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AIM CHA2 DS2 -VASc score has been proven to have great prognostic value in patients with acute coronary syndrome (ACS). We aimed to determine whether the addition of renal dysfunction in the CHA2 DS2 -VASc score would improve the prognostic impact of the scoring system to predict prognosis among ACS patients. METHODS A total of 3031 ACS patients were prospectively enrolled at 39 hospitals and followed for 1 year. The patients were divided into three groups based on estimated glomerular filtration rate (eGFR) (group 1, eGFR>90; group 2, eGFR between 60 and 90; and group 3, eGFR

Aims To investigate whether renal dysfunction is a useful predictor of postoperative atrial fibrillation (POAF) after cardiac surgery. We also aimed to determine whether the addition of renal dysfunction into the scoring system could improve diagnostic accuracy of the CHA2DS2-VASc score to predict POAF. Methods and results The study prospectively enrolled 350 consecutive patients who underwent cardiac surgery. Echocardiography was performed before cardiac surgery. Renal dysfunction was defined as estimated glomerular filtration rate < 60 mL min−1 1.73 m−2. All patients were monitored with continuous electrocardiographic telemetry for the occurrence of POAF until the day of hospital dismissal. Postoperative atrial fibrillation occurred in 103 of 350 patients (29%). Patients with POAF was associated with longer intensive care unit stay compared with those without POAF (3.7 ± 2.2 vs. 3.1 ± 1.4 days, P = 0.002). Both the CHA2DS2-VASc score and renal dysfunction were independent predictors of POAF in multivariate analysis. Renal dysfunction can further stratify patients with a CHA2DS2-VASc score of 0 or 1 into two groups with different POAF rates (3.1% vs. 68.8%, P < 0.001). A new scoring system (R-CHA2DS2-VASc score) derived by assigning an additional point representing renal dysfunction to the CHA2DS2-VASc score could improve its predictive accuracy. The area under the receiver operating characteristic curve increased from 0.68 to 0.71 ( P < 0.001). Furthermore, the rate of left ventricular diastolic dysfunction also increased with increasing renal dysfunction. Conclusion Renal dysfunction, associated with left ventricular diastolic dysfunction, was a significant risk factor for POAF after cardiac surgery and may improve the diagnostic accuracy of the CHA2DS2-VASc score.

We assessed the prognostic implications of low triiodothyronine (T3) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels in critically ill patients with acute heart failure. We acquired data for 144 critical care patients with acute decompensated heart failure, of which 106 were included in this study. Plasma thyroid hormones and NT-proBNP levels were determined within 48 hours of admission. We assessed these measures for predicting all-cause and cardiac mortalities. At a mean follow-up period of 25 ± 31 months, the all-cause mortality rate was 51% (54 of 106) and the cardiac mortality rate was 70% (38 of 54). A multivariate Cox regression model showed that log-transformed NT-proBNP levels (log NT-proBNP; hazard ratio [HR] 2.90, 95% confidence interval [CI] 1.38 to 6.08, p = 0.005) and T3 levels (HR 0.98, 95% CI 0.96 to 0.99, p = 0.008) were associated with all-cause mortality, and log NT-proBNP (HR 3.70, 95% CI 1.28 to 10.71, p = 0.02) and T3 (HR 0.98, 95% CI 0.96 to 0.99, p = 0.01) were associated with cardiac mortality. Based on cut-off values for NT-proBNP (10,685 pg/ml) and T3 (52.3 ng/dl), Kaplan-Meier analyses provided significant prognostic information with the highest risk for all-cause mortality in the low T3 (≤52.3 ng/dl)/high NT-proBNP (10,685 pg/ml) group (HR 8.54, 95% CI 4.19 to 17.40, p0.0001). In conclusion, T3 levels appear to be independent predictors for both all-cause and cardiac mortalities among critical ill patients with heart failure, and high NT-proBNP and low T3 levels predict a worse long-term outcome.

Aims/Introduction Admission hyperglycemia is associated with poor outcome in patients with myocardial infarction. The present study evaluated the relationship between admission glucose level and other clinical variables in patients with ST‐elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). Materials and Methods The 959 consecutive STEMI patients undergoing primary PCI were divided into five groups based on admission glucose levels of

Lung cancer cells express different chemokines and chemokine receptors that modulate leukocyte infiltration within tumor microenvironment. In this study we screened several mediators/growth factors on CXCL1 release in human carcinoma epithelial cells. Of the tested mediators, VEGF was found to have a robust increase in causing CXCL1 release. VEGF stimulated CXCL1 release and mRNA expression in a time- and concentration-dependent manner. The release was inhibited by the VEGF receptor antagonists and the JNK, PI-3K, tyrosine kinase, and transcription inhibitors. In parallel, VEGF induced JNK, PI3K and Akt activation. Strikingly, among these inhibitors only the JNK inhibitor could reduce VEGF-induced CXCL1 mRNA expression, suggesting that JNK participated in VEGF-induced CXCL1 synthesis, whereas PI-3K was responsible for cellular CXCL1 secretory process. In addition, the steroid dexamethasone and TGF-β suppressed CXCL1 release through a transcriptional regulation. We also showed that cells stimulated with VEGF significantly attracted monocyte migration, which could be abolished by CXCL1 B/N Ab, CXC receptor 2 antagonist, TGF-β, and dexamethasone. In summary, we provide here evidence showing JNK activation for VEGF-induced CXCL1 DNA transcription and PI-3K pathway for extracellular CXCL1 release in human carcinoma epithelial cells. The released CXCL1 was functionally linked to recruiting monocytes into lung cancer cell microenvironment.

Background: Renal dysfunction is associated with a higher rate of atrial fibrillation in clinical practice. This study investigated the associations between renal function, left ventricular (LV) diastolic dysfunction, and postoperative atrial fibrillation (POAF). Methods and Results: A total of 265 consecutive patients who underwent cardiac surgery were prospectively enrolled in the study. Echocardiography was performed before cardiac surgery. The patients were divided into 3 groups based on estimated glomerular filtration rate (eGFR) (group 1, ≥90ml·min–1·1.73m–2; group 2, 60–90ml·min–1·1.73m–2; and group 3, 15 – also increased (group 1, 19.0%; group 2, 38.1%; and group 3, 48.3%; P

Background Chemerin, a novel adipokine, plays a role in the inflammation status of vascular endothelial cells. Hypoxia causes endothelial-cell proliferation, migration, and angiogenesis. This study was aimed at evaluating the protein and mRNA expression of chemerin after exposure of human coronary artery endothelial cells (HCAECs) to hypoxia. Methods and Results Cultured HCAECs underwent hypoxia for different time points. Chemerin protein levels increased after 4 h of hypoxia at 2.5% O2, with a peak of expression of tumor necrosis factor-alpha (TNF-alpha) at 1 h. Both hypoxia and exogenously added TNF-alpha during normoxia stimulated chemerin expression, whereas an ERK inhibitor (PD98059), ERK small interfering RNA (siRNA), or an anti-TNF-alpha antibody attenuated the chemerin upregulation induced by hypoxia. A gel shift assay indicated that hypoxia induced an increase in DNA-protein binding between the chemerin promoter and transcription factor SP1. A luciferase assay confirmed an increase in transcriptional activity of SP1 on the chemerin promoter during hypoxia. Hypoxia significantly increased the tube formation and migration of HCAECs, whereas PD98059, the anti-TNF-alpha antibody, and chemerin siRNA each attenuated these effects. Conclusion Hypoxia activates chemerin expression in cultured HCAECs. Hypoxia-induced chemerin expression is mediated by TNF-alpha and at least in part by the ERK pathway. Chemerin increases early processes of angiogenesis by HCAECs after hypoxic treatment.

