Dr.S.Venkatesan MD

Dyspnea , Is it from the heart or lungs ? : A land mark paper in Internal medicine, JAMA 1982.

May 14, 2025 by dr s venkatesan

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.

Reference

 1.Wasserman K. Dyspnea on exertion. Is it the heart or the lungs? JAMA. 1982 Oct 22;248(16):2039-43. doi: 10.1001/jama.248.16.2039. PMID: 6811770.

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Difference between central and peripheral adrenergic alpha receptors

May 13, 2025 by dr s venkatesan

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.

Reference

1.Paul A. Insel, M.D Adrenergic Receptors- Evolving Concepts and Clinical Implications N Engl J Med 1996;334:580-585
2.Campbell lain C, McWilliam JR, Adamson P. Central adrenergic receptors. Journal of Psychopharmacology. 1987;1(2):55-66. doi:10.1177/026988118700100201

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Peripartum cardiomyopathy : Does the fetal gender influence the Incidence and recurrence ?

May 12, 2025 by dr s venkatesan

PPCM is a rare but an Important cardiac condition, that contribute to significant maternal and fetal morbidity and mortality.So many variables , triggers, back ground risks have been studied for decoding the pathogenesis of PPCM.

Does the sex of baby inside the mothers womb, in any way influence the incidence of PPCM ?

When searched in the literarure, I found almost no data on this simple parameter. While there is a lot of reference for PPCM relationships in twins and multigravida, none looked at gender specifically. From personal discussions with my Obstetrician colleagues, few suggested female babies are often seen to precipitate PPCM . I think it is an academic oversight, that we haven’t looked at the gender angle as yet, for this important entity.

Is there really no evidence ?

Yes, it is sursprisngly true . Gender as a variable may have been overlooked because it hasn’t shown up as a signal in preliminary data . Researchers often rely on patterns in existing data to guide hypotheses, and if no pattern suggests fetal gender matters, it may not be pursued. In some studies, gender data might be collected but not analyzed or reported.

It is a fertile research field. It may look like a simple study, but it can throw more light on this mystery myocardial disease that is directly related to pregnancy.

Could Fetal Gender Be Relevant in PPCM ?

While no evidence currently supports a link, there are theoretical reasons why fetal gender could be important.

Placental Differences: We know male and female fetuses have slightly different placental gene expression and responses to maternal stress, which could theoretically influence maternal cardiovascular load or immune responses.

Microchimerism: If fetal cells contribute to PPCM via immune mechanisms, sex-specific differences in cell behavior (e.g., Y-chromosome-related antigens) could be explored.( though this is speculative)

Hormonal Influence: Fetal sex might influence maternal hormonal profiles (e.g., via placental hormones), Female fetus are known to have more intense estrogenic effect in maternal circualtion.

Pregnancies with female fetuses may be associated with slightly higher levels of hCG or placental aromatase activity, which could theoretically enhance estrogen production or mimic an estrogenic effect in some contexts.(Ref 3)

What are the maternal diseases that are shown to be correlated with fetal sex ? (Ref 1, & 2)

Some maternal diseases, such as preeclampsia, gestational diabetes, preterm birth, hyperemesis gravidarum, autoimmune diseases, and asthma, have been associated with fetal gender in limited studies, with male fetuses often linked to slightly higher risks for preeclampsia and GDM, and female fetuses to hyperemesis and asthma exacerbations. However, these correlations are generally weak, and mechanisms are not fully understood. For PPCM, no evidence exists

Final message

Fetal gender is a simple, routinely collected variable, making it feasible to include in future studies without significant cost. If even a small association exists, it could refine risk stratification or guide mechanistic research (e.g., exploring sex-specific placental factors). The lack of data on this parameter represents a knowledge deficit in cardio obsterics that could be addressed in large registries or meta-analyses, especially as PPCM research has grown significantly in recent times.

*Request the fellows in O&G and cardiology to conduct a specific study on this topic and enrich the literature on PPCM. I think the data is already there in every PPCM paper. We just need to collate. (There is no copyright for this topic, but please acknowledge, if no one has done this aspect of a study in PPCM before)

Reference

1.Liu S, Joseph KS, Liston RM, Bartholomew S, Walker M, León JA, Kirby RS, Sauve R, Kramer MS; Maternal Health Study Group of the Canadian Perinatal Surveillance System (Public Health Agency of Canada). Incidence, risk factors, and associated complications of eclampsia. Obstet Gynecol. 2011 Nov;118(5):987-994. doi: 10.1097/AOG.0b013e31823311c1. PMID: 22015865.

