Regression Of Hypertrophy Research Articles

P6482Stress echocardiography in the assessment of long-term outcomes results of aortic valve replacement with mechanical prostheses of small size

Abstract Relevance Evaluation of the function of aortic mechanical prostheses of small size in the long-term period is an topical problem, due to the fact that a narrow fibrous ring occurs in 20–35% of cases of patients with aortic stenosis. Objective To study clinical and hemodynamic parameters of small size aortic prostheses using stress echocardiography in the long-term period after valve replacement Materials and methods The study included 89 patients (54 women, 35 men) who underwent aortic valve replacement with a landing diameter of 21 mm or less. The average was 48,1±11,3 years. BSA of 1,8 m2 (1.3 to 2.2). The following models of prostheses were used: On-X, ATS-AP, Carbomedics, St. Jude Medical. All patients after surgical correction in the long-term period (an average of 5,9±3,3 years from 1 to 11 years) underwent a comprehensive clinical and instrumental examination, including an ECG and stress - echocardiography with bicycle exercise. Results In the long-term period after aortic valve replacement of mechanical prostheses of small size, the ECG showed regression of hypertrophy and overload of the left ventricle. According to stress-echocardiography, there was a significant increase in load tolerance. At the peak of the load, the following were recorded: improvement of the pumping function and cardiac performance (stroke volume, cardiac output, cardiac index), improvement of myocardial work index (Tei - index), increase in speed parameters on the aortic valve prosthesis no more than 30% of the initial values. In repose, the maximum and mean pressure gradients were 26.3±9 mm Hg and 14.3±5.4 mm Hg, effective orifice area (EOA) 1,7±0,3 cm2, index effective orifice area (EOAi) 0,93±0,2 cm2/m2. When the submaximal load levels were reached, the maximum and mean pressure gradients were 33,5±6,0 mm Hg and 17,1±4,0 mm Hg, EOA - 1,5±0,4 cm2, EOAi - 0,79±0,6 cm2/m2. Conclusions The findings suggest that modern models of aortic prostheses with an increased effective orifice area provide good clinical results in the long term. Stress echocardiography is a necessary and highly informative method for assessing the parameters of mechanical aortic prostheses and heart function.

Regression of Left Ventricular Mass in Athletes Undergoing Complete Detraining Is Mediated by Decrease in Intracellular but Not Extracellular Compartments.

Background:Athletic cardiac remodeling can occasionally be difficult to differentiate from pathological hypertrophy. Detraining is a commonly used diagnostic test to identify physiological hypertrophy, which can be diagnosed if hypertrophy regresses. We aimed to establish whether athletic cardiac remodeling assessed by cardiovascular magnetic resonance is mediated by changes in intracellular or extracellular compartments and whether this occurs by 1 or 3 months of detraining.Methods:Twenty-eight athletes about to embark on a period of forced detraining due to incidental limb bone fracture underwent clinical assessment, ECG, and contrast-enhanced cardiovascular magnetic resonance within a week of their injury and then 1 month and 3 months later.Results:After 1 month of detraining, there was reduction in left ventricular (LV) mass (130±28 to 121±25 g; P<0.0001), increase in native T1 (1225±30 to 1239±30 ms; P=0.02), and extracellular volume fraction (24.5±2.3% to 26.0±2.6%; P=0.0007) with no further changes by 3 months. The decrease in LV mass was mediated by a decrease in intracellular compartment volume (94±22 to 85±19 mL; P<0.0001) with no significant change in the extracellular compartment volume. High LV mass index, low native T1, and low extracellular volume fraction at baseline were all predictive of regression in LV mass in the first month.Conclusions:Regression of athletic LV hypertrophy can be detected after just 1 month of complete detraining and is mediated by a decrease in the intracellular myocardial compartment with no change in the extracellular compartment. Further studies are needed in athletes with overt and pathological hypertrophy to establish whether native T1 and extracellular volume fraction may complement electrocardiography, echocardiography, cardiopulmonary exercise testing, and genetic testing in predicting the outcome of detraining.

