Ventricle Remodeling In Patients Research Articles

IMPACT OF RENAL DENERVATION TREATMENT ON LEFT VENTRICLE REMODELING IN RESISTANT HYPERTENSIVE PATIENTS: THREE YEARS FOLLOW-UP

Objective: Evaluation of effects of RDN on left ventricle remodeling in patients with resistant hypertension and heart failure with preserved ejection fraction. Design and method: The study enrolled 125 hypertensive patients, who after 3-week of standardized treatment with Losartan, Amlodipine and Indapamide and confirmation of their drug resistance, were randomly assigned into three groups depending on medication supplemented to previously administered: group I - selective I1-imidazoline agonist Moxonidine, group II - cardioselective beta-blocker Bisoprolol and group III - renal denervation. All patients underwent a transthoracic echocardiogram at baseline, one, two and three years follow-up. Renal denervation was performed in the main renal arteries and their branches. Results: Transthoracic echocardiography at baseline revealed LV hypertrophy in all patients. The majority of patients in all three research groups had concentric hypertrophy (52% versus 60% and 56% in group I, II and III, respectively), the normal pattern not being recorded in any group. An authentic reduction in LV mass index was noted from 1-year follow-up in all three observational groups, the progressive reduction being maintained until the end of the study, the group of patients undergoing renal denervation manifested a net superior effect to both pharmacological groups. So, at 3-years follow-up LV mass index was 128,57±4,91 g/m2 in Moxonidine group versus 126,0±5,34 g/m2 in Bisoprolol group and 94,44±3,90 g/m2 in RDN group, p < 0.001. Analyzing the impact of various therapeutic regimes on the geometric pattern of the LV, we can note the fact that both treatment schemes with SNS blockers and RDN favored LV reverse remodeling, its normal pattern being regained by 5 (10%) patients from group I and 7 (28%) patients from group III. This time as well RDN demonstrated absolute superiority over both pharmacological treatment regimens (Figure 1). Conclusions: The obtained data confirm the benefit of RDN treatment on the reverse remodeling of the LV by significantly reduction in LV mass index and inducing the recovery of its normal physiological pattern in practically a third of treated patients at 3 years post-procedurally.

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.

A Left ventricle remodeling in patients with bicuspid aortic valve.

We assessed the impact of bicuspid aortic valve (BAV), aortic stenosis (AS), and regurgitation (AR) on the metrics of left ventricular (LV) remodeling, as measured by electrocardiogram (ECG), transthoracic echocardiography (TTE), and cardiac magnetic resonance (CMR). This retrospective CMR study included 11 patients with both AS and AR (BAV-ASR), 30 with AS (BAV-AS), 28 with AR (BAV-AR), 47 with neither AS nor AR (BAV-no_AS/AR), and 40 with trileaflet aortic valve (TAV-no_AS/AR). CMR analysis included the LV end-diastolic volume index (LVEDVi), mass index (LVMi), and extracellular volume fraction (ECV). The Sokolow-Lyon and Cornell products by ECG and TTE-derived E/e' were measured. There were no differences in the ECG, TTE, and CMR parameters between BAV-no_AS/AR and TAV-no_AS/AR. However, the presence of aortic valve dysfunction resulted in an elevated Sokolow-Lyon product for BAV-ASR (p = 0.017) and BAV-AR (p = 0.001), as well as increased Cornell product (p = 0.04) and E/e' (p < 0.001) for BAV-AS compared with BAV-no_AS/AR. LVEDVi and LVMi were elevated in patients with BAV-ASR and BAV-AR compared with those with BAV-no_AS/AR (LVEDVi: 101 ± 29 ml/m2 and 112 ± 32 ml/m2 vs. 74 ± 15 ml/m2, p = 0.005 and p < 0.001, LVMi: 75 ± 7g/m2 and 64 ± 14g/m2 vs. 47 ± 9g/m2, respectively; p < 0.001). There was no difference in ECV between the BAV and TAV-no_AS/AR subgroups. Normally functioning BAV did not result in LV remodeling. However, concomitant AV dysfunction was associated with statistically significant morphological remodeling.

