Heart failure (HF)-related hospitalization is associated with significant mortality and morbidity and can be prevented by early intervention. Implantable sensors detect early pathophysiological changes in HF, using an accelerometer, a paced electrogram, impedance and pressure sensors in implanted intracardiac leads, or stand-alone devices. Such sensors monitor daily activity, QT and ST intervals, pulmonary fluid, and intracardiac pressures at various points. Sensor data are available either by patient’s or physician’s regular interrogation, or using remote patient monitoring. Different sensors have different levels of sensitivity and specificity for HF detection, and they have the ability to antedate HF exacerbation and thereby allow for the initiation of intervention to avert decompensation. Clinical studies suggest that alone or in combination, such sensors have a greater beneficial impact than conventional therapy on acute HF outcome.

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State-of-the-art, implantable, dual-chamber cardiac devices provide useful diagnostic information, including the number and duration of automatic-mode switch episodes in cases of atrial tachycardia and atrial fibrillation encountered in clinical practice. However, to acquire accurate diagnostic information, special attention must be paid to the device settings; to the presence or absence of ventriculoatrial conduction, which, when present, often represents repetitive non-reentrant synchrony (RNRVAS) or pacemaker-mediated tachycardia; to the post-ventricular atrial-blanking period and atrial sensitivity; and to the sensing of far-field R waves (FFRW) in the atrial channel. Physicians should be careful about the information gathered during the monitoring of patients with implantable devices.

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We investigated the direct action of angiotensin II (Ang II) on myocardial conduction and transmembrane action potential immediately after reoxygenation.
Method: After superfusion in a simulated ischemic solution, ventricular papillary muscle preparations of rat heart were washed with oxygenated Tyrode solution containing Ang II, Ang II plus CV-11974 (an AT₁ receptor blocker), or Ang II plus 5-hydroxydecanoic acid (mito-K_ATP blocker), under rapid electrical stimulation (RES) for 60 s.
Results: In the control experiments, the incidence of conduction delay and block was the highest within the first 10 s, and subsequently, 1:1 conduction was established after 40 s. Ang II significantly enhanced the 2:1 conduction block during the later phase of RES (40-60 s after reoxygenation). This effect of Ang II was abolished by either CV-11974 (P < 0.001) or 5-HD (P < 0.001).
Conclusion: RES-induced conduction delay and block immediately after reoxygenation were accelerated by Ang II, which could be relevant to the maintenance of reperfusion arrhythmias. The mito-K_ATP channel may participate in the mechanism underlying this phenomenon.

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Introduction: The long-term effect of angiotensin II receptor blockers (ARBs) on atrial fibrillation (AF) is unclear. In this study, we evaluated the change in the fibrillation cycle length (FCL) in patients under long-term ARB therapy for chronic AF.
Methods and results: The study population consisted of 25 chronic AF patients who were prescribed the same medication for more than 6 years and in whom specific ECG recording for FCL evaluation could be performed before and after the 6-year observation period. The patients were divided into 2 groups: those with and without ARB (ARB group and non-ARB group and n=15 and 10, respectively). FCL was calculated by the spectral analysis of the fibrillation waves in the surface ECG. There was no significant difference in the clinical characteristics between the 2 groups. In the ARB group, the mean FCL was prolonged from 154 ± 20 ms to 187 ± 37 ms (p=0.005), whereas it remained unchanged in the non-ARB group (150 ± 12 ms vs. 149 ± 10 ms). In the comparison between patients with and those without FCL prolongation (> 30 ms; n=6 and 19, respectively), a significant difference was observed only in those prescribed ARBs.
Conclusion: In cases of chronic AF, FCL might be prolonged under long-term ARB treatment.

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Atrial fibrillation (AF) has been gaining much attention as one of the major causes of cerebral infarction. It is imperative to establish antithrombotic treatment for AF patients. Thus far, guidelines for antithrombotic treatment in the management of AF patients, including the verification of the efficacy of direct thrombin and factor Xa inhibitors, have been published from the United States, Europe, Canada, and Japan. When we look at the Asia-Pacific region, antithrombotic treatment has not yet been defined, and no such guidelines have been published in this regard. The Asia-Pacific Heart Rhythm Society (APHRS) conducted a Web-based survey between June and August 2011, to elucidate the current status of antithrombotic treatment in 9 countries.
A total of 363 cardiologists in 9 countries examined 300 patients with cardiovascular disease per month on an average; of these patients, 37 (12%) had nonvalvular AF (NVAF; 6.5% in India to 16.9% in Australia).
The survey revealed that NVAF patients were not always administered appropriate antithrombotic treatment. These data give us a foothold for the next step, i.e., the formulation, of the APHRS practice guidelines.

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Cardiac-resynchronization therapy (CRT) improves the cardiac function of patients with left ventricular (LV) dyssynchrony. Maintenance of the biventricular pacing rate is very important in managing the hemodynamics in patients implanted with CRT devices. A low biventricular pacing rate, for example, in cases with atrial fibrillation or rapid intrinsic atrioventricular (AV) conduction, decreases the benefits of CRT. The LUMAX HF-T 540 device series (BIOTRONIK, Berlin, Germany) has a LV-triggered pace algorithm, which allows biventicular pacing rates to be maintained even during rapid intrinsic rhythms caused by shortened AV conduction and/or premature ventricular contraction (PVC) occurring in the right ventricle. We encountered a case of CRT device implantation with a defibrillator wherein this triggered pace algorithm caused a spike on T-wave due to T-wave oversensing. By remote monitoring, we were also able to determine that the T-wave oversensing was due to a PVC. The LUMAX 540 series allows for changes in the sensing threshold and filter settings of the device, which facilitated the elimination of T-wave oversensing in this case.

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Secondary long QT syndrome (LQTS) is caused by several drugs, cardiac conditions, and noncardiac conditions. One of the main metabolic causes is hypokalemia. We experienced treating a boy with secondary LQTS due to primary aldosteronism. The boy had been followed annually since he was 6 years old because his resting electrocardiogram (ECG) showed a prolonged QT interval. When he was 9 years old, he developed general fatigue and myalgia. The QT interval in his resting ECG became longer and serum data indicated rhabdomyolysis. The aldosterone level was high and renin activity was low. He was diagnosed with primary aldosteronism. When we, pediatricians, see children with LQTS, we are apt to think that their condition is congenital in nature. However, secondary or acquired LQTS should be always taken into consideration and be excluded not only in adults but also in the pediatric population.

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Adenosine-sensitive focal atrial tachycardia (AT) has been shown to originate in the confined area near the His-bundle. While several pieces of evidence support focal reentry as the primary underlying mechanism, few studies have clearly demonstrated entrainment. In this report, we present a case of adenosine-sensitive focal AT by focal reentry, wherein we were able to obtain clear evidence for entrainment.

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An 87-year-old woman with complete atrioventricular block was admitted for permanent pacemaker implantation. The patient had a large thoracic aortic aneurysm that had been conservatively treated. Lead placement was not possible via the superior vena cava or the epicardial route because of the aneurysm. Therefore, we implanted a VVI pacemaker via the femoral approach. A unit was placed in a pouch on the right lower abdominal wall, and a lead was introduced into the right ventricle via the right femoral vein. The femoral vein approach is rarely used; however, it should be recognized as an effective alternative when the usual approach is difficult or impossible to be performed.

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