Reduction In Left Ventricular Mass Research Articles

Echocardiographic findings following renal sympathetic denervation for treatment resistant hypertension, the ReShape CV-risk study

Objective The aim of this study was to describe and compare echocardiographic findings before renal sympathetic denervation (RDN) and 6 and 24 months after the procedure. Materials and methods Patients with treatment resistant hypertension (TRH) were included in this non-randomised intervention study. RDN was performed by a single experienced operator using the Symplicity Catheter System. Echocardiographic measurements were performed at baseline, and after 6 and 24 months. Results The cohort consisted of 21 patients with TRH, with a mean systolic office blood pressure (BP) of 163 mmHg and mean diastolic BP 109 mmHg. Mixed model analysis showed no significant change in left ventricular (LV) mass index (LVMI) or left atrium volume index (LAVI) after the RDN procedure. Higher LVMI at baseline was significantly associated with greater reduction in LVMI (p < 0.001). Relative wall thickness (RWT) increased over time (0.48 mm after two years) regardless of change in BP. There was a small but significant reduction in LV end-diastolic (LVIDd) and end-systolic (LVIDs) diameters after RDN, with a mean reduction of 2.6 and 2.4 mm, respectively, after two years. Progression to concentric hypertrophy was observed only in in patients who did not achieve normal BP values, despite BP reduction after RDN. Conclusion There was no reduction of LV mass after RDN. We found a small statistically significant reduction in LVIDd and LVIDs, which together with increase in RWT can indicate progression towards concentric hypertrophy. BP reduction after RDN on its own does not reverse concentric remodelling if target BP is not achieved.

Home Dialysis in Patients with Cardiovascular Diseases.

Kidney failure with replacement therapy and cardiovascular disease are frequently comorbid. In patients with kidney failure with replacement therapy, cardiovascular disease is a major contributor to morbidity and mortality. Conventional thrice-weekly in-center dialysis confers risk factors for cardiovascular disease, including acute hemodynamic fluctuations and rapid shifts in volume and solute concentration. Home hemodialysis and peritoneal dialysis (PD) may offer benefits in attenuation of cardiovascular disease risk factors primarily through improved volume and BP control, reduction (or slowing progression) of left ventricular mass, decreased myocardial stunning, and improved bone and mineral metabolism. Importantly, although trial data are available for several of these risk factors for home hemodialysis, evidence for PD is limited. Among patients with prevalent cardiovascular disease, home hemodialysis and PD may also have potential benefits. PD may offer particular advantages in heart failure given it removes volume directly from the splanchnic circulation, thus offering an efficient method of relieving intravascular congestion. PD also avoids the risk of blood stream infections in patients with cardiac devices or venous wires. We recognize that both home hemodialysis and PD are also associated with potential risks, and these are described in more detail. We conclude with a discussion of barriers to home dialysis and the critical importance of interdisciplinary care models as one component of advancing health equity with respect to home dialysis.

The effect of bariatric surgery type on cardiac reverse remodelling.

Bariatric surgery is effective in reversing adverse cardiac remodelling in obesity. However, it is unclear whether the three commonly performed operations; Roux-en-Y Gastric Bypass (RYGB), Laparoscopic Sleeve Gastrectomy (LSG) and Laparoscopic Adjustable Gastric Band (LAGB) are equal in their ability to reverse remodelling. Fifty-eight patients underwent CMR to assess left ventricular mass (LVM), LV mass:volume ratio (LVMVR) and LV eccentricity index (LVei) before and after bariatric surgery (26 RYGB, 22 LSG and 10 LAGB), including 46 with short-term (median 251-273 days) and 43 with longer-term (median 983-1027 days) follow-up. Abdominal visceral adipose tissue (VAT) and epicardial adipose tissue (EAT) were also assessed. All three procedures resulted in significant decreases in excess body weight (48-70%). Percentage change in VAT and EAT was significantly greater following RYGB and LSG compared to LAGB at both timepoints (VAT:RYGB -47% and -57%, LSG -47% and -54%, LAGB -31% and -25%; EAT:RYGB -13% and -14%, LSG -16% and -19%, LAGB -5% and -5%). Patients undergoing LAGB, whilst having reduced LVM (-1% and -4%), had a smaller decrease at both short (RYGB: -8%, p < 0.005; LSG: -11%, p < 0.0001) and long (RYGB: -12%, p = 0.009; LSG: -13%, p < 0.0001) term timepoints. There was a significant decrease in LVMVR at the long-term timepoint following both RYGB (-7%, p = 0.006) and LSG (-7%, p = 0.021), but not LAGB (-2%, p = 0.912). LVei appeared to decrease at the long-term timepoint in those undergoing RYGB (-3%, p = 0.063) and LSG (-4%, p = 0.015), but not in those undergoing LAGB (1%, p = 0.857). In all patients, the change in LVM correlated with change in VAT (r = 0.338, p = 0.0134), while the change in LVei correlated with change in EAT (r = 0.437, p = 0.001). RYGB and LSG appear to result in greater decreases in visceral adiposity, and greater reverse LV remodelling with larger reductions in LVM, concentric remodelling and pericardial restraint than LAGB.