DETERMINANTS OF LEFT VENTRICULAR HYPERTROPHY REGRESSION IN HYPERTENSIVE PATIENTS AFTER 5 YEARS FOLLOW-UP

Objective: Regression of left ventricular hypertrophy (LVH) is independently associated with improved cardiovascular outcome. In this setting, we examined the main factors influencing LVH regression and the prevention of LVH development in hypertensive subjects over time. Design and method: 2380 hypertensive subjects, (mean age 58 ± 12 years), 50.3% males, with baseline office blood pressure (BP) 143/89mmHg were followed for a mean period of 5.3 ± 3.3 years. At baseline and last follow-up visit all patients underwent office BP, laboratory and glomerular filtration rate (GFR) evaluation, echocardiographical determination of left ventricular mass index (LVMI) and albumin/creatinine ratio (ACR) assessment. Main outcome variable was LVH Regression/prevention (LVH Regr/prev), defined as: LVH at baseline visit with normal LVMI values at last visit or absence of LVH at baseline and last visit. BP control was considered optimal when the mean of office BP measurements during follow-up was <140/90mmHg. Results: 44.7% of study population presented LVH Regr/prev during follow-up period. Cox-regression analysis, after adjustment for clinical, biochemical and treatment variables, revealed that low levels of baseline LVMI (HR = 0.98, 95% CI 0.97–0.99, p < 0.0001), low baseline BMI levels (HR = 0.96, 95% CI 0.93–0.99, p = 0.008), optimal BP control during follow-up (HR = 1.26, 95% CI 1.01–1.56, p = 0.03), low baseline ACR levels (HR = 0.77, 95% CI 0.60–0.99, p = 0.04) and baseline GFR (HR = 1.03, 95% CI 1.02–1.04, p = 0.003) were independent predictors of LVH Regr/prev during follow-up. Conclusions: In conclusion, beyond optimal BP control, metabolic factors like BMI and the presence of other organ damages are significant predictors of LVH regression. Moreover, during the baseline evaluation of hypertensive subjects, renal dysfunction or albuminuria detection can offer information about the risk of structural cardiac alterations, LVH regression or development in the future.

Global longitudinal strain in prosthesis-patient mismatch: relation to left ventricular mass regression and outcomes.

Aortic prosthesis-patient mismatch (PPM) increases left ventricular (LV) afterload and prevents LV mass regression (LVMR) after surgery. This study was designed to investigate the association between the baseline global longitudinal strain (GLS) and the postoperative LVMR, and its relation to adverse outcomes. A total of 316 patients with aortic stenosis undergoing isolated mechanical prosthesis implantation were screened, and data from 91 patients with aortic PPM and 165 non-PPM patients were retrospectively collected. All 256 patients underwent measurement of GLS by two-dimensional speckle-tracking echocardiography preoperatively, and were followed up for postoperative changes of LV mass index (LVMi) and other clinical outcomes. During the follow-up, LVMi in PPM patients decreased significantly from 139.6 ± 20.8 to 119.6 ± 26.5 g/m (P < 0.001). These patients were divided into two groups according to the median value of the reduction rate of LVMi at final follow-up, and preoperative GLS markedly decreased in PPM patients with insignificant reduction in LVMi. Multivariate analysis identified preoperative GLS (odds ratio 3.45, 95% confidence interval 1.27-11.05, P = 0.002) and preoperative LVMi (odds ratio 2.87, 95% confidence interval 1.21-8.13, P = 0.012) as independently associated with an insignificant LVMR. Moreover, PPM patients with limited reduction in LVMi were at an increased risk of cardiac death and major adverse valve-related events. In patients with aortic PPM early after surgery, reduced preoperative GLS could be a novel sensitive risk factor for a limited regression of LV hypertrophy, and this is associated with an increased risk of adverse events in PPM patients.

