Left Ventricular Hypertrophy Group Research Articles

4091Mechanical dispersion by speckle tracking echocardiography in fabry disease

Abstract Background Fabry disease is a rare X-linked storage disorder caused by a deficiency of the lysosomal enzyme α-galactosidase A and generally causes multi-organ dysfunction. Heart disease is the main cause of death, due to severe left ventricular (LV) systolic dysfunction and sudden death. In several heart diseases, the LV systolic dysfunction and ventricular arrhythmias are associated with mechanical dispersion (MD). The presence of MD in patients with FD has not been studied yet. In this cross-sectional study, we investigated the prevalence of MD in patients with FD. Methods Complete echocardiographic and speckle tracking echocardiographic (STE) data were collected. MD is an index of inter-segmental discoordination of contraction which has been used to quantify LV dyssynchrony and was defined as the standard deviation (SD) of time to peak negative strain in 17 left ventricular segments. Patients were divided into two groups according to whether or not they had left ventricular hypertrophy (LVH). MD was defined as an SD >49 msec. Results We studied 108 patients with FD, 24 patients (22%) were excluded due to inadequate imaging quality or presence of comorbidities, so the final study population consisted of 84 patients (mean age 33.3±14.6 years, 60.7% women). LVH in FD appears at older ages than in patients without LVH (48±12.5 y/o vs 27.8±11.1 y/o, p<0.0001). Patients with FD without LVH (Group I) showed normal global longitudinal peak strain (GLPS) (21.2±2.5%) and no MD (32.7±8.8 msec). In Group II (n=23) patients with FD with LVH, 17 (73.9%) had MD >49 msec prolonged mechanical dispersion (73.3±20.7 msec) and reduced GLPS (13.6±4.0%). MD was more pronounced in Fabry patients with LVH than in patients without LVH (63.4±24.7 msec vs. 32.7±8.8 msec, p<0.0001). GLPS was lower in Fabry patients with LVH than in patients without LVH (15.3±4.7% vs 21.2±2.5%, p<0.0001). Figure 1 Conclusions To our knowledge, this is the first study to demonstrate the prevalence of mechanical dispersion in patients with FD. Mechanical dispersion was seen in 73.9% of patients with FD with LVH. This dyssynchrony should be taken into account in patients who develop heart failure or life-threatening ventricular tachyarrhythmias.

Early detection of left atrial dysfunction assessed by CMR feature tracking in hypertensive patients.

To evaluate whether early left atrial (LA) dysfunction in hypertension (HTN), with or without left ventricular hypertrophy (LVH), can be detected by cardiovascular magnetic resonance feature tracking (CMR-FT). Seventy-three HTN patients and 29 healthy controls were retrospectively recruited. HTN patients were divided into the LVH (n = 29) and non-LVH group (n = 44). LA performance was analysed using CMR-FT in 2- and 4-chamber cine images, including LA reservoir function (total ejection fraction [EF], total strain [εs], peak positive strain rate [SRs]), conduit function (passive EF, passive strain [εe], peak early negative strain rate [SRe]) and booster pump function (booster EF, active strain [εa], late peak negative strain rate [SRa]). One-way analysis of variance with post hoc LSD tests, Spearman analysis, receiver operating characteristic curve and intra-class correlation coefficient analysis were applied for statistical analyses. Compared with healthy controls, LA reservoir (LA total EF, εs, SRs) and conduit function (LA passive EF, εe, SRe) were significantly impaired in HTN patients with or without LVH, and these parameters significantly correlated with mitral E/A < 1 (all p < 0.05). However, LA booster pump function was relatively preserved in non-LVH patients, representing an intermediate stage between the LVH group and controls. Among LA deformation parameters, εe showed the highest diagnostic value for differentiation of HTN patients with healthy controls (AUC, 0.82; sensitivity, 80.82%; specificity, 72.41%). Observer reproducibility was good-excellent (ICC, 0.83-0.97) for all CMR-FT derived parameters. CMR-FT is a promising tool for quantification of LA function. LA reservoir and conduit dysfunction might be detected early by CMR-FT in HTN patients before the presence of LVH. • CMR-FT is a promising tool in quantifying LA function, including deformation and volumetric parameters. • LA reservoir and conduit dysfunction might be detected early by CMR-FT in HTN patients with or without LVH. • The LA booster pump function was relatively preserved in non-LVH patients.

