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2yr
Heart Failure Characteristics and Treatment Plan by Ejection Fraction

Heart failure with preserved ejection fraction (HFpEF) represents approximately half of all heart failure cases. It is characterized by EF >50%, as well as different pro-inflammatory and metabolic co-morbidities. HFpEF entails structural and cellular alterations such as cardiomyocyte hypertrophy, fibrosis, and inflammation. These factors render the left ventricle unable to relax properly. The 5-year survival rate of HFpEF is 35%, which is worse than most cancers. Additionally, most treatments for HFrEF are ineffective for HFpEF.

The other 50% of heart failure cases comprise heart failure with reduced ejection fraction (HFrEF) and heart failure with mid-range or mildly reduced EF (HFmrEF).

HFrEF is characterized by EF ≤ 40% and involves severe cardiomyocyte loss, therefore resulting in the development of systolic dysfunction, or contractility problems of the left ventricle. Heart failure with mid-range or mildly reduced EF (HFmrEF) represents a liminal stage—categorized by an EF between 40% and 49%.

In 25% of cases, HFmrEF progresses to HFpEF, and in 33% of cases, it progresses to HFrEF. HFmrEF is more akin to HFrEF than HFpEF in terms of ischemic etiology. Nevertheless, HFmrEF exhibits a higher chance of underlying coronary artery disease (CAD) and improved overall prognosis.

Hypertension, T2DM, obesity, and renal insufficiency occur before HFpEF. On the other hand, HFrEF occurs after acute or chronic loss of cardiomyocytes due to ischemia, genetic mutation, myocarditis, or valvular disease.

What important clinical differences do you observe in HFrEF vs. HFpEF (vs. HFmrEF)? How does your assessment and plan differ in HFrEF vs. HFpEF (vs. HFmrEF)?

  • 2yr
    ARNI ( or ace) , MRA , diuretic, SGLT inh, beta blocker for both types
  • 2yr
    I treat patients with HFmrEF similar to patients with HFrEF with beta-blockers, ARNi, spironolactone, diuretics, and SGLT2 inhibitors. I treat patients with HFpEF with diuretics, SGLT2 inhibitors, and blood pressure management.
  • 2yr
    The key clinical difference between HFrEF and HFpEF is the difference in EF, with HFrEF having an EF of ≤ 40%, while HFpEF has an EF > 50%. HFmrEF, with an EF between 40% and 49%, is a liminal stage between HFrEF and HFpEF. Additionally, HFrEF is characterized by systolic dysfunction or reduced contractility of the left ventricle, while HFpEF is characterized by diastolic dysfunction or impaired relaxation of the left ventricle.

