Kevin Cheng

@KevinCCheng

BHF Clinical Research Fellow | Cardiology registrar | Ex-NIHR ACF | REMEDY-PILOT Trial

London

Joined September 2020

281 Following

155 Followers

27 Posts

KevinCCheng retweeted

Stefano Garzon, MD

@stefano_garzon

3 months ago

Tsai et al. just published a very elegant core lab comparison of 5 angio-IMR methods against pressure wire IMR and continuous thermodilution Rmicro in JACC Interventions (@JACCJournals). The results were perhaps a bit disappointing: all 5 methods performed poorly — AUCs of 0.53–0.58 against PW-IMR ≥25. Essentially coin-flip territory. I guess everyone’s natural reaction is to blame angio-IMR. But maybe the real story here goes a bit deeper. So, before we condemn the index test, I wanted to look into the ruler. Tsai et al. compared 5 angio-IMR formulas from 3 software platforms (QAngio XA 3D, FlashAngio, AngioPlus Core) against PW-IMR in 274 vessels and Rmicro in 109 vessels, all analyzed by an independent core lab (CORRIB, Galway) with rigorous blinding. Three independent analysts, anonymized software, a dedicated matcher investigator selecting frames. Methodologically, this is as clean as it gets. The results well, were not good: correlations between angio-IMR and PW-IMR ranged from r = 0.04 to 0.12. Three methods massively overestimated IMR (mean bias –20 to –26 units). None discriminated PW-IMR ≥25 better than chance. Against Rmicro, three methods did somewhat better (AUC 0.68–0.70), but still clinically inadequate. IMR was introduced by Fearon et al. in 2003, validated in a porcine model where microspheres obliterated the microcirculation. The logic is Ohm's law: resistance = pressure / flow. Since flow ∝1/mean transit time, IMR = distal pressure × transit time during hyperemia. It was then tested in STEMI patients, where it correlated with infarct size (biomarkers, PET, CMR) and predicted mortality. In a registry of 253 patients, IMR >40 post-primary PCI was the only independent predictor of death or heart failure readmission at 1 year. From there, IMR became a widespread measurement method for microvascular resistance. But notice the leap: it was validated in extreme microvascular destruction. But what about other populations, including ANOCA where the measured differences might be more subtle? Gallinoro et al. (EuroIntervention 2023) performed duplicate bolus thermodilution measurements in 102 ANOCA patients. The test-retest variability of IMR was 24.2 ± 19.3%. What does that mean clinically? If a patient's true IMR is 22 (just below the threshold of 25), the 95% range on a repeat measurement spans roughly 17–27. That patient has about a 30% chance of being classified as "abnormal" on any given measurement. Conversely, a true IMR of 28 spans ~21 to 35 — roughly 25–30% chance of being called "normal." In STEMI, this noise actually doesn't matter as much. I mean, if your true IMR is 70, the 95% range is ~53–87. So the chance of this case be misclassified is very low. The signal (IMR values of 60–100 vs. 10–20) overwhelms the noise, with a very strong signal-to-noise ratio (3:1 to 10:1). In ANOCA, the population clusters right on the threshold. Median PW-IMR in Tsai et al. was 19.02, IQR 12.79–28.08. The "abnormal" ANOCA patients sit at ~28–40 and the "normal" ones at ~12–22. The between-group gap is 10–20 units. Apply 24% noise and the signal-to-noise ratio drops to ~1:1. Your discriminatory capacity shrinks considerably. When continuous thermodilution came along — validated against ¹⁵O-H₂O PET (the closest thing we have to a true gold standard for myocardial flow) — it provided absolute volumetric flow and resistance. It is in fact more reproducible: variability of ~12% vs. ~24% for bolus thermodilution. Now, here’s the thing: IMR does not correlate with absolute hyperemic microvascular resistance (Rμ-hyper) derived from continuous thermodilution. r = 0.06, P = 0.425 (Gallinoro et al., JACC Intv 2023). From another Gallinoro paper, published in EuroIntervention in 2023, reproducibility paper (n=102, ANOCA), in which they explicitly report reclassification rates for CFR, the percentage of disagreement between CFRcont and CFRbolus was 35.3%. So at the standard CFR ≤ 2.5 cutoff, the two methods disagree on classification in over a third of patients. For IMR vs. MRR specifically, the correlation was essentially zero (r = 0.1, P = 0.305), meaning binary agreement can't be much better. An article by Fawaz et al. (IJC Heart Vasc 2024, 96 patients, 116 vessels post-revascularization) confirmed this in a different population: when assessed at CFR cut-off values of 2.0 and 2.5, the methods disagreed in 35% and 39% of cases, respectively. An article by Jansen et al., published in the JAHA in 2023 (n=246 ANOCA) is explicit about the overall picture, finding a relatively high amount of classification disagreement between bolus and