Transthoracic echocardiography in patients with chronic kidney disease

Background: Evaluation of cardiac diseases in chronic kidney disease has been rarely investigated in Nepal.&#x0D; Objectives: Objective of this study is to evaluate cardiac lesions in admitted chronic kidney disease patients.&#x0D; Methodology: It is a prospective observational study of echocardiography of chronic kidney disease patients from April, 2007 to April, 2013 in Nepal Medical College Teaching Hospital.&#x0D; Results: One hundred chronic kidney disease patients were evaluated. Male to Female ratio was 1.8:1 and age ± SD was 46.3 ± 17.2 years. Forty eight percent of the chronic kidney disease patients had left ventricular hypertrophy. Patients with chronic kidney disease with left ventricular hypertrophy group had interventricular septum of 1.5 ± 0.3 cm vs. 1.1 ± 0.1 cm (p&lt;0.0001) and posterior wall of 1.1 ± 0.2cm vs. 1.0 ± 0.1cm (p&lt; 0.01) in comparison to chronic kidney disease without left ventricular hypertrophy. Forty one percent had left ventricular systolic dysfunction with left ventricular ejection fraction of 39 ± 9.9 %. Pulmonary arterial hypertension was noticed in 39% patients. Valvular regurgitant lesions were quite common (24.1%) usually as multivalvular lesions (4.4 lesions per patient). Mitral regurgitation was the commonest regurgitant lesion (81%).&#x0D; Conclusion: Echocardiographic cardiac evaluation is useful to diagnose concomitant cardiac lesions for standard care of chronic kidney disease patients.

The Potential Role of Circulating Endothelial Cells and Endothelial Progenitor Cells in the Prediction of Left Ventricular Hypertrophy in Hypertensive Patients.

BackgroundThe main aim of present study is to evaluate the potential role of circulating endothelial cells (CECs) and endothelial progenitor cells (CEPCs) – representing specific markers of endothelial damage, in the prediction of left ventricular hypertrophy (LVH) in hypertensive patients categorized into two groups; mild (MH) and resistant hypertension (RH).Materials and MethodsThirty patients with MH and 28 subjects with RH were involved in the study. In both groups, patients were divided into an LVH and non-LVH group. The control group included 33 age and sex-matched normotensive volunteers. Physical examination, laboratory tests and echocardiography were conducted.ResultsIn both the MH and RH group, patients with as well as without LVH demonstrated a higher number of CECs and a lower ratio of CEPCs/CECs as compared to the healthy control. Multiple linear regression analysis showed a positive association of CEPCs with left ventricular mass (LVM) and left ventricular mass index (LVMI), independently of other confounders.ConclusionOur results suggest that endothelial injury observed as an elevated CECs number and its impaired regeneration, reflected by a lowered CEPCs/CECs ratio, precede LVH occurrence and may play a significant role in LVH development regardless of the clinical severity of hypertension. Moreover, independent correlation of CEPCs with echocardiographic (ECG) incidences of LVH suggests their potential use as a screening biomarker to stratify the risk of LVH development.

Axl expression is increased in early stages of left ventricular remodeling in an animal model with pressure-overload.

BackgroundAXL is a receptor tyrosine kinase that has been related to kidney and vascular disorders. Heart failure patients with reduced ejection fraction have higher AXL in serum than controls. No information about Axl expression with HF progression is available.MethodsThoracic transverse aortic constriction (TAC) was successfully performed on male Wistar rats (n = 25) with different constriction levels. Controls underwent sham surgery (n = 12). Echocardiography measurements were performed 4–8 weeks after surgery. Collagen deposition was measured with picrosirius red staining. Axl mRNA levels in left ventricle (LV), left kidney (LK) and ascending aorta (aAo) and the LV expression of cardiac remodeling and fibrogenic factors were quantified with real-time PCR. AXL LV protein levels were quantified with western blot and localization was analyzed by immunohistochemistry. Soluble AXL levels in plasma were assayed with ELISA.ResultsSuccessful TAC rats were classified into LV hypertrophy (LVH) or heart failure (HF), modeling the progressive cardiac changes after pressure overload. Collagen deposition was increased only in the HF group. LV Axl mRNA levels were higher in LVH and HF than in Sham rats, and correlated with LVHi, and hypertrophic and fibrogenic mediators. However, no association was found with LV systolic function. AXL was expressed in LV myocytes and other cell types. Concentration of circulating sAXL in plasma was increased in the LVH group compared to Sham and HF rats. Axl mRNA levels were similar in all groups in the LK and aAo.ConclusionsAxl expression pattern suggests a role in the early progression of LV remodeling in HF but not in the later systolic dysfunction. The higher levels of circulating AXL found in HF patients most probably shed from the heart.

