Regression Of Left Ventricular Hypertrophy Research Articles

Abstract 4138292: Smoking cessation is linked to regression of electrocardiographic left ventricular hypertrophy

Introduction/Background: Electrocardiographic left ventricular hypertrophy is a strong predictor of cardiovascular morbidity and mortality. Further, smoking cessation provides a range of health benefits; however, its association with left ventricular hypertrophy is unclear. Research Questions/Hypothesis: What impact does smoking cessation have on left ventricular hypertrophy regression? Goals/Aims: We investigated the association between smoking cessation and regression of left ventricular hypertrophy. Methods/Approach: We compared electrocardiographic left ventricular hypertrophy between baseline and 6 years after smoking cessation follow-up visits in 752 non-hypertensive subjects (695 males, 47.8±9.2 years), from available datasets of 234 596 health check-ups. Left ventricular hypertrophy on ECG was assessed using the Sokolow-Lyon voltage criteria: SV1+RV5 (mV), with left ventricular hypertrophy defined as >3.5 mV. Results/Data: After 6 years of smoking cessation, body weight was found to increase (from 65.7±10.5 to 68.1±10.8 kg, p <0.0001) and systolic blood pressure also increased (from 112.9±12.7 to 122.0±14.2 mmHg, p <0.0001). Nevertheless, left ventricular hypertrophy on ECG regressed significantly (from 2.47 to 2.41 mV, p <0.0001), and the proportion fulfilling the criteria for left ventricular hypertrophy also decreased from 8.4 to 6.5%. In addition, the antihypertensive drug prescription rate due to elevated blood pressure after 6 years was 13.7% (103/752). Therefore, the regression of left ventricular hypertrophy with or without antihypertensive drug use was assessed. The results showed that left ventricular hypertrophy regressed significantly both [2.68→2.45 mV ( p <0.0001)] and [2.44→2.40 mV ( p =0.01)] in the groups administered (n=103) and not administered (n=649) antihypertensive drugs, respectively. Conclusions: Smoking cessation was found to be associated with regression of electrocardiographic left ventricular hypertrophy, despite being potentially associated with future weight gain, increased blood pressure, and with or without antihypertensive drugs. The results indicated that the health benefits of left ventricular hypertrophy regression from smoking cessation may outweigh the negative effects of weight gain and increased blood pressure from smoking cessation.

Significant regression of left ventricular hypertrophy in patient with arterial hypertension during antihypertensive treatment with perindopril and atorvastatin

Left ventricular hypertrophy (LVH) in arterial hypertension (AH) is one of the modifiable risk factors for cardiovascular events and serves as a justified goal for antihypertensive therapy. The article presents follow-up of a 60-year-old female with AH, hyperlipidemia, and discovered of LVH on the data of electrocardiography and echocardiography. In addition to the SokolowLyon and Cornell voltage criteria, the baseline echocardiographic examination revealed and increase in thickness of the ventricular septum and the left ventricular (LV) posterior wall, an increase in LV myocardial mass and LV myocardial mass index. The patient was recommended to take a drug of the class of angiotensin converting enzyme inhibitors perindopril and atorvastatin. The patient regularly received therapy and periodically underwent repeated echocardiographic examinations. After 40 months follow-up there are a significant decrease in septal hypertrophy (from 1.22 to 0.76 cm, -37.7%), LV posterior wall (from 1.05 to 0.49, -53.3%), as well as LV myocardial mass (from 197.9 to 96 g, -51.5%) and LV myocardial mass index (from 111.18 to 59.11 g/ m2, -51.5%). Thus, during the entire period of follow-up, the LV mass decreased almost twice. There was a decrease in the size of the left atrium, the relative wall thickness, with the same parameters of LV volumes, characteristics of systolic and diastolic function. Among the favorable factors contributing to significant LVH regression, high adherence to treatment, the efficacy of angiotensin converting enzyme inhibitors and the possible antihypertrophic influence of atorvastatin are discussed.

Impact of changes in left heart geometry on predicting new-onset atrial fibrillation in patients with hypertension

