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Drăgan, A.; Mateescu, A.D. Pathophysiology of Cardiac Dysfunction in Aortic Stenosis. Encyclopedia. Available online: (accessed on 21 June 2024).
Drăgan A, Mateescu AD. Pathophysiology of Cardiac Dysfunction in Aortic Stenosis. Encyclopedia. Available at: Accessed June 21, 2024.
Drăgan, Anca, Anca Doina Mateescu. "Pathophysiology of Cardiac Dysfunction in Aortic Stenosis" Encyclopedia, (accessed June 21, 2024).
Drăgan, A., & Mateescu, A.D. (2023, December 08). Pathophysiology of Cardiac Dysfunction in Aortic Stenosis. In Encyclopedia.
Drăgan, Anca and Anca Doina Mateescu. "Pathophysiology of Cardiac Dysfunction in Aortic Stenosis." Encyclopedia. Web. 08 December, 2023.
Pathophysiology of Cardiac Dysfunction in Aortic Stenosis

Aortic stenosis (AS) is a disease both of the valve and the myocardium, characterized by fibrosis and calcification of valve leaflets, progressive LV hypertrophy, and myocardial fibrosis. AS represents not only a valvular disease but a whole heart disease, often in patients with comorbidities.

aortic stenosis myocardial fibrosis remodeling left ventricle (LV) left atrium (LA)

1. Introduction

The prevalence of valvular diseases is increasing with the prediction of by 2050 [1], especially in developed countries. The aging population, the increasing availability of imaging techniques, and accessibility to diagnosis and treatment may be some reasons for this trend [2]. The prevalence of AS rises sharply with increasing age and approaches 25% of all adults older than 65 years [3], with 2–5% of patients having severe AS [3]. In the UK, one study reported a prevalence of 1.48% for severe AS with 31.7% asymptomatic cases for people aged ≥55 years [4]. Stewart et al. reported that 21% of men and 18.7% of women aged 65 years or older in Australia had evidence of mild-to-severe AS [5]. A percentage of 2.3% men and 1.9% women presented severe AS. They also demonstrated that not only severe AS but also mild and moderate AS might significantly reduce the longevity and quality of life of people aged 65 years or older [3][5].

Currently, the symptomatic status and left ventricular ejection fraction (EF) play a crucial role in the management of AS patients [6][7]. However, the symptoms are often subjective, and LVEF is not a sensitive marker of LV decompensation. As a consequence, the timing of aortic valve operations is often suboptimal. Research related to the cardiac structure and function in patients with AS has increased over the past years due to advanced imaging modalities and potential therapies, in particular the emergence of transcatheter aortic valve implantation (TAVI).
The progressive decrease in the area of the aortic valve determines a chronic pressure overload. The early adaptive manifestation of the ventricular myocardium is hypertrophy with LV diastolic dysfunction. Later, LV systolic dysfunction occurs, with myocardial contractile function and deformation becoming impaired. The left atrium (LA) also presents some morphological changes. The LA responds by increasing its volume to the chronic pressure overload, leading to a higher pulmonary venous and arterial pressure. The ventricular and atrial changes will result in heart failure, atrial fibrillation (AF), and symptom development. Thus, AS represents not only a valvular disease but a whole heart disease, often in patients with comorbidities. However, AS patients can be asymptomatic until the late stage of the disease.
The presence of symptoms in severe AS patients was reported to be associated with smaller aortic valve area, higher degree of LVH, increased levels of plasmatic brain natriuretic peptide, but also with impaired LV diastolic function parameters, including increased LA dimensions [8][9][10][11][12].
Since there is no other definitive treatment apart from AVR in AS, the time of intervention is crucial to optimizing the outcome for patients and their future quality of life. While for symptomatic severe AS patients, the AVR decision is clearly stipulated, the timing for intervention in asymptomatic severe AS patients is still subject to debate. Studies already reported that symptom development is associated with higher mortality, even after AVR. Asymptomatic patients with moderate-to-severe AS demonstrated unequivocal progression in the adverse cardiac remodeling within 12 months, with a significant increase in focal myocardial fibrosis (MF) [13]. A multi-center cardiac magnetic resonance (CMR) study reported that in AS patients, cellular hypertrophy and diffuse fibrosis progressed rapidly, but this change was reversible after AVR [14].
Once established, mid-wall late gadolinium enhancement (LGE) also accumulated rapidly, increasing by 75% each year on average, especially in patients with a high baseline fibrosis burden [14]. This change was irreversible following valve replacement [14]. Therefore, it is clinically relevant to better define the optimal timing of valve intervention in AS. The answer may not be found in one single assessment method but in a multi-parametric approach, which integrates imaging and serum biomarkers related to both ventricular and atrial myocardium function and structure, focusing on the potential reversal of structural changes, such as MF.

