Low LXA4, RvD1 and RvE1 levels may be an indicator of the development of hypertension.

Vascular structure and integrity are at the forefront of blood pressure regulation. However, there are many factors that affect the responses of the vessels. One of these is the inflammatory processes associated with high cholesterol and its modification. 15-lipoxygenase (15-LOX) is the critical enzyme in cholesterol oxidation, but this enzyme is also responsible for the synthesis of specialized proresoving lipid mediators (SPMs) called Lipoxin (Lxs) and Resolvin (Rvs). In this study, we determined serum LXA4, RvD1 and RvE1 levels in newly diagnosed hypertension (HT) and normotension (NT) cases. We evaluated how the presence of hypercholesterolemia (HC) in the follow-up changes the levels of these SPMs. We found that the three SPMs we measured decreased significantly in the presence of HC. In addition, we found a negative and significant correlation with systolic blood pressure and total cholesterol levels for the three SPMs. In conclusion, HT and HC are independent risk factors for cardiovascular death. However, the presence of HC may be an important factor for the development of HT. Increasing cholesterol levels may cause 15-LOX to shift towards LDL oxidation, thus leading to inflammation. This situation may negatively affect the vascular functions in the regulation of blood pressure. Serum LXA4, RvD1 and RvE1 measurements may provide clues that represent a shift of 15-LOX enzyme activity towards cholesterol.

The effect of fixed-dose combination of valsartan and amlodipine on nighttime blood pressure in patients with non-dipper hypertension.

OBJECTIVE: Failure to decrease blood pressure (BP) during the night is associated with higher cardiovascular (CV) morbidity and mortality. There is strong evidence that fixed-dose combinations (FDCs) of antihypertensive agents are associated with significant improvement and non-significant adverse effects. The aim of the present study was to evaluate whether FDC affected nocturnal BP favorably in patients with uncontrolled, non-dipper hypertension (HT). METHODS: All non-dipper hypertensives were either newly diagnosed with stage 2-3 HT or had HT uncontrolled with monotherapy. Patients (n=195) were consecutively assigned to 4 treatment groups: FDC of valsartan/amlodipine (160/5 mg), free-drug combination of valsartan 160 mg and amlodipine 5 mg, amlodipine 10 mg, and valsartan 320 mg. Ambulatory blood pressure monitoring (ABPM) was repeated at 4th and 8th week. RESULTS: Average 24-h (24-hour) and nocturnal BP were similar among the groups at baseline evaluation, and had significantly decreased by the fourth week of treatment. However, BP continued to decrease only slightly between the 4th and 8th weeks in the valsartan and amlodipine monotherapy groups, but continued to decrease significantly in both combination groups. After 4 weeks, day-night BP difference and day-night BP % change were significantly elevated in the combination and valsartan groups. Between the 4th and 8th weeks, however, day-night BP difference and day-night BP % change continued to rise only in the FDC group, nearly reducing to baseline levels in the free-drug combination and valsartan groups. An additional 2.2 mmHg decrease was observed in the FDC group, compared to the free-drug combination group. CONCLUSION: In non-dipper HT, FDC of valsartan and amlodipine improved diurnal-nocturnal ratio of BP and provided 24-h coverage.

Nebivolol versus Carvedilol or Metoprolol in Patients Presenting with Acute Myocardial Infarction Complicated by Left Ventricular Dysfunction.

OBJECTIVE: The aim of this study was to evaluate the efficacy of nebivolol, carvedilol or metoprolol succinate on the outcome of patients presenting with acute myocardial infarction (AMI) complicated by left ventricular dysfunction. SUBJECTS AND METHODS: Patients (n = 172, aged 28-87 years) with AMI and left ventricular ejection fraction ≤0.45 were randomized to the nebivolol (n = 55), carvedilol (n = 60) and metoprolol succinate (n = 57) groups. Baseline demographic and clinical characteristics and composite event rates of nonfatal MI, cardiovascular mortality, hospitalization due to unstable angina pectoris or heart failure, stroke or revascularization during the 12-month follow-up were compared among the groups using the x03C7;2 test, t test or log-rank test as appropriate. RESULTS: Baseline demographic and clinical characteristics were similar in the three groups. The composite end point during follow-up was lower in the patients treated with nebivolol than those treated with metoprolol (14.5 vs. 31.5%; p = 0.03). However, event rates were similar between the patients treated with carvedilol and those treated with the metoprolol (20.3 vs. 31.5%, p > 0.05) and between the patients treated with nebivolol and carvedilol (14.5 vs. 20.3%, p > 0.05). CONCLUSION: The patients treated with nebivolol experienced 12-month cardiovascular events at a lower rate than those treated with metoprolol succinate. However, event rates were similar between the carvedilol and the metoprolol succinate groups and between the nebivolol and the carvedilol groups.

