Relation between the Change in Mean Platelet Volume and Clopidogrel Resistance in Patients Undergoing Percutaneous Coronary Intervention.

We aimed to determine the association between the change in mean platelet volume (MPV) over time and aspirin/ clopidogrel resistance in patients undergoing percutaneous coronary intervention (PCI). The MPV and platelet function were analysed in 302 patients who underwent PCI. MPV changes were associated with increased aspirin reaction units (ARU, r = 0.114; P = 0.047), increased P2Y12 reaction units (PRU, r = 0.193; P = 0.001), and decreased P2Y12% inhibition (PI%, r = - 0.273; P < 0.001). The group with increasing MPV values showed significantly higher PRU values and lower PI% compared with the group with decreasing MPV values (222.5 ± 73.9 vs. 195.6 ± 63.7 PRU, P = 0.001; 24.1 ± 21.0 vs. 32.8 ± 18.5 PI%, P < 0.001, respectively). The clopidogrel resistant group (≥235 PRU or ≤15% of PI%) showed a significantly higher positive change in MPV (ΔMPV) values than the clopidogrel responder group (0.53 ± 0.78 vs. 0.13 ± 0.69 fL, P < 0.001). When the ΔMPV cut-off level was set at 0.20 fL using the receiver operating characteristic curve, the sensitivity and specificity for differentiating between the clopidogrel resistant and responder groups were 72.6% and 59.3%, respectively. After adjusting for traditional risk factors, the odds ratio in the clopidogrel resistant group with ΔMPV ≥0.2 fL was 4.10 (95% confidence interval; 1.84-9.17). In conclusion, ΔMPV was associated with PRU and PI%; a positive ΔMPV was an independent predictive marker for clopidogrel resistance after PCI.

Prediction of infarct severity from triiodothyronine levels in patients with ST-elevation myocardial infarction.

BACKGROUND/AIMS: The aim of the present study was to evaluate the relationship between thyroid hormone levels and infarct severity in patients with ST-elevation myocardial infarction (STEMI). METHODS: We retrospectively reviewed thyroid hormone levels, infarct severity, and the extent of transmurality in 40 STEMI patients evaluated via contrast-enhanced cardiac magnetic resonance imaging. RESULTS: The high triiodothyronine (T3) group (≥ 68.3 ng/dL) exhibited a significantly higher extent of transmural involvement (late transmural enhancement > 75% after administration of gadolinium contrast agent) than did the low T3 group (60% vs. 15%; p = 0.003). However, no significant difference was evident between the high- and low-thyroid-stimulating hormone/free thyroxine (FT4) groups. When the T3 cutoff level was set to 68.3 ng/dL using a receiver operating characteristic curve, the sensitivity was 80% and the specificity 68% in terms of differentiating between those with and without transmural involvement. Upon logistic regression analysis, high T3 level was an independent predictor of transmural involvement after adjustment for the presence of diabetes mellitus (DM) and the use of glycoprotein IIb/IIIa inhibitors (odds ratio, 40.62; 95% confidence interval, 3.29 to 502; p = 0.004). CONCLUSIONS: The T3 level predicted transmural involvement that was independent of glycoprotein IIb/IIIa inhibitor use and DM positivity.

Stroke prevention in patients with non-valvular atrial fibrillation: new insight in selection of rhythm or rate control therapy and impact of mean platelet volume.

The aim of this study was to determine the impact of mean platelet volume (MPV) on the strategy for treatment of atrial fibrillation (AF) with respect to stroke prevention. MPV was analyzed in 265 patients with AF who were undergoing treatment using rhythm or rate control. The primary endpoint was ischemic stroke or a transient ischemic attack (TIA) event. Kaplan-Meier analysis revealed a significantly higher stroke rate in the rate control group compared to the rhythm control group. A significantly higher stroke rate was observed in the higher tertile MPV group (≥7.9 fL) compared to the lower tertile MPV group (<7.3 fL). When the MPV cut-off level was set to 7.85 fL using the receiver operating characteristic curve, the sensitivity was 80.0% and the specificity was 70.4% for differentiating between the group with stroke and the group without stroke. In the Cox proportional hazard analysis, after adjusting for sex, treatment strategy for AF, high MPV level, antithrombotic treatment, and high CHADS2 score, higher MPV, rate control strategy for treatment of AF, and high CHADS2 score were found to be independent predictors of stroke risk. In addition, patients with AF who were treated using rate control had high stroke risk with an MPV over 7.85 fL and high CHADS2 score. The results of this study demonstrate that the MPV and the rate control strategy for treatment of AF were predictive markers for stroke; its predictive power for stroke was independent of female sex and high CHADS2 score in patients with AF.

