JP Mishra, MD, FACC

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JP Mishra, MD, FACC

JP Mishra, MD, FACC

@JPCardio

Upstate Cardiology. Rochester, NY. (seeking generosity, charity, friendship and passion for humanity).

Rochester, NY, USA Katılım Ocak 2010
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JP Mishra, MD, FACC
JP Mishra, MD, FACC@JPCardio·
@MJAckermanMDPhD @Hragy @EndeavorAir Lovely! She is officially not only ATP for herself but on a daily basis for you as well! You being in medicine/ cardiology, I don’t need to remind you what ATP stands for!! Your ATP: Better than coffee! Congratulations to all of you!!
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Michael J. Ackerman MD,PhD
Michael J. Ackerman MD,PhD@MJAckermanMDPhD·
Indulge me in one of those incredible proud dad days! Our daughter Grace earned her @EndeavorAir wings last Wednesday becoming an #Airline Transport #Pilot (ATP). She came home for #EasterWeekend2026 and today she flies her first CRJ900 jet flight ✈️! Love my Gracie girl 🤗😘🛫
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Arron Pearce
Arron Pearce@Arron_Pearce_·
@RobertHermanMD @BaoGTran @PMcardioApp @smithECGBlog @The_Nanashi_O This ECG is suspicious for a left arm ↔️ V2 reversal (both leads are yellow in the UK) I have simulated this kind of error before, see below. Note the what this error does to the frontal plane QRS axis. Do you have any other ECGs recorded for your patient?
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Milan Koštek
Milan Koštek@KostekMilan·
🟡 Fabry Cardiomyopathy 🟡
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JP Mishra, MD, FACC
JP Mishra, MD, FACC@JPCardio·
@TheECGMedic 1. Markedly inverted Ts give an impression as if the ECG is upside down! 2. These widely inverted Ts are as bad if not worse as the large, fresh Qs!!
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Arron Pearce
Arron Pearce@Arron_Pearce_·
Are you able to identify this patient's rhythm? 🧐
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Dr. Shiv_Kumar
Dr. Shiv_Kumar@Dr_Shiv_kumar_·
🚨 Endocrinology pearls you should never miss as a clinician 2️⃣ I diagnosed a patient with pheochromocytoma and started medical management and here’s the part may go wrong 👇 You DON’T start β-blockers first. You begin with α-blockade (e.g. Phenoxybenzamine). 🔻Why? Because catecholamines hit both: α → vasoconstriction ↑BP β2 → vasodilation β1 → tachycardia Block β first (e.g. Propranolol) → you remove β2 vasodilation → αlpha remains unopposed → severe vasoconstriction → hypertensive crisis. So we start with α-blockade → reduce vascular tone → stabilize BP. Only AFTER adequate α control → add β-blocker to manage reflex tachycardia. 🔻This ties into Dale’s vasomotor reversal: Block α → adrenaline’s effect flips → β2-mediated vasodilation dominates → BP falls instead of rising. 🔻Clinical takeaway: α first → prevents unopposed vasoconstriction β later → rate control Wrong sequence = dangerous BP surge Right sequence = controlled physiology #MedX #MedTwitter #Endocrinology
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Dr. Shiv_Kumar@Dr_Shiv_kumar_