Gamma glutamyltransferase, inflammation and cardiovascular risk factors in isolated coronary artery ectasia.

INTRODUCTION AND OBJECTIVE: There are conflicting data on the prevalence of cardiovascular risk factors in coronary artery ectasia (CAE). It is unclear whether CAE is associated with high-sensitivity C-reactive protein (hs-CRP) and gamma glutamyltransferase (GGT). We therefore investigated major cardiovascular risk factors, serum GGT and hs-CRP levels in a large population of patients with CAE. METHODS: A total of 167 patients with isolated CAE and 150 controls with normal coronary arteries were selected from 10505 patients undergoing coronary angiography. Serum GGT and hs-CRP levels were evaluated in addition to cardiovascular risk factors including family history, obesity, smoking, diabetes, hypertension and hyperlipidemia. RESULTS: Hypertension and obesity were slightly more prevalent in CAE patients than in controls, whereas diabetes was slightly less frequent in CAE patients. Other risk factors were similar. Serum GGT (22 [17-42] vs. 16 [13-21] U/l, p=0.001) and hs-CRP (2.9 [1.9-3.6] vs. 1.4 [1.1-1.8] mg/l, p=0.001) levels were higher in CAE patients than in controls. The presence of CAE was independently associated with diabetes (OR: 0.44, 95% CI: 0.20-0.95, p=0.04), obesity (OR: 2.84, 95% CI: 1.07-7.56, p=0.04), GGT (OR: 1.08, 95% CI: 1.03-1.12, p=0.001) and hs-CRP levels (OR: 3.1, 95% CI: 2.1-4.6, p=0.001). In addition, GGT and hs-CRP levels were higher in diffuse and multivessel ectasia subgroups than focal and single-vessel ectasia subgroups (each p<0.05). CONCLUSIONS: Our findings show that CAE can be independently and positively associated with obesity, GGT and hs-CRP levels, but inversely with diabetes. Moreover, its severity may be related to GGT and hs-CRP levels.

The effects of good glycaemic control on left ventricular and coronary endothelial functions in patients with poorly controlled Type 2 diabetes mellitus.

OBJECTIVE: Diabetics are at risk for developing overt heart failure and subclinical left ventricular (LV) dysfunction. Also, impaired coronary flow reserve (CFR) reflecting coronary microvascular dysfunction is common in diabetics. However, no substantial data regarding the effects of good glycaemic control on subclinical LV dysfunction and CFR are available. CONTEXT: To investigate whether good glycaemic control had favourable effects on subclinical LV dysfunction and CFR. DESIGN: Prospective, open-label, follow-up study. PATIENTS: Diabetics (n = 202) were classified based on baseline HbA1C levels: patients with good (group 1) (<7·0%) and poor glycaemic control (≥7·0%). MEASUREMENTS: All patients underwent echocardiographic examination at baseline evaluation, and it was repeated at months 6 and 12. Based on HbA1C levels obtained at month 6, the patients with poor glycaemic control were divided into two groups: achieved (group 2) and not achieved good glycaemic control (group 3). RESULTS: The groups were comparable with respect to diastolic function parameters including left atrium diameter, mitral E/A, Sm , Em /Am , E/E' and Tei index, and these parameters did not significantly change at follow-up in the groups. At baseline, CFR was slightly higher in group 1 than in group 2 and group 3, but it did not reach statistically significant level. At follow-up, CFR remained unchanged in group 1 (P = 0·58) and group 3 (P = 0·86), but increased in group 2 (P = 0·02: month 6 vs baseline and P = 0·004: month 12 vs baseline). CONCLUSIONS: Diabetics with poor and good glycaemic control were comparable with respect to echocardiographic parameters reflecting subclinical LV dysfunction, and good glycaemic control did not affect these parameters. However, good glycaemic control improved CFR.