continuous thermodilution measurements, of which the pathophysiological meaning is unknown. The Jansen et al. paper adds something else. CFR and IMR from bolus thermodilution did not correlate with anginal symptoms, while continuous thermodilution-derived parameters did. The Stanford transplant study (Circ Cardiovasc Interv 2025) added even more confusion, since in 20 transplant patients, IMR had excellent reproducibility (ICC 0.95) — far better than in ANOCA. So it appears that IMR behaves differently depending on the population. Now, I wanted to take a moment to think about the validation of IMR. To me, there’s some circular reasoning here, because the validation chain went something like this: 1. Tested in large microvascular destruction (animal models, acute STEMI) → IMR was able to differentiate injured from intact microvascular circulation in these very extreme scenarios. 2. Therefore, we assumed that IMR measures microvascular resistance accurately. 3. So, we assumed we can correctly measure & classify patients in other clinical settings. 4. So, we used it to measure other tools against because IMR works in all scenarios because it worked in extreme ones. I mean, to me it seems that we might be saying something like: I have this thermometer that can correctly tell ice from boiling water (it is). But I can’t say it's accurate at distinguishing 36.8°C from 37.2°C. Now let’s place angio-IMR in this context. It compounds multiple noisy inputs: contrast flow velocity from TIMI frame counts (which correlates poorly with true hyperemic velocity: r = 0.17–0.26 in Tsai et al.), angiographic contour detection (with known inaccuracies that get squared when converting diameter to area), estimated hyperemic pressure, and angio-FFR itself (which had only modest correlation with PW-FFR in this study: r = 0.33–0.38). Each error source multiplies through the formula. It's not surprising that the output is noisy. Maybe we’re measuring noise vs noise. The theoretical maximum AUC that any index test (even a perfect one) could achieve against PW-IMR ≥25, given PW-IMR's own ~25% misclassification rate around the threshold, is probably 0.80–0.85. The observed 0.53–0.58 is still below that ceiling (yes), so it appears that angio-IMR as a whole has real problems beyond reference noise. But the gap to "perfection" is much narrower than it looks at first glance. Now, someone might say: "But CorMicA proved IMR-guided therapy works in ANOCA." True, so true — randomized, stratified treatment based on IMR/CFR improved angina & quality of life at 1 year. But to me it seems that IMR probably works as a crude triage tool, not as a precise diagnostic test. You don't need a calibrated thermometer to know someone with a fever should take antipyretics — a hand on the forehead often suffices. CorMicA proved the hand-on-the-forehead approach to CMD management is better than guessing. It didn't prove the thermometer reads accurately. Now, where do we stand? Regardless of all of that, what Tsai et al. proves: → Current angio-IMR methods cannot replace invasive PW-IMR at the individual patient level. → The compounding of errors in frame-count-based formulas degrades signal below clinical utility. What Tsai et al. does NOT prove: → That angio-IMR is clinically useless. Prognostic value ≠ diagnostic accuracy. A noisy estimate that correlates with outcomes may still have clinical value as a screening or stratification tool, even if it can't match the absolute number. What I think is reasonable: → PW-IMR is not the stable, precise reference standard we treat it as. Its validation was built in high-signal environments and extrapolated without verification to low-signal ones. → Continuous thermodilution (Rmicro, MRR) is more reproducible and correlates with symptoms, but isn't widely available and has its own limitations. → We may be trying to reduce a complex, multidimensional pathophysiology (structural vs. functional vs. vasospastic CMD) to a single number. What should come next: → Validate angio-IMR (and any future wire-free tool) against Rmicro as the primary reference, not PW-IMR. → Prospective studies in pure ANOCA cohorts with full endotyping (including acetylcholine) and sufficient power. → Move from single-frame CFD equations to complete cine-run analysis with machine learning — the data is there in every angiogram, we're just not extracting it yet. → Accept that the microcirculation may require multiple measurements, not a single index. The story of angio-IMR isn't a story of failure. The same goes for IMR. It's a story of a field trying to measure something very subtle, very fragile, very complex. And to me this disposition to distill the complex interplay of cardiac disease and willingness to go deep into problems is something we should be proud of. #CardiologyX #InterventionalCardiology #IMR #JACC #angioIMR