Stroke or coronary artery disease prediction from mean platelet volume in patients with type 2 diabetes mellitus.

The aim of this study was to determine the association of mean platelet volume (MPV) with the development of stroke or coronary artery disease (CAD) in diabetes mellitus (DM). MPV was analyzed in 200 Korean patients with DM. The primary endpoint was composite of ischemic stroke/CAD events. The mean MPV was 7.6 ± 0.8 fl. There were 14 ischemic stroke events and 8 CAD events during a mean of 28.4 months of follow-up. The Kaplan-Meier analysis revealed that the higher tertile MPV group (≥7.9 fl) had a significantly higher stroke/CAD rate compared to the lower tertile MPV group (≤7.3 fl) (29.9% vs. 2.8%, log-rank: p < 0.001). Higher MPV was an independent predictor of stroke/CAD risk after adjusting for 10-year risk ≥10%, hypertension, dyslipidemia, and previous stroke or transient ischemic attack history (hazard ratio: 11.92, 95% confidence interval 2.68-52.92, p = 0.001) in the Cox proportional hazard analysis. When the MPV cut-off level was set to 7.95 fl using the receiver operating characteristic curve, the sensitivity was 91% and the specificity was 80% for differentiating between the group with stroke/CAD and the group without stroke/CAD. This value was more useful in patients with hypertension. The results of this study show that MPV is a predictive marker for stroke/CAD; its predictive power for stroke/CAD is independent of age, gender, hypertension, and hemoglobin A1C.

Predictive value of brachial-ankle pulse wave velocity for cardiovascular events.

BACKGROUND: The aim of this study was to determine the association of pulse wave velocity or left ventricular diastolic function with the development of cardiovascular (CV) events. METHODS: Brachial-ankle pulse wave velocity (baPWV) and E/E' were analyzed in 185 patients. The primary end point was CV events including ischemic stroke, coronary arterial disease (CAD), peripheral arterial disease and aortic dissection. RESULTS: There were 30 CV events during a mean follow-up period of 19.8 months. When the baPWV cutoff level was set to 1704 cm/s using the receiver operating characteristic curve, the sensitivity was 70/92% and the specificity 63/62% for differentiating between the group with and without CV events or ischemic stroke. In univariate analysis with the Cox proportional hazard model, higher baPWV was a predictor for CV events and ischemic stroke events. However, high E/E' (>15) was not a predictor for CV, ischemic stroke events or CAD. A higher baPWV was an independent predictor for CV and ischemic stroke risk after adjusting for age, sex, hypertension and diabetes in the Cox proportional hazard analysis. In subgroup analysis, diabetic patients with a baPWV >1704 cm/s had a high CV event and ischemic stroke risk. CONCLUSIONS: The results of this study show that higher baPWV was a predictive marker for CV events, especially ischemic stroke. The subgroup analysis suggests that antiplatelet therapy may be needed in diabetic patients with a high baPWV for prevention of ischemic stroke.

Stroke prediction using mean platelet volume in patients with atrial fibrillation.

