As we enter, another customary happy “New year” , a lingering “Old wish” remains largely unfulfilled. Let us try to return, to our forgotten home space, called patient’s bed side . Shall get Immersed in history taking , Intuitive clinical examination, and master the art of listening to our patient’s heart with our own ears. Investigations can wait unless it is a dire emergency.
Too often today, we bypass these foundations, relying blindly on Images, echocardiograms, angiograms, a deluge of scans, , multi-modality algorithms ,AI predictions. We have also become greedy servants to technology commerce , and increasingly intoxicating science as well. Let us not insist on investigations , driven by peer pressures or pride, in the process losing common sense in a flood of data.
Let us reclaim the intellect, that taught us listening and understanding to the patients symptoms (with kindness) is the highest form of Investigation .
Coming to scientific research, grow courage to question, debate , that ultimately would simplify complex problems .
Finally, seek the truth, which often hides behind the distorted evidence base and obsessive compulsive protocols.
“Every Interventional Cardiologist, realistically, need to be a preventive neurologist too!”
The concept a permanent ascending aortic porous membrane filter (PAA-PMF) is an extrapolation of the idea of mechanical thrombus capture, as proven by IVC filters for venous embolism prevention . Also we do have and temporary intra-aortic filters like Sentinel , Embol-X for arterial particulate capture.
Device Concept
The PAA-PMF would feature a self-expanding nitinol frame, with a fully porous head end. The device can be heparin-coated polyester or polyurethane mesh membrane, deployable via 12-14 Fr femoral sheath, similar to IVC filter designs but should be optimized for aortic pressures. Suggested pore size of 100-125 μm targets >100 μm emboli, akin to Embol-X filtration efficacy in capturing 95% of particulates (atheroma, fibrin) during aortic declamping. The essential requirement is that the porous membrane should not create an impedance gradient. How feasible it is, to be tested. Conical shape, the radial force will ensure good ascending aortic wall apposition.
Device location site
Site of placement is critical. Proximal ascending aorta, 2-3 cm distal to sinotubular junction/proximal to brachiocephalic trunk, as in Embol-X for maximal cardiac/aortic debris interception without coronary/arch compromis
Potential indications
(Only in patients with very high risk of cardioembolic stroke)
1.Chronic stroke reduction in patients with MVR/AVR/TAVR/MAVR
2.High-risk mobile LV mural thrombus
3.Chronic AF with visible and invisible clots in LA
4..High-risk procoagulant conditions with recurrent embolism
Definite Risks
*Occlusion and hemodynamic compromise is the most crucial issue. However, when compared to the incidence IVC filter clogging, the high pressure aortic flow is likely to self-wash the device (as happens in a prosthetic aortic valve)
Trapped emboli may enter into coronary circulation is a possibility. Putting a filter at ascending aorta precludes left heart catheterization.
*Migration , Hemolysis are other expected complications.
Intense anticoagulation would be required to prevent occlusion of the filte . (Still, stopping it temporarily doe not not increase the risk of stroke)
Final message : Is it Worth for a Preclinical trial ?
We do have temporary aortic filters. The concept of permanent or semi-permanent filters is largely theoretical, with potential risks being more than benefits. The device can take care of only cardio-aortic embolic stroke.
However, considering so many complex, risky intracardiac and intravascular devices being tested on a daily basis, it is not a big deal for the current generation of interventional cardiologists to try this.
More than our interventional appetite, we really need a device that prevents stroke in a permanent fashion. It is definitely worthy to do initial studies in a porcine model. Would be glad , if Edwards, Abbot or Medtronic and other new Innovators respond to this.
Shammas NW, et al. Embol-X Intra-Aortic Filtration System: Capturing Particulate Emboli in the Cardiac Surgery Patient. NIH. 2004. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC4682540/
Almanza DC, et al. Comparative Review of Large Animal Models for Suitability of Cardiovascular Devices. IJMS. 2024. Available from: https://ijms.info/IJMS/article/view/763/1645
Mohammadi H, et al. Simulation of blood flow in the abdominal aorta considering hyperelasticity of the wall. J Carme. 2021. Available from: https://jcarme.sru.ac.ir/article_1223.html
It would be silly to remind, it’s the same five liters of blood, that circulates across, both the arterial and venous system. But, its journey one away from the heart, and the other towards the heart are strikingly different. They are subjected to various hemodynamic forces, travels different terrains, at different speeds, thousands of kilometers of microvasculature along the cardiovascular highway, yet merging with each other every 15 seconds or so, at the pulmonary junction box. Have a look at the following images, to understand the distribution of the blood volume.
