




Michal Till
11.5K posts

@tillda
Fiscally conservative, socially democrat, sexually liberal. ♦ This is a personal account. 🇺🇦







After 13 years, I can distill all parenting advice to one variable: your kid’s closest friends.


At the request of the Russian government, @Apple removed numerous VPN services from the App Store - tools that had allowed Russians to bypass censorship. A remarkable stroke of luck for Putin to have such “friends” in Big Tech. Over the past few years, Russian authorities have blocked millions of websites, including independent media and opposition platforms. VPNs are now one of the few remaining ways for Russians to access truthful reporting on current events. Yet Apple has chosen to assist state censorship in Russia.








The whole Anglosphere is rotting from the inside out.





Can plaque regress? Yes—but only with aggressive lipid lowering 💢Atherosclerosis is not always a one-way road; under the right lipid targets, plaque can shrink and stabilize. Clinical Pearls Plaque regression is possible, but usually not with casual lipid control. The consistent message across intracoronary imaging trials is simple: the lower the LDL, the greater the plaque regression and stabilization. High-intensity statins do more than moderate statins. In REVERSAL, intensive atorvastatin halted plaque progression, while moderate pravastatin did not. In ASTEROID and SATURN, when LDL was brought into the ~60–70 mg/dL range, actual plaque regression was seen on IVUS. This established that treatment should aim not merely to “normalize” cholesterol, but to drive LDL to levels where arterial biology changes. Adding ezetimibe to statin therapy produced more regression than statin alone, showing that dual blockade of cholesterol synthesis and absorption is superior to monotherapy in higher-risk patients. With PCSK9 inhibitors, LDL can be pushed into the 20s to 30s, and plaque regression continues further. GLAGOV suggested no clear lower threshold of benefit within the studied range. Modern trials showed that benefit is not only about plaque volume. Aggressive lipid lowering also reduces lipid core, thickens fibrous cap, and therefore stabilizes vulnerable plaque—the plaque most likely to rupture and trigger acute coronary syndrome. After ACS, this becomes even more important. HUYGENS and PACMAN-AMI showed that very low LDL levels were associated with greater cap thickening, more lipid depletion, and greater plaque stabilization. A key modern lesson is that ApoB matters. LDL-C tells how much cholesterol is being carried; ApoB reflects the number of atherogenic particles. In patients with diabetes, insulin resistance, high triglycerides, or metabolic syndrome, ApoB may better represent residual risk. Practical Target Pearls LDL below 70 mg/dL: progression slows significantly. LDL around 60 mg/dL: plaque regression begins to appear reliably. LDL below 50 mg/dL: more dramatic regression and stabilization. ApoB below 65 mg/dL: may better predict structural plaque benefit in very high-risk patients. High-impact Bottom Line Do not ask only: “Is cholesterol normal?” Ask: “Is LDL low enough for plaque healing, and is ApoB at goal?” Final CME INDIA Take-home Message Plaque regression is real, but it requires intensity. For very high-risk ASCVD patients, especially post-ACS, the therapeutic aim should be early, aggressive, combination lipid lowering to achieve very low LDL and low ApoB, because that is where arteries begin to heal—not just stabilize. Key Point In preventive cardiology, lower LDL is not cosmetic biochemistry—it is vascular therapy. dralo.net/blog/reverse