Addition of N-acetyl cysteine to carvedilol decreases the incidence of acute renal injury after cardiac surgery.

BACKGROUND: Oxidative stress and inflammation during cardiac surgery may be associated with acute renal injury (ARI). N-acetyl cysteine (NAC) and carvedilol have antioxidant and anti-inflammatory properties. HYPOTHESIS: A combination of carvedilol and NAC should decrease the incidence of ARI more than metoprolol or carvedilol. METHODS: Patients undergoing cardiac surgery were randomized to metoprolol, carvedilol, or carvedilol plus NAC. End points were occurrence of ARI and change in preoperative to postoperative peak creatinine levels. RESULTS: ARI incidence was lower in the carvedilol plus NAC group compared with the metoprolol (21.0% vs 42.1%; P = 0.002) or carvedilol (21.0% vs 38.6%; P = 0.006) groups, but was similar between the metoprolol and carvedilol groups (P = 0.62). Preoperative and postoperative day 1 creatinine levels were similar among the metoprolol (1.02 [0.9-1.2] and 1.2 [0.92-1.45]) the carvedilol (1.0 [0.88-1.08] and 1.2 [0.9-1.5]) and the carvedilol plus NAC groups (1.06 [0.9-1.18] and 1.1 [1.0-1.21] mg/dL; all P values >0.05). Postoperative day 3, day 5, and peak creatinine levels were lower in the carvedilol plus NAC group (1.11 [1.0-1.23], 1.14 [1.0-1.25] and 1.15 [1.0-1.25]) as compared with the metoprolol (1.4 [1.3-1.49], 1.3 [1.0-1.54] and 1.3 [1.0-1.54]) or carvedilol groups (1.2 [1.0-1.52], 1.25 [1.0-1.52] and 1.25 [1.0-1.55] mg/dL; all P values <0.05), but were similar between the metoprolol and carvedilol groups (all P values >0.05). CONCLUSIONS: Combined carvedilol and NAC decreased ARI incidence as compared with carvedilol or metoprolol. No difference was detected between carvedilol and metoprolol.

Oxidative status, inflammation, and postoperative atrial fibrillation with metoprolol vs carvedilol or carvedilol plus N-acetyl cysteine treatment.

BACKGROUND: Atrial fibrillation is associated with inflammation and oxidative stress. HYPOTHESIS: Carvedilol and N-acetyl cysteine (NAC) combination decreases inflammation, oxidative stress, and postoperative atrial fibrillation (POAF) rates more than metoprolol or carvedilol. METHODS: Preoperative and postoperative total oxidative stress (TOS), total antioxidant capacity (TAC), and white blood cells (WBC) were measured in metoprolol, carvedilol, or carvedilol plus NAC groups, and association with POAF was evaluated. RESULTS: Preoperative TAC, TOS, and WBC levels were similar among the groups. Postoperative TAC levels were lower in the metoprolol group compared with the carvedilol group (1.0 vs 1.4) or the carvedilol plus NAC group (1.0 vs 1.9) and were also lower in the carvedilol group compared with the carvedilol plus NAC group (all P < 0.0001). Postoperative TOS levels were higher in the metoprolol group as compared with the carvedilol (29.6 vs 24.2; P < 0.0001) or the carvedilol plus NAC groups (P < 0.0001), and were also higher in the carvedilol group as compared with the carvedilol plus NAC group (24.2 vs 19.3; P < 0.0001). Postoperative WBC counts were lower in the carvedilol plus NAC group compared with the metoprolol group (12.9 vs 14.8; P = 0.004), were similar between the carvedilol and the metoprolol groups (13 vs 14.8) and between the carvedilol plus NAC group and the carvedilol group (both P > 0.05). Postoperative TAC, TOS, and WBC were associated with POAF. CONCLUSIONS: Carvedilol plus NAC reduced oxidative stress and inflammation compared with metoprolol and decreased oxidative stress compared with carvedilol. Postoperative TAC, TOS, and WBC were associated with POAF.

Increased mean platelet volume in hypertrophic cardiomyopathy.

