Ubiquitin Ligase Wwp1 Gene Deletion Attenuates Diastolic Dysfunction in Pressure Overload Hypertrophy

Background. Heart failure with a preserved left ventricular (LV) ejection fraction (HFpEF) often arises from a prolonged LV pressure overload (LVPO) and accompanied by abnormal extracellular matrix (ECM) accumulation. The E3 ubiquitin ligase WWP1 is a fundamental determinant ECM turnover. We tested the hypothesis that genetic ablation of Wwp1 would alter the progression of LVPO induced HFpEF. Methods/Results. LV echocardiography in mice with global Wwp1 deletion (n=41; Wwp1-/-) was performed at 12 weeks of age (Baseline) and then at 2 and 4 weeks following LVPO (transverse aortic banding) or surgery without LVPO induction. Age-matched wild type mice (Wwp1+/+; n=33) underwent identical protocols. LV EF remained constant and unchanged with LVPO and LV mass increased in both groups but was lower in the Wwp1-/- mice. With LVPO, the E/A ratio, an index of LV filling, was 3.97 + 0.46 in Wwp1+/+ but was 1.73 + 0.19 in the Wwp1-/- group (p<0.05). At the transcriptional level, mRNA for fibrillar collagens (types I and III) decreased by approximately 50% in Wwp1-/- compared to the Wwp1+/+ group at 4 weeks post-LVPO (p<0.05) and was paralleled by a similar difference in LV fibrillar collagen content as measured by histochemistry. Moreover, mRNA levels for determinants favoring ECM accumulation, such as transforming growth factor (TGF) increased with LVPO, but were lower in the Wwp1-/- group. Summary. The absence of Wwp1 reduced the development of LVH and subsequent progression to HFpEF. Modulating the WWP1 pathway could be a therapeutic target to alter the natural history of HFpEF.

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Abstract 297: Cardiac Transforming-growth-factor β-stimulated Clone 22 Gene Expression By Hypertrophic Stimuli

Circulation Research ◽

10.1161/res.113.suppl_1.a297 ◽

2013 ◽

Vol 113 (suppl_1) ◽

Author(s):

Annina Kelloniemi ◽

Jani Aro ◽

Elina Koivisto ◽

Heikki Ruskoaho ◽

Jaana Rysä

Keyword(s):

Growth Factor ◽

Gene Transfer ◽

Transforming Growth Factor ◽

Pressure Overload ◽

Transforming Growth Factor Β ◽

Left Ventricular ◽

Neonatal Rat ◽

Mrna Levels ◽

Ang Ii ◽

Sd Rats

Objectives: Transforming-growth-factor β-stimulated clone 22 (TSC-22) is a leucine zipper protein expressed in many tissues and possessing various transcription-modulating activities. However, its function in the heart remains largely unknown. The aim of the present study was to characterize the cardiac TSC-22 expression. Methods: Acute pressure overload was accomplished in conscious Sprague-Dawley (SD) rats by intravenous infusion of arginine 8 -vasopressin (AVP, 0.05 μg/kg/min) for 4 hours and subcutaneous infusion of angiotensin II (Ang II, 33 μg/kg/h) with and without Ang II receptor type 1 blocker losartan (400 μg/kg/h) by using osmotic minipumps for 2 weeks. Adenovirus-mediated intramyocardial gene transfer of TSC-22 was performed into left ventricle (LV) of SD rats. Experimental myocardial infarction (MI) was produced by ligation of the left anterior descending coronary artery. Cultured neonatal rat ventricular myocytes (NRVM) were treated with endothelin-1 (ET-1, 100 nM). Results: A significant 1.6-fold increase ( P <0.05) in LV TSC-22 mRNA levels was noted already after 1 hour AVP infusion. Moreover, Ang II infusion markedly upregulated TSC-22 expression, LV mRNA levels being highest at 6 hours (11-fold, P <0.001). Simultaneous infusion of losartan completely abolished Ang II-induced increase in TSC-22 mRNA levels. Adenovirus-mediated gene transfer of TSC-22 into LV resulted a 1.9-fold ( P <0.001) increase in TSC-22 mRNA levels, accompanied by upregulated BNP mRNA levels (1.4-fold, P <0.01). In response to experimental MI, TSC-22 mRNA levels were elevated 4.1-fold ( P <0.001) at 1 day and 1.9-fold ( P <0.05) at 4 weeks. In cultured NRVM, ET-1 treatment increased TSC-22 mRNA levels from 1 h to 24 h, the greatest increase being observed at 12 h (2.7-fold, P <0.001). TSC-22 protein levels were upregulated from 4 h to 24 h with the highest increase at 24 h (4.7-fold, P <0.01). Conclusion: These results indicate that TSC-22 expression is rapidly activated in response to pressure overload, MI and in ET-1 treated cultured NRVM. Moreover, adenovirus-mediated overexpression of TSC-22 mRNA was associated with elevated left ventricular BNP mRNA levels.