To study the association of renin gene polymorphism with essential hypertension in the Chinese population, 86 hypertensive and 107 normotensive subjects were enrolled from an epidemiologic survey. Leukocyte DNA was extracted and digested with Hind III and Bgl I restriction enzymes. Southern hybridization was done with digoxigenin-incorporated renin gene probes generated by polymerase chain reaction. The restriction fragments were detected by anti-digoxigenin antibody and enzyme methods. Two Hind III polymorphysms of the renin gene (8.7 kb and 6.2 kb) were identified. The allele frequences were 129(75%) and 43(25%), respectively, in hypertensives; they were 139(65%) and 75(35%), respectively, in normotensives (chi2 = 4.074, p = 0.044). The genotypes of 8.7/8.7,8.7/6.2 and 6.2/6.2 were significantly different between hypertensives and normotensives, being 45(52%), 39(45%), 2(3%) and 48(45%), 43(40%), and 16(15%), respectively (chi2 = 9.002, p = 0.11). The Bgl I polymorphism did not show a difference between hypertensives and normotensives. Thus, we conclude that the renin gene Hind III polymorphysm is associated with hypertension in this Chinese population.

Summary Background & aims Subjects with obesity had autonomic nervous abnormalities. This study investigated autonomic nervous modulation in subjects with obesity and its association with the indices of obesity, especially the body mass index and waist circumference, by heart rate variability analysis. Methods Forty-seven adults with a body mass index (in kg/m2) greater than 28 were recruited as the obese group and 30 subjects with a body mass index less than 23 were recruited as the control group. Anthropometric measures and heart rate variability measures were obtained for both groups. The correlation between heart rate variability measures and the anthropometric measures was assessed in subjects with obesity. Results Subjects with obesity had lower normalized low-frequency power and normalized high-frequency power than those of the control group. The body height, body weight, waist circumference and waist-to-hip ratio correlated significantly with the spectral heart rate variability measures in Asian subjects with obesity, whereas the body mass index did not. Conclusions Abdominal obesity, rather than general obesity, was related to autonomic nervous derangement in Asian subjects with obesity. The close relation between abdominal obesity and autonomic derangement may partially account for the close relationship between abdominal obesity and higher risk of mortality and morbidity in subjects with obesity.

In recent studies, aminoguanidine (AG), an inhibitor of advanced glycation endproducts, has been identified as a prominent agent that can prevent the age-related aortic stiffening and cardiac hypertrophy. The aim of this study was to determine whether AG had effects on the left ventricular (LV)-arterial coupling in aged Fisher 344 rats in terms of the ventricular and arterial chamber properties. Normotensive rats were treated from 18 to 24 months with AG (1 g l(-1) in drinking water) and compared with a control group. LV pressure and ascending aortic flow signals were recorded to construct the ventricular and arterial end-systolic pressure-stroke volume relationships to calculate LV end-systolic elastance (Ees) and effective arterial volume elastance (Ea), respectively. The optimal afterload (Qload) determined by the ratio of Ea to Ees was used to measure the efficiency of mechanical energy transferred from the left ventricle to the arterial system. In comparison with the 6-month-old rats, the 24-month-old animals had decreased Ees, at 567.4 +/- 26.7 vs 639.0 +/- 20.7 mmHg ml(-1), decreased Ea, at 411.5 +/- 18.6 vs 577.9 +/- 15.7 mmHg ml(-1), and decreased Q(load), at 0.9428 +/- 0.0024 vs 0.9962 +/- 0.0014. Treatment with AG for 6 months did not significantly affect Ees; however, when normalized to LV weight (i.e., Eesn = Ees/LV weight), Eesn showed a significant rise of 22.8%, suggesting that AG may retard the aging process on the intrinsic contractility of the left ventricle. On the other hand, the decrease in Ea in aging rats was prevented by AG, as reflected in the increase of 19.7% in this variable (P < 0.05). The 24-month-old treated rats also exhibited a significant rise of 21.6% in Ea/Ees, causing an increase of 5.2% in Qload (P < 0.05). We conclude that in healthy older Fisher 344 rats without diabetes, long-term treatment with AG may improve both the arterial and ventricular function and optimize the matching condition for the left ventricular-arterial coupling.

Surgically induced abnormalities in atrial conduction could result in unusual P wave changes. A 31-year-old woman underwent concomitant mitral valve surgery and atrial compartment operation for mitral stenosis and atrial fibrillation (AF). After operation, the AF was successfully converted to sinus rhythm, whereas an unusual electrocardiogram (ECG) with a discrete negative deflection before the T wave in V1 was noted. Electrophysiological study showed a marked conduction delay from the high right atrium (HRA) to the right atrial appendage (RAA) compartment, which resulted in a separation of P waves. The P wave preceding the QRS complex represented the activation of sinus node and the left atrial compartments, and the P at the vicinity of T wave represented the activation of RAA compartment. The conduction from HRA to RAA was worsened on HRA pacing at a faster rate, and improved after isoproterenol infusion. This report demonstrated that conduction across a surgically created isthmus in the atrium could be severely impaired and result in unusual P wave separation.

We determined the roles of maximal systolic elastance (Emax) and theoretical maximum flow (Qmax) in the regulation of cardiac pumping function in early streptozotocin (STZ)-diabetic fats. Physically, Emax can reflect the intrinsic contractility of the myocardium as an intact heart, and Qmax has an inverse relation to the systolic resistance of the left ventricle. Rats given STZ 65 mg/kg l.v. (n = 17) were divided into two groups, 1 week and 4 weeks after induction of diabetes, and compared with untreated age-matched controls (n = 15). Left ventricular (LV) pressure and ascending aortic flow signals were recorded to calculate Emax and Qmax, using the elastance-resistance model. After 1 or 4 weeks, STZ-diabetic animals show an increase in effective LV end-diastolic volume (Veed), no significant change in peak iso-volumic pressure (Pisomax), and a decline in effective arterial volume elastance (Ea). The maximal systolic elastance Emax is reduced from 751.5 ± 23.1 mmHg/ml in controls to 514.1 ± 22.4 mmHg/ml in 1- and 538.4 ± 33.8 mmHg/ml in 4-week diabetic rats. Since Emax equals PisomaxVeed, an increase in Veed with unaltered Pisomax may primarily act to diminish Emax so that the intrinsic contractility of the diabetic heart is impaired. By contrast, STZ-diabetic rats have higher theoretical maximum flow Qmax (40.9 ± 2.8 ml/s in 1- and 44.5 ± 3.8 ml/s in 4-week diabetic rats) than do controls (30.7 ± 1.7 ml/s). There exists an inverse relation between Qmax and Ea when a linear regression of Qmax on Ea is performed over all animals studied (r= 0.65, p < 0.01). The enhanced Qmax is indicative of the decline in systolic resistance of the diabetic rat heart. The opposing effects of enhanced Qmax and reduced Emax may negate each other, and then the cardiac pumping function of the early STZ-diabetic rat heart could be preserved before cardiac failure occurs.