FIXE FULL-DOSE COMBINATION PERINDOPRIL/INDAPAMIDE/AMLODIPINE IN SEVERE DIABETIC HYPERTENSIVES

Objective: Hypertension is worldwide spread and represents the leading cause of death. Diabetes rich epidemic levels in global population. Hypertension and diabetes are frequently present in the same patient and represents independent cardiovascular risk factors. Both hypertension and diabetes are associated with left ventricular hypertrophy and diastolic dysfunction. New ESC/ESH 2018 guidelines suggest the use of fixed-dose combination from the beginning of therapy, better in a single tablet, witch improves adherence. The most rationale combinations appear to be a blocker of renin-angiotensin system, a calcium antagonist and a diuretic. The aim of our study was to evaluate the efficacy of fix full-dose combination perindopril/indapamide/amlodipine 10/2.5/10 mg on blood pressure, left ventricular hypertrophy, and diastolic dysfunction in patients with grade 3 hypertension and type2 diabetes. Design and method: We performed a prospective study, lasting 3 months, in which 28 grade 3 hypertensives with type 2 diabetes, medium age 58 ± 10 years, received once a day, fix full-dose combination perindopril/indapamide/amlodipine 10/2.5/10 mg. Office blood pressure was measured at baseline, 1 month and 3 months. Left ventricular echocardiographic parameters ware assessed at baseline and after 3 months of treatment. We rated patient general condition or well-being as excellent, improved, appropriate or worse at baseline and after 3 months. Results: Both systolic (182 ± 16 vs 138 ± 11 mmHg, p < 0.01) and diastolic (112 ± 8.5 vs 84 ± 7 mmHg, p < 0.01) BP were significantly reduced. 85.71% of the patients reached blood pressure target. LVMI was decreased from155 ± 29 to 132.5 ± 18.9 g/m2 (p < 0.001). E/A ratio increased from 0.86 ± 0.21 to 1.27 ± 0.3 (p < 0.001). After 3 months of therapy, patient well-being was rated as excellent in 53.57%, improved in 35.72%, appropriate in 10.71% and worse in 0%. Conclusions: Treatment with fix full-dose combination perindopril/indapamide/amlodipine 10/2.5/10 mg in grade 3 hypertensives with type 2diabetes proved a good control of blood pressure, riched the therapeutic target, and was accompanied by regression of cardiac hypertrophy and improvement in left ventricular diastolic function. Treatment was well tolerated.

THE IMPACT OF LEFT VENTRICULAR HYPERTROPHY ON OPTIMAL BLOOD PRESSURE CONTROL

Objective:We aimed to investigate the determinant factors of blood pressure (BP) control achievement and in particular the impact of left ventricular hypertrophy (LVH) regression, determined by echocardiography, in hypertensive patients during a follow up period under treatment.Design and method:238

Dronedarone induces regression of coronary artery remodeling related to better global antioxidant status.

Our group previously demonstrated that dronedarone induces regression of left ventricular hypertrophy in spontaneously hypertensive rats (SHRs). We assessed changes in vascular remodeling and oxidative stress following short-term use of this agent. The coronary artery was isolated from 10-month-old male SHRs treated with 100 mg kg-1 dronedarone once daily for 14 days (SHR-D group), and age-matched untreated SHRs were used as hypertensive controls. We analyzed the geometry and composition of the artery and constructed dose-response curves for acetylcholine and serotonin (5-HT). We calculated a global score (OXY-SCORE) from plasma biomarkers of oxidative status: carbonyl levels, thiol levels, reduced glutathione levels, total antioxidant capacity, and superoxide anion scavenging activity. Finally, we analyzed asymmetric dimethylarginine (ADMA) concentrations in plasma. Dronedarone significantly decreased wall thickness (medial and adventitial layer thickness and cell count) and the cross-sectional area of the artery. Dronedarone significantly improved endothelium-dependent relaxation and reduced the contraction induced by 5-HT. The OXY-SCORE was negative in the SHR model group (suggesting an enhanced oxidative status) and was positive in the SHR-D group (suggesting enhanced antioxidant defense). Dronedarone significantly decreased the concentrations of ADMA. We conclude that dronedarone improves coronary artery remodeling in SHRs. The better global antioxidant status after treatment with dronedarone and decreased plasma ADMA levels could contribute to the cardiovascular protective effect of dronedarone.

