Rayees Ahmed Malik

Kashmiri | History Lover

[Rayees Ahmed Malik @imalikrayees]

❤❤❤

[Normal Guy @Normal_2610]

He explains quadratic equations in such a simple and effective way - honestly, even better than ChatGPT

[Gagandeep Singh @Gagan4344]

Youtube Link : https://t.co/O0Pepy9OvU

“I am still alive, but the film ‘Satluj’ shows me as dead.”

After 31 years, a key eyewitness in the Jaswant Singh Khalra case has broken his silence. Kikkar Singh, who says he personally fed Khalra while he was in police custody and later became a CBI witness, speaks out for the first time.

[Every Movie Plug @everymovieplug]

Christopher Nolan managed to create the most anxiety-inducing war movie opening in history using little to no dialogue and the literal ticking of his grandfather’s pocket watch.

[Rayees Ahmed Malik @imalikrayees]

😂😂😂😂

[Taimoor Zaman @taimoor_ze]

Vlogging has never been so good & accurate to be precise 😂🤣😭

[Rayees Ahmed Malik @imalikrayees]

@Jasonphilip8 @shekhar_lele Please use Inclisiran or PCSK 9 INHIBITOR

[Rayees Ahmed Malik @imalikrayees]

@DhruvMundhraYT Dr. Shamsheer Vayalil is the richest doctor in India, with an estimated net worth of approximately $3.7 billion (around Rs. 30,770 crore). He is a radiologist.

[Rayees Ahmed Malik @imalikrayees]

Titanic

[Tuğçe yıldız @tugce190333]

Bu resmi hatırlamıyorsanız , çok gençsiniz demektir.

[Rayees Ahmed Malik @imalikrayees]

🤣🤣🤣

[Akashhh @Hi_IamAkash]

Only true Bollywood fans will get this 😅😂

[Rayees Ahmed Malik @imalikrayees]

Amar Akbar Anthony. Secular Medical book 😅😅

[p. @dostoewhiskeyy_]

Medical version of "Amar,Akbar, Anthony".

[Rayees Ahmed Malik @imalikrayees]

@Jasonphilip8 Sorry to hear about your loss. Quacks are all over India. From Kashmir to Kanyakumari.

[Rayees Ahmed Malik @imalikrayees]

Jugaad

[Olivia 🎀🇺🇸 @Oliviaiie]

What would you call this ??

[Rayees Ahmed Malik @imalikrayees]

@IndiaHistorypic It still runs in few places. Have seen it in Pathankot.

[Rayees Ahmed Malik @imalikrayees]

@MohammedAlo Estimated price of Verve ?

[John Greenewald, Jr. @theblackvault]

Here is a thread of each of the UFO videos released today by the Department of War.

[Thomas Dayspring @Drlipid]

Lp(a) and Women: A MUST DOWNLOAD - "it is crucial that the risks associated with elevated Lp(a) levels in women are appropriately recognized by health care professionals to ensure the effective management of CVD risk and optimal CVD prevention in clinical practice" Open access at https://t.co/aL2Obn3bPA @nationallipid @MenopauseFnd @society_eas @ASPCardio @escardio @atherosociety @FamilyHeartFdn @MenopauseOrg @ErinMichos @MarlysLPA

[Pablo Corral MD @drpablocorral]

Lipoprotein(a), interleukin-6 and cardiovascular risk in a primary prevention setting

☝️New data from UK Biobank (n=34,092): In primary prevention, the cardiovascular risk associated with elevated Lp(a) was significantly influenced by IL-6, a key upstream inflammatory cytokine.

1️⃣ Higher Lp(a) increased MACE risk only when IL-6 was elevated (HR 1.17; 95% CI 1.07–1.28), while no significant association was seen when IL-6 was below median levels.

2️⃣ Inflammation appears to amplify Lp(a) pathogenicity, supporting the concept that not all elevated Lp(a) carries the same biological risk burden.

3️⃣ hs-CRP did not show the same modifying effect, suggesting IL-6 may be a more informative biomarker than conventional inflammatory markers for Lp(a)-related risk stratification.

