Aims: As arrhythmias in the long QT syndrome(LQTS) are triggered by heart rate deceleration or acceleration, we speculated that the sudden bradycardia and subsequent tachycardia that follow adenosine injection would u...Aims: As arrhythmias in the long QT syndrome(LQTS) are triggered by heart rate deceleration or acceleration, we speculated that the sudden bradycardia and subsequent tachycardia that follow adenosine injection would unravel QT changes of diagnostic value in patients with LQTS. Methods and results: Patients(18 LQTS and 20 controls) received intravenous adenosine during sinus rhythm. Adenosine was injected at incremental doses until atrioventricular block or sinus pauses lasting 3 s occurred. The QT duration and morphology were studied at baseline and at the time of maximal bradycardia and subsequent tachycardia. Despite simitar degree of adenosine- induced bradycardia(longest R- R 1.7± 0.7 vs. 2.2± 1.3 s for LQTS and controls, P=NS), the QT interval of LQT patients increased by 15.8± 13.1% , whereas the QT of controls increased by only 1.5± 6.7% (P< 0.001). Similarly, despite similar reflex tachycardia(shortest R- R 0.58± 0.07 vs. 0.55± 0.07s for LQT patients and controls, P=NS), LQTS patients developed greater QT prolongation(QTc=569± 53 vs. 458± 58 ms for LQT patients and controls, P< 0.001). The best discriminator was the QTc during maximal bradycardia. Notched T- waves were observed in 72% of LQT patients but in only 5% of controls during adenosine- induced bradycardia(P< 0.001). Conclusion: By provoking transient bradycardia followed by sinus tachycardia, this adenosine challenge test triggers QT changes that appear to be useful in distinguishing patients with LQTS from healthy controls.展开更多
Recent evidence suggests that atherosclerosis is an inflammatory disorder in which cytokines appear to play an important role. Special attention centered over the possible contribution of cytokines to the destabilizat...Recent evidence suggests that atherosclerosis is an inflammatory disorder in which cytokines appear to play an important role. Special attention centered over the possible contribution of cytokines to the destabilization of the plaque. IL-18 is a proinflammatory cytokine of the IL-1 family, recognized for its ability to promote IFN-γsecretion. It has recently been detected in human plaques and its administration was associated with increased atheros-clerosis in apolipoprotein E(apoE) mice concomitant with an increase in plaque infiltrating inflammatory cells. In our study, we investigated whether patients with established atherosclerosis, with either stable or unstable angina, possessed high levels of IL-18. Patients with stable angina(n=48) were from the outpatient clinic whereas patients with unstable angina(n=73) were recruited upon admission and prior to performance of coronary angiography. Control patients(n=19) were healthy subjects with no evidence of coronary artery disease. Serum levels of IL-18 were assayed by ELISA. Patients with stable and unstable angina exhibited higher serum levels of IL-18(77.1±7.2 and 61.5±5.1 pg/ml, respectively) in comparison to control subjects(p=0.002 and p=0.02, respectively). However, levels of IL-18 did not differ significantly between patients with stable and unstable angina. No differences were evident in the serum concentrations of IL-18 in patients with unstable angina(n=17) upon admission and 1-3 months later when the angina was already controlled. Although IL-18 serum levels appear elevated in the presence of coronary atherosclerosis, there is no evidence to associate this progression towards plaque instability.展开更多
文摘Aims: As arrhythmias in the long QT syndrome(LQTS) are triggered by heart rate deceleration or acceleration, we speculated that the sudden bradycardia and subsequent tachycardia that follow adenosine injection would unravel QT changes of diagnostic value in patients with LQTS. Methods and results: Patients(18 LQTS and 20 controls) received intravenous adenosine during sinus rhythm. Adenosine was injected at incremental doses until atrioventricular block or sinus pauses lasting 3 s occurred. The QT duration and morphology were studied at baseline and at the time of maximal bradycardia and subsequent tachycardia. Despite simitar degree of adenosine- induced bradycardia(longest R- R 1.7± 0.7 vs. 2.2± 1.3 s for LQTS and controls, P=NS), the QT interval of LQT patients increased by 15.8± 13.1% , whereas the QT of controls increased by only 1.5± 6.7% (P< 0.001). Similarly, despite similar reflex tachycardia(shortest R- R 0.58± 0.07 vs. 0.55± 0.07s for LQT patients and controls, P=NS), LQTS patients developed greater QT prolongation(QTc=569± 53 vs. 458± 58 ms for LQT patients and controls, P< 0.001). The best discriminator was the QTc during maximal bradycardia. Notched T- waves were observed in 72% of LQT patients but in only 5% of controls during adenosine- induced bradycardia(P< 0.001). Conclusion: By provoking transient bradycardia followed by sinus tachycardia, this adenosine challenge test triggers QT changes that appear to be useful in distinguishing patients with LQTS from healthy controls.
文摘Recent evidence suggests that atherosclerosis is an inflammatory disorder in which cytokines appear to play an important role. Special attention centered over the possible contribution of cytokines to the destabilization of the plaque. IL-18 is a proinflammatory cytokine of the IL-1 family, recognized for its ability to promote IFN-γsecretion. It has recently been detected in human plaques and its administration was associated with increased atheros-clerosis in apolipoprotein E(apoE) mice concomitant with an increase in plaque infiltrating inflammatory cells. In our study, we investigated whether patients with established atherosclerosis, with either stable or unstable angina, possessed high levels of IL-18. Patients with stable angina(n=48) were from the outpatient clinic whereas patients with unstable angina(n=73) were recruited upon admission and prior to performance of coronary angiography. Control patients(n=19) were healthy subjects with no evidence of coronary artery disease. Serum levels of IL-18 were assayed by ELISA. Patients with stable and unstable angina exhibited higher serum levels of IL-18(77.1±7.2 and 61.5±5.1 pg/ml, respectively) in comparison to control subjects(p=0.002 and p=0.02, respectively). However, levels of IL-18 did not differ significantly between patients with stable and unstable angina. No differences were evident in the serum concentrations of IL-18 in patients with unstable angina(n=17) upon admission and 1-3 months later when the angina was already controlled. Although IL-18 serum levels appear elevated in the presence of coronary atherosclerosis, there is no evidence to associate this progression towards plaque instability.