Thromboembolic events may be seen in patients with hypertrophic cardiomyopathy (HCM). We investigated the mean platelet volume (MPV), an indicator of platelet activation in patients with HCM. This study included 112 patients with HCM, in which 40 were patients with hypertrophic obstructive cardiomyopathy (HOCM), and 106 were control participants. The MPV was significantly higher in patients with HCM than in controls (9.1 ± 0.3 vs 7.9 ± 0.3 fL, P = .01). In the subgroup analyses, MPV was also higher in patients with HOCM compared to those with hypertrophic nonobstructive cardiomyopathy (HNCM; 9.3 ± 0.3 vs 9.0 ± 0.2 fL, P = .01). Similarly, patients with HNCM had higher MPV values than controls (9.0 ± 0.2 vs 7.9 ± 0.3 fL, P = .01). The MPV was significantly and positively correlated with left ventricular outflow tract (LVOT) obstruction (r = .42, P = .001) and septal thickness (r =.62, P = .001). In linear regression analysis, MPV was independently associated only with septal thickness (ß = .07, 95% confidence interval: 0.04-0.09, P = .001). The MPV can be elevated in patients with HCM regardless of the obstruction of LVOT and may be associated with the severity of septal thickness.

Evaluation of plasma oxidative status in patients with slow coronary flow.

BACKGROUND: Slow coronary flow (SCF) is a coronary microvascular disorder characterised by delayed opacification of coronary vessels in a normal coronary angiogram. Coronary endothelial dysfunction plays an important pathogenetic role in patients with SCF. Oxidative stress is associated with cardiovascular diseases. AIM: To assess the total antioxidant capacity (TAC) and total oxidative status (TOS) in patients with SCF. METHODS: The study included 36 patients with SCF. An age- and gender-matched control group was composed of 30 patients with normal coronary arteries and normal coronary flow. We measured plasma TAC and TOS levels and oxidative stress index(OSI) value in patients and control subjects. Linear regression analysis was performed to identify factors associated with the mean TIMI frame count (TFC). RESULTS: Plasma TOS level and OSI value were significantly higher in the SCF group compared to the control group (p = 0.005 and p = 0.004, respectively). However, there was no significant difference in plasma TAC levels between the groups (p = 0.104). Factors associated with mean TFC were plasma TOS levels (ß = 0.425, p = 0.002) and fasting glucose levels (ß = 0.099, p = 0.01) in linear regression analysis. CONCLUSIONS: We found that plasma TOS and OSI were significantly higher in SCF compared to the control group and plasma TOS levels were independently associated with mean TFC.

Effects of prediabetes and diabetes on left ventricular and coronary microvascular functions.

BACKGROUND: Coronary flow reserve (CFR) provides independent prognostic information in diabetic patients with known or suspected coronary artery disease. However, there have been no substantial data to evaluate CFR in prediabetics. Accordingly, we aimed to evaluate CFR in subjects with prediabetes using second harmonic transthoracic Doppler echocardiography. METHODS AND RESULTS: We measured CFR of 65 subjects with prediabetes, 45 patients with overt type 2 diabetes, and 43 sex and age matched normoglycemic healthy subjects with normal glucose tolerance. Ages, gender, existence of hypertension or hypercholesterolemia, smoking status were similar among the groups. CFR was significantly lower in diabetics (2.15 ± 0.39) than in prediabetics (2.39 ± 0.45) and controls (2.75 ± 0.35); in addition, it was significantly lower in prediabetics than controls. Only 2 (5%) of control subjects had abnormal CFR (<2) but 11 (17%) prediabetic subjects and 19 (42%) diabetic patients had abnormal CFR. We found that only age (ß=-0.31, P<0.01) and presence of the diabetes (ß=-0.57, P<0.01) were significant predictors of lower CFR in a multivariable model that adjusted for other variables. CFR was significantly and inversely correlated with age (r=-0.15, P=0.04), fasting glucose level (r=-0.27, P=0.001), postprandial glucose level (r=0.43, P<0.001), hemoglobin A1C level (r=-0.34, P<0.001), LDL cholesterol level (r=0.22, P=0.009), mitral A velocity (r=-0.27, P=0.001) and Tei index (r=-0.19, P=0.02), whereas mitral E/A ratio, mitral Em (r=0.18, P=0.02), mitral Em/Am ratio (r=0.23, P=0.004) were significantly and positively correlated with CFR. CONCLUSION: CFR is impaired in subjects with prediabetics, but this impairment is not as severe as that in diabetics.