Background MicroRNAs (miRs) play a role in cardiac remodelling, and acute myocardial infarction (AMI) can regulate miR expression. MiR-208a is essential for the expression of the genes involved in cardiac hypertrophy and fibrosis. MiR-208a activates endoglin expression and may result in cardiac fibrosis. The role of miR-208a and endoglin in AMI is not known. We sought to investigate the regulation of miR-208a and endoglin in AMI. Methods Ligation of the proximal left anterior descending artery was performed in adult Sprague-Dawley rats to induce AMI. Echocardiography was used to measure heart size and left ventricular function. The TaqMan miR real-time quantitative assay was used to quantitate miR-208a. Myocardial fibrosis was detected by Masson trichrome staining. Results AMI and overexpression of miR-208a in the sham group without infarction significantly increased myocardial miR-208a, endoglin, and β-myosin heavy chain (β-MHC) expression. Overexpression of antagomir-208a significantly inhibited the increase of myocardial endoglin and β-MHC protein expression induced by infarction. Overexpression of mutant miR-208a in the sham group did not induce myocardial endoglin and β-MHC expression. Pretreatment with atorvastatin and the angiotensin-receptor antagonist valsartan significantly attenuated the increase of endoglin and β-MHC induced by infarction. AMI and overexpression of miR-208a in the sham group significantly increased the area of myocardial fibrosis compared with the sham group. Overexpression of antagomir-208a and pretreatment with atorvastatin and valsartan in the AMI group significantly decreased the area of myocardial fibrosis induced by infarction. Conclusions MiR-208a increases endoglin expression to induce myocardial fibrosis in rats with AMI. Treatment with atorvastatin and valsartan can decrease myocardial fibrosis induced by AMI through attenuating miR-208a and endoglin expression.

BACKGROUND Repairing Ebstein's anomaly without correction of associated arrhythmia may result in sudden death. Catheter or surgical ablation is indicated for various symptomatic tachyarrhythmias in Ebstein's anomaly. METHODS Between October 1973 and October 1997, 30 patients with Ebstein's anomaly underwent surgical repair in our hospital. Tricuspid valve replacement was performed in 13 patients, tricuspid annuloplasty and valvuloplasty in the remaining 17 patients. Preoperative electrophysiological studies were performed in 11 patients after 1980. Concomitant arrhythmia ablation was done in 10 patients: 4 for Wolff-Parkinson-White syndrome, 2 for atrioventricular (AV) nodal reentrant tachycardia, one for ventricular tachycardia and 3 for paroxysmal atrial flutter and fibrillation. RESULTS No mortality or major morbidity occurred in those patients undergoing arrhythmia intervention. There were 7 deaths in total; 6 died suddenly, and the other died of purulent mediastinitis. None of the 6 sudden deaths underwent preoperative electrophysiological evaluation. The functional recovery was good in all survivals. CONCLUSIONS We conclude that detailed preoperative electrophysiological evaluation in patients with Ebstein's anomaly is mandatory. Aggressive surgical intervention of the associated arrhythmias in addition to anatomic correction can reduce the sudden death in Ebstein's anomaly.

Surgical treatment for atrial fibrillation is now feasible in selective cases. The aim of this study was to assess the electrophysiological properties of patients undergoing atrial compartment operation for chronic atrial fibrillation.Electrophysiological studies were performed in 20 mitral valve patients with atrial fibrillation who had been maintained in sinus rhythm for more than 1 year after atrial compartment operation. Intra-cardiac recording and programmed electrical stimulation were performed in various atrial compartments. The parameters studied included sinus node function, atrial conduction and refractoriness, atrioventricular conduction function and inducible arrhythmias if any. Intra-cardiac recordings showed that the rhythm was of sinus origin in all cases, with the earliest atrial activity located in the high right atrium. The mean sinus cycle length was 750 +/- 110 ms, AH time 106 +/- 29 ms, and HV time 53 +/- 7 ms. The sinus node function was normal in 18 patients (90%), and only two patients had prolonged sinus node recovery and sino-atrial conduction. The right atrial appendage compartment was driven by the sinus node in all patients. However, the conduction time from the high right atrium to the right atrial appendage compartment was markedly prolonged in 12 of 15 patients (80%) undergoing the three-compartment operation in which an incision was placed between the high right atrium and right atrial appendage compartments. On the other hand, the electrical activities in the left atrial compartment were much more varied. In 13 of 20 patients (65%), the left atrial compartment was driven by the sinus node; 11 of the 13 patients had a normal or mildly prolonged conduction time (ranged 75 to 146 ms), whereas two patients had a marked delay in conduction (200 ms and 266 ms, respectively). In the remaining seven patients, the left atrial compartments were dissociated from the rest of the heart; five of them had a quiescent left atrium, one a fluttering left atrial rhythm, and one a slow left atrial rhythm. The effective refractory period was longer in the left atrial compartment (242 +/- 47 ms) as compared to that of the high right atrium (224 +/- 26 ms, P0.01) and right atrial appendage compartments (219 +/- 25 ms, P0.01). Programmed electrical stimulation could not induce atrial fibrillation in any patient, whereas two patients had inducible atrial flutter and three repetitive atrial responses.(1) Atrial compartment operation does not impair sinus node function in most cases. (2) Elimination of atrial fibrillation while maintaining the electrical connection between different atrial compartments is feasible.

A 26-year-old woman with congenital mitral stenosis and embolic stroke was referred to our hospital. The echocardiogram showed a hypoplastic posterior mitral valve leaflet with short, unbalanced chordal attachments to the posteromedial papillary muscle. The mitral valve area was 0.9 cm2 by the pressure half-time method. There was no left atrial thrombus and spontaneous echo contrast. Percutaneous transvenous mitral commissurotomy was performed since the suggestion of surgical management was refused by her family members. A rupture at the chordae tendinae of the hypoplastic posterior papillary muscle developed during the procedure and needed mitral replacement. We advise that percutaneous transvenous mitral commissurotomy be avoided in adult patients with congenital mitral stenosis having an asymmetric and hypoplastic mitral valve.

We investigated the intrinsic cardiac mechanics of myocardium and changes in titin in insulin-resistant rats. Microsonometry and micromanometry were used to evaluate the maximal elastance (Emax) and myocardial stiffness constant (Km) of the left ventricle, in addition to the traditional systolic and diastolic cardiac function, with an isolated working heart preparation. Thirty 150 g Wistar rats were divided into three groups of 10. Group A was fed rat chow, while groups B and C were fed a 66% fructose diet for 7-8 months. Group C also received clonidine. Group B rats developed insulin resistance, as well as elevated plasma glucose and blood pressure. Group C rats also had insulin resistance and elevated plasma glucose, but not higher blood pressure. Group B rats had decreased Emax, decreased peak-dp/dt, prolonged Tau and increased Km compared to normal control rats. Group C rats, which mimicked the clinical condition of diabetic cardiomyopathy, maintained normal global left ventricular function as revealed by cardiac output, peak + dp/dt, peak-dp/dt and Tau of relaxation. However, they had a lower Emax slope (355 +/- 51 vs 535 +/- 56 mmHg.mm than group A rats, p0.05) and increased Km (81.6 +/- 9.9 vs 25.5 +/- 4.8 in group A, p0.001), even though the extent of elevation of plasma glucose was only mild (71.3 +/- 2.0 to 108.9 +/- 4.4 mg/dl, p0.001). Their left ventricular mass, myocyte size, interstitial fibrosis and vascular picture did not change. However, the content of myocardial titin decreased significantly (intensity ratio of titin/actin was 0.23 +/- 0.01 and 0.29 +/- 0.02 in group C and group A rats respectively, p0.05). These findings suggest that changes in titin play a role in the change in myocardial functional characteristics and may be one of the causes of diabetic cardiomyopathy.