Abstract Background Hypertension-induced left ventricular hypertrophy (LVH) increases end-diastolic LV pressure and contributes to left atrial enlargement (LAE), which are associated with development of atrial fibrillation (AF). However, the impact of LVH and LAE and their regression following antihypertensive therapy on AF incidence remains unclear. Purpose This study aimed to investigate the impact of changes in the LVH and LAE status on the occurrence of new-onset AF (NOAF). Methods This retrospective analysis included patients with sinus rhythm who underwent echocardiography at hypertension diagnosis and after 6–18 months. LVH was defined as LV mass index >115 g/m2 (men) and >95 g/m2 (women), and LAE was defined as LA volume index >42 ml/m2. LVH and LAE regression was defined as the absence of LVH and LAE on follow-up echocardiography, respectively. The occurrence of NOAF was assessed in relation to changes in LVH and LAE status. Results Among the 1,464 patients included in the study, 163 (11.1%) patients developed NOAF during a median follow-up of 63.8 months (interquartile range, 35.9–128.5 months). On average, 12 electrocardiograms per patient were reviewed for AF detection. New-onset LVH (adjusted HR 1.88, 95% CI 1.20–2.94, P=0.006) and LAE (adjusted HR 1.89, 95% CI 1.05–3.40, P=0.034) were significant predictors of NOAF. Conversely, regression of LVH (adjusted HR 0.51, 95% CI 0.280.91, P=0.022) or LAE (adjusted HR: 0.30, 95% CI 0.15–0.63, P=0.001) after antihypertensive therapy was associated with a reduced risk of NOAF. The risk of NOAF was higher in patients with LVH and LAE together (adjusted HR 4.30, 95% CI 2.81–6.56, P<0.001) than in those with either LVH or LAE, or those with neither, as determined by follow-up echocardiography. Conclusion In patients with hypertension and sinus rhythm, regression of LVH and LAE following antihypertensive therapy is associated with a decreased incidence of NOAF, whereas newly developed LVH or LAE is associated with a higher risk of NOAF. The changes in left heart geometry can serve as a predictive marker for NOAF in patients with hypertension.

Cardioprotective efficacy of combined therapy with azilsartan, indapamide, and nitrendipine in patients with essential hypertension

Abstract Objective To conduct a comparative assessment of the six-month cardioprotective efficacy of combined therapy using azilsartan with indapamide and nitrendipine in patients with essential hypertension (EH). Materials and Methods The study included 101 male and female patients with grade I–II arterial hypertension (AH) according to the classification (ESC/ESH, 2018), who were undergoing outpatient treatment at the Republican Specialized Scientific-Practical Medical Center of Cardiology. The mean age of the patients was 53.1±11.2 years, and the mean duration of AH was 8.5±7.2 years. Initially and after 6 months of therapy, echocardiography was performed to determine the left ventricular myocardial mass index (LVMMI) and left ventricular (LV) echo geometry types. Echocardiography (ECHO) was performed using the "En VisorC" ultrasound system (Philips, Netherlands). Statistical significance was considered for all analyses with p <0.05. Results All patients were divided into 2 groups: Group 1 - patients on combined antihypertensive therapy (AHT) with azilsartan and indapamide (n=50) and Group 2 - patients on therapy with azilsartan and nitrendipine (n=51). The mean daily dose of azilsartan was 49.3±6.0 mg, nitrendipine was 10.88±4.3 mg, and indapamide was 1.69±0.5 mg. In Group 1, the LVMMI initially was 127.4±32.9 g/m2, and after treatment, it was 110.3±29.0 g/m2 (p<0.001); in Group 2, it was 138.7±31.9 g/m2 and 116.6±30.3 g/m2, respectively (p<0.001). The degree of LVMMI reduction in Group 1 was -13.3±15.6% compared to Group 2, which was -14.4±17.9% (p>0.05). During therapy with azilsartan, indapamide, and nitrendipine, the reduction of LVMMI in EH patients was associated with a decrease in the concentric type of left ventricular hypertrophy (LVH) in both therapy groups: in both groups, a significant increase in the LV diastolic filling pattern index/LVMMI was observed, which was 0.51±0.07 ml/g before treatment and 0.57±0.14 ml/g after treatment in Group 1 (p<0.001), and 0.50±0.11 ml/g before treatment and 0.54±0.12 ml/g after treatment in Group 2 (p<0.02). Significant regression of LVH with 6-month combined therapy in both groups was accompanied by an improvement in LV echo geometry. Initially, there were 12 patients (11.9%) with unchanged LV echo geometry, concentric remodeling was detected in 9 patients (8.91%), eccentric LVH in 30 patients (29.7%), and concentric LVH in 50 patients (49.5%). In the dynamics, the number of patients with normal LV echo geometry increased to 41 patients (40.6%), with concentric LVH decreased to 34 patients (33.6%), with concentric remodeling decreased to 7 patients (7%), and with eccentric LVH decreased to 19 patients (18.8%) (χ2=21.635, p<0.001). Conclusion Achieving target blood pressure levels provided high cardioprotective efficacy of combined therapy with azilsartan, indapamide, and nitrendipine with improvement in LV echo geometry in both groups.

