In our case the LV
In our case, the LV-triggered pace algorithm had 2 modes: “RVs” and “RVs+RVEs”. In the “RVs” mode, LV pacing synchronizes with RV-sensed events. It aims to maintain the CRT benefits even if intrinsic AV conduction shortens with an increase in sympathetic nerve activity. In the “RVs+RVEs” mode, LV pacing synchronizes with both RV-sensed events as well as PVCs of RV origin. This algorithm is useful in minimizing the loss of a high biventricular pacing rate. The LV-triggered pacing mode applied in this case was “RVs+RVEs”. The T-wave was judged as a PVC because of T-wave oversensing. As a result, LV pacing occurred at the same time as that of the appearance of T waves. The spike on the T wave disappeared by changing the mode from “RVs+RVEs” to “RVs”. However, T-wave oversensing continued to be observed. T-wave oversensing is one of the causes of inappropriate ICD shocks [12–14]. LUMAX 540 series devices allow for changes in several parameters to prevent T-wave oversensing. This series has both upper and lower threshold segments of ventricular sensing after a constant blanking and/or ventricular refractory Chloroquine (Fig. 3). The nominal upper threshold setting is 50%, and the lower one is 25% of the QRS complex voltage. Each threshold can be selected from among 3 levels. The upper threshold can be set at 50, 75, or 87.5%, while the lower threshold can be set at 12.5, 25, or 50% of the QRS complex voltage. The threshold can also be set at a constant value of 2.0mV. Besides allowing for a selection of these thresholds, the device also permits the programming of the minimum threshold. In addition, the frequency of the high-cut and the low-cut filters can be changed. In this case, we changed the upper and the lower thresholds, fixing both at 2.0mV. The minimum threshold of 0.8mV was not changed. After the threshold parameters were changed, the PVCs that were apparent via remote home monitoring and turned out to be due to T-wave oversensing disappeared. Some patients with a low EF, who are considered candidates for CRT, have frequent PVCs. The LV-triggered pace algorithm is thought to be useful for synchronizing PVCs in such cases. If T-wave oversensing is observed, as was in this case, it is possible that the LV pacing occurs at the same time as the T wave because T waves are misjudged as PVCs. Therefore, programming of this algorithm must be done carefully. We first observed T-wave oversensing about 2 months after device implantation. It might have occurred due to an increase in the T-wave amplitude caused by a reduction in the LV dimension with CRT. However, T-wave oversensing could not have been predicted just after the operation. It should be noted that the shock lead position, RV-wave amplitude, and threshold did not change after device implantation. However, T-wave oversensing can be recognized early by remote home monitoring (Fig. 4), although a spike on T wave was observed on the electrocardiogram at the clinic in this case.
Conflict of interest
Introduction Hereditary long-QT syndrome (LQTS) is characterized by prolonged ventricular repolarization and an increased risk for ventricular tachyarrhythmias (torsades de pointes) and sudden cardiac death . It is caused by mutations that encode critical channel pore-forming alpha subunits and channel-interacting proteins [2,3]. LQTS is secondarily caused by several drugs (e.g., antiarrhythmics, antihistamines, psychotropics, and antimicrobials), cardiac conditions (myocardial infarction, heart failure, cardiomyopathy, hypertension, and bradycardia), and noncardiac conditions (diabetes mellitus, anorexia nervosa, metabolic causes, intracranial hemorrhage, and hypothyroidism) . One of the main metabolic causes is hypokalemia.
Case report He was unable to keep up with his peers since April 2008. In August 2008, he developed general fatigue and myalgia and visited the hospital on August 31, 2008. His resting ECG showed a QTc by Bazett\'s formula of 0.665 and by Fridericia\'s formula of 0.634 (Fig. 1a). Serum chemical data indicated rhabdomyolysis (Table 1). His aldosterone level was 1290 pg/ml, and renin activity was <0.1ngml−1h−1. Computed tomography and magnetic resonance imaging did not show any tumor-related change or hyperplasia in his adrenal gland. He was diagnosed with primary aldosteronism. Potassium and spironolactone were administered. Before the administration, his blood pressure was 140/99mmHg. A few days later, he recovered from general fatigue and myalgia. On the 23rd day of hospitalization, his ECG (Fig. 1b) and chemical data (Table 1) were normalized, and he was discharged. His corrected QT intervals by Fridericia\'s formula were significantly associated with serum potassium levels (Fig. 2). The final dosage of drugs was 60mg/d of spironolactone and 150mg/d of potassium aspartate, and his blood pressure after control was 120/85mmHg.