Changes in Cardiac Structure and Function Following Fistula Ligation in Kidney Transplant Recipients (Cohort Study)

Purpose: International guidelines recommend that haemodialysis access is provided by an arteriovenous fistula (AVF), which enables frequent, reliable access to the circulation, but there are no guidelines to suggest whether these AVFs need to be ligated after kidney transplantation. Cardiovascular morbidity and mortality remain high in recipients of a kidney transplant, the persistence of a patent arteriovenous fistula (AVF) after transplantation may contribute to ongoing maladaptive cardiovascular remodelling. The ability to reverse this maladaptive remodelling by ligation of this AVF is unknown. We conducted this trial to evaluate the effect of AVF ligation on cardiac structure and function in stable kidney transplant recipients. Also we studied the ability of preoperative echocardiographic and non-invasive hemodynamic measurements, including the effects of acute temporary occlusion of the fistula, to predict postoperative left ventricular diameter and mass reduction, by the closure of the fistula.&#x0D; Materials and Methods: Nonrandomized controlled trial. kidney transplant recipients (&gt;12 months after transplantation with stable graft function) were divided into 2 groups. The first referred for surgical arteriovenous fistula closure. The second group didn’t receive Fistula closure (control). Standard echocardiographic parameters, heart rate, and blood pressure were assessed preoperatively (fistula closure) at baseline. These measurements were repeated 6 months after surgical closure.&#x0D; Findings: Seventeen kidney transplant patients were prospectively studied with 11 case and 6 controls with no fistula closure. Surgical fistula closure decreased left ventricular end-diastolic diameter and mass indexes (29.9_2.4to 27.4_2.1 mm/m2, P&lt;0.001, and 141_37 to 132_39 g/m2, P&lt;0.05, respectively), whereas no changes were seen in controls after a similar delay. Postoperative left ventricular end-diastolic diameter and mass reductions correlated best with the increases in total peripheral resistance (r_0.85, P&lt;0.0001) and mean arterial blood pressure (r_0.64, P_0.006), respectively.&#x0D; Conclusions. Surgical closure of arteriovenous fistula reduces left ventricular diameter and mass in kidney transplant recipients. The best predictors of those morphological changes are the rise in blood pressure and total peripheral resistance induced by temporary occlusion of the fistula.&#x0D; Implications to Theory, Practice and Policy: Surgical closure of persistent AV fistula after renal transplantation to correct LV geometry and improve symptoms in terms of exertional dyspnea and palpitations.

The impact of outpatient pharmacological optimization on echocardiographic parameters in heart failure with reduced ejection fraction

Abstract Background The 2022 landmark STRONG-HF study demonstrated that aggressive uptitration of guideline directed medical therapy (GDMT) in patients recently hospitalized for heart failure leads to a reduction in the composite endpoint of heart failure hospitalization and mortality. However, the impact of optimization of GDMT on echocardiographic parameters in heart failure with reduced ejection fraction (HFrEF) is unknown. Purpose This goal of this study was to determine the impact of a virtual HFrEF optimization program for achieving GDMT uptake and its impacts of echocardiographic parameters. Methods We conducted a single center study at a Canadian community cardiovascular centre using a prospective pre-post design. NYHA class II/III HFrEF patients referred from inpatient and outpatient settings were enrolled in our virtual 3-month HFrEF optimization program. All participants underwent an initial consult with a nurse and cardiologist. After this, all patients were seen remotely by a nurse every two weeks for adjustment of HFrEF medications with the goal of maximally tolerated GDMT dosing within 3 months was. Transthoracic echocardiograms were performed prior to participation in the program &amp; after completion. Results Over 9 months, 284 NYHA class II/III HFrEF patients enrolled in the virtual HFrEF optimization program. Mean age was 67 and 70% were male. Mean ejection fraction was 34% and 54% had New York Heart Association Class II symptoms. At intake, the proportion of patients prescribed each class of GDMT was: 69% for Beta-blockers, 23% for Mineralocorticoid Receptor Inhibitors (MRA), 16% for Valsartan-Sacubitril and 7% for SGLT2 inhibitors. At 3-month follow-up, rates of GDMT prescription were improved: 90% for beta-blockers (p&amp;lt;0.01), 71% for MRA (p&amp;lt;0.01), 95% for ARNI (p&amp;lt;0.01) and 79% for SGLT2i (p&amp;lt;0.01). From baseline to follow-up echocardiogram, mean Left Ventricular End Diastolic Diameter improved from 5.51 to 5.13 cm (p&amp;lt;0.01). Mean Left Ventricular End Systolic Diameter improved from 4.33 to 3.75 cm (p&amp;lt;0.01). Mean Left Ventricular Mass Index was improved from 112.5 to 102.5 g/m2 (p&amp;lt;0.01). Mean Left Ventricular Ejection Fraction improved 34.4% to 49.8% (p&amp;lt;0.01). No hospitalizations due to medication-related adverse events were reported and 18 patients were hospitalized for HF exacerbation during study follow-up. Mean serum creatinine increased from 97.4 to 104.5 µmol/L (p&amp;lt;0.01); mean serum potassium increased from 4.48 to 4.58 (p&amp;lt;0.01). Conclusions This study demonstrates that a virtual program for GDMT optimization can safely and rapidly promote uptake of therapy in HFrEF patients. Furthermore, medical optimization was associated with significant reductions in left ventricular size, mass and ejection fraction. This provides a structural explanation for reductions in morbidity and mortality seen in STRONG-HF. Future studies should examine the effect of similar interventions on patient outcomes in a randomized setting.

