Heart Failure With Preserved Ejection Fraction

Published on 15/05/2015 by admin

Filed under Internal Medicine

Last modified 15/05/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1129 times

Chapter 24

Heart Failure with Preserved Ejection Fraction

1. What is diastolic dysfunction?

    Diastolic dysfunction occurs when there is an abnormality in the mechanical function of the myocardium during the diastolic phase of the cardiac cycle. This mechanical abnormality can occur with or without systolic dysfunction, as well as with or without the clinical syndrome of heart failure. Diastolic dysfunction may include abnormalities in left ventricular (LV) stiffness and relaxation that impair filling and/or result in elevated LV filling pressure to achieve adequate LV preload (end-diastolic volume) at rest or during physiologic stress.

2. What is diastolic heart failure?

    Whereas diastolic dysfunction describes abnormalities in mechanical function, diastolic heart failure is a clinical syndrome characterized by the signs and symptoms of heart failure, a preserved LV ejection fraction (LVEF ≥ 45% to 50%), and evidence of diastolic dysfunction. Earlier studies of patients with heart failure with preserved LVEF uniformly referred to this condition as diastolic heart failure, based on the premise that diastolic dysfunction was the sole mechanism for this syndrome. However, more recent studies suggest that a number of other abnormalities, both cardiac and noncardiac, may play an important role in the pathophysiology of heart failure with normal or near-normal LVEF. Therefore, the term heart failure with preserved ejection fraction (HFpEF) is more commonly used to refer to this clinical syndrome.

3. What is the prevalence of HFpEF?

    Approximately 5 million Americans currently have a diagnosis of heart failure, and more than half a million new cases of heart failure are diagnosed annually. Epidemiologic studies of various heart failure cohorts have documented a prevalence of HFpEF ranging from 40% to 71% (average approximately 50%). In addition, the prevalence of this condition is increasing as the population ages.

4. What is the morbidity and mortality associated with HFpEF compared with heart failure with reduced ejection fraction?

    Compared with age-matched controls without heart failure, patients with HFpEF have a significantly higher mortality. However, studies examining the risk of death in patients with HFpEF compared with patients with heart failure and reduced ejection fraction (LVEF < 40% to 50%), commonly known as systolic heart failure, show a somewhat lower or similar mortality in patients with HFpEF. Once hospitalized for heart failure, mortality in patients with HFpEF may be as high as 22% to 29% at 1 year and approximately 65% at 5 years. Although survival has significantly improved over time for patients with systolic heart failure, there has been no similar improvement in survival for HFpEF patients. In contrast to mortality, both the groups have similar morbidity as reflected by hospital admissions. Although the total or all-cause admissions are similar between the 2 groups, patients with HFpEF have higher non–heart failure related admissions that are driven by the higher prevalence of non-cardiac comorbidities in this population.

5. Which patients are at the highest risk for developing HFpEF?

    Patients with HFpEF are generally elderly and are predominantly women (60% to 70%). Reasons for the female predominance in HFpEF are not entirely clear but may be related to the fact that women have a greater tendency for the left ventricle to hypertrophy in response to load, and lesser predisposition for the ventricle to dilate. Hypertension is the most common cardiac condition associated with HFpEF. Hypertensive heart disease results in LV hypertrophy with resultant impairment in relaxation and increase in LV stiffness. Acute myocardial ischemia results in diastolic dysfunction, although its role in chronic diastolic dysfunction and chronic HFpEF remains uncertain. Valvular heart diseases, including regurgitant and stenotic aortic and mitral valve disease, can also result in the development of HFpEF. Other recognized risk factors associated with HFpEF include obesity, diabetes mellitus, and renal insufficiency. Onset of atrial fibrillation with rapid ventricular rate may precipitate decompensation of HFpEF, and the presence of diastolic dysfunction in general is also a risk factor for the development of this arrhythmia.

