¿Cuántas veces escribimos "haga ejercicio" en un informe y nos quedamos tan anchos?
El nuevo statement publicado en @JACCJournals
lo deja claro ➡️hay que preguntar, prescribirlo con dosis concreta y hacer seguimiento. Como cualquier tratamiento.
Y difícil convencer a nadie de algo que no hacemos nosotros. ¿ Has entrenado hoy? 🏃♀️
https://t.co/y14gLLILZB
Anatomical Approach from Aortic Sinus of Valsalva for Para-Hisian Premature Ventricular Contractions: Safety and Outcomes #OpenAccess
https://t.co/WOd74fontQ
🟥Acoplamiento Ventrículo-Arterial izquierdo [VAC]. 🔎🫀💥
🔴El VAC describe que tan bien están coordinados el ventrículo izquierdo y el sistema arterial durante la eyección. Esta relación se expresa como: VAC = Ea/Ees.
🔺️Ea (elastancia arterial): representa la carga arterial global o poscarga que enfrente el VI. Integra la resistencia vascular, distensibilidad arterial y FC. Una Ea ⤴️ sugiere mayor carga para el VI.
🔺️Ees (elastancia telesistólica): representa la capacidad contractil del VI para generar presión. Una Ees ⤵️ sugiere menor capacidad contractil.
📐Actualmente puede estimarse de forma no invasiva mediante ecocardiografía, utilizando el método se "un sólo latido", descrito por Chen et al.
📊Valores normales:
🔺️Ea: 2.2 ± 0.8 mmHg/mL.
🔺️Ees: 2.3 ± 1.0 mmHg/mL.
🔺️Ea/Ees: 1.0 ± 0.36
*En sujetos sanos, el sistema tiende fisiológicamente hacia un VAC ~0.5, asociado con una eficiencia metabólica óptima y una FEVI ~66%.
✅️VAC ~0.5 = máxima eficiencia energética. 👌🏻💓
⚠️VAC ~1.0 = máximo trabajo sistólico.
🚫VAC >1.3-1.4 = desacoplamiento.
https://t.co/rvQd0x1XtY
Class Ic antiarrhythmic therapy after PCI in new-onset atrial fibrillation: Safety and clinical outcomes from a nationwide cohort
https://t.co/3t3tNF3WFa
🫀 #EHRATopicWeek | Vascular access in EP
What are the main vascular closure techniques, and how should we choose between them?
🔹 Arterial access: Vascular closure devices are generally preferred over manual compression.
🔹 Venous access: Several effective options are available.
Both manual compression and subcutaneous figure-of-8 suture provide reliable hemostasis but require several hours of immobilization.
🔹 Venous closure devices (suture-based or collagen plug systems) enable very early ambulation, but at the expense of higher costs.
➡️ In everyday clinical practice, the choice of closure technique should be individualized according to the primary procedural goal (e.g. early ambulation, cost considerations, or workflow).
Read more 👉 https://t.co/Jw1CHjUzaD
@escardio #EHRA_ESC
🫀 #EHRAtopicweek | Vascular access in EP
Landmarks alone can deceive you. At lower inguinal punctures, the femoral vein sits posterior to the artery (>50% overlap) in ~24% of cases — and fully lateral in 6%. That's why palpation-guided access carries a real AV-fistula risk.
The fix? Ultrasound-guided access. Better success, fewer complications, especially in difficult or previously failed cases.
Know the anatomy. Image the vessel. Puncture with confidence. 🎯
Read more 👉 https://t.co/Jw1CHjUzaD
@escardio #EHRA_ESC
The rightward extension of Bachmann’s bundle
In this new #DaVinciAnatomyCorner@JACCJournals chapter, we explore its anatomy and clinical implications for physiological atrial pacing (BB pacing) @cardiac_anatomy
We hope you find it useful .
https://t.co/typfGFxizz
🚨 Can serial CMR redefine risk stratification in HCM?
A new study suggests that it may not be the amount of fibrosis alone that matters—but how quickly fibrosis progresses over time.
