Diastolic heart failure
Diastolic heart failure (DHF)
Description, Causes and Risk Factors:
Heart failure can arise from any condition that compromises the contractility of the heart (systolic heart failure) or that interferes with the heart's ability to relax (diastolic heart failure). Hospital- and community-based reports indicate that about one fourth to one half of patients with heart failure have normal left ventricular systolic function. Observational studies indicate that diastolic heart failure is more common in women and elderly persons. Although patients with diastolic heart failure have a lower annual mortality rate than patients with systolic heart failure, they have a higher rate than the general population. They also have hospitalization rates similar to those of patients with systolic heart failure. These observations emphasize diastolic heart failure as an important contributor to morbidity, mortality, and health care costs, and highlight the need for further research and clinical trials examining this condition.
Diastole is the process by which the heart returns to its relaxed state; it is also the time for cardiac perfusion. During diastole, drastic changes in cardiac pressure-volume relationships occur. The relaxation process has four identifiable phases: isovolumetric relaxation from the time of aortic valve closure to mitral valve opening; early rapid filling after mitral valve opening; diastasis, a period of low flow during mid-diastole; and late filling of the ventricles from atrial contraction.
In patients with isolated diastolic heart failure, the heart often is able to meet the body's metabolic needs, but at higher diastolic pressures. The left ventricle is stiff, with decreased compliance and impaired relaxation. Transmission of the higher end-diastolic left ventricular pressure to the pulmonary circulation may lead to pulmonary congestion, dyspnea, and other symptoms of heart failure.
Diastole is a complex process that is affected by a number of factors, including ischemia, heart rate, velocity of relaxation, cardiac compliance (i.e., elastic recoil and stiffness), hypertrophy, and segmental wall coordination of the heart muscle.
Ischemia: Relaxation of the ventricles involves the active transport of calcium ions into the sarcoplasmic reticulum, which allows the dissociation of myosinactin crossbridges. Hypoxia inhibits the dissociation process by altering the balance of the adenosine triphosphate-to-adenosine diphosphate ratio, which may contribute to diastolic dysfunction.
Atrial fibrillation: Patients with heart failure are at increased risk for atrial fibrillation. As the ventricle stiffens and develops higher end-diastolic pressures, the atria are distended and stressed; this situation often results in atrial fibrillation. The loss of atrial contraction worsens the symptoms of heart failure, because patients with diastolic dysfunction often are dependent on atrial filling of the left ventricle (“atrial kick”). Atrial fibrillation also can worsen symptoms if the ventricular rate is uncontrolled.
Ventricular load. At the end of normal systole, a small residual volume of blood remains in the left ventricle. If this residual volume increases, it interferes with the normal elastic recoil of the heart, the relaxation of the heart, and the development of a negative pressure gradient between the ventricle and atria. As a result, rapid early diastolic filling is impaired.
Chronic hypertension is the most common cause of diastolic heart failure. It leads to left ventricular hypertrophy and increased connective tissue content, both of which decrease cardiac compliance. The hypertrophied ventricle has a steeper diastolic pressure-volume relationship; therefore, a small increase in left ventricular end-diastolic volume (which can occur with exercise, for example) causes a marked increase in left ventricular end-diastolic pressure.
Cardiac catheterization remains the 'Gold standard' for demonstrating impaired relaxation and filling, because it provides direct measurement of ventricular diastolic pressure. However, the balance of benefit, harm, and cost argue against its routine use in diagnosing diastolic dysfunction.
Doppler echocardiography has assumed the primary role in the noninvasive assessment of cardiac diastolic function and is used to confirm the diagnosis of diastolic heart failure. For example, echocardiographic measurement of tau, the time constant of left ventricular pressure decay during isovolumetric relaxation, can be performed to assess left ventricular stiffness.
More importantly, Doppler echocardiography is used to evaluate the characteristics of diastolic transmitral valve blood flow. The peak velocities of blood flow during early diastolic filling (E-wave) and atrial contraction (A-wave) are measured, and the ratio is calculated. Under normal conditions, the early-filling E-wave velocity is greater than the A-wave velocity, and the E-to-A-wave ratio is about 1.5. In early diastolic dysfunction, this relationship reverses, because the stiffer heart relaxes more slowly, and the E-to-A-wave ratio drops below 1.0. As diastolic function worsens and left ventricular diastolic pressure rises, left ventricular diastolic filling occurs primarily during early diastole, because the left ventricular pressure at end-diastole is so high that atrial contraction contributes less to left ventricular filling than normal. At this point, the E-to-A-wave ratio rises, often to greater than 2.0. This so-called 'restrictive pattern' confers a poor prognosis.Recent studies also have shown that Doppler evaluation of myocardial velocities during ventricular relaxation predict elevated filling pressure.
The E-and A-wave velocities are affected by blood volume and mitral valve anatomy and function. Furthermore, these wave velocities are less useful in the setting of atrial fibrillation. Despite these limitations, Doppler echocardiography provides essential information about the anatomy and function of the heart, chamber size, hypertrophy, valvular function, regional wall abnormalities, and chamber pressures. It also allows the physician to identify and rule out other potential causes of the patient's symptoms, such as valvular lesions, pericardial disease, and pulmonary hypertension.
Treatment of diastolic heart failure is aimed to stop the progression of the disease, relieve its symptoms, eliminate exacerbations and reduce the mortality. The management should include antihypertensive treatment, maintenance of the sinus rhythm, prevention of tachycardia, venous pressure reduction, prevention of myocardial ischemia and prevention of diabetes mellitus. The treatment of diastolic heart failure is less well defined than the treatment of systolic heart failure. Current recommendations are based on disease-oriented evidence, including Pathophysiology, extrapolation of knowledge about other aspects of cardiovascular disease, data from small studies, and expert opinion. None of the treatment recommendations have been validated by randomized controlled trials (RCTs).
Treatment with diuretics and vasodilators often is necessary to reduce pulmonary congestion. However, caution is required to avoid excessive diuresis, which can decrease preload and stroke volume. Patients with diastolic dysfunction are highly sensitive to volume changes and preload.
The potential benefits of beta blockers stem from their ability to decrease heart rate, increase diastolic filling time, decrease oxygen consumption, lower blood pressure, and cause regression of left ventricular hypertrophy.
The multiple benefits of angiotensin-converting enzyme (ACE) inhibitors in the treatment of cardiovascular disease make them highly promising therapeutic agents. ACE inhibitors cause regression of left ventricular hypertrophy, decrease blood pressure, and prevent or modify cardiac remodeling; these actions provide strong theoretic support for the use of these agents in patients with diastolic dysfunction. So far, there have been few studies of ACE inhibitors in patients with diastolic dysfunction.
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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