Summary
Owing to modern epidemiology in Western countries, ageing represents a growing health burden. In general, because of age itself and comorbid conditions, all clinical cardiovascular manifestations have a higher mortality rate and a worse outcome in older people compared with in younger individuals. Diagnosis of the disease in the elderly in an emergency setting is particularly challenging for the practitioner. Age-related cardiovascular changes and comorbid conditions may alter signs, symptoms and adaptation to the disease and response to treatment. Bedside Doppler echocardiography is likely to play a major role in guiding diagnosis, therapeutic strategies and prognosis. The purpose of this review is to appraise the application of echocardiographic examination in helping the clinician facing emergency situations that involve the cardiovascular system in the older population.
Résumé
Du fait de l’épidémiologie moderne des pays occidentaux, le vieillissement représente un problème de santé publique majeur. L’âge avancé et les co-morbidités associées aggravent la mortalité et le pronostic des manifestations cardiovasculaires chez les sujets âgés. Poser le diagnostic d’une maladie chez le sujet âgé dans un contexte d’urgence est particulièrement complexe pour le praticien. Les modifications cardiovasculaires liées à l’âge et aux co-morbidités peuvent modifier les signes diagnostiques, les symptômes, l’adaptation à la maladie et la réponse au traitement. L’écho Doppler cardiaque au lit du patient joue un rôle majeur pour guider le diagnostic, la thérapeutique, les stratégies de prise en charge et ainsi le pronostic. Le but de cet article de synthèse est d’illustrer l’aide apportée par l’écho Doppler cardiaque au clinicien face aux situations urgentes qui impliquent le système cardiovasculaire chez le sujet âgé.
Background
Ageing represents a major public health burden. The proportion of people aged 65 years and older in Western Europe is projected to increase from 17% in 2008 to 30% in 2060. Cardiovascular disease remains the leading cause of morbidity and mortality in the elderly. Conversely, because of the age-associated alterations in cardiac and vascular properties, ageing remains a major risk factor for cardiovascular morbidity and mortality. Age is indeed one variable in various scores that predict poor outcome in different settings (e.g. the Global Registry of Acute Coronary Events or the Seattle Heart Failure Survival Model) . Where age alone results in pre-existing impaired left ventricular (LV) filling capacity and reduced renal function , for instance, myocardial infarction associated with minor myocardial damage is more likely to result in pulmonary congestion (Killip class ≥ II) and subsequent worse outcome in the older individual than in the younger individual.
Doppler echocardiography is a non-invasive, radiation-free, bedside tool that may be considered as a modern stethoscope. Extremely varied and undiscovered cardiovascular diseases, often at a very late stage of the disease, may be disclosed using Doppler echocardiography imaging in older people. Owing to the conveniences of modern life, sedentary older people may underestimate, ignore or not report their symptoms, or may reduce their level of physical activity to avoid or minimize symptoms. Moreover, diagnosis of an event such as an acute myocardial infarction is usually delayed in older people because of atypical symptoms (dizziness, fatigue, altered mental status, etc.), resulting in increased time to onset of therapy and poorer outcome than in the younger individual . In addition, because cardiovascular diseases are seldom seen in isolation in older people (half have at least two chronic medical conditions), non-specific symptoms such as dyspnoea may be caused by other concomitant diseases such as chronic lung disease or obesity. To this effect, besides other diagnostic procedures including biomarkers, electrocardiogram and chest X-ray, comprehensive bedside Doppler echocardiography appears to be an important tool for diagnosis, therapeutic management and risk stratification in older people presenting in the emergency room. The goal of this report is to review the usefulness of Doppler echocardiography imaging in treating older people in the emergency room. The operating room setting is also addressed.