2. Left Ventricular Response to Aortic Stenosis

Left ventricular hypertrophy (LVH) develops early, in response to pressure overload from AS. The LV remodeling pattern may vary between patients depending on sex, age, and co-existent coronary artery disease (CAD) or hypertension [15]. Although initially beneficial, the LV chronic hypertrophic response may be deleterious, with patients transitioning to symptoms, including heart failure, and adverse events. Stein et al. reported that LVH was independently associated with all-cause mortality in AS patients [16]. Myocyte degeneration, cell death, and fibrosis may be the structural changes responsible for this transition. The high myocardial oxygen demand is unbalanced in severe AS by the insufficient coronary capillary network, leading to impaired myocardial perfusion and cardiomyocyte cell death [17][18].
LVH and MF from chronically elevated LV systolic pressure result in diastolic LV dysfunction [19]. The gradual and often incomplete improvement in diastolic dysfunction (DD) follows LV remodeling after AVR [19]. Klein et al. draw attention to the timely detection of more advanced stages of DD in AS to identify the asymptomatic patients who would benefit from AVR, knowing that DD may be multi-factorial due to comorbidities, which impact diastolic LV function, such as hypertension and amyloidosis, particularly in elderly patients [20]. If the disease progresses, irreversible myocardial damage and interstitial fibrosis occur, leading to LV systolic dysfunction and a further decline in LVEF [21]. Stassen et al. recently demonstrated the importance of DD of LV in AS patients with preserved LVEF [22]. All-cause mortality was significantly dependent on DD of LV even in moderate AS [22].
The term fibrosis is used in the literature to describe the excessive deposition of extracellular matrix (ECM) proteins in parenchymal tissues and typically reflects inappropriate or unrestrained activation of a reparative program [23]. In AS, MF must be considered a dynamic process. To date, the mechanisms governing its development and progression in AS are incompletely understood. The contributors to the development of fibrosis in AS patients are an imbalance in matrix metalloproteinases and tissue inhibitors of matrix metalloproteinase (MMPs) activity, alongside increases in angiotensin-converting enzyme and transforming growth factor beta1 activity. Each of these mechanisms could be a potential target for aortic valve intervention [24][25].
In the early stages of the disease, the process involves the myocardium diffusely, is interstitial, reactive to pressure overload, and potentially reversible [26].
In the late stages of the disease, the fibrosis becomes substitutive and irreversible, with a focal distribution [26] due to the persistence of pressure overload. Progressive AS and LVH result in impaired myocardial blood flow, diminished coronary reserve, and compensatory vasodilation of the remaining vessels, with microvascular dysfunction and reduced capillary density ensuing. Thus, one driver of replacement fibrosis in AS was considered to be microvascular ischemia [15].
Frangogiannis identified the four mechanisms, which may induce the activation of the fibroblasts in heart failure associated with pressure overload [23]. Neurohumoral activation has an essential role in myofibroblast conversion [23][27]. The induction of matricellular proteins locally activates growth-factor-mediated signaling in fibroblasts, stimulating ECM protein synthesis [23][28][29]. The direct activation of mechanosensitive cascade and the release of inflammatory cytokines and growth factors by the stressed cardiomyocytes and immune cells contribute to fibroblast activation [23][30][31][32].
The gold standard for MF assessment is histological analysis obtained through endomyocardial biopsy, but non-invasive cardiac imaging may offer surrogate biomarkers [33].