Researchers followed 313 patients with hypertrophic cardiomyopathy (HCM) who underwent two CMR scans approximately 4 years apart, assessing changes in late gadolinium enhancement (LGE), a marker of myocardial fibrosis.
🔍 Key findings
📈 Myocardial fibrosis increased substantially over time:
Median LGE mass increased from 2.9 g to 8.3 g
LGE prevalence rose from 72% to 91%
Extensive fibrosis (LGE ≥15%) doubled from 7% to 15% of patients.
⚠️ Nearly 70% of patients without LGE at baseline developed fibrosis on follow-up CMR.
💡 The most important finding was the rate of fibrosis progression:
ΔLGE >1.5 g/year independently predicted adverse clinical outcomes
Patients with rapid fibrosis progression had more than a twofold increased risk of death, transplant, HF hospitalization, stroke, or aborted sudden cardiac death
Adding ΔLGE/year to conventional risk models significantly improved risk prediction and reclassification.
❤️ For hard endpoints (death, transplant, aborted SCD), a fibrosis progression rate of >3.75 g/year identified particularly high-risk patients.
🎯 Clinical implications
Current guidelines already recommend repeat CMR every 3–5 years in HCM. This study provides strong support for that recommendation and suggests that:
✅ Serial CMR should be viewed as a dynamic monitoring tool rather than a one-time assessment
✅ Fibrosis progression may identify high-risk patients who appear low-risk according to conventional risk scores
✅ Imaging intervals could potentially be personalised based on fibrosis progression rates.
📚 One particularly striking observation: patients considered "low risk" by traditional ESC or AHA/ACC criteria but showing rapid LGE progression often had worse outcomes than some patients classified as high risk with stable fibrosis.
🧬 The future of HCM risk stratification may therefore move beyond a static fibrosis threshold toward a dynamic assessment of myocardial fibrosis progression.
🏆 Premios a los mejores artículos publicados en #recintervcardiol.
El primer premio es para «Valor pronóstico del volumen global de placa valorado mediante reconstrucción 3D del árbol coronario en pacientes sin enfermedad coronaria significativa. Un estudio multicéntrico».
Recoge el premio Octavio Jiménez-Melo (@Octavio_JiMelo). ¡Felicidades, autores!
👉https://t.co/XzoF7Vrxp8
#ACISEC2026 @shci_sec@secardiologia
Transseptal puncture in cardiovascular interventions: a clinical consensus statement of the European Heart Rhythm Association, the Heart Failure Association, the European Association of Percutaneous Cardiovascular Interventions https://t.co/yjtcQGyqNz
👨🎓🧑🎓The knowledge of atrial anatomy and tissue disposition in these complex structures may enable the electrophysiologist to better understand the 👉🔹pathophysiology of left & right atrial flutter as well as 🔹to perform the ablation procedures.
🫀 Are we underestimating sudden cardiac death risk in HCM?
📊 For years, risk stratification in hypertrophic cardiomyopathy (HCM) has relied on clinical scores…
But are these models too simplistic for such a complex disease?
🔍 A recent editorial challenges the paradigm:
👉 Moving from risk scores → precision cardiology
⚠️ The problem with current models:
✔️ Based on static variables
✔️ Limited integration of imaging & genetics
✔️ “Low-risk” patients can still experience events
💡 Example:
A 5-year SCD risk of 4–6% translates to only ~0.8–1.2% per year…
👉 Small differences, big clinical uncertainty
🧠 New insight: the atrium matters
Traditionally, we focus on the LV… but:
➡️ The left atrium reflects chronic diastolic burden
➡️ Dysfunction may precede structural changes
📈 In “low-risk” HCM patients:
👉 Impaired LA strain (LA-GLS) predicted adverse outcomes
👉 Even when conventional scores were reassuring
🔬 Where are we heading?
The future of SCD prediction in HCM is multidimensional:
✔️ Advanced imaging (CMR, strain, LGE)
✔️ Genetics (variants, polygenic risk)
✔️ AI-driven ECG analysis
➡️ Not one tool… but integration of all
🚀 Take-home message:
We need to move beyond rigid risk categories and embrace a dynamic, patient-specific approach.