2.Schiff MA, Reed SD, Daling JR. The sex ratio of pregnancies complicated by hospitalisation for hyperemesis gravidarum. BJOG. 2004 Jan;111(1):27-30. doi: 10.1046/j.1471-0528.2003.00005.x. PMID: 14687048.

3.Steier JA, Myking OL, Bergsjø PB. Correlation between fetal sex and human chorionic gonadotropin in peripheral maternal blood and amniotic fluid in second and third trimester normal pregnancies. Acta Obstet Gynecol Scand. 1999 May;78(5):367-71. PMID: 10326878.

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Posted in pregnancy and heart disease | Tagged cardiology fellows research topic, cardiology research papers, dm cardiology research papers, ppcm recurrence rate, research topics in cardiology for drnb |

Can we really visualise macrophages in OCT Imaging of coronary plaques ?

May 8, 2025 by dr s venkatesan

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.

*USPIO:  ultra-small superparamagnetic particles of iron oxide (USPIOs) is an MRI contrast agent

**Nishimiya K, Poduval RK, Tearney GJ. OCT Emerging Technologies: Coronary Micro-optical Coherence Tomography. Interv Cardiol Clin. 2023 Apr;12(2):237-244. doi: 10.1016/j.iccl.2023.01.001. PMID: 36922064.

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.

Reference

1.Phipps J.E., Vela D., Hoyt T.et al. : “Macrophages and intravascular OCT bright spots: a quantitative study”. J Am Coll Cardiol Img 2015; 8: 63.

2.Li Z, Tang H, Tu Y. Molecular and Nonmolecular Imaging of Macrophages in Atherosclerosis. Front Cardiovasc Med. 2021 May 19;8:670639. doi: 10.3389/fcvm.2021.670639. PMID: 34095259; PMCID: PMC8169961.

3.Phipps JE, Vela D, Hoyt T, Halaney DL, Mancuso JJ, Buja LM, Asmis R, Milner TE, Feldman MD. Macrophages and intravascular OCT bright spots: a quantitative study. JACC Cardiovasc Imaging. 2015 Jan;8(1):63-72. doi: 10.1016/j.jcmg.2014.07.027. Epub 2014 Nov 5. PMID: 25499133; PMCID: PMC4297553.

Follow up question

Do the macrophages invade the stent metal ?

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.

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Bifurcation PCI : Which strut to cross, proximal or distal ?

April 30, 2025 by dr s venkatesan

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.

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Posted in Uncategorized | Tagged bbc trial, bifurcation pci, distal vs proximal strut crossing, dk crush cullotte, final kissing balloon inflation, lcx ostoium compromise, mini crush, pot technique, provisional single stent strategy, single vs double stent, tap t technique for pci, upfront two stent strategy, which cell to cross proximal or distal ? |

21 types of chest pain in STEMI : A rare study , that failed to enter mainstream cardiology academia.

April 29, 2025 by dr s venkatesan

It is an unusual study on STEMI ,yet profound, in adding clinical wisdom in this techno era. The study is titled : Symptoms Predictive of Acute Myocardial Infarction in the Troponin Era: Analysis From the TRAPID-AMI Study . Kudos to the Henry ford hospital team, for thinking to produce such a study .

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.

Reference

1.McCord J, Aurora L, Lindahl B, Giannitsis E, Calle-Muller C, Nowak R, Body R, Christ M, deFilippi CR, Christenson RH, Jacobsen G, Alquezar A, Panteghini M, Melki D, Plebani M, Verschuren F, French J, Bendig G, Weiser S, Mueller C; TRAPID-AMI Investigators. Symptoms Predictive of Acute Myocardial Infarction in the Troponin Era: Analysis From the TRAPID-AMI Study. Crit Pathw Cardiol. 2019 Mar;18(1):10-15. doi: 10.1097/HPC.0000000000000163. PMID: 30747759.

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Three questions (not so simple) on a 90% LAD lesion.

April 12, 2025 by dr s venkatesan

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. .

The famous dog experiment on the coronary flow on depressurisation (Ref 2)

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.

Reference

1.Johnson NP, Gould KL, De Bruyne B. Autoregulation of Coronary Blood Supply in Response to Demand: JACC Review Topic of the Week. J Am Coll Cardiol. 2021 May 11;77(18):2335-2345. doi: 10.1016/j.jacc.2021.03.293. PMID: 33958131.