Clinical outcome and hemodynamic performance of St. Jude Trifecta aortic prosthesis: short-term follow-up and risk factors analysis.

We retrospectively analysed the short-term outcome of the third-generation St. Jude Trifecta aortic prosthesis. Between December 2014 and December 2017, 177 patients (mean age 75.1±6.8 years, 95 males, 82 females) underwent aortic valve replacement with a St. Jude Trifecta aortic prosthesis and were followed up to 27±9 months. Preoperatively 92 patients (52.0%) were in NYHA class III-IV, EuroSCORE II was 3.2%±2.1%. Trifecta sizes implanted were 19 mm (n=46) (26%), 21 mm (n=69) (39%), 23 mm (n=46) (26%), 25 mm (n=16) (9%). Concomitant coronary artery bypass grafting was performed in 60 patients (34.0%). Operative mortality was 3.4% (1.7% for isolated aortic valve replacement versus 6.7% for combined aortic valve replacement and coronary artery bypass grafting) (P=0.084). The only independent predictor of mortality was the need for the mechanical ventilation greater than 24 hours (P=0.037); recently occurring myocardial infarction was risk factor for mortality at the univariate analysis only (P=0.013). Three-year survival was 84%±6%, freedom from cardiac death 98%±1%, freedom from prosthetic endocarditis 97%±1%. No thromboembolisms or structural valve degeneration were observed. Patient-prosthesis mismatch (PPM) was absent in 126 patients (71.2%), mild-to-moderate in 32 (18.1%), moderate in 19 (10.7%), severe in no any patient. Follow-up echocardiography showed an average mean and peak trans-aortic valve gradients reduction more than 70% in comparison with preoperative value (P<0.0001), and a significant regression of left ventricular hypertrophy (P<0.0001). Moderate PPM did not negatively affect survival. Concomitant severe coronary artery disease was found as an independent predictor of reduced survival (72%±12% versus 86%±6%) (P=0.015). Trifecta aortic prosthesis seems to provide very favourable clinical outcome and hemodynamic performance. At three years, survival was negatively affected by severe coronary artery disease detected at the time of operation. During short-term follow-up, no early structural valve degeneration was been observed. Due to low incidence of PPM and low peak and mean trans-prosthetic aortic valve gradients, third generation Trifecta aortic prosthesis should be considered as one of the best options in the setting of the aortic valve replacement surgery. However, a long-term follow-up is mandatory to confirm the early promising data.

Remote transplantation of human adipose-derived stem cells induces regression of cardiac hypertrophy by regulating the macrophage polarization in spontaneously hypertensive rats

Left ventricular hypertrophy (LVH) in hypertension has prognostic significance on cardiovascular mortality and morbidity. Recently, we have shown that n-butylidenephthalide (BP) improves human adipose-derived stem cell (hADSC) engraftment via attenuated reactive oxygen species (ROS) production. This prompted us to investigate whether remote transplantation of BP-pretreated hADSCs confers attenuated LVH at an established phase of hypertension. Male spontaneously hypertensive rats (SHRs) aged 12 weeks were randomly allocated to receive right hamstring injection of vehicle, clinical-grade hADSCs, and BP-preconditioned hADSCs for 8 weeks. As compared with untreated SHRs, naïve hADSCs decreased the ratio of LV weight to tibia, cardiomyocyte cell size, and collagen deposition independent of hemodynamic changes. These changes were accompanied by attenuated myocardial ROS production and increased p-STAT3 levels. Compared with naïve hADSCs, BP-preconditioned hADSCs provided a further decrease of ROS and LVH and an increase of local hADSC engraftment, STAT3 phosphorylation, STAT3 activity, STAT3 nuclear translocation, myocardial IL-10 levels, and the percentage of M2 macrophage infiltration. SIN-1 or S3I-201 reversed the effects of BP-preconditioned ADSCs increase on myocardial IL-10 levels. Furthermore, SIN-1 abolished the phosphorylation of STAT3, whereas superoxide levels were not affected following the inhibition of STAT3. Our results highlighted the feasibility of remote transplantation of hADSCs can be considered as an alternative procedure to reverse cardiac hypertrophy even at an established phase of hypertension. BP-pretreated hADSCs polarize macrophages into M2 immunoregulatory cells more efficiently than naïve hADSCs via ROS/STAT3 pathway.

