Heart failure with preserved ejection fraction (HFpEF) is known as diastolic heart failure.
Most rapidly increasing form of heart disease.
Prevalence is increasing by about 1% annually relative to heart failure with reduced ejection fraction.
The prevalence of this syndrome is progressively increased, and has become the most common form of heart failure, particularly an older persons, women, and Black individuals.
HFpEF affects more million people in the US and is associated with severe symptoms of exertional dyspnea and fatigue, impaired health related quality of life, severely reduced exercise capacity, and increased rates are we hospitalizations and deaths.
About 50% of patients have heart failure with reduced ejection fraction (HFrEF).
As the population ages the overall prevalence of patients with heart failure and a preserved ejection fraction is increasing.
The prevalence of HFpEF is increasing partly due to increased recognition and will continue to increase with reductions in deaths from other comorbidities they can lead to HFpEF, increasing age of the population, and increasing prevalence of obesity.
Older age and obesity are risk factors for HFpEF.
Patients with HFpEF and obesity have more adverse hemodynamic and clinical features, and a greater symptom burden, worse functional capacity, and more severely impaired quality of life if those with heart failure with preserved ejection fraction, but no obesity.
The incidence of HFpEF varies from 1 to 4 cases per thousand person years, depending on the cohort and time period study.
Risk factors include older age, diabetes, coronary artery disease and increased BMI.
Incidence of HFpEF is equal in men and women, but the incidence of HFrEF is lower in women.
Heart failure with preserved ejection fraction is associated with substantial functional and quality of life impairments that are at least equivalent to those of patients with heart failure and a reduced ejection fraction.
Exertional intolerance is a cardinal manifestation of heart failure with reduced left ventricular ejection fraction.
Exercise in tolerance is the cardinal, symptomatic manifestation of heart failure with preserved ejection fraction.
Increases in heart rate with exercise is characteristically reduced in patients with HFpEF.
HFpEF is a systemic syndrome initiated by circulating factors, and related to systemic inflammation arising from excess, maladaptive adipose tissue and resulting in widespread mitochondrial dysfunction and loss of tissue capillarity, which are critical to organ perfusion, and energy metabolism.
These factors impair the function of the heart and other organs, and indicates that HFpEF is a systemic multi organ disorder.
There is a current lack of interventions that consistently improve cardiovascular outcomes.
Nearly all drugs proven to reduce death and hospitalization in heart failure with reduced ejection fraction have been shown to be ineffective inHFpEF:notable, exception, or sodium glucose cotransporter 2 Inhibitors(SGLT-2).
Semaglutide, a glucagon like peptide 1 (GLP-1) agonist provides benefits for patients with heart failure with preserved ejection fraction through an upstream intervention that addresses metabolic drivers and differs from earlier treatment approaches that aim to reduce myocardial load, or induce neurohormonal blockade.
Pharmacologic agents shown to decrease clinical events in HFrEF have modest, if any, benefit on objectively measured exercise capacity: beta adrenergic receptor blockers, angiotensin converting enzyme inhibitors/angiotensin receptor blockers/angiotensin receptor-neprilysin inhibitors, mineralocorticoid receptor antagonists, sodium glucose cotransporter 2 inhibitors effects on exercise capacity compared with placebo are minimal.
Prevalence is between 1.1 and 5.5%.
Patients with heart failure with preserved ejection fraction have a high degree of medication complexity associated with polypharmacy, potentially inappropriate medications, and medications that lead to therapeutic competition.
Accounts for 40 to 70% of heart failure cases.
There is a negligible transition over time to heart failure with reduced ejection fraction.
Defined as heart falure with an ejection fraction of less than 40%
A value of LVEF of 40% does not distinguish patients with heart failure rate of normal LVEF from those who have abnormally low LVEF values.
Frequently there is no overt volume overload, on the EF is by definition normal making the diagnosis more difficult.
LVEF is a continuous variable, and the identification of normal values is dependent on age and sex.
Proportion of patients with heart failure with HFPEF increases about 1% a year.
Diagnosis is considered with ECG findings of left atrial large enlargement , right ventricular enlargement, or elevated pulmonary artery systolic pressure.
Associated with the high mobility and mortality, reduce quality-of-life, and no approved therapies
Will become the predominant phenotype of heart failure within the next decade.
Rate of growth most likely reflection of increased frequency of hypertension, obesity, atrial fibrillation, increased life expectancy, diabetes, coronary artery disease, sleep apnea and improved diagnosis.
Obesity scene him up to 75% of patients, while 95% of patients or overweight.