stefano_garzon's tweet photo. Tsai et al. just published a very elegant core lab comparison of 5 angio-IMR methods against pressure wire IMR and continuous thermodilution Rmicro in JACC Interventions (@JACCJournals). The results were perhaps a bit disappointing: all 5 methods performed poorly — AUCs of 0.53–0.58 against PW-IMR ≥25. Essentially coin-flip territory.
I guess everyone’s natural reaction is to blame angio-IMR. But maybe the real story here goes a bit deeper. So, before we condemn the index test, I wanted to look into the ruler.
Tsai et al. compared 5 angio-IMR formulas from 3 software platforms (QAngio XA 3D, FlashAngio, AngioPlus Core) against PW-IMR in 274 vessels and Rmicro in 109 vessels, all analyzed by an independent core lab (CORRIB, Galway) with rigorous blinding. Three independent analysts, anonymized software, a dedicated matcher investigator selecting frames. Methodologically, this is as clean as it gets.
The results well, were not good: correlations between angio-IMR and PW-IMR ranged from r = 0.04 to 0.12. Three methods massively overestimated IMR (mean bias –20 to –26 units). None discriminated PW-IMR ≥25 better than chance. Against Rmicro, three methods did somewhat better (AUC 0.68–0.70), but still clinically inadequate.
IMR was introduced by Fearon et al. in 2003, validated in a porcine model where microspheres obliterated the microcirculation. The logic is Ohm's law: resistance = pressure / flow. Since flow ∝1/mean transit time, IMR = distal pressure × transit time during hyperemia.
It was then tested in STEMI patients, where it correlated with infarct size (biomarkers, PET, CMR) and predicted mortality. In a registry of 253 patients, IMR >40 post-primary PCI was the only independent predictor of death or heart failure readmission at 1 year.
From there, IMR became a widespread measurement method for microvascular resistance. But notice the leap: it was validated in extreme microvascular destruction. But what about other populations, including ANOCA where the measured differences might be more subtle?
Gallinoro et al. (EuroIntervention 2023) performed duplicate bolus thermodilution measurements in 102 ANOCA patients. The test-retest variability of IMR was 24.2 ± 19.3%.
What does that mean clinically? If a patient's true IMR is 22 (just below the threshold of 25), the 95% range on a repeat measurement spans roughly 17–27. That patient has about a 30% chance of being classified as "abnormal" on any given measurement. Conversely, a true IMR of 28 spans ~21 to 35 — roughly 25–30% chance of being called "normal."
In STEMI, this noise actually doesn't matter as much. I mean, if your true IMR is 70, the 95% range is ~53–87. So the chance of this case be misclassified is very low. The signal (IMR values of 60–100 vs. 10–20) overwhelms the noise, with a very strong signal-to-noise ratio (3:1 to 10:1).
In ANOCA, the population clusters right on the threshold. Median PW-IMR in Tsai et al. was 19.02, IQR 12.79–28.08. The "abnormal" ANOCA patients sit at ~28–40 and the "normal" ones at ~12–22. The between-group gap is 10–20 units. Apply 24% noise and the signal-to-noise ratio drops to ~1:1. Your discriminatory capacity shrinks considerably.
When continuous thermodilution came along — validated against ¹⁵O-H₂O PET (the closest thing we have to a true gold standard for myocardial flow) — it provided absolute volumetric flow and resistance. It is in fact more reproducible: variability of ~12% vs. ~24% for bolus thermodilution.
Now, here’s the thing: IMR does not correlate with absolute hyperemic microvascular resistance (Rμ-hyper) derived from continuous thermodilution. r = 0.06, P = 0.425 (Gallinoro et al., JACC Intv 2023). From another Gallinoro paper, published in EuroIntervention in 2023, reproducibility paper (n=102, ANOCA), in which they explicitly report reclassification rates for CFR, the percentage of disagreement between CFRcont and CFRbolus was 35.3%. So at the standard CFR ≤ 2.5 cutoff, the two methods disagree on classification in over a third of patients. For IMR vs. MRR specifically, the correlation was essentially zero (r = 0.1, P = 0.305), meaning binary agreement can't be much better. An article by Fawaz et al. (IJC Heart Vasc 2024, 96 patients, 116 vessels post-revascularization) confirmed this in a different population: when assessed at CFR cut-off values of 2.0 and 2.5, the methods disagreed in 35% and 39% of cases, respectively. An article by Jansen et al., published in the JAHA in 2023 (n=246 ANOCA) is explicit about the overall picture, finding a relatively high amount of classification disagreement between bolus and continuous thermodilution measurements, of which the pathophysiological meaning is unknown.