    In terms of assessment and treatment, the management of HFrEF is well-established and effective. Treatment typically includes medications such as angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), beta-blockers, and mineralocorticoid receptor antagonists (MRAs), as well as implantable cardioverter-defibrillators (ICDs) and cardiac resynchronization therapy (CRT). In contrast, treatment options for HFpEF are limited, with no medications or therapies proven to improve outcomes in large randomized controlled trials. Nevertheless, lifestyle modifications, including weight loss, physical activity, and blood pressure control, can be beneficial. Diuretics and beta-blockers may be used to manage symptoms, and aldosterone antagonists may be beneficial in patients with comorbidities such as diabetes or hypertension. Patients with HFmrEF may benefit from treatment strategies that are similar to those used for HFrEF or HFpEF, depending on their clinical characteristics.
  • 2yr
    With the advent of ARNI added to BB, MRA I have found that many patients with HFref improve . Unless , the patients have LBBB then they may not improve and CRTs are good options. For hFpEF, I concur with the literature regarding the use of farxiga /jardiance.
  • 2yr
    I see little differences between the diagnoses. I feel that a thorough assessment and evaluation is important so that the correct medication is prescribed. I use the usual diuretics, CCBs, ARBs, SGLT2 inhibitors, nutrition, rehab, etc, plus education of both patient and family so they can understand the physiology and triggers of either condition in order for therapy to be most effective.
  • 2yr
    Control underlying co morbidities, HTN, DM, CKD. Medications like SGLT2, MRA are promising, along with Entresto, ICD.
  • 2yr
    in evaluating HFrEF I also recommend screening for amyloidosis for cause of symptoms not just HFrEF. we are using SGLT 2 inhibitors for management of the comorbidities however it is getting more expensive and there have been supply issues to access them! very frustrating.
  • 2yr
    HFrEF is easy-tons of therapies available including medications and devices. HFpEF and HFmrEF are more difficult, MRAs and SGLT-2 are options, HTN control crucial. And if we are talking HCM, new therapies coming up so stay tuned...
  • 2yr
    MRA and ICD are more beneficial in HF with reduced EF. Also definitely make sure that betablocker is XL in HF with reduced EF. In HF with preserved EF focus is on the etiology of HF such as HTN or volume control. Ther3e is no real mortality benefit in these for HF with preserved EF
  • 2yr
    MRA and ICD are more beneficial in HF with reduced EF. Also definitely make sure that betablocker is XL in HF with reduced EF. In HF with preserved EF focus is on the etiology of HF such as HTN or volume control. Ther3e is no real mortality benefit in these for HF with preserved EF
  • 2yr
    MRA and ICD are more beneficial in HF with reduced EF. Also definitely make sure that betablocker is XL in HF with reduced EF. In HF with preserved EF focus is on the etiology of HF such as HTN or volume control. Ther3e is no real mortality benefit in these for HF with preserved EF
  • 2yr
    on general I find volume control with diuretics and bp control work well in managing symptoms of chf with preserved lv function
    interesting that most traditional rx have not been shown to be effective.
    New rx with sglt2 inhibitors and entresto seem to improve prognosis
    I tend to treat hfmef in same manner as hfref.
  • 2yr
    The treatment guidelines are the same for medications at this point for the most part, ICDs reserved for thr patients with Hefref. The mid range reduction heart failure patients tend to have a similar profile the Hefref patients. Again it is important to treat any other underlying comorbidiites patient may have. Revascularization May improves LVEF
  • 2yr
    I think that the differences in etiology and treatment strategy are the most important to keep in mind; the 4 pillars are for HF(m)rEF patients, while we don't have quite as much for HFpEF patients (ARNI, SGLT2, +/- MRA). Also, the most common cause for HF(m)rEF is ischemic disease; for HFpEF, it's hypertension and depositional diseases, so the workup differs, as well.
  • 2yr
    When one looks at the veracity of the ability to define HFmrEF, it becomes apparent that the imaging tool is a critical piece for defining whether this unique pathophysiology does, in fact, exist. They higher resolved CV imaging tool such as Cardiac MRI, can distinguish between single digit versus 5–10% as opposed to Echo-based abilities. In our review of the literature and in our experience, the dichotomous distinction between hear failure ranges becomes more of a continuum than an actual distinct pathology when higher resolved imaging tools are used. Thus, HFmrEF may be just a bit of an artifact of the inexact tool.
  • 2yr
    The difference between HFrEF vs. HFpEF seems to be patients with HFrEF have suffered an event causing ischemia whereas patients HFpEF seem to have chronic conditions such as diabetes, obesity, lung disease, hypertension, kidney disease etc. Treatment for HFrEF and HFpEF includes management of contributing co-morbid conditions and the use of SGLT2 inhibitors. In HFrEF MRAs can then be added.
  • 2yr
    HFrEF has a lot of treatment options while there is no specific targeted treatment available for HFpEF. SGLT-2 inhibitors may offer some advantages. We could use beta blockers or calcium blockers to a reasonable extent. I believe device based therapies are in development, likely to create a left to right shunt to reduce the left atrial pressure.
  • 2yr
    Etiology is different for HFrEF vs HFpEF. Ischemic evaluation is always warranted. I tried to identify any reversible reasons. My preference is Entresto , carvedilol, spironolactonand Farxiga ( if covered by insurance ) I do the same for patients with HFmEF. My preference is to use spironolactoneplerenone for patients with HFpEF in addition to adequate BP control and life style modifications.
  • 2yr
    I agree with above comments but don’t forget to consider dx of ATTR Amyloidosis in some of your HFpEF patients especially if LVH seen - screen with strain polar map for the cherry on top sign but consider getting a pyrophosphate scan too.
  • 2yr
    HFrEF patients have treatment options including revascularization if severe CAD is present, diuresis, neurohumoral therapy (beta blocker, ACEI/ARB, MRA, SGLT2 inhibitor), and sometimes CRT if LBBB. Improvements is symptoms and outcomes can be expected with treatments in most patients. In HFpEF patients, fewer treatments are effective and outcomes are less likely improved Diuresis to lower cardiac filling pressures and thus reduce breathlessness and edema are the mainstay. Although recent studies such benefit from spironolactone, Entresto, and SGLT2 inhibitors, the benefits are less robus than with HFrEF. For example, outcome benefits from SGLT2 inhibitors in HFpEF are almost all reduction in CHF hospitalization with little improvement in mortality.
    Diagnosing that HFpEF (or HFmEF) is responsible for patient symptoms of breathlessness, fatigue, and edema is less straightforward. Many of these patients have other comorbid conditions which can be responsible including deconditioning, obesity sometimes with sleep apnea, or lung disease or kidney disease. So, patients are sometimes labeled as having HFpEF, are treated with loop diuretics and spironolactone, maybe Entresto and sometimes respond poorly with drops in BP, worsening renal function and less improvement in symptoms.
  • 2yr
    I am not quite so quick to 'assume' there is a distinct HFmrEF. When we look at more precise measures of LVEF such as cardiac MRI, we see loss of the distinct midrange group as a distinct prognostic entity. Thus, it might be artifactualdue more to our inabilities to define LVEF with more than a 5-10% decile.
  • 2yr
    I use guideline directed medical therapy for heart failure with reduced ejection fraction. I use the same treatment for mid range EF. It is still uncertain the treatment of preserved EF. Certainly, SG LT 2 inhibitors can be considered. I usually consider diuretics and ARB agents or calcium blockers. However, there is no real mortality benefit in any of these treatments for heart failure with preserved EF. It is more improved symptoms and reduced hospitalization rates which still are important.
  • 2yr
    Clinical symptomatology difficult to discern between the two entities. In both try to address underlying contributors, but medical therapy differs, now with medication actually available for HFPEF.
  • 2yr
    Treatment for reduced EF CHF is tailored towards controlling volume status, and attempting to reduce afterload to improve cardiac output. In patients with preserved EF CHF treatment is directed towards reducing LV contractility, and reducing edema. It is interesting that many of the same medication‘s are used to treat both conditions. Treatment for patients in the intermediate LVEF group is also comparable.
  • 2yr
    more specific treatment tailored to their EF status. One could take a more conservative approach towards HFmrEF if they have concomitant conditions that require less aggressive tx

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