Comparison of Left Ventricular Myocardial Structure and Function in Patients with Aortic Stenosis and Those with Pure Aortic Regurgitation

Cardiology ◽  
2015 ◽  
Vol 132 (2) ◽  
pp. 111-118 ◽  
Author(s):  
Vito Mannacio ◽  
Elia Guadagno ◽  
Luigi Mannacio ◽  
Mariarosaria Cervasio ◽  
Anita Antignano ◽  
...  

Objective: We aimed to support the structural and functional distinction between aortic stenosis (AS) and aortic regurgitation (AR). Methods: Biopsy specimens taken from 70 selected patients (35 with AS and 35 with AR) undergoing aortic valve replacement (AVR) were analyzed for their cardiomyocyte dimensions and structure, interstitial fibrosis and contractile function. To determine normal values of contractile function, 10 donor hearts were analyzed. Results: Cardiomyocyte diameter was higher in AS than in AR (22.7 ± 2.2 vs. 13.2 ± 0.7 µm, p < 0.001). Length was higher in AR (121.2 ± 9.4 vs. 95.6 ± 3.7 µm, p < 0.001). Collagen volume fraction was increased in both AS and AR, but was lower in the AS specimens (7.7 ± 2.3 vs. 8.9 ± 2.3, p = 0.01). Myofibril density was reduced in AR (38 ± 4 vs. 48 ± 5%, p < 0.001). Cardiomyocyte diameter and length were closely linked to the relative left ventricular (LV) wall thickness (R2 = 0.85, p < 0.001 and R2 = 0.68, p = 0.003). The cardiomyocytes of AS patients had higher Fpassive (6.6 ± 0.3 vs. 4.6 ± 0.2 kN/m2, p < 0.001), but their total force was comparable. Fpassive was also significantly higher in AS patients with restrictive rather than pseudo-normal LV filling (7.3 ± 0.5 vs. 6.7 ± 0.6, p = 0.004). In AS patients, but not in AR patients, Fpassive showed a significant association with the cardiomyocyte diameter (R2 = 0.88, p < 0.001 vs. R2 = 0.31, p = 0.6). Conclusions: LV myocardial structure and function differ in AS and AR, allowing for compensative adjustment of the diastolic/systolic properties of the myocardium.

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
M Fukui ◽  
M S Annabi ◽  
V E E Rosa ◽  
H B Ribeiro ◽  
F Tarasoutchi ◽  
...  

Abstract Background The clinical utility of comprehensive cardiac magnetic resonance (CMR) for the assessment of myocardial structure and function remains unknown in patients with low gradient (LG) aortic stenosis (AS). Purpose This study sought to compare CMR characteristics of myocardial structure and function according to different flow / gradient patterns of AS: classical low flow LG (LFLG); paradoxical LFLG; normal flow LG; and high gradient, and to evaluate their impact on the outcomes of these patients. Methods International multicentric prospective study included 147 patients with LG moderate to severe AS and 18 patients with high gradient severe AS who underwent comprehensive CMR evaluation of left ventricular global longitudinal strain (LVGLS), extracellular volume fraction (ECV), and late gadolinium enhancement (LGE). Results Patients with classical LFLG (n=90) had more LV adverse remodeling and impaired longitudinal function including higher ECV, and higher LGE and volume, and worst LVGLS, compared to other patterns of AS. Over a median follow-up of 2-years, 43 deaths and 48 composite outcomes of death or heart failure hospitalization occurred in LG AS patients. As LVGLS or ECV worsened, risks of adverse events also increased (per tertile of LVGLS: HR [95% CI] for mortality, 1.50 [1.02–2.20]; p=0.04; HR [95% CI] for composite outcome, 1.45 [1.01–2.09]; p&lt;0.05) (per tertile of ECV: HR [95% CI] for mortality, 1.63 [1.07–2.49]; p=0.02; HR [95% CI] for composite outcome, 1.54 [1.02–2.33]; p=0.04). LGE presence was also associated with higher mortality (HR [95% CI], 2.27 [1.01–5.11]; p&lt;0.05) and risk of the composite outcome (HR [95% CI], 3.00 [1.16–7.73]; p=0.02). The risk of all-cause death and of the composite outcome increased in proportion to the number of impaired components (i.e. LVGLS, ECV and LGE) (Figure) with and without adjustment for age, true severe AS, classical LFLG, and aortic valve replacement as a time-varying covariate. Conclusions In this international multicentric study of LG AS, comprehensive CMR assessment of myocardial structure and function provides independent prognostic value that is cumulative and incremental to clinical and echocardiographic characteristics. FUNDunding Acknowledgement Type of funding sources: None.