Relationship between plasma fibroblast growth factor-23 and subclinical cardiovascular damages in children with primary hypertension

Objective: To examine the plasma fibroblast growth factor-23 (FGF-23) concentration in children with primary hypertension and to investigate the association between plasma FGF-23 and subclinical cardiovascular damages,and to identify its predictive value for diagnosis. Methods: With prospective study,77 patients (61 males and 16 females) who were diagnosed as primary hypertension with the average age of (11.8±2.2) years were enrolled with informed consent in Children's Hospital,Capital Institute of Pediatrics from October 2016 to December 2017. Carotid wall intima-media thickness (cIMT) measured by Doppler ultrasound and left ventricular hypertrophy (LVH) identified by echocardiography were assessed as parameters of subclinical cardiovascular damages. Patients were divided into increased cIMT group (n=18) and normal cIMT group (n=46) (64 patients with complete data of cIMT). According to left ventricular geometry,patients were divided into LVH group (n=27) and normal geometry group (n=50). Concentration of plasma FGF-23 was detected in all children by enzyme linked immunosorbent assay test. Mann-Whitney U test was used to compare plasma levels of FGF-23 between groups. Kendall's tau-b correlation coefficient was used to analyze the correlation between plasma FGF-23 and cIMT/LVH. Receiver operating characteristic (ROC) curve was used to analyze the value of plasma FGF-23 in the prediction of subclinical cardiovascular damage. Results: The concentration of plasma FGF-23 in the increased cIMT group was higher than that in the normal cIMT group (55.6 (46.2,63.5) vs. 48.6 (39.4, 57.3) ×10(3) RU/L, Z=-2.143, P=0.032) . Also, plasma FGF-23 showed positive correlation with cIMT(r=0.222, P=0.032). According to ROC curve analysis,the cutoff value of plasma FGF-23 for prediction of increased cIMT was 53.9×10(3) RU/L (55.6% sensitivity and 71.7% specificity). The concentration of plasma FGF-23 in the LVH group was significantly higher than that in normal geometry group (55.0 (46.8, 65.7) vs. 48.2 (39.5, 56.0)×10(3) RU/L, Z=-2.375, P=0.018). And,plasma FGF-23 was correlated positively with LVH (r=0.224, P=0.018). The concentration of plasma FGF-23 in patients with concentric remodeling (n=10) was significantly higher than that of the normal geometry group (56.9 (49.6, 66.3) vs. 48.2 (39.5,56.0) ×10(3) RU/L, Z=-2.093, P=0.036). According to ROC curve analysis,the cutoff value of plasma FGF-23 for prediction of LVH was 49.1×10(3) RU/L (70.4% sensitivity and 60.0% specificity). Conclusion: The concentration of plasma FGF-23 in children with primary hypertension was correlated positively with LVH and cIMT and had certain predictive value of diagnosis for subclinical cardiovascular damages.

Circulating CTRP1 Levels Are Increased and Associated with the STOD in Essential Hypertension in Chinese Patients.

This study aimed to investigate the correlation between complement C1q tumor necrosis factor-related protein 1 (CTRP1) and subclinical target organ damage (STOD) in essential hypertension (EH). 720 patients were enrolled in this study, including 360 healthy subjects and 360 patients with EH. The EH group included 183 patients complicated with STOD and 177 patients without STOD. In the STOD group, there were 87 patients with left ventricular hypertrophy (LVH), 32 patients with microalbuminuria (MAU), and 58 patients with complication of LVH and MAU. Enzyme-linked immunosorbent assay (ELISA) was used to detect the CTRP1, adiponectin (APN), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). We found that CTRP1 levels were higher in patients with EH than those in healthy subjects; moreover, the level of CTRP1 of patients in the group complicated with EH and STOD was increased compared with EH patients without STOD. CTRP1 levels in the group complicated with LVH and MAU were significantly higher than those in the LVH group and the MAU group. Furthermore, APN, CTRP1, and IL-6 were three factors that influenced the STOD of EH patients, among which CTRP1 and IL6 were positively related with the complication of hypertension and STOD. In conclusion, CTRP1 levels are increased and associated with the STOD (heart and kidney) in essential hypertension, which can be regarded as a novel biomarker in the prediction of prognosis for patients with essential hypertension.

Deletion Polymorphism of Angiotensin Converting Enzyme Gene is Associated with Left Ventricular Hypertrophy in Uighur Hypertension-Obstructive Sleep Apnea Hypopnea Syndrome (OSAHS) Patients.

