Muhammad Asad Shabbir

Love for Iqbal Faiz & Zia Mohiuddin. 🇵🇰🇺🇸

[Muhammad Asad Shabbir @mashabbir7]

Weekend before ERAS deadline is as crazy for reviewers as it is for applicants. Best of luck everyone for #Match2027

[Zarrar Khuhro @ZarrarKhuhro]

"Your death will come on an ordinary day, in the middle of unfinished plans, and the world will continue without you."

[Muhammad Asad Shabbir @mashabbir7]

@fslsltn @UsmanHaiderMD This is massive. Congratulations!

[Muhammad Asad Shabbir @mashabbir7]

@Ramshaa97 Congratulations Ramsha

[NEJM @NEJM]

Presented at #ASCO26:

Among patients with previously treated metastatic pancreatic ductal adenocarcinoma, the RAS(ON) inhibitor daraxonrasib led to significantly longer overall survival and progression-free survival than chemotherapy. Full phase 3 RASolute 302 trial results: https://t.co/xwLWBZYRzq

@ASCO

[Muhammad Asad Shabbir @mashabbir7]

@UWorldMedical do we have to choose out of these options for the correct answer?

[Muhammad Asad Shabbir @mashabbir7]

@jasonryanmd My question: if not medicine then what else in this country?

[Muhammad Asad Shabbir @mashabbir7]

Beautiful article!

[Smita Barooah @smitabarooah]

The quiet grief of adult friendship: One of the most beautiful articles I've read in a while. Hits hard
https://t.co/qXi6UBaTs3

[Jason Ryan @jasonryanmd]

New name for PCOS. The new name makes pathophysiological sense but, like all these name changes, will lead to more confusion than clarity. Some of us will use the old name and some the new. Notes over time will be inconsistent and confusing to providers. Patients will get lost in all the letters. I'm not sure this is a net positive change.

[Anish Moonka @anishmoonka]

Winston Churchill fought his depression with bricks. He'd lay them for hours at his country home in Kent. He joined the bricklayers' union. And in 1921 he wrote about why it worked. It took psychology another 75 years to catch up.

He called his depression the "Black Dog." It followed him for decades. His method for fighting it back was as basic as it sounds: laying brick after brick, hour after hour.

Churchill spelled out his theory in a long essay for The Strand Magazine. People who think for a living, he wrote, can't fix a tired brain just by resting it. They have to use a different part of themselves. The part that moves the eyes and the hands. Woodworking, chemistry, bookbinding, bricklaying, painting. Anything that drags the body into a problem the mind can't solve by itself.

Modern psychology now calls this behavioral activation. It's one of the most-studied depression treatments out there. Depression sets a behavior trap. You feel bad, so you stop doing things, and doing less means less to feel good about. Feeling worse makes you do even less. The loop tightens until you can't breathe inside it.

Behavioral activation breaks the loop from the action side. You schedule the activity first, even when every part of you doesn't want to. Doing it produces small rewards: a wall gets straighter, a painting fills in, a messy room gets clean. Those small rewards slowly rewire the brain. Action comes first, and the feeling follows.

Researchers at the University of Washington put this to the test in 2006. They studied 241 adults with major depression and compared three treatments: behavioral activation, regular talk therapy, and antidepressants. For the people who were most severely depressed, behavioral activation matched the drugs. It beat the talk therapy. A 2014 review of more than 1,500 patients across 26 trials backed up the result.

Physical work like bricklaying does something extra on top of this. It crowds out rumination, the looping bad thoughts that grind people down during the worst stretches of depression. Bricklaying needs both hands and gives feedback brick by brick: each one is straight or crooked. After an hour you can see exactly how much wall you built. No room left for the mental chewing.

The line George Mack used in his post, "depression hates a moving target," is good poetry. The science behind it is sharper. Depression hates a brain that has somewhere else to be.

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

🫀Heart failure in 2026: we are no longer treating symptoms. We are redesigning the disease.

The latest evidence update reminds us of something profound:

Heart failure is no longer a single entity.
It is a spectrum, and now, finally, we are treating it as one.

Several paradigm shifts stand out.

1. SGLT2 inhibitors are no longer “add-on” therapy.
They are foundational across the entire EF spectrum.

From HFrEF to HFpEF, the data are now consistent.
Not just symptom improvement, but hard outcomes.

This may be the most important unifying therapy in modern HF.