Prognostic Utility of Cardiovascular Magnetic Resonance-Based Phenotyping in Patients With Muscular Dystrophy.

Background The prognostic utility of cardiovascular magnetic resonance imaging, including strain analysis and tissue characterization, has not been comprehensively investigated in adult patients with muscular dystrophy. Methods and Results We prospectively enrolled 148 patients with dystrophinopathies (including heterozygotes), limb-girdle muscular dystrophy, and type 1 myotonic dystrophy (median age, 36.0 [interquartile range, 23.0-50.0] years; 51 [34.5%] women) over 7.7 years in addition to an age- and sex-matched healthy control cohort (n=50). Cardiovascular magnetic resonance markers, including 3-dimensional strain and fibrosis, were assessed for their respective association with major adverse cardiac events. Our results showed that markers of contractile performance were reduced across all muscular dystrophy groups. In particular, the dystrophinopathies cohort experienced reduced left ventricular (LV) ejection fraction and high burden of replacement fibrosis. Patients with type 1 myotonic dystrophy showed a 26.8% relative reduction in LV mass with corresponding reduction in chamber volumes. Eighty-two major adverse cardiac events occurred over a median follow-up of 5.2 years. Although LV ejection fraction was significantly associated with major adverse cardiac events (adjusted hazard ratio [aHR], 3.0 [95% CI, 1.4-6.4]) after adjusting for covariates, peak 3-dimensional strain amplitude demonstrated greater predictive value (minimum principal amplitude: aHR, 5.5 [95% CI, 2.5-11.9]; maximum principal amplitude: aHR, 3.3 [95% CI, 1.6-6.8]; circumferential amplitude: aHR, 3.4 [95% CI, 1.6-7.2]; longitudinal amplitude: aHR, 3.4 [95% CI, 1.7-6.9]; and radial strain amplitude: aHR, 3.0 [95% CI, 1.4-6.1]). Minimum principal strain yielded incremental prognostic value beyond LV ejection fraction for association with major adverse cardiac events (change in χ2=13.8; P<0.001). Conclusions Cardiac dysfunction is observed across all muscular dystrophy subtypes; however, the subtypes demonstrate distinct phenotypic profiles. Myocardial deformation analysis highlights unique markers of principal strain that improve risk assessment over other strain markers, LV ejection fraction, and late gadolinium enhancement in this vulnerable patient population.

Effects of detraining on left ventricular mass in endurance-trained individuals: a systematic review and meta-analysis.

Detraining refers to a loss of training adaptations resulting from reductions in training stimulus due to illness, injury, or active recovery breaks in a training cycle and is associated with a reduction in left ventricular mass (LVM). The purpose of this study was to conduct a systematic review and meta-analysis to determine the influence of detraining on LVM in endurance-trained, healthy individuals. Using electronic databases (e.g. EMBASE and MEDLINE), a literature search was performed looking for prospective detraining studies in humans. Inclusion criteria were adults, endurance-trained individuals with no known chronic disease, detraining intervention >1 week, and pre- and post-detraining LVM reported. A pooled statistic for random effects was used to assess changes in LVM with detraining. Fifteen investigations (19 analyses) with a total of 196 participants (ages 18-55 years, 15% female) met inclusion criteria, with detraining ranging between 1.4 and 15 weeks. The meta-analysis revealed a significant reduction in LVM with detraining (standardized mean difference = -0.586; 95% confidence interval = -0.817, -0.355; P < 0.001). Independently, length of detraining was not correlated with the change in LVM. However, a meta-regression model revealed length of the detraining, when training status was accounted for, was associated with the reduction of LVM (Q = 15.20, df = 3, P = 0.0017). Highly trained/elite athletes had greater reductions in LVM compared with recreational and newly trained individuals (P < 0.01). Limitations included relatively few female participants and inconsistent reporting of intervention details. In summary, LVM is reduced following detraining of one week or more. Further research may provide a greater understanding of the effects of sex, age, and type of detraining on changes in LVM in endurance-trained individuals.