The Jansen et al. paper adds something else. CFR and IMR from bolus thermodilution did not correlate with anginal symptoms, while continuous thermodilution-derived parameters did. The Stanford transplant study (Circ Cardiovasc Interv 2025) added even more confusion, since in 20 transplant patients, IMR had excellent reproducibility (ICC 0.95) — far better than in ANOCA. So it appears that IMR behaves differently depending on the population.
Now, I wanted to take a moment to think about the validation of IMR. To me, there’s some circular reasoning here, because the validation chain went something like this:
1. Tested in large microvascular destruction (animal models, acute STEMI) → IMR was able to differentiate injured from intact microvascular circulation in these very extreme scenarios.
2. Therefore, we assumed that IMR measures microvascular resistance accurately.
3. So, we assumed we can correctly measure & classify patients in other clinical settings.
4. So, we used it to measure other tools against because IMR works in all scenarios because it worked in extreme ones.
I mean, to me it seems that we might be saying something like: I have this thermometer that can correctly tell ice from boiling water (it is). But I can’t say it's accurate at distinguishing 36.8°C from 37.2°C.
Now let’s place angio-IMR in this context. It compounds multiple noisy inputs: contrast flow velocity from TIMI frame counts (which correlates poorly with true hyperemic velocity: r = 0.17–0.26 in Tsai et al.), angiographic contour detection (with known inaccuracies that get squared when converting diameter to area), estimated hyperemic pressure, and angio-FFR itself (which had only modest correlation with PW-FFR in this study: r = 0.33–0.38). Each error source multiplies through the formula. It's not surprising that the output is noisy. Maybe we’re measuring noise vs noise.
The theoretical maximum AUC that any index test (even a perfect one) could achieve against PW-IMR ≥25, given PW-IMR's own ~25% misclassification rate around the threshold, is probably 0.80–0.85. The observed 0.53–0.58 is still below that ceiling (yes), so it appears that angio-IMR as a whole has real problems beyond reference noise. But the gap to "perfection" is much narrower than it looks at first glance.
Now, someone might say: "But CorMicA proved IMR-guided therapy works in ANOCA." True, so true — randomized, stratified treatment based on IMR/CFR improved angina & quality of life at 1 year. But to me it seems that IMR probably works as a crude triage tool, not as a precise diagnostic test. You don't need a calibrated thermometer to know someone with a fever should take antipyretics — a hand on the forehead often suffices. CorMicA proved the hand-on-the-forehead approach to CMD management is better than guessing. It didn't prove the thermometer reads accurately.
Now, where do we stand?
Regardless of all of that, what Tsai et al. proves:
→ Current angio-IMR methods cannot replace invasive PW-IMR at the individual patient level.
→ The compounding of errors in frame-count-based formulas degrades signal below clinical utility.
What Tsai et al. does NOT prove:
→ That angio-IMR is clinically useless. Prognostic value ≠ diagnostic accuracy. A noisy estimate that correlates with outcomes may still have clinical value as a screening or stratification tool, even if it can't match the absolute number.
What I think is reasonable:
→ PW-IMR is not the stable, precise reference standard we treat it as. Its validation was built in high-signal environments and extrapolated without verification to low-signal ones.
→ Continuous thermodilution (Rmicro, MRR) is more reproducible and correlates with symptoms, but isn't widely available and has its own limitations.
→ We may be trying to reduce a complex, multidimensional pathophysiology (structural vs. functional vs. vasospastic CMD) to a single number.
What should come next:
→ Validate angio-IMR (and any future wire-free tool) against Rmicro as the primary reference, not PW-IMR.
→ Prospective studies in pure ANOCA cohorts with full endotyping (including acetylcholine) and sufficient power.
→ Move from single-frame CFD equations to complete cine-run analysis with machine learning — the data is there in every angiogram, we're just not extracting it yet.
→ Accept that the microcirculation may require multiple measurements, not a single index.
The story of angio-IMR isn't a story of failure. The same goes for IMR. It's a story of a field trying to measure something very subtle, very fragile, very complex. And to me this disposition to distill the complex interplay of cardiac disease and willingness to go deep into problems is something we should be proud of.
#CardiologyX #InterventionalCardiology #IMR #JACC #angioIMR