BackgroundThis study aimed to explore the association of angiotensin converting enzyme (ACE) gene insertion/deletion polymorphisms with left ventricular hypertrophy (LVH) in Han and Uighur hypertension-OSAHS (obstructive sleep apnea hypopnea syndrome) patients in China.Material/MethodsA total of 162 Han and 72 Uygur patients with hypertension-OSAHS were independently subdivided into an LVH group and a non-LVH (NLVH) group based on the left ventricular mass index. The insertion/deletion polymorphisms of ACE gene were determined by polymerase chain reaction. The association of ACE gene insertion/deletion polymorphisms with LVH was assessed by chi-squared test. Logistic regression analysis was performed to obtain the odds ratios and 95% confidence intervals for the risk of LVH after adjusting for confounding factors.ResultsIn Uighur patients, the distributions of D allele and DD genotype showed significant differences between the LVH group and the NLVH group. The difference of DD genotype remained significant after multivariate adjustment. In contrast, no significant differences were observed in the distributions of D allele and DD genotype between the LVH group and the NLVH group in Han patients. Moreover, moderate-severe OSAHS was an independent risk factor for LVH.ConclusionsD allele and DD genotype of ACE gene are possible genetic markers for the risk of LVH in Uighur but not Han hypertension-OSAHS patients.

Plasma protein thiolation index (PTI) as a potential biomarker for left ventricular hypertrophy in humans.

BackgroundLeft ventricular hypertrophy (LVH) has been associated with oxidative stress, although not with the protein thiolation index (PTI). This study explored the potential use of PTI as a biomarker of oxidative stress in patients with LVH.MethodsWe recruited 70 consecutive patients (n = 35 LVH and n = 35 non-LVH) based on an echocardiography study in our institution (left ventricular mass indexed to body surface area). Plasma levels of both S-thiolated protein and total thiols were measured as biomarkers of oxidative stress by spectrophotometry, and PTI was calculated as the molar ratio between S-thiolated proteins and the total thiol concentration.ResultsValues for plasma S-thiolated proteins were higher in patients with LVH than in the control group (P = 0.01). There were no differences in total thiols between the LVH group and the control group. Finally, PTI was higher in patients with LVH than in the control group (P = 0.001). The area under the ROC curve was 0.75 (95% CI, 0.63–0.86; P<0.001), sensitivity was 70.6%, and specificity was 68.6%, thus suggesting that PTI could be used to screen for LVH. A multivariable logistic regression model showed a positive association (P = 0.02) between PTI and LVH (OR = 1.24 [95% CI, 1.03–1.49]) independently of gender (OR = 3.39 [95% CI, 0.60–18.91]), age (OR = 1.03 [95% CI, 0.96–1.10]), smoking (OR = 5.15 [95% CI, 0.51–51.44]), glucose (OR = 0.99 [95% CI, 0.97–1.01]), systolic arterial pressure (OR = 1.10 [CI 1.03–1.17]), diastolic arterial pressure (OR = 0.94 [CI 0.87–1.02]), dyslipidemia (OR = 1.46 [95% CI, 0.25–8.55]), estimated glomerular filtration rate (OR = 0.98 [95% CI, 0.96–1.01]), body mass index (OR = 1.03 [95% CI, 0.90–1.10]), and valvular and/or coronary disease (OR = 5.27 [95% CI, 1.02–27.21]).ConclusionsThe present study suggests that PTI could be a new biomarker of oxidative stress in patients with LVH.

Evaluation of left ventricular systolic function and synchrony in patients with essential hypertension by longitudinal strain and peak strain dispersion