Mean platelet volume may be elevated in mitral valve prolapse and associated with the severity of prolapse.

Thromboembolic events can be seen in patients with mitral valve prolapse (MVP). It is unclear whether platelet activation may contribute to these events in patients with MVP. Thus, we aimed to evaluate mean platelet volume (MPV) in patients with MVP and its association with the severity of MVP. This study included 312 patients with MVP and 240 control participants. Mean platelet volume was significantly higher in patients with MVP than in controls (8.9 ± 0.7 vs 7.9 ± 0.6 fL, P = .001). In linear regression analysis, MPV was independently associated with the degree of mitral regurgitation (ß = .23, 95% confidence interval (CI): 0.14-0.32, P = .001), maximal leaflet displacement (ß = .24, 95%CI: 0.17-0.31, P = .001), and mean thickness of the anterior (ß = .47, 95%CI: 0.27-0.61, P = .001) and posterior leaflets (ß = .22, 95%CI: 0.03-0.41, P = .02). Our findings show that MPV can be elevated in patients with MVP and may be independently associated with severity of mitral regurgitation, leaflet displacement, and thickness of the leaflets.

Metoprolol vs. carvedilol or carvedilol plus N-acetyl cysteine on post-operative atrial fibrillation: a randomized, double-blind, placebo-controlled study.

AIMS: Carvedilol and N-acetyl cysteine (NAC) have antioxidant and anti-inflammatory properties. Aim was to evaluate the efficacy of metoprolol, carvedilol, and carvedilol plus NAC on the prevention of post-operative atrial fibrillation (POAF). METHODS AND RESULTS: Patients undergoing cardiac surgery (n = 311) were randomized to metoprolol, carvedilol, or carvedilol plus NAC. Baseline characteristics were similar. The incidence of POAF was lower in the carvedilol plus NAC group compared with the metoprolol group (P < 0.0001) or the carvedilol group (P = 0.03). There was a borderline significance for lower POAF rates in the carvedilol group compared with the metoprolol group (P = 0.06). Duration of hospitalization was lower in the carvedilol plus NAC group compared to the metoprolol group (P = 0.004). Multivariate independent predictors of POAF included left-atrial diameter, hypertension, bypass duration, pre-randomization and pre-operative heart rates, carvedilol plus NAC group vs. metoprolol group, and carvedilol plus NAC group vs. carvedilol group. CONCLUSION: Carvedilol plus NAC decreased POAF incidence and duration of hospitalization compared with metoprolol and decreased POAF incidence compared with carvedilol.

Plasma lipoprotein(a) levels in patients with slow coronary flow.

INTRODUCTION: Slow coronary flow (SCF) is a microvascular disorder characterized by delayed opacification of coronary vessels with normal coronary angiogram. It may be due to endothelial dysfunction and diffuse atherosclerosis. Lipoprotein(a) [Lp(a)] is related to cardiovascular events. Plasma Lp(a) levels have not been studied previously in SCF patients. AIM: We investigated plasma Lp(a) and fibrinogen levels, and their relation to coronary flow rate in patients with SCF. MATERIAL AND METHODS: This cross-sectional study included 50 patients with SCF and 30 age- and sex-matched controls who had normal coronary arteries and normal flow. Coronary flow rates of patients and controls were counted with the thrombolysis in myocardial infarction (TIMI) frame count. Plasma Lp(a) and fibrinogen levels were measured in SCF patients and controls, with routine biochemical tests. RESULTS: There were no significant differences between the two groups with respect to plasma Lp(a) (21 mg/dl vs. 14 mg/dl, p = 0.11) and fibrinogen (278 mg/dl vs. 291 mg/dl, p = 0.48) levels. The TIMI frame count was not correlated with plasma Lp(a) (r = 0.13, p = 0.25) or fibrinogen (r = -0.14, p = 0.28) levels. CONCLUSIONS: Our results show that there is no significant association between SCF and Lp(a) and fibrinogen levels.

Plasma concentrations of asymmetric dimethylarginine, nitric oxide and homocysteine in patients with slow coronary flow.