The first image is taken from the maverick physiologist Dr. Guyton’s textbook of physiology, and the second one from the equally famous Dr. Ganong’s. Both images depict the distribution of blood volume, the corresponding pressures, and velocity. Every cardiology fellow should recall these two images even in their sleep. Also mind, they circulate around the body, lifelong without clotting or bleeding, assisted by the right balance of pro and antithrombotic forces.
Why some of patient’s blood is more likely to get frozen ?
Logic would suggest venous thrombosis should be more prevalent than arterial thrombosis at any point of time and location. This is due to the slowness of the circulation and the enormous volume within the venous reservoir. But is this the clinical reality? It is indeed true, that incidence of minor venous thrombosis exceeds arterial thrombosis. Since venous thrombosis often gets lysed or get stuck in the lungs, it’s frequently under-recognized. Arterial thrombosis causes more damage in an important sense, as it leads to target organ ischemia.
Apart from hemodynamic factors, the 200 year old Virchow’s triad is very much alive. The vessel wall integrity, intrinsic defects in the coagulation and anticoagulant/fibrinolytic molecules, the genetic susceptibility are the important determining factors. The RBC and platelet behaviour too changes, in high and low pressure environments.
How to diagnose a patient who is in a procoagulant state?
The topic is so complex .Many things are still poorly understood. We should have a checklist of all systemic conditions that can cause increased risk of thrombus. We know pregnancy is inherently a procoagulant state, as is manifest or concealed malignancy.
What we normally do ?
It is very easy to tick the coagulation profile/panel slip and pass it on to the nursing staff. Some of us take another easy route, referring such patients to a rheumatologist for the risk-stratifying job. This is probably because we strongly believe SLE and connective tissue disorders are the first culprits.
I think we need to engage the hematologist more often because thrombosis is not only due to excess coagulation. It is also due to a lack of enough circulating anticoagulants. (As a cardiologist, sometimes I feel awkward. to call myself an expert of the circulatory system, with almost zero knowledge of how the blood clots or dissolves.) This article tries to differentiate the risk factors operative on the venous and arterial sides. It is only a gross attempt; many risk factors are invisible and are common between arterial and venous thrombus.
Fortunately, identifying the thrombosis prone patients is complex , but the treatment is fairly simple. We have only few options: Aspirin, Warfarin, and NOACs *We need to choose one of them. The general rule is aspirin doesn’t work much on the venous side. I don’t know how far this is really true. (It has something to do with the shearing force of platelets? ) However, in obstetrics, the placental circulation is full of low pressure venous plexus where Aspirin is used as a norm.
Between Warfarin and NOACs, there is absolutely no doubt Warfarin is the clear winner on the arterial side. Because of monitoring issues and fear of bleeding, we are compelled to switch to NOACs in many situations. Beware, think twice before prescribing NOAC for prophylaxis against arterial thrombus. The venous side does not have much difference in choice. *Heparin (& its glamor sibling LMWH) is a unique molecule, which has ability to work on both arterial and venous sides.
The article doesn’t discuss the intra vascular metals, wires, devices, valves, pacemakers , related thrombosis. Here there is a known trigger. It is possible, they also influenced by the baseline factors of pro-coagulation discussed above.
“When we change the way we look at things, the things we look at change.”
Wayne Dyer
Standalone thrombolysis remains a potent, evidence-based, time tested lifeline for STEMI patients worldwide.It delivers rapid myocardial salvage. This is a rule,not an exception ,where primary PCI delays or pharmaco-invasive infrastructure falter, with absolute mortality reductions of 2-3% when administered early . The benefits holds on or often beats pPCI despite it’s relative edge in ideal settings.
STEMI : Time trumps technology
Fibrinolysis, as a modality has pioneered the science of myocardial reperfusion. It reduced the early mortality by >50% in landmark trials enrolling tens of thousands, and still stands tall. it carries (Class I-A Indication ) Pharmaco-invasive strategies reduce reinfarction by 2% absolute (NNT 50) over lysis-alone but show only uncertain 0.5% mortality gains (NNT -200, low-certainty), as per the 2025 PLOS ONE meta-analysis of 7 RCTs .