Objective To investigate the clinical application value of longitudinal peak strain(LPS) and peak strain dispersion(PSD) in evaluating left ventricular systolic function and synchrony in patients with essential hypertension. Methods Fifty-five patients with essential hypertension were enrolled, including 30 patients with non-left ventricular hypertrophy (NLVH), 25 patients with left ventricular hypertrophy (LVH), at the same time, 30 healthy volunteers were selected as the control group. Echocardiography was performed in all three groups, and two-dimensional dynamic images of the left ventricular apical four-chamber, three-chamber, and two-chamber′s long-axis views were collected for three consecutive cardiac cycles. The myocardial layer-specific strain was used to measure the LPS of the left ventricular myocardium of subendocardium, the middle layer, the subepicardium, and the myocardial strain and the PSD of the whole myocardial layers. Correlation analysis and ROC curve analysis were performed. Results The LPS in the control group, NLVH group and LVH group were decreased in turn from inner to out myocardial layers.Compared with the control group, the LPS in the subendocardial, middle, subepicardial, and whole myocardial layer of NLVH group were decreased (P 0.05). The LPS in the subendocardial, middle, subepicardial, and whole myocardial layer of LVH group were all reduced (P 0.05). Compared with the control group, the PSD of the NLVH group and the LVH group increased (P<0.05). Compared with the NLVH group, the PSD of the LVH group increased (P<0.05). Inter-ventricular septum thickness (IVSd) and the LPS in the subendocardial, middle, subepicardial, and whole myocardial layer were negatively correlated (r=-0.537, -0.518, -0.266, -0.471; all P<0.05), left ventricle posterior wall thickness (LVPWd) and the LPS in the subendocardial, middle, subepicardial, and whole myocardial layer were negatively correlated (r=-0.539, -0.524, -0.283, -0.478; all P<0.05). The area under the ROC curve (AUC) of the LPS in the subendocardial, middle, subepicardial, and whole myocardial layer and PSD for the diagnosis of hypertension were 0.685, 0.652, 0.510, 0.623, 0.995, respectively. The cut-off values were -21.70%, -18.90%, -16.95%, -19.45%, 46.50 ms, and the sensitivities were 94.4%, 83.3%, 77.8%, 94.4%, 100%, respectively, and the specificities were 47.8%, 52.2%, 39.1%, 39.1%, 95.7%, respectively. Conclusions The layer-specific strain can quantitatively evaluate myocardial longitudinal strain in patients with essential hypertension, provide a non-invasive test for early diagnosis of hypertensive heart disease, and the evaluation of left ventricular myocardial stratification. PSD for evaluating primary synchronous changes in left ventricular myocardial contraction in patients with hypertension has certain advantages. Key words: Echocardiography; Hypertension; Ventricular function; Layer-specific strain; Peak strain dispersion

COLOR M-MODE PROPAGATION VELOCITY (VP) TO ASSESS THE LEFT VENTRICULAR DIASTOLIC FUNCTION IN HYPERTENSION PATIENTS

Objective: To evaluate the color M-mode (Vp) propagation velocity parameter and the correlation between Vp and left ventricular diastolic function parameters in hypertension patients. Subjects and Methods: A echocardiography study of 51 hypertensive patients, admitted to the Department of Cardiology of Hue University of Medicine and Pharmacy Hospital. This is a cross-sectional study. Results: The Vp value was 63.34 ± 28.22 cm/s. In the left ventricular hypertrophy group, the Vp was lower (62.68 ± 28.08 cm/s) than Vp of the left ventricular non hypertrophy group but not significative (p &gt; 0.05). We found clearly a diminution of the Vp in the groupe with degree 2 of diastolic dysfunction (Vp = 36.18 ± 4.17 cm/s) in comparison with degree 1 (55.65 ± 21.43 cm/s). Vp was positively correlated with the left ventricular peak E-wave velocity (r = 0.304, p &lt; 0.05) and the E/A wave ratio (r = 0.319, p &lt; 0.05). In addition, Vp was inversely correlated with ventricular septal thickness (r = - 0.372, p &lt; 0.01) and left ventricular post wall (r = -0.347; p &lt; 0.01). Conclusion: The Vp parameter may be used as a complement parameters to assess the left ventricular diastolic function in hypertensive patients. This parameter is valuable in patients with 2 stage or more of diastolic function disorder. Key words: Hypertension, ventricular diastolic function, color M-mode propagation velocity

The prognostic value of circulating microRNA-29b in left ventricular hypertrophy in patients with hypertension

Objective: To analyze the relationship between the level of microRNA-29b in circulation and left ventricular hypertrophy in hypertensive patients. Methods: A total of 240 subjects from Henan Province People's Hospital from June 2015 to June 2018 were included in the present study. Among them, 160 were hospitalized patients, and were divided into two groups. Patients with simple hypertension and had no left ventricular hypertrophy (80 cases) were in the simple hypertension group (HBP-NLVH), and patients with hypertension combined with left ventricular hypertrophy (80 cases) were in the high blood pressure with left ventricular hypertrophy group (HBP-LVH). Normal control subjects (80 cases) were those with no hypertension and randomly selected from the medical center of Henan Province People's Hospital. Serum microRNA-29b expressions were detected by real time fluorescence quantitative PCR. The thickness of interventricular septum (IVSD) and left ventricular posterior wall thickness (LVPWD) were measured by echocardiography. Results: Compared with the normal control group (1.95±0.79), the relative expression of microRNA-29b in the patients both in the HBP-NLVH group (2.67±0.92) and the HBP-LVH group (5.12±1.23) was up-regulated, and the difference between normal control and patients was statistically significant (P<0.05). In patients, the microRNA-29b level in the HBP-LVH group was significantly higher than that in the HBP-NLVH group (P<0.05). The expression level of microRNA-29b was positively correlated with IVSD (r=0.71, P<0.05) and LVPWD (r=0.74, P<0.05), respectively. The sensitivity and specificity of serum microRNA-29b levels in the diagnosis of left ventricular hypertrophy in hypertension patients were 96.8% and 91.3%, respectively. Conclusion: Serum microRNA-29b level is elevated in hypertensive patients with left ventricular hypertrophy, and is positively correlated with left ventricular hypertrophy. The circulation microRNA-29b might be a useful biomarker with prognostic value in left ventricular hypertrophy in hypertension patients.

