Regression Of Left Ventricular Hypertrophy Research Articles

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

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

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>40 g/m^2.7 in girls >9 yrs of age and LVMi>45 g/m^2.7 in boys >9 yrs of age; in children <=9 yrs the LVH was defined as LVMi >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>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/

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.

Stricter Blood Pressure Control Is Associated With Lower Left Ventricular Mass in Children After Kidney Transplantation: A Longitudinal Analysis of the 4C-T Study.

We assessed the effect of blood pressure (BP) control on left ventricular mass index (LVMI) and left ventricular hypertrophy (LVH). Ninety-six patients (64 males) ≥9 months post-kidney transplantation from the 4C-T (Cardiovascular Comorbidity in Children with Chronic Kidney Disease and Transplantation) study were analyzed longitudinally (mean follow-up, 2.6±1.3 years). Cumulative systolic blood pressure (SBP)/diastolic BP exposure was calculated as a time-averaged area under the curve and categorized: ≤50th, 50th to ≤75th, 75th to ≤90th, and >90th percentile (pct). We performed adjusted linear and logistic mixed models for LVMI and LVH, respectively. At baseline, LVMI was 49.7±12.7g/m2.16 with 64% (n=61) kidney transplantation recipients displaying LVH. Compared with patients with cumulative SBP exposure >90th pct, patients with cumulative SBP of 50th to ≤75th showed a significant LVMI reduction of -5.24g/m2.16 (P=0.007). A similar tendency was seen for cumulative SBP≤50th (β=-3.70 g/m2.16; P=0.067), but patients with cumulative SBP of 75th to ≤90th pct showed no reduction. A post hoc analysis in patients with cumulative SBP≤75th revealed that median SBP exposure was at 57.5th pct. For cumulative diastolic BP, a significant LVMI reduction was seen in all 3 categories ≤90th pct compared with patients >90th pct. Patients with cumulative SBP of ≤50th or 50th to ≤75th pct showed 79% or 83% lower odds of developing LVH, respectively. Patients with cumulative diastolic BP ≤50th showed a tendency of 82% lower odds for LVH (95% CI, 0.03-1.07). Stricter BP control led to regression of LVMI and LVH. Our data suggest a BP target below the 60th pct, which needs to be substantiated in a randomized controlled trial.

Intensive Blood Pressure Lowering Improves Left Ventricular Hypertrophy in Older Patients with Hypertension: The STEP Trial.

Intensive systolic blood pressure (SBP) lowering has been increasingly used; however, its effect on cardiac remodeling remains not fully understood. This secondary analysis of the Strategy of Blood Pressure Intervention in the Elderly Hypertensive Patients trial aims to determine the changes in left ventricular hypertrophy (LVH) that occur in the context of intensive SBP lowering. A total of 7141 older patients with hypertension were randomly assigned to intensive treatment (SBP target, 110-130 mm Hg) or standard treatment (130 to 150 mm Hg). LVH was defined according to the Peguero-Lo Presti criteria on a standard 12-lead ECG. At baseline, the prevalence of LVH (16.6% versus 16.5%) and the mean Peguero-Lo Presti value (1811 versus 1808 μV) were comparable between the treatment groups. During a median follow-up of 3.24 years, intensive SBP lowering was associated with a significantly lower risk of new LVH occurrence (hazard ratio, 0.76 [95% CI, 0.66-0.89]; P=0.001) and slower progression of the mean Peguero-Lo Presti index value by -23.47 μV/y (95% CI, -34.93 to -12.01; P=0.000). However, the rates of regression of baseline LVH did not differ significantly. Of note, the beneficial effect of intensive SBP lowering in terms of cardiovascular events (hazard ratio, 0.75 [95% CI, 0.59-0.97]) was not markedly attenuated after adjusting for LVH as a time-varying covariate (hazard ratio, 0.76 [95% CI, 0.59-0.97]). Intensive SBP lowering protects against LVH development in older hypertensive patients, however, this favorable effect could not explain most of the reduction in cardiovascular events associated with intensive SBP lowering.

