Visceral fat and cardiometabolic future in children and adolescents: a critical update.

Cardiovascular disease (CVD) is a process whose pathogenetic mechanisms start very early in life. Recently, the importance of visceral adipose tissue (VAT) has been highlighted in the development of CVD. VAT does not always depend on body mass index (BMI) and has been implicated in unfavorable metabolic activity and cardiovascular adverse events. Abnormally high deposition of VAT is associated with metabolic syndrome, obesity-associated phenotype, and cardiometabolic risk factors. Although the importance of visceral fat has not been studied broadly or extensively in long-term studies in children and adolescents, it appears that it does not have the same behavior as in adults, it is related to the appearance of cardiac risk factors. In adolescents, it plays a role in the pathogenesis of CVD that occur later in adulthood. Excess body weight and adiposity may lead to the development of early myocardial and pathological coronary changes in childhood. The purpose of this review is to summarize the risk factors, the clinical significance, and the prognostic role of visceral obesity in children and adolescents. In addition, extensive reference is made to the most commonly used techniques for the evaluation of VAT in clinical settings. IMPACT: Visceral obesity, plays an important role in cardiovascular health from very early in an individual's life. Visceral adipose tissue (VAT) distribution is not entirely related to body mass index (BMI) and provides additional prognostic information. There is a need to pay more attention to the assessment of VAT in young people, to develop methods that would go beyond the measurement of only BMI in clinical practice and to identify individuals with excess visceral adiposity and perhaps to monitor its changes.

Early Left Ventricular Global Longitudinal Strain Deterioration After Aortic Aneurysm Repair: Impact of Aortic Stiffness.

PURPOSE: To associate the impact of aortic reconstruction using currently available grafts and endografts on pulse wave velocity in patients with abdominal aortic aneurysm (AAA) and to evaluate its effect on early cardiac systolic function indices. MATERIALS AND METHODS: Seventy-three consecutive patients with AAA (mean age 70±8 years; all men) who underwent open (n=12) or endovascular repair (EVAR; n=61) were prospectively enrolled in an observational cohort study. Left ventricular global longitudinal strain (GLS; an important diagnostic and prognostic index of early systolic dysfunction) and carotid-femoral pulse wave velocity (cf-PWV) were estimated 1 week preoperatively, as well as at 1 and 6 months postoperatively. RESULTS: A significant time effect was found for cf-PWV, which showed an increase at 1 month that remained through 6 months (p=0.007). Additionally, a deterioration in GLS values was revealed, with a significant change at 1 month that persisted 6 months later (p<0.001). No significant group effect was observed between EVAR and open repair (p=0.98), and there was no significant interaction (p=0.96). Notably, the difference in GLS between baseline and 6 months significantly correlated with the corresponding changes in cf-PWV (r=0.494, p<0.001). CONCLUSION: AAA repair leads not only to an increase in aortic stiffness, as measured by the increase in pulse wave velocity, but also to reduced cardiac systolic function. Our findings highlight the need for a more intense cardiac surveillance program after aortic reconstruction. Further studies are needed to investigate how this may translate into long-term manifestations of cardiovascular complications and symptomatology.

The long non-coding RNAs MHRT, FENDRR and CARMEN, their expression levels in peripheral blood mononuclear cells in patients with essential hypertension and their relation to heart hypertrophy.

Long non-coding RNAs (lncRNAs) participate in the modulation of cardiac hypertrophy, and they represent potential therapeutic targets in cardiovascular disease. We investigated the expression profiles of selected lncRNAs in peripheral blood mononuclear cells of patients with essential hypertension in relation to left ventricular hypertrophy. We assessed the expression levels of the lncRNAs MHRT, FENDRR and CARMEN using real-time reverse transcription polymerase chain reaction. Hypertensive patients showed significantly higher MHRT, FENDRR and CARMEN expression levels compared with healthy controls. In addition, we observed significant negative correlations of MHRT (r = -0.323, P = 0.003) and FENDRR (r = -0.380, P = 0.001) and a positive correlation of CARMEN (r = 0.458, P < 0.001) expression levels with left ventricular mass index. Our data reveal that the lncRNAs MHRT, FENDRR and CARMEN show distinct expression profiles in hypertensive patients and they possibly represent candidate therapeutic targets in hypertensive heart disease.

