Electrophysiology, we believe, is a field that contains a gamut of disorders of rate and rhythm defects, congenital or acquired, right from the SA node to the Purkinje fibers.The core principle of EP is interwined with LV function and preventing all preventable electrical SCD , should be be our primary aim. Unfortunately, nowadays if you open any EP journal, you will wonder whether electrophysiology is all about atrial fibrillation and pulmonary vein ablations.
Here is a table comparing the space allotted to AF and various ablation techniques in major EP journals between the years 2025 and 2026. It is clear that EP science is heavily biased towards AF. Meanwhile, PFA may be a genuine innovation in tissue ablation, but its overwhelming dominance in the EP literature is not acceptable and not in the best interest of patients.(Cryo and RF should not succumb to this inflated superiority of PFA) *The PACE journal should be appreciated as it seems to resist the peer pressure to promote pulsed field ablation (PFA).The editors deserve some complements.
Final message
Cardiac arrhythmias in ischemic structural heart disease are more critical than the more benign and nuisance arrhythmia of atrial fibrillation (AF), which can be effectively managed in 90% of the population with simple drugs and anti-arrhythmiclifestyle modifications.
An appeal to all stakeholders: Let us take a pause and bring back the original charm of electrophysiology (EP). Let us be inclusive.There are many more areas of crucial importance. Keep an upper limit for AF-related articles—maybe a maximum of 20% (even this appears liberal).
Bendopnea is a newer addition to the special forms of dyspnea, such as platypnea and trepnea.( Not exactly new .It was first reported by Jennifer T. Thibodeau from Texas in 2014 ) Though it initially appeared to be an inconsequential symptom, subsequent observations from many patients with heart failure have made this symptom highly significant. It seems to be a marker of high risk for decompensation. It occurs within 30 seconds of bending. In a patient with an already elevated left ventricular (LV) filling pressure, the act of sudden bending adds more stress by increasing the mean left atrial (LA) pressure further. A precise mechanical explanation for this phenomenon is not available.
The current literature attributes bendopnea to increased intra-abdominal pressure from bending forward, which pushes the diaphragm upward and forces congested splanchnic blood into the chest, causing a sudden surge in central venous return and pulmonary capillary wedge pressure. However, this fluid-shift mechanism does not explain why bendopnea correlates poorly with body mass index or abdominal girth.(Ref 1 the original paper do have BMI data)
The Mechanism of Bendopnea
The left atrium is the superior-most chamber of the heart in an erect posture, maintaining a strict superior-inferior relationship relative to the left ventricle.
Please realise a subtle relationship of LA to LV . LV may be the most crucial chamber of heart, but LV remains anatomically Inferior , that confers the humble LA, with some commanding powers over LV, especially in patients with LV compromised states.
In this upright position, LV filling is naturally assisted by gravity.When a patient bends forward more than 90 degrees, the LA-LV spatial relationship shifts from a vertical orientation to an almost horizontal one. Because of this shift, LA filling loses its gravitational advantage. The pressure must momentarily rise higher to compensate, resulting in acute stretch of the LA, pulmonary veins (PV), and J-receptors causes immediate dyspnea.
Clinical Implications
Though bendopnea is reproducible in many individuals, some patients can become accustomed to the sensation over time. Numerous papers also suggest that bendopnea serves as an excellent clinical marker for HFpEF, RV dysfunction, or pulmonary hypertension.
Final Message
Bendopnea is interesting new symptom . It is clear it can have multiple mechanisms. Posture-induced alteration in the LA-LV axis and the sudden elimination of gravity assistance can be an important factor in triggering dyspnea on bending. This can easily manifest in patients with advanced heart failure who have already exhausted all of their cardiac reserve mechanisms.
Reference
1.Thibodeau JT, Turer AT, Gualano SK, Ayers CR, Velez-Martinez M, Mishkin JD, Patel PC, Mammen PP, Markham DW, Levine BD, Drazner MH. Characterization of a novel symptom of advanced heart failure: bendopnea. JACC Heart Fail. 2014 Feb;2(1):24-31. doi: 10.1016/j.jchf.2013.07.009. Epub 2014 Jan 8. PMID: 24622115.
2.Karauzum K, Karauzum I, Kilic T, Sahin T, Baydemir C, Baris Argun S, Celikyurt U, Bildirici U, Agir A. Bendopnea and Its Clinical Importance in Outpatient Patients with Pulmonary Arterial Hypertension. Acta Cardiol Sin. 2018 Nov;34(6):518-525. doi: 10.6515/ACS.201811_34(6).20180528A. PMID: 30449993; PMCID: PMC6236562.
