A case of paroxysmal atrial fibrillation with a non-pulmonary vein trigger identified by intravenous adenosine triphosphate infusion.

A 54-year-old woman was referred to our institution with frequent chest discomfort and was diagnosed with drug-refractory paroxysmal atrial fibrillation. Radiofrequency catheter ablation (RFCA) was performed using a three-dimensional electroanatomic mapping system. After completion of left and right circumferential pulmonary vein isolation (CPVI), an intravenous bolus of adenosine triphosphate (ATP, 20 mg) was administered to evaluate the electric reconduction between the pulmonary vein (PV) and left atrium (LA). Although no PV-LA reconduction was observed, atrial fibrillation (AF) was reproducibly induced. As the duration of AF was very short (<20 s), no further RFCA to the LA was performed. One month later, the patient presented with frequent atrial tachyarrhythmias (ATs), and RFCA was repeated. Although no electric reconduction was observed in the left- or right-sided PVs, incessant ATs and AF were induced after an intravenous bolus administration of ATP. The earliest atrial activation site initiating ATs was consistently identified from electrodes positioned in the superior vena cava (SVC), and both ATs and AF were no longer inducible after electric isolation of the SVC. ATP-induced PV/non-PV ectopy may be a marker of increased susceptibility to autonomic triggers of AF and could potentially predict recurrent AF after CPVI.

Benefit to decrease esophageal damage using an ablation catheter with increased irrigation channels for pulmonary vein isolation.

INTRODUCTION: An ablation catheter has been developed with six additional irrigation channels at the proximal end of the ablating electrode. We investigated the potential improvement of esophageal damage when the number of irrigation channels of the ablation catheter was increased during pulmonary vein isolation (PVI). METHODS: This study included a total of 296 consecutive patients with atrial fibrillation. One hundred forty-eight patients were randomly assigned to receive PVI using an ablation catheter with six distal irrigation channels (6C) and 148 patients to receive PVI using an ablation catheter with 12 distal irrigation channels (12C). The luminal esophageal temperature (LET) was monitored in all patients. RESULTS: A total of 639 radiofrequency energy applications (in 225 out of 296 patients) reached the cut-off temperature. The time for the LET to reach the cut-off temperature was shorter for the 6C than the 12C group, and the 6C group had a higher T max of the LET than the 12C group. Some patients experienced a transient drop in the LET (TDLET) just before the delivery of the energy. The site that caused a TDLET before the energy delivery always reached the cut-off temperature. TDLET was more frequent in the 6C group than in the 12C group. CONCLUSIONS: The LET only showed a small difference between the 6C and 12C groups. In contrast, there may be a lower risk of esophageal injury with the 6C than the 12C if we use TDLET.

Measuring luminal esophageal temperature during pulmonary vein isolation of atrial fibrillation.

AIM: To investigate the luminal esophageal temperature (LET) at the time of delivery of energy for pulmonary vein isolation (PVI). METHODS: This study included a total of 110 patients with atrial fibrillation who underwent their first PVI procedure in our laboratory between March 2010 and February 2011. The LET was monitored in all patients. We measured the number of times that LET reached the cut-off temperature, the time when LET reached the cut-off temperature, the maximum temperature (T max) of the LET, and the time to return to the original pre-energy delivery temperature once the delivery of energy was stopped. RESULTS: Seventy-eight patients reached the cut-off temperature. It took 6 s at the shortest time for the LET to reach the cut-off temperature, and 216.5 ± 102.9 s for the temperature to return to the level before the delivery of energy. Some patients experienced a transient drop in the LET (TDLET) just before energy delivery. Ablation at these sites always produced a rise to the LET cut-off temperature. TDLET was not observed at sites where the LET did not rise. Thus, the TDLET before the energy delivery was useful to distinguish a high risk of esophageal injury before delivery of energy. CONCLUSION: Sites with a TDLET before energy delivery should be ablated with great caution or, perhaps, not at all.

Cardiac expression of placental growth factor predicts the improvement of chronic phase left ventricular function in patients with acute myocardial infarction.

OBJECTIVES: Our aim was to investigate cardiac expression of placental growth factor (PlGF) and its clinical significance in patients with acute myocardial infarction (AMI). BACKGROUND: Placental growth factor is known to stimulate wound healing by activating mononuclear cells and inducing angiogenesis. The clinical significance of PlGF in AMI is not yet known. METHODS: Fifty-five AMI patients and 43 control subjects participated in the study. Peripheral blood sampling was performed on days 1, 3, and 7 after AMI. Blood was also sampled from the coronary artery (CAos) and the coronary sinus (CS), before and after acute coronary recanalization. Cardiac expression of PlGF was analyzed in a mouse AMI model. RESULTS: In AMI patients, peripheral plasma PlGF levels on day 3 were significantly higher than in control subjects. Plasma PlGF levels just after recanalization were significantly higher in the CS than the CAos, which indicates cardiac production and release of PlGF. Peripheral plasma levels of PlGF on day 3 were negatively correlated with the acute phase left ventricular ejection fraction (LVEF), positively correlated with both acute phase peak peripheral monocyte counts and chronic phase changes in LVEF. Placental growth factor messenger ribonucleic acid expression was 26.6-fold greater in a mouse AMI model than in sham-operated mice, and PlGF was expressed mainly in endothelial cells within the infarct region. CONCLUSIONS: Placental growth factor is rapidly produced in infarct myocardium, especially by endothelial cells during the acute phase of myocardial infarction. Placental growth factor might be over-expressed to compensate the acute ischemic damage, and appears to then act to improve LVEF during the chronic phase.