Determinants of operator and patient radiation exposure during cardiac catheterization: Insights from the RadiCure (RADIation reduction during cardiac catheterization using real-timE monitoring) trial.

BACKGROUND: In the RadiCure study 505 catheterization procedures were 1:1 randomized to use or no use of real-time radiation monitoring. Use of the Bleeper Sv monitor resulted in a significant reduction in operator radiation exposure. METHODS: We examined the association between several baseline and procedural parameters with operator and patient radiation exposure using univariable and multivariable analysis in the 505 patients that were enrolled in RadiCure. All baseline demographic and procedure characteristics recorded were included in the univariable analysis. RESULTS: Median fluoroscopy time was 6.2 (2.5-12.5) minutes, median patient air kerma dose was 0.908 (0.602-1.636) Gray and median first operator exposure was 10 (5-22) µSv. For analysis purposes, the 505 procedures were dichotomized based on the median operator exposure (10 µSv) and median patient radiation dose (0.908 Gray). On multivariable analysis, factors associated with high (above median or >10 µSv) first operator radiation exposure included radial access (odds ratio [OR] 5.44, 95% Confidence Interval [CI] 2.88-10.76), chronic total occlusion (CTO) intervention (OR 12.78, 95% CI 4.42-43.60), real-time radiation monitoring (OR 0.42, 95% CI 0.26-0.66), and use of a radioabsorbent drape (OR 0.53, 95% CI 0.28-0.96). High patient radiation dose (above median or >0.908 Gray) was associated with body mass index>30 kg/m2 (OR 3.22, 95% CI 1.99-5.29), prior MI (OR 2.26, 95% CI 1.29-4.04), prior cerebrovascular disease (OR 0.34, 95% CI 0.15-0.75), hypertension (OR 2.40, 95% CI 1.05-5.82), prior coronary artery bypass graft surgery (OR 2.46, 95% CI 1.40-4.39) and CTO intervention (OR 12.93, 95% CI 3.28-87.31), but was not associated with real-time radiation monitoring and use of a radioabsorbent drape. CONCLUSIONS: Several clinical and procedural factors are associated with higher patient and operator radiation exposure. Real-time radiation monitoring and use of disposable radiation shields were associated with lower operator, but not patient, radiation dose. © 2015 Wiley Periodicals, Inc.

Peripheral Blood MicroRNA-21 as a Predictive Biomarker for Heart Failure With Preserved Ejection Fraction in Old Hypertensives.

BACKGROUND: Heart failure with preserved ejection fraction (HFpEF) is a major health issue with high morbidity and mortality. The epidemiology and the factors that cause HFpEF have not been fully clarified, while accurate predictive biomarkers are lacking. Our aim was to determine whether levels of microRNA-21 (miR-21) in peripheral blood monocytes, which play a critical role in many pathophysiological pathways of hypertensive heart disease, can predict the occurrence of HFpEF in older hypertensives, as well as the associated mortality and morbidity. METHODS: We enrolled 151 elderly patients >60 years old with essential hypertension but without HF at baseline. miRs expression levels in peripheral blood mononuclear cells had been quantified by real-time reverse transcription polymerase chain reaction. RESULTS: During a median follow-up of 8.2 years, 56 patients (37%) had an event. Levels of miR-21 in peripheral mononuclear blood cells proved to be significantly associated with the occurrence of HFpEF. More specifically, the median HFpEF-free period was 110 months for those with miR-21 >2.1 and 114 months for those with miR-21 <2.1. In addition, multivariate analysis showed that miR-21 (hazard ratio 11.14), followed by hemoglobin (Hg) (hazard ratio 0.56 for Hg >13.6 g/dl, a 45% risk reduction), were independent and the most significant predictors of HFpEF events. CONCLUSIONS: miR-21 levels in peripheral blood monocytes are associated with the development of future HFpEF. Our findings may alter the risk models of HFpEF and support the rationale for further research into the modulation of miRs as biomarkers and treatment targets for HFpEF.

