Valve Disease

Introduction

Mild degrees of valvular heart disease are very prevalent in adult patients with heart failure symptoms. Given that these are often patients with hypertension, aortic valve sclerosis and mitral annular calcification, frequently accompanied by some degree of mitral regurgitation, are extremely common. They need to be taken into consideration when assessing such patients. On the other hand, severe left-sided valvular heart disease may also lead to the clinical syndrome of heart failure. Naturally, the hemodynamic consequences of severe valvular lesions (e.g., in aortic stenosis) take priority over the assessment of myocardial diastolic function for making clinical decisions. Nevertheless, it is helpful to review the impact of such lesions on diastolic left ventricular (LV) pressure levels and diastolic function, and their echocardiographic correlates, since following valve replacement many patients will have persisting symptoms caused by the long-term effect of LV remodeling leading to diastolic dysfunction.

Epidemiology of Valvular Heart Disease

Valvular heart disease increases in prevalence with age. The most frequent valvular lesion requiring repair is aortic stenosis, followed by mitral regurgitation. Aortic stenosis is very prevalent (3%–5%) in the elderly population. Aortic regurgitation is considerably rarer, and severe mitral stenosis is almost exclusively rheumatic in origin and thus rare in developed countries. On the other hand, degenerative calcific mitral stenosis has become more frequent due to the aging of the general population, but mostly is hemodynamically mild. It does affect, however, parameters used in echocardiography to assess diastolic function, such as e′, and thus needs to be taken into account when interpreting such parameters.

Aortic Stenosis

In aortic stenosis with preserved ejection fraction, LV concentric remodeling or hypertrophy leads to slowed myocardial relaxation in early diastole, low chamber compliance, and increased myocardial stiffness, especially at a higher age (see Case Study 1). These changes are at least partially reversible after aortic valve replacement.

Additionally, long-standing aortic stenosis leads to myocardial interstitial fibrosis, and a considerable fraction of elderly patients with aortic stenosis also develop some degree of cardiac amyloidosis. The latter is impossible to differentiate by echocardiography from concentric remodeling due the valvular stenosis, but can be characterized by cardiac magnetic resonance imaging (cardiac MRI) or nuclear imaging. Fibrosis and amyloidosis are known to impair LV diastolic function; thus their detection suggests indirectly possible diastolic dysfunction. Global longitudinal echocardiographic strain has been shown to correlate modestly with diffuse myocardial fibrosis in patients with aortic stenosis.

On cardiac MRI, diffuse interstitial myocardial fibrosis leads to increased myocardial T1 values and increased extracellular volume estimates. Thus these parameters may be interpreted as markers of diastolic dysfunction, although the strength of the association between T1 values and histologic parameters of fibrosis, such as collagen volume fraction, is quite modest. Furthermore, replacement fibrosis, or the presence of localized increases in extracellular space, may be visible as midwall late enhancement after gadolinium (cardiac MRI contrast) application. The importance of such findings in the individual patient, however, is unclear.

As in all forms of hypertrophy, longitudinal function and thus e′, as well as longitudinal strain parameters, such as global longitudinal strain (GLS), are reduced in aortic stenosis, while ejection fraction is preserved until late in the progression of the disease (see Case Study 1). Diastolic dysfunction is probably the prime cause of the chief symptom of aortic stenosis, dyspnea. Signs of diastolic dysfunction are therefore expected in the context of significant aortic stenosis and should not be construed as necessarily indicating an additional disease. However, concomitant hypertension, coronary artery disease, myocardial fibrosis, amyloidosis, and others may be present and contribute to diastolic functional impairment. Thus increased left atrial (LA) volume, low e′ and high E/e′, as well as right-sided pressure increase are frequent in moderate or severe aortic stenosis and indicate LV diastolic dysfunction with increased diastolic pressures. Note that low longitudinal strain is also frequently present in spite of preserved ejection fraction. Other imaging modalities such as cardiac MRI are generally unnecessary to assess diastolic function.

Diastolic LV function contains prognostic information in aortic stenosis. In 125 patients with severe aortic stenosis who were not operated for diverse reasons, E/e′ was the best echo predictor of 1-year survival, both in symptomatic and asymptomatic patients. Recently, a retrospective study of 90 patients undergoing transcatheter intervention for severe aortic stenosis reported that (1) preoperative grade of diastolic dysfunction was a strong predictor of postinterventional 1-year morbidity and mortality, and (2) diastolic dysfunction tended to improve after intervention, but improvement was not clearly related to prognosis (which might be due to study size and/or missing data). In the largest such study ( n = 358), an effect of preoperative diastolic function grade on postinterventional mortality could not be shown; however, improvement in diastolic function after transcatheter intervention paralleled clinical improvement, and lack of improvement was associated with a worse prognosis. After aortic valve replacement or intervention, regression of LV hypertrophy and improvement of systolic LV function (by ejection fraction, as well as by longitudinal strain) occur. There is regression of myocardial T1, likely paralleling decrease in myocardial fibrosis. Diastolic function has been shown both invasively and noninvasively to improve over time. However, the degree of normalization varies. Patient-prosthesis mismatch is associated with persistent diastolic dysfunction and adverse prognosis.