Platelet size, measured as mean platelet volume (MPV), is associated with platelet reactivity. MPV has been identified as an independent risk factor for future stroke and myocardial infarction. The aim of this study was to determine the association of MPV with the development of stoke in patients with atrial fibrillation (AF). MPV, N-terminal pro B-type natriuretic peptide (NT-proBNP), and high-sensitivity C-reactive protein (hsCRP) were analysed in 200 patients with AF (mean age 69 years; 56% male). The primary endpoint was ischaemic stroke event. The mean MPV was 8.5 ± 1.0 fL and the median NT-proBNP was 1916.5 (IQR 810-4427) pg/mL. The median hsCRP was 0.47 (IQR 0.32-2.46) mg/dL. There were 14 stroke events during a mean of 15.1 months of follow up. Kaplan-Meier analysis revealed that the higher tertile MPV group (≥8.9 fL) had a significantly higher stroke rate compared to the lower tertile MPV group (<8.0 fL) (14.7% vs. 3.1%, log-rank: P = 0.01). A higher MPV was an independent predictor of stroke risk after adjusting for age, gender, and other CHADS(2) (congestive heart failure, hypertension, diabetes, and previous stroke or transient ischemic attack (TIA) history) score components (hazard ratio: 5.03, 95% CI 1.05-24.05, P = 0.043) in Cox proportional hazard analysis. When the MPV cut-off level was set to 8.85 fL using the receiver operating characteristic curve, the sensitivity was 71% and the specificity was 69% for differentiating between the group with stroke and the group without stroke. This value was more useful in patients with a low to intermediate traditional thromboembolic risk (CHADS(2) score <2). Furthermore, AF patients with an MPV over 8.85 fL had high stroke risk without anticoagulation, especially in the low thromboembolic risk group (Log-Rank <0.0001). The results of this study show that MPV was a predictive marker for stroke; its predictive power for stroke was independent of age, gender, and other CHADS(2) score components in patients with AF. These findings suggest that anticoagulation may be needed in patients with a high MPV, even if they have low to intermediate traditional thromboembolic risk (CHADS(2) score <2).

Non-invasive recognition of generalized coronary arteriosystemic fistulae by contrast echocardiography and multidetector CT.

Coronary artery fistulae, including generalized coronary arteriosystemic fistulae, are usually identified incidentally during invasive coronary angiographies. Generalized or multiple coronary arteriosystemic fistulae arise from all three major coronary arteries draining into the left ventricular chamber. In a patient with generalized coronary arteriosystemic fistulae, myocardial ischemia and diastolic volume overload of the left ventricle can be caused by a left-to-left shunt; however, the clinical and hemodynamic consequences are incompletely understood. We report the case of generalized coronary arteriosystemic fistulae in a 73-year-old female who presented with mild exertional dyspnea as an anginal equivalent. This case report represents the complementary, non-invasive role of transthoracic contrast echocardiography and multidetector computed tomography (MDCT) coronary angiography in the early recognition of generalized coronary arteriosystemic fistulae by demonstrating a plexus of multiple small vessels emptying exclusively into the left ventricle.

Effects of lovastatin on the pharmacokinetics of diltiazem and its main metabolite, desacetyldiltiazem, in rats: possible role of cytochrome P450 3A4 and P-glycoprotein inhibition by lovastatin.

OBJECTIVES: The purpose of this study was to examine the effects of lovastatin on cytochrome P450 (CYP) 3A4 and P-glycoprotein (P-gp) in vitro and then to determine the effects of lovastatin on the pharmacokinetics of diltiazem and its main metabolite, desacetyldiltiazem, in rats. METHODS: The pharmacokinetic parameters of diltiazem and desacetyldiltiazem were determined after orally administering diltiazem (12 mg/kg) to rats in the presence and absence of lovastatin (0.3 and 1.0 mg/kg). The effect of lovastatin on P-gp as well as CYP3A4 activity was also evaluated. KEY FINDINGS: Lovastatin inhibited CYP3A4 enzyme activity with a 50% inhibition concentration of 6.06 µM. In addition, lovastatin significantly enhanced the cellular accumulation of rhodamine-123 in MCF-7/ADR cells overexpressing P-gp. Compared with the control (given diltiazem alone), the presence of lovastatin significantly altered the pharmacokinetic parameters of diltiazem. The areas under the plasma concentration-time curve (AUC) and the peak concentration of diltiazem were significantly increased (P < 0.05, 1.0 mg/kg) in the presence of lovastatin. Consequently, the absolute bioavailability values of diltiazem in the presence of lovastatin (11.1% at 1.0 mg/kg) were significantly higher (P < 0.05) than that of the control group (7.6%). The metabolite-parent AUC ratio in the presence of lovastatin (1.0 mg/kg) was significantly (P < 0.05) decreased compared with the control group. CONCLUSIONS: It might be considered that lovastatin resulted in reducing the first-pass metabolism in the intestine and/or in the liver via inhibition of CYP3A4 and increasing the absorption of diltiazem in the intestine via inhibition of P-gp by lovastatin.