Postamble
Can bendopnea occur in a patient with a normal heart and normal LV function?
Yes, and here begins the problem. Many deconditioned, sedentary individuals do develop bendopnea. This is due to signals from the peripheral muscle spindle reflex. This condition is largely benign, but it implies that the person needs to improve their physical conditioning.
Today , September 29th is the World heart federation, backed official World Heart day.
Reclaiming the Soul of World Heart Day
Have you ever wondered why cardiologists, physicians, and big hospitals celebrate World Heart Day in a most sacred way as if it is festival of Diwali, Dussehra, or Onam? The scale of these celebrations and the accompanying mainstream media blitz have become truly overwhelming.
Originally, this day was meant to create genuine awareness about the rising global epidemic of heart disease. It was designed to propagate healthy lifestyle choices among the public and protect vulnerable hearts.
But it does not stop there. There is a concealed interest public rarely sees. Although we often emphasize that prevention is preferable to a cure , the explosive growth of high-tech diagnostics and aggressive therapeutic modalities has ironically become theenemy of true preventive care. World Heart Day has increasingly been hijacked as a marketing to drive hospital footfalls rather than to create true wellness.
The much glamourised , gadget based diagnostics , advanced screening packages, & biochemistry based “preventive heart checkups” have not yielded the desired results. In fact, by creating unnecessary anxiety and over diagnosing minor anomalies, they can have the exact opposite effect. As custodians of health, we must shift the focus away from lucrative diagnostic packages and return to the simple, low-cost fundamentals of diet, exercise and lifestyle modification.
I think, on this world heart day , We should make the public realise, it is absolutely possible they can prevent a heart attack in their life time, without fearing about their calcium scores, exotic lipid sub fractions or CT angiograms. Let us reclaim World Heart Day as a forum for genuine public health, not a corporate festival.
In the clinical practice of cardiology, some times, we are compelled to check our foundational concepts and refresh or reset the knowledge. Here is a two question challenge. The first question was in fact asked by one of my patients. Does negative TMT rule out CAD ? I thought it was a routine question, and told him no tests rule out CAD 100 % perfectly. It has only 70% accuracy. Some time later, after his consult , I was pondering over this 70 % accuracy . Very soon I realised , I was totally wrong with that answer as well. You can try to find the real truth about the validity of TMT in ruling out CAD.
1.Does negative TMT rule out CAD ?
A.No, It doesn’t
B.Yes, it rules out all significant CAD
C.Yes, it rules out obstructive CAD
D.No. It doesn’t rule out non-obstructive CAD .
Answer : To get the correct answer, go to the following question. (Response A,C,D are correct .B might appear right too , but it’s wrong.)
2.Which lesion often result in ACS in CAD population ?
A.Obstructive
B.Non obstructive
Answer : Both, (In fact, non obstructive CAD more often precipitates an ACS, because they are more in numbers)
So, what is the message from these two questions ?
TMT is in reality not useful to rule out ACS prone CAD. To include it in routine master health has little meaning , if that message is conveyed to our patients. (Of course a negative TMT rules out a severely obstructive lesion , that is really be a comforting news)
Read this Editorial from Dr Prem Pais for more insights.
Final message
What is significant CAD ? we can play with this word as long as we want. In the popular cardiology parlance , the word significance revolves around the flow limiting capacity only . So, be clear .The fact of the matter is, TMT can never rule out the presence of non flow limiting, ACS prone lesions at any level of exercise loads/METS . Hence the 70-80 % negative predictive value , we confer to it, is clearly misplaced in terms of ACS risk.
Wellens’ syndrome represents a unique pathophysiological subset in ACS. While typical ACS is characterized by dominant thrombotic luminal occlusion, Wellens’ syndrome is a prototype for a low-thrombus-load .Curiously it can even be termed as “Zero thrombus” ACS. This is not a new revelation. It was underscored by de Zwaan and Wellens in their original landmark 1989 angiographic study of about 180 patients. Notably, angiography performed days after stabilization revealed a ubiquitous absence of any visible, active thrombus burden. Instead, most of patients showed a severe, fixed mechanical stenosis ( 90-100 %) in LAD , some of them showing good collateral circulation.
However , the temporary total occlusions that cause the rest angina are either due to transient thrombus or dynamic epicardial vasospasm that make the occlusion complete , only to reopen later to maintain the UA/NSTEMI status.