KevinCCheng retweeted

Dr. Filippo Cademartiri

@FCademartiri

5 months ago

🫀🔥 Refractory angina redefined: beyond blocked arteries This 2025 European Heart Journal State-of-the-Art Review delivers a major conceptual shift in how we understand and manage refractory angina—arguing that persistent angina is not just a failure of revascularization, but often a failure of mechanism recognition . 🧠 A necessary redefinition Traditionally, refractory angina was limited to patients with obstructive epicardial CAD who remained symptomatic despite maximal drugs and revascularization. The authors show why this view is outdated. Today’s patients often have: Coronary microvascular dysfunction (CMD) Epicardial or microvascular vasospasm Myocardial bridging Or combinations of these—even after “successful” PCI or CABG Excluding these mechanisms leads to misclassification, undertreatment, and persistent suffering. 🔍 From anatomy to mechanisms The review proposes a systematic, mechanism-based diagnostic pathway, combining: Non-invasive imaging (PET, CMR, stress echo, CT) Invasive coronary physiology and provocation testing (CFR, IMR, ACh) The goal is not just to confirm ischaemia—but to identify where and why it occurs. 🎯 Stratified, not generic treatment Once mechanisms are defined, therapy must be tailored: Obstructive CAD → optimized pharmacology, selective revascularization CMD → targeted anti-ischaemic drugs, rehabilitation, emerging biologics Vasospastic angina → calcium antagonists, nitrates, trigger control Persistent symptoms → advanced options (EECP, CSR, neuromodulation, CBT) A key message: many patients labelled “refractory” are actually “misdiagnosed.” 👥 The Angina Heart Team Given complexity, the authors advocate for specialist multidisciplinary angina teams, focused on symptom relief, quality of life, and function—not just MACE. 🔮 Bottom line Refractory angina is not a dead end—it’s a call to think deeper. Moving from artery-centric to mechanism-centric care can transform outcomes for a large, neglected patient population ❤️

$FCademartiri's tweet photo. 🫀🔥 Refractory angina redefined: beyond blocked arteries This 2025 European Heart Journal State-of-the-Art Review delivers a major conceptual shift in how we understand and manage refractory angina—arguing that persistent angina is not just a failure of revascularization, but often a failure of mechanism recognition . 🧠 A necessary redefinition Traditionally, refractory angina was limited to patients with obstructive epicardial CAD who remained symptomatic despite maximal drugs and revascularization. The authors show why this view is outdated. Today’s patients often have: Coronary microvascular dysfunction (CMD) Epicardial or microvascular vasospasm Myocardial bridging Or combinations of these—even after “successful” PCI or CABG Excluding these mechanisms leads to misclassification, undertreatment, and persistent suffering. 🔍 From anatomy to mechanisms The review proposes a systematic, mechanism-based diagnostic pathway, combining: Non-invasive imaging (PET, CMR, stress echo, CT) Invasive coronary physiology and provocation testing (CFR, IMR, ACh) The goal is not just to confirm ischaemia—but to identify where and why it occurs. 🎯 Stratified, not generic treatment Once mechanisms are defined, therapy must be tailored: Obstructive CAD → optimized pharmacology, selective revascularization CMD → targeted anti-ischaemic drugs, rehabilitation, emerging biologics Vasospastic angina → calcium antagonists, nitrates, trigger control Persistent symptoms → advanced options (EECP, CSR, neuromodulation, CBT) A key message: many patients labelled “refractory” are actually “misdiagnosed.” 👥 The Angina Heart Team Given complexity, the authors advocate for specialist multidisciplinary angina teams, focused on symptom relief, quality of life, and function—not just MACE. 🔮 Bottom line Refractory angina is not a dead end—it’s a call to think deeper. Moving from artery-centric to mechanism-centric care can transform outcomes for a large, neglected patient population ❤️$

177

110

KevinCCheng retweeted

INOCA INTERNATIONAL @InocaInternati1

8 months ago

Just a few of the photos from the INOCA 2025 London Meeting - GREAT presentations, great networking, great organisation and GREAT live cases too! 🤩 You can read more about the meeting here - https://t.co/5mJ2h1rqhK

