Aortic stenosis and aortic regurgitation express different titin isoforms: Differences and relationships with functional and geometric characteristics

2018 ◽  
Vol 259 ◽  
pp. 138-144
Author(s):  
Vito Mannacio ◽  
Luigi Mannacio ◽  
Anita Antignano ◽  
Vincenzo De Amicis ◽  
Francesco Musumeci ◽  
...  
2019 ◽  
Vol 17 (2) ◽  
pp. 180-190 ◽  
Author(s):  
V. Katsi ◽  
G. Georgiopoulos ◽  
D. Oikonomou ◽  
C. Aggeli ◽  
C. Grassos ◽  
...  

Background: Hypertension (HT) is an important risk factor for cardiovascular disease and might precipitate pathology of the aortic valve. </P><P> Objective: To investigate the association of HT with aortic dysfunction (including both aortic regurgitation and stenosis) and the impact of antihypertensive treatment on the natural course of underlying aortic disease. </P><P> Methods: We performed a systematic review of the literature for all relevant articles assessing the correlation between HT and phenotype of aortic disease. </P><P> Results: Co-existence of HT with aortic stenosis and aortic regurgitation is highly prevalent in hypertensive patients and predicts a worse prognosis. Certain antihypertensive agents may improve haemodynamic parameters (aortic jet velocity, aortic regurgitation volume) and remodeling of the left ventricle, but there is no strong evidence of benefit regarding clinical outcomes. Renin-angiotensin system inhibitors, among other vasodilators, are well-tolerated in aortic stenosis. </P><P> Conclusion: Several lines of evidence support a detrimental association between HT and aortic valve disease. Therefore, HT should be promptly treated in aortic valvulopathy. Despite conventional wisdom, specific vasodilators can be used with caution in aortic stenosis.


JACC: Asia ◽  
2021 ◽  
Vol 1 (1) ◽  
pp. 105-111
Author(s):  
Jinghao Nicholas Ngiam ◽  
Nicholas W.S. Chew ◽  
Thanawin Pramotedham ◽  
Benjamin Yong-Qiang Tan ◽  
Ching-Hui Sia ◽  
...  

2001 ◽  
Vol 122 (1) ◽  
pp. 162-168 ◽  
Author(s):  
Emile A. Bacha ◽  
Gary M. Satou ◽  
Adrian M. Moran ◽  
David Zurakowski ◽  
Gerald R. Marx ◽  
...  

2021 ◽  
Author(s):  
Miriam S. Jacob ◽  
Brian P Griffin

Valvular heart disease is an important cause of cardiac morbidity in developed countries despite a decline in the prevalence of rheumatic disease in those countries. This chapter discusses the many etiologies of valvular heart disease and presents methods for assessment and management. Specific valvular lesions discussed include mitral stenosis, mitral regurgitation, mitral valve prolapse, aortic stenosis, aortic regurgitation, and tricuspid and pulmonary disease. The section on tricuspid disease includes a discussion of mechanical prostheses (ball-in-cage and tilting-disk) and biologic prostheses (xenografts, allografts, and autografts) and their complications.  This review contains 5 figures, 9 tables, and 53 references. Keywords: Valvular heart disease, stenosis, regurgitation, mitral regurgitation, mitral valve prolapse (MVP), aortic stenosis, congenital bicuspid valve, senile valvular calcification, aortic regurgitation, chordae or papillary muscles


2016 ◽  
Vol 8 (3) ◽  
pp. 267
Author(s):  
Ihsen Zairi ◽  
Khadija Mzoughi ◽  
Miriem Jabeur ◽  
Alaedine El Jary ◽  
Fethia Ben Moussa ◽  
...  

2019 ◽  
Vol 20 (10) ◽  
pp. 1105-1111
Author(s):  
E Mara Vollema ◽  
Gurpreet K Singh ◽  
Edgard A Prihadi ◽  
Madelien V Regeer ◽  
See Hooi Ewe ◽  
...  

Abstract Aims Pressure overload in aortic stenosis (AS) and both pressure and volume overload in aortic regurgitation (AR) induce concentric and eccentric hypertrophy, respectively. These structural changes influence left ventricular (LV) mechanics, but little is known about the time course of LV remodelling and mechanics after aortic valve surgery (AVR) and its differences in AS vs. AR. The present study aimed to characterize the time course of LV mass index (LVMI) and LV mechanics [by LV global longitudinal strain (LV GLS)] after AVR in AS vs. AR. Methods and results Two hundred and eleven (61 ± 14 years, 61% male) patients with severe AS (63%) or AR (37%) undergoing surgical AVR with routine echocardiographic follow-up at 1, 2, and/or 5 years were evaluated. Before AVR, LVMI was larger in AR patients compared with AS. Both groups showed moderately impaired LV GLS, but preserved LV ejection fraction. After surgery, both groups showed LV mass regression, although a more pronounced decline was seen in AR patients. Improvement in LV GLS was observed in both groups, but characterized by an initial decline in AR patients while LV GLS in AS patients remained initially stable. Conclusion In severe AS and AR patients undergoing AVR, LV mass regression and changes in LV GLS are similar despite different LV remodelling before AVR. In AR, relief of volume overload led to reduction in LVMI and an initial decline in LV GLS. In contrast, relief of pressure overload in AS was characterized by a stable LV GLS and more sustained LV mass regression.


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