2021 ◽  
Author(s):  
Guozhu Shao ◽  
Yukun Cao ◽  
Yue Cui ◽  
Xiaoyu Han ◽  
Jia Liu ◽  
...  

Abstract Background: The purpose of this study is to dynamically monitor the myocardial structure and function changes in diabetic mini-pigs by 1.5T cardiac magnetic resonance. Methods: Cardiac magnetic resonance (CMR) T1 mapping was performed in three male streptozotocin-induced diabetic mini-pigs. T1-mapping and ECV-mapping were acquired at basal, mid and apical segments. CMR feature-tracking (CMR-FT) is used to quantify left ventricle global longitudinal (LVGLS), circumferential (LVGCS) and radial strain(LVGRS). Epicardial adipose tissue (EAT) was evaluated using a commercially available software.Results: Left ventricular mass (LVM), myocardial T1 value and extracellular volume (ECV) value increased gradually after 3, 4.5 and 6 months of modeling, while LVGLS decreased gradually after 3 months of modeling(Modeling 3M VS 1.5M:LVM,34.0 ± 1.9 VS 26.4 ± 1.3,P=0.027;T1,1012.3 ± 9.6 VS 1002.2 ± 11.4, P=0.014; ECV,24.3 ± 1.6 VS 22.4 ± 1.6,P=0.014;GLS:-20.8 ± 1.3 VS -23.0 ± 1.6,P=0.014;Modeling 4.5M VS 3M:LVM,37.5 ± 1.3 VS 34.0 ± 1.9,P=0.005;T1, 1017.8 ± 9.5 VS 1012.3 ± 9.6, P<0.001;ECV,26.2 ± 1.5 VS 24.3 ± 1.6,P=0.037;GLS:-19.4 ± 1.4 VS -20.8 ± 1.3,P=0.016;Modeling 6M VS 4.5M:LVM,42.9 ± 1.6 ± 1.9 VS 37.5 ± 1.3,P=0.008;T1,1026.6 ± 10.2 VS 1017.8 ± 9.5, P=0.003;ECV,28.6 ± 1.8 VS 26.2 ± 1.5,P=0.016;GLS:-17.9 ± 1.1 VS -19.4 ± 1.4,P=0.019). EAT did not increase significantly until the sixth month (Modeling 6M VS 4.5M, EAT: 24.1 ± 3.1 VS 20.2 ± 2.4, P= 0.043).Conclusion: The progressive impairments in LV structure and myocardial deformation occurs in diabetic mini-pigs. T1 mapping and CMR-FT technology are promising to monitor abnormal changes of diabetic myocardium in early stage of diabetic cardiomyopathy.


2005 ◽  
Vol 33 (1_suppl) ◽  
pp. 30A-38A ◽  
Author(s):  
AO Conrady ◽  
IO Kiselev ◽  
NI Usachev ◽  
AN Krutikov ◽  
OI Yakovleva ◽  
...  

The aim of the present study was to assess the effect of treatment with the angiotensin II receptor blocker telmisartan for 24 weeks on myocardial structure and function in patients with essential hypertension, and the relationship between this effect and the structural polymorphism of the angiotensin-converting enzyme (ACE) gene. Thirty-five patients with essential hypertension and left ventricular hypertrophy (LVH) without other associated morbidity were included in an open-label, non-comparative study. The patients were treated with telmisartan 40-80 mg once daily. In the final analysis, there were 29 patients who received the full course of treatment and were evaluated echocardiographically before and after treatment by the same blinded investigator, and myocardial structure and function were analysed. The myocardial mass of the left ventricle was determined in M-mode. Assessment of diastolic function of transmitral blood flow was performed using pulsed Doppler echocardiography. All patients were genotyped for insertion/deletion (I/D) polymorphism of the ACE gene. Telmisartan produced a significant reduction in left ventricular mass index from 140.4 ± 48.6 to 128.7 ± 40.6 g/m2 that was accompanied by an improvement in characteristics of diastolic function. The decrease in LVH was more significant in the ID genotype group than in the II and DD groups. Thus, prolonged treatment with telmisartan is accompanied by an improvement in myocardial structure, expressed as a reduction in left ventricular mass and function that is more marked in patients with ID genotype of the ACE gene.


