Ejection fraction

ECG shows normal sinus rhythm with anterior Q waves, a narrow QRS, and no acute ST segment or T wave changes.

Repeat transthoracic echocardiogram shows an LVEF of 30%.

What is the most appropriate next step? The answer choices are as follows.

A, switch Valsardin to Sacubrital Valsardin.

So the correct answer is B, consider implantable cardioverter defibrillator ICD placement.

Generally, arrhythmic complications increase both morbidity and mortality rates in patients after ACS.

Patients who present with EMI with reduced LVEF as in less than or equal to 40% have increased risk of new onset atrial fibrillation, radiarrhythmias, and ventricular arrhythmias.

Ventricular arrhythmias are common after ACS and more common in patients with reduced LVES.

It was a non-inferiority margin, and the margin they chose was minus 10% points, and it was an intention to treat primary analysis.

Secondary endpoints were left ventricular ejection fraction, QRS duration, NT-proBNP symptoms, six minute walk, capture thresholds, and device implant measures.

Crossover was permitted.

So let's talk about the crossover part.

CSP turned out to be worse than Byvi.

All the other trials point towards the direction that that this is non-inferior.

The way I look at it until we have a much larger randomized trial is try by V in this classic situation, left bundle reduced ejection fraction.

And if the anatomy, the CS anatomy is poor, then just jump straight, not even try putting a CS lead in because the anatomy is so bad.

She has atrial fibrillation, and she's actually on a Pixaban and amiodarone for that.

She has hypertension, hyperlipidemia, not obstructive coronary artery disease, chronic kidney disease with a baseline creatinine around 1.2, Heart failure with improved EF, and now the most recent EF, was 60 to 65, and a remote history of breast cancer, and she got a mastectomy and lumpectomy many years ago.

And for her meds, like I mentioned, she's on anticoagulation with apixaban, amiodarone, amlodipine, atorvacetin, and dipagliflozin, and she said she took all of her medications in the morning prior to admission.

Her family history is non-contributory.

So we got an echocardiogram.

It showed that her TAVR was well-seated, very minimal regurgitation, no issues with the TAVR.

Her EF was 60 to 65%, same as previous, and there was no vegetations noted.

Otherwise, her echo essentially looked completely normal with a well-seated TAVR.

Emergent coronary angiography demonstrates ninety percent stenosis of proximal to mid LAD, and he's treated with two drug-eluting stents.

Transthoracic echocardiograms during hospitalization showed an LVEF of twenty-five percent with anterior and apical wall motion abnormalities.

He is discharged on dual antiplatelet therapy, along with metoprolol, valsartan, spironolactone, SGLT2 inhibitor, and rosuvastatin.

At follow-up three months later, he reports home blood pressure readings in the nineties over fifties millimeters of mercury with intermittent shortness of breath and lightheadedness.

Blood pressure in the office is ninety-two over fifty-four millimeters of mercury.

ECG shows normal sinus rhythm with anterior Q waves, a narrow QRS, and no acute ST segment or T wave changes.

Repeat transthoracic echocardiogram shows an LVEF of thirty percent.

What is the most appropriate next step? The answer choices are as follows.

Because there's only 4,400 patients in this cohort who had a GLP-1 exposure compared to 470,000 patients who didn't.

And so they just took everybody who had the exposure and which of the 470,000 was the closest based off of, um, the history of diabetes, obesity, their age, their sex, their LVEF, their blood pressure, lactate, creatinine, bilirubin, bicarb, those were their propensity scores, and said, "Okay, who's the closest in this group to my, to my person?"

Yeah.

"That's the person I'm gonna use to match" And they did it for all, for all 4,400 patients there.

And it's important to emphasize that at this point, the patient had already established on good medical therapy and he was clinically stable and no chest pain and his ECG was stable at this point.

So to summarize, this is an 88-year-old with NSTEMI, preserved EF, and complex coronary anatomy, including distal left main disease and CTO of RCA.

So, Mina, Faryal, can you please take us through your thinking process in terms of the medical therapy and the next steps of the management?

Yeah, so at that point, he was pain-free and we can see that he has complex coronary anatomy.

But whenever I use support, honestly, I haven't regretted it.

One thing I would do for this case is since patient is stable and we have time, I would assess the access sites to make sure we have appropriate access and it's not going to add additional complications to the case.

But otherwise, I think I would also go for support given multivascular disease, frailty, even though EF is normal.

I would also get an LVDP to see what the left-sided filling pressures are.

So it could be that both drugs were effective and fell on either side of that significance level.

Or aficamten could be a slightly better drug based on its shorter half-life, uh, that allows, you know, a better ability to uptitrate and may be able to stop the drug sooner if the LVEF drops.

And there are also fewer drug-drug interactions with aficamten.

The thing that seems reasonable to conclude is that both drugs affect the biology of HCM as echo and biomarkers do go in the right direction.

I'm just a neutral Martian looking in at this interesting data, but I'm struck by the short-term nature of these trials.

I mean, both drugs work by creating negative inotropy.

That's a little worrisome, isn't it? I mean, LVEF fell below fifty percent in ten point five percent of aficamten patients versus zero point eight on placebo, and serious heart failure events occurred in four point three versus zero point four.

So that's a lot higher.

Cardiac structural abnormalities can also qualify.

Cardiac structural abnormalities can include increased left ventricular mass, increased chamber sizes, such as increased left atrial volume, increased wall thickness, reduced LVEF, wall motion abnormalities, or abnormal global longitudinal strain.

Evidence suggesting elevated filling pressures, such as an average E over E prime of at least fifteen, can also be relevant.

Let's make this practical.