Emmanuel Daniel

Cardiovascular disease fellow @Wayne cardio | former CMR @ Trinity Health Ann Arbor | Interested in interventional/critical care card + MedEd #cardiorounds

[Emmanuel Daniel @eodanielmd]

Starting a #cardioround series. Will aim for 1-2 tweets per day.

[Emmanuel Daniel @eodanielmd]

#cardiorounds

[Emmanuel Daniel @eodanielmd]

🫀 The "square root sign" (√) on cath:
• Sharp early-diastolic DIP in ventricular pressure
• Rapid rise to an elevated PLATEAU the rest of diastole
• 👉 to impaired ventricular filling
Ddx ➡️constrictive pericarditis or RCM

To tell apart ? Look for ventricular dependency

[Emmanuel Daniel @eodanielmd]

#cardiorounds

[Emmanuel Daniel @eodanielmd]

Tachycardia & mitral stenosis 🫀
• ⬇️⏱️ in diastole → less time to cross a narrow valve.
• Incomplete LA emptying → mean LA pressure ⬆️. MG (LAP - LVP) ⬆️.
• Sx- 🫁 edema.
• Cath hallmark: persistent LA–LV diastolic gradient, no diastasis.
• 💊 Rate control - BB.

[Emmanuel Daniel @eodanielmd]

#cardiorounds

[Emmanuel Daniel @eodanielmd]

🫀 The Treppe (Bowditch) effect:
• ↑ HR → ↑ contractile force

• Mech: faster pacing → more Ca²⁺ influx/time → more Ca²⁺ in the cytosol vs SR→ stronger contraction

• ≠ Frank-Starling (that's preload driven, not HR-driven)
• In failing 🫀 the staircase reverses

[Emmanuel Daniel @eodanielmd]

#cardiorounds

[Emmanuel Daniel @eodanielmd]

Post-extrasystolic potentiation (PESP) 🫀

• Sinus beat after a PVC contracts harder → higher systolic BP
• Driven by Ca²⁺ force-interval relationship
• Pause loads the SR → bigger next Ca²⁺ transient
• High PESP + fewer "ejecting" PVCs may flag PVC-cardiomyopathy

[Emmanuel Daniel @eodanielmd]

🔊 Why ultrasound gel?
• Air between probe & skin = huge impedance mismatch → ~100% of the beam bounces back, no image
• Gel fills the gap & matches skin, so sound passes cleanly I&Out
• Result: better penetration + sharper image
• Kills air-gap artifacts ! #cardiorounds

[Emmanuel Daniel @eodanielmd]

#cardiorounds

[Emmanuel Daniel @eodanielmd]

🫀 The Brockenbrough–Braunwald���Morrow sign — a hallmark of dynamic LVOT obstruction in HOCM
- Noted after a premature beat

- See previous tweet on post-extrasystolic potentiation (PESP)

[Emmanuel Daniel @eodanielmd]

🫀 When NOT to close a VSD:

🚫 Eisenmenger physiology (Class 3: Harm)
🚫 Nonrestrictive VSD w/ PVR >10 WU — prohibitive surgical risk
🚫 Qp:Qs <1.5 & no other indication (Class 3: No Benefit)
⚠️ PVR 5–8 WU = gray zone → treat-and-repair, close only if PVR <5 WU

#cardiorounds

[Emmanuel Daniel @eodanielmd]

Spotting a CTO on cath🫀
🔴 Blunt/tapered proximal cap, no lumen (TIMI 0)
🔴 No fresh thrombus or contrast staining
🔴 Calcification along the occluded segment
🔴 Well-developed, mature collaterals filling the distal vessel
🔴 Hard, resistant cap on wiring
#cardiorounds

[Emmanuel Daniel @eodanielmd]

@aldoferly Ablate when medications are ineffective

[Emmanuel Daniel @eodanielmd]

Fascicular VT 🫀
The most common idiopathic LV VT — seen in young, structurally normal hearts. Classically verapamil-sensitive (Purkinje re-entry).
📈 ECG: RBBB with a narrow-ish QRS (<140ms), leftward axis usually
▪️ Acute Rx: IV verapamil
▪️ Ablation: >90% success
#cardiorounds

[Emmanuel Daniel @eodanielmd]

@anishgeorgephi1 Yes you can visualize the distance on different views

[Emmanuel Daniel @eodanielmd]

🫀 Arrhythmic Mitral Valve Prolapse

‼️ MVP subset where SCD risk is INDEPENDENT of MR severity—even mild MR can kill.
🔑 Watch for:
• Bileaflet prolapse + MAD
• Young women, EKG- inferior TWI, PVCs/NSVT
• "Pickelhaube sign" (>16 cm/s)
• CMR fibrosis: basal inferolat wall

[Emmanuel Daniel @eodanielmd]

#cardiorounds

[Emmanuel Daniel @eodanielmd]

🫀 Gerbode Defect
• ���️ Typical VSD → L→R shunt → LA + LV enlarge (not RV)
• 🔄 Why not RV? Systolic jet ejects straight to PA — RV is a conduit; volume returns via lungs → LA → LV
• 💠 Gerbode = LV→RA shunt → RA + RV enlarge
• ⚠️ Mimics severe TR / pulmonary HTN

[Emmanuel Daniel @eodanielmd]

#cardiorounds

[Emmanuel Daniel @eodanielmd]

Turner Syn & Aortic Risk 🧵
~100x ⬆️ risk of dissection. Cos of short stature, index aortic area to BSA
📋 Baseline TTE + cMRI at diagnosis
🔁 Screen q5–10y (more if RF: BAV, coarctation, HTN, growth >3mm/yr) & before🤰
📅 Annual imaging if ASI >2.3 cm/m²
🔪 referral at ASI >2.5

[Davide Capodanno @DFCapodanno]

The day after the announcement of the neutral results of HORIZON Lp(a), and while keeping in mind that nobody has yet seen the final results (although, in practical and regulatory terms, that may matter little), much of the discussion is focusing on Lp(a) as a prognostic risk-stratification marker.
The argument goes: “If you, as a patient, have high Lp(a), then you are a high-risk patient, and I will intensify the therapies I have available”—starting from the assumption that, without knowing your Lp(a), I would somehow not have done so based on other available biomarkers and clinical features.
But this raises at least two other questions.
First: what therapy has evidence specifically in patients with elevated Lp(a)? Are there trials of non-Lp(a)-lowering drugs conducted specifically in patients with elevated Lp(a) (all patients, not just a subgroup—no cheating)?
Second: if universal Lp(a) screening is indeed useful even though we have no evidence that lowering Lp(a) improves outcomes, are there at least studies showing that knowing the Lp(a) level improves outcomes? In other words, are there trials in which physicians—not patients—are randomized to know versus not know the Lp(a) value, and therefore to act accordingly (e.g., prescribing exercise or other therapies that physicians in the control group would presumably consider anyway)?