Japanese heart journal最新文献

To clarify whether inflammation is a cause or consequence of atrial fibrillation (AF), we measured high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) before and after pharmacological cardioversion in 15 patients with paroxysmal AF. Levels of hs-CRP, IL-6, and TNF-alpha after cardioversion were significantly higher than those in controls (P < 0.05). Furthermore, the levels of these indices did not differ significantly even at 24 hours and 2 weeks after cardioversion. These results suggest that inflammation is a causative agent of paroxymal AF.

The present study was designed to investigate the incidence of benign joint hypermobility syndrome (BJHMS) in mitral valve prolapse (MVP) and the correlation between the echocardiographic features of the mitral valve and elastic properties of the aortic wall and Beighton hypermobility score (BHS) in patients with MVP and BJHMS. Fourty-six patients with nonrheumatic, uncomplicated, and isolated mitral anterior leaflet prolapse (7 men and 39 women, mean age; 26.1 +/- 5.9) and 25 healthy subjects (3 men and 22 women, mean age, 25.4 +/- 4.3) were studied. Patients were divided into two groups according to their BHS (group I, MVP+BJHMS; group II, MVP-BJHMS). Individuals with accompanying cardiac or systemic disease were excluded. Echocardiographic examination was performed in all subjects. The presence of BJHMS was evaluated according to Beighton's criteria. The incidence of BJHMS in patients with MVP was found to be significantly higher than that of controls (45.6%, (21/46) vs 12% (3/25), P < 0.0001). Group I (MVP + BJHMS) had significantly increased anterior mitral leaflet thickness (AMLT, 3.4 +/- 0.4 vs 3.1 +/- 0.3; P < 0.005), maximal leaflet displacement (MLD, 2.4 +/- 0.4 vs 1.7 +/- 0.4; P < 0.005), and degree of mitral regurgitation (DMR, 17.1 +/- 7.2 vs 11.2 +/- 4.4; P < 0.01) compared to group II. However, the index of aortic stiffness (IAOS) was found to be lower (17.6 +/- 6.9 vs 23.9 +/- 7.6; P < 0.005) and aortic distensibility (AOD) to be higher (0.0035 +/- 0.007 vs 0.0024 +/- 0.005; P < 0.005) in group I. There was a significant correlation between AMLT, MLD and DMR, and BHS (r = 0.57/P = 0.007, r = 0.55/P < 0.009, r = 0.51/P < 0.01, respectively). In addition, AOD correlated positively with BHS (r = 0.53/P < 0.005), but the index of aortic stiffness correlated inversely with BHS (r = -0.49/P < 0.007). The incidence of BJHMS in patients with MVP was more frequent than the normal population and there was a significant correlation between the severity of BJHMS (according to BHS) and echocardiographic features of the mitral leaflets and elastic properties of the aortic wall.

A whole-heart coverage MRI sequence, which employes a hybrid of fast gradient echo and echo planar acquisition imaging (FastCard EchoTrain), has recently been developed. Using this sequence, a first-pass myocardial perfusion MRI was shown to be a good noninvasive modality for detecting coronary artery disease (CAD) in a clinical setting. In addition, the clinical usefulness of delayed enhanced MRI has recently been reported. The objectives of this study were (1) to investigate the accuracy of dipyridamole stress first-pass myocardial perfusion MRI for diagnosing CAD (> 50% stenosis) and (2) to clarify whether additional delayed enhancement MRI has any clinical significance. We performed first-pass myocardial perfusion MRI in 102 consecutive patients (66 +/- 9 years old) suspected to have CAD or new lesions in patients with well-documented prior myocardial infarction (MI). Using a 1.5 T cardiac MR imager (GE CV/i), eight short axis MR images of the left ventricle were acquired by injecting gadolinium (0.1 mmol/kg) under dipyridamole infusion stress (0.56 mg/kg). Fifteen minutes later, aminophylline (250 mg) was injected and first-pass perfusion MRI was repeated in the resting state in order to evaluate both the presence of perfusion defect and delayed enhancement. The presence of perfusion defect and delayed enhancement was determined based on a visual qualitative analysis by the agreement of two separate readers who were blinded to any clinical information. Based on the stress and rest findings, no defect, reversible defect, or fixed defect with or without delayed enhancement was recorded in any patient. The MR findings revealed 76 CAD patients, including 24 MI patients with new lesions and 26 patients without CAD on coronary angiography. The presence of stress perfusion defect had a 93% sensitivity and an 85% specificity for diagnosing CAD. A fixed defect showed an 86% sensitivity and a 66% specificity for diagnosing a prior MI. Patients with a fixed defect with delayed enhancement had more significant stenosis in the infarct related artery than in those without any enhancement (11/26 vs 15/20, P < 0.05). Dipyridamole stress first-pass myocardial perfusion MRI using the FastCard EchoTrain was found to be a clinically useful and accurate modality for diagnosing CAD.