2. HFpEF is no longer a therapeutic desert.

For the first time, we have real disease-modifying options:

Finerenone → outcome reduction across EF ranges

GLP-1 / dual incretin therapies → targeting the obesity phenotype

Structural and metabolic mechanisms are finally being addressed

We are moving from “HFpEF frustration” → HFpEF phenotyping.

3. Acute heart failure is no longer about stabilization.
It is about early transformation.

The new paradigm:

Start GDMT in-hospital

Optimize rapidly

Treat beyond congestion

Decongestion is still important, but it is no longer the goal.
Disease modification starts on day 1.

4. Decongestion is becoming precision medicine

Urine sodium-guided therapy

Early escalation of loop diuretics

Sequential nephron blockade

Not just “give furosemide”, but measure, adjust, and target response.

5. Devices are no longer rescue therapy, they are integrated care

TEER expanding from mitral → tricuspid

Pulmonary artery pressure monitoring reducing hospitalizations

Remote hemodynamics shaping outpatient management

The boundary between ICU, ward, and home is dissolving.

6. The biggest problem is no longer evidence.
It is implementation.

We already have:

Quadruple therapy

Proven outcome benefits

Yet many patients never reach target doses.

The gap is no longer science.
It is execution.

🤓Final message

Heart failure care has entered a new era:

Mechanism-based therapy

Early aggressive optimization

Phenotype-driven treatment

And perhaps most importantly:
We are no longer chasing symptoms.
We are altering the trajectory of the disease.

📃Reference
Liori S, et al. Heart failure evidence update 2026. Heart Failure Reviews. 2026. https://t.co/T4MVjK0vGd

[Muhammad Asad Shabbir @mashabbir7]

Beyond thankful! Alhamdulillah.
#Match2026

[Muhammad Asad Shabbir @mashabbir7]

@goin_nuts_ Its emotional intelligence

[Muhammad Hussnain Sadiq, M.D @drhussnainsadiq]

And sometimes, against all odds, against all logic, we hope.

[Muhammad Asad Shabbir @mashabbir7]

@SeeFisch @MDaniyalNadeem1 Chief is a gentleman!

[Muhammad Asad Shabbir @mashabbir7]

@GovSherrillNJ Why were all NJ transit outbound from Penn New York cancelled without a prior notice at 7 pm EST? Suspension was supposed to go into affect at 9 pm. It has not even snowed an inch yet and your system has started to give up? Please investigate.

[Dr. Chokri Ben Lamine @abouabdrahman0]

Credits for sharing to Dr. Abdulrahman Nassiri 💐👌🤝

100 concise pearls from the 2026 AHA/ACC Guideline for Acute PE

🫀 Acute PE – 100 Pearls

1️⃣ PE risk stratification is mandatory before therapy.
2️⃣ New AHA/ACC Acute PE Clinical Categories A–E introduced.
3️⃣ Category A = incidental, asymptomatic PE.
4️⃣ Category B = symptomatic, low severity score.
5️⃣ Category C = elevated severity score ± RV strain.
6️⃣ Category D = incipient cardiopulmonary failure.
7️⃣ Category E = cardiopulmonary failure.
8️⃣ Use validated clinical probability tools.
9️⃣ Wells score remains practical.
🔟 Revised Geneva score validated.

1️⃣1️⃣ PERC rule avoids unnecessary imaging in very low-risk.
1️⃣2️⃣ Always assess pretest probability before imaging.
1️⃣3️⃣ Age-adjusted D-dimer recommended.
1️⃣4️⃣ Threshold = age ×10 μg/L (FEU).
1️⃣5️⃣ <2% failure acceptable for PE exclusion.
1️⃣6️⃣ YEARS algorithm reduces imaging burden.
1️⃣7️⃣ D-dimer strategies unsafe if already anticoagulated.
1️⃣8️⃣ Pregnancy-adapted YEARS supported.
1️⃣9️⃣ Avoid over-testing in low probability patients.
2️⃣0️⃣ CTPA is first-line imaging.

2️⃣1️⃣ Positive CTPA confirms PE.
2️⃣2️⃣ High-probability V/Q is diagnostic.
2️⃣3️⃣ Prefer CTPA over planar V/Q.
2️⃣4️⃣ V/Q SPECT better than planar V/Q.
2️⃣5️⃣ Echo cannot rule in or rule out PE.
2️⃣6️⃣ RV/LV ratio should be reported numerically.
2️⃣7️⃣ RV/LV ≥1 suggests RV strain.
2️⃣8️⃣ TAPSE <1.6 cm abnormal.
2️⃣9️⃣ McConnell’s sign indicates RV dysfunction.
3️⃣0️⃣ Report chronic thromboembolic signs on CT.

