Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • There have been some case reports of

    2019-04-15

    There have been some case reports of RNRVAS [3,4], but the present case is the first report of RNRVAS exacerbating heart failure. After RNRVAS was avoided with NCAP, the state of his heart failure improved, indicating that RNRVAS was the trigger for the worsening heart failure. His bradycardia parameters (a relatively rapid base rate, a long AV interval, and a long PVARP) had been programmed to minimize ventricular pacing and to prevent atrial fibrillation based on the results of the previous studies. The Dual Chamber and VVI Implantable Defibrillator trial suggested that unnecessary ventricular pacing might promote heart failure and worsen clinical patient outcome [6]. Sweeney et al. [7] found that the risk of atrial fibrillation increased with increased cumulative percent ventricular pacing. Unfortunately, in the present case, those parameters programmed to decrease ventricular pacing rate created, in the contrary, an environment that could easily lead to RNRVAS and exacerbate heart failure. Therefore, we must be careful not to cause RNRVAS especially in patients with pacemaker parameters such as a relatively rapid base rate, a long AV interval, and a long PVARP. In such cases, the NCAP algorithm is effective to prevent RNRVAS, although there is a possibility that NCAP could also induce RNRVAS [4].
    Introduction Left atrial myxoma is the most frequently occurring type of heart tumor [1–3]. Patients often require pacemaker implantation after cardiac surgery for treatment of myxomas [1–3]. The superior septal approach (SSA) is one of the surgical approaches used for myxoma resection. Cases that require pacemaker implantation after SSA have been reported to be very rare [4,5]. We herein describe the case of a patient who required pacemaker implantation after surgery with the SSA for the treatment of a left atrial myxoma. Moreover, this case involved a complex endocardial electrogram that affected the pacemaker implantation procedure.
    Case report The patient was a 64-year-old woman with a history of hypertension, who experienced a near-syncopal episode after developing transient palpitations and dyspnea. A 12-lead electrocardiogram (ECG) (Fig. 1b) and a Holter ECG recorded upon her arrival at our hospital showed the presence of a normal sinus rhythm with no significant arrhythmias. Normal sinus nodal function and normal mps1 conduction were estimated according to the Holter ECG findings of a maximum heart rate of 150bpm and maximum 1:1 AV conduction rate of >120bpm. In addition, coronary angiography showed no significant stenosis. However, the echocardiographic findings revealed the presence of a large left atrial tumor. Surgery was performed under cardiopulmonary bypass. Use of the SSA and removal of a large part of the atrial septum followed by patch closure were required in order to resect the tumor because the tumor was large, multilobular, myxomatous, and attached to the thick stalk arising from the interatrial septum near the fossa ovalis. A 12-lead ECG recorded after surgery revealed the presence of sinus arrest with backup ventricular pacing by epicardial temporary pacing leads (Fig. 1a and c), and sometimes showed an ectopic atrial rhythm or prolonged R–R intervals following the termination of paroxysmal atrial fibrillation. Therefore, a diagnosis of bradycardia–tachycardia syndrome was made. Because the ectopic atrial rhythm and sinus arrest were sustained, and the patient did not recover a normal sinus rhythm within 2 weeks of the operation, a permanent pacemaker (REPLY™ DR; Sorin Group, Milan, Italy) was implanted into the left precordial region. The atrial bipolar lead (model 5076-45cm; Medtronic Inc., MN, USA) was screwed into the free wall of the right atrium. The atrial pacing threshold was 0.5V/0.5ms, lead impedance was 604Ω at 5V, and P wave amplitude was 0.6mV at the implanted site. Concerning the position of the atrial lead, no other location in the right atrium satisfied the standard sensing and pacing threshold criteria. Pacing thresholds and P-wave amplitudes were more than 5V/0.5ms and 0.1mV at the high septal wall; more than 5V/0.5ms, 0.3mV at the posterior septum; more than 5V/0.5ms, 0.2mV around the right atrial appendage; and more than 5V/0.5ms, 0.4mV at the cavotricuspid isthmus. The ventricle bipolar lead (model Screwvine-52cm; Japan Lifeline Co., Ltd., Tokyo, Japan) was screwed into the septum of the right ventricle. A 12-lead ECG recorded during pacemaker implantation showed an ectopic atrial rhythm with a very broad P-wave morphology (Fig. 1d). Moreover, the timing of the intrinsic waves at the atrial and ventricular leads was almost simultaneous (Fig. 2a). Although the atrial lead on the free wall was located apart from the AV valve, we could not rule out the possibility that the intrinsic wave of the atrial lead was a far-field potential of the intrinsic R wave. To address this point, intravenous adenosine triphosphate (ATP) (20mg) was administered to induce an AV block (Fig. 2b). As expected, the pacing from the atrial lead captured only the atrium and not the ventricle (Fig. 2b). In addition, electromapping of the right atrium and the coronary sinus (CS), using the atrial pacemaker lead, revealed that the CS ostium was the earliest site of activation of the ectopic P rhythm in the right atrium and that the activation sequence in mps1 the CS was distal to the proximal site. These results suggest that the ectopic P rhythm originated from the left atrium (most likely from the lateral wall), and the conduction time of the ectopic P wave from the origin to the tip of the atrial lead on the free wall of the right atrium was very long (Fig. 3a). In addition, the conduction time of the right free wall to the left atrium was also very long (Fig. 3a). These observations suggested a severe conduction delay between the left and right atria.