Regular tachycardia terminated by ventricular anti-tachycardia pacing in an ICD recipient. What is the mechanism?

This is the case of a misdiagnosed atrioventricular nodal reentry tachycardia (AVNRT) with occasionally 2:1 atrioventricular block terminated by delivery of an inappropriate ventricular antitachycardia pacing scheme, in an ICD recipient. The detailed analysis of stored electrograms facilitated the revelation of the arrhythmic mechanism.

Chronic skeletal muscle ischemia preserves coronary flow in the ischemic rat heart.

Chronic skeletal muscle ischemia confers cytoprotection to the ventricular myocardium during infarction, but the underlying mechanisms remain unclear. Although neovascularization in the left ventricular myocardium has been proposed as a possible mechanism, the functional capacity of such vessels has not been studied. We examined the effects of chronic limb ischemia on infarct size, coronary blood flow, and left ventricular function after ischemia-reperfusion. Hindlimb ischemia was induced in 65 Wistar rats by excision of the left femoral artery, whereas 65 rats were sham operated. After 4 wk, myocardial infarction was generated by permanent coronary artery ligation. Infarct size was measured 24 h postligation. Left ventricular function was evaluated in isolated hearts after ischemia-reperfusion, 4 wk after limb ischemia. Neovascularization was assessed by immunohistochemistry, and coronary flow was measured under maximum vasodilatation at different perfusion pressures before and after coronary ligation. Infarct size was smaller after limb ischemia compared with controls (24.4 ± 8.1% vs. 46.2 ± 9.5% of the ventricle and 47.6 ± 8.7% vs. 80.1 ± 9.3% of the ischemic area, respectively). Indexes of left ventricular function at the end of reperfusion (divided by baseline values) were improved after limb ischemia (developed pressure: 0.68 ± 0.06 vs. 0.59 ± 0.05, P = 0.008; maximum +dP/dt: 0.70 ± 0.08 vs. 0.59 ± 0.04, P = 0.004; and maximum -dP/dt: 0.86 ± 0.14 vs. 0.72 ± 0.10, P = 0.041). Coronary vessel density was markedly higher (P = 0.00021) in limb ischemic rats. In contrast to controls (F = 5.65, P = 0.00182), where coronary flow decreased, it remained unchanged (F = 1.36, P = 0.28) after ligation in limb ischemic rats. In conclusion, chronic hindlimb ischemia decreases infarct size and attenuates left ventricular dysfunction by increasing coronary collateral vessel density and blood flow.

ULnar Artery Transient Compression Facilitating Radial Artery Patent Hemostasis (ULTRA): A Novel Technique to Reduce Radial Artery Occlusion After Transradial Coronary Catheterization.

AIMS: To evaluate the safety and efficacy of a novel technique with simultaneous compression of the ulnar artery in order to reduce the incidence of radial artery occlusion (RAO) after transradial cardiac catheterizations. METHODS AND RESULTS: Ipsilateral ulnar artery transient compression for 1 hour facilitating radial artery patent hemostasis (ULTRA) was performed in all patients treated transradially in October 2015 and was compared with patients treated with conventional patent hemostasis in September 2015. The primary endpoint of the study was to evaluate the incidence of RAO within 1 hour after removing the closure device, confirmed by the absence of palpation and the consecutive absence of flow signal with Doppler examination. A total of 119 patients were treated with the ULTRA method and 121 patients with conventional patent hemostasis. None of the patients treated with ULTRA had RAO compared with 6 patients (5%) of those treated with conventional patent hemostasis (P=.01). No hematomas EASY class ≥3, nerve injury, or ischemic pain complications were recorded in either group. CONCLUSION: The ULTRA technique may reduce the incidence of RAO in patients treated with the radial approach compared with conventional patent hemostasis.