Sharing our state-of-the-art review on beta blockers just published in @JACCJournals! Thanks @rcstarling @DLBHATTMD @WilfriedMullens @AndreaRussoEP @MAbdeljawadmd for your expertise!

Key points:
1. Beta-blockers should no longer be prescribed by reflex. The modern question is: Which beta-blocker, for which patient, for which indication, and for how long? We propose an indication- and phenotype-based approach.

2. Beta-blockers do more than slow the heart rate. Blocking cardiac β1 receptors reduces heart rate, contractility and oxygen demand, while blocking β1 receptors in the kidney’s juxtaglomerular apparatus suppresses renin release.
3. Beta-blocker selectivity is relative and varies substantially among agents and is dose dependent. Nebivolol and bisoprolol are our most β1-selective agents. Didn't include this figure in the article, but this is a *rough* breakdown of selectivity.

4. A little-known reason patients respond differently to metoprolol: CYP2D6 genetics. Poor metabolizers can develop substantially higher metoprolol exposure and greater heart-rate reduction.

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Sorry @venkmurthy @onco_cardiology @IbrahimMSaeed1 and others but #WhyCMR is not on this algorithm. Though, it is used frequently as a “catch all” diagnostic test for various cardiomyopathies. 17/
I use cardiac MRI frequently for non-invasive evaluation in AL. Still, you will need biopsy proof of amyloid somewhere in the body before most hematologists will treat.

Amazing summary image by NAC group in London: ncbi.nlm.nih.gov/pubmed/29929616

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As #ESCCongress nears, I thought I would do a #tweetorial on amyloidosis. Exciting times for the field and new data/treatments expected next week.

#FITSurvivalGuide #CardioTwitter @tony_breu @rodney_falk @marthagrogan1 @amyloidosisfdn @AmyloidosisSupp @Amyloidosis_ARC 2/
What is amyloidosis?

A protein misfolding disorder in which one of thirty-five distinct proteins pathologically misfolds and aggregates extracellularly as insoluble amyloid fibrils, ultimately leading to organ dysfunction.