6. What are proposed pathophysiologic mechanisms of HFpEF?

    Diastolic dysfunction has been thought to be the major mechanism contributing to HFpEF, with abnormalities in active LV relaxation and in LV passive diastolic stiffness. LV relaxation is an active, energy-dependent process that may begin during the ejection phase of systole and continue throughout diastole. Animal studies and various models have shown that impaired LV relaxation can contribute to elevated mean LV diastolic filling pressures in HFpEF when the heart rate is increased (as during exercise or uncontrolled atrial fibrillation). On the other hand, LV stiffness consists of the passive viscoelastic properties that contribute to returning the ventricular myocardium to its resting force and length. These viscoelastic properties are dependent on both intracellular and extracellular structures. The greater the stiffness of the LV myocardium, for any given change in LV volume during diastolic filling, the higher the corresponding filling pressures. In other words, when comparing a left ventricle with normal diastolic function with that of a left ventricle with diastolic dysfunction, for any given left ventricle volume during diastole, LV pressure will be higher in the ventricle with diastolic dysfunction compared with normal. The net result of these processes is that LV diastolic pressures and left atrial pressures become elevated at rest and/or during exercise, with resultant elevation of pulmonary capillary wedge pressure and pulmonary vascular congestion.

    Clinically, this manifests as dyspnea at rest or with exertion, paroxysmal nocturnal dyspnea, and orthopnea. Furthermore, these stiffer hearts have an inability to increase end-diastolic volume and stroke volume via the Frank-Starling mechanism despite significantly elevated LV filling pressure. The resultant decrease in augmentation of cardiac output, which normally occurs with exercise, results in reduced exercise tolerance and fatigue.

    In addition to diastolic dysfunction, a number of additional factors are now thought to contribute to the development of HFpEF. For example, increased arterial vascular stiffness along with LV systolic stiffness may increase systolic blood pressure sensitivity to circulating intravascular volume and may predispose to rapid-onset pulmonary edema. On the other hand, vascular-ventricular stiffening also predisposes to the hypotensive effects of preload or afterload reduction, thus potentially limiting the efficacy of vasodilators or diuretics in HFpEF. Neurohormonal activation may result in increased venous vascular tone, which in turn may result in a shift of the blood volume to the central circulation. Concomitant renal dysfunction may contribute to sodium and water retention and may precipitate symptoms of volume overload and heart failure in patients with the above substrate. Concurrent atrial dysfunction may result in further elevation in left atrial pressures and pulmonary vascular congestion.

    In the elderly, chronotropic incompetence with exercise is more commonly seen and may contribute to limitation in exercise cardiac output with resultant exertional fatigue. Pulmonary hypertension is common in HFpEF. The pulmonary hypertension may be related to both pulmonary venous as well as reactive pulmonary arterial hypertension in both HFpEF and systolic heart failure. As the right ventricle is very sensitive to afterload, resting and exercise-induced pulmonary hypertension may contribute to progressive right ventricular dysfunction.

7. What factors may precipitate decompensated HFpEF?

    In patients with underlying diastolic dysfunction and other abnormalities detailed in Question 6, acute decompensation of heart failure may often be contributed to by uncontrolled hypertension, atrial fibrillation or flutter (especially with rapid ventricular rates), myocardial ischemia, hyperthyroidism, medication noncompliance (especially diuretics and antihypertensives), dietary indiscretion (e.g., high-sodium foods), anemia, and infection.

8. How is the diagnosis of HFpEF made?

    The clinical diagnosis of HFpEF depends on the presence of signs and symptoms of heart failure and documentation of normal or near-normal LVEF (greater than 45% to 50%) by echocardiography, radionuclide ventriculography, or contrast ventriculography.

9. What common tests are useful in the diagnosis of HFpEF, and what do they often reveal?

Buy Membership for Internal Medicine Category to continue reading. Learn more here

Related posts:

Diabetes and Cardiovascular Disease Electrocardiogram Percutaneous Coronary Intervention Echocardiography Preoperative Cardiac Evaluation Cardiovascular Physical Examination