In three adult patients, two with atrial septal defect and one with Ebstein's anomaly, chronic atrial fibrillation was documented for 13, 21, and 3 years, respectively. Atrial compartment surgery was performed for ablation of the atrial fibrillation concomitant with repair of the cardiac defects. The operation was performed with traditional cardiopulmonary bypass and crystalloid cardioplegia myocardial protection. A U-shaped incision was made in the right atrium: a longitudinal incision 1 cm lateral and parallel to the sulcus terminalis, extending along the borders of the atrial septum to 3 cm (upper margin) and 1 cm (lower margin) distant to the tricuspid anulus. Cryolesions of the atrial isthmus between the upper incision margin and the tricuspid valve anulus were created at -60o C for 180 seconds at a time. After the operation, all three patients had restored and maintained normal sinus rhythm during follow-up periods of 32, 16, and 3 months. Doppler echocardiography detected the recovery of atrial contractility in all three patients. Atrial compartment surgery is a simple and effective method for elimination of chronic atrial fibrillation associated with congenital heart defects. (J THORAC CARDIOVASC SURG 1996;111:231-7)

Despite major success in the treatment of atrioventricular (AV) node reentrant tachycardia using either catheter ablation or surgery, the morphologic basis underlying AV node reentry is not yet clear. A canine model of AV node reentrant tachycardia was used to examine the histologic features of the reentry circuit. AV node reentrant tachycardia was created in 4 of 8 dogs by a right atrial division which divided the right atrial free wall and the atrial septum into upper and lower portions on a plane between the mid-right atrial free wall and the fossa ovalis. The AV junctional area of all dogs were serially sectioned on a plane that was perpendicular to the AV annulus and the septum. The slices were stained with Masson's trichrome technique. The connections between atrial fibers and the compact AV node and the common AV bundle were examined, and comparison of the histologic features between dogs with and without AV nodal re-entry was made. The histologic examinations showed that, in all dogs, the operation scar was remote from the AV junctional area leaving the Koch's triangle intact. The compact node received its atrial inputs mainly from the anterosuperior and posterior aspects of the Koch's triangle. However, both atrial inputs gave off superficial (subendocardial) fibers that by-passed the compact node to terminate at the base of tricuspid valve. These superficial fibers might function as the proximal link between the dual AV nodal inputs by means of lateral connections. There was no bypass connection between atrial fibers and the common AV bundle. The histologic features of the AV junctional area was not different between dogs with and without AV nodal reentry. In conclusion, AV nodal reentry involves the anterior and posterior atrio-nodal inputs which function as dual AV nodal pathways, and the superficial bypass fibers form the proximal linkage between the two inputs. These structures, together with the compact node, complete the reentry circuit.

BACKGROUND--A specific local indicator in the Koch's triangle could be critical to the complication-free treatment of atrioventricular nodal reentrant tachycardia by transcatheter radiofrequency ablation. Recording of perinodal slow potential reflects a slow conduction area, and probably indicates the location of the slow pathway component of the circuit. Specific ablation of the slow pathway would carry the least risk of atrioventricular block. METHOD AND RESULTS--Guided by the mapped perinodal slow potential, atrioventricular nodal reentrant tachycardia was successfully eliminated in all of 55 consecutive patients in one session. Fifty two patients (94.5%) had confirmed slow potential at the final success sites. Despite the good result, the underlying electrophysiological mechanisms of early success from slow-potential-guiding catheter ablation were heterogeneous: selective slow pathway eradication in 31 patients (56.4%, group A), selective slow pathway modification in 18 patients (32.7%, group B), inadvertent fast pathway damage in six patients (10.9%, group C). Group B patients had the preservation of dual atrioventricular nodal pathways, adequate atrio-Hisian delay, fast pathway facilitation, and a higher frequency of inducible, single non-conducted nodal echo (15/18, 83.3% v 6/31, 19.4% in group A, P << 0.001). The upper communicating path of the circuit was implicated as another site of radiofrequency destruction. Three recurrences were documented in follow up study. However, reablation by the same approach caused complete atrioventricular block in one patient (1.7%, 1/58 procedures). None of the local characteristics of ablation sites was an independent predictor of procedure outcome. CONCLUSIONS--Perinodal slow potential is not a specific slow pathway indicator in transcatheter radiofrequency ablation of atrioventricular nodal reentrant tachycardia. Multiple strategic sites of the reentry circuit may be damaged through similar local signals.

To investigate the circadian variations of plasma atrial natriuretic peptide (ANP) and its relationship to arterial blood pressure, plasma renin activity and aldosterone level, we determined 24-h blood pressure in 14 healthy volunteers. Plasma ANP concentration, renin activity and aldosterone levels were measured every 3 h by radioimmunoassay. We found no significant circadian variation of plasma ANP level (pg/ml) (daytime level, 62 +/- 24 vs. nighttime level, 57 +/- 19, P = 0.146) and plasma renin level (ng/ml/h) (1.32 +/- 0.78 vs. 1.15 +/- 0.57, P = 0.148), but there was diurnal change of blood pressure (mmHg) (systolic, 122 +/- 7 vs. 116 +/- 11, P0.001; diastolic, 80 +/- 11 vs. 72 +/- 11, P = 0.025) and plasma aldosterone level (pg/ml) (86 +/- 42 vs. 62 +/- 37, P0.001). The blood pressure and aldosterone levels reached maxima (11:00 h and 08:00 h, respectively) before that of ANP (17:00 h) and then decreased together until the nadir at 02:00 h. This might indicate that elevation of arterial blood pressure and plasma aldosterone level stimulate release of ANP under normal physiological conditions.

To study the correlation between ambulatory blood pressure and target organ complications of hypertension, ambulatory blood pressure monitoring was performed on 290 patients with mild to moderate essential hypertension before treatment. Their target organ complications of hypertension were assessed by ECG, chest X-ray, urinalysis and an eye-fundus examination. An average ambulatory diastolic blood pressure value greater than the casual diastolic blood pressure was found in 35% of subjects with ECG evidence of left ventricular hypertrophy (LVH) and 5. 2% of subjects without (P

BACKGROUND Gastrointestinal bleeding is a hemorrhagic complication after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction (STEMI). OBJECTIVES To determine predictors of gastrointestinal bleeding and the impact of gastrointestinal bleeding on outcomes in STEMI patients undergoing primary percutaneous coronary intervention. METHODS AND RESULTS Gastrointestinal bleeding occurred in 18 (3.5%) of 519 consecutive patients with STEMI undergoing primary percutaneous coronary intervention. Univariate predictors of gastrointestinal bleeding were previous gastrointestinal bleeding (33% vs 4%, P < .001), impaired renal function (89% vs 37%, P