Changes in left atrial function, left ventricle remodeling, and fibrosis after septal myectomy for obstructive hypertrophic cardiomyopathy

BackgroundThis study aimed to investigate the impact of septal myectomy on left atrial function, left ventricle remodeling, and fibrosis in patients with obstructive hypertrophic cardiomyopathy. MethodFrom May 2012 to September 2016, preoperative cardiac magnetic resonance imaging of 507 adult patients who underwent septal myectomy at Fuwai Hospital was retrospectively collected. Until October 2019, 57 patients were followed up with postoperative cardiac magnetic resonance imaging at 11.9 months (interquartile range, 6.4-25.3). Preoperative and postoperative left atrium and left ventricle changes, as well as late gadolinium enhancement as a surrogate of myocardial fibrosis, were analyzed. ResultsPatients with hypertrophic cardiomyopathy requiring myectomy showed increased left atrium volume, stroke volume, left ventricular ejection fraction, and left ventricle mass, as well as decreased left ventricle end-systolic volume. Echocardiography demonstrated that myectomy decreased the left ventricle outflow tract gradient, left atrium diameter, left ventricular ejection fraction, and posterior wall thickness. Postoperative cardiac magnetic resonance imaging showed that the minimal left atrium volume (P < .001), stroke volume (P = .009), left ventricle ejection fraction (P < .001), and left ventricle mass (166.9 [interquartile range, 135.8] vs 149.3 [interquartile range, 100.5] g, P < .001) decreased, whereas the left ventricle end-systolic volume (P = .001) and left atrium ejection fraction (37.9% ± 14.6% vs 47.8% ± 14%, P < .001) increased. However, left ventricle myocardial fibrosis, as detected by late gadolinium enhancement, still progressed after myectomy in patients with obstructive hypertrophic cardiomyopathy (15.2% ± 9.6% vs 18.6% [interquartile range, 21.6], P = .009). ConclusionsSeptal myectomy alleviated left ventricle hypertrophy and reversed left atrium and left ventricle remodeling in patients with obstructive hypertrophic cardiomyopathy. Late gadolinium enhancement in the left ventricle increased despite myectomy in patients with obstructive hypertrophic cardiomyopathy.

P778Valsartan reduces level of soluble ST2 and left ventricle remodeling in patients with dual chamber pacemaker

Abstract Introduction Permanent right ventricle pacing leads to left ventricle remodeling, its systolic dysfunction and symptomatic heart failure in the long run. Valsartan is well known for its preventive anti-remodeling function in the post infarction heart remodeling. Objectives To assess the effect of valsartan on left ventricle remodeling in patients with second and third degree atrioventricular block with first-time implantation of dual chamber pacemaker. Methods This was a randomized, double-blind, placebo controlled single center study. One hundred eligible patients were assigned in a 1:1:1 fashion to receive placebo, valsartan 80mg or 160mg once daily, respectively. Echocardiographic assessment of left ventricle geometry, its systolic and diastolic function was performed at baseline and at twelve months. One patient from placebo group suffered stroke. We present the baseline date for 100 enrolled patients and follow-up data for 88 patients who have completed the study. Data in valsartan arms are pooled in one group. Concentration of soluble ST2 was measured in duplicates with Aspect Reader (Critical Diagnostics). Results Results are presented in table. Data are presented as mean and standard deviation. Table 1 Placebo (n=28) Valsartan (n=60) ANOVA Baseline 12 mths Baseline 12 mths sST2, ng/mL 36.0±16.0 39.4±15.3 35.1±15.2 19.9±6.5 0.01 LVEF, % 60±8 55±9 60±8 58±8 0.01 LVEDD, mm 48±5 50±4 48±6 49±5 NS LVESD, mm 29±4 32±5 29±5 31±4 NS LVEDV, mL 79±12 84±13 80±12 81±13 NS LVESV, mL 32±5 38±7 31±5 34±6 0.01 E/A 0.94±0.12 0.92±0.13 0.94±0.15 0.95±0.15 NS DecT, ms 211±38 226±43 223±45 218±37 0.01 IVRT, ms 98±14 108±17 101±17 99±18 0.01 Conclusion Valsartan has protective effect of left ventricle remodeling and function. It may be useful in prevention of pacing induced heart failure. Decrease in soluble ST2 concentration may help explain the alternative mechanism for protective role of valsartan. (NCT01805804)

Особливості ремоделювання лівого шлуночка у хворих артеріальною гіпертензією на фоні первинної подагри в залежності від функціонального стану нирок

Особливості ремоделювання лівого шлуночка у хворих артеріальною гіпертензією на фоні первинної подагри в залежності від функціонального стану нирок

Left ventricle remodeling in patients with β-thalassemia major. An emerging differential diagnosis with left ventricle noncompaction disease

To differentiate left ventricle non-compaction (LVNC) from hypertrabeculated myocardium due to LV remodeling in β-thalassemia major (β-TM) patients, cardiac magnetic resonance (CMR) images of 38 β-TM patients and 10 LVNC patients were compared using 3 diagnostic criteria: ratio of diastolic segmental non-compacted to compacted myocardium (NC/C ratio) >2.5, percentage of non-compacted LV mass (NC-LVM%) >20% and >25% of global LV mass. Specificity of NC/C ratio of >2.5 was the lowest (58%) and of NC-LVM% of >25% the highest (93%). A NC-LVM% >20% showed sensitivity 100% and specificity 87%. Disease differentiation depends on the selected CMR criterion and is better with NC-LVM%.