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Left ventricular apical mass after myocardial infarction—not always a thrombus: a diagnostic dilemma

BMJ Case Reports ◽

10.1136/bcr-2021-245963 ◽

2021 ◽

Vol 14 (10) ◽

pp. e245963

Author(s):

Jayanty Venkata Balasubramaniyan ◽

Judah Nijas Arul ◽

Jebaraj Rathinasamy ◽

Thangavel Periyasamy

Keyword(s):

Myocardial Infarction ◽

Systolic Dysfunction ◽

Anterior Wall ◽

Left Ventricular ◽

Prior History ◽

Surgical Removal ◽

Diagnostic Dilemma ◽

Echocardiographic Evaluation ◽

Lv Mass ◽

History Of

Myxomas arising from the left ventricle (LV) are extremely rare and can be easily mistaken for a thrombus. We report a case of a 35-year-old man who presented with an acute cerebrovascular accident, having had a prior history of an anterior wall myocardial infarction 2 years back with an echocardiographic evaluation showing mild LV systolic dysfunction. His present prothrombotic workup revealed hyperhomocystinaemia and elevated levels of factor VIII. Present echocardiography revealed a mass arising from a scarred LV wall. Considering the possibility of a thrombus, he was initially started on parenteral anticoagulation. Unfortunately, consequent echocardiogram evaluation showed no reduction in size of the LV mass hence surgical removal was done. Histopathological evaluation unveiled the mass to be a myxoma.

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Abstract 14664: Reduced Activin Like Kinase 1 Activity Promotes Cardiac Fibrosis in Heart Failure

Circulation ◽

10.1161/circ.132.suppl_3.14664 ◽

2015 ◽

Vol 132 (suppl_3) ◽

Author(s):

Kevin Morine ◽

Vikram Paruchuri ◽

Xiaoying Qiao ◽

Emily Mackey ◽

Mark Aronovitz ◽

...

Keyword(s):

Heart Failure ◽

Cardiac Remodeling ◽

Cardiac Fibrosis ◽

Type I Collagen ◽

Transforming Growth Factor ◽

Left Ventricular ◽

Lv Function ◽

Type I ◽

Mrna Levels ◽

Protein Levels

Introduction: Activin receptor like kinase 1 (ALK1) mediates signaling via transforming growth factor beta-1 (TGFb1), a pro-fibrogenic cytokine. No studies have defined a role for ALK1 in heart failure. We tested the hypothesis that reduced ALK1 expression promotes maladaptive cardiac remodeling in heart failure. Methods and Results: ALK1 mRNA expression was quantified by RT-PCR in left ventricular (LV) tissue from patients with end-stage heart failure and compared to control LV tissue obtained from the National Disease Research Interchange (n=8/group). Compared to controls, LV ALK1 mRNA levels were reduced by 85% in patients with heart failure. Next, using an siRNA approach, we tested whether reduced ALK1 levels promote TGFb1-mediated collagen production in human cardiac fibroblasts. Treatment with an ALK1 siRNA reduced ALK1 mRNA levels by 75%. Compared to control, TGFb1-mediated Type I collagen and pSmad-3 protein levels were 2.5-fold and 1.7-fold higher, respectively, after ALK1 depletion. To explore a role for ALK1 in heart failure, ALK1 haploinsufficient (ALK1) and wild-type mice (WT; n=8/group) were studied 2 weeks after thoracic aortic constriction (TAC). Compared to WT, baseline LV ALK1 mRNA levels were 50% lower in ALK1 mice. Both LV and lung weights were higher in ALK1 mice after TAC. Cardiomyocyte area and LV mRNA levels of BNP, RCAN, and b-MHC were increased similarly, while SERCa levels were reduced in both ALK1 and WT mice after TAC. Compared to WT, LV fibrosis (Figure) and Type 1 Collagen mRNA and protein levels were higher among ALK1 mice. Compared to WT, LV fractional shortening (48±12 vs 26±10%, p=0.01) and survival (Figure) were lower in ALK1 mice after TAC. Conclusions: Reduced LV expression of ALK1 is associated with advanced heart failure in humans and promotes early mortality, impaired LV function, and cardiac fibrosis in a murine model of heart failure. Further studies examining the role of ALK1 and ALK1 inhibitors on cardiac remodeling are required.

