A technique for diagnosis of accessory pathway using the H-H and A-A intervals of the first entrained cycle during ventricular overdrive pacing

Although advancement of succeeding atrial activation by a ventricular extrastimulus (VES) on His refractoriness during supraventricular tachycardia (SVT) has been used as evidence of an accessory pathway (AP), the sensitivity of this method is suboptimal. This study was designed to compare the His-His (H-H) and atrial-atrial (A-A) intervals of the first entrained cycle during ventricular overdrive pacing (VOD) for the diagnosis of AP, in comparison to the conventional VES method. In 55 patients with SVT, a VES was elicited on His refractoriness during SVT. VOD was subsequently performed at cycle lengths 30 to 40 ms shorter than SVT cycle lengths. When the A-A interval became equal to the pacing cycle length after some beats of VOD, the cycle was considered the first entrained cycle and the H-H interval preceding the A-A interval was measured. VES advanced the next atrial activation in 16 patients (52%) with an AP, but in no patient without an AP. The H-H interval of the first entrained cycle was longer than the pacing cycle length by > or =15 ms in all patients with an AP, but was equal to the pacing cycle length in all patients without an AP. The criterion of H-H greater than A-A by > or =15 ms for the first entrained cycle provided higher diagnostic yield for AP compared with the VES method(100% vs 52%, p <0.001). In conclusion, this new criterion reliably diagnoses the presence of an AP in patients with SVT, with higher sensitivity compared with the VES method.     

Risk factors of thrombotic recurrence and major bleeding in patients with intermediate-risk for recurrence of venous thromboembolism

Journal of Thrombosis and Thrombolysis - Prolonged anticoagulation therapy is recommended for patients with intermediate-risk for recurrence of venous thromboembolism (VTE). The current study aimed...     

Microvascular resistance in response to iodinated contrast media in normal and functionally impaired kidneys

Contrast‐induced nephropathy (CIN) is considered to result from intrarenal vasoconstriction, and occurs more frequently in impaired than in normal kidneys. It was hypothesized that iodinated contrast media would markedly change renal blood flow and vascular resistance in functionally impaired kidneys. Thirty‐six patients were enrolled (32 men; mean age, 75.3 ± 7.6 years) undergoing diagnostic coronary angiography and were divided into two groups based on the presence of chronic kidney disease (CKD), defined as an estimated glomerular filtration rate (eGFR) of < 60 mL/min per 1.73 m² (CKD and non‐CKD groups, n = 18 in both). Average peak velocity (APV) and renal artery resistance index (RI) were measured by Doppler flow wire before and after administration of the iodinated contrast media. The APV and the RI were positively and inversely correlated with the eGFR at baseline, respectively (APV, R = 0.545, P = 0.001; RI, R = ?0.627, P < 0.001). Mean RI was significantly higher (P = 0.015) and APV was significantly lower (P = 0.026) in the CKD than in the non‐CKD group. Both APV (P < 0.001) and RI (P = 0.002) were significantly changed following contrast media administration in the non‐CKD group, but not in the CKD group (APV, P = 0.258; RI, P = 0.707). Although renal arterial resistance was higher in patients with CKD, it was not affected by contrast media administration, suggesting that patients with CKD could have an attenuated response to contrast media.     

Caspase activation and neuroprotection in caspase-3- deficient mice after in vivo cerebral ischemia and in vitro oxygen glucose deprivation

Caspase-3 is a major cell death effector protease in the adult and neonatal nervous system. We found a greater number and higher density of cells in the cortex of caspase-3(-/-) adult mice, consistent with a defect in developmental cell death. Caspase-3(-/-) mice were also more resistant to ischemic stress both in vivo and in vitro. After 2 h of ischemia and 48 h of reperfusion, cortical infarct volume was reduced by 55%, and the density of terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling-positive cells was decreased by 36% compared with wild type. When subjected to oxygen-glucose deprivation (2 h), cortical neurons cultured from mice deficient in caspase-3 expression were also more resistant to cell death by 59%. Mutant brains showed caspase-specific poly(ADP-ribose) polymerase cleavage product (85-kDa fragment) in vivo and in vitro, suggesting redundant mechanisms and persistence of caspase-mediated cell death. In the present study, we found that caspase-8 mediated poly(ADP-ribose) polymerase cleavage in caspase-3(-/-) neurons in vivo and in vitro. In addition, mutant neurons showed no evidence of compensatory activation by caspase-6 or caspase-7 after ischemia. Taken together, these data extend the pharmacological evidence supporting an important role for caspase-3 and caspase-8 as cell death mediators in mammalian cortex and indicate the potential advantages of targeting more than a single caspase family member to treat ischemic cell injury.