Severe aortic stenosis is associated with left atrial prothrombotic flow changes that persists despite successful aortic valve replacement

Abstract Background Severe aortic stenosis (AS) is associated with ischaemic stroke independently of atrial fibrillation (AF) or other causes. Even after aortic valve replacement (AVR), patients remain affected by up to 15% five-year rate of incident ischaemic strokes independently of AVR-related complications and with knowledge gaps in the underlying pathophysiology. Purpose To assess whether severe AS leads to prothrombotic left atrial (LA) flow changes with reduction of LA velocities and vorticity which do not normalise after AVR. Methods Seventy-seven participants without history of AF were recruited in this study: N=40 with severe AS (60% male; age 73 ±10 years, BMI 28 ±5 Kg/m2, median CHA2DS2VASc = 3) and N=37 controls with similar clinical risk profile (51% male; age 71 ±6 years, BMI 28 ±5 Kg/m2, median CHA2DS2VASc = 3). All participants underwent a cardiovascular magnetic resonance (CMR) scan to quantify left ventricular (LV) volumes, mass, and ejection fraction (LVEF), LV global longitudinal strain (GLS) as a sensitive marker of longitudinal dysfunction, LA maximum volume and emptying fraction (LAEF), LA blood flow peak velocity and vorticity by 4-dimensional flow CMR. Out of the 40 patients with severe AS, N=23 (58%) underwent a successful AVR and were followed-up with a repeat CMR scan at approximately 6 months after surgery. Results When compared to matched controls, patients with severe AS displayed significantly higher LV mass, smaller LA and LV volumes (i.e. concentric LV hypertrophy), significantly reduced GLS but higher (more hyperdynamic) LVEF (all p<0.05), as expected. LAEF (i.e. global LA function) was not significantly different from controls but despite this, severe AS was associated with slightly lower LA peak flow velocity (mean 0.25 vs. 0.28 m/sec respectively) and lower LA flow vorticity (mean 16.6 vs. 21.1 radians) compared to controls (both p<0.05). Successful AVR led to complete regression of LV hypertrophy (p<0.05) with LV mass that was no longer different from controls (p>0.05). Nevertheless, post-AVR patients displayed a persistent adverse morpho-functional phenotype characterised by persistently smaller LA and LV volumes, persistently hyperdynamic LV function with reduced GLS (all p<0.05), as well as adverse LA flow changes with significantly lower velocity (mean 0.24 vs 0.28 m/sec, p=0.003) and vorticity when compared to controls (17.1 vs 21.1 radians, p<0.001). Conclusions Patients with severe AS display adverse LA physiology and structure (prothrombotic LA flow characteristics in smaller LA size) and LV changes (smaller size with reduced longitudinal function and hyperdynamic function), which persist after successful AVR despite normalisation of the LV hypertrophy.Figure 1

Left Ventricular Hypertrophy Regression Following Transcatheter Aortic Replacement: A Comparison of Self-Expanding Versus Balloon-Expandable Prostheses

There are limited reports on the impact of prosthesis-patient mismatch (PPM) on the regression of left ventricular hypertrophy (LVH) after transcatheter aortic valve replacement (TAVR). We compared the relative effects of supra-annular, self-expanding (SE) versus intra-annular, balloon-expandable (BE) prostheses on TAVR LVH regression. Regression of left ventricular mass index (LVMi) was evaluated in 168 consecutive TAVR patients, including 60 treated with SE valves (Evolut series) and 108 treated with BE valves (Sapien 3). All patients had LVH determined at baseline by echocardiography and had repeat LVMi measurements at a mean follow-up time of 707 ± 528 days. SE patients were more likely female (68.3% vs 46.3%, p = 0.007), but otherwise, the 2 cohorts did not differ with respect to baseline demographics and Society of Thoracic Surgeons risk score. SE patients had a higher effective orifice area indexed to body surface area after TAVR (0.98 ± 0.29 vs 0.86 ± 0.25 cm²/m², p = 0.006), with lower mean aortic valve gradients (9.9 ± 6.5 vs 12.8 ± 5.8 mm Hg, p = 0.003) and a lower prevalence of moderate/severe PPM (33.3% vs 49.1%, p = 0.049). On follow-up, changes in LVMi were similar between the SE and BE groups, with similar absolute changes in LVMi (19.2 ± 26.8 vs 21.9 ± 31.7 g/m2, p = 0.578) and relative LVMi decrease (14.0 ± 19.5 vs 16.2% ± 24.2%, p = 0.547). No difference in LVMi regression was also noted comparing combined SE/BE patients with moderate/severe PPM versus those without PPM. In conclusion, despite differences in effective orifice area indexed to body surface area, mean aortic valve gradient, and PPM after TAVR, the degree of LVH regression during intermediate follow-up did not differ between patients receiving supra-annular SE and intra-annular BE prostheses.

Impact of changes in left heart geometry on predicting new-onset atrial fibrillation in patients with hypertension.