A case of iatrogenic aortic valve leaflet perforation after closure of a ventricular septal defect.

Aortic regurgitation caused by leaflet perforation is most frequently seen in association with infective endocarditis that involves the aortic valve. There have been occasional reports of iatrogenic aortic regurgitation caused by aortic valve injury after cardiac surgery with the use of the transaortic approach or invasive cardiac procedures. Suture-related aortic valve injury can develop during periaortic cardiac surgery, but this has been very rarely reported. Inadvertent injury to an aortic valve leaflet caused by a stitching needle or surgical forceps can produce leaflet perforation with aortic regurgitation. This report describes a case of aortic regurgitation that was caused by iatrogenic aortic valve leaflet perforation, and this occurred in a 22-year-old woman who underwent repair of a ventricular septal defect (VSD) 15 years previously. Transthoracic echocardiography (TTE) showed a defect located at the aortic annulus close to the infundibular septum on a two-dimensional echocardiographic study and we observed an eccentric jet flow into the left ventricle in early diastole on the continuous wave and color flow Doppler studies. A small perforation in the body of the right aortic cusp and mild to moderate aortic regurgitation were confirmed by the use of transesophageal echocardiography (TEE) and ascending aortography.

Effects of lovastatin on the pharmacokinetics of verapamil and its active metabolite, norverapamil in rats: possible role of P-glycoprotein inhibition by lovastatin.

This study was to investigate the effect of lovastatin on the bioavailability or pharmacokinetics of verapamil and its major metabolite, norverapamil, in rats. The pharmacokinetic parameters of verapamil and norverapamil in rats were measured after the oral administration of verapamil (9 mg/kg) in the presence or absence of lovastatin (0.3 or 1.0 mg/kg). The pharmacokinetic parameters of verapamil were significantly altered by the presence of lovastatin compared to the control group (given verapamil alone). The presence of lovastatin significantly (p < 0.05, 0.3 mg/kg; p < 0.01, 1.0 mg/kg) increased the total area under the plasma concentration-time curve (AUC) of verapamil by 26.5-64.8%, and the peak plasma concentration (C(max)) of verapamil by 34.1-65.9%. Consequently, the relative bioavailability (R.B.) of verapamil was increased by 1.27- to 1.65-fold than that of the control group. However, there was not significant change in the time to reach the peak plasma concentration (T(max)) and the terminal half-life (t(1/2)) of verapamil in the presence of lovastatin. The AUC and C(max) of norverapamil were significantly (p < 0.05) higher than those of presence of 1.0 mg/kg of lovastatin compared with the control group. However, there was no significant change in the metabolite-parent ratio (M.R.) of norverapamil in the presence of lovastatin. The presence of lovastatin significantly enhanced the oral bioavailability of verapamil. The enhanced oral bioavailability of verapamil may be due to inhibition both of the CYP3A-mediated metabolism and the efflux pump P-glycoprotein (P-gp) in the intestine and/or in liver by the presence of lovastatin.

Effects of resveratrol on the pharmacokinetics of diltiazem and its major metabolite, desacetyldiltiazem, in rats.

