Dyspnea is one of the commonest symptoms in medical practice. Whatever be the trigger, ultimately, it is a sensory perception, felt at the level of the cortex (to be specific, the Amygdala nucleus) decides the intensity . The initiating receptor usually arises from the muscle spindles , due to mismatch in the length and tension . These spindles are located widespread in intercostal and other respiratory muscles. The afferent pathways are complex, as are the brain stem processing centers and cortical modifications—all matters.
(* A proposed definition with mechanism :Both physiological and pathological dyspnea are the unpleasant breathing awareness (In time), till for the oxygen debt is repaid to the depleted mitochondrial, ATP treasury , for the cost of excess respiratory work done, is one popular definition )
The complexity of the neural circuit for dyspnea can be judged, even if the cranial or spinal pathways i.e., vagus or spinal transection, dyspnea is not fully relieved (experiments on post-vagotomy, quadriplegic patients, and transverse myelitis). The answer might look simple in one way. Please mind, we don’t need an intact nervous system to carry afferent dyspnea signals to the brain centers. It can simply be carried by blood, to the central chemoreceptor in biochemical form.
The uniqueness of this symptom is , it can be entirely physiological , or a harbinger of Instant fatality as in acute pulmonary embolism or LVF. Resting dyspnea is always a concern, unlike exertional which has more benign cause. As a cardiologist, we always equate dyspnea to elevated LVEDP and possible LVF . Though RV failure can also cause dyspnea.
Generally, young fellows might ignore non -cardiac non- pulmonary cause of dyspnea. It is better to reemphasize ,the commonest cause of dyspnea missed in ERs and ICUs are metabolic or systemic in nature . (We have seen Kusmaul’s breathing of DKA raising false cardiac alarm )
Systemic causes of dyspnea (With normal PCWP)
Metabolic dyspnea*
Bio-chemical dyspnea*
Anemia*
Most lung diseases
*Chemo receptors are as important as baro- recptors of heart and J receptors in lungs
Is cardiac dyspnea possible with normal PCWP ?
Pre capillary Pulmonary HT (Isolated Arterial PH)
RV infarction.
Classical Hypoxic dyspnes in cyanotic heart disease (TOF,)
Any RV failure , can trigger RV baro-receptors(similar to LV but less concentrated)
Final message
Dyspnea: is it from the heart or lungs? This popular debate has been going on for decades and was answered in a landmark review published four decades ago.(JAMA 1982).Every one of us, must go through this to understand critical cause of dyspnea that arise from heart and lungs.
However, if the question is, which is the commonest cause for exertional dyspnea? Is it from the heart or lungs? The answer is neither of the two. The commonest cause of dyspnea as a whole is neither from the heart nor lungs. It is probably anemia, physical deconditioning, fragility, or sluggish systemic skeletal muscle respiratory status due to a sedentary lifestyle. This explains why a marathon runner can run 42 km without stopping, while a healthy middle-aged man struggles to climb even three floors because of sedentary activity.
Paclitaxel: Is a highly lipophilic, and rapidly absorbed by vessel walls and retained for days to weeks, making it ideal for DEBs, which deliver the drug during brief balloon inflation (30–60 seconds). Its cytotoxic action, disrupting microtubules and arresting cells in the M-phase, effectively inhibits neointimal hyperplasia without requiring prolonged drug release.
Sirolimus: Less lipophilic, sirolimus requires sustained release to achieve therapeutic levels, as it acts cytostatically by inhibiting the mTOR pathway, arresting cells in the G1 phase. This suits DESs, which provide continuous drug elution over weeks via polymer coatings. Its lower tissue retention makes it less effective for short-contact DEBs.
Paclitaxel hurts the endothelium with DES, but it heals with DEB ? How is this possible ?
Paclitaxel’s association with delayed healing and inflammation raised concerns about long-term safety in DESs, particularly after reports of late and very late stent thrombosis. It is abandoned in DES platform.