👉 Precision cardiology is no longer a concept—it’s becoming a necessity.
#Cardiology #HCM #SuddenCardiacDeath #CardioImaging #CMR #StrainImaging #CardioGenetics #PrecisionMedicine #AIinMedicine #CardiologyResearch #PhDLife 🧬✨
The Empirical Evidence in the Successful Anatomical Ablation of Idiopathic LV Summit Ventricular Arrhythmias: Lessons From Endocardial Mapping | JACC: Clinical Electrophysiology https://t.co/0lxZAre8a1
✨ Mitral annular disjunction (MAD): are we focusing on the right marker for arrhythmic risk? ✨
📄 Read the discussion:
📌 DOI: 10.1093/eurheartj/ehag242
💡 A thought-provoking discussion challenges a key concept in arrhythmic MVP:
👉 Is “true-MAD” really the best marker for ventricular arrhythmic risk?
⚠️ What we thought
Patients with MVP + true inferolateral MAD → ↑ risk of ventricular arrhythmias
(even after mitral valve surgery)
🤔 But here’s the problem…
🔍 MAD is extremely common
– detected in up to 96% of individuals with advanced imaging
📉 Imaging limitations
– TTE may miss true-MAD, especially small disjunctions
– poor agreement between echo and CMR
🧠 Key paradigm shift
👉 It’s not just presence of MAD
👉 It’s the mechanical consequences that matter
✔️ Systolic extent of MAD
✔️ Dynamic systolic–diastolic changes
✔️ Mechanical traction on myocardium
➡️ Leading to fibrosis and arrhythmias
❤️ Role of fibrosis
📌 Myocardial fibrosis (LGE-CMR) strongly linked to malignant arrhythmias
But often not systematically assessed
👉 So what is driving risk?
– Persistent mechanical stress?
– Pre-existing fibrosis?
🚨 Critical questions raised
• Are we overemphasizing true-MAD as a binary marker?
• Should we instead focus on quantitative and dynamic metrics?
• Do we need multimodality imaging + rhythm monitoring for proper risk stratification?
📊 Notably:
👉 No clear increase in sudden cardiac death in true-MAD group
→ challenges a simplistic interpretation of risk
🚀 Take-home message
MAD is not just anatomy — it’s mechanics + substrate + phenotype
🧩 Future direction
• Integrate CMR + echo
• Quantify systolic MAD dynamics
• Assess fibrosis systematically
• Improve arrhythmic monitoring
💬 This discussion reminds us:
👉 In cardiomyopathies and valvular disease, structure alone is rarely enough
#MVP #MAD #Arrhythmias #CardiacImaging #CMR #Echocardiography #Cardiology #Electrophysiology #CardioTwitter 💙
Recognizing the septopulmonary region not as an isolated “bundle,” but as a functional 3D myocardial architecture, is essential for interpreting mapping data & optimizing ablation strategies
@JACCJournals@DrRoderickTung@davidgzcasal@DamianSanc1955
https://t.co/nnirFWiTnc
🔍 #EHRATopicWeek on Atrial Tachycardias
Atrial Tachycardia is more complex than we once thought
Traditionally, rapid regular atrial arrhythmias were divided into “atrial tachycardia” and “atrial flutter” based mainly on ECG appearance. Today, high-resolution mapping shows these distinctions are often oversimplified.
📌 Current concepts classify all regular atrial rhythms >100 bpm as AT:
• Non-reentrant AT
• Reentrant AT (localized or macro-reentrant)
Importantly, many arrhythmias previously labeled as “flutter” may actually represent different AT mechanisms.
⚡ Differentiating AT from organized AF can be challenging, especially in scarred atria or after ablation. ECGs, EP studies, intracardiac mapping, and even wearable devices all play an important role in diagnosis.
💡 Precise classification matters — for diagnosis, treatment strategy, and improving ablation outcomes.
Find out more in the #EHRA_ESC Consensus document on Management of patients with atrial tachycardia 🔗https://t.co/T5EGaHI51q
@escardio@EuropaceEiC