Prevalence and Risk Factors of Heart Failure

EP: 1.Challenges in Heart Failure Management

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EP: 2.Prevalence and Risk Factors of Heart Failure

EP: 3.Quadruple Therapy for Patients With Heart Failure

EP: 4.Use of SGLT-2 Inhibitors in Heart Failure

EP: 5.Personalizing Quadruple Therapy in Heart Failure

EP: 6.Unmet Needs in the Management of Heart Failure

EP: 7.Clinical Trials of Sacubitril/Valsartan in Heart Failure

EP: 8.The Future of Heart Failure Therapy

Anuradha Lala-Trindade, MD: I think our understanding as to the prevalence of heart failure across the spectrum of ejection fraction has evolved tremendously over the past decade. We used to think heart failure with reduced ejection fraction was the only really meaningful heart failure. And what we know now from large registry and observational studies is that the prevalence of heart failure with reduced ejection fraction and preserved ejection fraction is actually equivalent. And they also, for different reasons, have similar profiles in terms of prognosis.

In terms of my clinical practice, because we're an advanced heart failure and transplant and LVAD [left ventricular assist devices] center, I tend to see a greater proportion of about two-thirds of individuals with reduced ejection fraction. I would say it’s difficult to exactly measure or quantify proportion, but a smaller one certainly with mildly reduced ejection fraction, and then approximately 25% to 30% with preserved ejection fraction.

In terms of what I see differently, I think it ranges, of course, based on the individual, but certainly with those patients with reduced ejection fraction, I am trying to first and foremost optimize all 4 pillars of guideline-directed medical therapy. Fortunately, in those patients who I am able to accomplish that in, we do see very meaningful differences in improvement in quality-of-life functional capacity. My practice has now evolved to ensure that those patients with improved ejection fraction to what is now maybe mildly reduced or is mildly reduced from the get-go, that they, too, are optimized on guideline-directed medical therapy across the pillars.

With the preserved ejection fraction folks, I'm really focusing foremost on the SGLT2 [sodium-glucose cotransporter-2] inhibitors, which I know we'll speak later about. When appropriate, mineralocorticoid receptor antagonists. And then, really, I am steering away from beta-blockers. I'm actually asking myself, ‘Why is this patient with heart failure with preserved ejection fraction on a beta-blocker? Is there a specific reason?’ If not, then I'll try and peel that away because we know that they don't do so well on beta-blockers. In terms of how I manage them differently, I think there's a wide array, as we know, of differences in functional capacity that has really nothing to do with ejection fraction. So I spend a lot of my time talking about that principle because a lot of patients will say, ‘My ejection fraction is 10%, I'm not going to be able to do anything.’ And then you have people with an ejection fraction, let's say, of 60% who are highly symptomatic and then are very frustrated by the fact that they are symptomatic. So, I spend a good deal amount of time talking about that disconnect.

I think the other way that things have evolved for me as a clinician is that I, first and foremost, as I mentioned, try to optimize all pillars of guideline-directed medical therapy across that spectrum. I really try to address comorbid conditions as well. I try to ensure adequate volume status and I'll use device-based therapies to help enable that. So, whether it's PA [pulmonary artery] pressure sensor monitors or other device-based therapeutic interventions, I think I'm thinking about them more alongside pharmacologic therapy than I did before.

In terms of seeing differences in the different types of heart failure, I think what we do see is certainly a greater prevalence of women who present with mildly reduced or preserved ejection fraction. We know that to be true. Now seen repeatedly. I think we tend to see more men with more of ischemic cardiomyopathy with reduced ejection fraction. I think we see a higher prevalence of individuals of black race with a nonischemic cardiomyopathies with reduced ejection fraction as well. So those are some of the overt sex- and race-based differences that we see in clinical practice.

In terms of how I assess a patient's risk factors and the possible etiologies of their heart failure, I try to be pretty holistic about it. We know that hyperlipidemia, hypertension, and coronary disease are precursors to the development of heart failure. So, those are some of the ones that I look to identify first and foremost. And then, concomitant diabetes, 40% of the population with heart failure ends up having diabetes, and that's likely an underestimate. Certainly, at our institution that is an underestimate. So, I think addressing the heart failure, the symptoms, the appropriate medical therapy, but also ensuring that key comorbid conditions are addressed and optimized as equally important. So, like I said, the hypertension, the coronary disease, the diabetes, the obstructive sleep apnea or pulmonary or sleep disordered breathing present, atrial fibrillation, chronic kidney disease, I think all of these comorbid conditions are incredibly common and warrant special attention while we're treating an individual's heart failure because the trajectories are the same.

And then, with regards to working up the etiology, I think going back old school, I still rule out ischemia as a primary cause of an underlying myopathy if present, by way of a cardiac catheterization, but depending on the individual, may use CT imaging as well. And once that has been ruled out, if it is a younger individual or certainly if there's a family history of any kind of familial cardiomyopathy, I'm very quick to pursue genetic testing, which is now endorsed by the guidelines as well. I think it's incredibly informative. Sometimes if you see a specific mutation, it may render you a little bit more ready to pursue the implantation of ICD [implantable cardioverter-defibrillator]. For example, if it's a desmoplakin mutation, we know that those tend to be more proarrhythmic. So that's just one example.

So, I would say, I rule out ischemic disease, I pursue genetic testing, and I really go after comorbid conditions in terms of ideology workup. I also, importantly, assess for iron deficiency. I have increasingly become astutely aware of how important it is to rule out amyloid disease, specifically in those patients along the lines of the higher ejection fractions spectrum, but still relevant across the spectrum of ejection fraction.

Transcript edited for clarity