The association of plasma oxidative status and inflammation with the development of atrial fibrillation in patients presenting with ST elevation myocardial infarction.

Atrial fibrillation (AF) is the most common supraventricular arrhythmia following ST elevation myocardial infarction (STEMI). Oxidative stress and inflammation may cause structural and electrical remodeling in the atria making these critical processes in the pathology of AF. In this study, we aimed to evaluate the association between total oxidative status (TOS), total antioxidative capacity (TAC) and high-sensitivity C-reactive protein (hs-CRP) in the development of AF in patients presenting with STEMI. This prospective cohort study consisted of 346 patients with STEMI. Serum TAC and TOS were assessed by Erel's method. Patients were divided into two groups: those with and those without AF. Predictors of AF were determined by multivariate regression analysis. In the present study, 9.5% of patients developed AF. In the patients with AF, plasma TOS and oxidative stress index (OSI) values were significantly higher and plasma TAC levels were significantly lower compared to those without AF (p = .003, p = .002, p < .0001, respectively). Multivariate regression analysis results showed that, female gender (Odds ratio [OR] = 3.07; 95% Confidence Interval [CI] = 1.26-7.47; p = .01), left atrial diameter (OR =1.28; 95% CI =1.12-1.47; p < .0001), hs-CRP (OR =1.02; 95% CI =1.00-1.03; p = .001) and OSI (OR =1.10; 95% CI =1.04-1.18; p = .001) were associated with the development of AF in patients presenting with STEMI. The main finding of this study is that oxidative stress and inflammation parameters were associated with the development of AF in patients presenting with STEMI. Other independent predictors of AF were female gender, left atrial diameter and hs-CRP.

Relationship between Fragmented QRS Complex and Aortic Stiffness in Chronic Hemodialysis Patients.

OBJECTIVE: This study aimed to evaluate the correlation between fragmented QRS complex (fQRS), aortic stiffness, and diastolic dysfunction in hemodialysis patients. SUBJECTS AND METHODS: A sample of 56 patients who received hemodialysis treatment was stratified into 2 groups according to their electrocardiography (ECG) patterns with or without fQRS. Baseline characteristics and laboratory parameters of patients were documented. Conventional echocardiographic and Doppler echocardiographic procedures were performed in all patients. The mean early (Em) diastolic and late (Am) diastolic myocardial velocities were calculated. These tests were performed before dialysis. The Student t test, Mann-Whitney U test, χ2 test, Spearman correlation, and multivariate linear regression analysis were used to analyze parameters where appropriate. RESULTS: Of the 56 patients under hemodialysis, fQRS in ECG was detected in 26 (46.4%). Echocardiographic evaluation showed that deceleration time (237.57 ± 40.10 ms; p = 0.030), isovolumic relaxation time (126.84 ± 15.62 ms; p < 0.001), early (E)/late (A) ventricular filling velocity (E/A) ratio (1.15 ± 0.40; p ≤ 0.001), and aortic stiffness index value (9.62 ± 4.53; p = 0.016) exhibited a statistical increase in hemodialysis patients with fQRS compared to patients without fQRS. E (58.23 ± 19.96 m/s; p = 0.004), and Em (5.96 ± 2.08 cm/s; p = 0.023) velocity levels were significantly lower in hemodialysis patients with fQRS than patients without fQRS. Aortic stiffness closely correlated with diastolic dysfunction (deceleration time r = 0.273, p = 0.042; isovolumic relaxation time r = 0.497, p < 0.001; E/A ratio r = -0.449, p = 0.001). On multivariate linear regression analysis, fQRS and aortic stiffness were independently associated in hemodialysis patients (ß = 0.321, p = 0.049). CONCLUSIONS: Increased aortic stiffness and left ventricular systolic dysfunction were observed more frequently in hemodialysis patients with fQRS than in patients without fQRS. fQRS is an important determinant of aortic stiffness in hemodialysis patients.

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.

Relationship Between Mean Platelet Volume and Pulmonary Embolism in Patients With Deep Vein Thrombosis.