Differences in MicroRNA Expression in Pericoronary Adipose Tissue in Coronary Artery Disease Compared to Severe Valve Dysfunction.

Pericoronary adipose tissue (PCAT) is a source of microRNAs (miRs) that act as messengers for intercellular communication. We investigated whether the PCAT surrounding significant coronary atherosclerotic lesions shows specific miR expression patterns compared with PCAT surrounding plaque-free segments. We included 49 patients with 3-vessel coronary artery disease (CAD) and 19 patients with severe valvular disease but no CAD, who underwent elective cardiac surgery. The PCAT was harvested from two sites: adjacent to a significant atherosclerotic coronary lesion and from plaque-free segments. miR-133a, miR-21, miR-26b, miR-9, and miR-143 levels in PCAT cells were quantified by real-time reverse transcription polymerase chain reaction (data expressed as arbitrary units). Expression of miR-133, miR-21, and miR-26b in adipose tissue at a site without atherosclerotic lesion was much lower in patients with CAD than in those without CAD (0.82 ± 1.37 vs 1.86 ± 0.52, P < .001, 0.45 ± 1.3 vs 1.51 ± 1.11, P < .001, 0.3 ± 1.25 vs 1.2 ± 0.73, P = .02, respectively). In addition, miR-133, miR-21, and miR-143 in CAD patients showed significantly greater expression in PCAT from atherosclerotic lesion compared with plaque-free segments (1.32 ± 0.96 vs 0.82 ± 0.37 (P = .011), 0.91 ± 1.7 vs 0.3 ± 1.25 (P = .012), 1.2 ± 1.59 vs 0.43 ± 0.54 (P < .001), respectively). Our findings open new perspectives for the role of PCAT in the pathophysiology of atherosclerosis and should be further investigated.

Effects of Sodium-Glucose Cotransporter-2 Inhibitors on Cardiac Structural and Electrical Remodeling: From Myocardial Cytology to Cardiodiabetology.

Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have changed the clinical landscape of diabetes mellitus (DM) therapy through their favourable effects on cardiovascular outcomes. Notably, the use of SGLT2i has been linked to cardiovascular benefits regardless of DM status, while their pleiotropic actions remain to be fully elucidated. What we do know is that SGLT2i exert beneficial effects even at the level of the myocardial cell and that these are linked to an improvement in the energy substrate, resulting in less inflammation and fibrosis. SGLT2i ameliorates myocardial extracellular matrix remodeling, cardiomyocyte stiffness and concentric hypertrophy, achieving beneficial remodeling of the left ventricle with significant implications for the pathogenesis and outcome of heart failure. Most studies show a significant improvement in markers of diastolic dysfunction along with a reduction in left ventricular hypertrophy. In addition to these effects, there is electrophysiological remodeling, which explains initial data suggesting that SGLT2i have an antiarrhythmic action against both atrial and ventricular arrhythmias. However, future studies need to clarify not only the exact mechanisms of this beneficial functional, structural, and electrophysiological cardiac remodeling but also its magnitude to determine whether this is a class or a drug effect.

Artificial intelligence-based opportunistic screening for the detection of arterial hypertension through ECG signals.

OBJECTIVES: Hypertension is a major risk factor for cardiovascular disease (CVD), which often escapes the diagnosis or should be confirmed by several office visits. The ECG is one of the most widely used diagnostic tools and could be of paramount importance in patients' initial evaluation. METHODS: We used machine learning techniques based on clinical parameters and features derived from the ECG, to detect hypertension in a population without CVD. We enrolled 1091 individuals who were classified as hypertensive or normotensive, and trained a Random Forest model, to detect the existence of hypertension. We then calculated the values for the Shapley additive explanations (SHAP), a sophisticated feature importance analysis, to interpret each feature's role in the Random Forest's results. RESULTS: Our Random Forest model was able to distinguish hypertensive from normotensive patients with accuracy 84.2%, specificity 78.0%, sensitivity 84.0% and area under the receiver-operating curve 0.89, using a decision threshold of 0.6. Age, BMI, BMI-adjusted Cornell criteria (BMI multiplied by RaVL+SV 3 ), R wave amplitude in aVL and BMI-modified Sokolow-Lyon voltage (BMI divided by SV 1 +RV 5 ), were the most important anthropometric and ECG-derived features in terms of the success of our model. CONCLUSION: Our machine learning algorithm is effective in the detection of hypertension in patients using ECG-derived and basic anthropometric criteria. Our findings open new horizon in the detection of many undiagnosed hypertensive individuals who have an increased CVD risk.