OBJECTIVES: Slow coronary flow (SCF) is slow progression of contrast agent in the coronary arteries in the absence of stenosis in epicardial coronary vessels. Endothelial dysfunction and diffuse atherosclerosis have been proposed for the etiology of SCF. Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthesis, levels are associated with an increased risk of endothelial dysfunction and atherosclerosis. ADMA levels may be increased by homocysteine. The aim of this study was to evaluate the relationship between ADMA, nitric oxide and homocysteine in patients with SCF. METHODS: The study group consisted of 50 patients with SCF. An age- and gender-matched control group was composed of 30 patients with normal coronary arteries and normal coronary flow on coronary angiography. We measured ADMA, nitric oxide and homocysteine plasma concentrations in all patients. RESULTS: Plasma nitric oxide concentrations were significantly lower in the SCF group than in the control group (11.4 ± 6, 16.1 ± 9, p = 0.02). Plasma ADMA concentrations (0.9 ± 0.3, 0.7 ± 0.3, p = 0.01) and plasma homocysteine concentrations (12.4 ± 5, 9.8 ± 2, p = 0.03) were significantly higher in the SCF group than control group. The mean TIMI frame count (TFC) was significantly correlated with plasma ADMA (r = 0.26, p = 0.02) and homocysteine (r = 0.28, p = 0.02) concentrations, but not with nitric oxide concentrations (r = - 0.18, p = 0.13). In linear regression analysis, plasma ADMA concentrations (ß = 4.6, p = 0.005) and homocysteine concentrations (ß = 0.2, p = 0.03) were independently and positively associated with mean TFC. CONCLUSION: Our results suggest that plasma concentrations of ADMA and homocysteine are increased in SCF and also that these are independent predictors of SCF.

Elevated carbohydrate antigen 125 levels in patients with aortic stenosis: relation to clinical severity and echocardiographic parameters.

OBJECTIVES: Carbohydrate antigen 125 (CA 125), known as a tumor marker for ovarian cancer, has been reported to increase in relation to disease severity in heart failure patients with systolic dysfunction. Aortic stenosis (AS) has a wide clinical spectrum that often includes heart failure symptoms. The purpose of the present study is to evaluate the serum levels of CA 125 in patients with AS and its relation to clinical severity and echocardiographic parameters. STUDY DESIGN: The study group consisted of 42 patients (20 males, 22 females, mean age 62.5 ± 14.9 years) with AS and 35 healthy controls (17 men, 18 women; mean age 59.0 ± 9.1 years). All patients and control subjects underwent chest X-ray and echocardiographic evaluation. We measured serum CA 125 values in patients with AS and control subjects. RESULTS: The median (interquartile range) CA 125 level was significantly higher among AS patients than in the control group in covariate analysis (9.4 [2.5-38.1] vs. 6.8 [4.4-13.9] U/ml respectively; p=0.001). Spearman correlation analysis in the whole group indicated that CA 125 was positively correlated with aortic mean gradient (p=0.007, r=0.30) and creatinine levels (p=0.02, r=0.26). CONCLUSION: We found that CA 125 levels were elevated in patients with AS and were correlated with mean gradient and creatinine levels.

Percutaneous mitral balloon valvuloplasty reduces mean platelet volume in patients with rheumatic mitral stenosis.

BACKGROUND: Rheumatic mitral stenosis (RMS) is associated with increased thromboembolic event, especially in the presence of concomitant atrial fibrillation. In addition, increased platelet activity including elevated mean platelet volume (MPV) has been demonstrated in patients with RMS. It has also been reported that percutaneous mitral balloon valvuloplasty (PMBV) attenuates platelet activity. However, the impact of PMBV on MPV has never been studied. Accordingly, we aimed to investigate whether PMBV decreases MPV in patients with RMS. METHODS: In the present study, MPV was measured in 20 patients with RMS planned for PMBV just before and 1 month after the procedure. Twenty sex- and age- matched apparently healthy controls were used for comparison. Mitral valve area (MVA), transmitral gradient (TMG) and pulmonary artery pressure (PAP) were measured using transthoracic echocardiography. RESULTS: As compared to apparently healthy controls, patients with RMS had higher MPV (9.05 ± 1.26 vs. 7.56 ± 0.74 fl, p < 0.001). All patients with RMS underwent successful PMBV. One month after the procedure, MVA, TMG and PAP were reduced significantly (p < 0.0001). As compared to values obtained before the procedure, white blood cell count, hemoglobin concentration and hematocrit remained unchanged. However, 1 month after the procedure platelet count had increased (p < 0.05) and MPV decreased significantly (to 7.78 ± 0.59, p < 0.0001). PMBV induced an absolute decrease in MPV more than 0.2 fl in 19 of 20 patients (95%). CONCLUSIONS: As compared to apparently healthy controls, patients with RMS have higher MPV reflecting increased platelet activity, and PMBV is associated with a significant decrease in MPV 1 month after the procedure.