BACKGROUND: Mean platelet volume (MPV) has been demonstrated to be associated with deep vein thrombosis (DVT). However, its role in the prediction of pulmonary embolism (PE), which is a major complication of DVT, is still unclear. Therefore, we investigated the association of MPV values with acute PE in patients with DVT. METHOD: The study included three groups: patients with DVT and PE (n=98); patients with DVT without PE (n=97); and control group (No DVT, No PE, n=98). We also evaluated DVT patients according to the MPV values on admission and categorised them into two groups: MPV≤9.15 fL (n=82) and MPV>9.15 fL (n=113). RESULTS: MPV was significantly higher in all DVT patients than controls (9.3±0.9 fL vs 7.9±0.7 fL, p<0.001) and in DVT patients with PE than DVT patients without PE (9.9±0.6 fL vs 8.7±0.7 fL, p<0.001). The rate of PE was higher in patients with DVT with MPV>9.15 fL than those with MVP≤9.15 fL (75.2% vs 15.9%, p<0.001). The presence of PE in patients with DVT was independently associated with MPV (OR: 22.19, 95%CI: 9.39-53.19, P<0.001). CONCLUSION: Although our findings should be considered within the limitations of the study, they suggest that MPV measures may be elevated in DVT patients and a higher MPV may be associated with PE in patients with DVT.

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.

Evaluation of total oxidative status and total antioxidant capacity in patients with endemic fluorosis.

The objective of the present study was to determine the plasma total oxidative status (TOS) and total antioxidant capacity (TAC) in patients with endemic fluorosis. A total of 79 (35 males and 44 females; mean age 44.0 ± 11.9 years) patients with endemic fluorosis and 55 (23 males and 32 females; mean age 48.3 ± 8.5 years) age-, sex- and body mass index-matched healthy controls were included in this study. The urine fluoride levels and plasma TOS and TAC levels were measured. The urine fluoride levels of fluorosis patients were significantly higher than control subjects as expected (1.91 ± 0.15 vs. 0.49 ± 0.13 mg/L, respectively; p < 0.001). TOS was significantly higher in fluorosis group than in control group (17.55 ± 3.82 vs. 15.06 ± 4.31 µmol H(2)O(2) Eq/L, respectively; p = 0.001). TAC was significantly lower in fluorosis group than in control group (1.60 ± 0.36 vs. 1.82 ± 0.51 mmol Trolox Eq/L, respectively; p = 0.004). Oxidative stress index (OSI) was significantly higher in fluorosis group than in control group (11.5 ± 3.8 vs. 8.8 ± 3.7, respectively; p < 0.001). Correlation analysis in all the groups indicated that TAC was negatively correlated with urine fluoride (r = -0.25, p = 0.003), TOS was positively correlated with urine fluoride (r = 0.34, p < 0.001) and OSI was positively correlated with urine fluoride (r = 0.36, p < 0.001). The results of our study demonstrate that oxidative stress plays an important role in the pathogenesis of the endemic fluorosis.

Mean platelet volume is increased in infective endocarditis and decreases after treatment.

OBJECTIVES: The aim of this study was to assess the mean platelet volume (MPV), an indicator of platelet activation in patients with infective endocarditis. SUBJECTS AND METHODS: Twenty-nine patients with infective endocarditis and 29 healthy subjects were studied. Plasma MPV values in patients and control subjects were measured on admission and after 2 weeks of specific treatment of infective endocarditis. RESULTS: The MPV was significantly higher among patients with infective endocarditis when compared with the control group (9.86 ± 1.1 vs. 8.0 ± 1.0 fl, respectively; p < 0.01). The MPV values of patients with infective endocarditis decreased significantly after treatment from 9.86 ± 1.1 to 7.86 ± 1.0 fl (p < 0.01). Total platelet counts increased significantly after treatment from 193.4 ± 96.5 × 10(9) to 243.7 ± 92.4 × 10(9) (p = 0.04). CONCLUSION: MPV values were higher in patients with infective endocarditis and decreased significantly after treatment. Elevated MPV values indicate that patients with infective endocarditis have increased platelet activation and infective endocarditis treatment decreases this platelet activation by decreasing MPV.