Hypertension-induced left ventricular hypertrophy (LVH) increases end-diastolic LV pressure and contributes to left atrial enlargement (LAE), which are associated with development of atrial fibrillation. However, the impact of LVH and LAE and their regression following antihypertensive therapy on atrial fibrillation incidence remains unclear. This retrospective analysis included consecutive patients with sinus rhythm who underwent echocardiography at hypertension diagnosis and after 6-18 months between 2006 and 2021 at tertiary care centres in Korea. LVH was defined as LV mass index greater than 115 g/m2 (men) and greater than 95 g/m2 (women), and LAE was defined as LA volume index greater than 42 ml/m2. The occurrence of new-onset atrial fibrillation (NOAF) was assessed in relation to changes in LVH and LAE status. Among the 1464 patients included, 163 (11.1%) developed NOAF during a median 63.8 [interquartile range (IQR) 35.9-128.5] months of surveillance period. New-onset LVH [adjusted hazard ratio (aHR) 1.88, 95% confidence interval (CI) 1.20-2.94, P = 0.006] and LAE (aHR 1.89, 95% CI 1.05-3.40, P = 0.034) were significant predictors of NOAF. Conversely, regression of LVH (aHR 0.51, 95% CI 0.28-0.91, P = 0.022) or LAE (aHR 0.30, 95% CI 0.15-0.63, P = 0.001) was associated with a reduced risk for developing NOAF. Patients with both LVH and LAE at follow-up echocardiography had a higher risk for NOAF (aHR 4.30, 95% CI 2.81-6.56, P < 0.001) than those with either LVH or LAE or those with neither. The changes in left heart geometry can serve as a predictive marker for NOAF in patients with hypertension.

Electrocardiographic tracking of left ventricular hypertrophy in hypertension: incidence and prognostic outcomes from the SPRINT trial

BackgroundThis study explores the impact of intensive blood pressure (BP) control on left ventricular hypertrophy (LVH) incidence and evaluates the prognostic implications of LVH status (pre-existing/new-onset/persistent/regression) using Systolic Blood Pressure Intervention Trial (SPRINT) Electrocardiogram Data.MethodsPoisson regression was used to assess new-onset LVH and LVH regression rates. Multivariable-adjusted Cox proportional hazard models determined the risk of adverse cardiovascular events (ACE), a composite of myocardial infarction (MI), non-MI acute coronary syndrome, stroke, heart failure, or cardiovascular death, alongside safety adverse events.ResultsIn 8,016 participants, intensive BP control significantly reduced new-onset LVH (8.27 vs. 14.79 per 1000-person years; adjusted p<0.001) and increased LVH regression (14.89 vs. 11.89 per 1000-person years; adjusted p<0.001). Elevated ACE risk was notable in participants with pre-existing LVH [adjusted HR: 1.94 (95% CI: 1.25–2.99); p = 0.003], new-onset LVH [adjusted 1.74 (95% CI: 1.16–2.60); p = 0.007], and persistent LVH[adjusted HR: 1.96 (95% CI: 1.11–3.46); p = 0.020], compared to those without LVH. Intriguingly, LVH regression attenuated this risk increment [adjusted HR: 1.57 (95% CI: 0.98–2.53); p = 0.062]. Achieving a BP target of < 120/80 mmHg nullified the increased ACE risk in those with pre-existing LVH.ConclusionsIntensive BP control is instrumental in both reducing the emergence of LVH and fostering its regression. Pre-existing, new-onset LVH and persistent LV remain a predictor of adverse cardiovascular prognosis, whereas LVH regression and achieving on-treatment BP < 120/80 mmHg in pre-existing LVH individuals may further mitigate residual cardiovascular risk.Clinical trial registrationURL: ClinicalTrials.gov Unique Identifier: NCT01206062.

Left Ventricular Hypertrophy After Renal Transplantation: Systematic Review and Meta-analysis.

Left ventricular hypertrophy (LVH) in patients with end stage renal disease undergoing renal replacement is linked to an increased risk for cardiovascular diseases. Dialysis does not completely prevent or correct this abnormality, and the evidence for kidney transplantation (KT) varies. This analysis aims to explore the relationship between KT and LVH. MEDLINE and Scopus were systematically searched in October 2023. All cross-sectional and longitudinal studies that fulfilled our inclusion criteria were included. Outcome was left ventricular mass index (LVMI) changes. We conducted a meta-analysis using a random effects model. Meta-regression was applied to examine the LVMI changes dependent on various covariates. Sensitivity analysis was used to handle outlying or influential studies and address publication bias. From 7416 records, 46 studies met the inclusion criteria with 4122 included participants in total. Longitudinal studies demonstrated an improvement of LVMI after KT -0.44 g/m2 (-0.60 to -0.28). Blood pressure was identified as a predictor of LVMI change. A younger age at the time of KT and well-controlled anemia were also associated with regression of LVH. In studies longitudinally comparing patients on dialysis and renal transplant recipients, no difference was detected -0.09 g/m2 (-0.33 to 0.16). Meta-regression using changes of systolic blood pressure as a covariate showed an association between higher blood pressure and an increase in LVMI, regardless of the modality of renal replacement treatment. In conclusion, our results indicated a potential cardiovascular benefit, defined as the regression of LVH, after KT. This benefit was primarily attributed to improved blood pressure control rather than the transplantation itself.