Abstract P304: Coronary Flow Reserve In Primary Aldosteronism

Introduction: Primary aldosteronism (PA) is characterized by excess cardiovascular risk, underpinned by evidence of microvascular dysfunction. Whether this extends to the coronary vasculature and, as such, regresses after appropriate treatment remains to be determined. Aim: To investigate the presence of coronary microvascular dysfunction and its reversibility in PA patients. Methods: Fifteen PA patients with evidence of lateralized aldosterone overproduction at adrenal vein sampling underwent Doppler echocardiography for the assessment of Coronary flow reserve (CFR: diastolic peak flow on the anterior descending coronary artery during pharmacological [dipyridamole, n=14] or physical stress [n=1] -induced hyperaemia/basal flow) and the ratio between diastolic peak flow and left ventricle mass (FMR), at the time of diagnosis (after withdrawal of RAAS-interfering drugs and normalization of kalemia with K supplementation) and 4-6 months after specific treatment. In case CFR was ≤ 2.5 or the stress protocol suggested potential ischemia, regardless of CFR, a coronary CT angiography (coroCT) was performed to exclude underlying macrovascular coronary artery disease. Results: Out of 15 PA patients (5F; 52±10 yo; BP:149/91±17/11 mmHg; sK + =3.5±0.6 at diagnosis and 3.8±0.3 mmol/L on KCl supplements; DRC=3.0 [2.0-5.5] mIU/L; PAC=747 [417-1430] pmol/L), 14 were cured by unilateral adrenalectomy (127/81±13/11 mmHg; sK + =4.3±0.4 mmol/L; DRC=11.8 [6.7-19.2] mIU/L; PAC=200 [136-244] pmol/L, p&lt;0.05 for all); one patient experienced incomplete biochemical cure and was managed with long-term mineralocorticoid receptor antagonism. At the time of diagnosis, n=7 (46%), n=3 (20%) and n=1 (7%) patients showed CFR ≤ 3.0, 2.5 and 2.0, respectively; none had evidence of macrovascular disease at coroCT. In parallel to a reduction in left ventricular mass (trend; p=0.084), both CFR and FRM significantly increased after treatment (CFR=3.1 [2.6-3.3] vs. 3.4 [3.1-4.6], p=0.013; FMR=0.71±0.33 vs. 0.91±0.32 cm x g/sec x m 2 , p=0.038). Conclusions: Treatment of PA improves coronary microvascular function, as assessed by established prognostic indices like CFR and FMR.

Abstract P2072: Chronic Treatment With An Androgen Receptor Antagonist Promotes Maladaptive Structural And Functional Cardiac Remodeling In Aging Male Mice

Testosterone levels decrease with age in men, while the risk for cardiovascular diseases (CVD) increases dramatically. Indeed, low circulating testosterone levels in men are associated with diseases such as heart failure. Testosterone exerts its effects via androgen receptors, which are even present in the heart. In addition, androgen receptor antagonists are used to treat prostate cancer in older men who may also have CVD. We investigated the effects of the androgen receptor antagonist flutamide on cardiac structure and function in aged mice. Twenty-month-old male C57BL/6 mice were treated with flutamide for 90 days (slow-release pellet implant; ~20mg/kg/day). In-vivo heart structure/function was assessed using echocardiography and then hearts were Langendorff-perfused to assess load-independent ventricular function ex-vivo . Androgen receptor blockade via flutamide caused maladaptive ventricular remodeling. In-vivo studies showed that flutamide-treated mouse hearts had smaller left ventricular inner diameters when compared to vehicle-treated mice ( e.g. , diastolic: 4.7 ± 0.1 vs. 4.4 ± 0.1 mm; p=0.01; n=8,7). Flutamide also caused left ventricular (LV) atrophy with thinner posterior walls (0.91 ± 0.07 vs. 0.74 ± 0.04 mm; p=0.05) and reduced LV mass when compared to vehicle controls (140 ± 12 vs. 105 ± 6 mg; p=0.03). Ex-vivo functional assessment showed a marked reduction in LV developed pressure in the flutamide-treated mice (111 ± 11 vs. 71 ± 3 mmHg; p&lt;0.01). These mice also had significantly slower rates of LV pressure rise (+dP/dT=2219 ± 263 vs. 1406 ± 95 mmHg/s; p&lt;0.01) as well as LV pressure decay (-dP/dT=-1975 ± 263 vs. -1327 ± 132 mmHg/s; p=0.04). This indicates that flutamide-treated mice had defects in both systolic and diastolic cardiac function. These results demonstrate that suppressing the effects of testosterone by blocking androgen receptors promotes maladaptive structural remodeling of the left ventricle and promotes systolic and diastolic dysfunction in hearts from aged male mice. This study suggests that chronic treatment with androgen receptor antagonists may induce cardiac dysfunction in older men, which has implications for individuals taking these medications for prostate cancer treatment.

