Groundbreaking Insight in Preventive Cardiology
For the first time in humans, we’ve directly tracked coronary artery disease at its earliest and most dangerous stage and have shown the benefits of early treatment: non-calcified (soft) plaque — with a zero - calcium score before the plaque even hardens.
This overturns the long-held assumption that “no calcium = no disease.”
Using AI-assisted quantitative coronary CT angiography (AI-QCT), we followed non-calcified plaque volume in a patient for a decade. The plaque continued to grow and remained biologically active for years before any calcium appeared. AND IT CAN BE TREATED!!!
Key breakthrough:
When intensive lipid-lowering therapy (e.g., high-dose statins) was started, plaque progression slowed dramatically.
This is direct imaging proof that we can:
• Detect disease earlier
• Treat it earlier
• Stabilize it before irreversible damage occurs
— rather than relying only on blood tests or indirect risk markers.
Even more striking:
Large studies now show that non-calcified plaque volume outperforms every traditional risk factor in predicting heart attacks and death, including:
• Age and sex
• Cholesterol levels
• Blood pressure
• Diabetes
• Smoking
• Calcium scores
• Standard ASCVD risk calculators
When AI-derived plaque metrics are added to clinical models, risk prediction improves substantially.
Bottom line:
Non-calcified plaque volume is not just another marker — it is the true, quantifiable measure of a person’s coronary disease burden. It directly drives future cardiac events, and now we can measure it and change its trajectory over time.
This enables true personalized prevention.
We can now identify the dominant drivers of plaque in each individual:
• Lipids
• Inflammation
• Metabolic dysfunction / insulin resistance
• Hypertension
• Smoking
• Sedentary lifestyle
• Poor diet
• Stress
• Sleep disorders
— usually in combination
Lifestyle changes can now be judged by their direct effect on plaque itself, not just surrogate lab values.
And new therapies are accelerating this shift:
• Advanced lipid-lowering agents
• Anti-inflammatory therapies
• Metabolic treatments
• Gene-silencing therapies that target plaque biology directly
This moves cardiology away from one-size-fits-all population risk — toward treating the actual disease in each person.
The takeaway is simple:
• Visualize the disease with coronary CTA
• Measure it precisely with AI-QCT
• Treat it directly
• Track response over time
That’s the future of preventive cardiology — and a realistic path toward dramatically reducing, and perhaps one day preventing, coronary artery disease.
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