InocaInternati1's tweet photo. Just a few of the photos from the INOCA 2025 London Meeting - GREAT presentations, great networking, great organisation and GREAT live cases too! 🤩

You can read more about the meeting here -
https://t.co/5mJ2h1rqhK https://t.co/KZxmqQReo3

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KevinCCheng retweeted

INOCA INTERNATIONAL @InocaInternati1

12 months ago

Is INOCA a consideration in post-oncotherapy? It certainly is! And thanks to the recent JACC article from Philip Macanovic, Kevin Cheng Anantharaman Ramasamy John Baksi and Ranil De Silva, we now know how and why! 😃 https://t.co/tPDJME9TCM INOCA - https://t.co/HEjyjSwz2Q

InocaInternati1's tweet photo. Is INOCA a consideration in post-oncotherapy?

It certainly is! And thanks to the recent JACC article from Philip Macanovic, Kevin Cheng Anantharaman Ramasamy John Baksi and Ranil De Silva, we now know how and why! 😃

https://t.co/tPDJME9TCM

INOCA - https://t.co/HEjyjSwz2Q https://t.co/LLNp1ifIkK

Who to follow

Kalpa De Silva

@K_DeSilva

Interventional cardiologist, complex PCI, researcher, social mobility 💪🏾, lifelong learner, 🎧 Motown, Prince, Marvin Gaye. 🐕🏎🏏 ⚽️ fan. 🇱🇰🇬🇧

Chris Allen

@dr_chrisallen

Structural & Coronary Interventional Fellow @CedarsSinai | Past President @thebjca | https://t.co/Q29nJQnb3X

Aish Sinha

@AishSinha1

Cardiology Registrar, NIHR academic clinical lecturer interested in coronary physiology

KevinCCheng retweeted

INOCA INTERNATIONAL @InocaInternati1

12 months ago

Not just an academic paper but a blueprint for improving outcomes for thousands of patients who’ve been told: ❌ Your angiogram is clear ❌ We’ve done all we can ❌ It’s probably just stress ✅ Let’s do better ✅ Let’s look deeper ✅ Let’s treat smarter https://t.co/vA9X2b2oAx

KevinCCheng retweeted

INOCA INTERNATIONAL @InocaInternati1

12 months ago

What do you do if your patient's angina is not responding to treatment? An author group including several members of the INOCA International Medical Advisory Board, have written a state of the art review on Refractory Angina - and what a review it is! 😍 https://t.co/sSnI52lOnj

$InocaInternati1's tweet photo. What do you do if your patient's angina is not responding to treatment? An author group including several members of the INOCA International Medical Advisory Board, have written a state of the art review on Refractory Angina - and what a review it is! 😍 https://t.co/sSnI52lOnj https://t.co/6vOsH0jyko$

514

KevinCCheng retweeted

Diego Segura-Rodríguez @SeguraCardio

12 months ago

🔥 Refractory Angina: What really drives it, and how can we treat it better? 🫀 Obstructive and non-obstructive chronic myocardial ischaemia—explored. 📌 Dive into the latest #StateOfTheArt #Review👇

$SeguraCardio's tweet photo. 🔥 Refractory Angina: What really drives it, and how can we treat it better? 🫀 Obstructive and non-obstructive chronic myocardial ischaemia—explored. 📌 Dive into the latest #StateOfTheArt #Review👇 https://t.co/LJchlfQlOx$

189

124

12K

KevinCCheng retweeted

ranil de silva @ranildesilva2

12 months ago

Refractory angina is a growing clinical challenge increasingly encountered in daily practice. We provide a re-definition of refractory angina, frameworks for precision diagnosis, stratified treatment and propose a comprehensive model for patient care. https://t.co/ogXh2IVIcE

235

KevinCCheng retweeted

Dr. Martha Gulati ♥️🫀❤️‍🩹🇨🇦

@DrMarthaGulati

12 months ago

Important paper released today @ehj_ed @ESC_Journals Refractory angina: mechanisms and stratified treatment in obstructive & non-obstructive chronic myocardial ischaemic syndromes. Honoured to be a part of this work led by @ranildesilva2 #angina 📎 https://t.co/BHFQbp0qmz

