Objectives:The aim of this study was to investigate the effects of the menstrual cycle on QT interval dynamics and the autonomic tone in healthy women.Methods: Holter ECGs were recorded in 11 healthy women aged 18-32 years during the follicular and luteal phases of their regular menstrual cycle. The interval from QRS onset to the apex (QaT) and to the end of the T-wave (QeT), the interval between the apex and the end of the T-wave (Ta-e), and RR intervals were measured automatically in the course of 24 hours by Holter ECGs. The QeT/RR, QaT/RR, and Ta-e/RR relationships were evaluated in each subject. The autonomic tone was assessed by the serum catecholamine level at rest and heart rate variability was measured by Holter ECGs.Results: (1) The follicular and luteal phases did not differ significantly with respect to the slopes of the QeT/RR, QaT/RR, and Ta-e/RR relationships. However, QeT and QaT intervals were significantly shorter for all RR intervals in the luteal than in the follicular phase (P < 0.0001). (2) The serum progesterone concentration was significantly higher in the luteal than in the follicular phase (P < 0.001). (3) Noradrenaline was significantly higher in the luteal than in the follicular phase (P < 0.05). There was no significant difference in the follicular and luteal phases with respect to heart rate variability measurements.Conclusions: Our results suggest that the menstrual cycle affects the QT intervals. The observed shorter QT interval during the luteal than the follicular phase may be attributable to the increase in serum progesterone and sympathetic tone. (PACE 2006; 29:607-613) QT interval, menstrual cycle, sex hormone, gender difference, QT/RR relationship, autonomic tone IntroductionPrevious studies have reported a gender difference in the incidence of various types of ventricular arrhythmias. Torsades de pointes associated with long QT syndrome is more common in women than in men, 1-3 whereas the incidence of Brugada syndrome 4 or sudden death 5 is higher in men than in women. We reported that genderspecific differences exist in the incidence of various types of idiopathic ventricular tachycardia (VT) and that VT originating from the right ventricular outflow tract (RVOT) is more common in women than in men. 6 It is important to consider the potential significance of endogenous, menstrual cycle-related sex hormones in various cardiovascular diseases. 7,8 The early follicular phase, during which serum estrogen is at its lowest level in the menstrual cycle, might be a time when premenopausal women with coronary artery disease are particularly susceptible to ischemic events. 7,8 On the other hand, Marchlinski et al. 9 reported that the hormonal flux that occurs during pre-

This randomized trial did not show a reduction in the incidence of slow flow following low-speed RA as compared with high-speed RA (UMIN ID: UMIN000015702). © 2016 Wiley Periodicals, Inc.

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SummaryCompared to acute myocardial infarction (AMI) with single vessel disease (SVD) or double vessel disease (DVD), AMI with triple vessel disease (TVD) is associated with higher mortality. The aim of this study was to identify the determinants of in-hospital death in AMI with TVD. We identified AMI patients with TVD in our tertiary medical center between January 2009 and December 2014. Baseline patient characteristics including laboratory data, echocardiograms, and coronary angiograms were collected from our hospital records. We divided our study population into a survivor group and non-survivor group. Multivariate stepwise logistic regression analysis was performed to identify the determinants of in-hospital death. A total of 138 AMI patients with TVD were identified and included as the final study population. Fifteen patients died during the hospitalization (mortality rate, 10.9%). Mean systolic blood pressure (134 ± 27 mmHg) was significantly greater in the survivor group compared with the non-survivor group (114 ± 31 mmHg) (P = 0.02). The prevalence of shock on admission was significantly less in the survivor group (15.4%) than in the non-survivor group (66.7%) (P < 0.001). Multivariate stepwise logistic regression analysis revealed that shock status on admission (OR 11.50, 95% CI 3.21-41.14, P < 0.001), the left anterior descending artery (LAD) as the infarct related artery (IRA) (OR 3.83, 95% CI 1.04-14.09, P = 0.04), and serum albumin on admission (OR 0.26, 95% CI 0.08-0.84, P = 0.02) were significantly associated with in-hospital death. In conclusion, shock status on admission, the LAD as the IRA, and a low serum albumin level were the determinants of in-hospital death in AMI patients with TVD. ( 1,2) The in-hospital mortality rates of AMI complicated with cardiogenic shock with SVD, DVD, and TVD were reported to be 32.8%, 45.1%, and 58.2%, respectively. 1) Furthermore, the long-term mortality of AMI with TVD is poorer than that with DVD.2) Although several groups studied the determinants of poor clinical outcomes in AMI with multivessel disease, 3,4) the determinants of in-hospital death in AMI with TVD have not been fully investigated. It is clinically important to identify such determinants in order to obtain a better understanding of AMI with TVD, because the mortality of AMI with TVD is the greatest among AMI.