Associated with conditions that drive endothelial inflammation and diastolic dysfunction.
Hallmark is large artery stiffness and heart stiffness whether related to fibrosis myocardial based stiffness.
Involves abnormalities in left ventricular diastolic function, leading to increased left atrial and pulmonary venous pressure associated with additional cardiovascular and non-cardiovascular pathophysiological abnormalities.
Likely to be associated with widespread micro vascular dysfunction involving all cardiac chambers and other organs including the lungs, kidneys, and skeletal muscles, indicating that it is a systemic disorder.
Left ventricular systolic function is often abnormal, global left ventricular ejection fraction is preserved, and left ventricular longitudinal fiber systolic function is frequently impaired.
Patients with HFPEF commonly have marked reduced reserve capacity.
Cardiac, vascular and skeletal muscle dysfunction become apparent during exertion.
Increasing incidence worldwide is due to improved the recognition, aging population, increases in the prevalence of comorbid diseases such as hypertension, chronic kidney disease, and diabetes.
Patients with obesity driven HFpEF Frequently have the greatest disconnect between symptoms and objective measures of heart failure with the lowest left atrial size and natural Radick peptide levels despite having the poorest quality-of-life and symptoms of heart failure.
Diagnostic criteria: Symptoms and signs consistent with heart failure, nondilated left ventricle with preserved ejection fraction of 50% or greater and evidence of structural heart disease such as diastolic dysfunction on echocardiography.
Managing HFPEF as a single clinical syndrome is incorrect, as in reality it is a combination of multiple disease stthat require unique approaches.
Impairment of myocardial relaxation and stiffness of the ventricle resulting in reduced left ventricular filling, elevated diastolic pressures, and heart failure symptoms.
Hemodynamic measurements chemistry prolonged isovolumetric pressure decline as well as upward shift in the pressure volume loop, consistent with aberrant myocardial relaxation.
The heart’s ability to cope with exercise induced hemodynamic overload is restricted in this situation.
Passive stiffness in the indices are characteristically high in patients with HFPEF.
Exercise produces abrupt rise and pulmonary and left atrial pressure, the main driver of dyspnea in patients with heart failure with preserved ejection fraction.
Exercise intolerance is the main symptom and the major reason for reduced quality of life, with exertional dyspnea the most common complaint.
Dyspnea is highly distressing and the main reason for frequent hospitalizations in these patients.
More than 40% of patients admitted to the hospital for decompensated heart failure have preserved systolic function ( heart failure with preserved injection fraction-HFPEF and diastolic dysfunction.
Associated with normal or near normal systolic function.
Among patients with HFPEF coronary artery disease, diabetes, atrialfibrillation, hyperlipidemia are highly prevalent.
Pathophysiology of HFPEP is complex and related to a combination of elements of ventricula dye synchrony, atrial dysfunction, atrial fibrillation, right ventricular dysfunction, pulmonary vascular disease, vascular stiffening and dysfunction and alterations in chronotropic reserve and autonomic tone.
Associated with effort intolerance, which is associated with profound and rapid increase in left atrial pressure during exercise, indicating impaired left ventricular diastolic reserve, with consequent pulmonary congestion.
Disproportionate rise in left atrial pressure provoke symptoms and contributes to increase morbidity and mortality in HFPEF.
Prevalence increasing and accounts for approximately half the cases of heart failure.
Occurs primarily in older women.
Associated with high rates of morbidity,mortality, and health care expenditures.
More than 80% of HFPEF patients are overweight or obese.
Prevalence increases with age and especially affects individuals older than 70 years.
Diastolic dysfunction as assessed by echocardiography highly prevalent in the elderly with mild diastolic dysfunction present in more than 21% of patients age 45 for older, and 7% have evidence of moderate to severe diastolic dysfunction.
Majority of patients with diastolic dysfunction have no symptoms of heart failure.
Echocardiographic markers of diastolic dysfunction are absent in a significant proportion of patients with heart failure and preserved ejection fraction.
Patients older than patients with systolic heart failure, more females, more have hypertension and fewer have previously known coronary artery disease, and myocardial infarctions.
Other comorbid risk factors for diastolic heart failure include: obesity, coronary heart disease, diabetes, atrial fibrillation, and hyperlipidemia.
Heterogeneous disorder with multiple pathophysiological processes.
Traditionally attributed to a primary cardiac abnormality of myocardial stiffening from hypertrophy and fibrosis, abnormal calcium handling and venous turgor.
Heart failure with preserved ejection fraction is a syndrome involving volume overload, exertional intolerance and myocardial stiffness.