🚨 Endocrinology pearls you should never miss as a clinician 1️⃣ If you see elevated calcium, this is how you should think as a clinician? Most people remember “Stones, Bones, Groans & Psychiatric Overtones.” But that mnemonic doesn’t help you find the cause. What matters is a structured approach. When you see hypercalcemia, pause! think systematically. 🟢 FIRST RULE - CHECK PTH Your first lab is PTH. Don’t shotgun investigations. Don’t jump to imaging. PTH divides hypercalcemia into two diagnostic pathways. 🟢 INTERPRET THE PTH Only two possibilities: 🔻 PTH ↑ / inappropriately normal → PTH-mediated hypercalcemia 🔻 PTH ↓ → Non-PTH mediated hypercalcemia This single fork determines the entire work-up. 🟢 PATHWAY 1 : PTH HIGH → THINK PARATHYROID 🔴 Primary Hyperparathyroidism (Most common outpatient cause) Usually due to parathyroid adenoma (~85%). 🟢Mechanism :- PTH acts at three sites: 🔺Bone → osteoclast activation → calcium release 🔺Kidney → ↑ calcium reabsorption 🔺Kidney → ↑ vitamin D activation → ↑ gut absorption Net effect → persistent hypercalcemia. 🔻Typical Labs ↑ Calcium ↑ PTH ↓ Phosphate ↑ ALP ↑ Urinary calcium 🔻Why phosphate low? PTH causes phosphaturia by inhibiting Na-phosphate transporters in proximal tubule. 🔴 Familial Hypocalciuric Hypercalcemia (FHH) Mutation in calcium-sensing receptor. 🔻Typical Labs Mild ↑ Calcium Normal / mild ↑ PTH LOW urinary calcium ← key clue Normal phosphate Patients are asymptomatic → no surgery needed. 🔴 Tertiary Hyperparathyroidism Seen in long-standing CKD. Chronic stimulation → parathyroid glands become autonomous. 🔻Typical Labs ↑ Calcium ↑↑ PTH ↑ Phosphate ↓ Vitamin D 🟢 PATHWAY 2 :- PTH LOW → NON-PTH CAUSES If PTH is suppressed, calcium is coming from somewhere else. 🔴 Malignancy-Associated Hypercalcemia (Most common inpatient cause) Mechanisms: PTHrP secretion Osteolytic metastasis Excess vitamin D (lymphoma) 🔻Labs ↑ Calcium ↓ PTH ↑ PTHrP ↑ ALP 🔴 Multiple Myeloma Due to osteolytic bone destruction. 🔻Labs ↑ Calcium ↓ PTH ↑ ESR ↑ Total protein M-spike on SPEP CRAB C → Calcium R → Renal failure A → Anemia B → Bone lesions 🔴 Vitamin D Toxicity Usually from supplement overdose. 🔻Labs • ↑ Calcium • ↓ PTH • ↑ 25-OH Vitamin D • ↑ Phosphate 🔴 Granulomatous Diseases (Sarcoidosis, TB) Macrophages produce excess 1-α hydroxylase → ↑ active vitamin D. 🔻Labs ↑ Calcium ↓ PTH ↑ 1,25-OH Vitamin D ↑ ACE 🔴 Milk-Alkali Syndrome Excess calcium + absorbable alkali. Common sources: Calcium carbonate antacids Calcium supplements Calcium + vitamin D tablets Classic triad Hypercalcemia Metabolic alkalosis Renal dysfunction 🟢 CLINICAL CHEAT CODE If Calcium ↑ Step 1 → Check PTH PTH ↑ → Parathyroid causes PTH ↓ → Malignancy, Vitamin D excess, Granulomatous disease, Drugs One lab directs the entire diagnostic pathway. #MedTwitter #MedX #Endocrinology