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Inhibition of Smurf2 translation by miR-322/503 modulates TGF-β/Smad2 signaling and intestinal epithelial homeostasis

Molecular Biology of the Cell ◽

10.1091/mbc.e13-09-0560 ◽

2014 ◽

Vol 25 (8) ◽

pp. 1234-1243 ◽

Cited By ~ 39

Author(s):

Shan Cao ◽

Lan Xiao ◽

Jaladanki N. Rao ◽

Tongtong Zou ◽

Lan Liu ◽

...

Keyword(s):

Ubiquitin Ligase ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Cellular Responses ◽

Mrna Levels ◽

Intestinal Epithelial ◽

Regulatory Factor ◽

Epithelial Homeostasis ◽

Repressive Effect ◽

Single Binding Site

Smad ubiquitin regulatory factor 2 (Smurf2) is an E3 ubiquitin ligase that regulates transforming growth factor β (TGF-β)/Smad signaling and is implicated in a wide variety of cellular responses, but the exact mechanisms that control Smurf2 abundance are largely unknown. Here we identify microRNA-322 (miR-322) and miR-503 as novel factors that regulate Smurf2 expression posttranscriptionally. Both miR-322 and miR-503 interact with Smurf2 mRNA via its 3′-untranslated region (UTR) and repress Smurf2 translation but do not affect total Smurf2 mRNA levels. Studies using heterologous reporter constructs reveal a greater repressive effect of miR-322/503 through a single binding site in the Smurf2 3′-UTR, whereas point mutation of this site prevents miR-322/503–induced repression of Smurf2 translation. Increased levels of endogenous Smurf2 via antagonism of miR-322/503 inhibits TGF-β–induced Smad2 activation by increasing degradation of phosphorylated Smad2. Furthermore, the increase in Smurf2 in intestinal epithelial cells (IECs) expressing lower levels of miR-322/503 is associated with increased resistance to apoptosis, which is abolished by Smurf2 silencing. These findings indicate that miR-322/503 represses Smurf2 translation, in turn affecting intestinal epithelial homeostasis by altering TGF-β/Smad2 signaling and IEC apoptosis.

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Alterations of Left Ventricular Hypertrophy in and Survival of Patients Receiving Hemodialysis: Follow-up of an Interventional Study

Journal of the American Society of Nephrology ◽

10.1681/asn.v12122759 ◽

2001 ◽

Vol 12 (12) ◽

pp. 2759-2767 ◽

Cited By ~ 5

Author(s):

Gérard M. London ◽

Bruno Pannier ◽

Alain P. Guerin ◽

Jacques Blacher ◽

Sylvain J. Marchais ◽

...