Paclitaxel born again as DEB avatar
It is claimed, Paclitaxel’s rapid uptake and lipophilicity make it suitable for DEBs, while sirolimus’s need for sustained release and favorable long-term profile suits DESs. It is very hard to believe, the published evidence, however robust they are. Only thing I can guess is, Paclitaxel enjoys a safety net in DEB , as the drug disappears so quickly before any useful effect or side effect could manifest. Ongoing research into sirolimus-coated balloons may shift this paradigm. Till then, we have to trust Paclitaxel, that remains the standard for DEBs due to pure scientific reasons.
Final message
Paclitaxel, which was at its crowning glory during the SYNTAX times , was phased out in DES due to various/ serious untoward effects.
Please bear with this highly biased opinion. I suspect, as a face-saving measure, the industry accommodated Paclitaxel into the DEB platform when it was chucked out of DES. I think we must learn to find truthful pathways of research.
Understanding sympathetic nervous had never been easy. (It doesn’t in any way mean, we have mastered para-sympathetic !). As physicians and cardiologists, we are expected to know the updated adrenergic, dopaminergic, imidazoline receptors etc. We need to know at-least an overview of its current nomenclature, area of distribution, benefits of blocking and stimulating them. Unfortunately, many of us consider it as student stuff and too theoretical for a busy cardiologist.
A realistic scenerio
Then one fine day, an I-pad wielding ,medical representative would come, late in night and teach us about a new drug called Moxonidine. “Sir this is a combined alpha and Imidazoline-1 agonist. Just .2 mg is enough sir to treat any refractory HT” We nod our heads sheepishly, wondering what is that Imidazoline ? Why is this guy is saying alpha agonist* ?
*So far I had been thinking only alpha blockers, have anti-hypertensive action. It took few moments to make some sense . Oh, okay, I got it, Clonidine and Prazosin are entirely different groups of drugs, though they act on alpha receptors—one stimulating and other blocking at different sites.
This post is meant to avoid such embarrassing situations.
Final message
Let us learn new things every day , but never think, reviewing what we read in the past is a mean academic activity.
The answer is, yes, but a crude yes. A lot of OCT literature has taken this aspect casually. Macrophages, both resident and blood borne monocyte-macrophage, lay the foundation for the athersclerotic plaques. Currently, cardiology imaging specialists tell us, that bright spots in OCT, beneath the Intima are believed to be macrophages, based on a few histological correlation studies. If you go through these studies (Ref 1), it is almost guessing like tossing a coin .It finds 57% of bright spots were macrophages. The rest 43 % can be any of the following 7 in the list.
The causes of bright spots in OCT are too many
1.Lipid Pools/Necrotic Core: Lipid-rich areas or necrotic cores in plaques can appear as hyperreflective spots.These may mimic macrophage infiltration but are typically larger and less discrete.
2.Cholesterol Crystals: Resemble macrophage-related foci but are often linear or needle-like.
3.Calcifications: We know calcium is always a bright spotin any Imaging. Same with OCT Microcalcifications or early calcium deposits in plaques can appear as bright easily mistake formacrophage. But, unlike macrophages, calcifications are often accompanied by acoustic shadowing.
4.Fibrous Tissue: Dense fibrous tissue in stable plaques may occasionally produce bright spots, particularly if imaging artifacts enhance their reflectivity.
5.Neovascularization: Reflection due to red blood cell content or vessel wall components, mimick macrophage accumulation.
6.Thrombus: Small thrombi (red or white) within plaques can appear as bright spots.
7.Imaging Artifacts: Motion artifacts, stent strut reflections, or incomplete blood clearing during OCT imaging can produce spurious hyperreflective spots that mimic macrophages.
Please note :The most important factor in the above list, is the last one, ie technical and Imaging artifact.
Can we identify true macrohoages with emerging technologies ?
We are in the era of virtual histology. It may come true in the future. Current generation OCTs have 10 to 20 micron resolution.