Body surface potential maps were obtained in 50 normal adults using the heart potential map system designed by Yamada. Group A (younger adult group) consisted of 30 persons whose ages ranged from 20 to 39 years. Group B (middle-aged group) included 20 persons whose ages ranged from 40 to 59 years.Although there were slight variations in the pattern of isopotential distribution among the subjects studied, a consistent pattern with a similar sequence was observed in both study groups. However, there were some parameters which significantly differed between groups A and B, including the earliest appearance time of the anterior negative potential (p

Previous studies have shown that an increased intake of dietary flavonoids is associated with a decreased risk of cardiovascular diseases (CVDs). PDGF is a major mitogen for vascular smooth muscle cell (VSMC) and participates in the pathogenesis of many CVDs. The study investigated whether the flavone chrysin affected PDGF functions in VSMCs and neointma formation in rat artery. We found that chrysin concentration-dependently inhibited PDGF-induced proliferation and chemotaxis and reduced PDGF signaling in VSMCs. Chrysin attenuated H 2 O 2 signaling and PDGF-induced reactive oxygen species production and NADPH oxidase activation but did not interfere with PDGF binding to VSMCs . The further analyses revealed that chrysin relieved PDGF-induced inhibition on activity of protein tyrosine phosphatase (PTP) and reduced PDGF-induced oxidation of PTP cysteinyl active site. Moreover, it inhibited PDGF receptor autophosphorylation induced by low-dose vanadate (an inhibitor for PTP). The effect of chrysin, but not of the flavonoid (-)-epigallocatechin-3-gallate and antioxidant N-acetylcysteine, on PDGF signaling and PTP activity was reversed by depletion of intracellular glutathione (GSH), suggesting an involvement of chrysin on GSH/glutaredoxin system for PTP reactivation. Finally, to demonstrate the effectiveness of chrysin in vivo, we showed that oral administration of chrysin before and after angioplasty could reduce neointima formation in balloon-injured carotid artery in rats. In conclusion, we provide here evidence that chrysin can regulate intracellular PTP activity during PDGF signaling, inhibits PDGF-induced VSMC proliferation and chemotaxis, and reduces arterial intima hyperplasia in vivo.

Background/PurposeKnowledge concerning subacute stent thrombosis (SST) following primary stenting for ST-elevation myocardial infarction (STEMI) is not widely available. We studied the incidence, predictors, and clinical outcomes of SST following STEMI.MethodsWe analyzed data from 455 consecutive patients who underwent primary stenting for STEMI. Baseline clinical characteristics, coronary angiographic features, medication and outcome were compared in patients with and without SST.ResultsSST occurred in 17 patients, and the incidence was 3.7%. Univariate predictors of SST were being a current smoker (53.0% vs. 82.4%, p = 0.01), Killip class ≥ II (38.4% vs. 58.8%, p = 0.05), no coronary re-flow after stenting (6.2% vs. 17.6%, p = 0.05) and lack of coprescription with a statin (39.5% vs. 5.9%, p

Left circumflex (LC)-related acute myocardial infarction (AMI) presenting without ST-T changes has been underdiagnosed in the emergency department. There is little information on its clinical features and significance.The aims of the study were to investigate the clinical characteristics and outcomes of LC-related AMI without ST-T changes.Ninety-six patients were admitted for LC-related AMI. Comparisons between those with and without ST-T changes were analyzed.Twenty-two patients (23%) did not have ST-T changes, whereas 74 patients (77%) had them. Patients without ST-T changes had younger age (55.6 + or - 16.8 vs 62.6 + or - 12.0 years, P = .03), fewer presented as Killip III/IV (4.5% vs 27.4%, P = .02) and with lower creatine kinase (1647.3 + or - 1602.2 vs 2778.2 + or - 2343.3 IU/L, P = .037) and creatine kinase-MB (136.8 + or - 130.3 vs 247.7 + or - 200.0 IU/L, P = .017), and more were with concurrent culprit lesion in the middle or distal LC and right- or balanced-dominant coronary circulation (86.4% vs 44.6%, P.001). During follow-up, the need for repeat percutaneous coronary intervention (48.6% vs 45.5%, P = .40) and recurrent infarction (13.5% vs 13.6%, P = .62) were similar between the 2 groups. The 30-day mortality (0% vs 5.4%, P = .35) and overall mortality rate (4.5% vs 12.2%, P = .28) between them were not different statistically.The relatively lower prevalence of LC-related AMI without ST-T changes in the study might be underestimated. These patients have smaller infarct size than patients with ST-T changes without differences in the short- and long-term outcomes between them.

AIM: To demonstrate the prevalence of sonographic fatty liver, overweight and ischemic heart disease (IHD) among the male workers in Taiwan, and to investigate the possible association of these three factors. METHODS: From July to September 2003, a total of 2 088 male aircraft-maintenance workers aged from 22 to 65 years (mean 40.5) underwent an annual health examination, including anthropometrical evaluation, blood pressure measurement, personal medical history assessment, biochemical blood analysis, abdominal ultrasonographic examination and digital electrocardiography (ECG). The Student’s t-test, χ2 test and multivariate logistic regression analysis were utilized to evaluate the relationship between IHD and salient risk factors. RESULTS: The all-over prevalence of overweight was 41.4%, and that of fatty liver was 29.5% (mild, moderate and severe fatty liver being 14.5%, 11.3%, and 3.7%, respectively); while the prevalence of ischemic changes on ECG was 17.1% in this study. The abnormal rates for conventional IHD risk factors including hypertension, dyslipidemia, hyperglycemia and overweight increased in accordance with the severity of fatty liver. Overweight and severity of fatty liver were independently associated with increased risks for developing IHD. Overweight subjects had a 1.32-fold (95%CI: 1.01-1.73) increased IHD risk. Participants with mild, moderate, and severe fatty liver had a 1.88-fold (95%CI: 1.37-2.6), 2.37-fold (95%CI: 1.66-3.37) and 2.76-fold (95%CI: 1.62-4.72) increased risk for developing IHD. The prevalence of ischemic ECG for the fatty liver-affected subjects with or without overweight was 30.1% and 19.1%, while that of overweight subjects free from fatty liver was 14.4%. Compared to the subjects without fatty liver nor overweight, IHD risk for the three subgroups above was as follows: OR: 2.95 (95%CI: 2.31-4.09), OR: 1.60 (95%CI: 1.07-2.39) and OR: 1.11 (95%CI: 0.78-1.56), respectively. CONCLUSION: The presence of fatty liver and its severity should be carefully considered as independent risk factors for IHD. Results of the study suggest the synergistic effect between fatty liver and overweight for developing IHD. Abdominal sonographic examination may provide valuable information for IHD risk assessment in addition to limited report about liver status, especially for overweight males.