This is major evidence stress an important hidden truth , that standalone lysis is not “obsolete” in low-risk, well-reperfused cases where PCI risks (bleeding, microvascular injury) may offset slim benefits.(Soriano-Moreno DR 2025 PLOS ONE meta analysis)
Real-world registries confirm this. In >70% of global STEMI (LMICs, rural/high-transfer areas), lysis achieves TIMI 3 flow in 50-60% and can beat the delayed PCI prognostically., if door-to-needle <30 minutes . More importantly (& not so-scientifically too) TIMI 2 flows are not considered as success in most of these studies. In reality, an early TIMI 2 flow, which can be achieved with lytics easily, is more than good enough to prevent myocardial necrosis. This is in contrast to the fact, that even a glorious TIMI 3 flow, after PCI does not guarantee complete myocardial reperfusion.
Systems reality: Equity vs PCI hegemony
Population-based registries indicate primary PCI utilization rates below 20% for STEMI cases in India, or other developing countires.
Compulsive mandates, that prioritise PCI, increase total ischemic time, elevate no-reflow incidence, and raise mortality compared to systems enabling universal early fibrinolysis. The most troubling truth is, non-PCI centers hesitate to deliver timely fibrinolysis , due to perceived Inferiority, peer pressure , potentially forgoing established mortality benefits.
Commercial undercurrents: Incentives could Injure the myocardium
PCI ecosystem prioritizes procedural volume metrics, cardiologist’s Incentives, reimbursements (10-20 times higher than fibrinolysis costs), and institutional performance indicators, resulting in under-investment in fibrinolysis infrastructure. This systemic bias potentially compromising overall STEMI outcomes by deprioritizing rapid reperfusion strategies.
Final message
Cardiology Literature Needs a Scientific Distillation & a Philosophical Kick
Modern cardiology’s PCI dogma is trying to blind thrombolysis’s enduring truth. A village PHC’s or ER crew’s humble hand injections at 30 minutes could salvage more myocardium than a helicopter transferred PCI, in a star rated cathlab.
Standalone lysis fights STEMI fiercely, early, equitably, economically, unless commercial narratives, transfer dogma, and selective trials confer them a cult status, exposing millions of ACS patients to prolonged ischemia.
Are we reqdy to revive and embrace the truth? Population-based pPCI can wait. It is a futile to set wrong goals like “stent for every STEMI”; not only in a country like India, it applies to even the developed nations. Let us, prioritize lysis-first systems, especially the pre-hospital or ultra-fast in-hospital lysis. Reserve pharmaco-invasive PCI for failures or high-risk, especially with built in harm seen with routine early PCI post-lysis.
References
Bouyaddid S, Bouchlarhem A, Bazid Z, Ismaili N, El Ouafi N. Pharmaco-invasive Therapy: A Continued Role for Fibrinolysis in the Primary PCI era. Clin Appl Thromb Hemost. 2023;29:10760296231221549. doi:10.1177/10760296231221549. https://pubmed.ncbi.nlm.nih.gov/38145624/pmc.ncbi.nlm.nih
Armstrong PW, Gershlick AH, Goldstein P, et al. Fibrinolysis or primary PCI in ST-segment elevation myocardial infarction. N Engl J Med. 2013;368(15):1379-1387. doi:10.1056/NEJMoa1304062. https://www.nejm.org/doi/full/10.1056/NEJMoa1304062ncbi.nlm.nih
Assessment of the Safety and Efficacy of a New Thrombolytic Regimen (ASSENT)-4 PCI investigators. Primary versus tenecteplase-facilitated percutaneous coronary intervention in patients with ST-segment elevation acute myocardial infarction (ASSENT-4 PCI): randomised trial. Lancet. 2006;367(9510):569-578. doi:10.1016/S0140-6736(06)68148-0. https://pubmed.ncbi.nlm.nih.gov/16488800/pubmed.ncbi.nlm.nih
McDonald MA, Fu Y, Zeymer U, et al. Adverse outcomes in fibrinolytic-based facilitated percutaneous coronary intervention: insights from the ASSENT-4 PCI electrocardiographic substudy. Eur Heart J. 2008;29(7):871-879. doi:10.1093/eurheartj/ehm599. https://academic.oup.com/eurheartj/article/29/7/871/483738academic.oup
Pinto DS, Kirtane AJ, Ruocco TA Jr, et al. Facilitated percutaneous coronary intervention following fibrinolysis: the path to redemption? Insights from BRAVE, GRACIA, and beyond. Rev Cardiovasc Med. 2007;8(4):187-194. https://pubmed.ncbi.nlm.nih.gov/18192961/pmc.ncbi.nlm.nih
This is an editorial submitted by this author to a leading cardiology journal, which was returned within 24 hours , with a comment that article is unsuitable for publication .Want to know, whether the readers agree with the journal editorial team
The Unfinished Story of “Successful” Primary PCI
