🫀⚡ CCTA is no longer “just a test.” It is becoming the operating system of modern cardiology.
This review makes something very clear: Coronary CT has crossed a threshold.
It is no longer simply about detecting stenosis.
It is now integrating:
👉 anatomy
👉 physiology
👉 plaque biology
👉 inflammation
👉 procedural planning
👉 AI-driven prediction
—all inside one examination.
For years, cardiac imaging was fragmented:
- stress test for ischemia
- angiography for anatomy
- IVUS/OCT for plaque
- separate risk scores for prognosis
Now CCTA is starting to merge all of these layers together.
The paradigm shift is obvious
From: ❌ “Is there obstructive CAD?”
To: 👉 “What is the biological trajectory of this patient?”
The paper highlights how modern CCTA now provides:
✅ plaque characterization
✅ quantitative plaque burden
✅ CT-FFR
✅ PCAT inflammatory analysis
✅ radiomics
✅ AI-driven phenotyping
And Photon Counting CT accelerates everything.
Because PCCT is solving one of the oldest problems in coronary imaging:
👉 blooming
👉 limited spatial resolution
👉 poor stent evaluation
👉 calcium interference
With PCCT:
⚡ spatial resolution approaches ~0.25 mm
⚡ calcium blooming is dramatically reduced
⚡ stent lumen visualization improves substantially
But here’s the deeper implication
We are moving away from: ❌ lumen-centric cardiology
toward: 👉 multi-dimensional atherosclerosis phenotyping
And AI becomes critical here.
Not because it “replaces” physicians.
But because humans cannot realistically integrate:
✅ plaque texture
✅ morphology
✅ inflammation
✅ radiomics
✅ flow dynamics
✅ longitudinal progression
at scale.
My take
The future cardiac CT exam will not answer:
👉 “Is there a stenosis?”
It will answer:
👉 “How dangerous is this artery biologically?”
👉 “How will this patient evolve?”
👉 “Which therapy changes the trajectory most?”
Bottom line
CCTA is evolving from:
👉 diagnostic imaging
to:
👉 computational cardiovascular phenotyping
⚡ And once imaging becomes biology + AI + prediction…
the entire architecture of cardiology changes.
#CCTA #Cardiology #PhotonCounting #AI #PrecisionMedicine #Atherosclerosis #CardiacCT #PlaqueImaging #yesCCT
🗣️El Dr. Valentín Fuster será protagonista de una de las conferencias más esperadas del congreso, abordando un tema clave para el futuro de la cardiología.
➡️ Rosario- 28 de mayo
➡️Más información en nuestra web.
#CNC2026#FAC#Cardiología#PrevenciónCardiovascular
Queríamos invitarlos a las jornadas presenciales binacionales que realizaremos con el Dist. Formosa de @SAC_54 🇦🇷, en conjunto con @SPCyCC 🇵🇾 y @sac_pais . El sábado 25/4 con el @SACemergencias sumado al de Emergencias de Paraguay llevaremos a cabo 3 sesiones de C. critica.
CRISPR deleted the extra chromosome behind Down syndrome.
In a groundbreaking world-first, researchers have successfully used CRISPR gene-editing technology to remove the extra chromosome responsible for Down syndrome, opening a potential path toward treating genetic disorders previously considered incurable.
Down syndrome, or trisomy 21, occurs when a person has three copies of chromosome 21 instead of the usual two. It is one of the most common genetic conditions, affecting about 1 in 700 babies worldwide, and leads to intellectual disability, developmental delays, and various health issues. Until now, no treatment has been able to correct the underlying cause.
That may soon change.
In a new proof-of-concept study, scientists applied CRISPR-Cas9 to cells taken from people with Down syndrome—including skin cells and pluripotent stem cells—and successfully eliminated the extra chromosome 21. The edited cells showed a striking return to normal gene expression patterns and cellular function. To improve precision, the team briefly disabled certain DNA-repair pathways during the process, making the chromosome removal cleaner and more effective.
At this stage, the technique has only been demonstrated in laboratory cell cultures and is far from ready for human use. Removing an entire chromosome carries significant risks, including possible off-target effects, so extensive safety work lies ahead. If those challenges can be overcome, however, the approach could one day be applied to brain cells or even used during early fetal development.
The implications extend beyond Down syndrome. The same strategy might eventually treat other life-limiting trisomies, such as trisomy 13 and trisomy 18, which are often fatal in infancy or cause severe disability. For the first time, a tool exists that could, in principle, correct the root chromosomal abnormality rather than merely managing symptoms.
["Trisomic rescue via allele-specific multiple chromosome cleavage using CRISPR-Cas9 in trisomy 21 cells." PNAS Nexus, 2025]