Regular consumption of green tea improves pulse pressure and induces regression of left ventricular hypertrophy in hypertensive patients.

This study characterized the effects of regular green tea (GT) and hot water (HW) ingestion on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and left ventricular hypertrophy (LVH) in two equal, sex‐ and age‐matched groups; Grp1 and Grp2 (n = 100 each; age 53 ± 4 years) of hypertensive patients. Grp1 had regular GT treatment, followed by HW ingestion, whereas Grp2 had HW ingestion followed by GT treatment for periods of 4 months each. Electrocardiographic (ECG) and echocardiographic assessments of LVH were made before and at the end of both periods. SBP was lowered significantly by 6.6%; DBP by 5.1%, and PP by 9.1% by the end of month 4 of GT treatment in Grp1. Upon GT cessation and HW ingestion, SBP, DBP, and PP returned to pretreatment levels over 4 months. In Grp2, SBP, DBP, and PP were reduced insignificantly by 1.5%, 1.0%, and 2.3% by the end of the 4th month of HW ingestion. Conversely, over 4 months of GT treatment, SBP, DBP, and PP were significantly lowered by 5.4%, 4.1%, and 7.7% from the baseline values, respectively. ECG and echocardiographic evidence of LVH was shown in 20% of Grp1 and 24% of Grp2 patients before intervention. This was significantly lowered to 8% and 10% in Grp1 and Grp2 by GT treatment. However, this increased to 16% following HW ingestion in Grp1. HW ingestion did mot induce regression of LVH in Grp2. Thus, regular GT ingestion has cardiovascular protective effects.

Treatment of Hypertensive Left Ventricular Hypertrophy.

The development and risk potential of hypertension-induced left ventricular (LV) hypertrophy has been well described in epidemiological studies. Regression of LV hypertrophy reduces cardiovascular morbidity and mortality. However, the best treatment strategy is still debated, as well as the appropriate blood pressure target in these patients. We here review the treatment of LV hypertrophy and the potential benefit on clinical outcomes, against a background of the epidemiology and pathophysiology. Both hemodynamic and non-hemodynamic mechanisms contribute to hypertensive LV hypertrophy, which is characterized by an inappropriate myocardial fibrosis. Stringent blood pressure control reduces LV hypertrophy. Blockers of the renin-angiotensin-aldosterone system may have valuable effects on cardiac and electrophysiological remodelling beyond the effects of blood pressure reduction. Thus, they represent a cornerstone in the treatment of hypertensive LV hypertrophy, but most often other antihypertensive drug classes need to be added. Current guidelines indicate a blood pressure target in most patients with hypertensive LV hypertrophy of 120-130/80 mmHg. LV hypertrophy and myocardial fibrosis are important characteristics of hypertensive heart disease and associated with untoward prognosis. Regression of LV hypertrophy reduces cardiovascular morbidity and mortality. New drugs under development may add additional benefit.