Age-related changes in health (‘normal’ ageing process)
Cellular and molecular mechanisms (cardiomyocyte size, number and function, key steps of excitation-contraction coupling, composition and distribution of elastin and collagen, vascular endothelial and smooth muscle cell function and structure, nitric oxide pathway, etc.) that account for changes in the ageing heart and vessels are multiple and complex. The reader can refer to the excellent review articles published previously on this topic . Arterial alterations include mainly decreased endothelial-mediated vasodilation, increased central vascular stiffening and aortic pulse wave velocity and faster reflected pulse waves, leading to an age-associated increase in LV wall stress and metabolic demand ( Fig. 1 ) . Increased late-systolic reflected waves due to the marked decrease in arterial compliance result in a fall in diastolic blood pressure and a rise in systolic blood pressure, and therefore higher pulse pressure. The marked increase in systolic contribution to total coronary blood flow suggests that systolic blood pressure may have a greater role in myocardial perfusion in the elderly than in the younger individual. Besides the progressive increase in cardiac workload with advancing age, myocardial fibrosis promotes prolonged LV diastolic relaxation. Blunted beta-adrenergic arterial vasodilation and inotropic and heart rate response , in addition to the changes mentioned above, contribute to the decreased aerobic capacity in older people. Lastly, decline in renal function and atrial fibrillation also contribute to a decrease in the stress response.
Echocardiographic features in normal ageing
The structural echocardiographic changes associated with normal ageing include a progressive increase in LV wall thickness that does not exceed the upper limit of normal (≤ 11 mm), with a minor decrease or no change in LV internal dimensions, resulting in a mild increase in cardiac mass and concentric LV remodelling . A significant increase in the aortic root dimension occurs with age and predicts incident heart failure (HF), stroke, and cardiovascular and all-cause mortality . Left atrial enlargement, which promotes stroke and atrial fibrillation (frequent illnesses in older people), also occurs with age . Sclerosis due to myxomatous degeneration, collagen infiltration and calcifications of both aortic and mitral valves are observed frequently in the elderly. Changes at the mitral level include from a few spicules of calcium to a large mass located behind the posterior leaflet, forming a half ring that may interfere with annular motion and decrease atrioventricular compliance, serve as a substrate for thromboembolism, heart block, valvular dysfunction or infective endocarditis ( Video Loop 1 ) . There is also a statistically significant decrease in LV outflow tract diameter and velocity that parallels a decrease in aortic valve area and an increase in aortic velocity . Paralleling the increased arterial stiffening and systemic vascular resistance, an aortic flow mid-systolic notch is seen frequently in the elderly population ( Fig. 2 ). Importantly, LV diastolic function declines with ageing, while LV ejection fraction remains preserved. There is a progressive decrease in early diastolic peak flow velocity (E), deceleration and early diastolic peak flow velocity/late diastolic peak flow velocity (E/A) ratio . As a result, 87% of the elderly population exhibit an E/A ratio < 1 ( Fig. 3 ) . Similarly, tissue Doppler early diastolic mitral and tricuspid annular velocities (Ea) are lower in older people than in younger individuals. In addition, Ea is inversely related to late systolic load, which is mediated predominantly by the increased systolic wave reflections brought by age, thereby leading to an increased E/Ea ratio . However, it is not known whether other cut-off values for ‘normal’ age-specific E/Ea ratios should be used. In contrast, tissue Doppler late diastolic velocities are not altered with age. It is worth noting that tissue Doppler systolic mitral annular velocity (a measure of longitudinal contractility of the LV myocardium) is also lower in the elderly, demonstrating subclinical LV systolic dysfunction . However, the compensatory increase in radial thickening normalizes LV ejection fraction, which remains stable with age . Systolic pulmonary artery pressure, estimated from the tricuspid regurgitant velocity, increases progressively with age , probably due to the age-related increase in pulmonary arterial stiffening and/or heightened LV end-diastolic pressure. Both systolic and early diastolic velocities of the tricuspid annulus are lower in older people than in younger individuals . It is worth noting that systemic hypertension, a common condition in older people , exacerbates the changes related to ageing, such as LV hypertrophy, alterations in LV diastolic function, longitudinal systolic function and pulmonary pressure .
Heart failure setting
HF is the most frequent hospital discharge diagnosis among the elderly . The reader can refer to a recently published comprehensive review on the role of echocardiography in the management of HF .