Influence of renin-angiotensin-aldosterone system block on the systemic inflammation activity and left ventricle remodeling in patients with Q-myocardial infarction after thrombolysis

Aim. Inflammatory cytokines play a role in adaptive postinfarction remodeling of the heart. In order to study the influence of treatment on the condition of systemic inflammatory markers, the incidence of post-infarction aneurysm and thrombus formation in the left ventricle of patients with Q-wave myocardial infarction after thrombolytic therapy serum levels of interleukin-6, interleukin-1-beta, von-Willebrand factor, fibrinogen were studied in 92 patients with immunoassay analysis. Results and discussion. Remodeling, systolic and diastolic function of the heart were evaluated with echocardiography. Under the influence of the treatment reduction of systemic inflammatory markers activity was showed, which accompanied by improvement of left ventricular systolic function and low frequency of left ventricle aneurysm and thrombus formation.

Randomized placebo controlled blinded study to assess valsartan efficacy in preventing left ventricle remodeling in patients with dual chamber pacemaker — Rationale and design of the trial

BackgroundDual chamber pacing is known to have detrimental effect on cardiac performance and heart failure occurring eventually is associated with increased mortality. Experimental studies of pacing in dogs have shown contractile dyssynchrony leading to diffuse alterations in extracellular matrix. In parallel, studies on experimental ischemia/reperfusion injury have shown efficacy of valsartan to inhibit activity of matrix metalloproteinase-9, to increase the activity of tissue inhibitor of matrix metalloproteinase-3 and preserve global contractility and left ventricle ejection fraction. PurposeTo present rationale and design of randomized blinded trial aimed to assess whether 12month long administration of valsartan will prevent left ventricle remodeling in patients with preserved left ventricle ejection fraction (LVEF≥40%) and first implantation of dual chamber pacemaker. MethodsA total of 100 eligible patients will be randomized into three parallel arms: placebo, valsartan 80mg/daily and valsartan 160mg/daily added to previously used drugs. The primary endpoint will be assessment of valsartan efficacy to prevent left ventricle remodeling during 12month follow-up. We assess patients' functional capacity, blood plasma activity of matrix metalloproteinases and their tissue inhibitors, NT-proBNP, tumor necrosis factor alpha, and Troponin T. Left ventricle function and remodeling is assessed echocardiographically: M-mode, B-mode, tissue Doppler imaging. ConclusionIf valsartan proves effective, it will be an attractive measure to improve long term prognosis in aging population and increasing number of pacemaker recipients. ClinicalTrials.org (NCT01805804).

Perindopril treatment promote left ventricle remodeling in patients with heart failure screened positive for autoantibodies against angiotensin II type 1 receptor

BackgroundAutoantibodies specific to the angiotensin II type I receptor (anti-AT1-AR) have been implicated in the pathology of congestive heart failure (CHF). Anti-AT1-AR may be associated with left ventricular function in CHF patients treated with perindopril.MethodsSynthetic angiotensin II type 1 receptor (AT1-R) peptides served as the target antigen. ELISA was used to screen the sera of 156 CHF patients, which were divided into positive and negative groups based on their anti-AT1-AR reactivity. Echocardiography and a 6-minute walk test were performed at baseline and after one year of perindopril therapy. The end-point events were compared over a 5-year follow-up.ResultsFinal analysis covered 138 patients, including 82 positive and 56 negative. The frequency and geometric mean titre of anti-AT1-AR were significantly lower in the positive group after one year of treatment (all P < 0.01, from 100% to 73.2% and from 1:125.3 ± 1.0 to 1:69.2 ± 1.1). Of these, 22 patients showed no antibodies. Both groups showed improvement in left ventricular end-diastole, end-systolic dimensions, ejection fraction, and a 6-minute walk test by perindopril in combination with standard treatment regime for one year (all P < 0.01). However, the 82 patients positive for anti-AT1-AR showed more pronounced improvement than the 56 negative patients (all P < 0.05). However, after 5 years of follow-up, the rate of all causes and cardiovascular mortality attributable to any cause and the re-hospitalisation rate showed no significant differences between the two groups (all P > 0.05).ConclusionsPerindopril treatment significantly decreased the frequency and geometric mean titre in patients positive for anti-AT1-AR, even to complete ablation. These patients showed greater improvement in left ventricular remodeling and heart function than negative that in patients after one year of perindopril treatment in combination with standard treatment, but no significant differences in endpoint events were observed in the following 5 years. Anti-AT1-AR might be a useful biomarker of over-activation of the renin-angiotensin-aldosterone system for clinical medication.