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Dr. Shiv_Kumar
Dr. Shiv_Kumar@Dr_Shiv_kumar_·
@DrNikhilMD Complete Heart Block (3rd-degree AV block) with AV dissociation ( Ventricular rate is 35-40bpm & atrial rate is more than the ventricular rate ) both are marching independent of each other + Severe bradycardia + Likely ventricular escape rhythm.
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Dr. Shiv_Kumar
Dr. Shiv_Kumar@Dr_Shiv_kumar_·
@JPCardio I totally missed that Inverted T’s in the lead aVL sir, thanks for pointing it out🙏🏼
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Dr. Shiv_Kumar
Dr. Shiv_Kumar@Dr_Shiv_kumar_·
🫀 Cardio- ECG pearls you should never miss as a clinician 🚨 8️⃣ One ECG. Same ST elevation. Two completely different diagnoses. One needs reassurance One needs treatment Can you tell the difference in seconds? ST Elevation: BER vs Pericarditis Diffuse ST elevation… 👉 Normal variant or pathology? This is a classic ECG dilemma most of us get stuck, let’s break it down. 🔹 1️⃣ Definition Early Repolarization (BER) → Normal ECG variant in healthy individuals Acute Pericarditis → Inflammation of pericardium affecting epicardium Both can look similar on ECG 🔹 2️⃣ Presentation BER : Chest pain & can be asymptomatic, Incidental finding Pericarditis: Chest pain (pleuritic, positional) May have pericardial rub Fever SOB 🔹 3️⃣ Physiology (Why ST changes?) Phase 2 - Calcium influx balanced by K+ efflux ST segment = plateau phase Normally flat Changes → altered repolarisation/ inflammation 🔹 4️⃣ Pericarditis ECG Breakdown 🔸 Diffuse ST elevation → Multiple leads involved - Widespread concave ST elevation and PR depression throughout most of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6) 🔸 PR elevation in aVR - Reciprocal ST depression and PR elevation in lead aVR (± V1) 🔸 Spodick sign → Downsloping TP segment (clinical add-on) 🔸 Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial effusion 🔸 Evolution over time- Stages of Pericarditis: Pericarditis is classically associated with ECG changes that evolve through four stages. 🔻Stage 1 – widespread STE and PR depression with reciprocal changes in aVR (occurs during the first two weeks) 🔻Stage 2 – normalisation of ST changes; generalised T wave flattening (1 to 3 weeks) 🔻Stage 3 – flattened T waves become inverted (3 to several weeks) 🔻Stage 4 – ECG returns to normal (several weeks onwards) (Less than 50% of patients progress through all four classical stages and evolution of changes may not follow this typical pattern) 🔹 5️⃣ Early Repolarization (BER) ECG specifications 🔸 J-point elevation (J-wave) → Notching/slurring - Widespread concave ST elevation, most prominent in the mid-to-left precordial leads (V2-5) 🔸 ST elevation : T wave height ratio in V6 < 0.25 + No reciprocal ST depression to suggest OMI. 🔸 Fish-hook sign (V4) → Classic notch at J point 🔸 Prominent T waves → Tall, symmetric 🔸 No PR depression 🔸 Stable ECG (no evolution) 🔹 6️⃣ How to Think Fast (ECG) PR depression (diffuse) → Think pericarditis Fish-hook J-point (V4) → Think BER Tall T waves? - Not specific→ Could be BER / hyperkalemia / early MI Still unsure? Look for reciprocal changes Check ST morphology Repeat ECG + correlate clinically 🔅Final Takeaway Pericarditis = inflammatory process BER = normal variant Same ECG pattern Completely different meaning ECG suggests. Clinical context decides. #MedTwitter #MedX
Dr. Shiv_Kumar tweet mediaDr. Shiv_Kumar tweet mediaDr. Shiv_Kumar tweet mediaDr. Shiv_Kumar tweet media
Dr. Shiv_Kumar@Dr_Shiv_kumar_

🚨Cardio-emergency pearls you should never miss as a clinician 7️⃣ In hypertensive crisis, the number misleads. The organs tell the real story lets break this down 🟥 HYPERTENSIVE EMERGENCY 🟨 SEVERE BP (NO ORGAN DAMAGE) 🔻1. Definition (Get this right first) Hypertensive crisis = BP ≥180/120 mmHg ⚠️ But classification depends on END-ORGAN DAMAGE, not the number: 🟥 Emergency → Acute target-organ injury 🟨 Severe BP → No injury 👉 Same BP. Completely different management. 🔻2. Terminology update 🟨 “Hypertensive urgency” → ❌ obsolete / discouraged 👉 Why? Misleading → overtreatment → harmful rapid BP lowering ✔️ Use: → Severe asymptomatic hypertension → Severe BP without organ damage 🔻3. Before labeling a crisis - verify BP. Pseudo-elevation is common. ✔️ Correct cuff size ✔️ Repeat after 5 min rest (seated, back supported) ✔️ Measure both arms (>15 mmHg difference → suspect vascular disease) ✔️ Check for: pain, anxiety, full bladder, recent caffeine/nicotine 👉 Many normalize → avoid unnecessary IV therapy 🔻4. Pathophysiology Chronic HTN → right-shifted autoregulation Acute rise → endothelial injury → fibrinoid necrosis + capillary leak → microangiopathy + ischemia Rapid BP fall → hypoperfusion → infarction 🔻5. Target Organ Damage (Defines EMERGENCY) 🧠 Neuro → encephalopathy, stroke, seizures ❤️ Cardiac → ACS, LV failure, pulmonary edema 🧂 Renal → AKI, hematuria/proteinuria 👁 Eye → papilledema, flame hemorrhages 🫀 Vascular → aortic dissection 🤰 Obstetric → preeclampsia/eclampsia 🔻6. MAP : what organs actually care about MAP = DBP + \frac{1}{3}(SBP - DBP) 👉 All targets are based on MAP reduction, not SBP alone. 🟨 SEVERE BP (NO ORGAN DAMAGE) 🔻7. Management (Do less, but do it right) ❌ No IV antihypertensives ❌ No rapid BP reduction ✔️ Start/adjust oral therapy ✔️ Identify triggers (pain, NSAIDs, steroids, non-adherence) ✔️ Reinforce compliance ✔️ Follow-up in 24–72 hrs ⚠️ Rapid lowering here → stroke / syncope risk 🟥 HYPERTENSIVE EMERGENCY 🔻8. Core principle - Controlled reduction: • 1st hour → ↓ MAP ≤25% • Next 2–6 hrs → ~160/100–110 mmHg (slight correction) • 24–48 hrs → gradual normalization ❌ Never normalize immediately 🔻9. Why this matters Chronic HTN → shifted autoregulation Rapid drop → hypoperfusion → → Stroke → MI → AKI 🔻10. Condition-specific targets 🫀 Aortic dissection → SBP <120 + HR <60 (within minutes) → IV beta-blocker FIRST (then vasodilator) 🧠 Ischemic stroke → No thrombolysis: allow ≤220/120 → Thrombolysis:  Before: <185/110  After: <180/105 🧠 ICH → Target SBP ≈ 140 → Avoid <130 💦Pulmonary edema → IV nitroglycerin + diuretics 🤰 Preeclampsia/eclampsia → Labetalol / Hydralazine → MgSO₄ (seizure prophylaxis) sympathomimetic → ❌ Avoid pure β-blockers → Use benzodiazepines + vasodilators 🔻11. IV drugs (Know your weapons) ✔️ Nicardipine ✔️ Labetalol ✔️ Esmolol ✔️ Clevidipine ✔️ Nitroglycerin ⚠️ Nitroprusside → last resort (cyanide toxicity & sudden hypotension) 🔻12. Investigations (Don’t miss organ damage) 🧪 Labs: CBC, creatinine, electrolytes Troponin, LDH Urinalysis (protein/hematuria) Imaging: ECG CXR CT brain (if neuro signs) Echo (if cardiac involvement) 🔻BEDSIDE CLINICAL EXAM (MUST DO) General Mental status → encephalopathy? Seizures / confusion Vitals BP in BOTH arms Pulse deficit → Aortic dissection Eye (Fundoscopy) Papilledema → emergency Hemorrhages/exudates Cardiac S3 → LV failure New murmur → dissection (AR) Respiratory • Crackles → pulmonary edema Neuro • Focal deficits → stroke Peripheral • Weak/absent pulses → vascular cause 🔻14. Pitfalls (Exam + real life traps) ❌ Treating numbers blindly ❌ Overcorrection (>25% drop early) ❌ Missing aortic dissection ❌ Giving IV drugs in non-emergency ❌ Not doing fundoscopy #MedTwitter #MedX #Cardiology