STRICTER AMBULATORY BLOOD PRESSURE CONTROL IS POSSIBLE IN PATIENTS AFTER KIDNEY TRANSPLANTATION AND IS ASSOCIATED WITH REGRESSION OF LEFT VENTRICULAR HYPERTROPHY: POST HOC ANALYSIS

Objective: The recently published analysis of the 4C-T study demonstrated an association of stricter cumulative office blood pressure (BP) control with lower left ventricular mass (LVM) in children after kidney transplantation. The aim of our study was to investigate whether stricter control of ambulatory BP is also associated with improved LVMI and regression of left ventricular hypertrophy (LVH) in pediatric kidney transplant recipients. Design and method: A post-hoc analysis of nineteen patients (median age at baseline 9.7 years, range 3.3–15.1, median time after transplantation 4.3 years, range 1.0-13.1) from our previous ESCORT trial who had echocardiography performed at baseline (T0), 1 (T1), 2 (T2) and 3 (T3) years was performed. Cumulative 24-hour mean arterial pressure (MAP) Z-scores (CMAPz) were calculated according to 4C-T study (Sugianto et al. 2023). Left ventricular hypertrophy (LVH) was defined as LVMi&gt;40 g/m^2.7 in girls &gt;9 yrs of age and LVMi&gt;45 g/m^2.7 in boys &gt;9 yrs of age; in children &lt;=9 yrs the LVH was defined as LVMi &gt;95th percentile (Khoury et al 2009). Results: The median CMAPz decreased from a median +0.27 (IQR=-0.09 to +0.38) in the 1st year down to -0.06 (IQR=-0.26 to +0.32) in the 2nd year (p=0.02) and to +0.05 (IQR=-0.32 to 0.27) in the 3rd year (p=0.04) of follow-up. The prevalence (number) of children with LVH was 26% (5/19) at T0, 16% (3/19) at T1, 23% (3/13) at T2 and 0% (0/11) at T3 (trend in proportions p=0.06). All 5 children with elevated LVMi&gt;0.9 at T0 decreased / normalized their LVMi at T3 (p=0.07), on contrary children without LVH at baseline did not significantly change their LVMi during follow-up. Conclusions: This first prospective interventional study demonstrated an association between stricter cumulative ambulatory MAP and regression of LVH in patients after kidney transplantation. Our data suggest that aiming stricter ambulatory BP can improve the often unfavourable cardiac phenotype in these patients. However, randomized control trial is required to confirm our findings.

Features of The Dynamics of Profibrotic Markers and Regression of Left Ventricular Hypertrophy After Renal Denervation in Patients With Resistant Hypertension and Stenosing Atherosclerosis of the Coronary Arteries.

To compare the changes in serum concentrations of matrix metalloproteinases (MMPs) and their tissue inhibitor (TIMP) to the dynamics of blood pressure (BP) and parameters of left ventricular hypertrophy (LVH) 6 months after renal denervation (RD) in patients with resistant arterial hypertension (RAH) and complicated coronary atherosclerosis. In 22 RAH patients with complicated coronary atherosclerosis (revascularization and/or history of myocardial infarction (MI)), 24-hour BP monitoring, echocardiography, and measurement of blood MMPs and TIMP were performed at baseline and six months after RD. The comparison group consisted of 48 RAH patients without a history of coronary revascularization or MI. In 6 months after RD, BP was decreased comparably in both groups. In the group of complicated atherosclerosis, there were no significant changes in profibrotic markers or LVH parameters. Thus, at baseline and after 6 months, the values of the studied indicators were the following: left ventricular myocardial mass (LVMM) 233.1±48.1 and 243.0±52.0 g, LVMM index 60.6±14.5 and 62.8±10 .9 g/m2.7, proMMP-1 4.9 [2.1; 7.7] and 3.6 [2.0; 9.4] ng/ml, MMP-2 290.4 [233.1; 352.5] and 352.2 [277.4; 402.9] ng/ml, MMP-9 220.6 [126.9; 476.7] and 263.5 [82.9; 726.2] ng/ml, TIMP-1 395.7 [124.7; 591.4] and 424.2 [118.2; 572.0] ng/ml, respectively. In the comparison group, on the contrary, there was a significant decrease in LVMM from 273.6±83.3 g to 254.1±70.4 g, LVMM index from 67.1±12.3 to 64.0±14.4 g/m2.7, proMMP-1 from 7.2 [3.6; 11.7] to 5.9 [3.5; 10.9] ng/ml, MMP-2 from 328.9 [257.1; 378.1] to 272.8 [230.2; 343.2] ng/ml, MMP-9 from 277.9 [137.0; 524.0] to 85.5 [34.2; 225.9] ng/ml, and the MMP-9/TIMP-1 ratio from 0.80 [0.31; 1.30] to 0.24 [0.07; 0.76]. The BP dynamics in this group was inversely correlated with MMP-2 at 6 months (r=-0.38), and the MMP-9/TIMP-1 ratio was correlated with LVMM and the LVMM index at baseline (r=0.39 and r=0.39) and at 6 months (r=0.37 and r=0.32). The change in TIMP-1 from 543.9 [277.5; 674.1] to 469.8 [289.7; 643.6] ng/ml was not significant (p=0.060). In RAH patients with complicated coronary atherosclerosis, the dynamics of profibrotic biomarkers and LVH parameters after RD was absent despite the pronounced antihypertensive effect, probably due to the low reversibility of cardiovascular remodeling processes or more complex regulatory mechanisms of the MMP system.