The P wave in the surface ECG represents atrial electrical activation and may be altered in certain pathological conditions. Atrial compartment operation has been used to convert chronic AF to sinus rhythm. However, this procedure may result in changes of impulse conduction in various atrial compartments and alters the P wave morphology. This study sought to elucidate the P wave changes after the atrial compartment operation for AF. Fifteen patients undergoing the atrial compartment operation for chronic AF were studied. In the operation, the atrium was divided into three compartments, namely the left atrium, the atrial septum including sinus and AV nodes, and the right atrial compartment. The anatomic connection between adjacent compartments were preserved at the posterior lower margin of incisions. The surface lead P waves were correlated with intracardiac recording and stimulation in various atrial compartments. Fifteen age- and sex-matched control patients without structural heart diseases were compared. The results showed that patients undergoing the atrial compartment operation had a prolonged P wave duration (190 +/- 27 v s95 +/- 14 ms, P0.001), a prolonged PR interval (207 +/- 23 vs 155 +/- 20 ms, P0.001), and a shortened PR segment (17 +/- 19 vs 60 +/- 17 ms, P0.001). The increase in P wave duration was primarily due to a conduction delay from the sinus node to the other atrial compartments as the conduction time from the high right atrium to the right atrial appendage was 132 +/- 57 ms(vs 21 +/- 6 ms for control,P0.001), and the conduction time from the high right atrium to the distal coronary sinus was 140 +/- 55 ms(vs 70 +/- 15 ms, P0.001). However, the conduction from the high right atrium to the low septal right atrium, which were located in the same compartment, was not impaired. Also, the conduction in the AV node and His-Purkinje system were not impaired. The mean axis of P waves varied greatly, but was not statistically different from that of the control group (60 +/- 48 degrees vs 52 +/- 18 degrees,P0.05). Although the patients undergoing atrial compartment operation had a larger left atrial size, their P wave amplitude was smaller (1.0 +/- 0.3 vs 1.3 +/- 0.3 mm, P0.01), and an increased negative terminal force in V1 was not seen (0.02 +/- 0.02 vs 0.02 +/- 0.01 mm/s, P0.05). Alteration in P wave morphology was seen in 14 patients. All the P waves showed a biphasic configuration with an initial positive and a terminal slurred negative deflection in leads II, III, and aVF. The terminal components represented the activation of right atrial appendage in 5 patients, the left atrium in 1, and the combined activation of right atrial appendage and the left atrium in 8 patients. The P wave morphology suggested that activation of both the right atrial appendage and the left atrial compartments proceeded in a caudocranial direction as a result of the atrial incisions. In conclusion, atrial compartment operation altered the conduction time and direction in the atria and resulted in characteristic P wave changes.

Conjoined twins occur in approximately 1 in 50,000 births, and most of them have major junctions at the levels of chest and upper abdomen (thoracopagus). 1 It is difficult to separate twins with conjoined hearts. Only a single instance of successful separation in one of a set of twins with conjoined atria has been reported. 2 Therefore, preoperative documentation of the existence of conjoined hearts is crucial. We report herein a set of conjoined twins, in whom evaluation by echocardiography and angiography failed to define the conjoined hearts because the chambers and circulation were separate. Electrophysiologic studies demonstrated an atrial electromyocardial continuity resulting in synchronized heart beats of the twins.

To examine which recumbent position can lead to the highest vagal modulation in patients during the acute phase of myocardial infarction.Descriptive study.Intensive care unit in a medical center.A total of 52 patients admitted to the intensive care unit because of acute myocardial infarction (AMI), 41 patients with coronary artery disease (CAD), and 28 patients with patent coronary arteriogram.None.Heart rate variability analysis was performed in patients with AMI, patients with CAD, and patent coronary controls in supine, left lateral decubitus, and right lateral decubitus positions in random order. In the right lateral decubitus position, the vagal modulation was the highest and the sympathetic modulation was the lowest among three recumbent positions in three groups of patients. When the position was changed from supine to right lateral decubitus, the increase in vagal modulation was greater in patients who had more severely depressed vagal modulation in the supine position and the rate of increase was the greatest in patients with AMI, followed by patients with CAD and patent coronary controls. Detailed analysis showed that the vagal enhancing and sympathetic suppression effect of the right lateral decubitus position applied to patients with Q wave myocardial infarctions.The right lateral decubitus position can lead to the highest vagal modulation and the lowest sympathetic modulation among three recumbent positions in patients with Q wave myocardial infarction. The right lateral decubitus position can be used as an effective vagal enhancer in patients with Q wave myocardial infarction but without severe bradycardia or atrioventricular block.

The objective of the present study was to investigate the characteristics of body surface potential map (BSPM) findings during ventricular repolarization in patients with coronary artery disease (CAD). A total of 108 consecutive patients, 99 men and 9 women with angina pectoris and positive treadmill exercise test results as well as angiographically documented CAD underwent BSPM study in a fasting state. Their ages ranged from 30 to 70 years. There were 13 patients with right coronary artery (RCA) lesions, 37 with left anterior descending artery (LAD) lesions, 5 with left circumflex artery (LCX) lesions, 17 with both RCA and LAD lesions, 12 with both LCX and LAD lesions, and 24 with 3-vessel disease, The BSPMs were obtained by using the heart potential map system designed by Toyama et al. There were 59 lead points on the anterior chest wall and 28 on the back. The BSPMs in isopotential distribution were made every one msec throughout the ventricular activation period. The distribution of positive and negative potentials, potential maximum and potential minimum, polarity of potential distribution, and the reversal of potential distribution during ventricular repolarization were analyzed. The following information on BSPMs was obtained: (1) In early ventricular repolarization, the negative potential and the potential minimum appeared abnormally on the anterior thorax. The potential abnormality displayed on the right portion or the inferior portion in patients with RCA lesions, on the middle portion or the left portion in patients with LAD lesions, and on the left-superior portion or the left-middle portion in patients with LCX lesions. In patients with multi-vessel disease, the abnormal potential distribution showed a combined pattern of individual vessel lesions, (2) In some cases, the multipolar potential distribution appeared abnormally during the initial stage and the peak of the T wave. (3) The reversal of potential distribution was observed in about half of the patients. The characteristic findings of the BSPM during ventricular repolarization, including abnormal potential distribution, multipolar potential distribution and reversal of potential distribution, will be of clinical value in patients with CAD.

Effect of acupuncture at Nei-Kuan (EH-6) on left ventricular ejection fraction (LVEF) was examined in 22 patients with angiographically proved coronary artery disease (CAD) and 22 normal subjects. Serial equilibrium radionuclide angiography was done to measure LVEF at 4 different times (at baseline, at 1 to 15 minutes, and 16 to 30 minutes during acupuncture, and immediately after acupuncture). One week later, each patient had an identical imaging protocol with acupuncture performed at a dummy point. Our results showed that in normal subjects, the mean values of LVEF did not change significantly during or after acupuncture. In contrast, in patients with CAD, the mean values of LVEF in the initial 15 minutes of acupuncture significantly increased from baseline (42.5 ± 15.6% vs. 40.6 ± 15.4%, p < 0.05). The increase persisted through the next 15 minutes of acupuncture and 15 minutes after acupuncture, but became insignificant at one week. Thus, acupuncture at Nei-Kuan can temporarily improve LV function in patients with CAD.

In the presence of a normal atrial systole and optimal AV delay, atrial kick contributes to a significant fraction of the stroke volume. This atrial contribution may be lost during atrial asystole or mismatch in the timing of atrial and ventricular contraction. A patient received atrial compartment operation for his chronic AF. Although the AF was successfully converted to sinus rhythm, the conduction from the right to left atrium was markedly delayed so that the left atrial and ventricular activations occurred almost simultaneously. This delay in left atrial activation resulted in impaired cardiac performance.