Image source (Ref 2)OCT cross-section images of the atherosclerotic vessel lumen, the location indicated by the white arrow is, rather susspected the macrophage. (C,D)
Advanced techniques like USPIO*-enhanced OCT and μOCT** show promise for more precise macrophage detection, but they are not yet standard in clinical practice. For now, OCT remains a valuable tool for assessing plaque vulnerability, in which we believe macrophages are playing a key trigger.
What is purpose of identifying these macrophages with such costly technology?
Not much really. May be a feel of scientific enthrallment. Of course, it can help monitor plaque healing, which is going to happen anyway whether we visulaize it or not if proper medications are taken (Intensive dose statin). Ofcoure ,these imaging modes do have a role , if we want to know how the macrophages are going to feed on the bio-absorbable stents.
Final message
All that blinks bright in OCT, are not macrophages. Virtual histology-based interventions are great scientific tools, but have little value in cath lab interventions as of now.
The answer is an unequivocal yes. The catch is, DES , tends to whip out the macrophages from its vicinty . BMS welcomes it . Which is good ? Think about it , answer will be very surprising.
I am neither an active or inactive Interventional cardiologist. But, I have sat through numerous sessions of complex PCI workshops. I used to wonder why they give so much importance to the side branch crossing. Obviously, it must be for some good reason. I did this brief write-up, trying to comprehend some sense. Hope the experts would agree with this.
This study looked into the clinical characters of STEMI presentation and correlated with various aspects including Troponin levels with reference tothe clinical factors.
Reproducing just one sample data about the character of chest pain. Please go through the complete paper.
Few observations need a comment
The pull or catchining type of pain has 0% likelyhood of STEMI.The last in the list is mentioned as dyspnea is of great importance.It is the angina equivalnet ,which is reported to be 50 % is quiet high.
One observation, and an unlikely miss I could found, is the incidence of epigastric pain and rare abdominal pain in some of those pateints with inferio posterior MI where it direct intimacy with diaphgram and whcih can radiate downwrds.We have missed some cases as acute abdomen, as pancreatitis , later on proven to be RCA STEMI.
Final message
We keep talking at length, dozens of listless trials fighting between single or two stent strategies in bifurcation lesions in every compulsive interventional workshop. Currently, I don’t think any conference would give a stage space to discuss trials such as TRAP-AMI which can infuse fresh thoughts in youngsters’ minds. It is an unrealistic wish though; any cardiology scientific committee should be mandatorily instructed to allot at least 30% of time to clinical cardiology that can bring back the field of cardiology, on the righteous track again.
1.Is systemic HT an advantage ?so that high pressure head aids in pushing the blood across the lesion. ?
I don’t know whether I can say Yes*, physiologically, the high proximal pressure and low distal pressure help maintain the flow. The distal drop happens due to the tightness of the lesion itself, but that is counterproductive, unless tone of the distal microvascular bed is intact and dilates fully.
*Mind you, IABP during cardiogenic shock, essentially does this – keep the coroanry diastolic pressure high.
However, there are significant caveats.
There is law of diminishing Returns : In a 90% lesion, the resistance is so high that even elevated Pa may not substantially increase flow due to the fixed obstruction. Hypertension increases left ventricular afterload, raising myocardial oxygen demand. In a 90% LAD lesion with compromised flow, this can worsen ischemia, outweighing any flow benefit from higher pressure.
2.What happens to trans-lesion flow during hypotension ?
This has direct implications when a patient with a significant lesion develops hypotension due to a systemic cause like dehydration or postoperative hypovolemia. We have often observed transient ST/T changes in a postoperative patient that may or may not lead to full-blown ACS.
To know what exactly happens across a lesion, we need to understand coronary autoregulation and its limits. Coronary autoregulation maintains stable myocardial blood flow despite changes in coronary perfusion pressure. Its limits and range are as follows. .