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JP Mishra, MD, FACC
JP Mishra, MD, FACC@JPCardio·
@Dr_Shiv_kumar_ Excellent breakdown of this ECG description. I just wanted to say that the very small voltage in lead I that you mentioned here is described in some books as Lead I Sign, something easier for the cardiology fellows and the residents to remember!
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Dr. Shiv_Kumar
Dr. Shiv_Kumar@Dr_Shiv_kumar_·
Sinus tachycardia, 110/min Biatrial enlargement Right superior axis deviation This ECG shows typical findings seen in patient with chronic lung disease: 🔻Tall peaked P waves in the inferior leads: right atrial enlargement 🔻The prominent negative component of the P in V1 (commonly seen in patients with chronic lung disease) may be due to shift of the cardiac position due the lower diaphragm, rather than to left atrial enlargement. 🔻Right axis deviation 🔻Small QRS voltage in leads 1 and aVL 🔻Delayed R/S transition point in the precordial leads (the R becomes taller than the S in V5)  #MedTwitter #MedX
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C.Alberto Ortega@albertoortegana

A 65-year-old man with severe chronic obstructive lung disease has been admitted to the intensive care unit for treatment of broncho-pneumonia. @dr_manish_ydv @Dr_Shiv_kumar_ @DrMedica_13 @drobiy12 @DrsansariOrd @hemo_shk @MiguelP23970914 @shakilED