Heart failure with preserved left ventricular ejection fraction
HF with preserved ejection fraction (HFpEF) increases in prevalence in older populations (about 50% of older people with HF) . HFpEF is particularly common in elderly women with longstanding hypertension, type 2 diabetes mellitus and obesity . However, before categorizing a patient as having HFpEF, several causes (such as severe cardiac valvular diseases, restrictive, infiltrative or hypertrophic cardiomyopathy, isolated right ventricular failure, pericardial diseases, intracardiac masses, pulmonary vein stenosis, congenital heart diseases, presence of prosthetic heart valve, bradycardia related to atrioventricular or sinoatrial blocks, myocardial ischaemia related to coronary artery disease, high-output HF, dialysis-dependent and end-stage renal failure, liver cirrhosis, nephrotic syndrome, and transient LV systolic dysfunction related to tachyarrhythmia) need to be excluded by thorough clinical and echocardiographic examination, laboratory data and eventually other diagnostic procedures. In HFpEF patients, echocardiography shows the characteristic combination of LV hypertrophy or concentric remodelling and left atrial enlargement, which is a harbinger of chronically elevated LV filling pressure in older people presenting with signs and symptoms of congestive HF ( Video Loop 2 ) . The acute rise in E/Ea ratio and pulmonary pressure is common in the setting of acute HF. Importantly, transmitral inflow recording may, nevertheless, show the pattern of ‘hyperabnormal relaxation’ in decompensated older people ; in these cases, heightened LV filling pressure is easily uncovered by calculating the E/Ea ratio ( Fig. 4 ). In steady state, despite vasodilator and diuretic therapy, the averaged levels of the E/Ea ratio and pulmonary pressure remain higher compared with controls . Similarly, right ventricular enlargement and functional mitral regurgitation may be observed transiently in the overloaded state, although this reduces or disappears with cardiac load reduction ( Video Loops 3A and 3B ) . Importantly, besides severe coronary artery or valve disease, HFpEF may be an unrecognized cause of mechanical ventilatory weaning failure in the intensive care unit. Abrupt and unprepared ventilatory weaning can result in an acute increase in LV wall tension, and increased venous return and thereby LV preload, promoting increased pulmonary capillary wedge pressure and secondary mitral regurgitation, and eventually precipitating pulmonary oedema in HFpEF patients ( Fig. 5 ) . Prior vasodilator and diuretic therapy is likely to help ventilatory weaning in this setting. Of note, after the acute HF episode, exercise echocardiography often unmasks LV abnormal response or induced functional mitral regurgitation .
Heart failure with reduced LV ejection fraction
HF with reduced ejection fraction is also common in elderly populations ( Video Loop 4 ). Coronary artery disease, hypertension, sustained excess tachycardia and cardiac valvular disease, such as aortic stenosis, are the main causes of HF with reduced ejection fraction in older people. Segmental wall motion abnormalities and LV scarring suggest underlying coronary artery disease. Coronary angiography provides the definitive diagnosis.
