Deepak Choudhry

Consultant Anaesthetist and Perioperative medicine and Regional Anaesthesia enthusiast. Trekking and mountaineering. All views my own.

[Deepak Choudhry @drdeeps76]

@ARanganathan72 राहत इंदौरी साहेब ने इस पे बहुत उम्दा शेर कहा था

जो दौर है दुनिया का उसी दौर से बोलो,
बहरों का इलाक़ा है, ज़रा ज़ोर से बोलो।

[Deepak Choudhry @drdeeps76]

@vulturetrades Guide

[Deepak Choudhry @drdeeps76]

@usludurkizim 40

[Afshine Emrani MD FACC @afshineemrani]

I'm a cardiologist. I've held dying hearts in my hands in the cath lab at 3 AM. And I need to tell you something that changes everything about how we prevent heart attacks.

For decades, the entire field was built on one target: lower LDL cholesterol. Statins save lives — that's settled science. But too many of my patients did everything right — took their statins, hit their numbers, lived clean — and still ended up on my table with a ruptured artery.

We were treating the smoke while the fire kept burning.
The fire is inflammation. And the evidence is now overwhelming.

The CANTOS trial proved it first — lowering inflammation independent of cholesterol reduced cardiac events. But the newer data is what keeps me up at night.

AI-enhanced CT angiography can now detect inflamed arteries by measuring changes in the fat surrounding your coronary vessels — the perivascular fat attenuation index. Higher inflammation in the fat around even one artery independently predicts cardiac death. When multiple arteries show inflammation, the risk multiplies dramatically — even in patients whose cholesterol looks perfect.

This isn't theoretical. This is measurable. Right now. On a scan you can get this month.

Low-dose colchicine — a drug that's been around for centuries for gout — is now FDA-approved specifically for reducing cardiovascular events. It works by quieting the inflammatory cascade that destabilizes the plaque sitting in your arteries. A pill that costs pennies is saving lives the statins couldn't reach.

And the next wave is already in Phase 3 trials. Ziltivekimab — an IL-6 inhibitor — targets the central inflammatory pathway driving atherosclerosis. Phase 2 data showed a 90% reduction in hsCRP. The ZEUS cardiovascular outcomes trial is enrolling now, with results expected late 2026 into 2027. If positive, anti-inflammatory therapy will become standard in managing heart disease alongside lipid-lowering. The era of inflammation-targeted cardiology is arriving.
But it goes deeper than drugs. AI is now predicting heart failure and cardiac events 5+ years before symptoms — integrating CT imaging, electronic health records, and genetic data with accuracy that jumps far beyond traditional risk calculators.

And polygenic risk scores — a simple genetic test that flags inherited cardiovascular risk — are now formally recognized as a risk-enhancing factor in the 2026 ACC/AHA guidelines. A single blood draw can reveal risk that's been silently building since birth. Decades before the first chest pain.

Here's what this means for you right now — today:
Ask your doctor for a high-sensitivity CRP test. It's cheap, routine, and measures the systemic inflammation that standard cholesterol panels completely miss. You can have perfect LDL and inflamed arteries that are quietly preparing to rupture.
If your hsCRP is elevated, discuss low-dose colchicine with your physician. It's FDA-approved for exactly this.
Push for a coronary CT angiography with AI plaque and inflammation analysis if you have risk factors. This isn't the stress test your parents got. This is 3D visualization of your actual arteries — with AI quantifying not just how much plaque you have, but what kind it is and whether the surrounding tissue is inflamed.
Consider polygenic risk score testing — especially with a family history of early heart disease. It's now guideline-supported.

And the foundation that never changes: move daily, eat real food, sleep 7-9 hours, manage stress, and know your numbers — ApoB, Lp(a), hsCRP, fasting insulin.
I left Iran as a child with nothing. I rebuilt everything in a country that gave me the freedom to become a physician. I've spent twenty years watching patients get second chances.

