Previous noninvasive measurements of the pulse waveform of the radial artery have not employed standard positioning procedures. Here, we propose a new noninvasive measuring apparatus that has a two-axis mechanism and employs a standard positioning procedure for detecting the optimal site for accurately measuring the pressure pulse waveform (PPW). A modified sensor was designed to simultaneously measure the arterial diameter changed waveform (ADCW) and PPW. Considering the artery as a cylinder, the measured waveform would be distorted if the sensor were not at the middle of arterial width. Moreover, a blood vessel is elastic, and its compliance changes with the transmural pressure, being maximal when the transmural pressure is equal to zero. The sensor should detect the PPW with the lowest possible distortion and, hence, an analysis of the vascular geometry and an arterial model were used to design a standard positioning procedure based on the ADCW for the X and Z axes. In order to verify the resolution of the X axis scanning procedure, the echo method was used to measure the radial artery outer diameter in ten healthy subjects. The difference between the scanning width and the actual arterial diameter was 0.36 +/- 0.23 mm (mean +/- SD). Finally, the PPW as measured at the optimal position was used to diagnose myocardial ischemia symptoms in 60 elderly subjects whose chief complaint was chest pain, with the exercise electrocardiogram being used as a reference to compare between individuals with and without myocardial ischemia. The PPW analysis used the harmonic components in the frequency domain. We found that the fourth harmonic of the Fourier series differed significantly between the groups (p = 0.0039), which is consistent with previous studies. The results indicate that our noninvasive measurement apparatus is very suitable for analyzing the PPW of the radial artery.

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trial tachycardia (AT) originating focally from diverse anatomical structures in both atria has been well described. [1][2][3][4][5][6][7][8] Focal AT is distinguished from macroreentrant AT by its electrophysiological characteristics and electropharmacological responses, and by the approaches to mapping and ablation of the tachycardia. 7,8 The underlying mechanism of focal AT is thought to be automaticity, triggered activity or atrial microreentry. 7,8 Recently, Tsai et al reported an unusual form of focal atrial fibrillation (AF) triggered by ectopic beats originating from the superior vena cava (SVC), and radiofrequency (RF) ablation of the triggering SVC focus was safe and highly effective in eliminating the focal AF. 9 Theoretically, it is possible that focal electrical firing in the SVC could initiate AT in addition to AF; however, the mechanism of this type of focal AT remains unclear. In this study, we describe the distinct electrocardiograms and electrophysiological characteristics in 3 patients with focal AT originating from various parts of the SVC. The location of the successful RF site in the SVC was proven by multi-plane SVC angiography. All 3 patients underwent uneventful ablations of their SVC foci within a few seconds of RF current application. Methods PatientsThe study group were 3 patients with drug-refractory atrial tachyarrhythmias who were admitted for electrophysiological study and RF ablation therapy. Each patient had a focal AT originating from the SVC that had been diagnosed and confirmed by the electrophysiological study, SVC angiography and RF ablation. Two (cases 1 and 2) of the 3 patients did not have significant organic heart diseases detectable by physical examination, chest roentgenograms, echocardiography, and coronary angiography. The other patient (case 3) had one-vessel coronary artery disease. The definition of focal AT was based on previously established criteria. 7,10-12 Electrophysiological Study and RF AblationThe electrophysiological study was performed in a postabsorptive state after each patient gave written informed consent. All antiarrhythmic drugs except amiodarone were discontinued for at least 5 half-lives before the study. Two 6F quadripolar electrode catheters with a 5-mm interelectrode spacing were positioned at the high right atrium and the right ventricular apex, respectively, for pacing and recording. Another 6F quadripolar electrode catheter with a 10-mm interelectrode spacing was positioned across the tricuspid annulus to record the His bundle potential. A 6F decapolar electrode catheter with a 2-10-2-mm interelectrode spacing (Daig Corp) was positioned in the coronary sinus for recording and pacing. A 7F deflec- Electrophysiological Characteristics and Radiofrequency Ablation of Focal Atrial Tachycardia Originating From the Superior Vena CavaKuan-Cheng Chang, MD; Yu-Chin Lin, MD; Jan-Yow Chen, MD; Hsiang-Tai Chou, MD, PhD; Jui-Sung Hung, MDThe initiation of focal atrial tachycardia (AT) from the superior vena cava (SVC) remains unclear. In 3 patients (2...

There is increasing evidence that green tea polyphenols can protect against myocardial damage. Recently, we showed that they bind to cardiac troponin C and alter myofilament Ca(2+) sensitivity in cardiac muscle. In the present study, we examined whether green tea extract (GTE) could prevent the progressive remodeling seen in ischemic myocardium and improve cardiac function by modulation of the contractile apparatus utilizing a myocardial infarction (MI) model in the rat involving ligation of the left anterior descending branch. Using this model, severe myocardial injury was found, including altered cardiac performance and the appearance of extensive fibrosis and left ventricular (LV) enlargement. Supplementation with 400 mg/kg/day of GTE for 4, 18, or 46 days had beneficial effects in preventing the hemodynamic changes. Histopathological studies showed that GTE attenuated the progressive remodeling seen after myocardial injury. Echocardiography confirmed that GTE prevented LV enlargement and improved LV performance in post-MI rats. In addition, we showed that GTE supplementation for 18 or 46 days increased the myofilament Ca(2+) sensitivity of the ischemic myocardium in post-MI rats. These results validate the novel action of green tea polyphenols in protecting against myocardial damage and enhancing cardiac contractility by modulating myofilament Ca(2+) sensitivity in post-MI rats.