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JP Mishra, MD, FACC
JP Mishra, MD, FACC@JPCardio·
@hyderabaddoctor A beautiful positive story with truly a great outcome! Congratulations to you for your hard work as well. Well composed writing! Thanks for sharing!
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Dr Sudhir Kumar MD DM
Dr Sudhir Kumar MD DM@hyderabaddoctor·
When a Little Toe Moved Menaka was 25. She had just started her dream job at a leading technology company. A bright B. Tech graduate from a reputed college. Her parents were proud. She was excited. Life had just begun to unfold beautifully. Two weeks before everything changed, she had a mild fever. It lasted three days. It was labeled a “viral fever.” She recovered and moved on. Then, suddenly, over just two days, she became weak. First her legs. Then her hands. Then she could barely move. By the time she reached a nearby hospital, her condition worsened dramatically. She became unresponsive. Her breathing failed. She was intubated and placed on a ventilator. That was when she was referred to us. MRI brain, MRI spine, and cerebrospinal fluid analysis pointed to Acute Disseminated Encephalomyelitis (ADEM), a rare, immune-mediated inflammatory condition of the brain and spinal cord. It often follows a viral infection. The body’s immune system, instead of settling down, mistakenly attacks the brain. And in Menaka’s case, it was fulminant. We had very little time. We explained everything to her family; the diagnosis, the uncertainty, the risks. She was deeply comatose. We started high-dose intravenous steroids, the standard first-line treatment for ADEM. Five days passed. There was no improvement. In fact, she worsened. Her parents sat outside the ICU, waiting for hope in every footstep that came toward them. We decided to escalate treatment. Plasma exchange (plasmapheresis), a procedure that removes harmful antibodies from the blood, is recommended in severe, steroid-refractory ADEM. After the first session, something extraordinary happened. Her little toe moved. It was subtle. Almost invisible. But we saw it. Her eyes opened briefly. She was not following commands. She was not making eye contact. But we knew, something had shifted. With each plasma exchange session, there were small, fragile signs of improvement. Every morning during rounds, we spoke to her. “Menaka, open your eyes.” Silence. “Menaka, move your hand.” Nothing. After rounds, the hardest part was facing her family. Telling them, again and again, that she was still deeply unconscious. Watching hope struggle against fear in their eyes. Two weeks passed in the ICU. She was still on the ventilator. And then, one morning, during rounds, I said, “Menaka, open your eyes.” She opened them. “Raise your hand.” Her fingers trembled. Just slightly. But they moved. That was enough. I walked out of the ICU faster than usual that day. Her parents were standing there. I said only one sentence: “She responded.” The relief on their faces, that mixture of disbelief and gratitude, is something no textbook can teach. Over the next two weeks, she gradually improved. She was weaned off the ventilator. She was discharged with significant limb weakness, but alive, conscious and recovering. We advised intensive physiotherapy and rehabilitation. One month later, she walked into my OPD. Not in a wheelchair. Not on a stretcher. Walking. I asked, “What problems are you facing now?” She looked thoughtful and said, “Doctor, my nails are dark. They don’t look nice.” “Anything else?” “No, Doctor. I am absolutely fine. I want to rejoin office, but I feel awkward with dark nails. Can you give me medicine for that?” In that moment, I realized something profound. A month ago, we were fighting for her life. Now, she was worried about how her nails looked at work. I smiled and said, “There is a simple solution. Apply nail polish. Any color you like. You can even change it every month.” She smiled widely and freely, the kind of smile that belongs to someone who has unknowingly crossed the edge of life and come back. And I felt something every doctor knows but rarely speaks about: There is no greater reward than seeing a patient and family smile after surviving what once felt impossible. Sometimes recovery announces itself loudly. Sometimes it begins with a little toe. Dr Sudhir Kumar @hyderabaddoctor (Note: The name has been changed to protect privacy. Image is AI-generated)
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Dr. Shiv_Kumar
Dr. Shiv_Kumar@Dr_Shiv_kumar_·
ECG alert 🚨 A 58-year-old male presents with: • Intermittent palpitations for 3 months • Occasional lightheadedness • No chest pain • No syncope • BP well controlled on medications • No known structural heart disease Physical examination is unremarkable. ECG below 👇 What’s the diagnosis? 🔍 #MedTwitter #MedX #CardioTwitter #ECGChallenge @GangulySho56067 @Ecgloverr @DocPriyamMD @albertoortegana @ECG_BUDDY_ARPI @ecgandrhythmRoe @ecgrhythms @aldoferly @drobiy12 @usernamee389 @DrAGernsback @_mehdibennis @MedLearnHub @medcrux @Medzonetv @BodyExplained @khannaa @momochaname @chi_no_usagi
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JP Mishra, MD, FACC
JP Mishra, MD, FACC@JPCardio·