The effect of intensive blood pressure lowering on left ventricular hypertrophy in patients with hypertension: a systematic review and meta-analysis of randomized controlled trials

Background We conducted a comprehensive systematic review to examine the efficacy of intensive blood pressure lowering on the risk of left ventricular hypertrophy (LVH). Methods We searched PubMed, Scopus, Web of Science, Cochrane Central, and EMBASE for all relevant randomized controlled trials. The primary outcome was the incidence of left ventricular hypertrophy. We used the risk ratio (RR) and hazard ratio (HR) with a 95% confidence interval as our effect sizes. Results Four studies, comprising 20,747 patients, were included. Intensive blood pressure lowering was linked with a diminished LVH incidence (RR: 0.66, 95% CI [0.56–0.77]). We also found that intensive blood pressure lowering increased the risk of LVH regression in patients with baseline LVH (RR: 1.21, 95% CI [1.11–1.32]). Finally, intensive blood pressure lowering was linked with a reduced risk of cardiovascular disease (HR: 0.71, 95% CI [0.60–0.85]). No significant heterogeneity was seen in either outcome. Conclusion Our study suggests that intensive blood pressure lowering effectively reduces the risk of LVH and cardiovascular disease. An interactive version of our analysis can be accessed here: https://databoard.shinyapps.io/lvh_hypertophy/

Regression of left ventricular hypertrophy in patients with resistant hypertension after renal denervation: the role of hemodynamic and antifibrotic effects

Regression of left ventricular hypertrophy in patients with resistant hypertension after renal denervation: the role of hemodynamic and antifibrotic effects

Perceval sutureless bioprosthesis versus Perimount sutured bioprosthesis for aortic valve replacement in patients with aortic stenosis: a retrospective, propensity-matched study

BackgroundRapid-deployment aortic valve replacement (RDAVR) is an alternative to conventional AVR (cAVR) for aortic stenosis. Benefits include a reduction in operative times, facilitation of minimal access surgery and superior haemodynamics compared to conventional valves. However, further evidence is required to inform guidelines, preferably in the form of propensity-matched studies that include mid-term follow-up data.MethodsThis was a single-centre, retrospective, propensity-matched cohort study comparing the Perceval and conventional Perimount Magna Ease valve for short- and mid-term clinical parameters and size-matched mid-term echocardiographic parameters (n = 102 in both groups) from 2014 to 2020. Data were extracted from a nationally managed dataset.ResultsThere were no demographic differences between the matched groups. The Perceval group had shorter cross-clamp time (Perceval 62 [49–81] minutes; Perimount 79 [63–102] minutes, P < 0.001), shorter bypass time (Perceval 89 [74–114] minutes; Perimount 104 [84–137] minutes, P < 0.001), and more frequent minimally-invasive approaches (Perceval 28%; Perimount 5%, P < 0.001). Size-matched haemodynamics showed initially higher gradients in the Perceval group, but haemodynamics equalised at 12 + months. The Perceval group had a more favourable % change in the left ventricular posterior wall dimension at 2 + years (Perceval − 4.8 ± 18; Perimount 17 ± 2).ConclusionsThe Perceval facilitated shorter operations, which may benefit intermediate-high-risk, elderly patients with comorbidities requiring concomitant procedures. It also facilitated minimally invasive surgery. Size-matched haemodynamic performance was similar at mid-term follow-up, with the Perceval possibly better facilitating regression of left ventricular hypertrophy.

Age-dependent implications of left ventricular hypertrophy regression in patients with hypertension.

Left ventricular hypertrophy (LVH) is a significant risk factor for cardiovascular mortality and morbidity in patients with hypertension. However, the effect of age on LVH regression or persistence and its differential prognostic value remain unclear. Therefore, we investigated the clinical implications of LVH regression in 1847 patients with hypertension and echocardiography data (at baseline and during antihypertensive treatment at an interval of 6-18 months) according to age. LVH was defined as a left ventricular mass index (LVMI) > 115 g/m2 and >95 g/m2 in men and women, respectively. LVH prevalence at baseline was not different according to age (age < 65 years: 42.6%; age ≥65 years: 45.7%; p = 0.187), but LVH regression was more frequently observed in the younger group (36.4% vs. 27.5%; p = 0.008). Spline curves and multiple linear regression analysis showed a significant relationship between reductions in systolic blood pressure and LVMI in the younger group (β = 0.425; p < 0.001), but not the elderly group (β = 0.044; p = 0.308). LVH regression was associated with a lower risk of the study outcome (composite of cardiovascular death and hospitalization for heart failure) regardless of age. In conclusion, the association between the reduction in blood pressure and LVH regression was prominent in patients with age < 65 years, but not in those with age ≥65 years. However, an association between LVH regression and lower risk of cardiovascular death and hospitalization for heart failure was observed regardless of patient age, suggesting the prognostic value of the LVH regression not only in the younger patients but also in elderly patients.