Remodeling and regression of left ventricular hypertrophy in patients with arterial hypertension (literature review)

The article contains literature information concerning the pathogenesis of hypertrophy and remodeling of the left ventricle (LV) of the heart in patients with arterial hypertension (AH), regression of left ventricular hypertrophy (LVH) under the influence of anti-hypertensive treatment. Remodeling of the heart is its structural geometrical changes occurring under the influence of pathological factors: increasing the number of sarcomeres, length and thickness of cardiomyocytes, increasing or decreasing the wall thickness, and enlargement of the ventricular cavity. The renin-angiotensin-aldosterone system (RAAS) plays a central role in the pathogenesis of hypertrophy and remodeling of the myocardium with AH and heart failure. LVH is one of the most significant predictors of cardiovascular events, including myocardial infarction, stroke, life-threatening ventricular arrhythmias, mortality from cardiovascular diseases, and general mortality. Treatment with angiotensin-converting enzyme inhibitors (ACEI), dihydropyridine calcium channel blockers (CCB), АТ ІІ receptor blockers (ARB) promotes reverse development of LVH and regression of the processes of the heart muscle remodeling. ACEIs are found to be more effective in achieving regression of LVH in patients with AH compared to CCB and beta-blockers. An early beginning of anti-hypertensive therapy and attention to metabolic aspects are critically important to avoid irreversible LVH. The ESH/ESC recommendations (2018) indicate that ACEI and ARB are effective for the prevention or regression of LVH in patients with AH, and beta-blockers are less effective than RAAS blockers and CCB.Objective: to systematize literature data about the pathogenesis of the left ventricle remodeling in patients with arterial hypertension, and the role of anti-hypertensive therapy in the regression of left ventricular hypertrophy. Conclusion. Today, the concept about the role of the renin-angiotensin-aldosterone system in the pathogenesis of hypertrophy and remodeling of the left ventricle in patients with arterial hypertension has been formulated. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers are the most effective in the prevention or regression of left ventricular hypertrophy in patients with arterial hypertension.

Hypertensive heart: from left ventricular hypertrophy to chronic heart failure

Objective. The purpose of this review is to highlight the pathophysiological mechanisms of the sequential formation of left ventricular hypertrophy (LVH), left ventricular dysfunction and chronic heart failure (CHF) in patients with hypertension (HTN), diagnostic and therapeutical issues of CHF with both reduced and preserved ejection fraction (EF). HTN is the main risk factor for cardiovascular diseases and is accompanied by damage of target organs, among which LVH is of particular importance. On the one hand, development of LVH is the consequence of increased load on the heart muscle and neurohumoral stimuli, and on the other hand, it is an independent risk factor for myocardial infarction, stroke, cardiac arrhythmias and CHF. HTN precedes newly developed heart failure in 91 % of patients with a predominance of CHF with a preserved EF according to the Framingham Heart Study. To date, different drugs can improve the prognosis of patients with HTN, CHF with reduced EF and to induce LVH regression. However, the issues of effective treatment of patients with CHF with preserved EF are still insufficiently studied.

Physical Activity and Cardiac Morphologic Adaptations

Chronic and intense exercise programs lead to cardiac adaptations, followed by increased left ventricular wall thickness and cavity diameter, at times meeting the criteria for left ventricular hypertrophy (LVH), commonly referred to as “athlete’s heart”. Recent studies have also reported that extremely vigorous exercise practices have been associated with heightened left ventricular trabeculation extent, fulfilling noncompaction cardiomyopathy criteria, as part of exercise-induced structural adaptation. These changes are specific to the exercise type, intensity, duration, and volume and workload demands imposed on the myocardium. They are considered physiologic adaptations not associated with a negative prognosis. Conversely, hypertrophic cardiac adaptations resulting from chronic elevations in blood pressure (BP) or chronic volume overload due to valvular regurgitation, lead to compromised cardiac function, increased cardiovascular events, and even death. In younger athletes, hypertrophic cardiomyopathy (HCM) is the usual cause of non-traumatic, exercise-triggered sudden cardiac death. Thus, an extended cardiac examination should be performed, to differentiate between HCM and non-pathological exercise-related LVH or athlete’s heart. The exercise-related cardiac structural and functional adaptations are normal physiologic responses designed to accommodate the increased workload imposed by exercise. Thus, we propose that such adaptations are defined as “eutrophic” hypertrophy and that LVH is reserved for pathologic cardiac adaptations. Systolic BP during daily activities may be the strongest predictor of cardiac adaptations. The metabolic demand of most daily activities is approximately 3–5 metabolic equivalents (METs) (1 MET = 3.5 mL of O2 kg of body weight per minute). This is similar to the metabolic demand of treadmill exercise at the first stage of the Bruce protocol. Some evidence supports that an exercise systolic BP response ≥150 mmHg at the end of that stage is a strong predictor of left ventricular hypertrophy, as this BP reflects the hemodynamic burden of most daily physical tasks. Aerobic training of moderate intensity lowers resting and exercise systolic BP at absolute workloads, leading to a lower hemodynamic burden during daily activities, and ultimately reducing the stimulus for LVH. This mechanism explains the significant LVH regression addressed by aerobic exercise intervention clinical studies.