2009 ◽  
Vol 297 (5) ◽  
pp. H1744-H1751 ◽  
Author(s):  
Santhosh K. Mani ◽  
Sundaravadivel Balasubramanian ◽  
Juozas A. Zavadzkas ◽  
Laura B. Jeffords ◽  
William T. Rivers ◽  
...  

Cardiac pathology, such as myocardial infarction (MI), activates intracellular proteases that often trigger programmed cell death and contribute to maladaptive changes in myocardial structure and function. To test whether inhibition of calpain, a Ca2+-dependent cysteine protease, would prevent these changes, we used a mouse MI model. Calpeptin, an aldehydic inhibitor of calpain, was intravenously administered at 0.5 mg/kg body wt before MI induction and then at the same dose subcutaneously once per day. Both calpeptin-treated ( n = 6) and untreated ( n = 6) MI mice were used to study changes in myocardial structure and function after 4 days of MI, where end-diastolic volume (EDV) and left ventricular ejection fraction (EF) were measured by echocardiography. Calpain activation and programmed cell death were measured by immunohistochemistry, Western blotting, and TdT-mediated dUTP nick-end labeling (TUNEL). In MI mice, calpeptin treatment resulted in a significant improvement in EF [EF decreased from 67 ± 2% pre-MI to 30 ± 4% with MI only vs. 41 ± 2% with MI + calpeptin] and attenuated the increase in EDV [EDV increased from 42 ± 2 μl pre-MI to 73 ± 4 μl with MI only vs. 55 ± 4 μl with MI + calpeptin]. Furthermore, calpeptin treatment resulted in marked reduction in calpain- and caspase-3-associated changes and TUNEL staining. These studies indicate that calpain contributes to MI-induced alterations in myocardial structure and function and that it could be a potential therapeutic target in treating MI patients.


Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Zhenyu Xiong ◽  
Jiaying Li ◽  
Xiaodong Zhuang ◽  
Xinxue Liao

Background and aims: To measure the association between intensity of hypertensive exposure and myocardial structure and function during a 25-year period in young adulthood. Methods: The Coronary Artery Risk Development in Young Adults (CARDIA) Study enrolled 5,115 healthy black and white American aged 18-30 years at baseline (March 1985 to May 2011). Intensity of hypertensive exposure was estimated based on their durations of hypertension over 25 years. Myocardial structure and function was identified by echocardiogram at year 25. Results: Of 2027 participants, 1315 were women (64.9%) and 906 were black (44.7%); mean (SD) age was 24.9 (3.6) at baseline. Duration of stage 1 hypertension was associated with higher left ventricular (LV) structure: LV mass (β [SE], 3.69 [1.80], P < 0.001), relative wall thickness (β [SE], 0.009 [0.003], P = 0.001), worse longitudinal strain (β [SE], 0.27 [0.008], P < 0.001), worse diastolic function: e’ (β [SE], -0.25 [0.07], P < 0.001), E/e’ (β [SE], 0.23 [0.007], P < 0.001). Duration of stage 2 hypertension was associated with higher left ventricular (LV) structure: LV mass (β [SE], 7.30 [2.23], P = 0.001), worse longitudinal strain (β [SE], 0.44 [0.13], P = 0.001), worse diastolic function: e’ (β [SE], -0.77 [0.12], P < 0.001), E/e’ (β [SE], 0.48 [0.13], P < 0.001). Conclusions: In early adulthood, more severe intensity of hypertensive exposure is associated with myocardial structure and diastolic dysfunction in middle age. Key Words: cardiac structure, cardiac dysfunction, hypertension, young adult


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