Influence of Antihypertensive Drugs on Left Ventricular Hypertrophy Regression in Hypertensive Patients

Background: Hypertension and its effect on heart in the form of left ventricular hypertrophy are the important predictors of heart failure. Hypertension treatment and left ventricular hypertrophy regression is crucial in the prevention of cardiovascular disease. However, the impact of antihypertensive treatment on left ventricular hypertrophy is less studied and which particular class of antihypertensive medicine is more effective is largely unexplored in our population. We designed this study to explore this issue in subjects taking treatment by evaluation initial and after six months echocardiography findings. Methods: One hundred fifty subjects aged 25-75 years, taking antihypertensive medicine were enrolled in the study. Along with basic demographic and epidemiological data, initial and after 6 months echocardiographic findings were analyzed for the presence of LV hypertrophy regression. Choice of medicine and necessary changes for the achievement of blood pressure targets were done on treating physician’s discretion.Results: Out of 150 subjects, data for 130 subjects were available for final analysis. Mean age was 54.4 years with standard deviation of 12.3 years. Apart from age, smoking, overweight and obesity, dyslipidemia, and diabetes were the important risk factors with a prevalence of 28%, 26%, 22% and 20% respectively. Although the decrease in rates of LV hypertrophy over the duration of 6 months were not significant in overall and in subjects treated with various antihypertensive medicines, the reductions in LV mass index (108.76+/-11.3 to 98.46+/-11.23) in overall and in different antihypertensives were significant (p&lt;0.001). The decrease in LV mass index was statistically significant in subjects taking angiotensin converting enzyme inhibitors or angiotensin receptor blockers when compared to subjects taking calcium channel blockers (p&lt;0.05). This decrease in LV mass index was not significant when compared between CCBs and mixed drugs.Conclusion: There was regression in LV hypertrophy among subjects taking antihypertensive treatment. It was more obvious in subjects taking angiotensin converting enzyme inhibitors/angiotensin receptor blockers when compared with subjects taking calcium channel blockers or both.

Abstract 17679: Prognostic Implications of Left Ventricular Hypertrophy Regression Based on 4-Tiered Classification of Left Ventricular Hypertrophy

Introduction: 4-tiered classification of left ventricular (LV) hypertrophy (LVH), which accounts for increased LV wall thickness and LV volume, has been suggested to identify subgroups of patients at differential risk. This study was conducted to evaluate prognostic impact of 4-tiered classification of LVH in newly diagnosed hypertension patients with LVH. Methods: We retrospectively enrolled patients who had LVH on echocardiography at the time of diagnosis and had serial echocardiography taken within a 6-18-month interval with anti-hypertensive medication. Patients were divided into 5 groups based on 4-tiered LVH classification (eccentric LVH with dilatation or without dilatation, concentric with dilatation or without dilatation), and LVH regression group by the follow up echocardiography. The primary outcome was the composite of adverse cardiovascular (CV) outcomes, including CV death, hospitalization for heart failure, coronary revascularization, stroke, and aortic events. Results: Among the 837 patients in the five groups the concentric LVH group and dilated eccentric group demonstrated significantly higher incidence of CV outcomes. Compared with LVH regression group, those with dilated concentric (adjusted hazard ratio [adjHR]: 8.95; 95% confidence interval [CI]: 4.34 to 18.48), dilated eccentric (adjHR: 6.24; 95% CI: 2.96-13.18), non-dilated concentric (adjHR: 2.04; 95% CI: 1.26-3.32) LVH exhibited increased in CV risk according to multivariable cox-regression analysis. However, the non-dilated eccentric LVH group did not demonstrate a significant increase in CV risk (adjHR: 0.75; 95% CI: 0.24-2.35). Conclusions: In patients with hypertension, regression of LVH during anti-hypertensive treatment is associated with better CV outcomes. However, non-dilated eccentric group were not increase CV risk compared with regression group. The 4-tiered LVH classification can be helpful to stratifying CV risk in patients with hypertension.