HFPEF associated with vascular and renal dysfunction, chronotropic incompetence, metabolic derangements, and contractile abnormalities.
HFPEF associated with normal heart contraction, but ventricles do not relax properly and less blood enters the heart.
Associated with increased risk of stroke and thromboembolism.
HFPEF have similar mortality rates and rehospitalization rates as with systolic heart failure.
The severity of exercise intolerance which is the primary symptom and major contribution to reduced quality of life of patients with chronic HFPEF is significantly correlated with increased body adiposity and skeletal muscle adipose infiltration.
In patients with HFREF treatment with sacubitril-valsartan, the reduction in NT-pro BNP was weekly yet significantly correlated with improvements in markers of cardiac volume and function at 12 months.
Treatment with secubitril-valsartan did not result in reduced hospital admissions for cardiovascular associated heart failure impatiens with preserved ejection fraction.
Systolic heart mortality rates are decreasing but diastolic heart failure mortality rates have remained the same.
The mortality in HFPEF may be as high as in heart failure with reduced ejection fraction or systolic heart failure.
There is no proven therapy.
No effective pharmacotherapeutic treatment.
Drug therapies have not shown improvements in diastolic dysfunction, cardiac remodeling or cardiovascular outcome.
There is significant overlap between heart failure with preserved ejection fraction (HFPEF) and heart failure with reduced ejection fraction (HFREF).
Diastolic dysfunction and impaired systolic contractility occur in both HFREF and HFPEF.
Renin-angiotensin-aldosterone system and other neurohormonal activations occur in both HFREF and HFPEF.
Associated with hypertensive episodes and onset of atrial fibrillation.
Older patients with HFPEF and heart rate of 70 beats or a greater per minute have a higher risk of all cause mortality.
In patients with HFPEF and heart rate of 70 beats or greater per minute, high dose of beta blocker use significantly lowered risk of death.
About 1/3 of patients with symptomatic CHF have a “normal” Ejection Fraction (EF at least >40%) and experience symptoms that are entirely or predominantly the result of diastolic dysfunction.
About 50-60% of elderly persons with heart failure have adequate ventricular contractile function and are thus experiencing mainly diastolic dysfunction (Kitzman, 2002).
CHF secondary to diastolic dysfunction is the result of an impairment in heart’s ability to relax.
There is an increase in the ventricular diastolic pressure at any given diastolic volume.
Heart failure with preserved ejection fraction diagnosed when the clinical syndrome of HF with volume overload, dyspnea, exertional intolerance is associated with preserved systolic function and evidence of diastolic dysfunction by heart catheterization, echocardiography or cardiac biomarkers.
HF-PEF mimicked by constrictive cardiomyopathy, pericardial disease, dynamic mitral regurgitation, ischemic heart disease, and exercise induced pulmonary hypertension.
No universally agreed upon diagnostic criteria for diagnosis of HP-PEF.
Causes include restrictive and hypertrophic cardiomyopathies, ischemic states, hypertension, and senile cardiac amyloid.
Control of hypertension and minimizing ischemia are important goals for treatment and ACE inhibitors and Angiotensin Receptor Blocking agents appear to be indicated for both diastolic and systolic heart failure.
No class of drugs consistently provide benefits with heart failure with preserved ejection fraction.
However, in a randomized trial of 6263 patients treatment with Dapagliflozin resulted in a lower risk of worsening heart failure in patients with a preserved ejection fraction and those that had improved ejection fraction by 10 to 40%.
The renin- angiotensin-aldosterone system (RAAS) contributes to fibrosis of hypertensive heart disease and treatment with lisinopril decreases myocardial fibrosis in the left ventricle hypertrophy with concomitant improvement in left ventricular diastolic function.
Digoxin might be considered in systolic dysfunction, mainly now when there is atrial fibrillation, it may not be as effective in diastolic dysfunction because it increases contractility rather than relaxation.
Beta blockers also may be indicated in diastolic dysfunction.
With diastolic dysfunction, venous return and adequate ventricular filling are very important to maintaining cardiac output.
Mineralocorticoid receptor activation by aldosterone contributes to the pathophysiology of heart failure, regardless of ejection fraction: This occurs due to sodium retention, potassium loss, endothelial dysfunction, vascular inflammation, fibrosis, and hypertrophy.
Among patients with heart failure and preserved ejection fraction and recent decompensation, treatment with vericiglut compared with placebo did not improve the physical limitations score.
In patients with HFpEF and chronotropic incompetence, implantation of a pacemaker to enhance exercise heart rate did not result in improvement in exercise capacity, and was associated with increased adverse events (ReddyVNV).