*Quantifying the content of the lesion in ACS is tricky . STEMI we know there is definitely thrombus dominates. In NSTEMI it is combination of both . But in Wellens , it is pre-dominatly mechanical for sure.
Clinical implication of low thrombus load
While the original study by Wellen’s did not mention about thrombus at all, the OCT based study Arteaga et al from Mexico documents thrombus in only about 20%.
OCT image shows significant, eccentric, lipid-rich plaque in a patient with Wellens ( Ref 3)
This raises a highly provocative clinical question. If a meaningful thrombus burden is fundamentally absent during the stable phase of of Wellens , do these patients truly derive any clinical benefit from aggressive heparin infusions and dual antiplatelet therapy (DAPT)? It is still more concerning, many of text call Wellens as STEMI equivalent or occlusive myocardial infarction , suggesting a huge thrombus load which it rarely show.
Final message
Wellens’ syndrome demands better clinical , pathological and therapeutic reasoning.It probably demands an urgent PCI Some times, we have labelled them as refractory UA go on to receive given 2B -3A blockers* as well increasing the bleeding risk .The lesson learnt is , aggressive anti-thrombotic strategy is largely out of place and risky in Wellens.(Ironically, after the stenting the patient will require rigorous anti-platelet agents )
Cardiogenic shock occurs in 5% to 10% of all STEMI cases. The prefix “cardio” bothers us for all the wrong reasons. Though the shock component is initially triggered by primary cardiac pump failure, it soon spirals downward into a tissue level shock threatening the body’s 30 trillion cells. As cardiologists, we repeatedly fail to comprehend this. Instead, we aggressively attempt to revascularise the myocardium using multi-vessel PCI, IABP, ECMO, and LVADs. Yet, nothing seems to work. When tissues are irreversibly damaged a non-stop lactate ooze begins to ring a final pre death biochemical SOS call.
What is the Time Window for Tissue Perfusion?
For myocardial cell death, we have a defined therapeutic window of 12 hours, with under 6 hours being ideal. In cardiogenic shock, however, we face an unknown time window. During this uncertain period, cells within vital organs like the kidneys, liver, and lungs lose their structural integrity and face irreversible injury.
As far as I know, there is no defined timeline for intervention in cardiogenic shock. The inflection point between reversible and irreversible shock varies individually because it is a complex, systemic spiral. But, one thing we must be clear. The clock does not start at the moment of infarct-related artery (IRA) occlusion. Rather, it starts when cardiac index drops below critical threshold required to sustain cellular respiration. Note the emphasis on flow. Beyond a certain point, blood pressures have nothing to do with actual flow. This explains why systolic and mean arterial pressures do not correlate well with the severity of shock. We must never forget the concept of nomotensive shock .
Current Criteria to Diagnose Cardiogenic Shock
We have known this for a long time. To establish a diagnosis of cardiogenic shock, a patient must meet a triad of criteria:
Note the dramatic (& ironic)changes in the current guidelines : Neither the blood presure not the filling pressure matters in the diagnosis of cardiogenic shock
Myocardial No-Reflow vs. Tissue level No-Reflow
This concept has some evidence back up. Even if you somehow manage to revive the heart In CS, it does not guarantee full systemic tissue recovery. This failure of organ perfusion at the systemic level behaves exactly like the no-reflow phenomenon we witness at the myocardial microvascular bed.
So, what shall we do to tame this dreaded condition ?
We really don’t know. Preventing the onset seems to be the most effective Intervention.
How to prevent?
Have a close look at the table to gain some insights. Focus the third and last column. Ask this question. Why the incidence remains high even in the modern Interventional era,with little improvements in outcomes ?
It is prudent, we make every attempt to revive the heart, paradoxically, we must realise healing can still take place without myocardial excesses*Some times, attempting a cure , will interfere with prevention of the event, we aim to cure.
Final Message
The cardiac component in cardiogenic shock becomes less relevant when vascular and tissue-level shock sets in, making PCIs or MCS devices almost redundant. I think , in the overall interest of the patients , It is advisable for cardiologists to transfer them early to an intensivist or anesthetist, as they are better equipped to manage shock syndromes including the cardiogenic ones.
*Postamble: The missing link in the SHOCK trial
When we look back at the landmark 1999 SHOCK Trial, we find an quixotic truth to ponder over.Nearly 34% of the patients randomized to the medical arm survived to one year without any emergency revascularisation.If cardiogenic shock were purely a mechanical problem that survival rate should have been zero. This study throws two facts, many of us will be reluctant to accept.