Range of Autoregulation: In healthy coronary arteries, autoregulation operates effectively between perfusion pressures of approximately 50–60 mmHg to 120–140 mmHg. Within this range, vascular smooth muscle in coronary arterioles adjusts resistance to maintain near-constant blood flow.Lower Limit: Below 50–60 mmHg, autoregulation fails, and blood flow becomes pressure-dependent. This can lead to ischemia, especially in the subendocardium, which is most vulnerable due to higher oxygen demand.Upper Limit: Above 120–140 mmHg, maximal vasodilation is reached, and further increases in pressure do not significantly increase flow.
However , we don’t know how this autoregulatory biological servo control, is tampered in the presence of a single or a tandem lesions.
3.How does FFR gets altered during exertion in such lesion ?
We have very limited data available on this and are essentially ignorant . FFR during exertion typically decreases compared to rest due to the amplified pressure gradient across the stenosis driven by increased flow demand and limited reserve.However collaterals can mitigate this fall in FFR.
Final message
Putting a stent across 90% lesion surely is a childish task, when compared to understanding complex hemodynamic vortices that happen across it.
We know, stress tests can give false positive results suggesting ischemia in at least 20% of patients for various reasons . It can occur with systemic (Anemia) and cardiac conditions such as HT, LVH, baseline ECG changes, or myocardial disease.
Here is a middle-aged man who went for an annual health check and ended up with this TMT. His exercise capacity was good at 11 METs, stopped at early stage 4 standard Bruce. He was asymptomatic, and every other parameter was normal.
Images: Resting, Peak, severe positive response, in lead V5 and V6. Every cardiologist advised some form of CAG. Opinions were so diverse, ranging between silent left main, tight proximal LAD to innocuous false positive.
What is your inference ? The patient seeked by advice It was indeed an academic stress test. There is a frightening ST depression I said. yes the rest is very likely to be false positive but I don’t have the courage to commit so. Mostly, you can’t escape from a coronary angiogram” . Next option is CT angiogram, Thallium or dobutamine stress.
It was indeed an academic stress test. There is a frightening ST depression . Very difficult to Ignore. May be, it could be false positive but I don’t have the courage to commit so. Mostly, you can’t escape from a coronary angiogram” .Other options are CT angiogram, Thallium or dobutamine stress.
He smiled and said, “You are absolutely right, doctor. Out of 5 cardiologists I consulted, 4 asked me to go for an immediate angiogram. Still, I escaped because of one Egyptian cardiologist.”
I was eager to see what he did . This is the test he did.
Yes. It was indeed a smart move. The shrewd cardiologist did a bicycle ergometry and simultaneous echocardiogram without any drugs or injections. He could confidently rule out significant CAD (by absence of any wall motion defect). Hats off to him. Lets earn some courage from such truely learnt cardiologist.
Final message
Most of us (Cardiologists) find it difficult to trust the physiological data that come from history, ie excercise capcity . We are obsessed with anatomy. Though, we eloborately debate about physiology-based intervention inside cathlab in every conference.
Our flawed intellect keeps asking this question: How can I trust physiology (Flow) without documenting a good anatomy? In fact, truth is the other way around. A good epicardial anatomy rarely guarantee good physiology. (It is worth recalling, CAG, the investigation we celebrate as the gold standard, images only about 2% of the entire coronary vasculature.)
A well-documented near physiologically flowing coronary circulation, negates the need to document anatomy through whihc it flows,however shabby or good it may be. (For the FFR & iFR guys, it must be mentioned that a negative stress test implies a net combined three-vessel FFR of > 0.9.)
Postamble
There was a well-accepted holistic, yet scientific concept roaming around in cardiology academic circles in the 1990s. (Of course, now it is thrown to the dustbin.) It said, if anybody crosses 10 METs in TMT, he or she is unlikely to harbor a significant lesion; even if there is one, it usually doesn’t require a metallic fix.
In pregnant women with significant heart disease : A quick LSCS or a potentially prolonged natural delivery,which is more safe ?
In pregnant women with significant heart disease, the choice between natural vaginal birth and a cesarean section (LSCS) depends on several factors, including the specific type and severity of the heart condition, the overall health of the mother and fetus, and the recommendations of a multidisciplinary medical team (typically involving obstetricians, cardiologists, and anesthesiologists). There’s no one-size-fits-all answer.