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Effect of sodium-glucose cotransporter protein-2 inhibitors on left ventricular hypertrophy in patients with type 2 diabetes: A systematic review and meta-analysis.

This systematic review and meta-analysis was performed to compare the effect of sodium-glucose cotransporter protein-2 inhibitors (SGLT-2i) and placebo on left ventricular hypertrophy (LVH) in patients with type 2 diabetes. Randomized controlled trials (RCTs) comparing the LVH parameters of SGLT-2i to placebo in patients with type 2 diabetes were included. Our primary outcomes were the changes in left ventricular mass (LVM) and left ventricular mass index (LVMI) from baseline to the study endpoint. Secondary outcomes were the changes in left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular ejection fraction (LVEF), and the ratio of early mitral inflow velocity to atrial inflow velocity (E/A). Summary odds ratios were estimated using a fixed-effect or random-effect model. A total of 11 articles were included. Data were extracted from 11 original studies matching our inclusion criteria. In our meta-analysis, there were significant improvement in LVM (SMD -0.23, 95% CI -0.44 to -0.02, I 2 = 22.6%, p = 0.034), LVMI (SMD -0.25, 95% CI -0.38 to -0.12, I 2 = 0.0%, p = 0.000), LVEDV (SMD -0.19, 95% CI -0.36 to -0.01, I 2 = 62.3%, p = 0.035), and LVESV (SMD -0.21, 95% CI -0.39 to -0.04, I 2 = 32.9%, p = 0.017) in the SGLT-2i group compared with the placebo group. Furthermore, no significant differences were found in LVEF (SMD 0.13, 95% CI 0.00 to 0.26, I 2 = 0.0%, p = 0.050) and E/A (SMD -0.01, 95% CI -0.22 to 0.20, I 2 = 0%, p = 0.908) between the two groups. This meta-analysis confirmed the beneficial effects of SGLT-2i on reversal of left ventricular remodeling. The LVH regression was more pronounced in studies of type 2 diabetes patients receiving SGLT-2i than placebo.

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.

PS-BPC05-10: DIASTOLIC DYSFUNCTION, HYPERTROPHY AND HYPERTENSION VENTRICULAR-ARTERIAL UNCOUPLING TREATMENT

Objective: the aim of this study was to evaluate the effects of hypertension ventricular-arterial uncoupling treatment on left ventricular hypertrophy and diastolic dysfunction regression. Design and method: observational prospective study, consecutive hypertension patients. Left ventricle mass index measured by Devereux 2D echocardiography method and diastolic function by conventional and tissue Doppler following the Guidelines from Echocardiography from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Left ventricular end systolic elastance (Ees) was measured by Guarracino calculator, the effective arterial elastance (Ea) and ventricular-arterial coupling (VAC) measured by Sunagawa et al single beat method adapted by Chen et al in human ventricles. The sample was analyzed in quartiles (Q) according to VAC (Q1 worst VAC to Q4 best VAC). Follow-up 2 years. Results: 288 patients, mean age 56.3 + 12.5 years and 168 patients (58.3%) males. VAC increased from 0.303 + 0.07 to 0.54 + 0.25 (p &lt; 0.005) in Q1 mainly due to a reduction in Ees from 5.25 + 2.3 to 3.68 + 0.25 mm Hg/ml (p &lt; 0.01) while Ea increased from 1.5 + 0.53 to 1.64 + 0.56 mm Hg/ml (p = NS); on the other side VAC was reduced from 0.87 + 0.15 to 0.68 + 0.26 (p &lt; 0.05) in Q 4 with an increase in Ees from 2.28 + 0.6 to 2.67 + 1.07 mm Hg/ml (p = NS) and a reduction of Ea from 1.94 + 0.41 to 1.69 + 0.67 mm Hg/ml (p = NS) (Figure). The frequency of LVH was reduced from 31.9% to 10.8% in Q1 (p &lt; 0.025) while moved from 14.7 to 17.9% (p = NS) in Q2, 22.9% to 13.9% (p = NS) in Q3 and 11.3 % to 23.7% (p = NS) in Q4. The frequency of normal diastolic function increased from 75% to 94.6% (p &lt; 0.01) in Q1, from 78.7% to 100% in Q2 (p &lt; 0.005), from 87.1% to 100% (p &lt; 0.025) in Q3 and from 88.7% to 100% (0,025) in Q4. Conclusions: 1) patients with the worst ventricular-arterial uncoupling (Q1) are the most VAC benefited from hypertension treatment; 2) regression of left ventricular hypertrophy was observed only in the group of patients with the worst ventricular-arterial uncoupling (Q1); 3) improvement in diastolic function was demonstrated in all Q of ventricular-arterial coupling. This study shows that achieving an optimal mechanical efficiency measured as ventricular-arterial coupling by hypertension treatment is essential for left ventricular hypertrophy and diastolic dysfunction regression.