3️⃣1️⃣ LMWH preferred over UFH initially.
3️⃣2️⃣ DOACs preferred over VKAs.
3️⃣3️⃣ DOACs reduce major bleeding.
3️⃣4️⃣ Extended anticoagulation if unprovoked PE.
3️⃣5️⃣ Treat first episode ≥3–6 months minimum.
3️⃣6️⃣ Persistent risk → continue beyond 6 months.
3️⃣7️⃣ Evaluate bleeding risk regularly.
3️⃣8️⃣ IVC filters not routine.
3️⃣9️⃣ Use IVC filter only if anticoagulation contraindicated.
4️⃣0️⃣ Remove IVC filter when safe.

4️⃣1️⃣ Category A patients can be discharged.
4️⃣2️⃣ Category B often early discharge.
4️⃣3️⃣ Category C requires hospitalization.
4️⃣4️⃣ Category D needs close monitoring.
4️⃣5️⃣ Category E needs aggressive intervention.
4️⃣6️⃣ Persistent hypotension defines high risk.
4️⃣7️⃣ Use biomarkers for risk stratification.
4️⃣8️⃣ Troponin elevation signals myocardial injury.
4️⃣9️⃣ BNP elevation suggests RV strain.
5️⃣0️⃣ PE Response Teams (PERT) recommended.

5️⃣1️⃣ Systemic thrombolysis for high-risk PE.
5️⃣2️⃣ Consider advanced therapy in D1–D2.
5️⃣3️⃣ Catheter-directed thrombolysis reasonable.
5️⃣4️⃣ Mechanical thrombectomy evolving option.
5️⃣5️⃣ Surgical embolectomy when indicated.
5️⃣6️⃣ ECMO for refractory shock.
5️⃣7️⃣ Avoid routine thrombolysis in low-risk PE.
5️⃣8️⃣ Evaluate for contraindications before lytics.
5️⃣9️⃣ Monitor for intracranial hemorrhage risk.
6️⃣0️⃣ Early recognition saves mortality.

6️⃣1️⃣ Assess hemodynamics continuously.
6️⃣2️⃣ Monitor oxygenation closely.
6️⃣3️⃣ HFNC or NIV may be required.
6️⃣4️⃣ Mechanical ventilation cautiously.
6️⃣5️⃣ Avoid aggressive fluid overload.
6️⃣6️⃣ Use vasopressors if hypotension.
6️⃣7️⃣ Norepinephrine preferred.
6️⃣8️⃣ Reassess category over time.
6️⃣9️⃣ Clinical status can evolve rapidly.
7️⃣0️⃣ Repeat imaging only if clinically indicated.

7️⃣1️⃣ Ask about dyspnea at every follow-up visit.
7️⃣2️⃣ Screen for CTEPD at least 1 year.
7️⃣3️⃣ Persistent symptoms need evaluation.
7️⃣4️⃣ Chronic RV strain needs specialist input.
7️⃣5️⃣ Exercise intolerance must be addressed.
7️⃣6️⃣ Educate patients about recurrence risk.
7️⃣7️⃣ Travel guidance important.
7️⃣8️⃣ Activity resumption individualized.
7️⃣9️⃣ Avoid routine thrombophilia testing acutely.
8️⃣0️⃣ APS alters anticoagulation choice.

8️⃣1️⃣ Cancer-associated PE requires special planning.
8️⃣2️⃣ Pregnancy PE requires low-dose protocols.
8️⃣3️⃣ Avoid over-radiation in pregnancy.
8️⃣4️⃣ Avoid under-treatment of high-risk PE.
8️⃣5️⃣ Document RV strain in report.
8️⃣6️⃣ Quantify clot burden cautiously.
8️⃣7️⃣ Clot burden alone not treatment determinant.
8️⃣8️⃣ Clinical severity score essential.
8️⃣9️⃣ Hemodynamics trump imaging.
9️⃣0️⃣ Biomarkers add prognostic

[Jay Giri @jaygirimd]

2/ ⭐️ Use d-dimer and CTA in pts with high diagnostic suspicion to rule out PE.

⭐️ CTA is optimal diagnostic test.

⭐️ Quantitatively report RV:LV ratio with all PE CTA

⭐️ Specific reccs for TTE performance &amp; reporting also included.

[Muhammad Asad Shabbir @mashabbir7]

@LIRR &gt; @NJTRANSIT

[Muhammad Asad Shabbir @mashabbir7]

@fasc1nate @MaryamMaqsood_ Looks like a cross sectional study 😂