Association between plasma microRNA-29a and left ventricular hypertrophy in patients with hypertension

Objective: Previous studies have shown that plasma microRNA-29a (miRNA-29a) is associated with myocardial fibrosis and the degree of cardiac hypertrophy in patients with hypertrophic cardiomyopathy. However, the relationship between plasma miRNA-29a and hypertensive left ventricular hypertrophy (LVH) has not yet been reported. So the purpose of this study is to investigate the relationship between the plasma miRNA-29a and hypertensive LVH. Method: Enrolled 168 hypertensive patients and classified the patients into 2 groups: those with LVH (LVH group, n=41) and those without LVH (NLVH group, n=127). All patients underwent echocardiography examination. Left ventricular mass index (LVMI) was calculated by interventricular septal thickness (IVSd), left ventricular posterior wall thickness(LVPWTd), left ventricular end diastolic dimension (LVEDD) and left ventricular mass index (LVMI) were obtained. Plasma levels of miRNA-29a were assessed by quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between plasma miRNA-29a levels and LVH was analyzed. Results: Plasma miRNA-29a was significantly higher in LVH group than in NLVH group (0.52±0.10 vs. 0.37±0.07, t=9.788, P<0.01) . Pearson correlation analysis evidenced a positive correlation between plasma miRNA-29a levels and IVSd(R=0.459, P<0.01), LVPWTd (R=0.398, P<0.01), and LVMI (R=0.745, P<0.01). After adjustment for gender, age, systolic blood pressure, diastolic blood pressure, body mass index, hypertension duration, antihypertensive drugs, multiple regression analysis showed that there were still positive correlations between plasma miRNA-29a level and IVSd (β=0.535, P<0.01), LVPWTd (β=0.085, P<0.01), and LVMI (β=0.806, P<0.01). Conclusion: Plasma miRNA-29a level is positively associated with LVH in hypertensive patients, and future studies are warranted to explore if miRNA-29a could be used as a potential biomarker for LVH assessment in hypertensive patients.

Impact of Left Ventricular Hypertrophy on Peak Serum Troponin T Levels in Patients With Acute Myocardial Infarction

Previous studies have reported that peak serum troponin I levels were disproportionately elevated in patients with acute anterior ST-segment elevation myocardial infarction (STEMI) and left ventricular (LV) hypertrophy (LVH) compared with those with normal LV mass. The purpose of this retrospective study was to assess the relation of peak serum troponin T levels in patients with normal LV mass and in subjects with mild, moderate, and severe LVH in patients with acute STEMI or non-ST segment elevation myocardial infarction (NSTEMI) when stratified on variables that might be expected to affect serum troponin T levels. The study population consisted of 262 patients; 91 with STEMI and 161 with NSTEMI. Serum troponin levels and 2-dimensional echocardiograms were obtained within the first 24 hours of hospitalization for STEMI or NSTEMI. There was no significant difference in serum troponin T levels in LV mass and/or LVH groups (p = 0.3210). There was no significant difference in serum troponin T levels in LV mass and/or LVH groups when these data were stratified on third variables including serum creatinine >1.2 mg/dl (p = 0.3681), LV ejection fraction <60% (p = 0.0978), STEMI (p = 0.2576), NSTEMI (p = 0.4994), and location of severe coronary stenosis (p = 0.1981). The results of this study suggest that there is no association between peak serum troponin T levels and LV mass and/or LVH groups when such groups are stratified on a third variable that may influence peak serum troponin T levels.

Residual left ventricular hypertrophy with adverse clinical outcomes in patients with severe aortic stenosis and asymmetric septal hypertrophy after aortic valve replacement.