Primary percutaneous coronary interventions (PCI) have been developed to improve clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI). In primary PCI, the door-to-balloon time (DTBT) is closely associated with mortality and morbidity. The purpose of this study was to find determinants of short and long DTBT. From our hospital record, we included 214 STEMI patients, and divided into the short DTBT group (DTBT < 60 min, n = 60), the intermediate DTBT group (60 min ≤ DTBT ≤ 120 min, n = 121) and the long DTBT group (DTBT > 120 min, n = 33). In-hospital mortality was highest in the long DTBT group (24.2%), followed by the intermediate DTBT group (5.8%), and lowest in the short DTBT group (0%) (< 0.001). Transfers from local clinics or hospitals (OR 3.43, 95% CI 1.72-6.83, P < 0.001) were significantly associated with short DTBT, whereas Killip class 3 or 4 (vs. Killip class 1 or 2: OR 0.20, 95% CI 0.06-0.64, P = 0.007) was inversely associated with short DTBT in multivariate analysis. In conclusion, transfer from local clinics/hospitals was associated with short DTBT. Our results may suggest the current limitation of ambulance system, which does not include pre-hospital ECG system, in Japan. The development of pre-hospital ECG system would be needed for better management in STEMI.

BackgroundRhythm outcomes after the pulmonary vein isolation (PVI) using the cryoballoon (CB) are reported to be excellent. However, the lesions after CB ablation have not been well discussed. We sought to characterize and compare the lesion formation after CB ablation with that after radiofrequency (RF) ablation.MethodsA total of 42 consecutive patients who underwent PVI were enrolled (29 in the CB group and 13 in the RF group). The PVI lesions were assessed by late gadolinium enhancement magnetic resonance imaging 1–3 months after the PVI. The region around the PVs was divided into eight segments: roof, anterior‐superior, anterior‐carina, anterior‐inferior, bottom, posterior‐inferior, posterior‐carina, and posterior‐superior segment. The lesion width and lesion gap in each segment were compared between the two groups. Lesion gaps were defined as no‐enhancement sites of >4 mm.ResultsAs compared to the RF group, the overall lesion width was significantly wider and lesion gaps significantly fewer at the anterior‐superior segment of the left PV (LAS) and anterior‐inferior segment of the right PV (RAI) in the CB group (lesion width: 8.2 ± 2.2 mm vs 5.6 ± 2.0 mm, P = .001; lesion gap at LAS: 7% vs 38%, P = .02; lesion gap at RAI: 7% vs 46%, P = .006).ConclusionsThe PVI lesions after CB ablation were characterized by extremely wider and more continuous lesions than those after RF ablation.

It has been shown that orally administered geranylgeranylacetone (GGA), an anti-ulcer drug, induces expression of heat shock protein 72 (HSP72) and provides protection against ischemia-reperfusion in rat hearts. The underlying protective mechanisms, however, remain unknown. Mitochondria have been shown to be a selective target for heat stress-induced cardioprotection. Therefore, we hypothesized that preservation of mitochondrial function, owing to an opening of a putative channel in the inner mitochondrial membrane, the mitochondrial ATP-sensitive potassium (mitoKATP) channel, could be involved in GGA- or heat stress-induced cardioprotection against ischemia-reperfusion. Rats were treated with oral GGA or vehicle. Twenty-four hours later, each heart was isolated and perfused with a Langendorff apparatus. GGA-treated hearts showed better functional recovery, and less creatine kinase was released during a 30-min reperfusion period, after 20 min of no-flow ischemia. Concomitant perfusion with 5-hydroxydecanoate (5-HD, 100 μM) or glibenclamide (10 μM) abolished the GGA-induced cardioprotective effect. GGA also showed preserved mitochondrial respiratory function, isolated at the end of the reperfusion period, which was abolished with 5-HD treatment. GGA prevented destruction of the mitochondrial structure by ischemia-reperfusion, as shown by electron microscopy. In cultured cardiomyocytes, GGA induced HSP72 expression and resulted in less damage to cells, including less apoptosis in response to hypoxia-reoxygenation. Treatment with 5-HD abolished the GGA-induced cardioprotective effects but did not affect HSP72 expression. Our results indicate that preserved mitochondrial respiratory function, owing to GGA-induced HSP72 expression, may, at least in part, have a role in cardioprotection against ischemia-reperfusion. These processes may involve opening of the mitoKATP channel.