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Symptomatic Presentations of Severe Aortic Stenosis

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Symptomatic Presentations of Severe Aortic Stenosis Precision and Future Medicine 2017;1(3):122-128 REVIEW https://doi.org/10.23838/pfm.2017.00156 ARTICLE pISSN: 2508-7940 · eISSN: 2508-7959 Symptomatic presentations of severe aortic stenosis Sung-Ji Park Division of Cardiology, Department of Internal Medicine, Cardiovascular Imaging Center, Heart Vascular Stroke Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea Received: August 2, 2017 Revised: September 12, 2017 Accepted: September 19, 2017 ABSTRACT Aortic stenosis (AS) is the most common type of valvular heart disease. A manifestation Corresponding author: Sung-Ji Park of ageing, the disorder is becoming more frequent as the average age of the population Division of Cardiology, increases. Onset of cardinal manifestation of AS—angina, syncope, and heart failure— Department of Internal remains the major demarcation point in the disease’s course. It has been well described Medicine, Cardiovascular that patients’ survival is limited once they develop symptoms from AS and survival after Imaging Center, Heart Vascular the onset of a symptom depends on what type of symptom a patient develops. Know- Stroke Institute, Samsung ing how the pathophysiology of AS causes typical symptoms and death is paramount to Medical Center, Sungkyunkwan understanding the disease. We discuss these issues in this review. University School of Medicine, 81 Irwon-ro, Gangnam-gu, Keywords: Aortic valve stenosis, Chest pain, Dyspnea, Echocardiography, syncope Seoul 06351, Korea Tel: +82-2-3410-3419 E-mail: [email protected] INTRODUCTION Aortic stenosis (AS) is the most common valvular heart disease in the elderly characterized by fixed aortic valve narrowing, left ventricular (LV) remodeling with hypertrophy, and progressive diastolic dysfunction [1]. The cardinal manifestations of AS include syncope, chest pain, and dyspnea. It has been well described that patients’ survival is limited once they develop symp- toms from AS and survival after the onset of a symptom depends on what type of symptom a patient develops [2]. Therefore, the onset or presence of these symptoms are the class I indica- tion for surgical indication [3], but without any distinction among symptoms. Is there any significant correlation between the severity of AS and development of symp- toms? The development of symptoms in asymptomatic AS was predicted by aortic jet velocity at baseline, the rate of change in aortic jet velocity, and baseline functional status [4]. However, there was a large overlap between symptomatic and asymptomatic patients, consistent with This is an Open Access article the known heterogeneous response to the pressure load of AS [5]. Therefore, the occurrence distributed under the terms of the and severity of cardiac symptoms may correlate poorly with the severity of AS (aortic valve Creative Commons Attribution area [AVA] and transvalvular pressure gradients), and symptoms often occur despite preserved Non-Commercial License (http:// creativecommons.org/licenses/ LV ejection fraction (EF) [6,7]. by-nc/4.0/). 122 Copyright © 2017 Sungkyunkwan University School of Medicine Sung-Ji Park THE EFFECT OF LEFT VENTRICULAR HY- active LV relaxation, and compromised coronary flow re- PERTROPHY ON SYMPTOMS STATUS IN serve. All of these changes may affect diastolic and systolic AS function and be associated with increased mortality [9,10]. The magnitude of LVH did not by itself explain the presenta- Hypertrophy is considered one of the major mechanisms of tions of symptoms of AS [7]. Pressure gradient nor AVA are the myocardium for adapting to hemodynamic overload. not predictive of symptom onset because those factors alone More muscle mass provides more contractile elements for do not by themselves control the myocardium’s response to generating the extra work required by the overload. In pres- AS [11]. It is thus possible that the development of symptoms sure overload of AS, concentric LVH normalizes wall stress, a in AS reflects alterations in LV morphology and function, key determinant of ejection performance [8]. leading to increased filling pressures and left atrial (LA) dila- Afterload is often expressed as ventricular wall stress (δ). In tation, hemodynamic, and morphological changes that may this way, the high systolic pressure required to drive blood occur without any change in LVEF. through a very stenotic aortic valve and it can be consistent with normal afterload and normal EF. Since afterload is a key ASYMPTOMATIC VERSUS SYMPTOMATIC AS determinant of ejection performance, its normalization is important in maintaining normal EF and stroke volume. LV The basic question is which echocardiographic parameters pressure overload may induce LV hypertrophy. Unfortunate- differentiate the presence of symptoms in severe AS? ly, hypertrophy is a double-edged sword. Although it helps to The hemodynamic consequence of AS is LV pressure over- preserve ejection performance, hypertrophy also impairs load, causing morphological changes of the LV characterized coronary blood flow reserve inducing myocardial fibrosis, by LV hypertrophy, concentric remodeling, and myocardial which in turn leads to increased chamber stiffness, delayed fibrosis. As a consequence of increased afterload [8] and LV 100 100 40 ) ) 2 80 2 80 30 60 60 E/e’ 20 40 40 SVI (mL/m LAVI (mL/m LAVI 10 20 20 0 A 0 B 0 C Syncope DOE Chest pain Syncope DOE Chest pain Syncope DOE Chest pain Fig. 1. (A) Left atrial volume index (LAVi), (B) stroke volume index (SVI), and (C) E/e’ ratio in patients with different symptoms. Adapted from Park et al. [7]. DOE, dyspnea on exertion. 