Salt-induced effects on microvascular function: A critical factor in hypertension mediated organ damage.

Salt has been linked very closely to the occurrence and complications of arterial hypertension. A large percentage of patients with essential hypertension are salt-sensitive; that is, their blood pressure increases with increased salt intake and decreases with its reduction. For this reason, emphasis is placed on reducing salt intake to better regulate blood pressure. In day-to-day clinical practice this is viewed as mandatory for hypertensive patients who are judged to be salt-sensitive. Previous studies have highlighted the negative effect of high-salt diets on macrovascular function, which also affects blood pressure levels by increasing peripheral resistances. More recent studies provide a better overview of the pathophysiology of microvascular disorders and show that they are largely due to the overconsumption of salt. Microvascular lesions, which have a major impact on the functioning of vital organs, are often not well recognized in clinical practice and are not paid sufficient attention. In general, the damage caused by hypertension to the microvascular network is likely to be overlooked, while reversion of the damage is only rarely considered as a therapeutic target by the treating physician. The purpose of this review is to summarize the impact and the harmful consequences of increased salt consumption in the microvascular network, their significance and pathophysiology, and at the same time to place some emphasis on their treatment and reversion, mainly through diet.

Platelet microRNAs in hypertensive patients with and without cardiovascular disease.

Platelets contain abundant microRNAs (miRs) that regulate gene expression and protein synthesis and may reflect platelet activation. We assessed platelet levels of miR-223, miR-126, and miR-22 in 82 patients with essential hypertension and 28 healthy individuals, using real-time reverse transcription polymerase chain reaction, and evaluated their relation with the patients' clinical profile. Hypertensives had significantly lower platelet miR-22 and miR-223 levels (97.6 ± 170.3 in hypertensives versus 193.8 ± 228.9 in normotensives, p = 0.011, for miR-22; 91.3 ± 154.1 in hypertensives versus 189.9 ± 266.3 in normotensives, p = 0.022, for miR-223). Significant differences in platelet miR levels were also observed between hypertensives who had cardiovascular disease and those who did not (4.1 ± 3.6 versus 75.1 ± 85.2 for miR-126, 24.3 ± 62.9 versus 122.8 ± 187.9 for miR-22, and 10.1 ± 10.4 versus 119.3 ± 169.0 for miR-223, respectively; p < 0.001 for all). In addition, we found a significant negative correlation with systolic blood pressure (SBP) (r = -0.43, p < 0.001, for miR-22; r = -0.47, p < 0.001, for miR-223 in hypertensives; and r = -0.54, p < 0.001, for miR-126). Finally, receiver operating characteristic analysis showed that platelet miR levels were also strong prognostic markers for cardiovascular disease in these patients. In conclusion, platelet miR-22 and miR-223 levels are reduced according to the hypertension status and they are negatively correlated with SBP levels. Platelet miR levels are also related to the presence of overt cardiovascular disease in this population. Further studies are needed to elucidate the exact role of platelet miRs in platelet function and their utility as novel biomarkers of atherothrombotic risk in those patients.

Long-term outcome of hypertensive patients with heart failure with mid-range ejection fraction: The significance of blood pressure control.