The ones who haunt me aren't the ones who died on my table. They're the ones who survived but never acted on what the science was telling them — years before the event that didn't have to happen.

You can have perfect cholesterol and still have a heart attack. Inflammation plus genetics can drive plaque rupture in arteries that look "fine" on a standard panel.
The myth that normal cholesterol means you're safe has cost more lives than I can count.

We now have the tools to detect the fire — not just the smoke. AI to see it. Genetics to predict it. Drugs to quiet it. And the ancient basics — movement, real food, sleep, purpose — to prevent it from starting.

Prevention is the new cure. And the science to make it real is no longer coming.
It's here.

[Knowledge & History @xKnowledgeBANK]

The best way to teach people critical thinking

🎥: Jordan.b.peterson

[Deepak Choudhry @drdeeps76]

@dpradhanbjp one of the ways NEET can be fool-proofed is to make it compulsorily computer based and take out the examiners setting the questions and instead use AI to set the questions and ensure that the set of paper is released only an hour before so that there is no leak

[Anand Ranganathan @ARanganathan72]

Supreme court when Nupur Sharma repeats what is written in Islamic scriptures: You have ignited India. You possess a loose tongue. Power has gone to your head. You should apologise.

Supreme court when Udhayanidhi Stalin repeats his call to eradicate Sanatana Dharma: Silence.

[anand mahindra @anandmahindra]

When I saw this video, my first thought was that the earth, very often, sends us messages.

This tree, facing constant winds, is still standing, & has neither fallen nor been uprooted.

Instead it’s been shaped by it.

And developed its own unique aesthetic & identity.

We have to recognize & accept that tough times & tragedies are part of the journey.

They don’t define us, they simply give us our own unique personalities & capacities…

#MondayMotivation

[Prasad @theprasad_]

In 1984, Jiddu Krishnamurti explained how to end every form of fear known to humankind.

No psychologist or philosopher ever came close to him.

His frameworks:
• Thought creates fear
• Time sustains fear
• Escape strengthens fear

13 lessons on ending fear completely:

[Deepak Choudhry @drdeeps76]

@MapleStax CBC

[Deepak Choudhry @drdeeps76]

@TradingWarz Me

[Deepak Choudhry @drdeeps76]

@felixprehn Workbook

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🩺 Arterial line ≠ just a number on the monitor

If you’re only looking at MAP…
you’re missing most of the physiology.

🧠 Invasive BP is a real-time hemodynamic language

Every component tells a different story:

▪️ MAP → organ perfusion
▪️ DAP → vascular tone
▪️ SAP → LV afterload
▪️ Pulse Pressure (PP) → stroke volume surrogate

➡️ It’s not one number.
It’s a dynamic physiological system

⚠️ First rule, often ignored:

👉 If the waveform is wrong → everything is wrong

Before interpreting:

✔️ Check damping
✔️ Perform fast flush test
✔️ Look for:

Rapid upstroke

Dicrotic notch

Smooth diastolic decay

➡️ Bad waveform = bad decisions

📉 MAP alone is NOT enough

We target MAP ≥65 mmHg…
but:

▪️ Duration of hypotension matters
▪️ Individual physiology matters
▪️ CVP matters

👉 Think instead:

🎯 Perfusion pressure = MAP − CVP (MPP)

➡️ A “normal MAP” can still mean hypoperfusion

🔥 DAP = your vasopressor trigger

Low DAP = low vascular tone

▪️ Septic shock → ↓ DAP
▪️ Early signal before MAP collapses

👉 Use it to:

✔️ Start norepinephrine earlier
✔️ Avoid delayed vasopressor therapy

➡️ It’s one of the most underused variables in ICU

⚡ Pulse Pressure = hidden CO monitor

PP reflects:

▪️ Stroke volume
▪️ Arterial stiffness

👉 Dynamic changes = key:

✔️ PLR
✔️ Fluid challenge
✔️ Ventilator cycles (PPV)

➡️ You can track CO trends without a CO monitor

🧬 Next-level physiology (very underrated):

New indices:

▪️ DSI = HR / DAP
→ identifies vasoplegia early

▪️ VNERi = DAP / (HR × NE dose)
→ detects norepinephrine resistance

👉 These may define who needs vasopressin early

💡 Mindset shift

Don’t ask:

❌ “What’s the MAP?”