Elevated mean platelet volume is associated with impaired coronary microvascular function in patients with idiopathic dilated cardiomyopathy.

Attenuated coronary flow reserve (CFR) has been reported in patients with idiopathic dilated cardiomyopathy (IDC). On the other hand increased platelet activity has been demonstrated in patients with congestive heart failure and left ventricular dysfunction. Accordingly, we aimed to investigate whether mean platelet volume (MPV) is increased in patients with IDC and increased MPV correlates with the degree of coronary microvascular dysfunction. MPV was measured in 37 patients with IDC. Each patient with IDC also underwent echocardiographic examination including CFR measurement. Patients with IDC were divided into two groups based on median CFR value (lower CFR group and normal CFR group). MPV was significantly higher in the lower CFR group than in the normal CFR group (9.00 ± 0.56 vs. 8.25 ± 0.76 fl; respectively, p = 0.001). CFR correlated significantly and inversely to MPV (r = -0.475, p = 0.003). Logistic regression analysis revealed that MPV level was the independent predictor of lower CFR (ß = -0.750, p = 0.002). Furthermore, MPV was an accurate predictor of low CFR (p = 0.001); Area under the curve was 82% (95% CI 0.67-0.96). The best cut-off value of MPV to predict low CFR was 8.3 fl with 95% sensitivity and 69% specificity. In conclusion, the present study showed a negative correlation between MPV and CFR in patients with IDC.

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.

Increased plasma neopterin and hs-CRP levels in patients with endemic fluorosis.

Although fluoride induced inflammatory reactions have been shown in animals and in vitro humans, there are few studies about fluoride induced inflammatory reactions in human beings at clinical setting. We aimed to measure the plasma neopterin, a marker of activation of the monocyte/macrophage system, and high sensitivity C-reactive protein (hs-CRP) levels in patients with endemic fluorosis to investigate the possible role of inflammatory processes (monocyte/macrophage activity) in the underlying pathophysiology of fluoride toxicity at clinical level. Plasma neopterin and hs-CRP levels were determined in endemic fluorosis patients and control subjects. Plasma neopterin levels were significantly higher among patients with endemic fluorosis when compared with control group (2.40 ± 0.66 vs. 1.63 ± 0.27 ng/mL respectively; p < 0.001) and plasma hs-CRP levels were also significantly higher among patients with endemic fluorosis when compared with control group (2.41 ± 1.23 vs. 1.93 ± 0.64 mg/L respectively; p < 0.001). Plasma neopterin levels were positively correlated with urine fluoride levels (r = 0.67, p < 0.001) and serum hs-CRP levels were positively correlated with urine fluoride levels (r = 0.36, p < 0.001). We have found that plasma neopterin and hs-CRP levels are increased in patients with endemic fluorosis. We have concluded that inflammation play an important role in the pathophysiology of fluoride toxicity in patients with endemic fluorosis.

Platelet indices in patients with acute pulmonary embolism.

Previous studies have demonstrated that platelet activation occurs in patients with acute pulmonary embolism (PE). The aim of this study was to assess the mean platelet volume (MPV), an indicator of platelet activation in patients with acute PE. The study group consisted of 107 patients with acute PE. Seventy subjects matched for age, gender, body mass index (BMI) and frequency of concomitant diseases served as control group. All patients and control subjects underwent physical examination and echocardiography. We measured MPV values and platelet counts on admission. MPV was significantly higher among patients with acute PE when compared with control group (9.6 ± 1.0 vs. 8.1 ± 0.8 fL respectively; < 0.001). Platelet count was significantly lower among acute PE patients when compared with control group (227.1 ± 77.0 vs. 268.7 ± 58.4 × 10(9)/L, respectively; < 0.001). MPV was correlated with right ventricular (RV) diameter (p < 0.001, r = 0.33) in correlation analysis. In linear regression analysis, MPV was independently correlated with RV dimension (ß = 0.29, p = 0.001). We have shown that MPV, an indicator of platelet activation, was increased in patients with acute PE and it was correlated with RV diameter. Platelet count was decreased in patients with acute PE.

