Hey CEOs:

When people don’t want to work long hours, it doesn’t mean they’re lazy. It means they have lives beyond work.

A team delivering 40 hours of excellence is worth more than one offering 50 of mediocrity.

What counts is the value people create, not the time they put in.

sciencedirect.com/science/articl…

In toxic cultures, rest is taking your foot off the gas. You're forced to push yourself to exhaustion—burnout is a price to pay for excellence.

In healthy cultures, rest is a supply of fuel. You're expected to take regular reprieves—breaks are vital to gain and sustain energy.

Is Peripartum Cardiomyopathy an inflammatory disease?Jana Lovell ⁦serum proteomics analysis says: yes! Points to immunomodulatory cholesterol metabolism related pathways as regulators of recovery⁩JACC Journals⁩ Johns Hopkins Cardiology⁩ #cardiacimmunology sciencedirect.com/science/articl…

The Promise and Risks of mHealth in Heart Failure Care onlinejcf.com/article/S1071-…

Fresh in press 🔥 🔥 🔥

SCALE-HF 1 is the first study to develop and evaluate the performance of a composite index derived from noninvasive hemodynamic biomarkers measured from a cardiac scale in predicting worsening HF events.

Open access Circ: Heart Failure

Marat Fudim, MD MHS Adam DeVore, MD, MHS

ahajournals.org/doi/full/10.11…

Very exciting to begin 1 year tenure as President of SCAI Now #SCAI2023 Icahn School of Medicine at Mount Sinai Mount Sinai Health System Mount Sinai Fuster Heart Hospital American College of Cardiology AHAMeetings

⁦Muthu Vaduganathan⁩ presenting a prespecified analysis of #PARAGON and #PARAGLIDE

Sac/Val reduces clinical events in acute or recently acute HFpEF particularly in those with EF <60%

#Heartfailure2023

Grateful to share results of PARAGLIDE-HF on behalf of tremendous team effort.
Sac/Val vs Val in 466 pts w HF and EF>40% with recent WHF.
Positive trial for NTproBNP reduction; CV & renal endpts favored esp in EF<|=60% jacc.org/doi/10.1016/j.…

To sum it all up?
⚫️Check iron panel in symptomatic HFrEF
⚫️ IDHF = ferritin <100 μg/L or ferritin 100-300 with Tsat <20%
⚫️ Treat with IV iron (not oral)
⚫️ Improves functional capacity and quality of life
⚫️ Stay tuned for role in HFpEF, impact of SGLT2i, long-term outcomes

This is a rapidly evolving field with many unknown answers. There are several ongoing studies evaluating various repletion strategies, outcomes, and populations. The interaction between SGLT2i and IV iron also remains unknown.

What dose? Historically, the Ganzoni equation was used to calculate patient-specific iron deficits. More recent studies use fixed doses. The average dose needed over 1 year in CONFIRM-HF: ~1500mg. Most patients in CONFIRM-HF, AFFIRM-AHF, and IRONMAN did not require > 2 infusions.

Back to IV iron, which agent to choose? FCM has the greatest amount of evidence in HF, but ACC guidelines do not specify which formulation to use. Agents can generally be chosen based on formulary considerations/access, AEs and convenience of administration/scheduling.

Wouldn't oral be a lot easier? Maybe, but oral iron has not been associated with improvements in outcomes in IDHF. Remember, hepcidin decreases absorption; patients with higher hepcidin saw the least improvement in iron indices in IRONOUT-HF.

Improvements in functional capacity with IV iron are especially notable. Even GDMT (which we should still definitely use!) has not been consistently associated with as much improvement in this outcome compared to IV iron (although our friends the MRAs are a close second 😎).

How should we treat IDHF? The key is IV (not oral!) iron. IV iron has consistently been shown to improve functional capacity and QOL in HFrEF. There is also some evidence for ⬇️risk of hospitalizations; ongoing trials maybe able to provide clarity around larger outcomes.

Who should be screened for IDHF? Any patient with symptomatic HFrEF *independent* of whether or not they are anemic. Up to 40% of patients with IDHF are *not* anemic at baseline and benefits of therapy are seen independent of anemia.

So how do we define IDHF? The most commonly used definition (ferritin <100 μg/L or ferritin 100-300 with Tsat <20%) includes a higher ferritin cutoff due to its nature as an acute phase reactant (ie, likely chronically elevated in HF independent of iron stores).

The mechanism of IDHF is multifactorial, but largely due to ⬆ hepcidin (protein involved in iron homeostasis) secondary to chronic inflammation. Increased hepcidin leads to ⬇️ iron absorption from the gut and mobilization from both the liver and reticuloendothelial system.