We investigated the use of a catheter-based cryoablation system on atrioventricular (AV) junction ablation in dogs. In five dogs, the cryoablation catheter was introduced to the AV junction area in order to create transient high degree or complete AV block. Cryo-freezing energy was applied by lowering the temperature to -75 degrees C for five minutes as a single cycle. This cycle was repeated until significant impairment of the AV conduction appeared. Transient high degree and complete AV block was obtained in all five dogs without any adverse effects. The iceball formation was identified by intracardiac echocardiography. Ablation of the AV junction is effective with several freeze-thaw cycles using a transvenous catheter cryoablation system.

Few data have been published on the reproducibility of baseline subtracted peak intensity obtained from intravenous intermittent triggered myocardial contrast echocardiography. We investigated the reproducibility of the peak intensity measured from intravenous intermittent triggered myocardial contrast echocardiography in 10 young healthy males. The contrast echocardiography was obtained using the second harmonic mode with an intravenous bolus injection of Levovist (first study). The same myocardial contrast echocardiography was repeated after the first study (second study). The myocardial opacification and peak intensity in the 12 segments of the apical 4 and 2 chamber views were assessed visually and quantitatively. The differences in the peak intensity between the initial and repeated measurements in the first study (intraobserver reproducibility) and between the initial measurements in the first and second studies (interinjection reproducibility) were assessed using the Bland and Altman method. The degree of opacification was good or intermediate in 207/228 (91%) of the segments. The agreement of myocardial opacification between the first and second studies was 87/114 (76%). However, significantly higher peak intensity was obtained in apical septal (8200 +/- 6300 au2) and mid septal (8500 +/- 6000 au2) segments in the 4 chamber view and in the mid inferior (12400 +/- 9300 au2) and apical inferior (10700 +/- 6300 au2) segments in the 2 chamber view compared with other segments. The mean differences of the peak intensities according to the Bland and Altman analysis was -1600 +/- 5000 au2 in the intraobserver reproducibility study, and -1100 +/- 5300 au2 in the interinjection reproducibility study. Thus, the measurement error was determined to range from 8400 au2 to 9500 au2 in both studies. We conclude that the peak intensity obtained from intravenous intermittent triggered myocardial contrast echocardiography using Levovist varies significantly among segments in the left ventricular myocardium. Large intraobserver and interinjection variability exists in the measurement of peak intensity, suggesting that the reproducibility of this technique is limited for quantitative assessment of myocardial perfusion.

Although the damage in myocardial infarction has been demonstrated to be related with the magnitude and number of ST elevation, its relation with terminal distortion of QRS is unclear. The relationship between terminal QRS distortion in ECGs on admission and the results of early low dose dobutamine stress echocardiography (LDSE) performed 6 +/- 2 days later was investigated. Patients admitted to our clinic within the first six hours of their chest pain and without a prior infarction diagnosis were divided into two groups based on the admission electrocardiogram as the absence (QRS-, n = 33) or presence (QRS+, n = 29) of distortion of the terminal portion of the QRS in > or = 2 leads (QRS+; J point at > 50% of the R wave amplitude in lateral leads or presence of ST elevation without S wave in leads V1-V3). There were no significant differences between the groups with respect to thrombolytic therapy or reperfusion criteria. During LDSE, the infarct zone wall motion score index (WMSI) in the QRS- group was significantly decreased relative to baseline (from 2.93 +/- 0.65 to 2.37 +/- 0.84, P = 0.02), and it was significantly different compared with WMSI in the QRS+ group (P = 0.005). Improvement of akinetic regions to hypokinetic regions in the infarct zone (IZ) was found to be 33.5% (44/131) in the QRS- group and 17.8% (27/151 P = 0.004) in the QRS+ group. Furthermore, 55.1% (10/29) of the patients in the QRS+ group and only 18.1% (6/33) of those in the QRS- group did not respond to LDSE (P < 0.05). In multiple logistic regression analysis, while there was no relationship between good left ventricular functions (WMSI < 2) and terminal QRS distortion under basal conditions (P = 0.07), an independent relation was observed to exist between them after LDSE (P = 0.03, OR 4.48, 95% CI, 1.13-17.7). Moreover, plasma CK levels were higher in the QRS+ group (P = 0.03), whereas the ejection fraction was worse (P = 0.01). In both groups, there was no correlation between the Selvester score and left ventricle WMSI at baseline, but this correlation was significantly improved with LDSE (QRS-; r = 0.39 P = 0.02 and QRS+; r = 0.44 P = 0.01) The viability in the IZ is relatively less in those patients with terminal QRS distortion observed in their ECG on admission. This simple classification would be useful in predicting left ventricular function at the time of discharge.