$DrMarthaGulati's tweet photo. Important paper released today @ehj_ed @ESC_Journals Refractory angina: mechanisms and stratified treatment in obstructive & non-obstructive chronic myocardial ischaemic syndromes. Honoured to be a part of this work led by @ranildesilva2 #angina 📎 https://t.co/BHFQbp0qmz https://t.co/PrbU5KbUr6$

KevinCCheng retweeted

ranil de silva @ranildesilva2

12 months ago

@ehj_ed @escardio @ESC_Journals The culmination of a great team effort! @KevinCCheng @HenrytTimothy @divaka_perera Ana Abreu Fabienne Vervaat @VTaqMD @DrMarthaGulati Hiroaki Shimokawa Felicita Andreotti @jckaski

641

KevinCCheng retweeted

EHJ Editor-in-Chief

@ehj_ed

12 months ago

Refractory angina: mechanisms and stratified treatment in obstructive and non-obstructive chronic myocardial ischaemic syndromes. Read more in EHJ. https://t.co/ti1T7wmUAW @ESCardio @ESC_Journals

$ehj_ed's tweet photo. Refractory angina: mechanisms and stratified treatment in obstructive and non-obstructive chronic myocardial ischaemic syndromes. Read more in EHJ. https://t.co/ti1T7wmUAW @ESCardio @ESC_Journals https://t.co/mcILdrHZsf$

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KevinCCheng retweeted

ranil de silva @ranildesilva2

about 1 year ago

Excited about #EuroPCR in Paris next week. Strong presence from our team. If you are interested in refractory angina, coronary sinus reducer and assessment of INOCA #fullphysiology, please do come along! @ImperialNHLI @RBandH @TheBHF @ShockwaveIVL @JNJMedTech @AbbottGlobal

$ranildesilva2's tweet photo. Excited about #EuroPCR in Paris next week. Strong presence from our team. If you are interested in refractory angina, coronary sinus reducer and assessment of INOCA #fullphysiology, please do come along! @ImperialNHLI @RBandH @TheBHF @ShockwaveIVL @JNJMedTech @AbbottGlobal https://t.co/lMfnK2HLud$

KevinCCheng retweeted

ABME

@ABMEjournal

about 1 year ago

Why atherosclerosis, an important risk factor for heart disease and heart attacks, involves certain arteries and spares others has remained a stubborn mystery. Researchers analyzed blood flow dynamics in moving coronary arteries and compared them to known locations of early atherosclerotic lesions. They found that relative residence time – a metric combining low flow and multidirectional shear – best explains where lesions form, outperforming traditional measures like oscillatory shear index. This work brings us closer to predicting, and ultimately preventing, where heart disease begins. 𝗥𝗲𝗮𝗱 𝗺𝗼𝗿𝗲: https://t.co/T1sBcVXOtv 𝗦𝘁𝘂𝗱𝘆: Relative Residence Time Can Account for Half of the Anatomical Variation in Fatty Streak Prevalence Within the Right Coronary Artery 𝗔𝘂𝘁𝗵𝗼𝗿𝘀: Pratik Kandangwa, @KevinCCheng, Miten Patel, Spencer J. Sherwin, @ranildesilva2, and Peter D. Weinberg @imperialcollege @ImperialBioeng @aeroimperial @ImperialNHLI @RBandH 𝗦𝘂𝗯𝗺𝗶𝘁 𝘆𝗼𝘂𝗿 𝗺𝗮𝗻𝘂𝘀𝗰𝗿𝗶𝗽𝘁: https://t.co/Gyz8DNneUg

ABMEjournal's tweet photo. Why atherosclerosis, an important risk factor for heart disease and heart attacks, involves certain arteries and spares others has remained a stubborn mystery.

Researchers analyzed blood flow dynamics in moving coronary arteries and compared them to known locations of early atherosclerotic lesions. They found that relative residence time – a metric combining low flow and multidirectional shear – best explains where lesions form, outperforming traditional measures like oscillatory shear index.

This work brings us closer to predicting, and ultimately preventing, where heart disease begins.