Ask:

✔️ “What is the physiology behind this waveform?”

🧠 Take-home

Arterial line monitoring is not passive.

It’s:

▪️ Diagnostic
▪️ Therapeutic
▪️ Predictive

➡️ If you read it correctly…
it becomes a precision resuscitation tool

📚 Bertrand M et al. (2025)Annals of Intensive Care
DOI: 10.1186/s13613-025-01608-y

[Deepak Choudhry @drdeeps76]

@Simi_2210_ 179

[Deepak Choudhry @drdeeps76]

@Simi_2210_ 170

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🤓🫀We keep asking: “What’s the cardiac output?”
But maybe the better question is:
“How efficiently is the heart working?”

In septic shock, we often focus on:

Preload
Cardiac output
MAP

But we forget something fundamental:

👉 The heart doesn’t work alone.
👉 It works against the arterial system.

1. The missing concept: Ventriculo–arterial coupling (LVAC)

LVAC = interaction between:

Ees → contractility

Ea → arterial load

👉 Expressed as Ea / Ees

This ratio reflects:

How efficiently the heart converts energy into forward flow

2. What is “normal”?

LVAC ≈ 0.5 → optimal efficiency

LVAC ≈ 1 → maximal stroke work

LVAC > 1 → uncoupling (inefficient system)

But here’s the twist:

👉 In septic shock, LVAC is often >1
👉 Not just due to vasodilation—but also myocardial dysfunction

3. Why this matters clinically

Two patients can have:

Same MAP

Same CO

But completely different physiology:

✔ One → efficient coupling
❌ One → energy wasted, poor flow generation

4. The key insight

Septic shock is NOT just:

❌ “low preload”
❌ “vasodilation”

It is:

👉 A mismatch between heart and arterial system

5. Therapy changes the balance

Fluids → may improve coupling (↓ LVAC)

Norepinephrine → can improve OR worsen coupling

Inotropes → target Ees

Important:

👉 Increasing MAP ≠ improving flow
👉 Increasing pressure can worsen afterload

6. The most interesting part

From the data:

LVAC >1 can predict response to norepinephrine

But improving LVAC ≠ guaranteed tissue perfusion and outcomes follow a U-shaped curve

👉 Both too high AND too low LVAC can be harmful

7. The limitation we must respect

Even if you “optimize” LVAC:

👉 Microcirculation may still be impaired
👉 Lactate may still rise
👉 Shock may persist

Because: Macro ≠ micro

🤓Final message

We need to move from:

❌ “Fix the blood pressure”

To:

✅ “Optimize the interaction between heart and vessels”

LVAC doesn’t replace hemodynamics.
It completes it.

📃Reference
Caicedo Ruiz JD et al. Journal of Critical Care, 2026. https://t.co/1ZNMHqwBl4

[Mindset Machine  @mindsetmachine]

This is where real relationships are actually tested.

[Shabnam Parveen @shabnam_774]

In 2019, a legendary MIT lecture quietly changed how the smartest people communicate.

Most people still ignore it.

Patrick Winston didn’t just teach speaking he exposed why people fail to be understood.

18M+ views later… it’s still ahead of its time.

His frameworks:
• Your ideas are like your children
• The 5-minute rule for job talks
• Why jokes fail at the start

15 lessons on communication:

[Sonal Kalra 🇮🇳 @sonalkalra]

Why confuse pride in our national identity with ideology? Aapka kya kehna hai is baare mein?

[Zahack Tanvir — ضحاك تنوير @ZahackTanvir]

It’s not Hindu vs. Muslim. It’s Nativists Vs. Foreigners clash! My comments on Impact Stories!