4️⃣ Clinical implication: Future Lp(a)-lowering therapies may yield greatest benefit in individuals with concomitant elevated IL-6, enabling more precise preventive targeting.

👉 Elevated Lp(a) appears to confer its greatest cardiovascular hazard in the presence of heightened IL-6–mediated inflammation, supporting a biologically integrated model in which inherited atherothrombotic burden and residual inflammatory risk act synergistically

@ATHjournal
@society_eas

🔗 https://t.co/dEWhC0JpAm

[Dr. Deepak L. Bhatt @DLBHATTMD]

PCSK9 inhibitor treatment and outcomes in patients with atherosclerotic #cardiovascular disease but without prior ischemic events: an observational study https://t.co/uIDcZN08UJ #cardiology #prevention @ESC_Journals @escardio @ehj_ed @TokgozogluLale

[Samuel Hume @DrSamuelBHume]

With Novartis' Lp(a) readout expected any day now, here's a great figure to explain the thesis:

[Pablo Corral MD @drpablocorral]

👉 Update on familial hypercholesterolemia: An expert clinical consensus from the National Lipid Association

👆 FH is common (≈1:311) and systematically underdiagnosed → the real problem is not rarity, it’s detection

👆 Driven by lifelong LDL-C exposure, not a single value → risk = LDL-C × time

👆 Genetics help, but phenotype rules → treat based on LDL-C burden, not just mutations

📍 Diagnosis
LDL-C ≥190 mg/dL (adults) → think FH, but confirm clinically
Genetic testing = useful for cascade screening, not mandatory
Always exclude secondary causes before labeling

📍 Screening
Universal pediatric screening (9–11 yrs) is not optional—it’s delayed prevention
Cascade screening = highest yield strategy (and still underused)

📍 Risk
Standard risk calculators? Useless in FH → they underestimate risk
Risk depends on:
Lifetime LDL exposure
Lp(a)
Family history
Timing of treatment

📍 Treatment (no shortcuts)
Lifelong, early, aggressive
Targets:
<55 mg/dL (secondary prevention)
<70 mg/dL (primary prevention)
Start with:
High-intensity statin, ezetimibe, PCSK9i / others as needed
≥50% LDL reduction is the floor, not the goal

📍 Take-home
FH is not a lipid disorder.
It’s a time-dependent vascular disease.
Diagnose early, treat hard, treat forever.

🔗 🔓 Open Access https://t.co/mt2c3QNp9y

@nationallipid
@LipidJournal
@society_eas

[Dr. Filippo Cademartiri @FCademartiri]

🫀🔥 LDL is controlled. Statins are optimized.
And yet… patients still have events.

This study addresses one of the most important unanswered questions in cardiology:
👉 What really drives residual cardiovascular risk?

📊 In >9,400 statin-treated patients with LDL <70 mg/dL undergoing PCI:
Patients were stratified by:
Triglycerides (TG ≥150 mg/dL)
Inflammation (hs-CRP ≥2 mg/L)

💡 The result is striking:
👉 Inflammation—not triglycerides—drives risk
Residual inflammatory risk → ~1.8x higher MACE
Combined TG + inflammation → ~1.9x higher MACE
Residual TG risk alone → NO significant increase

⚠️ And what’s driving this?
👉 Mostly all-cause mortality
Not subtle. Not marginal.
👉 Clinically meaningful.

🧠 Let’s be clear:
We’ve spent decades optimizing:
✔ LDL
✔ Lipid profiles
✔ Cholesterol targets

But this study shows:
👉 You can win the lipid battle… and still lose the war
🔥 Because atherosclerosis is not just lipid-driven.
👉 It’s an inflammatory disease

🎯 Clinical implication
Risk stratification cannot stop at LDL.
We need to integrate:
hs-CRP
Inflammatory burden
Systemic biology

🚀 Paradigm shift
From:
❌ “How low is LDL?”
➡️ to
✅ “How active is the disease?”

🧠 Bottom line
Lowering LDL is necessary.
👉 But it is NOT sufficient.

If inflammation persists:
👉 Risk persists.
⚡ The future of prevention?
Not just lipid control.
👉 Inflammation-guided precision cardiology.