PS-C22-11: EFFICACY OF TRI-COMBINATION ACEI PLUS AMLODIPINE AND INDAPAMIDE VERSUS ARB AMLODIPINE AND THIAZIDE IN DIABETES WITH HYPERTENSION PATIENTS

Introduction: Global Burden of Disease (GBD) Study has estimated that Hypertension leads to 1.6 million deaths and 118 million disability-adjusted life years in INDIA1 40% of diagnosed Hypertension patients are treated1. The poor control rates among treated Hypertension patients are around 40% in Indian3. Plausible reasons for poor Hypertension control rates in INDIA. This is mainly because most treated patients only receive monotherapy despite guidelines recognizing that most patients require combination therapy 2 and 3. ISH 2020 guidelines support initiating with A+C SPC in Hypertension patients For patients uncontrolled on two drugs, recommended approaches are to increase doses as step 2 and add a third drug as step 3. 4 Every third Hypertension patient needs three or more drugs to reach the BP Perindopril + Amlodipine + Indapamide offers better blood pressure control. In studies such as the ADVANCE CCB study5. Active treatment with Perindopril + Indapamide + CCB reduced the relative risk of death by -28%. -The recent Mazza et al. study provides evidence for Cardiovascular risk reduction with Perindopril + Indapamide + Amlodipine combination. Left ventricular hypertrophy (LVH) regression was greater in the SPC group of Perindopril+ Indapamide+ Amlodipine vs. the FCT group (43.5% vs. 30.4%, P &lt; 0.05).6 In our Indian study from 2019 to 2022, 110 patients with Diabetes with Moderate to severe Hypertension on Perindopril with Amlodipine and Indapamide were able to achieve a blood pressure target of &lt; 130/80 mmHg with Minimum 6 months to a maximum of 2 years on this combination therapy, whereas Target of &lt; 130/80 mmHg with ARB with Amlodipine and thiazide were achieved in 54% only, which was significant (Figure 1). Indian patients are well Tolerated with triple single Pill, and adherence to therapy was Good.

Prognostic implication of left ventricular hypertrophy regression after antihypertensive therapy in patients with hypertension.

Left ventricular (LV) hypertrophy (LVH) in patients with hypertension is a significant risk factor for cardiovascular mortality and morbidity. However, the prognostic implication of LVH regression after antihypertensive therapy has not been clearly investigated. Patients who underwent echocardiography at the time of the diagnosis of hypertension and repeated echocardiography at an interval of 6-18 months were retrospectively identified. LVH was defined as LV mass index (LVMI) >115 g/m2 (men) and >95 g/m2 (women). LVH regression was defined as LVH at initial echocardiography with normal geometry or concentric LV remodeling at follow-up echocardiography. Cardiovascular mortality, hospitalization for heart failure (HHF), coronary revascularization, stroke, and aortic events were analyzed according to changes in LVMI and geometry. Of 1,872 patients, 44.7% (n = 837) had LVH at the time of diagnosis; among these, 30.7% showed LVH regression. The reduction in LVMI was associated with the reduction in BP, especially in those with LVH at baseline. During follow up (median, 50.4 months; interquartile range, 24.9-103.2 months), 68 patients died of cardiovascular causes, 127 had HHF, and 162 had vascular events (coronary revascularization, stroke, and aortic events). Persistent or newly developed LVH during antihypertensive therapy was a significant predictor of cardiovascular mortality and events, especially HHF. On multivariable analysis, women, diabetes, atrial fibrillation, coronary artery disease, larger LVMI and end-diastolic dimension, and less reduction in systolic BP were associated with persistent or newly developed LVH. LVH regression in patients with hypertension is associated with a reduction in cardiovascular events and can be used as a prognostic marker.