The Effect of Glycemic Control on Left Ventricular Function in Clinical and Experimental Diabetes

BackgroundGlycemic control in diabetes mellitus (DM) has not improved cardiovascular outcomes with normal left ventricular (LV) function. We assessed the effect on LV dysfunction using a canine model of LV dysfunction and DM, and in patients with DM and LV dysfunction. MethodsChronic LV dysfunction was produced by coronary microsphere embolization in 34 canines (15-25 kg). Following 8 weeks of stabilization, DM was induced in 24 canines and randomized to good or poor glycemic control for 3 months. Ten canines without DM were controls. Hemodynamic and Doppler echocardiographic data were obtained prior to and following pressure loading. We reviewed the Doppler-echocardiography at baseline and follow-up in 207 patients with DM with reduced ejection fraction (EF; median follow-up = 612 days) and 60 age- and sex-matched non-DM patients with normal EF. Laboratory results, medications, and incident adverse events from medical records were obtained. ResultsEF = 43.8% ± 11.2% for all canines at 8 weeks. Canines with poor glycemic control (hemoglobin [Hb]A1c = 8.05% ± 3.02%) demonstrated reduced LV mass and rate-corrected velocity of circumferential fiber shortening, compared to those with LV dysfunction (1.36 ± 0.73 vs 0.88 ± 0.13 circumference per second, P < 0.01). Good glycemic control (HbA1c = 3.88% ± 0.89%) demonstrated similar LV parameters, compared to controls (HbA1c = 2.99% ± 0.44%). EF was similar among groups. Patients with vs without DM were followed for up to 3 years. Patients with DM and poor glycemic control had reduced EF, lower rate-corrected velocity of circumferential fiber shortening = 0.93 ± 0.26 vs 1.11 ± 0.26, P < 0.001), and greater incidence of heart failure. ConclusionsPoor glycemic control had an adverse effect on preexisting LV dysfunction experimentally and in patients with type 2 diabetes.

Left ventricular mass predicts cardiac reverse remodelling in patients treated with empagliflozin

BackgroundThe cardiovascular (CV) benefits of sodium-glucose transport protein 2 inhibitors have been attributed, in part, to cardiac reverse remodelling. The EMPA-HEART CardioLink-6 study reported that sodium-glucose cotransporter-2 inhibition for 6 months with empagliflozin was associated with a significant reduction in left ventricular mass indexed to body surface area (LVMi). In this sub-analysis, we evaluated whether baseline LVMi may influence how empagliflozin affects cardiac reverse remodelling.MethodsA total of 97 patients with type 2 diabetes and coronary artery disease were randomized to empagliflozin (10 mg/d) or matching placebo for 6 months. The study cohort was divided into those whose baseline LVMi was ≤ 60 g/m2 and those who had a baseline LVMi > 60 g/m2. Subgroup comparisons were conducted using a linear regression model adjusted for baseline values (ANCOVA) that included an interaction term between LVMi subgroup and treatment.ResultsBaseline LVMi was 53.3 g/m2 (49.2–57.2) and 69.7 g/m2 (64.2–76.1) for those with baseline ≤ 60 g/m2 (n = 54) and LVMi > 60 g/m2 (n = 43) respectively. The adjusted difference of LVMi regression between those randomized to empagliflozin and placebo were − 0.46 g/m2 (95% CI: −3.44, 2.52, p = 0.76) in the baseline LVMi ≤ 60 g/m2 subgroup and − 7.26 g/m2 (95% CI: −11.40, −3.12, p = 0.0011) in the baseline LVMi > 60 g/m2 subgroup (p-for-interaction = 0.007). No significant associations were found between baseline LVMi and 6-month change in LV end systolic volume-indexed (p-for-interaction = 0.086), LV end diastolic volume-indexed (p-for-interaction = 0.34), or LV ejection fraction (p-for-interaction = 0.15).ConclusionsPatients with higher LVMi at baseline experienced greater LVM regression with empagliflozin.

Left ventricular cellular regression occurs without matrix changes at two months post aortic valve replacement in severe aortic stenosis