1.00 P=0.006 Asymptomatic Symptomatic P<0.001 0.75 100 1 41 80 0.50 60 Sensitivity Age % 19 35 Age+AVmax 7 0.25 Age+AVmax+LAVi 40 114 Age+AVmax+LAVi+LAMi Age+AVmax+LAVi+LAMi+DT 20 0 2 0 A 0 0.25 0.50 0.75 1.00 B Normal Grade 1 Grade 2 Grade 3 1-Specificity Fig. 2. (A) Symptomatic status as a function of diastolic grade, (B) Incremental information of age, maximum aortic valve velocity (AVmax), left atrial volume index (LAVi), LVMi, and deceleration time in predicting symptom status. Adapted from Dahl et al., with permission from Wolters Kluwer Health [17]. https://doi.org/10.23838/pfm.2017.00156 123 Symptoms in aortic stenosis remodeling [12-14], AS will lead to LV diastolic dysfunction, lumic relaxation, in turn delaying mitral valve opening and increased filling pressures, and heart failure (HF) symptoms. shortening the time for the LV to fill. Passive filling in patho- The development of HF symptoms has previously been logic LVH is characterized by a shift in the diastolic pres- demonstrated to be associated with measures of AS severity sure-volume relation of the LV upward and leftward, thus re- and LV hypertrophy [15,16]. In contrasts, Park et al. [7] recent- quiring increased filling pressure to fill the LV to any given ly demonstrated that compared with the asymptomatic volume because the LV is stiffer than normal. Increased LV group, symptomatic patients were older and had lower car- stiffness in pathologic LVH accrues both from intrinsic and diac output, and higher E/e’ ratio while having a similar AVA extrinsic factors. Intrinsically, myocytes are thicker and filled and gradient in 498 severe AS and normal LVEF. Syncope with a denser than normal cytoskeleton [21], in turn causing group displayed smaller LV dimension, stroke volume, cardi- the myocyte to be stiffer than normal. Increased chamber ac output, left atrial volume index (LAVi), and E/e’ ratio. Con- stiffness is also due to increased extracellular components versely, dyspnea group was found to have the worst diastolic including the collagen network that holds the LV together function with largest LAVi and highest E/e’ ratio (Fig. 1). Dahl and that connects the myocyte to the chamber [22]. In se- et al. [17] also compared clinical characteristics and echocar- vere AS patient, at least four factors—LV thickness, active re- diographic parameters in 99 symptomatic and 139 asymp- laxation, myocyte structure, and extracellular matrix—can tomatic patients with severe AS and normal LVEF. This study vary from patient to patient. Those four factors can alter dia- demonstrated that symptomatic status was associated with stolic function [11]. This complexity and augmented diastolic LVH, concentric remodeling, diastolic dysfunction, and dila- dysfunction leads to pulmonary congestion and dyspnea in tation of LA. An LV diastolic grade of 2 or 3 was highly associ- severe AS. ated with the presence of symptoms and model including age, maximum aortic valve velocity, left ventricular mass in- SYNCOPE dex (LVMi), LAVi, and deceleration time provided incremental information on symptomatic status (Fig. 2). Syncope is one of the most urgent clinical symptoms, occur- ring suddenly without warning. Syncope occurs when there DYSPNEA is inadequate systemic blood pressure to support cerebral blood flow. Three mechanisms have been suggested to ex- Onset of dyspnea and other symptoms of HF presage the plain exertional syncope in patients with AS: (1) cardiac ar- worst outlook for the patient with AS [18]. The first question rhythmias, (2) sudden failure of an overloaded LV during the is what causes the dyspnea in severe AS? In the patients with stress of exercise, (3) peripheral vasodilatation occurring severe AS who develop dyspnea, markedly altered LV diastol- suddenly and inappropriately in the face of fixed cardiac out- ic function with increased filling pressure was present (Fig. 1) put [23]. Inappropriate vasodilation, the result of reflexes [7]. Left-sided filling pressures seem to have a good correla- triggered by LV baroreceptors [24] and occurring during or tion with the symptom [19]. Diastolic dysfunction, which in- just after exercise, is thought to be the mechanism in most creases LV filling pressure, predicted dyspnea in severe AS cases [25]. The exact mechanism of syncope in AS still re- patients. The second question is what causes the diastolic mains unclear. dysfunction in severe AS? Diastole is typically divided into The prevalence of AS has increased with aging.
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