Heart failure (HF) with mid-range ejection fraction (HFmrEF) is a newly suggested entity in HF. Since it has been inadequately addressed, there is an urgent need to determine the profile of HFmrEF patients and the optimal approach to their management. The present study aimed to assess the long-term clinical outcomes of hypertensive patients with HFmrEF and the impact of blood pressure (BP) on their mortality and cardiovascular outcome. We performed a retrospective observational study that included 121 hypertensive patients with HFmrEF and 149 hypertensives with heart failure and preserved ejection fraction (HFpEF). The median follow-up was 84 months (22-122). Our analysis did not reveal any statistically significant difference between the two groups in total mortality (P = 0.34) or cardiovascular mortality (P = 0.54). The total mean survival time was 102.9 months (100.5-110.1), while the mean survival time was 105.3 months (80.4-90.2) in HFpEF and 97.6 months (92.7-102.6) in HFmrEF. An office systolic BP > 139 mm Hg and diastolic BP > 89 mm Hg were significantly associated with both all-cause mortality (P = 0.02 and P = 0.013, respectively) and cardiovascular mortality (P = 0.02 for both). In HFpEF patients, no significant association was found between outcome and office BP. HFpEF and HFmrEF have similar long-term outcomes. Suboptimal BP levels are a significant risk factor for an adverse outcome in HFmrEF. Our results emphasize the importance of good BP control in order to achieve better outcomes in hypertensives with impaired EF and HF symptomatology.

MicroRNAs in Peripheral Mononuclear Cells as Potential Biomarkers in Hypertensive Patients With Heart Failure With Preserved Ejection Fraction.

BACKGROUND: MicroRNAs (miRs) regulate gene expression and play an important role in ventricular and vascular remodeling. However, there are limited data regarding their role in heart failure with preserved ejection fraction (HFpEF). The aim of this study was to assess gene expression of miR-1, miR-133a, miR-21, miR-208b, miR-499, and miR-26b in peripheral blood mononuclear cells (PBMCs) in hypertensive patients with HFpEF and to evaluate their association with their exercise capacity. METHODS: We included 56 hypertensive patients with HFpEF (age 67.29 ± 7.75 years). Forty-two hypertensive patients without HFpEF (age 66.83 ± 7.17 years) served as controls. All subjects underwent a cardiopulmonary exercise test (CPXT). PBMCs were isolated and levels of miRs were determined by quantitative real-time reverse transcription polymerase chain reaction. RESULTS: For hypertensive patients with HFpEF, higher expression levels in PBMCs were found only for miR-26b (7.6 ± 7.3 vs. 4.0 ± 3.6, P = 0.002), miR-208b (28.8 ± 35.3 vs. 7.5 ± 13.3, P < 0.001), and miR-499 (14.2 ± 22.4 versus 3.5 ± 2.9, P = 0.001). The strongest correlations with CPXT parameters were found for miR-208b levels, which had a positive correlation with maximal oxygen uptake (peakVO2) (r = 0.671, P < 0.001), exercise duration (r = 0.445, P = 0.001), and minute ventilation-carbon dioxide production relationship (VE/VCO2) (r = 0.437, P = 0.001) in the HFpEF group. CONCLUSIONS: miR-26b, miR-208b, and miR-499 show a distinct in profile in hypertensive patients with HFpEF that is related with functional capacity. Further studies are needed to assess the role of miRs as prognostic tools or as therapeutic targets in those patients.

Endothelial progenitor cells as markers of severity in hypertrophic cardiomyopathy.

AIMS: Endothelial progenitor cells (EPCs) are bone marrow-derived cells that are mobilized into the circulation to migrate and differentiate into mature endothelial cells contributing to post-natal physiological and pathological neovascularization. In this study, we evaluated circulating EPCs in patients with hypertrophic cardiomyopathy (HCM) and examined a potential association with clinical parameters of the disease. METHODS AND RESULTS: We included 40 HCM patients and 23 healthy individuals. Using flow cytometry we measured EPCs in peripheral blood as two subpopulations of CD45-/CD34+/VEGFR2+ and CD45-/CD34+/CD133+ cells. Circulating CD45-/CD34+/VEGFR2+ cells were significantly increased in HCM patients in comparison with the controls (0.000238 ± 0.0003136 vs. 0.000057 ± 0.0001316, respectively, P = 0.002). However, there was no significant difference in the number of circulating CD45-/CD34+/CD133+ cells (0.003079 ± 0.0033288 vs. 0.002065 ± 0.0022173, respectively, P = 0.153). The CD45-/CD34+/VEGFR2+ subpopulation revealed a moderate correlation with LV mass index (r = 0.35, P = 0.026), while both EPC subpopulation levels showed strong positive correlations with th E/e' ratio (r = 0.423, P = 0.007 for CD45-/CD34+/VEGFR2+ and r = 0.572, P < 0.001 for CD45-/CD34+/CD133+). CONCLUSION: HCM patients showed an increased mobilization of EPCs compared with healthy individuals that correlated with diastolic dysfunction. Our findings may open up new dimensions in the pathophysiology, prognostication, and treatment of HCM.