Mean platelet volume is elevated in patients with myocardial infarction with normal coronary arteries, as in patients with myocardial infarction with obstructive coronary artery disease.

Although the majority of cases of acute myocardial infarction are caused by atherosclerotic coronary artery disease (CAD), it can also occur in people with normal coronary arteries. One of the possible mechanisms causing myocardial infarction with normal coronary arteries (MINC) is transient occlusion of the infarct-related artery owing to platelet hyperactivity and thrombosis. Mean platelet volume (MPV), an indicator of platelet activation, has been shown to be elevated in patients with unstable angina and myocardial infarction in the setting of obstructive CAD. However, the value of MPV in patients with MINC is not known. The aim of this study was to assess the MPV in patients with MINC. We retrospectively studied 47 patients with MINC, 63 patients with myocardial infarction resulting from single coronary artery disease (MISC) and 55 control subjects. MPV values were recorded in all study patients and control subjects. The MPV values of patients with MINC and MISC were significantly higher than those of the control group (9.1+/-1.8 and 9.4+/-1.0 versus 8.3+/-1.4 fl; p<0.05 and p<0.001, respectively). There were no significant differences in MPV values between the MINC and MISC groups. We show for the first time that MPV is significantly higher in patients with MINC compared with control subjects. Concurring with previous studies, we also show that MPV is significantly higher in patients with MISC compared to control subjects.

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.

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.

Increased Mean Platelet Volume in Familial Hypercholesterolemia.

Familial hypercholesterolemia (FH) is a genetic disorder of lipoprotein metabolism and increases the risk of premature cardiovascular diseases. In patients with FH, platelet function may be activated; however, the extent of this activation and its etiology are unclear. We aimed to evaluate the mean platelet volume (MPV), a marker of platelet activation, in patients with FH. The study group consisted of 164 patients with FH and 160 control patients. Controls were matched for age, gender, hypertension, and smoking. The MPV was significantly higher in patients with FH than in controls (9.2 ± 0.4 vs 7.9 ± 0.6 fL, respectively; P < .001). Platelet count was significantly lower among patients with FH when compared to control patients (259 ± 51 vs 272 ± 56 × 10(3)/L, respectively; P = .03). In linear regression analysis, MPV was independently associated only with total cholesterol (ß = .6, 95% confidence interval: 0.004-0.008, P < .001). We have shown that MPV was increased in patients with FH and that it was independently associated with total cholesterol level.

Ivabradine on aortic stiffness in patients with heart failure.

AIM: The aim of this study was to evaluate the effect of ivabradine treatment on aortic stiffness by measuring aortic elastic parameters in patients with heart failure (HF) receiving ivabradine treatment. MATERIALS AND METHODS: The study included clinical patients who were diagnosed with HF (ejection fraction, <35%), had sinus rhythm and persistent symptoms despite full medical treatment. The study group consisted of patients with a heart rate greater than 70 beats per minute and the control group consisted of patients with a heart rate less than 70 beats per minute. Echocardiographic measurements were conducted and aortic strain, aortic distensibility, and aortic stiffness index were calculated. RESULTS: By the end of the twelfth month, a decrease was observed in the left ventricular end-diastolic and end-systolic volumes, whereas ejection fraction was increased (P < 0.001). When aortic elastic parameters were evaluated between the 2 groups, there was no significant difference regarding aortic strain, aortic distensibility, and aortic stiffness index at the time of enrollment and during the visit at 3 months. At the twelfth month visit, aortic strain (P < 0.001) and distensibility (P < 0.001) were significantly increased, whereas there was a significant decrease in the aortic stiffness index (P < 0.001). CONCLUSIONS: During the follow-up at 12 months, significant improvements were observed in the left ventricular functions and aortic elastic parameters along with decreased heart rate in patients with HF receiving ivabradine treatment. This outcome may indicate that ivabradine treatment may correct aortic stiffness and may reduce aortic stiffness after 1 year of follow-up.

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.