Hemodynamics of normal delivery
Natural delivery involves the physiological stress of labor, which includes increased cardiac output, blood pressure fluctuations, and oxygen demand, peaking at 50-80% above baseline during contractions and pushing. For women with significant heart disease (e.g., severe mitral stenosis, pulmonary hypertension, or cardiomyopathy), prolonged labor could strain the heart excessively, potentially leading to decompensation, heart failure, or arrhythmias. The unpredictability of labor duration is a key concern, as it might delay intervention if complications arise.
A planned C-section, on the other hand, offers a controlled environment with predictable timing and monitored anesthesia (often regional, like spinal ,graded spinal or epidural, which can minimize hemodynamic shifts compared to general anesthesia). It avoids the prolonged cardiac stress of labor and allows immediate access to surgical intervention if needed. However, it’s not risk-free: C-sections increase the risk of bleeding, infection, and fluid shifts post-delivery, which can also challenge a compromised heart. Recovery might also be tougher on someone with limited cardiac reserve.
Evidence leans toward individualized decisions rather than a universal preference. For example, women with conditions like Marfan syndrome and aortic dilatation (>4 cm) or Eisenmenger syndrome often have C-sections recommended due to the risk of aortic rupture or acute heart failure during labor. In contrast, women with well-managed, less severe conditions (e.g., repaired congenital defects) might safely attempt vaginal delivery with careful monitoring and a low threshold for intervention.
The American Heart Association and European Society of Cardiology guidelines suggest that for high-risk cardiac patients (e.g., WHO Class III or IV), a planned C-section under controlled conditions is often safer, especially if labor could become prolonged or unpredictable. Epidural anesthesia and assisted vaginal delivery (e.g., forceps) can sometimes bridge the gap, reducing labor strain while avoiding surgery, but this requires a stable patient and skilled team.
Is LSCS really more safe ?
Ultimately, “more safe” hinges on the specific case. A quick C-section in a monitored setting often edges out natural delivery for significant heart disease because it minimizes uncertainty and prolonged stress—but it’s not without trade-offs. The medical team would weigh the patient’s cardiac function (e.g., ejection fraction, symptoms), fetal status, and delivery logistics. If you’re asking about a specific scenario, feel free to give me more details, and I can refine the answer further
Dictums can’t dictate
Is the generally accepted dictum, that ceserain section is meant only for obsterical Indication, still valid in most cardiac patients?
It is true , cesarean section is reserved for obstetric indications—like fetal distress, breech presentation, or failure to progress in labor, has historically been rooted in minimizing surgical risks and prioritizing natural delivery when possible. However, in the context of pregnant women with cardiac disease, this principle isn’t universally upheld as a strict rule. For cardiac patients, the decision often shifts from purely obstetric factors to a broader risk-benefit analysis that includes maternal cardiac safety, sometimes overriding the “obstetric indication only” guideline.
In women with significant heart disease, the physiological demands of labor (e.g., increased cardiac output, blood pressure spikes, and oxygen consumption) can pose a direct threat to maternal survival, even if the pregnancy itself is obstetrically uncomplicated. Conditions like severe pulmonary hypertension, advanced heart failure, or critical aortic stenosis carry high maternal mortality risks during labor—sometimes 30-50% in extreme cases like Eisenmenger syndrome. Here, a planned C-section isn’t just about the baby; it’s about keeping the mother alive. This makes maternal cardiac status a valid indication for C-section, challenging the traditional obstetric-only framework.
However, the dictum still holds some relevance for cardiac patients with milder or well-controlled conditions (e.g., WHO Class I or II, like a repaired atrial septal defect with normal function). In these cases, vaginal delivery is often preferred if obstetric factors don’t demand otherwise, as it avoids surgical risks like bleeding, infection, or anesthesia-related complications that could still tax a less-severe cardiac condition. Assisted vaginal delivery (e.g., with forceps or vacuum) and epidural anesthesia can further reduce labor strain, making natural birth feasible and safe.