@hyderabaddoctor A cup of coffee: 100-200 mg caffeine. 1 cup of tea: 50-75 mg caffeine. How come then study revealed we need a fewer cups of tea than coffee to get the same effect when the effect is mostly caffeine driven?
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Dr Sudhir Kumar MD DM
Dr Sudhir Kumar MD DM@hyderabaddoctor·
That morning cup of coffee might be doing more than just waking you up; it could be a powerful tool for long-term brain health. A massive new study just published in JAMA (following 131,000+ participants for over 40 years) reveals a significant link between moderate caffeine intake and a lower risk of dementia. Main findings: 1. The "Sweet Spot" for Protection The most pronounced benefits were seen in those consuming: ✅Coffee: 2 to 3 cups of caffeinated coffee per day. ✅Tea: 1 to 2 cups of caffeinated tea per day. 2. The 18% Advantage Participants with the highest intake of caffeinated coffee had an 18% lower risk of dementia compared to non-consumers. They also reported significantly lower rates of subjective cognitive decline. 3. It’s All About the Caffeine Interestingly, the study found no protective effect from decaffeinated coffee. This suggests that caffeine itself is the active neuroprotective agent, likely due to its ability to block adenosine receptors which reduces inflammation and cellular damage in the brain. 4. Long-Term Evidence This was not a short-term trial. With data spanning 4 decades, the results held steady even after adjusting for age, smoking, and genetics. For those under 75, the risk reduction was even more striking, reaching up to 35%. ✅The Takeaway: Dementia has no cure, making preventive lifestyle choices critical. If you already enjoy a few cups of coffee or tea daily, your brain may be reaping the benefits. Dr Sudhir Kumar @hyderabaddoctor #Health #Neurology #DementiaPrevention #Coffee #BrainHealth #MedicalNews #Longevity
Dr Sudhir Kumar MD DM tweet mediaDr Sudhir Kumar MD DM tweet media
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JP Mishra, MD, FACC
JP Mishra, MD, FACC@JPCardio·
@RitikaTuliMD Sometimes our collective wisdom gives us mixed signals: 1. The guidelines would say NOT to do a stress test until symptoms. 2. Do a plain treadmill 1st. 3. Many health insurance co. won’t allow Nuclear stress tests. 4. I wonder PET now: superior to SPECT?
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JP Mishra, MD, FACC
JP Mishra, MD, FACC@JPCardio·
@physiosign Please read the red and the blue circles annotations. Is there typo (reverse changes noted, text vs the image) or am I not understanding the concept here? Thank you.
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Benny Lau
Benny Lau@physiosign·
*WPW with CAD* In routine clinical practice, standard electrocardiograms (ECGs) identify common conduction and rhythm abnormalities such as premature beats, atrial fibrillation or flutter, bundle branch blocks, atrioventricular blocks, Wolff-Parkinson-White (WPW) syndrome, tachycardias, and bradycardias. These patterns frequently represent secondary electrical phenomena. Critically, they can obscure the underlying primary pathology: acute coronary syndromes, including ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and acute coronary syndrome (ACS)—encompassing myocardial infarction and unstable angina. This diagnostic limitation stems from the technical focus of conventional ECG acquisition, which primarily captures high-frequency electrical signals. Since the 1970s, a period marked by the rising prevalence of coronary artery disease, clinicians have faced the persistent challenge that these prominent high-frequency patterns can mask the more subtle, often low-voltage, electrocardiographic signs of acute, evolving, or prior myocardial ischemia and infarction. Example: A 52-year-old man undergoing two ECG synchronization tests prior to angiography. Coronary angiography (CAG) subsequently confirmed the findings, revealing a 95% blockage in the LCx and 65% stenosis with generalized plaque in the RCA. [A] Existing ECG: Only demonstrates the WPW pattern (delta wave), with no clear signs of myocardial infarction or ischemia. [B] new ECG: While this does not alter the standard (ECG) itself, it allows for the recording of detailed local electrical signals. In the atrial area (red circle), the technique clearly delineates the HV interval. A side-by-side comparison reveals that this specific signal is embedded within the Delta wave. This marks the first time in cardiac electrophysiology that the precise local signals folded into the Delta wave—and the reason for its appearance—have been clearly demonstrated. In the ventricular area (blue circle): Reveals epicardial injury currents and allows precise measurement of the ST segment duration (exact time length - ST segment 209.36ms) - ST segment < 120ms**considered the gold standard in textbooks. [C] Back in the 1980s, experts already recognized that the duration of the ST segment (i.e., its time length along the X-axis) is important for diagnosing ischemia — rather than just ST-segment elevation or depression (Y-axis amplitude). Annotation: “S-T interval = ST segment + T wave, but traditional ECGs cannot measure it accurately. PhysioSign USA #Cardiology #ECG
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