A Simple Method to Differentiate Atrioventricular Node Reentrant Tachycardia from Orthodromic Reciprocating Tachycardia.

Discrimination between atrioventricular node reentry tachycardia (AVNRT) and orthodromic reciprocating tachycardia (ORT) during an electrophysiological study is sometimes challenging. This study aimed to investigate if the difference in the local VA (ventricle-atrium) interval during ventricular entrainment pacing and during tachycardia (DVA, defined as the shortest local VA interval of coronary sinus [CS] during entrainment minus the shortest local VA interval of CS during tachycardia) was different in patients with AVNRT and patients with ORT.Diagnoses of AVNRT or ORT through a concealed accessory pathway (AP) were made according to conventional electrophysiological criteria and ablation results. Entrainment by right ventricular (RV) pacing was performed in each patient before ablation and patients with successful entrainment were included in the study. The DVA was compared between patients with AVNRT and patients with ORT. The DVA in patients with AVNRT was significantly longer than that in patients with ORT (120 ± 20 versus 5.7 ± 9; P < 0.001). In each patient with AVNRT of slow-fast type, fast-slow type, and slow-slow type, the DVA was more than 48 ms. In each patient with ORT using a left free wall accessory pathway (AP), right free wall AP, and septal AP, the DVA was less than 20 ms.DVA was found to be a rapid, useful test in distinguishing patients with AVNRT from those with ORT.

Combination of C-reactive protein and cardiac troponin I for predicting adverse cardiac events after sirolimus-eluting stent implantation.

AIMS: We assessed the predictive value of a combination of C-reactive protein (CRP) and cardiac troponin I (cTnI) in a 2-year prospective study in patients undergoing sirolimus-eluting stents (SES) implantation. METHODS AND RESULTS: CRP and cTnI levels were examined 1 day before and after SES implantation in 322 patients. CRP level greater than 3.0 mg/l (defining the high serum CRP levels) and cTnI level greater than 1.0 microg/l (defining the high serum cTnI levels) were considered abnormal. Major adverse cardiac events were defined as nonfatal myocardial infarction (MI), target vessel revascularization (TVR), and cardiac death. After 2+/-0.2 years of follow-up, there were 11 MI, 19 TVR, and 11 cardiac deaths. After adjustment for relevant risk factors, the combination of high CRP and cTnI remained predictive of adverse cardiac events, with the presence of both elevated CRP and cTnI associated with the highest risks of MI [relative risk (RR): 4.0, 95% confidence interval (CI): 2.3-6.4], TVR (RR: 3.3, 95% CI: 2.8-5.3), and cardiac death (RR: 4.2, 95% CI: 2.6-6.0). The presence of either a high CRP or cTnI was associated with an intermediated risk of MI (RR: 1.7, 95% CI: 1.2-2.2), TVR (RR: 1.5, 95% CI: 1.2-2.7), and cardiac death (RR: 2.8, 95% CI: 2.2-3.6). CONCLUSION: The combination of elevated CRP and cTnI increased the risk of adverse cardiac events, demonstrating the additive impacts of active inflammation and myocardial injury on prognosis after SES implantation.

[Elevated serum high sensitivity C-reactive protein and endothelial dysfunction in silent myocardial ischemia].

OBJECTIVE: To explore the association between silent myocardial ischemia (SMI) and high sensitivity C-reactive protein (hsCRP) and endothelial dysfunction. METHODS: 148 asymptomatic patients (103 men and 45 women) with known CAD were recruited. According to the results of ambulatory electrocardiography recording (AECG), patients were divided into two groups: SMI group and non-SMI group. All the patients underwent assessment of endothelial dependent flow mediated dilation (FMD) with high resolution ultrasound for the evaluation of endothelial function and 24-hour three-lead ambulatory electrocardiography recording for the detection of SMI. Serum hsCRP, blood glucose, HDL cholesterol, LDL cholesterol and triglycerides were measured. RESULTS: Sixty of the 148 patients had SMI, with a relatively high prevalence of 40.5%. The serum concentration of hsCRP in SMI group was higher than that in non-SMI group (1.86 +/- 0.52 vs 0.91 +/- 0.36, P < 0.05) and FMD was lower in SMI group than that in non-SMI group (3.02 +/- 1.46 vs 6.36 +/- 3.79, P < 0.05). In logistic regression analysis, SMI was found to be related only to FMD (beta = -0.452, P = 0.046, OR = 1.572) and hsCRP (beta = 1.233, P = 0.036, OR = 1.632). CONCLUSIONS: SMI shows a relatively high prevalence in patients with known stable CAD; it is suggested that this population still needs to be carefully evaluated with risk stratification. SMI may be caused by inflammation and endothelial dysfunction. FMD and hsCRP may serve as the surrogate markers in screening SMI in patients with known CAD.