The aim of this study is to describe the temporal pattern of left atrial (LA) and left ventricular (LV) reverse remodelling and to evaluate the impact of residual LV hypertrophy on the prognosis of patients with severe aortic stenosis and asymmetric septal hypertrophy undergoing aortic valve replacement (AVR). We retrospectively reviewed 59 consecutive patients who underwent AVR for severe aortic stenosis and asymmetric septal hypertrophy. They were divided into the normal LV mass group and the residual LV hypertrophy group according to the LV mass index (LVMI) 2 years after AVR. Thirty patients were eligible for analysis of the time-dependent changes in LA and LV reverse remodelling. The interventricular septal thickness and LVMI gradually decreased and reached their lowest points 2 years after operation, whereas the LA dimension rapidly decreased in the early postoperative period and plateaued at 3 months. The multivariable analysis revealed a higher preoperative LVMI [odds ratio 6.36 (1.678-24.11); P = 0.007] as an independent predictor of residual hypertrophy 2 years after operation. The Cox proportional hazards model showed that a higher postoperative peak velocity [hazard ratio 6.715 (1.405-32.104); P = 0.017] was an independent predictor of long-term non-fatal cardiovascular hospitalization. Patients with residual hypertrophy 2 years after AVR had a higher rate of non-fatal cardiovascular hospitalization (P = 0.014). For patients with severe aortic stenosis and asymmetric septal hypertrophy, maximum LA recovery occurred 3 months after AVR, whereas maximum LV recovery occurred 2 years thereafter. A higher preoperative LVMI may lead to postoperative residual hypertrophy, which is associated with adverse clinical outcomes.

Heart Rate and Heart Rate Variability of Rhesus Macaques (Macaca mulatta) Affected by Left Ventricular Hypertrophy.

Hypertrophic cardiomyopathy (HCM) is frequently associated with sudden cardiac death, presumably due to the development of malignant arrhythmias. The risk of sudden cardiac death due to HCM has been reported to be predicted by assessing electrocardiographic (ECG) changes including frequencies and complexities of arrhythmias as well as heart rate variability (HRV) as an assessment of autonomic balance. Sudden cardiac death in association with naturally-occurring left ventricular hypertrophy (LVH) has been reported in a colony of rhesus macaques and is under investigation as a potential non-human primate model of human HCM. In the present study, 10 rhesus macaques with LVH and 10 without the signs of LVH confirmed by an echocardiographic examination were recruited for assessing ECG and HRV parameters. ECG morphology on 10-s, 6-lead ECG analysis, and the frequency and complexity of arrhythmias as well as HRV on 20-h ambulatory ECG Holter analyses were assessed. On the standard 10-s 6-lead ECG analysis, P wave and QRS complex duration as well as the QRS complex amplitude were significantly increased in the LVH-affected rhesus macaques compared to control rhesus macaques. Analysis of 20-h Holter monitoring revealed no statistically significant differences in the frequency or the complexity of arrhythmias between the LVH and the control groups. Several HRV parameters were smaller in the LVH group than the control group throughout the majority of Holter recordings showing periods of reduced variability, however, no statistically significant differences were achieved across groups and/or time points. These findings indicate that ECG analysis and Holter monitoring of rhesus macaques are feasible and that ECG morphological changes in association with LVH could be used as a possible component of an antemortem screening tool. The rhesus macaques of this study did not reveal clear indications of risk for sudden cardiac death. Further studies are necessary to determine the etiology of sudden cardiac death due in LVH affected rhesus macaques and identify if any parameters of arrhythmia assessment or HRV can be used to predict the development of sudden cardiac death.

Aortic-flow propagation velocity is associated with proteinuria and left ventricular hypertrophy in newly diagnosed hypertensive patients.

Subclinical target organ damage (TOD) is an important long-term complication of hypertension and is associated with cardiovascular events and death. Aortic-flow propagation velocity (APV) is one of the arterial stiffness parameters. The aim of this study was to investigate the predictive value of APV on left ventricular hypertrophy (LVH) and proteinuria. A total of 149 newly diagnosed HT patients were included in the study. Urine samples and blood tests were obtained from each patient for diagnosis of proteinuria. All patients underwent echocardiographic examination. All patients' APV measurements, carotid intima-media thicknesses (CIMT), and ankle-brachial indexes (ABI) were measured and recorded. The LVH (+) group consisted of 47 patients, and the LVH (-) group consisted of 102 patients. The proteinuria (+) group consisted of 32 patients, and the proteinuria (-) group consisted of 117 patients. Average CIMT was significantly higher in both proteinuria (+) and LVH (+) groups compared with the (-) groups. ABI and APV were significantly lower in both proteinuria (+) and LVH (+) groups compared with the (-) groups. APV was negatively correlated with LVH, proteinuria, and CIMT and positively correlated with ABI. In the multivariate binary logistic regression analysis, APV was the significant independent predictor of proteinuria. Additionally, APV and ABI were found to be independent predictors of LVH or/and proteinuria. Hypertensive patients who had TOD had worse consequences of APV, CIMT, and ABI. APV had a powerful predictive value to identify the patients with higher risk of TOD among newly diagnosed hypertensive patients.

