1/4 The patient was labeled as 'NSTEMI' in the ED. Once a patient is labeled 'NSTEMI', clinical inertia can begin. Troponin: 96–120 (ULN: 14). Not dramatically elevated. Plan? CAG within 24h. Admitted to CCU, but no beds were available, so monitoring continued in the ED.

Beyond stenosis: imaging phenotyping and risk stratification in nonobstructive coronary artery disease shorturl.at/fI2bu @pamelapina_s @AnnalisaFiltz @danilorenzatti @Ankurdee1 @JaideepBha35378 @Piotr_JSlomka @danielbermanmd @damini_dey @MonteHeart @MontefioreNYC @EinsteinMed

🫀Before calling septic shock “refractory,” look again. A patient remains hypoperfused. Norepinephrine requirements continue to rise. Additional vasopressors are being considered. It is tempting to conclude that we are dealing with refractory septic shock, but high vasopressor requirements do not necessarily mean true refractoriness. Melo et al propose a framework for distinguishing an apparent refractory trajectory from established refractory septic shock. The question at the bedside therefore becomes: What potentially reversible mechanism is still sustaining hypoperfusion or increasing vasopressor requirements? The authors describe these mechanisms as the “usual suspects.” First comes the foundation: adequate antimicrobial therapy and source control. Without control of the infectious stimulus, optimization of fluids and vasoactive drugs cannot eliminate the underlying inflammatory and vasoplegic drive. Then comes fluid status, but with an important evolution beyond simply asking whether the patient is “fluid responsive.” We should evaluate three different concepts ALWAYS fluid Responsiveness, Tolerance, cardiac efficiency. A patient can therefore be fluid responsive but fluid intolerant, and even an initial hemodynamic response may disappear rapidly. Fluid responsiveness alone is not an indication for fluid administration. Persistent vasoplegia should also trigger evaluation of potentially reversible endocrine, metabolic and iatrogenic contributors. Corticosteroid insufficiency, relative vasopressin deficiency, severe acidemia and excessive sedation may all increase apparent catecholamine resistance. Importantly, sedation itself can reduce venous tone, venous return, myocardial contractility and vascular tone, potentially increasing preload dependence and vasopressor requirements. Sepsis induced myocardial dysfunction may involve LV systolic or diastolic dysfunction, RV dysfunction or hyperdynamic phenotypes. The authors also emphasize VAC. Increasing arterial pressure by increasing effective arterial elastance may improve pressure and flow when ventricular reserve is adequate, but in another patient it may create afterload mismatch: MAP rises while stroke volume and tissue perfusion deteriorate. Dynamic LVOT obstruction represents another easily missed mechanism. Low preload, low afterload and hypercontractility can generate obstruction and paradoxically reduce stroke volume despite an apparently excellent ejection fraction. More catecholamine stimulation can make the problem worse. Reference 📚 Melo, P., Wendel-Garcia, P. D., Leone, M., Khanna, A. K., Morales, S., Ospina-Tascón, G. A., Castro, R., Hernández, G., & Kattan, E. (2026). The usual suspects: A pragmatic framework to identify and address reversible contributors in apparent refractory septic shock. Critical Care, 30, 378. doi.org/10.1186/s13054-026-0…

I trained in a residency program without fellows, and we consulted subspecialists when something was truly beyond the scope of general internal medicine. Our attendings expected us to build a strong foundation and make decisions grounded in that knowledge. That foundation has served me throughout my career, and I sometimes find it surprising how often we now consult for problems that most internists should be comfortable managing. Atrial fibrillation in sepsis. Community-acquired meningitis. Many of these situations benefit more from thoughtful generalist care than an automatic specialty consult. I remember one of my first ICU admissions as a fellow in Seattle. The diagnosis was classic Pneumocystis pneumonia in a patient with advanced HIV. We discussed why he needed TMP-SMX, when steroids were indicated, and what to expect clinically. The immediate question from the residents was, “When do we consult ID?” My response was, “For what?” If the consult is to help with ART planning and longitudinal HIV care, absolutely. If it’s because we’re uncomfortable treating a textbook presentation ourselves, that’s a different issue. I worry we’ve gradually trained generations of physicians to seek subspecialty input before they’re comfortable applying their own knowledge. Some of that is appropriate because medicine is more complex than ever. Some is driven by fear, culture, or medicolegal concerns. But there is a cost. The best subspecialists are built on a strong foundation in general internal medicine. If trainees never develop the confidence to manage common problems independently, we risk weakening the very foundation that makes excellent specialists possible.