3. Left Atrial Response to Aortic Stenosis

In AS, the increased pressure and wall stress are also present at the atrium level. The LA plays an important role in modulating LV filling and maintaining an optimal LV stroke volume, especially in patients with AS and LVH, through several different mechanisms. The LA acts as a reservoir during LV systole and isovolumic relaxation, filling with blood from the pulmonary veins; as a conduit during early LV diastole and diastasis, transferring blood into the LV via a small pressure gradient during early diastole and passively from the pulmonary veins during diastasis; as a booster pump during late LV diastole, contributing to LV stroke volume by 20–30% in normal subjects and significantly more when LV diastolic properties are impaired; and as a suction source, which refills itself in early systole [34]. LV diastolic dysfunction is an independent predictor of cardiovascular events in the general population, being associated with adverse outcomes [35]. The LA volume index is one of the four parameters currently recommended for the evaluation of LV diastolic function by echocardiography [36].
MF at the LA level is very important, leading to LA dysfunction with symptom occurrence and/or atrial fibrillation (AF). The remodeling process becomes irreversible if this LA fibrosis is extensive. Thus, early detection of LA dysfunction is mandatory for initiating specific therapeutic interventions [37].
The increased LA pressure and wall stretch lead to the renin–angiotensin–aldosterone system (RAAS) and leukocyte activation—the main pathways to atrial fibrosis and cardiomyocyte hypertrophy [38].
RAAS activation promotes the activation of hydrolysis phospholipase C (PLC), the activation of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, the release of reactive oxygen species (ROS), and it regulates the expression of profibrotic factors (TGF, CTGF) [38]. PLC activation leads to intracellular Ca2+ overload and fibroblast proliferation [38]. The mitogen-activated protein kinase is stimulated by Ang II–AT1–R interaction, further regulating the transcription of some genes: MMP, PAI-1, CTGF, and TGF-β [37]. Smad 2/3 phosphorylation, with Smad complex translocation into the cell nucleus—and TGF-β synthesis are also induced by Ang II [37]. Ang II can also increase ROS production and cause cardiac hypertrophy through the Rho G pathway [37]. Sygitowicz et al. reported Ang II-MAPK, TGF-β-Smad signaling pathways, and Rac1-dependent CTGF activation to be the mechanisms in atrial remodeling and fibrosis in AF [37]. Ang II was also demonstrated to have an epigenetic-dependent prohypertrophic effect on atrial cardiomyopathy through the regulation of histone acetylation via the cytoplasmic-nuclear shuttling of HDACs [39]. Thus, the MEF2 binding to the promoter of hypertrophy-related genes is produced. This constitutes a novel mechanism of atrial hypertrophy regulation reported by Zheng et al., which might provide a promising therapeutic strategy for atrial cardiomyopathy [39].
Leukocyte activation is also triggered at the LA level with the subsequent release of inflammatory stimuli [38]. Fibroblast proliferation and differentiation into the myofibroblast phenotype are activated. Thus, the extracellular matrix (ECM) components are released, including fibronectin, procollagen, laminin, elastin, fibrillin, proteoglycans, glycoproteins matrix metalloproteinases (MMPs), and tissue inhibitors of MMPs [38].
Structural remodeling is one of the factors influencing the AF pathophysiology in AS, in addition to ion channel dysfunction, Ca2+-handling abnormalities, and autonomic neural dysregulation [40]. Fragão-Marques et al. studied, for the first time, the atrial remodeling in AS patients with chronic AF through fibrosis quantification and target extracellular matrix protein gene expression analysis. In AF patients, an increased collagen type III and decreased TIMP1 and TIMP2 gene expressions were found, accompanied by anincreased cardiomyocyte area and atrial fibrosis discovered during the histologic quantification [40]. The atrial expressions of collagen I, collagen ratio I/III, MMP2, MMP9, MMP16, TGFβ1, and TIMP 4 genes were similar in AF and non-AF patients. The MMP16/TIMP4 ratio was decreased, while serum TIMP1 and TIMP2 were increased in AF patients [40]. In AS, the occurrence of AF may lead to misclassification of severity because it associates lower maximum and mean pressure gradients [40]. Researchers reported that the aortic valve mean gradient was inversely correlated with the MMP2/TIMP1 ratio, collagen type I gene expression, collagen type I/III ratio, and serum TIMP1 levels [40]. Collagen type I gene expression and collagen type I/III ratio were associated with the aortic valve area [40].


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