Clinical efficacy of a fixed-dose combination of amlodipine/indapamide/perindopril in patients with hypertension and multiple risk factors

Aim. To evaluate the antihypertensive and organ protective efficacy of the triple fixed-dose combination of amlodipine/indapamide/perindopril in patients with hypertension (HTN) who did not achieve target blood pressure (BP) on previous antihypertensive therapy (AHT).Material and methods. The study included 47 patients with HTN and multiple risk factors who did not achieve target blood pressure during previous AHT. They were prescribed triple fixed-dose combination of amlodipine/indapamide/perindopril with preliminary prescription of amlodipine, indapamide and perindopril in the free-dose combination. At baseline and after 3 months of AHT, 24-hour ambulatory blood pressure monitoring (ABPM), echocardiography and arterial stiffness were analyzed.Results. Initially, in patients included in the study, the main ABPM parameters were increased, while non dipper and reduced dipper (66% of patients) patterns prevailed. The results of echocardiography indicated left ventricular (LV) hypertrophy (LVH) by left ventricular mass index (LVMI), left ventricular posterior wall thickness (LVPWT), interventricular septum (IVS) and its diastolic dysfunction by E/A, while an increase in CAVI and biological vascular age reflected an increase in arterial stiffness. After 3 months of AHT, significant (p£0,05) ABPM changes and a predominance of the dipper-type 24-hour BP pattern were recorded in more than half of the patients (53%). A decrease in LVMI, LVPWT and IVS by 7%, 12% and 8%, respectively (p£0,05), while an E/A increase by 12% reflected LVH regression and LV diastolic function improvement. A decrease in arterial stiffness was evidenced by a decrease (p£0,05) in CAVI by an average of 10% and biological vascular age by 4 years.Conclusion. Triple fixed-dose therapy of amlodipine/indapamide/perindopril after 3-month treatment made it possible to achieve target blood pressure in 78% of patients, improved ABPM parameters and ensured pronounced cardioand vasoprotective effects, reflected in LVH regression, improvement of LV diastolic function and reduction of arterial stiffness.

ТАКТИКА ЛЕЧЕНИЯ ТЯЖЕЛОЙ РЕФРАКТЕРНОЙ АРТЕРИАЛЬНОЙ ГИПЕРТЕНЗИИ У ПОДРОСТКА С ГИПОПЛАЗИЕЙ БРЮШНОЙ АОРТЫ И СТЕНОЗАМИ ПОЧЕЧНЫХ АРТЕРИЙ: КЛИНИЧЕСКОЕ НАБЛЮДЕНИЕ

Renovascular arterial hypertension (AH) is one of the most common and prognostically most serious secondary hypertensions in children, however, descriptions of renal artery stenosis as part of middle aortic syndrome are quite rarely described Worldwide, and the etiology of this syndrome remains unclear in more than half of all the cases. Treatment approaches include a combination of complex conservative and surgical endovascular techniques that require constant monitoring of effectiveness. A clinical case observation and treatment tactics for refractory hypertension in an adolescent patient with hypoplasia of the abdominal aorta, stenosis of both renal arteries, a progressive decline in the function and volume of the left kidney (a picture of shrinkage of the left kidney on scintigraphy, an increase in hyperazotemia) and left ventricular (LV) hypertrophy is presented. Due to the ineffectiveness of drug antihypertensive therapy, the patient subsequently underwent aortoaortic bypass surgery of the abdominal aorta with prosthetics and implantation of the left renal artery into the shunt, balloon vasodilation with the installation of stents in the lower pole artery of the left kidney and the right renal artery. Over time, there was an improvement in the velocity parameters of the vessels of both kidneys, a decrease in blood pressure to values close to normal and regression of LV hypertrophy. Conclusion: the treatment tactics for a patient with renovascular hypertension and hypoplasia of the abdominal aorta, including drug methods in combination with two-stage surgical correction - the application of an aortoaortic shunt and endovascular treatment - turned out to be the most effective in terms of controlled hypertension.

Understanding the Position of Beta-blockers in the Management of Hypertension among Patients with Different Clinical Comorbidities: An Expert Opinion of Cardiologists from India

Abstract Background: Elevated blood pressure (BP) increases the risk of cardiovascular mortality, underscoring the vital importance of effective management in individuals with hypertension (HTN) and cardiovascular disease. However, lack of clear guidance on the utilization of the new beta-blockers has caused hesitation among doctors in using them effectively. The objective of this expert opinion was to understand the role and current position of beta-blockers in the management of patients with HTN and different clinical comorbidities. Methods: A collective of 828 cardiologists throughout India were invited to participate in an online survey and virtual meetings. Their clinical insights were gathered on approaches in managing these patients and their understanding of the role of beta-blockers. Results: The panel of experts recommended that in patients with HTN and angina, the BP target should be 130/80 mmHg (40.70%), and the use of a combination of telmisartan and cardio-selective beta-blockers should be used to lower BP (63.29%). A combination of telmisartan and a beta-1 blocker was recommended for effective BP control and structural regression of left ventricular hypertrophy (52.78%). For intensive BP control, combination therapy of telmisartan and beta-blockers should be used in patients with HTN and atrial fibrillation (59.18%). The panel of experts opined (60.02%) that different BP targets should be considered for different stroke subtypes. Telmisartan (44.44%) and selective beta-1 blockers (29.35%) are recommended to manage BP variability in patients with HTN and recurrent stroke. Conclusion: In patients with HTN and cardiovascular disease, individualized decision-making is necessary for beta-blocker use in HTN management. Selective beta-blockers should be considered first-line therapy or combined with telmisartan when indicated.