Diabetes causes coronary atherosclerotic disease by reducing nitric oxide (NO) production and increasing thromboxane A2 activity which cause endothelial dysfunction. As we age, NO levels also decrease which is associated with cardiovascular disease, loss of immune and neural function. Control your sugar levels, eat well and exercise regularly. 🏃🏻‍♂️

What is interesting in this ECG?#EPeeps

Eugene Braunwald, ‘Icon’ of Modern Cardiology 🫀, Dies at 96. What a legacy. tctmd.com/news/eugene-braunw…

What a wonderful session on PVCs at #ACC26 ⚡🫀 ❓Should every patient with frequent PVCs get a cardiac MRI? ❓What to do with Asymptomatic PVCs? Key insights below 👇 #CardioTwitter #EPeeps #ACCEP

This might seem inappropriate, but Japanese electronic bidet toilets blew me away 😅 heated seat and water. 🤯 What is the purpose of the top part though..?

Temporary pacing can be accomplished by: 1. Transcutaneous (TCP) 2. transvenous 3. epicardial This lead is from a TCP capture with a Zoll monitor-defibrillator. It has a square pacing spike, other external pacemakers may have a different pacing artifact. Kudos to few of you who got it!

Clopidogrel is superior to aspirin for cardiac outcomes beyond 1-year up to 5-years. Results from the STOPDAPT-2 ACS and STOPDAPT-2 Total Cohort. Should it be a lifelong maintenance therapy? @HirotWatanabeMD @MNatsuaki @KoYamamoto7 ahajrnls.org/3PlxLhD

左室前乳頭筋起源のPVC（VT）の場合、 「下壁誘導がdiscordant pattern、つまりⅡ（−）Ⅲ（＋）」になるのがポイント🫀 起源推定で覚えておくべきめちゃつよ所見📝✨ しっかり覚えたはずなのに復習しないと忘れるー！🥲

What causes coronary thrombosis? 1. White plaques/ thrombus (Plaque erosion)⚪️ 🔹Platelet-rich 🔹Intact fibrous cap 🔹often presents as NSTEMI/ UA. 2. Red plaques/ thrombus (Plaque rupture)🔴 🔹Fibrin-rich, lipid-rich necrotic core ➡thin-capped fibroatheroma (TCFA) 🔹Rupture of this vulnerable plaque often results in STEMI due to transmural ischemia. Inflammation increases breakdown of collagen fibrils that protect the plaque from rupture, and increases fibrinogen. Statins don't just lower LDL, they limit inflammation. This is why we give high intensity statins before the LDL even comes back from the lab.

66yo man in the ICU, what happened here? 🤔

Finally published: the COBRRA trial, the first randomized head-to-head comparison of major DOACs — something the companies would never have done themselves, as a direct confrontation goes beyond their commercial interests. This was driven by independent investigators. The results somewhat support the idea of apixaban being the “safer” DOAC. That said, the list of study limitations is long, and for me, labeling something as “safe” is not enough — after all, even placebo is “safe” when it comes to bleeding. nejm.org/doi/full/10.1056/NE…

When QRS complex is wide, look for the "slow start". In VT, electricity travels through the muscle instead of the Purkinje highway. This creates the delay at the beginning of the QRS. In blue (🔵)here, Josephson's sign. - notching/ slurring near the lowest point of S wave. - usually more obvious in precordial leads (V1-V3). In green (🟢), Brugada's sign. - RS interval >100ms (2.5 small boxes) in any precordial leads (V1-V6). - due to slow, inefficient cell-to-cell conduction of a ventricular focus (in contrast, SVT with aberrancy conducts down the bundle branches fast enough that the RS is <100ms).

Typical Counterclockwise (CCW) Atrial Flutter〰️🫀 🔹Inferior leads: Classic negative "sawtooth" pattern. Look for slow downstroke followed by a rapid upstroke. 🔹Lead V1: Upright (positive) P waves with distinct isoelectric segment between them. In our case, the ventricular rhythm is IRREGULAR. This means you have variable AV conduction. 💡Tip for counting flutter waves: Grab a pencil✏️, put the tip at the end of the QRS complex and count every downward dip of the "V" as one flutter wave, including the "V" that goes into the next QRS complex. This patient has alternating 5:1 and 4:1 block.

Ace of Spade is found in⁉️

Pacing for AVB.🫀 What falls under the ominous Infrahissian (Infranodal) block category? 🔹Second-degree Mobitz II 🔹High degree AVB 🔹Infranodal 2:1 AVB 🔹Complete AVB (specifically when the anatomical block is below the AVN, usually with wide QRS escape). According to @escardio, pacing is CLASS I indication for Mobitz II, high degree, and third-degree AVB irrespective of symptoms! 2:1 AVB can be Type I (nodal) or Type II (infranodal). If the patient is asymptomatic, put them on a treadmill 🏃🏻‍♀️ ⒈ Nodal (Type I): Exercise increases sympathetic and reduces vagal tone, improving AV nodal conduction.✅ ⒉ Infranodal (Type II): the diseased His-Purkinje system cannot handle the increased atrial demand. Conduction worsens (e.g. drops to 3:1 block).❌