Hypertrophic and antihypertrophic microRNA levels in peripheral blood mononuclear cells and their relationship to left ventricular hypertrophy in patients with essential hypertension.

MicroRNAs regulate several aspects of physiological and pathologic cardiac hypertrophy, and they represent promising therapeutic targets in cardiovascular disease. We assessed the expression levels of the microRNAs miR-1, miR-133a, miR-26b, miR-208b, miR-499, and miR-21, in 102 patients with essential hypertension and 30 healthy individuals. All patients underwent two-dimensional echocardiography. MicroRNA expression levels in peripheral blood mononuclear cells were quantified by real-time reverse transcription polymerase chain reaction. Hypertensive patients showed significantly lower miR-133a (5.06 ± 0.50 vs. 13.20 ± 2.15, P < .001) and miR-26b (6.76 ± 0.53 vs. 9.36 ± 1.40, P = .037) and higher miR-1 (25.99 ± 3.07 vs. 12.28 ± 2.06, P = .019), miR-208b (22.29 ± 2.96 vs. 8.73 ± 1.59, P = .016), miR-499 (10.06 ± 1.05 vs. 5.70 ± 0.91, P = .033), and miR-21 (2.75 ± 0.15 vs. 1.82 ± 0.20, P = .002) expression levels compared with healthy controls. In hypertensive patients, we observed significant negative correlations of miR-1 (r = -0.374, P < .001) and miR-133a (r = -0.431, P < .001) and significant positive correlations of miR-26b (r = 0.302, P = .002), miR-208b (r = 0.426, P < .001), miR-499 (r = 0.433, P < .001) and miR-21 (r = 0.498, P < .001) expression levels with left ventricular mass index. Our data reveal that miR-1, miR-133a, miR-26b, miR-208b, miR-499, and miR-21 show distinct expression profiles in hypertensive patients relative to healthy individuals and they are associated with clinical indices of left ventricular hypertrophy in hypertensive patients. Thus, they may be related to heart hypertrophy in hypertensive patients and are possibly candidate therapeutic targets in hypertensive heart disease.

Evolution of the American College of Cardiology/American Heart Association Clinical Guidelines.

BACKGROUND: The American College of Cardiology (ACC) and the American Heart Association (AHA) have been developing clinical guidelines to assist practicing clinicians. OBJECTIVES: The goal of this study was to evaluate changes in ACC/AHA guideline recommendations between 2008 and 2014. METHODS: The previous and current ACC/AHA guideline documents that were updated between 2008 and June 2014 were compared to determine changes in Class of Recommendation (COR) and Level of Evidence (LOE). Each recommendation was classified as new, dropped, revised, or unchanged, and the changes in evidence were examined. RESULTS: During the study period, 11 guideline documents (9 disease based and 2 interventional procedure based) were updated. The total number of recommendations decreased from 2,067 to 1,869 (321 fewer recommendations in disease-based guidelines and 123 additional recommendations in interventional procedure-based guidelines). The recommendation class distribution of the updated guidelines was 50.1% Class I (previously 50.8%), 39.4% Class II (previously 35.4%), and 10.4% Class III (previously 13.8%) (p = 0.001). The LOE distribution among updated versions was 15.0% for LOE: A (previously 13.3%), 50.8% for LOE: B (previously 41.4%), and 34.2% for LOE C (previously 45.3%) (p < 0.001). Among all guidelines, 859 recommendations were new, 1,339 were dropped, 881 were unchanged in COR and LOE, and 129 were revised. Of the revised guidelines, 75 recommendations had an increase in LOE (the majority from LOE: C to LOE: B); 34 recommendations had a decrease in LOE; and 20 recommendations had class changes. LOE increases were justified by introduction of new randomized controlled trials, new studies, and new meta-analyses. CONCLUSIONS: The ACC/AHA guideline recommendations are undergoing significant changes, becoming more evidence based and scientifically robust with a tendency to exclude recommendations with insufficient scientific evidence.