Recent studies have shown that percutaneous coronary intervention (PCI) activates systemic hemostatic activity, reflecting platelet activation and thrombin formation in the coronary arteries. The present study compared systemic levels of hemostatic markers induced by plain old balloon angioplasty (POBA), coronary stenting (STENT), and cutting balloon (CB) angioplasty. Sixty-one patients with stable angina pectoris, who underwent elective PCI or diagnostic coronary angiography (CAG) alone, were investigated. Patients who underwent PCI were divided into the POBA group (n = 11), the STENT group (n = 27), and the CB group (n = 11). Patients who underwent CAG alone were assigned to the CAG group (n = 12). Blood samples were collected before, 24 hours after, and 3 days after PCI or CAG. Plasma concentrations of prothrombin fragment 1+2 (F1+2), fibrinopeptide A (FPA), thrombin-antithrombin III complex (TAT), and plasminogen activator inhibitor-1 (PAI-1) were measured. In the CB group, the F1+2 (1.23 +/- 0.4 nmol/L) level 3 days after PCI was significantly smaller than that of the POBA group (2.37 +/- 0.5 nmol/L) (P < 0.05). The FPA (1.81 +/- 0.9 ng/mL), TAT (3.36 +/- 1.2 ng/mL) and PAI-1 (23.0 +/- 4.1 ng/mL) levels in the CB group 3 days after PCI were significantly smaller than those of the POBA group (P < 0.05, respectively) and STENT group (P < 0.05, respectively), but similar to the CAG group. Systemic hemostasis is activated to a greater extent after POBA and stenting than it is after CB angioplasty of the coronary arteries. This may contribute to the favorable long-term outcome of CB angioplasty.

Several studies claim that prothrombin 20210GA and factor V Leiden mutations are related to arterial thrombosis. We investigated the frequencies of these mutations and their significance in the development of early atherosclerosis in acute myocardial infarction (AMI) patients younger than 55 years of age. We investigated 96 patients with AMI and 77 control subjects. The diagnosis of AMI was established by typical chest pain and ST elevations on the presentation electrocardiogram and characteristic cardiac enzyme elevations. None of the control subjects had evidence of cardiovascular disease. DNA samples were isolated from all subjects and prothrombin 20210GA and factor V Leiden mutations were determined by the RealTime PCR technique with the aid of a Light Cycler device. The prevalence of factor V Leiden mutation was 6.3% and 5.2% in the patient and control groups, respectively (OR 0.6 [95% CI 0.1- 3.9], P = 0.6), whereas the prevalence of prothrombin G20210A mutation was 4.2% and 2.6% in the patient and control groups, respectively (OR 2.8 [95% CI 0.2 - 32.2], P = 0.4). None of the patients had both mutations. Prothrombin 20210GA and factor V Leiden mutations are not significant risk factors for the development of myocardial infarction in patients less than 55 years old in Southern Turkey.

Radiofrequency (RF) catheter ablation has become standard therapy for many types of arrhythmias. RF energy may cause deterioration in left ventricular function by damaging the myocardium. The aim of the present study was to assess the changes in left ventricular function after catheter ablation using various echocardiographic parameters. Forty patients (22 women), aged 37 +/- 14 years (range, 15-76 years), underwent catheter ablation for various tachycardias. Routine echocardiogaphic examination was done in all patients. Left ventricular systolic function was evaluated by the modified Simpson method and tissue Doppler. With regard to left ventricular diastolic function parameters, diastolic early (E) and late (A) transmitral filling velocities, deceleration time (DT), isovolumetric relaxation time (IVRT), and tissue Doppler parameters were assessed. All ventricular function parameters were assessed before, and 1 hour, 1 day, and 1 month after the catheter ablation procedure. To avoid any influence of heart rate on diastolic function parameters, the E/A ratio, DT, and IVRT were adjusted to heart rate (cE/A, cDT, cIVRT). No changes in left ventricular systolic function after the ablation were observed. After the ablation procedure (1 hour, 1 day, and 1 month) the cE/A ratio decreased from 1.42 +/- 0.43 to 1.19 +/- 0.40, 1.18 +/- 0.40, and 1.30 +/- 0.33 (P = 0.009), respectively. cDT increased from 210 +/- 54 to 272 +/- 64, 255 +/- 60, 240 +/- 64 (P = 0.001), respectively. Likewise cIVRT increased from 113 +/- 22 to 133 +/- 54, 123 +/- 27, 117 +/- 19 (P = 0.007), respectively. Significant changes were also observed concerning tissue Doppler parameters in assessing diastolic function. Although no significant changes were observed in systolic function after RF ablation, this procedure may have some detrimental effects on ventricular diastolic function para-meters.