Keyword(s):

Confidence Interval ◽

Left Ventricular ◽

Independent Effect ◽

Lv Mass ◽

History Of ◽

Cv Disease ◽

Stage Renal Disease ◽

End Stage

ABSTRACT. Left ventricular (LV) hypertrophy (LVH) is a risk factor for mortality in patients with end-stage renal disease (ESRD). Whether the attenuation of LVH has a positive effect on survival of patients with ESRD has not been documented. The aim of this study was to determine the effect of parallel treatment of hypertension and anemia on LV mass (LVM) and to determine the effect of LVM changes on survival. A cohort of 153 patients receiving hemodialysis was studied. The duration of follow-up was 54 ± 37 mo. All patients had echocardiographic determination of LV dimensions and LVM at baseline and regular intervals until the end of the follow-up period. During the study, BP decreased from (mean ± SD) 169.4 ± 29.7/90.2 ± 15.6 to 146.7 ± 29/78 ± 14.1 mmHg (P< 0.001), and hemoglobin increased from 8.65 ± 1.65 to 10.5 ± 1.45 g/dl (P< 0.001). The LV end-diastolic diameter and mean wall thickness decreased from 56.6 ± 6.5 to 54.8 ± 6.5 mm (P< 0.001), and from 10.4 ± 1.6 to 10.2 ± 1.6 mm (P< 0.05), respectively. The LVM decreased from 290 ± 80 to 264 ± 86 g (P< 0.01). Fifty-eight deaths occurred, 38 attributed to cardiovascular (CV) disease and 20 attributed to non-CV causes. According to Cox analyses after adjustment for age, gender, diabetes, history of CV disease, and all nonspecific CV risk factors, LVM regression positively affected the survival. The hazard risk ratio associated with a 10% LVM decrease was 0.78 (95% confidence interval, 0.63 to 0.92) for all-causes mortality and 0.72 (95% confidence interval, 0.51 to 0.90) for mortality due to CV disease. These results show that a partial LVH regression in patients with ESRD had a favorable and independent effect on patients’ all-cause and CV survival.

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Abstract 184: Pressure Overload Activates Left Ventricular (LV) Intramyocardial Vascular Endothelial Cells and induces T Cell Infiltration into the LV

Circulation Research ◽

10.1161/res.113.suppl_1.a184 ◽

2013 ◽

Vol 113 (suppl_1) ◽

Author(s):

Pilar Alcaide ◽

Anna Grodecki-Pena ◽

Andrew Knapp ◽

Tanya Kershaw ◽

Mark Aronovitz ◽

...

Keyword(s):

T Cells ◽

Endothelial Cells ◽

T Cell ◽

Vascular Endothelium ◽

Pressure Overload ◽

Left Ventricular ◽

T Cell Subsets ◽

Mrna Levels ◽

Flow Conditions ◽

Cell Recruitment

Left ventricular dysfunction and Heart Failure (HF) are associated with systemic inflammation with clinical data showing that HF patients have higher levels of circulating pro-inflammatory cytokines. Recruitment of circulating T cells to tissues across the vascular endothelium is a key event in the inflammatory response, but whether it plays a role in the heart in HF is unknown. We hypothesized that pressure overload induced HF activates cardiac endothelial cells resulting in T cell recruitment into the left ventricle (LV). Using transverse aortic constriction (TAC), quantitative flow cytometry, immunohistochemistry, qPCR and real time live cell videomicroscopy, we examined mRNA and protein expression levels of endothelial cell adhesion molecules and the presence of T cell infiltrates in the LV in vivo , and also studied the T cell interactions with primary mouse heart endothelial cells (MHEC) under flow conditions in vitro , comparing Sham and TAC operated mice (6-10/group) during the course of HF. 48h after TAC, in the pre-hypertrophic state, no differences were observed in the recruitment of T cells in the LV. Interestingly, two and four weeks after TAC, when mice developed LVH and LV dysfunction (Fractional Shortening 25±13%), E-Selectin, VCAM-1 and ICAM-1 mRNA levels were significantly upregulated in the LV as compared to Sham mice (2.3, 2.8 and 4 fold, respectively), with notable enhancement of endothelial ICAM-1 protein levels in the LV intramyocardial vessels, and T cells infiltrated in the LV in response to TAC (P≤0.05 TAC vs Sham). Furthermore, T cells isolated from mice 2 and 4 weeks after TAC adhered to MHEC under flow conditions in significantly higher numbers than T cells from Sham mice (P≤0.01 TAC vs Sham). Systemically, the frequency of three different T cell subsets in the peripheral lymphoid organs was increased in TAC vs Sham mice, indicating activation of the adaptive immune response to pressure overload. Taken together, our studies indicate that activation of the heart vascular endothelium occurs in response to pressure overload resulting in T cell recruitment into the LV. Further studies will be needed to determine in the extent to which T cell recruitment into the heart contributes to the pathogenesis of HF.