Circulating mesenchymal stem cells in patients with hypertrophic cardiomyopathy.

BACKGROUND: This study examines the mobilization of mesenchymal stem cells (MSCs) in patients with hypertrophic cardiomyopathy (HCM) compared to healthy individuals. The pathogenesis of myocardial hypertrophy in HCM is not fully understood. MSCs are involved in the process of neovascularization, fibrosis, and ventricular wall remodeling. METHODS AND RESULTS: We included 40 patients with HCM and 23 healthy individuals. Using flow cytometry, we measured MSCs in peripheral blood, as a population of CD45-/CD34-/CD90+ cells and also as a population of CD45-/CD34-/CD105+ cells. The resulting MSC counts were expressed as percentages of the total cells. Patients with HCM were found to have a greater percentage of circulating CD45-/CD34-CD34-/CD90+ cells compared to controls (0.0041±0.005% vs. 0.0007±0.001%, respectively, P<.001). No significant difference in circulating CD45-/CD34-/CD105+ cells in the peripheral blood was found between HCM patients and controls (0.016±0.018% vs. 0.012±0.014%, respectively, P=.4). Notably, circulating CD45-/CD34-/CD90+ cells were positively correlated with left ventricular mass index (r=0.54, P<.001). CONCLUSIONS: Patients with HCM reveal an increased mobilization of MSCs compared to healthy individuals. Although further research is needed to reveal the clinical significance of our findings, our data open a new dimension in the pathophysiology of the disease and may indicate new future therapeutic possibilities.

Increased mobilization of mesenchymal stem cells in patients with essential hypertension: the effect of left ventricular hypertrophy.

Stem cells have great clinical significance in many cardiovascular diseases. However, there are limited data regarding the involvement of mesenchymal stem cells (MSCs) in the pathophysiology of arterial hypertension. The aim of this study was to investigate the circulation of MSCs in patients with essential hypertension. The authors included 24 patients with untreated essential hypertension and 19 healthy individuals. Using flow cytometry, MSCs in peripheral blood, as a population of CD45-/CD34-/CD90+ cells and also as a population of CD45-/CD34-/CD105+ cells, were measured. The resulting counts were translated into the percentage of MSCs in the total cells. Hypertensive patients were shown to have increased circulating CD45-/CD34-/CD90+ compared with controls (0.0069%±0.012% compared with 0.00085%±0.0015%, respectively; P=.039). No significant difference in circulating CD45-/CD34-/CD105+ cells was found between hypertensive patients' and normotensive patients' peripheral blood (0.018%±0.013% compared with 0.015%±0.014%, respectively; P=.53). Notably, CD45-/CD34-/CD90+ circulating cells were positively correlated with left ventricular mass index (LVMI) (r=0.516, P<.001). Patients with essential hypertension have increased circulating MSCs compared with normotensive patients, and the number of MSCs is correlated with LVMI. These findings contribute to the understanding of the pathophysiology of hypertension and might suggest a future therapeutic target.

Circulating endothelial progenitor cells in hypertensive patients with increased arterial stiffness.

The potential association between arterial stiffening and circulating endothelial progenitor cells (EPCs) in patients with essential hypertension was investigated. Pulse wave velocity (PWV) was used to evaluate arterial stiffness in 24 patients with essential hypertension and 19 healthy controls. Blood samples were taken and immunostained with antibodies against the cell surface markers CD34, CD45, and CD133. Using flow cytometry, EPCs as a population of CD45-/CD34+/CD133+ cells were measured. Hypertensive patients were not found to have higher levels of circulating CD45-/CD34+/CD133+ compared with the control group (0.0026%±0.0031% vs 0.0023%±0.0023%, respectively; P=.7). Correlation analysis revealed a strong association between the number of CD45-/CD34+/CD133+ cells and PWV (r=0.58, P<.001), indicating that hypertensive patients with increased PWV have a greater percentage of CD45-/CD34+/CD133+ cells. Data showed a correlation between the number of circulating CD45-/CD34+/CD133+ cells and arterial stiffness, suggesting that those cells might have a role in arterial remodeling.