Acute changes in cardiac structural and tissue characterisation parameters following haemodialysis measured using cardiovascular magnetic resonance

In patients with chronic kidney disease (CKD), reverse left ventricular (LV) remodelling, including reduction in LV mass, can be observed following long-term haemodialysis (HD) and has been attributed to regression of LV hypertrophy. However, LV mass can vary in response to changes in myocyte volume, edema, or fibrosis. The aims of this study were to investigate the acute changes in structural (myocardial mass and biventricular volumes) and tissue characterization parameters (native T1 and T2) following HD using cardiovascular magnetic resonance (CMR). Twenty-five stable HD patients underwent non-contrast CMR including volumetric assessment and native T1 and T2 mapping immediately pre- and post-HD. The mean time between the first and second scan was 9.1 ± 1.1 hours and mean time from completion of dialysis to the second scan was 3.5 ± 1.3 hours. Post-HD, there was reduction in LV mass (pre-dialysis 98.9 ± 36.9 g/m2 vs post-dialysis 93.3 ± 35.8 g/m2, p = 0.003), which correlated with change in body weight (r = 0.717, p < 0.001). Both native T1 and T2 reduced significantly following HD (Native T1: pre-dialysis 1085 ± 43 ms, post-dialysis 1072 ± 43 ms; T2: pre-dialysis 53.3 ± 3.0 ms, post-dialysis 51.8 ± 3.1 ms, both p < 0.05). These changes presumably reflect acute reduction in myocardial water content rather than regression of LV hypertrophy. CMR with multiparametric mapping is a promising tool to assess the cardiac changes associated with HD.

Comparison of the Reverse-Remodeling Effect of Pharmacological Soluble Guanylate Cyclase Activation With Pressure Unloading in Pathological Myocardial Left Ventricular Hypertrophy.

Background: Pressure unloading induces the regression of left ventricular myocardial hypertrophy (LVH). Recent findings indicate that pharmacological activation of the soluble guanylate cyclase (sGC) – cyclic guanosine monophosphate (cGMP) pathway may also exert reverse-remodeling properties in the myocardium. Therefore, we aimed to investigate the effects of the sGC activator cinaciguat in a rat model of LVH and compare it to the “gold standard” pressure unloading therapy.Methods: Abdominal aortic banding was performed for 6 or 12 weeks. Sham operated animals served as controls. Pressure unloading was induced by removing the aortic constriction after week 6. The animals were treated from week 7 to 12, with 10 mg/kg/day cinaciguat or with placebo p.o., respectively. Cardiac function and morphology were assessed by left ventricular pressure-volume analysis and echocardiography. Additionally, key markers of myocardial hypertrophy, fibrosis, nitro-oxidative stress, apoptosis and cGMP signaling were analyzed.Results: Pressure unloading effectively reversed LVH, decreased collagen accumulation and provided protection against oxidative stress and apoptosis. Regression of LVH was also associated with a full recovery of cardiac function. In contrast, chronic activation of the sGC enzyme by cinaciguat at sustained pressure overload only slightly influenced pre-established hypertrophy. However, it led to increased PKG activity and had a significant impact on interstitial fibrosis, nitro-oxidative stress and apoptosis. Amelioration of the pathological structural alterations prevented the deterioration of LV systolic function (contractility and ejection fraction) and improved myocardial stiffness.Conclusion: Our results indicate that both cinaciguat treatment and pressure unloading evoked anti-remodeling effects and improved LV function, however in a differing manners.

Сlinical and anamnestic features and their prognostic value in assessment of treatment effiiency of arterial hypertension with comorbidity