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): British Heart Foundation Background Increased left ventricular mass (LVM) in severe aortic stenosis (AS) is a result of the combined expansion of myocardial cellular and extracellular compartments in response to chronic pressure overload. Upon relief of pressure overload by aortic valve replacement (AVR), LVM regresses significantly however patients remain at risk of post-AVR heart failure and mortality. T1 mapping, by cardiovascular magnetic resonance (CMR), can quantify the proportion of cellular and extracellular volume. Purpose We sought to determine the relative contributions of cellular and extracellular remodelling early after AVR to gain insight into potential post-AVR mechanisms of heart failure. Methods Patients with severe symptomatic AS underwent CMR (volumes, function, pre- and post-contrast T1 mapping using 0.1mmol/kg Dotarem) prior to and 8-weeks after surgical or transcatheter AVR. Global extracellular volume fraction (ECV%) was quantified from pre- and post-contrast T1 mapping and synthetic haematocrit. ECV% was used to calculate cellular compartment volume (CellVol) and extracellular volume (ECVol) from total LV volume (LVM/1.05[specific gravity of myocardium]). Segments with focal LGE were excluded from ECV% calculation. Statistical analysis was via paired t-test denoted by standard deviations (SD), or Wilcoxon signed-rank test with reported interquartile ranges (IQR). Results 27 patients (age 71.2 SD±9.8, male 70.3%) returned for repeat investigation at median 8.5 [IQR 7.1–11.6] weeks post-AVR (surgical: 16 / transcatheter: 11). Aortic valve peak velocity significantly improved (4.5 SD±0.5m/s to 2.4 SD±0.4m/s; p&amp;lt;0.001) alongside median NYHA class (2 [IQR 0] to 1 [IQR 0.5]; p&amp;lt;0.001). LVM regressed 10.3% (170.8 SD±36.6g to 153.2 SD±39g; P&amp;lt;0.001), which comprised of a 13.8% reduction in CellVol (134.8 SD±29.4mL to 116.2 SD±30.5mL; P&amp;lt;0.001). However, ECVol remained unchanged (44.4 SD±10.2mL to 44.7 SD±11.2mL; P=0.78) resulting in an ECV% increase of 3.1% (24.8 SD±2.4% to 27.9 SD±2.1%; P&amp;lt;0.001). Summary We show for the first time that the rapid early LVM reduction after AVR is driven entirely by regression of cardiomyocyte hypertrophy. The extracellular compartment volume is unchanged at two months post-AVR. This relative increase in the ratio of fibrosis and cell volume may result in early worsening myocardial stiffness and could be a contributing factor to post-AVR diastolic dysfunction and heart failure.

Mapping the Unseen: In Vivo CEST-MRI of Creatine Reveals Improved Cardiac Energetics in Subjects with Obesity Following Bariatric Surgery.

Obesity is associated with derangement of cardiac metabolism and the development of subclinical cardiovascular disease. This prospective study examined the impact of bariatric surgery on cardiac function and metabolism. Subjects with obesity underwent cardiac magnetic resonance imaging (CMR) at Massachusetts General Hospital before and after bariatric surgery between 2019 and 2021. The imaging protocol included Cine for global cardiac function assessment and creatine chemical exchange saturation transfer (CEST) CMR for myocardial creatine mapping. Thirteen subjects were enrolled, and 6 subjects [mean BMI 40.5 ± 2.6] had completed the second CMR (i.e. post-surgery), with a median follow-up of 10 months. The median age was 46.5 years, 67% were female, and 16.67% had diabetes. Bariatric surgery led to significant weight loss, with achieved mean BMI of 31.0 ± 2.0. Additionally, bariatric surgery resulted in significant reduction in left ventricular (LV) mass, LV mass index, and epicardial adipose tissue (EAT) volume. This was accompanied by slight improvement in LV ejection fraction compared to baseline. Following bariatric surgery, there was a significant increase in creatine CEST contrast. Subjects with obesity had significantly lower CEST contrast compared to subjects with normal BMI (n = 10), but this contrast was normalized after the surgery, and statistically similar to non-obese cohort, indicating an improvement in myocardial energetics. CEST-CMR has the ability to identify and characterize myocardial metabolism in vivo non-invasively. These results demonstrate that in addition to reducing BMI, bariatric surgery may favorably affect cardiac function and metabolism.

Two innovative aortic bioprostheses evaluated in the real-world setting. First results from a two-center study.

The increasing use of biological substitutes for surgical aortic valve replacement (AVR), has led to the development of new bioprostheses with improved hemodynamics and expected durability. In this observational retrospective two-center cohort study, two innovative bioprostheses, INSPIRIS Resilia and AVALUS were analyzed. We analyzed early and 2.4-year follow-up results in terms of safety, clinical outcome and hemodynamic performance. From November 2017 to February 2021, 148 patients underwent AVR with INSPIRIS Resilia (N.=74) or AVALUS (N.=74) bioprosthesis. The 30-day and mid-term mortality was comparable (1% vs. 3%, P=0.1 and 7% vs. 4%, P=0.4, respectively). Valve-related mortality was observed in one AVALUS patient. Three (4%) patients of the AVALUS group developed prosthetic endocarditis and two of them died after reoperation. No other cases of prosthetic endocarditis were observed. No cases of structural valve degeneration or significant paravalvular leak were detected at follow-up. Median follow-up peak pressure gradient was 21 vs. 23 mmHg (P=0.4) and the mean pressure gradient was 12 vs. 13 mmHg (P=0.9) for Inspiris and AVALUS, respectively. The effective orifice area (EOA) and indexed EOA were 1.5 cm2 vs. 1.4 cm2 (P=0.4) and 0.8 vs. 0.7 cm2/m2 (P=0.5), respectively. Indexed left ventricular mass regression was -33 vs. -52 g/m2 for the Inspiris and AVALUS groups, respectively, (R2-adjusted =0.14; P<0.01). INSPIRIS Resilia and AVALUS bioprostheses were reliable with comparable results in safety, clinical outcome and hemodynamic performance. After statistical adjustment, AVALUS was associated with better left ventricular mass reduction. Long-term follow-up would provide definitive comparative results.