The purpose of this study was to investigate the effects of resveratrol, an antioxidant, on the pharmacokinetics of diltiazem and its active metabolite, desacetyldiltiazem, in rats. The pharmacokinetic parameters of diltiazem and desacetyldiltiazem were determined after an oral administration of diltiazem (15 mg/kg) to rats in the presence and absence of resveratrol (0.5, 2.5, and 10 mg/kg). Compared to the control group, the presence of resveratrol significantly (P < 0.05) increased the area under the plasma concentration-time curve (AUC) of diltiazem, except for resveratrol 0.5 mg/kg. Consequently, the absolute bioavailability (AB) of diltiazem in the presence of resveratrol (2.5 and 10 mg/kg) was significantly (P < 0.05) higher (10.2-11.1%) than that of the control (6.9%). The relative bioavailability (RB) of diltiazem in the presence of resveratrol (2.5 and 10 mg/kg) was increased by 1.48- to 1.60-fold. Resveratrol did not alter absorption rate constant (K(a)) and the time to reach the peak concentration (T(max)) of diltiazem. The AUC of desacetyldiltiazem was increased significantly (P < 0.05) in the presence of 10 mg/kg of resveratrol. The metabolite-parent AUC ratio (MR) in the presence of resveratrol was decreased but did not show significant change. In conclusion, resveratrol significantly increased the bioavailability of diltiazem due to the inhibition of both the cytochrome P450 (CYP) 3A4-mediated metabolism and the efflux pump P-glycoprotein (P-gp) in the intestine and/or liver. Based on these results, if these results would be confirmed in clinical experiments, the dosage of diltiazem should be readjusted when diltiazem is used concomitantly with resveratrol.

N-terminal pro B-type natriuretic peptide and the evaluation of cardiac dysfunction and severity of disease in cirrhotic patients.

PURPOSE: Cardiac dysfunction and hyperdynamic systemic circulation may be present in patients with cirrhosis. The purpose of this study was to identify relations between plasma levels of N-terminal-proBNP (NT-proBNP), reflecting early ventricular dysfunction, and the severity of liver disease and cardiac dysfunction in cirrhotic patients. MATERIALS AND METHODS: Sixty-three cirrhotic patients and 15 controls (group 1) were enrolled in this study. Plasma levels of NT-proBNP were determined in echocardiographically examined patients, which were allocated to 1 of 3 groups according to Child-Pugh classification or into 2 groups, i.e., a compensated group without ascites (group 2) and decompensated group with ascites (group 3). RESULTS: Plasma NT-proBNP levels were significantly higher in cirrhotic patients (groups 2 and 3) than in age-matched controls (155.9 and 198.3 vs. 40.3 pg/mL, respectively, p < 0.05). NT-proBNP levels were significantly increased in Child class C patients than in classes B and A (250.0 vs. 168.6 and 119.6 pg/mL, respectively, p < 0.05). Left atrial dimension, wall thickness of left ventricle, and EF or E/E' were significantly increased, and EDT was prolonged in cirrhotic patients than in controls. Increased LVMI and decreased E/A ratio were noted in the group of patients with ascites as compared with the other groups. CONCLUSION: Plasma NT-proBNP levels were high in cirrhotic patients and are likely to be related to the severity of disease. Advanced cirrhosis is associated with advanced cardiac dysfunction, and NT-proBNP levels has predictive value for concomitant cardiac dysfunction and cirrhosis progression.

Effect of atorvastatin on the intravenous and oral pharmacokinetics of verapamil in rats.

The present study aimed to investigate the effect of atorvastatin on the intravenous and oral pharmacokinetics of verapamil in rats. The pharmacokinetic parameters of verapamil were measured after an oral (9 mg/kg) or intravenous (3 mg/kg) administration of verapamil to rats in the presence and absence of atorvastatin. Compared with the control given verapamil alone, the concurrent use of 1.5 mg/kg of atorvastatin significantly increased the oral exposure of verapamil in rats. The AUC and C(max) of verapamil increased by 70% and 61%, respectively in the presence of atorvastatin (1.5 mg/kg), while there was no significant change in T(max) and the terminal plasma half-life (T(1/2)) of verapamil. Accordingly, the presence of atorvastatin significantly (p<0.05) increased the bioavailability of verapamil in rats. In contrast, atorvastatin had no effect on any pharmacokinetic parameters of verapamil given intravenously, implying that atorvastatin may improve the oral bioavailability of verapamil by reducing the prehepatic extraction of verapamil most likely mediated by P-gp and/or CYP3A4. In conclusion, coadministration of atorvastatin significantly enhanced the oral exposure of verapamil in rats without a change in the systemic clearance of intravenous verapamil, suggesting a potential drug interaction between verapamil and atorvastatin via the modulation of prehepatic extraction.