𝗥𝗲𝗮𝗱 𝗺𝗼𝗿𝗲: https://t.co/T1sBcVXOtv

𝗦𝘁𝘂𝗱𝘆: Relative Residence Time Can Account for Half of the Anatomical Variation in Fatty Streak Prevalence Within the Right Coronary Artery

𝗔𝘂𝘁𝗵𝗼𝗿𝘀: Pratik Kandangwa, @KevinCCheng, Miten Patel, Spencer J. Sherwin, @ranildesilva2, and Peter D. Weinberg

@imperialcollege
@ImperialBioeng
@aeroimperial
@ImperialNHLI
@RBandH

𝗦𝘂𝗯𝗺𝗶𝘁 𝘆𝗼𝘂𝗿 𝗺𝗮𝗻𝘂𝘀𝗰𝗿𝗶𝗽𝘁: https://t.co/Gyz8DNneUg

341

KevinCCheng retweeted

ranil de silva @ranildesilva2

about 1 year ago

Excellent work by @KevinCCheng and CMR Unit @RBandH providing new insights into mechanism of action of @ShockwaveIVL CS Reducer. https://t.co/MzaZbpdqoD @GreggWStone @HenrytTimothy

201

KevinCCheng retweeted

ranil de silva @ranildesilva2

over 1 year ago

Delighted to share our recent publication using diffusion tensor cardiovascular magnetic resonance in the European Heart Journal @ESC_Journals @ehj_ed led by our outstanding fellow @RRajakulasingam. https://t.co/yocAHIHEIs

KevinCCheng retweeted

EHJ Editor-in-Chief

@ehj_ed

over 1 year ago

Biphasic diffusion tensor cardiovascular magnetic resonance identifies microstructural alterations after STEMI and predicties adverse left ventricle remodelling. https://t.co/xO9GMMxtY3 #STEMI #remodelling #cardiotwitter @ESC_Journals @escardio

ehj_ed's tweet photo. Biphasic diffusion tensor cardiovascular magnetic resonance identifies microstructural alterations after STEMI and predicties adverse left ventricle remodelling.
https://t.co/xO9GMMxtY3
#STEMI #remodelling #cardiotwitter @ESC_Journals @escardio https://t.co/XT2DJIw7jw

KevinCCheng retweeted

Ramzi Khamis @rkhamis

over 1 year ago

Join us online for day three of #VPM2024 . Exceptional presentations from the day 3 Faculty. @imperialcollege @ImperialNHLI . @GreggWStone @ranildesilva2 @ColletCarlos @ekedhi

rkhamis's tweet photo. Join us online for day three of #VPM2024 . Exceptional presentations from the day 3 Faculty. @imperialcollege @ImperialNHLI . @GreggWStone @ranildesilva2 @ColletCarlos @ekedhi https://t.co/Af35u3ERXx

KevinCCheng retweeted

Shockwave Medical

@ShockwaveIVL

almost 2 years ago

Hot off the press for international physicians! 🔥📰 Congratulations to Drs @KevinCCheng, @DrJMHill and @ranildesilva2 for publishing their new review on the #ShockwaveReducer. In #ICR3Journal, read their great summary on the available evidence and the Reducer’s role in contemporary interventional practice: https://t.co/09xrAEVEBA @radcliffeCARDIO ISI https://t.co/t2NKOrlaSj: Investigational Device. Limited by U.S. and Canadian law to investigational use. The Reducer is commercially available in certain countries outside the U.S. and Canada. Please contact your local representative for specific country availability.

ShockwaveIVL's tweet photo. Hot off the press for international physicians! 🔥📰 Congratulations to Drs @KevinCCheng, @DrJMHill and @ranildesilva2 for publishing their new review on the #ShockwaveReducer.

In #ICR3Journal, read their great summary on the available evidence and the Reducer’s role in contemporary interventional practice: https://t.co/09xrAEVEBA

@radcliffeCARDIO
ISI https://t.co/t2NKOrlaSj: Investigational Device. Limited by U.S. and Canadian law to investigational use. The Reducer is commercially available in certain countries outside the U.S. and Canada. Please contact your local representative for specific country availability.

KevinCCheng retweeted

INOCA INTERNATIONAL @InocaInternati1

almost 2 years ago

Take a look at the newly released publication on the use of the Coronary Sinus Reducer in refractory angina. https://t.co/fYtWKeisLn

$InocaInternati1's tweet photo. Take a look at the newly released publication on the use of the Coronary Sinus Reducer in refractory angina. https://t.co/fYtWKeisLn https://t.co/zhTrC0uWNR$

KevinCCheng retweeted

BNCS_imaging @bncs_imaging

about 2 years ago

Interesting. MRI didn’t show any change in transmural perfusion in orbita cosmic.

Kevin Cheng

@KevinCCheng

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