Cellular Resilience: The human cells do possess ancient survival mechanisms. When the coronary flow crtically drops, some individuals have the microvascular mechanism to tolerate severe ischemia and “hibernate” until the native heart recovers.
The harm of hyper-Intervention could be real . Every extra wire, balloon, and large bore mechanical device we insert brings its own dose of strqin, vascular trauma, and reperfusion injury. The reason for the lucky 30% who survived in SHOCK trial, may simply because they were spared from the toxicity of excess Intervention.
Nothing happens without energy cost both in physics and biology. How much is the metabolic cost of an extra systole ? While an occasional VPD is benign and has a negligible effect, a high burden of VPDs can consume extra energy and drain myocardial metabolic reserves.
Three ways it can happen
Inefficiency: VPDs cause premature contractions before AV valves fill and hence there is a mechanically wasted work However the electrical cost is small.
Dyssynchrony: dys or desynchrony due to the VPDs also hikes myocardial oxygen consumption (MVO₂) for identical workloads.
Post-Extrasystolic Potentiation: We know, the beat following a VPD shows increased force due to calcium accumulation. This can elevates contractility and wall tension, increasing energy demands.
Molecular basis of energy depletion
At the cellular level, the variable timing of VPDs disrupts calcium homeostasis in phase 2 of action potential within the myocytes. The sarcoplasmic reticulum must continuously pump calcium ions against concentration gradients via SERCA2 channels, a process requiring ATP hydrolysis. Additionally, the chronic workload mismatch induces mitochondrial oxidative stress, which damages the electron transport chain, impairs ATP synthesis resulting in energy consumption mis mamtch.
What is the cut off number ?
A high VPD burden* (10% to 20% all heart beats in day ) is considered a chronic strain, leading to cardiomyopathy and heart failure.First step is a Holter monitor assessment. Yet, we are not clear about the exact number For example : Does bigeminy counted then 50 % of all beats )
*VPDS and elEctrical SCD is different topic , and is not discussed here.
Does suppression help ?
We think so. If and only if we can document porgressive LV dysfunction.
Final message
VPDs are usually benign unless linked to LV dysfunction, which complicates prognosis. The electrical energy cost of VPDs is negligible . But its impact on the mechanical behaviour on myocardial contractility is the issue. It’s crucial to determine if they are primarily electrical or secondary to associated LV dysfunction. Treatment is based on individual assessment.
While the term “pre & post capillary pulmonary hypertension” is useful for hemodynamic understanding , it creates a false impression biologically. Pre-capillary PH is a pan-vasculopathy where the capillary bed is routinely remodeled, congested, or even entirely destroyed. Please mind, this happens in almost in all the 4 groups of PH , at least in the advanced stages.
Heart disease in pregnancy is the third important cause for maternal mortality in most part of the world. (Apart from Bleeding, Infection and obstetrical complications) We know pregnancy is hemodynamic stress test for any mother and obviously it is a challenge in a compromised heart. Most heart disease encountered are mild and the mother has natural capability to walk through the pregnancy. It is the high risk subset that pose a real challenge. It is surprising ,even in the high risk, most women touch the finish line. The MMR review committee from USA has come out with clear data about the time line of mortality in various heart disease*.In this comprehensive analysis , the fact that 88% of mortality occur after delivery is too striking and is to be considered a core concept around which cardiac care of pregnant women should be addressed.
The figure shows the percentage of pregnancy-related deaths with an MMRC-identified underlying cause of death of cardiovascular conditions at 5 time periods from pregnancy to 1-year postpartum.(Ref 1) Note : The percentages are displayed for total cardiovascular conditions, and then for cardiomyopathy and other cardiovascular conditions individually. Percentages might not sum to 100 because of rounding.
Why this data is important ?
Though the peak hemodynamic stress happens around 24-28 weeks, it is the post partum period after the baby is out is very critical. In fact, nearly 40 to 50 % event happen up to one year. Some of them doesn’t even come under the definition of maternal mortality.
Is there any thing we can do during pregnancy , that can mitigate the post partum events?
Also, this delayed events give us a window of opportunity to act on these adversity.Postpartum care for patients with heart disease, including PIH, should be provided in a specialized unit at major hospitals that manage a high volume of pregnancies.
*We are not yet clear , whether PIH(Gestational HT) related cardio- vascular complications to be included in the heart disease basket. Logically and scientifically it should.
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