Effect of atorvastatin on the pharmacokinetics of diltiazem and its main metabolite, desacetyldiltiazem, in rats.

The purpose of this study was to investigate the effect of atorvastatin, HMG-CoA reductase inhibitor, on the pharmacokinetics of diltiazem and its active metabolite, desacetyldiltiazem, in rats. Pharmacokinetic parameters of diltiazem and desacetyldiltiazem were determined in rats after oral administration of diltiazem (15 mg x kg(-1)) to rats pretreated with atorvastatin (0.5 or 2.0 mg x kg(-1)). Compared with the control (given diltiazem alone), the pretreatment of atorvastatin significantly altered the pharmacokinetic parameters of diltiazem. The peak concentration (Cmax) and the areas under the plasma concentration-time curve (AUC) of diltiazem were significantly (p < 0.05, 0.5 mg x kg(-1); p < 0.01, 2.0 mg x kg(-1)) increased in the presence of atorvastatin. The AUC of diltiazem was increased by 1.40-fold in rats pretreated with 0.5 mg x kg(-1) atorvastatin, and 1.77-fold in rats pretreated with 2.0 mg x kg(-1) atorvastatin. Consequently, absolute bioavailability values of diltiazem pretreated with atorvastatin (8.4-10.6%)were significantly higher (p < 0.05) than that in the control group (6.6%). Although the pretreatment of atorvastatin significantly (p < 0.05) increased the AUC of desacetyldiltiazem, metabolite-parent AUC ratio (M.R.) in the presence of atorvastatin (0.5 or 2.0 mg x kg(-1)) was significantly decreased compared to the control group, implying that atorvastatin could be effective to inhibit the metabolism of diltiazem. In conclusion, the concomitant use of atorvastatin significantly enhanced the oral exposure of diltiazem in rats.

Effect of anabasine on catecholamine secretion from the perfused rat adrenal medulla.

OBJECTIVES: The present study was designed to investigate the characteristic effects of anabasine on secretion of catecholamines (CA) from the isolated perfused rat adrenal gland and to establish its mechanism of adrenomedullary secretion. METHODS: The adrenal gland was isolated by a modification of the Wakade method, and perfused with normal Krebs-bicarbonate solution. The content of CA was measured using fluorometry. RESULTS: The perfusion of anabasine(30-300 microM) into an adrenal vein for 60 min resulted in great increases in CA secretions in a dose-dependent fashion. Upon repeated injection of anabasine (100 microM) at 120 min-intervals, CA secretion was rapidly decreased after the third injection of anabasine. However, there was no statistical difference between the CA secretory responses of both 1st and 2nd treated groups by the successive administration of anabasine at 120 min-intervals. Tachyphylaxis to the releasing effects of CA evoked by anabasine was observed by repeated administration. Therefore, in all subsequent experiments, anabasine was not administered successively more than twice at only 120 min-intervals. The CA-releasing effects of anabasine were depressed by pretreatment with chlorisondamine (selective neuronal nicotinic receptor antagonist, 1 microM), atropine (muscarinic receptor antagonist, 2 microM), nicardipine (L-type dihydropyridine Ca2+ channel blocker, 1 microM), TMB-8 (anti-releaser of intracellular Ca2 +, 30 microM), and perfusion of EGTA (Ca2+ chelator, 5 mM) plus Ca2+ -free medium. In the presence of anabasine (100 microM), the CA secretory responses induced by acetylcholine (5.32 mM), high K+ (direct membrane-depolarizer, 56 mM), DMPP(selective neuronal nicotinic receptor agonist, 10(-4) M), and McN-A-343 (selective muscarinic M1 receptor agonist, 10(-4) M) were maximally enhanced in the first 4 min. However, as time elapsed, these responses became more inhibited at later periods. Furthermore, the perfusion of nicotine (30 microM) into an adrenal vein for 60 min also caused a great increase in CA secretion, leading to peak response in the first 0-5 min period. In the presence of nicotine (30 microM), the CA secretory responses induced by acetylcholine, high K+, DMPP and McN-A-343 were also enhanced for the first 4min, but later reduced to less than the control release. CONCLUSIONS: Taken together, these experimental results indicate that anabasine affects rat adrenomedullary CA secretion in a calcium-dependent fashion. This facilitatory effect of anabasine may be mediated by activation of both cholinergic nicotinic and muscarinic receptors, which is relevant to both stimulation of Ca2+ influx into adrenomedullary chromaffin cells and Ca2+ release from cytoplasmic Ca2+ Anabasine may be less potent than nicotine in rat adrenomedullary CA secretion. Anabasine, in addition to nicotine, alkaloids present in tobacco smoke may be a risk factor in causing cardiovascular diseases.