The body surface potential map (BSPM) may reflect regional myocardial electrical activity. This technique can thus provide information regarding the excitation of ventricles. This study is an attempt to evaluate the usefulness of BSPM in determining the sites of the atrioventricular (AV) accessory pathway (AP) in patients with Wolff-Parkinson-White (W-P-W) syndrome. The BSPMs were obtained from 40 consecutive patients with W-P-W syndrome in a fasting state, using the heart potential map system designed by Toyama et al. Unipolar electrocardiograms were recorded simultaneously from 87 lead points on the chest surface, including 59 lead points on the anterior chest and 28 on the back. Wilson's central terminal was used as a voltage reference and BSPMs in an isopotential distribution pattern were made every millisecond throughout ventricular activation from these unipolar ECGs with the use of a microcomputer system. All patients underwent an electrophysiologic study (EPS) at cardiac catheterization. We analyzed the potential distribution during ventricular depolarization and compared the results between EPS and BSPM findings. The following results were obtained: (1) seven types of BSPM pattern were identified in accordance with the sites of the AV AP confirmed by EPS; (2) the location of the potential minimum of ventricular depolarization and the direction of the excitation wavefront during early ventricular depolarization, the reversal pattern of ventricular potential distribution, the epicardial right ventricular breakthrough and the dynamic change of ventricular potential distribution were useful for the detection of the ventricular pre-excitation site; (3) epicardial right ventricular breakthrough occurred in nearly all patients with left ventricular free wall accessory AV connections; (4) the abnormal early reversal pattern of ventricular potential distribution did not occur in patients with left ventricular AV connections but did appear in most patients with right ventricular free wall AV connections. Accordingly, BSPM is a reliable non-invasive procedure to determine the ventricular pre-excitation sites of patients with W-P-W syndrome.

Atrial dissociation with segmental atrial arrhythmia is an interesting electrophysiological phenomenon. It was rarely reported before to be caused by anatomical exit block after cardiac surgery. We report the case of a 28-year-old patient who developed atrial disassociation after a surgical method for correcting atrial fibrillation--atrial compartment operation. The segmental atrial flutter was first found by Doppler echocardiography and proved later by detailed intracardiac mapping.

The relation between left ventricular (LV) endsystolic wall stress (sigma es) and rate-corrected velocity of circumferential fiber shortening (Vcfc), which is independent of heart rate (HR) and loading conditions has previously been used to assess cardiac contractility in insulin dependent diabetes mellitus (IDDM). This study is the first report in which this relation has been utilized with data obtained by echocardiography in addition to the traditional indices, to evaluate the cardiac function in asymptomatic, middle-aged patients with noninsulin dependent diabetes mellitus (NIDDM) at baseline and during dobutamine stimulation. There were 16 NIDDM patients in our study and these patients were classified into 2 groups. Group 1 consisted of 11 patients without microvascular complications. Group 2 consisted of the remaining 5 patients with microvascular complications. Ten age- and sex-matched normal subjects were enrolled as a control group. At baseline, diabetic patients tended to have a faster HR and a greater LV enddiastolic dimension, though these values were not significantly different from the normal subjects. Ejection fraction (EF) in group 1 was significantly higher than that of the normal controls (73 +/- 2% vs 65 +/- 2%, p0.005). Mitral inflow pattern was normal (E/A1) in the normal subjects (1.11 +/- 0.06), but reversed in group 1 (0.87 +/- 0.07) and group 2 (0.95 +/- 0.12). Isovolumic relaxation time corrected for HR (IVRTc) and the slope of relation between sigma es and Vcfc were similar among the 3 groups. Comparing Vcfc at 50 g/cm2 of sigma es, it tended to increase from the normal subjects (0.883 +/- 0.057 cir/sec) to 0.969 +/- 0.048 in group 1 and 1.034 +/- 0.101 in group 2, though this result was not statistically significant. During dobutamine stimulation, EF increased and IVRTc shortened significantly only in the normal subjects. E/A became normalized in both diabetic groups. The increment in Vcfc representing cardiac reserve of contractility was significantly lower in the diabetics (0.110 +/- 0.040 in group 1 and 0.057 +/- 0.043 in group 2) than in normal subjects (0.244 +/- 0.044). In conclusion, using the index of relation between sigma es and Vcfc, the cardiac contractility of NIDDM was not impaired at baseline, and even had a tendency to increase. However, during dobutamine stimulation, the inadequate reserve of contractility was exposed, especially in those patients who had microvascular complications. These results indicate the importance of controlling diabetes, not only to prevent the development of microvascular complications but also to preserve cardiac function.

To examine the association of the molecular variants of the angiotensinogen (AGT) gene with essential hypertension in Taiwanese.We conducted a case-control study concerning 151 subjects, 102 hypertensives and 49 normotensives. We created a rapid mini-sequencing method based on dye-terminator cycle sequencing to simultaneously detect the M235T and T174M variants of the AGT gene for each subject.The genotype and allele distribution of the M235T variant differed significantly in hypertensives and normotensives (chi 2 = 11.106, P = 0.004 and chi 2 = 6.453, P = 0.011, respectively), whereas those of the T174M variant did not differ (chi 2 = 0.004, P = 0.998 and chi 2 = 0.032, P = 0.858, respectively). The odds ratio for hypertension was 3.64 (95% confidence interval 1.56-8.49) for subjects with the C/C genotype of the M235T variant compared with other genotypes of 2.87 (95% confidence interval 1.76-4.68) for those carrying allele C versus those carrying allele T.The molecular variant M235T, but not T174M, of the AGT gene is associated significantly with essential hypertension in this Taiwanese population. The genotype C/C or allele C is a risk factor for hypertension. The underlying mechanism of this association needs to be elucidated further.

Insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been postulated as a risk factor for coronary heart disease. We conducted a case-control study of 271 Chinese, including 114 subjects with coronary artery disease (CAD), 42 with non-CAD and 115 apparently normal controls to examine the association of I/D polymorphism and CAD. The genotypes were identified by polymerase chain reaction and the plasma ACE activity was assayed by spectrophotometry. The allele and genotype frequencies were not different among the CAD, non-CAD and apparently normal groups (p = 0.42 and 0.63). Plasma ACE activity was not different among the three groups (p = 0.32). The D-allele and DD genotype were not more prevalent in subjects with low risk CAD (p = 0.07 and 0.16) and subjects with myocardial infarction (p = 0.79 and p = 0.35). No association was found between I/D polymorphism and severity of CAD (p = 0.42 and 0.70). In conclusion, the deletion polymorphism of the ACE gene may not be an independent risk factor in the development of CAD or myocardial infarction in this Chinese population. The unique or synergistic effect of other genes needs further study.

To examine the association between insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene and essential hypertension in a Chinese population, a case-control study was conducted using 157 hypertensive and 115 normotensive subjects. The I/D polymorphism of the ACE gene was identified by polymerase chain reaction. Plasma ACE activity was determined using spectrophotometry. The difference of allele frequencies between normotensives and hypertensives was statistically significant (X2 = 4.467, P = .035), while the gentotype distribution was not different between normotensive and hypertensive subjects (X2 = 3.954, P = .138). Plasma ACE activity was highest in the DD genotype, followed by the ID genotype, and the lowest in the II genotype (P = .0001 in normotensives and P = .163 in hypertensives, respectively). Thus, we conclude that the ACE gene polymorphism is not associated with essential hypertension in this Chinese population, but plasma ACE activity is genetically determined in the normotensive Chinese.