Parathyroidectomy versus oral cinacalcet on cardiovascular parameters in peritoneal dialysis patients with advanced secondary hyperparathyroidism (PROCEED): A randomized trial.

This trial aimed to evaluate oral cinacalcet versus total parathyroidectomy with forearm autografting (PTx) on cardiovascular surrogate outcomes and health-related quality of life (HRQOL) measures in dialysis patients with advanced SHPT. In this pilot prospective randomized trial conducted in two university-affiliated hospitals, 65 adult peritoneal dialysis patients with advanced SHPT were randomized to receive either oral cinacalcet or PTx. Primary endpoints were changes in left ventricular (LV) mass index by cardiac magnetic resonance imaging and coronary artery calcium scores (CACS) over 12 months. Secondary endpoints included changes in heart valves calcium scores, aortic stiffness, biochemical parameters of chronic kidney disease-mineral bone disease (CKD-MBD) and HRQOL measures over 12 months. Changes in LV mass index, CACS, heart valves calcium score, aortic pulse wave velocity and HRQOL did not differ between-groups or within-groups, despite significant reductions in plasma calcium, phosphorus and intact parathyroid hormone in both groups. Cinacalcet-treated patients experienced more cardiovascular-related hospitalizations than those who underwent PTx (P=0.008) but the difference became insignificant after adjusting for baseline difference in heart failure (P=0.43). With the same monitoring frequency, cinacalcet-treated patients had fewer hospitalizations due to hypercalcemia (1.8%) than patients who underwent PTx (16.7%) (P=0.005). No significant changes were observed in HRQOL measures in either group. Both cinacalcet and PTx effectively improved various biochemical abnormalities of CKD-MBD and stabilized but did not reduce LV mass, coronary artery and heart valves calcification, arterial stiffness or improve patient-centered HRQOL measures in PD patients with advanced SHPT. Cinacalcet may be used in place of PTx for treating advanced SHPT. Long-term and powered studies are required to evaluate PTx versus cinacalcet on hard cardiovascular outcomes in dialysis patients.

Cardiovascular Magnetic Resonance Demonstrates Myocardial Inflammation of Differing Etiologies and Acuities in Patients with Genetic and Inflammatory Myopathies.

Myopathies are heterogeneous neuromuscular diseases of genetic and/or inflammatory etiology that affect both cardiac and skeletal muscle. We investigated the prevalence of cardiac inflammation in patients with myopathies, cardiovascular symptoms, and normal echocardiography using cardiovascular magnetic resonance (CMR). We prospectively evaluated 51 patients with various genetic (n = 23) and inflammatory (n = 28) myopathies (median age, IQR: 12 (11-15) years, 22% girls; 61 (55-65) years, 46% women, respectively) and compared their CMR findings to corresponding age- and sex-matched controls (n = 21 and 20, respectively) and to each other. Patients with genetic myopathy had similar biventricular morphology and function to healthy controls but showed higher late gadolinium enhancement (LGE), native T1 mapping, extracellular volume fraction (ECV), and T2 mapping values. Collectively, 22 (95.7%) patients with genetic myopathy had a positive T1-criterion and 3 (13.0%) had a positive T2-criterion according to the updated Lake Louise criteria. Compared with healthy controls, patients with inflammatory myopathy showed preserved left ventricular (LV) function and reduced LV mass, while all CMR-derived tissue characterization indices were significantly higher (p < 0.001 for all). All patients had a positive T1-criterion, and 27 (96.4%) had a positive T2-criterion. A positive T2-criterion or T2-mapping > 50 ms could discriminate between patients with genetic and inflammatory myopathies with a sensitivity of 96.4% and a specificity of 91.3% (AUC = 0.9557). The vast majority of symptomatic patients with inflammatory myopathies and normal echocardiography show evidence of acute myocardial inflammation. In contrast, acute inflammation is rare in patients with genetic myopathies, who show evidence of chronic low-grade inflammation.

Fabry Disease: Switch from Enzyme Replacement Therapy to Oral Chaperone Migalastat: What Do We Know Today?