Cardiac valvular diseases
Cardiac valvular diseases are common in the general population and increase with age . Aortic valve stenosis affects 2% of patients older than 65 years (mean age 82 years) . The pathophysiological consequences of aortic valve stenosis include LV hypertrophy, elevated LV diastolic pressure and progressive decline in LV systolic function . Aortic valve replacement is warranted in the absence of severe comorbid conditions when patients develop symptoms or LV systolic dysfunction . It is worth noting that percutaneous procedures in older people need further validation (ongoing REVIVE, REVIVAL and PARTNERS trials) before wide acceptance in routine practice. Low-dose dobutamine is useful for assessing the presence of contractile reserve and differentiating true severe from pseudosevere stenosis in the challenging subset of patients with low LV ejection fraction and low transvalvular gradient . Exercise stress echocardiography may be envisioned in patients with aortic valve stenosis and equivocal symptoms and normal ejection fraction . In the elderly, the narrowed valvular orifice is often combined with underlying LV systolic and diastolic dysfunction that may be related to other cofactors such as coronary artery disease or longstanding hypertension, thereby adding a level of complexity to the assessment of these patients. In addition, low transvalvular gradients are frequently observed in these elderly patients, despite a calculated aortic valve area below 1.0 cm 2 or 0.60 cm 2 /m 2 , questioning the true severity of the stenosis. In some patients, the discrepancy between relatively low transvalvular gradients and decreased aortic valve area may be explained by the pressure recovery phenomenon . A significant rise in static pressure downstream from the orifice occurs (due to reconversion of kinetic energy into potential energy) if the ascending aorta is narrow (diameter of the aortic sinotubular junction < 30 mm) and leads to an overestimation of Doppler-derived transvalvular gradients. The use of the Doppler-derived energy loss index, which takes account of the diameter of the aorta to calculate aortic effective orifice area, helps to reconcile discrepancies between Doppler transvalvular pressure gradient data and effective orifice area obtained by the Doppler continuity equation . Recently, Hachicha et al. demonstrated that low-flow (stroke volume index ≤ 35 mL/m 2 ), low-gradient but severe aortic valve stenosis despite normal ejection fraction is prevalent in older people, especially in hypertensive women with concentric LV remodelling or hypertrophy and high systemic vascular resistances ( Fig. 6 , Video Loop 5 ) . Despite a low transvalvular pressure gradient , these patients are indeed at a severe stage of the disease, associated with a high global LV afterload (the sum of arterial and valvular loads) . The low survival observed in patients managed conservatively advocates identification of this challenging subgroup of aortic valve stenosis patients and consideration of aortic valve replacement. Concomitant significant mitral regurgitation or left-to-right shunt related to an atrial septal defect may occasionally cause low transvalvular gradients despite severe aortic valve stenosis and normal ejection fraction .
Concomitant mitral regurgitation and HF requires comprehensive assessment. The reader can refer to the review article published previously on this topic . Mitral valve prolapse is a common cause of mitral regurgitation ( Video Loops 6A and 6B ) and is often combined with mitral annular calcification in older people, which otherwise complicates valve surgery significantly. Large calcific deposits in the posterior mitral annulus may themselves restrict posterior leaflet motion and produce mitral regurgitation ( Video Loops 7A and 7B ) . In contrast, extensive mitral calcifications that extend onto the base of the mitral leaflets may produce a significant increase in transvalvular velocity-derived gradients, suggesting severe mitral stenosis ( Video Loop 8 ) . Using transoesophageal echocardiography, in contrast to the thickening at the leaflet tips and commissural fusion seen with rheumatic disease, these large calcifications spare the edges of the leaflets and the commissures, often resulting in moderate stenosis and thus allowing conservative management in the elderly. Of note, heightened LV diastolic pressure, related to ageing, hypertension or concomitant aortic valve disease, may result in relatively low transmitral gradient despite severe mitral stenosis. Of note, patients with true severe calcific mitral stenosis are not good candidates for percutaneous valvotomy . In older people with LV systolic dysfunction, functional/ischaemic mitral regurgitation is usually mild or moderate but may be severe, especially in the case of severe posterior leaflet tethering ( Video Loop 9 ). Patients with ischaemic mitral regurgitation associated with a high posterior leaflet angle should not undergo restrictive annuloplasty . Drug-induced valvular disease (with the anti-Parkinson disease dopamine receptor agonist pergolide) has been reported but is uncommon.
Intra-left ventricular obstruction
The presence of LV obstruction should be ruled out systematically in the setting of HF and normal or supranormal ejection fraction, even in the absence of hypertrophic cardiomyopathy ( Fig. 7 , Video Loop 10 ). Dynamic LV outflow tract obstruction affects both systolic and diastolic LV function. Pre-existing LV concentric remodelling, associated with specific conditions such as inappropriate or excessive use of positive inotropic therapy or relative hypovolaemia, may facilitate the occurrence of intra-LV obstruction and produce mitral leaflet systolic anterior motion and hence unexpected (‘paradoxical’) pulmonary oedema. Fluid challenge, discontinuation of inotropic therapy and possibly initiation of beta-blockade therapy are indicated in this situation.