Objectives The presence of postoperative atrial fibrillation predicts a higher short- and long-term mortality rates; however, no scoring system has been used to discriminate patients at high risk for this complication. The aim of this study was to investigate whether the CHADS 2 and CHA 2 DS 2 -VASc scores are useful risk assessment tools for new-onset atrial fibrillation after cardiac surgery. Methods A total of 277 consecutive patients who underwent cardiac surgery were prospectively included in this risk stratification study. We calculated the CHADS 2 and CHA 2 DS 2 -VASc scores from the data collected. The primary end point was the development of postoperative atrial fibrillation within 30 days after cardiac surgery. Results Eighty-four (30%) of the patients had postoperative atrial fibrillation at a median of 2 days (range, 0-27 days) after cardiac surgery. The CHADS 2 and CHA 2 DS 2 -VASc scores were significant predictors of postoperative atrial fibrillation in separate multivariate regression analyses. The Kaplan-Meier analysis obtained a higher postoperative atrial fibrillation rate when based on the CHADS 2 and CHA 2 DS 2 -VASc scores of at least 2 than when based on scores less than 2 (both log rank, P 2 DS 2 -VASc scores could be used to further stratify the patients with CHADS 2 scores of 0 or 1 into 2 groups with different postoperative atrial fibrillation rates at a cutoff value of 2 (12% vs 32%; P = .01). Conclusions CHADS 2 and CHA 2 DS 2 -VASc scores were predictive of postoperative atrial fibrillation after cardiac surgery and may be helpful for identifying high-risk patients.

Objectives. The purpose of the study was to investigate the hypothesis that nodal approaches of both anterior and posterior atrial input sites of the atrioventricular (AV) node contribute to part of the circuit of AV node reentrant tachycardia. Thus, tachycardia might be elicited by a premature atrial impulse that arrived at the AV node through one input site while blocked at another. Background. Atrioventricular node reentrant tachycardia is the most common supraventricular tachycardia in humans, yet the exact pathway of the reentrant circuit is unknown. Methods. In eight dogs, an operation that blocked atrial impulses from the anterior input site to the AV node was performed through a right thoracotomy with the inflow occlusion method. The right atrial free wall and the anterior atrial septum between the sinoatrial node and the AV node were completely divided, whereas the tissues within the triangle of Koch remained intact. Thus, atrial impulses were blocked from the anterior input site in the right atrium and the atrial septum and were conducted only through the left atrial free wall to the posterior atrial septum into the AV node. Results. In a baseline electrophysiologic study before operation, dual AV conduction pathways were demonstrated in seven of eight dogs, but none of the seven had inducible AV node reentrant tachycardia. A repeat study 1 week postoperatively revealed that 1) both PR and AH intervals were prolonged during sinus rhythm (p < 0.01); 2) anterograde and retrograde conduction of the AV node showed no significant changes; and 3) AV node reentrant tachycardia was induced in four dogs (50%), of which three had sustained tachycardia. Conclusions. These results are compatible with the hypothesis that both nodal approaches of atrial input sites of the AV node contribute to part of the circuit of AV node reentrant tachycardia. They also confirm Moe's hypothesis of the existence of a brake system that prevents sustained AV node reentry. Our data suggest that the brake system is located in the anterior atrial septum.

In a search for features predictive of ventricular arrhythmias in myocardial ischemia, the body surface potential maps of 17 dogs with coronary artery occlusion were studied. Ventricular tachycardia occurred in 9 (53%) of the 17 dogs. Multiple distribution of the abnormal potential minimum was found in 6 (67%) of the 9 dogs with (group A) and none of the 8 dogs without ventricular tachycardia (group B). The difference was statistically significant (p less than 0.01). The abnormal "early reversal" phenomenon of potential distribution was observed in 6 (67%) of group A and 7 (88%) of group B. The difference was not statistically significant (p greater than 0.05). The area of abnormal negative potential was 28.0 +/- 8.5 cm2 for group A and 14.5 +/- 5.5 cm2 for group B (p less than 0.001). The abnormal negative potential lasted for 25.4 +/- 3.5 ms in group A and 10.1 +/- 5.1 ms in group B (p less than 0.001). The abnormally early appearance of potential minimum lasted for 24.2 +/- 5.1 ms in group A and 10.5 +/- 5.4 ms in group B (p less than 0.001). The data suggest that the distribution, area, and duration of the abnormal negative potential of the body surface potential map are useful in the prediction of ventricular tachycardia associated with coronary artery occlusion.

The exact site of reentrant circuit involved in the atrioventricular node reentrant tachycardia was questioned. Seven patients (6 females and 1 male), aged 21 to 64 years (mean = 40 +/- 17 years), with refractory nodal reentry, underwent surgical treatment. The associated cardiac diseases included rheumatic valvar disease in two and an atrial septal defect. Electrophysiologic studies before surgery showed dual nodal pathways in 4 patients. Right atrial endocardial mapping was performed and the earliest retrograde atrial activation during tachycardia was mapped to the apex of the triangle of Koch in 6 patients and near the orifice of coronary sinus in one. Perinodal dissection was performed according to the location of earliest retrograde atrial activity. Care was taken to preserve as much of the atrioventricular node and its arterial supply as was possible. Immediately after surgery, conduction in an antegrade direction recovered and the tachycardia could no longer be reproduced. There was no surgical mortality or morbidity. At 10 to 26 months of follow-up, all patients remain free of tachycardia without antiarrhythmic drugs. Four patients underwent repeated electrophysiologic studies at 2 weeks to 6 months after surgery. Dual nodal pathways were no longer demonstrated. It is concluded that the perinodal atrial tissue plays a part in the atrioventricular nodal reentry, and that surgical dissection is a simple and effective treatment for patients with refractory atrioventricular node reentrant tachycardia.

We evaluated the effects of dicentrine on the physical properties of systemic arterial trees. Dicentrine, isolated from Lindera megaphylla, was identified as a potent, selective alpha 1-adrenoceptor antagonist. We used high-fidelity multisensor catheter to measure the ascending aortic pressure and flow signals in 9 mongrel dogs. A succinct T-tube model with vascular nonuniformity was adopted to relate the pulsatile pressure and flow waves. The model-estimated parameters were capable of representing the mechanical properties of the blood vessel walls. Dicentrine had a beneficial effect on the rigidity of head and body circulation, respectively. There were great improvements not only in the tube distensibility and wave transmission time, but also in the peripheral load compliance and resistance. In global circulation that was defined as the parallel combination of head and body circulation, dicentrine significantly reduced values in characteristic impedance of the ascending aorta from 164 +/- 67 to 105 +/- 43 dynes/s/cm5, and in wave reflection factor from 0.46 +/- 0.14 to 0.36 +/- 0.13, and in total peripheral vascular resistance from 4,751 +/- 1,226 to 3,581 +/- 1,277 dynes/s/cm5. On the other hand, total peripheral load compliance was increased from 0.2950 +/- 0.1794 to 0.4457 +/- 0.2199 ml/mm Hg. Cardiac output (CO) and heart rate (HR) remained unchanged, however. Dicentrine had an impact on the mechanical properties of Windkessel vessels and resistance vessels in the systemic circulation.