Antihypertensive treatment leads to regression of left ventricular hypertrophy, reduces the incidence of cardiovascular complications and improves survival rates, and this occurs regardless of the degree of lowering of blood pressure (BP). The aim of the study was to determinate the prognostic significance of clinical and anamnestic factors in the evaluation of effectiveness of therapeutic correction of arterial hypertension (AH) associated with obesity and diabetes mellitus by angiotensin II receptors blocker, telmisartan. Material and methods. 135 patients were examined, diagnosed with AH stage I–II associated with obesity of 1–2 degrees (mean age 61.6 ± 6.7 years). Duration of study was 3 month. Chronic heart failure was no worse than II functional class by NYHA. Evaluation of prognostic properties of the studied factors was carried out using sequential hypothesis by Wald–Genkin, according to which all the indices were ranged with the subsequent determination of the prognostic coefficient (PC) and the general informativeness of the index (I). The groups were matched by sex, age, severity of the clinical condition, concomitant pathology. The control group consisted of 20 practically healthy persons of similar age and sex without signs of disease. Results . In the study, the predictive value of clinical and anamnestic parameters of the effectiveness of antihypertensive treatment was analyzed. The results show that some clinical and anamnesis factors of the disease can be used to determine the telmisartan effectiveness in the treatment of hypertension with obesity. The most informative criteria (I > 1.0) are the duration (more than 11 years) of arterial hypertension, as well as the age of the patient and the presence of concomitant pathology, in particular type 2 diabetes and obesity. Conclusions . Based on the obtained data about the value of clinical and anamnestic factors’ significance in assessing of the antihypertensive therapy in patients with co-morbid pathology, it is assumed that patients with hypertension duration of more than 11 years with concomitant obesity and type 2 diabetes and those older than 71 years require special tactics in the selection of antihypertensive therapy. And, most likely, such patients need more frequent adjustment of the doses of the drug.

Reduction of left ventricular mass, left atrial size, and N-terminal pro-B-type natriuretic peptide level following alcohol septal ablation in patients with hypertrophic obstructive cardiomyopathy.

Alcohol septal ablation (ASA) is an alternative to surgical treatment in patients with hypertrophic obstructive cardiomyopathy (HOCM). Through alcohol-induced necrosis, ASA leads to an increase in left ventricular outflow tract (LVOT) diameter and a decrease in LVOT pressure gradient. We sought to assess the effect of ASA on left ventricular (LV) wall thickness and mass, left atrial (LA) size, and N-terminal pro-B-type natriuretic peptide (NT-proBNP) level. The study cohort consisted of 50 patients with HOCM (30 in the ASA group, 20 in the optimal pharmacotherapy group [OPG]). Transthoracic echocardiography (TTE), cardiac magnetic resonance (CMR), and NT-proBNP level analysis were performed at baseline and at six months. All parameters are presented as means. In the ASA group, the maximal LVOT pressure gradient decreased from 122.7 to 54.8 mmHg directly after ASA and to 37.2 mmHg after a further six months (p < 0.0001). The NT-proBNP level decreased from 2174.4 to 1103.4 pg/mL (p < 0.001). On TTE, the interventricular septum (IVS) thickness decreased to from 23.6 to 19.4 mm (p < 0.0001) and the lateral wall (LW) thickness decreased from 15.9 to 14.2 mm (p < 0.007). On CMR, basal IVS thickness decreased from 23.7 to 18.0 mm (p < 0.0001) and the LW thickness decreased from 13.2 to 12.2 mm (p = 0.02). IVS mass reduced from 108.9 to 91.5 g (-16%; p < 0.001). All of the above parameters remained unchanged in the OPG. Successful ASA reduces LV hypertrophy and improves parameters of the LV overload, resulting in LV wall hy-pertrophy regression, and LA size and NT-proBNP level reduction. The above parameters may be as useful in assessing the efficacy of ASA as the LVOT gradient itself.

Kv4.3 expression abrogates and reverses norepinephrine-induced myocyte hypertrophy by CaMKII inhibition