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Abstract 18822: Endoglin Selectively Modulates TRPC Expression in Response to Left or Right Ventricular Pressure Overload

Circulation ◽

10.1161/circ.130.suppl_2.18822 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Kevin J Morine ◽

Vikram Paruchuri ◽

Xiaoying Qiao ◽

Duc T Pham ◽

Gordon S Huggins ◽

...

Keyword(s):

Transforming Growth Factor Beta ◽

Cardiac Fibrosis ◽

Transient Receptor Potential ◽

Transforming Growth Factor ◽

Pressure Overload ◽

Receptor Potential ◽

Left Ventricular ◽

Transient Receptor ◽

Novel Target ◽

The Right

Introduction: Endoglin is an accessory receptor for the cytokine transforming growth factor beta. Reduced endoglin activity limits cardiac fibrosis due to left ventricular (LV) pressure overload. Recently, we reported that reducing endoglin activity also limits upregulation of the profibrogenic transient receptor potential canonical channel 6 (TRPC6) in the right ventricle (RV) during pressure overload. Few studies have compared TRPC channel expression in the RV versus LV. Hypothesis: We hypothesized that endoglin regulates TRPC upregulation in response to RV and LV pressure overload. Methods: To explore a functional role for endoglin as a regulator of TRPC expression in response to RV or LV pressure overload, endoglin haploinsufficient (Eng+/-) and wild-type (Eng+/+) mice were exposed to thoracic aortic (TAC) or pulmonary arterial (PAC) constriction for 10 weeks. Biventricular tissue was then analyzed by real-time polymerase chain reaction. Results: After TAC, LV levels of TPRC1 and 6 were increased in both Eng +/+ and Eng +/- mice compared to sham controls. LV levels of TRPC4 were increased in Eng +/+, not Eng +/- mice after TAC. After PAC, RV levels of TRPC1, 3, 4, and 6 were increased in Eng +/+ compared to sham controls. In contrast, chronic RV pressure overload did not increase RV levels of TRPC1, 3, 4, and 6 in Eng +/- mice compared to sham controls. Conclusions: Pressure overload induces distinct profiles of TRPC expression in the RV and LV and these effects in the RV require full endoglin activity. Taken together, these data support that endoglin may be an important and novel target of therapy to modulate RV responses to injury.

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Left ventricular mass and myocardial scarring in women with hypertensive disorders of pregnancy

Open Heart ◽

10.1136/openhrt-2020-001273 ◽

2020 ◽

Vol 7 (2) ◽

pp. e001273

Author(s):

Odayme Quesada ◽

Ki Park ◽

Janet Wei ◽

Eileen Handberg ◽

Chrisandra Shufelt ◽

...

Keyword(s):