Echocardiographic predictors of progression from prehypertension to hypertension.

BACKGROUND: Prehypertension (PHT) was recently introduced by replacing former categories of high-normal and above-optimal blood pressure (BP). The rationale for redefining this new category was to emphasize the excess cardiovascular risk associated with BP in this range and to focus high risk for developing hypertension (HT). However, no clear definite markers to identify prehypertensive patients at high risk of progressing to HT have been established yet. Accordingly, we aimed to establish echocardiographic predictors of progression from PHT to HT. METHODS AND RESULTS: The study population consisted of 98 eligible prehypertensive patients. All patients underwent echocardiographic examination including coronary flow reserve (CFR) at baseline. Twenty-nine (30%) patients developed HT during the 3-year follow-up period. Creatinine level, left ventricular mass index (LVMI), mitral Em and Em/Am had a trend towards a significant crude odds ratio (OR) for the development of HT; however, only baseline SBP [OR = 1.18, 95% confidence interval (CI) = 1.06-1.31; P = 0.002), having metabolic syndrome (OR = 3.75, 95% CI = 1.43-9.78; P = 0.007), high-density lipoprotein (HDL) cholesterol (OR = 0.92, 95% CI = 0.86-0.98; P = 0.01), presence of microalbuminuria (OR = 3.53, 95% CI = 1.11-11.2; P = 0.03) and CFR (OR = 0.65, 95% CI = 0.53-0.77; P = 0.02) were significant independent predictors of progression of PHT into HT. The best cutoff value of CFR to predict incident HT was 1.98 with 94% sensitivity and 79% specificity. CONCLUSION: This prospective study suggested that baseline SBP, having metabolic syndrome, HDL cholesterol level, presence of microalbuminuria and CFR reflecting coronary microvascular function, but not left ventricular diastolic function parameters, were significant independent markers to identify participants with PHT at high risk for incident HT.

The effects of continuous positive airway pressure therapy on mean platelet volume in patients with obstructive sleep apnea.

Previous studies have reported increased platelet activation and aggregation in patients with obstructive sleep apnea (OSA). Continuous positive airway pressure (CPAP) treatment has been shown to decrease platelet activation. We aimed to study the effects of nasal CPAP therapy has on MPV values in patients with severe OSA. Thirty-one patients (21 men; mean age 53.8 ± 9.2 years) with severe OSA (AHI > 30 events/hour) constituted the study group. An age, gender and body mass index (BMI) matched control group was composed 25 subjects (14 men; mean age 49.6 ± 8.5 years) without OSA (AHI < 5 events/hour). We measured MPV values in patients with severe OSA and control subjects and we measured MPV values after 6 months of CPAP therapy in severe OS patients. The median (IQR) MPV values were significantly higher in patients with severe OSA than in control group (8.5 [8.3-9.1] vs. 8.3 [7.5-8.8] fL; p = 0.03). The platelet counts were significantly lower in patients with severe OSA than in control group (217.8 ± 45.9 vs. 265.4 ± 64.0 × 109/L; p = 0.002). The six months of CPAP therapy caused significant reductions in median (IQR) MPV values in patients with severe OSA (8.5 [8.3-9.1] to 7.9 [7.4-8.2] fL; p < 0.001). Six months of CPAP therapy caused significant increase in platelet counts when compared with baseline values (217.8 ± 45.9 to 233.7 ± 60.6 × 109/L; p < 0.001). We have found that the MPV values of patients with severe OSA were significantly higher than those of the control subjects and 6 months CPAP therapy caused significant reductions in the MPV values in patients with severe OSA.