A large MFLA and a higher BVI number are powerful predictors of in-hospital complications after acute type B aortic dissection.

There is evidence for a negative correlation between green tea consumption and cardiovascular diseases. The aim of the present study was to examine whether green tea extract (GTE) given before regional myocardial ischemia could improve depression of myocardial contractility by preventing cytosolic Ca(2+) overload. Regional ischemia-reperfusion (IR) was induced in rats by ligating the left anterior descending branch for 20 min, then releasing the ligature. Ligation induced ventricular arrhythmias in rats without GTE pretreatment, but decreased arrhythmogenesis was seen in rats pretreated 30 min earlier with GTE (400 mg/kg). During reperfusion, arrhythmias only occurred during the initial 5 min, and GTE pretreatment had no effect. After overnight recovery, serum cTnI levels were greatly increased in control post-IR rats but only slightly elevated in GTE-pretreated post-IR rats. Myocardial contractility measured by echocardiography was still depressed after 3 days in control post-IR rats, but not in GTE-pretreated post-IR rats. No myocardial ischemic injury was seen in post-IR rats with or without GTE pretreatment. Using freshly isolated single heart myocytes, GTE was found to attenuate the post-IR injury-associated cytosolic Ca(2+) overload and modulate changes in the levels and distribution of myofibril, adherens junction, and gap junction proteins. In summary, GTE pretreatment protects cardiomyocytes from IR injury by preventing cytosolic Ca(2+) overload, myofibril disruption, and alterations in adherens and gap junction protein expression and distribution.

SUMMARYMultiple intracardiac catheters are often necessary for electrophysiological study (EPS) and radiofrequency (RF) ablation therapy. Therefore, multiple venous sheath placement in one femoral vein is always required for multiple intracardiac catheter insertion. The vascular complications incurred by placement of multiple sheaths have not been fully studied. We utilized duplex ultrasonography to assess the femoral veins before and after the procedure. This study consisted of 52 patients (68 femoral veins) who underwent EPS and RF ablation therapy. Up to three sheaths were inserted into a single femoral vein. Nonocclusive deep vein thrombosis (DVT) occurred in 12/68 veins (17.6%) of 11 patients on the day following the procedure. Thrombosis regressed spontaneously in 11 veins and persisted in 1 vein at 1-week follow-up. The venous diameter significantly decreased the day after the procedure (8.7 ± 1.2 mm vs 5.3 ± 1.5 mm, P < 0.001), but recovered by the 1-week follow-up (7.9 ± 1.7 mm, P = 0.07) in the 12 veins. Short-term placement of multiple venous sheaths in a single femoral vein appears to be safe. Nonetheless, nonocclusive DVT does occur in a significant number of patients. Although thrombosis regressed and the outcome appeared to be benign in most patients, close follow-up to avoid potential vascular complications is necessary. (Jpn Heart J 2004; 45: 257-264)

BackgroundIt is well known that familial sick sinus syndrome (SSS) is caused by functional alterations of ion channels and gap junction. Limited information is available on the mechanism of age-related non-familial SSS. Although evidence shows a close link between arrhythmia and the renin-angiotensin system (RAS), it remains to be determined whether the RAS is involved in the pathogenesis of non-familial SSS.MethodsIn this study, 113 patients with documented non-familial SSS and 125 controls were screened for angiotensinogen (AGT) and gap junction protein-connexin 40 (Cx40) promoter polymorphisms by gene sequencing, followed by an association study. A luciferase assay was used to determine the transcriptional activity of the promoter polymorphism. The interaction between nuclear factors and the promoter polymorphism was characterized by an electrophoretic mobility shift assay (EMSA).ResultsAssociation study showed the Cx40 -44/+71 polymorphisms are not associated with non-familial SSS; however, it indicated that four polymorphic sites at positions -6, -20, -152, and -217 in the AGT promoter are linked to non-familial SSS. Compared to controls, SSS patients had a lower frequency of the G-6A AA genotype (OR 2.88, 95% CI 1.58–5.22, P = 0.001) and a higher frequency of the G allele at -6 position (OR 2.65, 95% CI 1.54–4.57, P = 0.0003). EMSA and luciferase assays confirmed that nucleotide G at position -6 modulates the binding affinity with nuclear factors and yields a lower transcriptional activity than nucleotide A (P<0.01).ConclusionG-6A polymorphism, which modulates the transcriptional activity of the AGT promoter, may contribute to non-familial SSS susceptibility.