Subendocardial systolic dysfunction in hypertensive patients with strain ST-T changes on ECG by speckle tracking

Objective The aim of this study was to evaluate longitudinal strain by speckle tracking in hypertensive patients with strain ST-T on ECG. Background Hypertension causes ST-T changes on ECG which may predict subclinical systolic dysfunction detected by two-dimensional speckle tracking. Patients and methods Longitudinal strain analysis was done in 82 hypertensive patients, who were divided into three groups: the first group included 30 hypertensive patients with echocardiographic evidence of left ventricular hypertrophy (LVH) and strain ST-T changes on ECG (group 1), the second included 31 hypertensive patients with echocardiographic evidence of LVH but without changes on ECG (group 2), and the third control group included 21 hypertensive patients without echocardiographic evidence of LVH (group 3). Results A high significant difference was detected in relation to hypertension duration, which divided into two categories (>10 and ≤10 years) (P Conclusion Subtle LV systolic dysfunction evident by speckle tracking was present in hypertensive patient with strain ST-T changes on ECG independent of left ventricular ejection fraction percentage.

Cardio-omentopexy Reduces Cardiac Fibrosis and Heart Failure After Experimental Pressure Overload

The pedicled greater omentum has been shown to offer benefit in ischemic heart disease for both animal models and human patients. The impact of cardio-omentopexy in a pressure overload model of left ventricular hypertrophy (LVH) is unknown. LVH was created in rats by banding the ascending aorta after right thoracotomy (n= 23). Sham surgery was performed in 12 additional rats. Six weeks after banding, surviving LVH rats were assigned to cardio-omentopexy by left thoracotomy (LVH+Om, n= 8) or sham left thoracotomy (LVH, n= 8). Sham rats also underwent left thoracotomy for cardio-omentopexy (Sham+Om, n= 6); the remaining rats underwent sham left thoracotomy (Sham, n= 6). Echocardiography 10 weeks after cardio-omentopexy revealed LV end-systolic diameter, cardiomyocyte diamter, and myocardial fibrosis in the LVH group were significantly increased compared with the LVH+Om, Sham+Om, and Sham groups (p < 0.01). LV ejection fraction of the LVH group was lower than the LVH+Om group (p < 0.01). Gene expression analysis revealed significantly lower levels of sarcoendoplasmic reticulum calcium adenosine triphosphatase 2b in LVH rats than in the LVH+Om, Sham+Om, and Sham groups (p < 0.01). In contrast, collagen type 1 α 1 chain, lysyl oxidase-like protein 1, nuclear protein-1, and transforming growth factor- β1 in the LVH group were significantly higher than in the LVH+Om cohort (p < 0.01), consistent with a reduced fibrotic phenotype after omentopexy. Lectin staining showed myocardial capillary density of the LVH group was significantly lower than all other groups (p < 0.01). Cardio-omentopexy reduced cardiac dilation, contractile dysfunction, cardiomyocyte hypertrophy, and myocardial fibrosis, while maintaining other molecular indicators of contractile function in this LVH model.

Technical feasibility of semiautomatic three-dimensional threshold-based cardiac computed tomography quantification of left ventricular mass.

Semiautomatic three-dimensional (3-D) threshold-based cardiac computed tomography (CT) quantification has not been attempted for left ventricular mass. To evaluate the technical feasibility of semiautomatic 3-D threshold-based cardiac CT quantification of left ventricular mass in patients with various degrees of left ventricular hypertrophy. In 99 patients, cardiac CT was utilized to quantify ventricular volume and mass by using a semiautomatic 3-D threshold-based method. Left ventricular mass values were compared between the end-systole and the end-diastole. Volumetric parameters were compared among three left ventricular hypertrophy groups (definite, borderline, none). The reproducibility was assessed. The t-test, one-way analysis of variance and Pearson correlation were used. There were no technical failures. The left ventricular mass between the two sessions exhibited a small mean difference of 2.3±1.1% (mean±standard deviation). The indexed mass values were significantly higher at the end-systole than at the end-diastole (71.4±42.9g/m2 vs. 65.9±43.3g/m2, P<0.001), with significant correlation (R=0.99, P<0.001). The definite group (83.5±41.3g/m2) showed statistically significantly higher indexed mass values than the borderline and none groups (64.7±26.9 and 55.6±23.9g/m2, respectively; P<0.03), while demonstrating no statistically significant difference between the latter two groups (P>0.05). Left ventricular volume-mass and mass-volume ratios could be calculated in all three groups. CT quantification of left ventricular mass using semiautomatic 3-D threshold-based segmentation is feasible with high reproducibility and the mass values and its ratios with ventricular volumes may be used in patients with various degrees of left ventricular hypertrophy.