart Association. Circulation. 2015 May 19;131(20):1806-18.
  2. Templin C, et al. Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy. N Engl J Med. 2015;373(10):929-38.
  3. Lanza GA, Crea F. Primary coronary microvascular dysfunction: clinical presentation, pathophysiology, and management. Circulation. 2010 Jun 1;121(21):2317-25.
  4. Nishimura RA, et al. Mitral Valve Prolapse. N Engl J Med. 2007;356(26):2641-9.
  5. Sliwa K, et al. Peripartum Cardiomyopathy. Circulation. 2010;121(8):840-50.
  6. Dunlay SM, et al. Heart Failure with Preserved Ejection Fraction: Drivers and Therapies. JACC. 2017;69(17):1919-1932.
  7. Johnston SL, Lock RJ, Gompels MM. Takayasu arteritis: a review. J Clin Pathol. 2002;55(7):481-6.
  8. Abramowitz Y, et al. Mitral Annular Calcification. J Am Coll Cardiol. 2015;66(17):1934-41.
  9. Warnes CA. Adult congenital heart disease: Specific considerations for women. J Am Coll Cardiol. 2016;68(7):747-760.
  10. Hoffman JI, Kaplan S. The incidence of congenital heart disease. J Am Coll Cardiol. 2002;39(12):1890-900.

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