Fabry disease is a lysosomal storage disorder caused by the deficiency of the α-galactosidase-A enzyme. The result is the progressive accumulation of complex glycosphingolipids and cellular dysfunction. Cardiac, renal, and neurological involvement significantly reduces life expectancy. Currently, there is increasing evidence that clinical response to treatment improves with early and timely initiation. Until a few years ago, treatment options for Fabry disease were limited to enzyme replacement therapy with agalsidase alfa or beta administered by intravenous infusion every 2 weeks. Migalastat (Galafold®) is an oral pharmacological chaperone that increases the enzyme activity of "amenable" mutations. The safety and efficacy of migalastat were supported in the phase III FACETS and ATTRACT studies, compared to available enzyme replacement therapies, showing a reduction in left ventricular mass, and stabilization of kidney function and plasma Lyso-Gb3. Similar results were confirmed in subsequent extension publications, both in patients who started migalastat as their first treatment and in patients who were previously on enzyme replacement therapy and switched to migalastat. In this review we describe the safety and efficacy of switching from enzyme replacement therapy to migalastat in patients with Fabry disease and "amenable" mutations, referring to publications available to date.

Effect of Migalastat on cArdiac InvOlvement in FabRry DiseAse: MAIORA study

BackgroundA small but significant reduction in left ventricular (LV) mass after 18 months of migalastat treatment has been reported in Fabry disease (FD). This study aimed to assess the effect...

Effect of Spironolactone on QRS Duration in Patients at Risk for Heart Failure (from the HOMAGE Trial)

The QRS duration can be easily obtained from a 12-lead electrocardiogram. Increased QRS duration reflects greater ventricular activation times and often ventricular dyssynchrony. Dyssynchrony causes an impairment of the global cardiac function and adversely affects the prognosis of patients with heart failure (HF). Little is known about the impact of pharmacologic therapies on the QRS duration, particularly for patients with presymptomatic HF with a preserved left ventricular (LV) ejection fraction (i.e., stage B HF with preserved ejection fraction [HFpEF]). The HOMAGE (Heart OMics in AGEing) trial enrolled patients at risk factors for developing HF and assigned them to receive either spironolactone or the usual care for approximately 9months in a randomized manner. This analysis reports the effect of spironolactone on the QRS duration. A total of 525 patients was included in the analysis. The median (percentile25-75) QRS duration at baseline was 92 (84 to 106) ms. Spironolactone reduced the QRS duration at month 9 by -2.8, 95% confidence interval -4.6 to -1.0 ms, p=0.003. No significant associations were found between month 9 changes in the QRS duration and corresponding changes in the LV ejection fraction, LV mass, LV end-diastolic volume, blood pressure, N-terminal pro-brain natriuretic peptide, and procollagen type I carboxy-terminal propeptide (all p >0.05). This analysis shows that for patients with stage B HFpEF, therapy with spironolactone for 9months shortened the QRS duration, an effect that was not associated with reductions in LV mass or volume, supporting the hypothesis that spironolactone has direct beneficial effects to improve myocardial electrical activation in patients with stage B HFpEF.

S-50-6: HOW TO ASSESS BENEFICIAL EFFECTS OF ANTIHYPERTENSIVE TREATMENTS

Most hypertensive patients could have hypertension mediated organ damage (HMOD) at the moment of the diagnosis. Even in low 10-year cardiovascular risk patients HMOD is frequent. The presence of HMOD is related to increased cardiovascular risk and mortality, so, at the same time HMOD should be considered as a therapeutic target and a surrogate marker of blood pressure un/controlled. The effects of impaired renal function and left-ventricular hypertrophy could identify patients at a mortality very high risk. Guidelines considered arterial stiffening evaluated as high carotid-femoral pulse wave velocity a factor influencing cardiovascular risk, and a documented carotid artery stenosis &gt; 50 % as a marker of very high cardiovascular risk. The Shiga Epidemiological Study of Subclinical Atherosclerosis (SESSA) showed that 50% of the participants at risk category one had a mean of one atherosclerotic plaque, and 80.7 % of individuals at category two had a mean of 2.2 atherosclerotic plaques. The hazard ratio of having a vascular event could increase by 50% in the presence of one HMOD and by 3.8 times when three HMOD are present. In this scenario, to prevent that at least some patients could be misclassified as low risk, screening of HMOD as modifiers of cardiovascular risk estimated by different scores could be recommended in hypertensive patients. The non-significant net reclassification improvement of cardiovascular risk and the lack of evidence suggesting a relationship between vascular images biomarkers regression independently of blood pressure lowering and a reduction in cardiovascular events precludes the routine search of arterial stiffness or carotid atherosclerotic plaques out of research scenarios. A reduction in left ventricular mass during treatment is a favorable prognostic marker that predicts lesser risk for subsequent cardiovascular morbidity and mortality. The association between left ventricular mass regression and cardiovascular outcomes is independent of baseline left ventricular mass, baseline clinic and ambulatory blood pressure, and degree of blood pressure reduction. Suboptimal blood pressure control is a significant covariate of persistent left ventricular hypertrophy, independent of the number and class of antihypertensive drugs. RAS blockade is recommended as the initial treatment of hypertension in patients with reduced glomerular filtration rate or albuminuria since they are the most effective at reducing progression to end stage kidney disease, but a combination with calcium channel blockers or diuretics is recommended due to the difficulties to achieve the targets with monotherapy.