BackgroundDown-regulation of Kv4.3 protein is a general feature of cardiac hypertrophy. Based on our recent studies, we propose that Kv4.3 reduction may be a hypertrophic stimulator. ObjectiveWe tested whether Kv4.3 expression can prevent or reverse cardiac hypertrophy induced by norepinephrine (NE). Methods and resultsIncubation of 20 μM NE in cultured neonatal rat ventricular myocytes (NRVMs) for 48 h and 96 h induced myocyte hypertrophy in a time-dependent manner, characterized by progressive increase in cell size, protein/DNA ratio, ANP and BNP, along with an progressive increase in the activity of CaMKII and calcineurin and reduction of Kv4.3 mRNA and proteins. Interestingly, PKA-dependent phosphorylation of phospholamban (PLB) at Ser16 was increased at 48 h but reduced to the basal level at 96 h NE incubation. CaMKII inhibitors KN93 and AIP blunted NE-induced hypertrophic response and caused regression of hypertrophy, which is associated with a reduction of CaMKII activity and calcineurin expression. Kv4.3 expression completely suppressed the development of NE-induced hypertrophy and led to a regression in the hypertrophic myocytes. These effects were accompanied by a reduction in CaMKII autophosphorylation, PLB phosphorylation at Thr-17 without changing PLB phosphorylation at Ser-16. NFATc3 was also reduced by Kv4.3 expression. ConclusionsOur results demonstrated that Kv4.3 reduction is an important mediator in cardiac hypertrophy development via excessive CaMKII activation and that Kv4.3 expression is likely a potential therapeutic strategy for prevention and reversion of adrenergic stress-induced cardiac hypertrophy.

Diuretics and left ventricular hypertrophy regression: The relationship that we commonly forget.

Diuretics and left ventricular hypertrophy regression: The relationship that we commonly forget.

Abstract 011: Regression of Left Ventricle Hypertrophy and Improvement of Ventricular Dysfunction After Renal Revascularization is Dependent of Blood Pressure Response and Etiology of Renal Artery Stenosis

Background: Renovascular hypertension promotes humoral and hemodynamic overload on the cardiovascular system and it is unknown the clinical impact of the correction of renal artery stenosis (RAS) on the structure and function of the heart.We aimed to evaluate the effect of RAS correction on blood pressure (BP) and left ventricle (LV) morphology, function and mass index (LVMI). Methods: Ninety-eight hypertensive patients with significant RAS (&gt; 70%) undergoing percutaneous intervention (26%) or surgical treatment (74%) with a minimum follow-up of 12 months entered the study. We analyzed echocardiographic measurements , including LVMI and ejection fraction (EF) before and after correction of RAS. The BP response after treatment was based on AHA guidelines: cured (BP&lt;140/90 without drugs), improved (BP &lt;140/90 with reduction of number of drugs) and failure. Results: The mean age was 46 ±17 years and 60% were female. The etiology of RAS was atherosclerosis (59%), arteritis (21%) and dysplasia (20%). Before treatment, echocardiography showed LVMI=162 ± 60 g/m2, 73.5% had LV hypertrophy (LVMI &gt; 125 g/m2) and 13 patients had systolic dysfunction (EF&lt;50%). In a mean follow-up of 51 ± 40 months, 62% were considered cured or improved (Benefit group) and 38% as Failure. In the Benefit group, mean LVMI in the follow-up was lower than in Failure group (129 ±44 vs 169 ±42 g/m2, p&lt;.05). The reduction of LVMI was significantly greater in Benefit than in Failure group (23 ±5 vs. 9±9 g/m2, p&lt;.03). The systolic function normalized in 10 from 13 patients with previous dysfunction. The mean LVMI reduction was higher in patients with arteritis than in those with atherosclerosis or dysplasia. Conclusion: Successful renal revascularization promotes significant reduction of LV hypertrophy and normalize previously impaired systolic dysfunction in patients with RAS. The regression of ventricle mass is dependent of BP response after treatment and is more impressive in patients with arteritis.

Atrial changes after kidney transplant: what diagnostic and therapeutic perspectives?

Kidney transplant is known to be the first choice therapy for end stage chronic kidney disease, also for its positive effects on kidney transplant recipients cardiovascular morbidity and mortality. Several evidences evaluated the morphological changes of the left ventricle before and after transplantation, demonstrating a positive effect of at least partial regression of left ventricular hypertrophy (LVH) in kidney transplant recipients. This article is protected by copyright. All rights reserved.

P4756Remote transplantation of human adipose-derived stem cells induces regression of cardiac hypertrophy by regulating the macrophage polarization in spontaneously hypertensive rats

P4756Remote transplantation of human adipose-derived stem cells induces regression of cardiac hypertrophy by regulating the macrophage polarization in spontaneously hypertensive rats