In vitro efficacy of the combination of ciprofloxacin and cefotaxime against Vibrio vulnificus.

We performed time-kill studies of antimicrobial combinations that included minocycline, cefotaxime, and ciprofloxacin with Vibrio vulnificus ATCC 27562. Cefotaxime-plus-ciprofloxacin combinations acted synergistically against V. vulnificus in vitro, and this combination regimen can be a good choice as the empirical treatment for suspected necrotizing fasciitis due to V. vulnificus.

Familial isolated noncompaction of the ventricular myocardium in asymptomatic phase.

Isolated noncompaction of the ventricular myocardium (INVM) is a rare cardiomyopathy resulting from a failure of normal endomyocardial embryogenesis and it has been categorized as a form of unclassified cardiomyopathy. The disorder is characterized by an excessively prominent trabecular meshwork with deep intertrabecular recesses. Although the disorder is sporadic, familial incidence may occur. Clinical symptoms and prognosis of INVM may differ markedly, and range from an asymptomatic course to a severe cardiac disability. The diagnostic method of choice for IVNM is echocardiography, which reveals multiple prominent trabeculations with deep intertrabecular spaces communicating with the left ventricular cavity in the middle and apical segments of the left ventricle. The authors report a case of INVM in a family in which three adult members (a brother and two sisters) were found to be affected by this disorder. They were all asymptomatic. The diagnosis of the disorder was made first in the 36-year-old brother by transthoracic echocardiography (TTE) and multidetector CT (MD CT), during the process of preoperative evaluation for surgical treatment of low back intervertebral herniated disc. TTE and MD CT showed similar and peculiar findings of INVM. Echocardiographic screening in all first-degree relatives of this patient, in order to identify asymptomatic patients, demonstrated INVM in two elder sisters.

Comparison of green tea extract and epigallocatechin gallate on blood pressure and contractile responses of vascular smooth muscle of rats.

The present study was conducted to investigate the effects of green tea extract (GTE) on arteral blood pressure and contractile responses of isolated aortic strips of the normotensive rats and to establish the mechanism of action. The phenylephrine (10(-8) approximately 10(-5) M)-induced contractile responses were greatly inhibited in the presence of GTE (0.3 approximately 1.2 mg/mL) in a dose-dependent fashion. Also, high potassium (3.5 x 10(-2) approximately 5.6 x 10(-2) M)-induced contractile responses were depressed in the presence of 0.6 approximately 1.2 mg/mL of GTE, but not affected in low concentration of GTE (0.3 mg/mL). However, epigallocatechin gallate (EGCG, 4 approximately 12 microg/mL) did not affect the contractile responses evoked by phenylephrine and high K+. GTE (5 approximately 20 mg/kg) given into a femoral vein of the normotensive rat produced a dose-dependent depressor response, which is transient. Interestingly, the infusion of a moderate dose of GTE (10 mg/kg/30 min) made a significant reduction in pressor responses induced by intravenous norepinephrine. However, EGCG (1 mg/kg/30 min) did not affect them. Collectively, these results obtained from the present study demonstrate that intravenous GTE causes a dose-dependent depressor action in the anesthetized rat at least partly through the blockade of adrenergic alpha1-receptors. GTE also causes the relaxation in the isolated aortic strips of the rat via the blockade of adrenergic alpha1-receptors, in addition to the unknown direct mechanism. It seems that there is a big difference in the vascular effect between GTE and EGCG.