Effects of delayed percutaneous coronary intervention on left ventricle remodeling in patients with acute myocardial infarction

ObjectiveTo assess the effect of delayed percutaneous coronary intervention (PCI) on left ventricle remodeling after acute myocardial infarction (AMI).MethodsNinety six patients with ST-segment elevation acute interior wall myocardial infarction (AAMI)...

437 Ultrasonic myocardial tissue characterization by cyclic variation of integrated backscatter in patients with aortic stenosis

s S63 Eur J Echocardiography Abstracts Supplement, December 2006 437 Ultrasonic myocardial tissue characterization by cyclic variation of integrated backscatter in patients with aortic stenosis M. Fijalkowski 1 ; A. Koprowski 1 ; R. Galaska 1 ; W. Dubaniewicz 1 ; J. Rogowski 1 ; A. Rynkiewicz 1 1Medical University Of Gdansk, 1St Department Of Cardiology, Gdansk, Poland Background: Ultrasonic myocardial tissue characterization by cyclic variation of integrated backscatter (CVIBS) has been successfully used for the differentiation of various myopathies from normal myocardium. Aim: The aim of the study was ultrasonic myocardial tissue characterization in patients with aortic stenosis (AS) by cyclic variation of integrated backscatter. Methods: The study population consisted of 128 patients (42 women; mean age 65±10 years). In the parasternal long-axis view two regions of interest were chosen to estimate CVIBS: the mid-septum and the mid-posterior wall. Types of left ventricular remodeling in our group were classified according to left ventricular mass index (LVMI) and relative wall thickness (RWT): normal LV (N), LV concentric remodeling (CR), LV concentric hypertrophy (CH) and LV excentric hypertrophy (EH). Results: The mean echocardiographic parameters were: the aortic valve area (AVA) 0.8±0.3 cm2, maximal pressure gradient (PG max) 86±29 mm Hg and mean pressure gradient (PG mean) 54±20 mm Hg, LVEF 71±14%, fractional shortening (FS) 35±10%, left LVMI 146±47 mg, circumferential end-systolic wall stress (cESS) 102±48 kdynes/cm2; CVIBS septum 5.6±2.3 db, CVIBS posterior wall 5.4±2.0 dB. We found inverse correlation between mean CVIBS and LVMI (r=-0.29; r=-24; p<0.05; for septum and posterior wall respectively) and cESS (r=-0.28; r=-32; p<0.05; for septum and posterior wall respectively) and direct correlation between mean CVIBS and LVEF (r=0.28; r=-25; p<0.05; for septum and posterior wall respectively) and FS (r=0.26; r=-22 p<0.05; for septum and posterior wall respectively). In addition mean CVIBS for both septum and posterior wall was significantly lower in group with LV excentric hypertrophy compared to patients with LV concentric remodeling and LV concentric hypertrophy (Table 1). There were no significant correlations between mean CVIBS and NYHA, AVA, PG max, PG mean and diastolic function indices. Conclusion: The severity of myocardial dysfunction and left ventricle remodeling in patients with aortic stenosis are associated with alterations in myocardial ultrasonic reflectivity detected by integrated backscatter analysis.

Neurohormonal modulation in heart failure of ischemic etiology: Correlates with left ventricular remodeling

The natural progression of heart failure (HF) is accompanied by the compensatory activation of cardiac and extracardiac neurohormonal systems and changes in the anatomy and function of the left ventricle. The processes of ventricular remodeling and neurohormonal activation are mutually influenced so that strong associations may be observed between circulating concentrations of biomarkers (especially the natriuretic peptides originating from the heart) and parameters of left ventricle size and function. Temporal changes in the concentration of natriuretic peptides convey incremental prognostic value compared with a single determination and are usually related to concomitant changes in markers of left ventricle remodeling in patients with chronic HF. Whether knowledge of biomarkers' concentration can improve the clinical outcome of patients with HF by helping in guiding and monitoring their therapy treatment is a stimulating working hypothesis still to be verified.