Current guidelines, from the American College of Cardiology and European Society of Cardiology, reflect this changing perception . They recommend individualized plans rather than blanket rules. For high-risk cardiac patients (WHO Class III or IV), a C-section is frequently favored—often scheduled around 34-36 weeks if preterm delivery is tolerated—regardless of obstetric status, because the controlled setting trumps the unpredictability of labor. For lower-risk patients, the obstetric indication rule still guide us, unless cardiac monitoring suggests otherwise.
It must me emphasised , the discipline of the multidisciplinary team , especially the egoless ineractions of all members is the key. Type of anesthesia and their cooperation and expertise will be a defining factor many times.
Final message
So, the dictum is no longer valid in all cardiac patients” anymore—it’s just sort of entered our minds and refuse to go away. (There are set of contions and absolute indication for LSCS in heart disese. Every one agrees on that) The purpose of this write up is to look beneath those established Indications.
There is an urgent need for some “academic tinkering” to this decades old, much revered dictum, for the beenfit of mother and baby May be , It applies where cardiac risk is low and obstetric needs dominate, but for severe heart disease, maternal cardiac indication alone can justify a C-section. The shift reflects better understanding of cardio-obstetric interplay and prioritizes outcomes over tradition.
Counterpoint
Guidelines are still dilly-dallying between choices of delivery , based on tradition, technology, expertise & experince (Ref 2 : vouch against LSCS), I think, the obstetrician who is the captain of the multidisciplinary team along with her anesthetist and intensivist are the best persons to take the call. Cardiologist’s role is generally minimal in most situations except for that critical moral support , few management advices and ofcourse for legal protection.
This is the Image of JVP wave forms from the famous original paper by BORST JG, MOLHUYSEN JA. in 1954 paper in Lancet.(Ref 1)
JVP typically has three positive waves and two negative waves. The “A” waves are due to atrial contraction while V waves are due to passive atrial filling. A waves are timed prior to S1 and V waves peak around S2. A tiny c wave interrupts the “x” descent . The word “c” could refer either to the RV contractile force or carotid contamination in the neck or simply a controversial wave.
The downward waves are X and Y descent. The major X descent is due to systolic atrial filling*, when the tricuspid valve is closed. Y descent is diastolic atrioventricular filling.
One interesting echocardiographic correlation has been observed. The force, power, and amplitude of X descent indirectly reflect RV contractility, and it can be referred to as poor man’s TAPSE.
One clinical question often asked in cardiology boards for fellows.
What are the difference between V waves that occur in ASD and Tricuspid regurgitation ?
V waves in ASD vs Tricuspid regurgitation
V wave is due to passive filling wave of atria when the ventricle is contracting and Tricuspid valve is closed.This physiological v wave . In ASD*, this wave just gets exaggerated as the right atrium receives the shunted blood from left atrium when the trisupid valve is closed. Since it almost resembles normal atrial flow pattern , both X descent and Y descent are retained ,and y may be slighly prominent in ASD.
In Tricuspid regurgitation , the V waves are truly pathological in terms of opened tricuspid valve and timing of TR jet which fills the atria in systole rather thanin diastole. (Note this is different from the excessive diastolic filling of atria as in ASD )
While Y descent is prominent in both ASD and TR ,the X descent in TR is lost for simple reason. tricuspid valve is leaking and TR jet abolish the systolic X descend, rather it becomes a X-ascent (Conventionaly called CV waves)
*Please note, the v waves of ostium primum ASD, may not follow this rule as MR from cleft mitral valve further modifies the v wave.
Final message
When we analyse the V waves in JVP , it is important to assess its timing, relative to 2nd sound and also the both the descents to derive maximum hemodynamic information.
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Please Note
The author acknowledges all the queries posted by the readers and wishes to answer them .Due to logistic reasons only few could be responded. Inconvenience caused is regretted.
Dr.S.Venkatesan MD 