Absolutely practice changing!! One of the most stunning developments in the treatment of patients with metastatic pancreatic cancer !! It is one of the rare moments in oncology which you will always remember ! Like the imatinib, trastuzumab presentations @ASCO #ASCO26 @OncoAlert

🎉 Monday night's #SHOCKTalks NYC was everything we hoped for — and more! 40 critical care cardiology professionals packed the room at Tara Mor for ~3 hours of lively, case-based discussion. The energy was incredible. Thank you to the planning team and to every faculty member, trainee, and enthusiast who joined us. This is exactly why we do what we do. 🫀 Support provided by @MedicalZoll @ChiesiGroup @jjmt_heartrecov #CriticalCareCardiology #CICU #CardiacCare #C3E #MedTwitter

🙌 Our last manuscript is out. 👉“Safety of Very Low LDL-Cholesterol: Ten Common Concerns, Misconceptions, and Evidence-Based Clarifications” 📍Very low LDL-C levels continue to generate debate, fear, and misinformation in clinical practice. 📍In this review, we critically examined 10 of the most frequent concerns related to intensive LDL-C lowering: — Cognitive decline — Hemorrhagic stroke — Cancer — Cataracts — Hormonal dysfunction — Diabetes risk — Muscle symptoms — Older adults — Sex differences — Overall cardiovascular benefit 📍The key message is clear: RCTs, meta-analyses, and genetic evidence consistently support the safety profile of very low achieved LDL-C levels in appropriately selected high-risk patients. 📍Some adverse effects are real — particularly statin-associated dysglycemia and muscle symptoms — but their absolute risk is generally modest compared with the magnitude of ASCVD risk reduction. 📍Therapeutic inertia and misinformation remain major barriers in preventive cardiology. Evidence-based communication matters. 📍Lower LDL-C. Earlier. Longer. Safer than many still believe. ☝️Proud to collaborate with outstanding colleagues from Latin America, Europe, and beyond in this international effort. 🔗 doi.org/10.1016/j.atheroscle… @society_eas @ATHjournal

Maternal Cardiac Disease and Heart Disease Risk in Offspring jamanetwork.com/journals/jam…

We’re excited to invite you to our upcoming SHOCK TALKS Dinner! 📅 May 4 📍 Tara Mor, NYC 🔗 bit.ly/4sml4Rx Join us for an engaging evening bringing together critical care cardiology faculty, trainees, and enthusiasts for dynamic, case-based discussions. Together, we’ll explore the care of critically ill cardiac patients, compare approaches across institutions, and dive into complex cases from the CICU, cath lab, cardiac OR, and emergency department. Looking forward to a night of learning, collaboration, and great conversation. #CriticalCareCardiology #Cardiology #MedEd #CICU #ShockTalks

The American Heart Association mourns the passing of the legendary cardiologist Eugene Braunwald, M.D., widely recognized as one of the most influential figures in the history of cardiovascular medicine. Over seven decades, his work reshaped the understanding and treatment of heart disease, leading many to call him the father of modern cardiology. Braunwald was a lifelong contributor to the American Heart Association, helping advance its research and scientific mission, and was honored with some of the Association’s highest honors for his lasting influence on cardiovascular care and research. His influence extended well beyond his own discoveries, as generations of Association‑supported investigators, clinicians and academic leaders were trained by Braunwald or guided by the clinical trial standards and mentorship models he helped establish. newsroom.heart.org/news/amer…