2.Smalling RW, Kelley K, Kirkeeide RL, Fisher DJ. Regional myocardial function is not affected by severe coronary depressurization provided coronary blood flow is maintained. J Am Coll Cardiol. 1985 Apr;5(4):948-55. doi: 10.1016/s0735-1097(85)80438-1. PMID: 3973297.

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Posted in Uncategorized | Tagged coronary autoregulation, coronary perfusion pressure, ffr, iapb, ifr, lad flow, qfr |

Defining optimism is not an easy task in science.

April 9, 2025 by dr s venkatesan

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Posted in cardiology -Therapeutics, Ethics in Medicine | Tagged dr s venkatesan, dr venkatesan sangareddi, ethics, optimism, optimism vs pessimism, optimist, positive vs negative thinking, venkat quotes, venkatesan sangareddi, widom quotes |

Glorifying FAME 3, is an academic mischief ! “PCI, in isolation can’t beat CABG, but with FFR it can”

April 9, 2025 by dr s venkatesan

Cardiologists have been trying for the last two decades to prove PCI is superior or at least equal, to CABG in multivessel CAD. We desperately needed studies to prevail over FREEDOM and SYNTAX which favored CABG.

FAME series , though never had an intention to compare PCI vs CABG , now we have used the platform to upend it to take on the CABG in multivessel CAD. ( FAME 3)

FAME 1 (Fractional Flow Reserve Versus Angiography for Multivessel Evaluation)

Purpose

The FAME 1 study aimed to compare the efficacy of FFR-guided PCI versus angiography-guided PCI in patients with multivessel coronary artery disease (CAD). The goal was to determine whether using FFR to identify functionally significant stenoses (FFR ≤ 0.80) for stenting, rather than relying solely on angiographic appearance.

Inference

Established that FFR-guided PCI is superior to angiography-guided PCI in multivessel CAD, reducing unnecessary revascularizations and improving outcomes.

FAME 2

Purpose

FAME 2 sought to evaluate whether FFR-guided PCI plus optimal medical therapy (OMT) was superior to OMT alone in patients with stable CAD and at least one functionally significant stenosis (FFR ≤ 0.80).

The study concluded that FFR-guided PCI is beneficial in stable CAD when ischemia is present, reducing the need for subsequent urgent revascularizations compared to OMT alone, though it did not significantly reduce rates of death or MI

FAME 3

Purpose
FAME 3 aimed to determine whether FFR-guided PCI using contemporary drug-eluting stents was non-inferior to CABG in patients with three-vessel CAD. The study sought to compare these two revascularization strategies in terms of clinical outcomes, testing the hypothesis that FFR-guided PCI could achieve similar results to CABG by targeting only functionally significant lesions.

Conclusion

At 1 year, FFR-guided PCI did not meet the criterion for non-inferiority compared to CABG for the primary endpoint of MACE (death, MI, stroke, or repeat revascularization), with event rates of 10.6% for PCI vs. 6.9% for CABG.

5 years later in 2025

FAME 3 : 5 year follow up data , released in 2025, tries to confirm the non inferiorty of PCI over CABG in a larger sense.

The study concluded that in patients with three-vessel CAD, FFR-guided PCI is not non-inferior to CABG, with CABG remaining superior for reducing MI and repeat revascularization. However, FFR guidance still refined PCI by limiting interventions to functionally significant lesions.

Did the FAME 3 study compare FFR guided CABG vs FFR guided PCI ?

No, none of the FAME studies (FAME 1, FAME 2, or FAME 3) directly compared FFR-guided CABG versus FFR-guided PCI. Each study had a distinct focus involving FFR-guided PCI, but none incorporated FFR guidance into CABG as a primary comparator. Here’s why this comparison could be meaningless.

Final message

Truths express themselves. We can’t force it to happen.

Reference

1.Fearon WF, Zimmermann FM, Ding VY, Takahashi K, . Outcomes after fractional flow reserve-guided percutaneous coronary intervention versus coronary artery bypass grafting (FAME 3): 5-year follow-up of a multicentre, open-label, randomised trial. Lancet. 2025 Mar 28:S0140-6736(25)00505-7. doi: 10.1016/S0140-6736(25)00505-7. Epub ahead of print. PMID: 40174598.

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Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology therapeutics |

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