#HFpEF pearl of the day: Once the Dx of HFpEF is made, the 1st step is looking for and Rx'ing congestion, then Rx'ing comorbidities, and then exercise/weight loss program. I use sequential nephron blockade to minimize loop diuretic dose, always try to use MRAs when possible.
If strictly following TOPCAT protocol for MRA use in HFpEF, here is an algorithm published here (with @SumeetMitter): pubmed.ncbi.nlm.nih.gov/26408016/
MRAs can also be very useful for patients with HFpEF on 3+ anti-HTN meds. Hyperaldo state can be unmasked with MRA treatment. I've had patients on 3-4 drugs for HTN come off of all or most of them after starting MRA treatment.
In the HFpEF management algorithm above, for treating HFpEF comorbidities: concomitant lung disease (e.g., COPD, ILD) is common and difficult to treat. O2 sat can ⬇️⬇️ with even mild pulmonary venous congestion b/c of poor lung reserve, so maintaining euvolemia very important.
Implantable hemodynamic monitoring can reduce respiratory hospitalizations in HF patients, as seen with #CardioMEMS. See: ncbi.nlm.nih.gov/pmc/articles/P…

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More from @HFpEF

21 Dec
#HFpEF pearl of the day: Eval of filling pressures is critical for HFpEF management. Use entire echo and integrate info for filling pressures assessment: E, E/A, decel time, pulm vein flow, LA volume, LA strain, PASP, PR end-diastolic gradient, IVC, hepatic vein, tricuspid E/e'.
⬆️E, ⬇️DT, ⬆️E/A, and D-dominant pulm vein flow (in older pts); ⬆️E/e’, ⬆️LA volume (esp. ⬆️LA min volume), ⬇️LA reservoir strain; ⬆️PASP, ⬆️PREDP gradient (in absence of PAH); ⬆️tricuspid E/e’ > 6, ⬆️size ⬇️collapsibility of IVC, hep. vein flow reversal all = ⬆️filling pressures
Alternatively, continuous flow by 2D doppler into RA (in RV inflow views) or continuous forward flow on hepatic vein tracing can be helpful signs of normal RA pressure.
Read 9 tweets
19 Dec
#HFpEF pearl of the day: speckle-tracking strain bullseye map of the LV can help determine etiology of HFpEF. Here's an example: 58-year-old man with HTN, CKD presents with SOB, leg swelling, elevated JVP. Echo shows normal LVEF. Image
What did his ECG show?
The answer is deep T wave inversions due to apical HCM. Image
Read 8 tweets
18 Dec
#HFpEF pearl of the day: Always look at echo LVOT VTI when eval. HFpEF pts. Normal 18-22 cm at HR 60-100. ⬆️LVOT VTI: look for NASH, anemia, cirrhosis, AVMs, etc. If ⬇️LVOT VTI: infiltrative/restrictive CM, constriction, LA failure, PAH, RV failure, obstructive lung dz, MS, etc.
If ⬆️LVOT, measure volumes/dimensions of all 4 cardiac chambers to look for enlargement. Case: 31 yo woman previously healthy presents with dyspnea, leg swelling, BNP 166 pg/ml. Training for a marathon. Urine pregnancy test negative.
Echo shows normal LVEF (65%). E/e’ = 6. Lateral e’ velocity = 15 cm/s. LV dilated (LVEDVI = 85 ml/m2) and LA dilated (LA volume index = 50 ml/m2). ⬆️LVOT VTI = 30 cm.
Read 6 tweets
16 Dec
#HFpEF pearl of the day: In HFpEF pts with #CardioMEMS devices, bike stress echo + continuous CardioMEMS PA pressure recording can help evaluate underlying pathophysiologic abnormalities.
Case: 71 yo woman w/apical HCM, AF s/p ablation, pacemaker, HTN, CKD with cardiorenal syndrome and PH-HFpEF presents with worsening overload. Echo shows preserved LVEF with apical HCM, PASP 85 mmHg, RAP 15 mmHg, RVOT PW notching consistent with ⬆️PVR.
Read 17 tweets
15 Dec
#HFpEF pearl of the day: Bike stress echo is very helpful in the evaluation of HFpEF. In 1 test you can diagnose HFpEF (E/e') and evaluate for CAD (WMA), health of the LA (Δ LA strain), LV contractile reserve (Δ LV strain), dynamic MR, and dynamic LV outflow tract obstruction.
If RV free wall strain goes down with exercise, could be a sign of dynamic pulmonary vasoconstriction during exercise (i.e., ⬆️PVR with exercise) or intrinsic RV dysfunction.
Here is an example. 72 yo woman w/HFpEF. With just 25W exercise, E velocity goes way up. And a' velocity goes down dramatically, indicative of LA contractile dysfunction and ⬆️LV end-diastolic stiffness. Image
Read 12 tweets
12 Dec
Answer to today's case: the pt had a very stiff LA, poss. due to AF ablation. But stiff LA alone cannot cause big V waves. Sympathetic activation➡️splanchnic vasoconstriction w/redistribution of volume from gut/liver➡️lungs/heart with minimal exertion + stiff LA = big V waves.
This pt also had significant coronary microvascular dysfxn. Exercise➡️myocardial ischemia➡️LV diastolic dysfunction➡️increased load on LA. I tried everything to treat him, nothing worked for 7 years. And then he got an IASD as part of the @corviamedical REDUCE LAP-HF I trial.
Huge improvement in symptoms, now NYHA class I-II.
Read 4 tweets

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