Primary percutaneous coronary intervention (pPCI) has revolutionized the management of ST-elevation myocardial infarction (STEMI) and remains the gold standard for restoring coronary perfusion. Angiographic success defined as achieving Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow in the infarct-related artery occurs in more than 90–95% of cases. (1,3)However, this measure reflects epicardial recanalization alone and falls short as an indicator of effective myocardial reperfusion..(5)
Cardiac magnetic resonance (MRI/CMR) imaging, myocardial contrast echocardiography, and nuclear perfusion techniques consistently reveal that adequate tissue-level reperfusion occurs in only 60–70% of patients with angiographically successful PPCI. This disparity highlights a critical gap between procedural endpoints and true myocardial salvage.(6)
The Persistent Challenge of Microvascular Obstruction
Despite apparent angiographic success, up to 20–30% of patients exhibit microvascular obstruction (MVO) or “no-reflow.” The pathophysiology of MVO involves distal microembolization, capillary edema, and endothelial dysfunction. (2)
MRI studies have demonstrated MVO in 10–15% of PPCI-treated patients with TIMI 3 flow, often associated with larger infarct size, lower left ventricular (LV) ejection fraction, and worse long-term outcomes. (4,6)
Redefining the Endpoints: From Epicardial Patency to Microvascular Integrity
Left ventricular function remains the most clinically relevant indicator of therapeutic success in STEMI. Persistent LV dysfunction in up to 40% of successfully revascularized patients underscores the inadequacy of angiography based assessment. (3)
TIMI grading system is the universally adopted most popular angiographic flow grading. It has its limitations . It confines with epicardial flow . The max grade is TIMI 3 , and it sort of falsely reassures
The concept of TIMI 4 flow was originally suggested by Dr Gibson in 1999 , calling hyperemic flow with a low TIMI fame count, as TIMI 4 flow. For some reason this concept was never adopted, though this term extends the traditional TIMI grading system to include microcirculatory perfusion.
This proposed category reflects optimal tissue level reperfusion, measurable through myocardial blush grade, the index of microcirculatory resistance (IMR), or perfusion-based MRI parameters. (8,10)TIMI 4, therefore, would define the ultimate therapeutic endpoint in the physiological perfusion at the myocyte level.
Emerging Tools and Strategies for Microvascular Optimization
Several strategies can favorably influence microvascular flow. Intracoronary vasodilators such as adenosine, verapamil, and sodium nitroprusside mitigate microvascular constriction and distal embolization. Deferred stenting techniques may reduce reperfusion injury in selected cases.
Recalibrating the Definition of Successful pPCI
Given the growing evidence base, it is time to reconsider what constitutes “success” in pPCI. A restored epicardial lumen without adequate tissue perfusion represents an incomplete therapeutic achievement.
A Call to Global Cardiovascular Leadership
It is good, if the major professional societies like the American College of Cardiology (ACC), European Society of Cardiology (ESC), and Society for Cardiovascular Angiography and Interventions (SCAI) reassess the criteria used to define procedural success in STEMI interventions. Integrating TIMI 4 flow as a recognized endpoint, along with preservation of maximal left ventricular function, will more accurately define the true success of pPCI.
van ‘t Hof AW, et al. Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction: myocardial blush grade. Circulation. 2001 Aug 28;104(9):1130-4. https://pmc.ncbi.nlm.nih.gov/articles/PMC2810032/pmc.ncbi.nlm.nih
*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.
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. )
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
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.
Comparative studies that looked into LV function following pPCI
Study (Year, Location)
Sample Size
LV Dysfunction Definition
Incidence (%)
Key Predictors
Khaled et al. (2022, Saudi Arabia)
2863
LVEF ≤30% (early, <24h echo)
36%
Anterior STEMI, high troponin, renal impairment, multi-vessel disease
Liu et al. (2023, China)
186
LVEF decline (long-term, 4y)
54 %
High peak troponin I, anterior STEMI, prior MI, low baseline LVEF
Kim et al. (2018, Korea)
1736
LVEF ≤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 cited
Anterior MI, large infarct size
HORIZONS-AMI (2011)
Large RCT
Heart failure post-PCI
5-9%
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
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.pdfj-saudi-heart
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
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
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
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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