What's Moving the Needle Right Now
Three things worth paying close attention to this month.
Senescent cells accumulate in atherosclerotic plaques. The D+Q combo clears them — early trials show reduced arterial stiffness. Radiation accelerates cellular senescence. This could be a direct RICAD countermeasure.
ClinicalTrials.gov →Two injections per year can cut LDL by 50%+. For radiation-induced CAD where plaques are fibrotic and aggressive, aggressive LDL lowering matters more than in typical CAD. Game-changer for compliance.
ORION-10 Trial (NEJM) →The SELECT trial showed 20% reduction in MACE in non-diabetic overweight patients. The cardiac benefit appears independent of weight loss — likely anti-inflammatory. RICAD patients may have direct benefit even at healthy weight.
SELECT Trial (NEJM) →Cardiovascular Interventions for RICAD Survivors
From approved standards to frontier experiments. Always discuss with your cardio-oncologist before changing your protocol.
| Intervention | Status | Mechanism | RICAD Relevance |
|---|---|---|---|
| High-intensity statinsRosuvastatin, Atorvastatin | Approved | LDL reduction + plaque stabilization | First-line for RICAD. Fibrotic plaques may respond differently — higher dose often warranted. |
| PCSK9 InhibitorsEvolocumab, Alirocumab, Inclisiran | Approved | Block PCSK9 protein → more LDL receptors | For statin-insufficient LDL control. Inclisiran (RNA-based) requires only 2 injections/year. |
| ColchicineLow-dose, 0.5mg daily | Approved | Anti-inflammatory (NLRP3 inhibition) | COLCOT & LoDoCo2 trials showed 31% reduction in MACE. Radiation drives vascular inflammation — colchicine directly targets this. |
| Senolytics (D+Q)Dasatinib + Quercetin | Experimental | Clears senescent cells from vessel walls | Radiation creates senescent cells. D+Q removes them. Phase I/II trials in progress. Intermittent dosing protocol (not daily). |
| GLP-1 AgonistsSemaglutide (Ozempic/Wegovy) | Approved | Cardiac inflammation reduction + metabolic | SELECT trial: 20% MACE reduction independent of weight loss. Anti-inflammatory mechanism may be especially relevant post-radiation. |
| CAR-T for AtherosclerosisEarly-stage research | Emerging | T cells engineered to clear arterial foam cells | Penn/Penn Medicine research. Conceptually revolutionary. Years from clinical use but the direction points toward reversing established disease — not just stopping it. |
| ZiltivekimabIL-6 ligand inhibitor — RESCUE trial | Clinical Trial | IL-6 pathway blockade → vascular inflammation | Targets the same inflammatory axis as CANTOS (IL-1β) but via IL-6. Radiation-induced vascular inflammation is likely IL-6 mediated. |
| CRISPR / Gene TherapyInclisiran → CRISPR-PCSK9 | Emerging | Permanent PCSK9 knockout via single treatment | Intellia Therapeutics leading. A one-time treatment for LDL reduction — lifetime effect. Not yet approved but pivotal trials running. |
| Rapamycin (mTOR inhibition)Longevity off-label use | Off-label | mTOR inhibition → autophagy, anti-senescence | Used by some longevity physicians weekly (intermittent). May slow vascular aging and reduce plaque progression. Active research in aging context. |
| AI-Enhanced CAC ScreeningCleerly AI, Elucid | Approved | Deep learning plaque characterization | Goes beyond a simple CAC score — characterizes plaque composition (fibrotic vs. lipid-rich vs. calcified). Especially useful for RICAD where fibrotic plaques are common. |
Scientists & Physicians at the Edge
The researchers and clinicians doing the most relevant work. Follow them, read them, advocate for their research.
One of the world's leading cardiologists and the foremost voice on AI in medicine. His work on deep learning for cardiac imaging is directly relevant to earlier, better RICAD detection.
The physician most responsible for mainstreaming atherosclerosis prevention as a longevity priority. His framework of ApoB, LP(a), and early aggressive intervention applies directly to RICAD survivors.
Leading researcher on coronary artery calcium scoring and CT angiography. His work on CAC progression and plaque characterization is essential reading for any RICAD survivor managing their disease.
One of the most prolific researchers in cardio-oncology. Focused specifically on cardiovascular toxicity from cancer treatment — his publications are a direct resource for understanding RICAD mechanisms and management.
Specifically focused on radiation-induced cardiovascular damage at the molecular level. Her research into mitochondrial dysfunction and reactive oxygen species in radiation-exposed vascular tissue is foundational RICAD science.
The information theory of aging, NAD+ biology, and sirtuins. While not RICAD-specific, his framework for understanding accelerated aging — which radiation induces — is directly relevant to why RICAD happens and how to counter it.
Studies That Changed How We Think
The trials and papers every RICAD survivor should know about.
COLCOT Trial — Colchicine in Coronary Artery Disease (NEJM, 2019)
Low-dose colchicine (0.5mg/day) reduced MACE by 23% in post-MI patients. First major trial to validate anti-inflammatory therapy as a cardiovascular intervention beyond lipid lowering. RICAD plaques are inflammation-driven — this applies directly.
SELECT Trial — Semaglutide in Cardiovascular Prevention (NEJM, 2023)
Semaglutide reduced major cardiovascular events by 20% in non-diabetic, overweight patients with established CVD. The mechanism appears to involve direct anti-inflammatory effects on the arterial wall — independent of weight or glucose effects.
Radiation-Induced Cardiovascular Disease — ESC Cardio-Oncology Guidelines (2022)
The first comprehensive European Society of Cardiology guidelines specifically for cardiovascular complications of cancer treatment. Covers screening timelines, risk stratification, and management recommendations for RICAD. Essential reference.
Clearance of Senescent Cells Reverses Radiation-Induced Damage (Nature Medicine, 2021)
Senolytic treatment reversed radiation-induced physical dysfunction and metabolic disruption in mouse models. Provides direct mechanistic support for using senolytics in RICAD survivors. Translational work is ongoing in humans.