Congratulations, Dr. Klein, on this incredibly high honor! It has been an everlasting privilege to learn under your mentorship. A well-deserved recognition of your lasting contributions to cardiovascular research that has shaped key clinical practice guidelines! @ACCinTouch

HARP study: OCT + CMR identified an underlying cause in 79% of MINOCA presentations; clinical factors had limited utility in predicting imaging abnormalities. #ACC26 Download slides here: clinicaltrialresults.org/wp-…

Presented at #ACC26: Among patients with atherosclerotic cardiovascular disease, targeting an LDL cholesterol level below 55 mg per deciliter led to a lower 3-year risk of cardiovascular events than targeting a level below 70 mg per deciliter. Full Ez-PAVE trial results: nejm.org/doi/full/10.1056/NE… Editorial: Paving the Road toward Targeted Lipid Lowering nejm.org/doi/full/10.1056/NE… @ACCinTouch

Presented at #ACC26: In patients with pulmonary embolism, ultrasound-facilitated, catheter-directed fibrinolysis led to a lower risk of a composite of major adverse outcomes than anticoagulation alone. Full HI-PEITHO trial results: nejm.org/doi/full/10.1056/NE… Editorial: Advanced Therapy for Intermediate-Risk Pulmonary Embolism nejm.org/doi/full/10.1056/NE… @ACCinTouch

#ACVC 2026: Mixed shock: the reality behind cardiogenic shock An outstanding session by Dr. David Morrow. Morrow highlighting a critical and often under-recognized concept: 👉 Pure cardiogenic shock is rare. Mixed shock is common. 🔍 Key messages: SVR is not always elevated in cardiogenic shock → Wide variability, often with vasoplegia (SIRS component) Mixed shock = low CO + inappropriately low SVR → A combination of cardiac failure + vasodilatory physiology 📊 Epidemiology (SHARC data): .Cardiogenic shock (isolated): ~65% .Mixed shock: ~17% .Mortality highest in mixed shock (~48%) 🧠 Common phenotypes: -Cardiogenic shock → secondary vasoplegia -Cardiac arrest → stunned myocardium + vasodilation -Sepsis + cardiac dysfunction -Toxic cardiomyopathy (e.g., Ca-blockers, BBs) -Post-cardiotomy vasoplegia ⚙️ Pathophysiology: Inflammation (SIRS) plays a central role Microcirculatory dysfunction + iNOS activation Loss of vascular tone despite vasopressors ⚠️ Clinical implication: 👉 Hemodynamics must be interpreted dynamically, not assumed 👉 SVR ≠ always high → avoid “one-size-fits-all” approach 🛠️ Management principles: Phenotype-guided therapy Combine: Vasopressors (norepinephrine first-line) Inotropes when needed Careful fluid strategy Consider: .Methylene blue / hydroxocobalamin in refractory vasoplegia .CIRCI (steroids) in selected patients 📌 Take-home message: Cardiogenic shock is not purely cardiac. Recognizing the vasoplegic component is key to survival. #ACVC26 #CardiogenicShock #MixedShock #CriticalCare #Hemodynamics #ShockManagement

1/9 The 2026 ACC/AHA Dyslipidemia Guidelines are officially here! Replacing the 2018 guidelines, these new updates bring major shifts in risk assessment, novel lipid markers, and cholesterol targets. Here are the most salient features you need to know. 🧵👇 #Cardiology #MedTwitter

1/8: The cardiology world is buzzing! Two major randomized trials—HeartSync-LBBP and PhysioSync-HF—recently compared Conduction System Pacing (CSP) vs. Biventricular Pacing (BiVP) in heart failure patients with LBBB. Surprisingly, they reached opposite conclusions! Let’s break them down. 🧵👇

Excellent video explaining cardiac axis determination