* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download 11_Skarvan_The aging heart: what can echocardiography tells us
Cardiac contractility modulation wikipedia , lookup
Saturated fat and cardiovascular disease wikipedia , lookup
Cardiovascular disease wikipedia , lookup
Artificial heart valve wikipedia , lookup
Antihypertensive drug wikipedia , lookup
Electrocardiography wikipedia , lookup
Heart failure wikipedia , lookup
Lutembacher's syndrome wikipedia , lookup
Arrhythmogenic right ventricular dysplasia wikipedia , lookup
Coronary artery disease wikipedia , lookup
Cardiac surgery wikipedia , lookup
Myocardial infarction wikipedia , lookup
Hypertrophic cardiomyopathy wikipedia , lookup
Aortic stenosis wikipedia , lookup
Echocardiography wikipedia , lookup
Dextro-Transposition of the great arteries wikipedia , lookup
The aging heart: what can echocardiography tells us about it? K. Skarvan Prof. emer., Cardiovascular Research Group, Department of Anaesthesia University Hospital Basel, Spitalstrasse 21, 4031 Basel, Switzerland [email protected] [email protected] Structural changes of the aging heart In the course of the natural aging process the heart undergoes a structural remodelling, which inevitably results in alterations of cardiac function. While in aging women left ventricular (LV) myocardial mass as well as myocyte number, size and volume are preserved, in men there is a progressive loss of LV both myocyte number and mass. The remaining myocytes are subjected to an increased stress and exhibit an increase in volume and stiffness. The LV walls become thicker and the LV changes its shape to a more spherical one. There is also an increase in focal myocardial fibrosis and diffuse or multifocal deposits of amyloid can be found both in the atria (isolated atrial) and ventricles (systemic senile amyloidosis). Thickening and calcification of cardiac valve leaflets and their supporting apparatus as well as dilation of the aortic root and the aorta are other characteristic features of the aging process. The simultaneous aging of the arteries exposes the LV to an increased systolic load. This is related to the increased stiffness of the aortic wall, late systolic pressure augmentation caused by increased pulse wave velocity and reflected pressure waves increased systolic pressure. Although the pressure overload represents a trigger of LV hypertrophy, the myocytes growth is limited in the aging heart and may not be able to compensate for the lost myocardium. There is no convincing evidence that the LV mass consistently increases with age. The LV end diastolic (ED) size remains unchanged and the left atrial size does not increase until the 8th decade. Changes in the function of the aging LV. The LV contraction velocity is decreased and the duration of the contraction is prolonged. However, the global and regional LV systolic functions remain well preserved. In contrast, the diastolic function is altered and results in a progressive impairment of the early diastolic filling. Consequently, the LV filling depends progressively more on the booster pump function of the left atrium. Both end systolic (ES) and ED LV chamber stiffness (Ees and Eed, respectively) are increased and likely reflect the structural changes in the aging myocardium. The increase in Ees with age matches the parallel increase in vascular stiffening (described by effective elastance Ea: systolic blood pressure:stroke volume) and preserves the normal ventricular-vascular coupling (Ea/Ees). The real loss of cardiac function, however, becomes evident only under exercise, which will unmask the progressive decrease in cardiac output reserve (1). Echocardiography of the aging heart The 2-D echocardiography typically finds a normal global LV systolic function expressed as fractional shortening (FS%), fractional area change (FAC%) or ejection fraction (EF%). However, the mid-wall shortening corrected for LV afterload shows a weak decline and the systolic velocity of the mitral annulus (S’) is also reduced in higher age groups. This is associated with a decreasing longitudinal and radial LV strain and strain rate. The preload indices, such as LV ED diameter, ED area or ED volume remain within the normal ranges. The LV wall thickness is usually increased, particularly in the ventricular septum. The changes in the sphericity index (length: width ratio) and the relative wall thickness (2x ED wall thickness: ED diameter) point to the presence of LV concentric remodeling. The leaflets of the mitral and aortic valves are thickened and there will be a varying amount of calcium deposits in the mitral and aortic annulus. However, not more than a mild valvular regurgitation should be present. The diameter of the aortic root is usually increased and an atheromatosis of the ascending aorta of varying grade is usually found. Doppler measurements of transmitral and pulmonary venous flow velocity demonstrate prolonged isovolumic relaxation time (IVRT), decreased E, D, and increased A velocity, prolonged deceleration time of the E wave, reduced E/A ratio, increased S/D ratio, increased atrial emptying ratio as well as atrial ejection force. The left atrial size (diameter, area or volume) may be increased in the very old. The early diastolic mitral annular velocity E’ decreases with age but the E/E’ quotient should remain in the normal range (<8). These findings correspond to a grade I of diastolic dysfunction called „impaired relaxation“. In subjects with marked concentric remodeling, increased LV intraventricular velocities may be found in systole by CW Doppler. The presence of mild tricuspid and pulmonic valve regurgitation allows the estimation of the systolic and diastolic pulmonary artery pressures that should be normal. The calculation of the stroke volume from the cross-sectional area and velocity time integral of the blood flow velocity of the LV outflow tract should confirm the presence of a still normal stroke volume. Nevertheless, a decline in resting cardiac index of 6-7 ml/min/m2 and year can be expected. Echocardiographic diagnosis of heart disease in the elderly The echocardiography is the most important diagnostic tool for the detection of heart disease in the aging population. The most common heart diseases of the advanced age include heart failure (HF), calcified aortic stenosis, hypertension and coronary artery disease (CAD). The disease related changes in the structure and function of the heart become superimposed on the substrate of the aging heart. In patients with HF, the echocardiography should confirm the diagnosis based on clinical and laboratory findings (BNP) and provide additional information on the mechanism of the HF (2). The systolic HF can be separated from the aging heart by the findings of chamber dilation, abnormal global and/or regional LV function and signs of increased filling pressures. The common causes include CAD, valvular heart disease, cardiomyopathy and hypertension. In the elderly, the most common form of HF is the diastolic HF with preserved ejection fraction. However, the separation between diastolic HF and the aging heart with diastolic dysfunction is not easy and should be based on the recently updated recommendations for the diagnosis of diastolic HF (3). The CAD can be detected by abnormal LW wall motion, reflecting ischemia, postinfarction scars with remodeling and aneurysms at rest or by ischemia provoked by dobutamine stress test. The valvular lesions are assessed according to the published guidelines (4). A calcified aortic valve without any signs of outflow obstruction is known as aortic valve sclerosis and can be found in up to 1/3 of subjects older than 65 years. It is associated with atheromatosis of the aorta and increased risk of all cause and cardiovascular mortality. The patients with superimposed hypertensive heart disease can be identified by pronounced LV hypertrophy and increased LV mass. References 1. Lakatta EG Heart Failure Reviews 2002;7:29-497 2. ACCF/AHA Guidelines Circulation 2009;119:e391-e-479 3. EAE/ASE Recommendations Eur J Echocardiogr 2009;10:165-193 4. European Society of Cardiology Guidelines Eur Heart J 2007; 28:230-268