Vascular Dysfunction ◽

Obstructive Coronary Artery Disease ◽

Left Ventricular ◽

Hypertensive Disorders Of Pregnancy ◽

Similar Frequency ◽

Hypertensive Disorders ◽

Lv Mass ◽

Scar Size ◽

History Of ◽

And Function

AimsHypertensive disorders of pregnancy (HDP) predict future cardiovascular events. We aim to investigate relations between HDP history and subsequent hypertension (HTN), myocardial structure and function, and late gadolinium enhancement (LGE) scar.Methods and resultsWe evaluated a prospective cohort of women with suspected ischaemia with no obstructive coronary artery disease (INOCA) who underwent stress/rest cardiac magnetic resonance imaging (cMRI) with LGE in the Women’s Ischemia Syndrome Evaluation-Coronary Vascular Dysfunction study. Self-reported history of pregnancy and HDP (gestational HTN, pre-eclampsia, toxaemia and eclampsia) were collected at enrollment. In our cohort of 346, 20% of women report a history of HDP. HDP history was associated with 3.2-fold increased odds of HTN. Women with a history of both HDP and HTN had higher cMRI measured left ventricular (LV) mass compared with women with HDP only (99.4±2.6 g vs 87.7±3.2 g, p=0.02). While we found a similar frequency of LGE scar, we observed a trend towards increased LGE scar size (5.1±3.4 g vs 8.0±3.4 g, p=0.09) among the women with HDP history compared to women without.ConclusionIn a high-risk cohort of women with suspected INOCA, 20% had a history of HDP. Women with HDP history were more likely to develop HTN. Our study demonstrates higher LV mass in women with HDP and concomitant HTN. Although the presence of LGE scar was not different in women with and without HDP history, we observed a trend towards larger scar size in women with HDP. Future studies are needed to better assess the relationship of HDP and cardiac morphology and LGE scarring in a larger cohort of women.

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IL-1β dysregulates cGMP signaling in the newborn lung

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00382.2019 ◽

2020 ◽

Vol 319 (1) ◽

pp. L21-L34

Author(s):

Ying Zhong ◽

Kristina Bry ◽

Jesse D. Roberts

Keyword(s):

Mrna Expression ◽

Transforming Growth Factor ◽

Critical Role ◽

Lung Epithelial Cells ◽

Lung Fibroblasts ◽

Transcriptional Level ◽

Mrna Levels ◽

Iκb Kinase ◽

Primary Mouse ◽

Cgmp Signaling

Cyclic guanosine monophosphate (cGMP) signaling is an important regulator of newborn lung function and development. Although cGMP signaling is decreased in many models of newborn lung injury, the mechanisms are poorly understood. We determined how IL-1β regulates the expression of the α1-subunit of soluble guanylate cyclase (sGCα1), a prime effector of pulmonary cGMP signaling. Physiologic levels of IL-1β were discovered to rapidly decrease sGCα1 mRNA expression in a human fetal lung fibroblast cell line (IMR-90 cells) and protein levels in primary mouse pup lung fibroblasts. This sGCα1 expression inhibition appeared to be at a transcriptional level; IL-1β treatment did not alter sGCα1 mRNA stability, although it reduced sGCα1 promoter activity. Transforming growth factor-β (TGFβ)-activated kinase-1 (TAK1) was determined to be required for IL-1β’s regulation of sGCα1 expression; TAK1 knockdown protected sGCα1 mRNA expression in IL-1β-treated IMR-90 cells. Moreover, heterologously expressed TAK1 was sufficient to decrease sGCα1 mRNA levels in those cells. Nuclear factor-κB (NF-κB) signaling played a critical role in the IL-1β-TAK1-sGCα1 regulatory pathway; chromatin immunoprecipitation studies demonstrated enhanced activated NF-κB subunit (RelA) binding to the sGCα1 promoter after IL-1β treatment unless treated with an IκB kinase-2 inhibitor. Also, this NF-κB signaling inhibition protected sGCα1 expression in IL-1β-treated fibroblasts. Lastly, using transgenic mice in which active IL-1β was conditionally expressed in lung epithelial cells, we established that IL-1β expression is sufficient to stimulate TAK1 and decrease sGCα1 protein expression in the newborn lung. Together these results detail the role and mechanisms by which IL-1β inhibits cGMP signaling in the newborn lung.

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Time course of left ventricular remodelling and mechanics after aortic valve surgery: aortic stenosis vs. aortic regurgitation

European Heart Journal - Cardiovascular Imaging ◽

10.1093/ehjci/jez049 ◽

2019 ◽

Vol 20 (10) ◽

pp. 1105-1111

Author(s):

E Mara Vollema ◽

Gurpreet K Singh ◽

Edgard A Prihadi ◽

Madelien V Regeer ◽

See Hooi Ewe ◽

...

Keyword(s):

Aortic Valve ◽

Aortic Stenosis ◽

Aortic Regurgitation ◽

Time Course ◽

Pressure Overload ◽

Volume Overload ◽

Left Ventricular ◽

Valve Surgery ◽

Aortic Valve Surgery ◽

Lv Mass

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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