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  • A year old male was referred to our hospital in

    2019-04-15

    A 59-year-old male was referred to our hospital in cardiogenic shock. A 12-lead electrocardiogram showed abnormal Q-waves in V1–V4 leads and complete atrioventricular block; the patient was diagnosed with acute myocardial infarction (AMI) (Fig. 1). Upon arrival, the patient was unconscious, and his blood pressure was 60mmHg; therefore, endotracheal intubation and ventilation were immediately performed. Emergency percutaneous coronary intervention (PCI) was performed under temporary pacing for the left main coronary trunk (75% stenosis→0%) and left anterior descending artery (90% stenosis→0%). Left ventricular wall motion showed severe hypokinesis at the anteroseptal region with an ejection fraction of 33%. Sinus rhythm was restored after PCI; however, atrioventricular block frequently occurred, and we considered the patient\'s condition an indication for permanent pacemaker implantation. Echocardiography showed severely impaired left ventricular wall motion with low EF of 33.6% and cardiac dyssynchrony. The QRS duration was widened to 145ms and showed a right bundle branch block configuration. The patient was on β-blockade, ACE-inhibitor, and amiodarone. Mexiletine was also given intravenously for frequent ventricular tachycardia (VT). Despite the use of these antiarrhythmic agents, VT still occurred frequently and cardioversion was performed several times. Cardiac resynchronization therapy defibrillator (CRT-D) therapy was selected for this patient and the device was implanted on June 3, 2008, 1 week after PCI. We performed this chk1 inhibitor in the acute stage of MI because the patient had an advanced AV block and needed pacing therapy. At first, the right ventricular (RV) lead was inserted into RV apex. However, RV sensing was not satisfactory (<3.0mV) and only the RV septum area yielded a slightly better result. After insertion of the RV lead, we performed coronary venography and selected a preferred site for LV pacing in the posterior coronary vein. Ultimately, the atrial pacing lead was located in the right atrial (RA) appendage with sensing 4.1mV, the RV pacing lead was located in the ventricular septum area with sensing 4.3mV, and the LV pacing lead was located in the posterior coronary vein (generator: Medtronic CONCERTO C154DWK; RV lead: 6947 Sprint Quatro Secure; LV lead: 4194 Attain; right atrial lead: 5554 CapSure). The RA pacing threshold was 0.2V at 0.5ms, RV pacing threshold was 0.6V at 0.5ms, and LV pacing threshold was 1.9V at 0.5ms without phrenic nerve stimulation. Defibrillation threshold (DFT) testing was not performed because the patient had not fully recovered after PCI. The patient\'s condition improved gradually after CRT-D implantation and follow up CAG was performed on June 7, 2008. No significant stenosis was seen, including in the region of previous PCI. Echocardiography 1 week after CRT-D implantation showed a slightly increased EF of 41%. On June 11, 2008, DFT testing was planned to confirm the CRT-D system. Interrogation data did not show remarkable change compared to the data at implantation. Ventricular fibrillation (VF) was induced by T wave shock; however, defibrillation was not achieved due to VF undersensing (under the setting of RV sensing, 1.2mV), and sinus rhythm was manually restored after 30–60s with a shock of 20J (Fig. 2). We repeated DFT testing after changing the RV sensing sensitivity from 1.2 to 0.6mV. Fine VF wave sensing was obtained, and VF was successfully converted with a shock of 20J. After DFT testing, the patient complained of headache and nausea, and his blood pressure dropped to 60mm Hg. Chest X-ray showed significant congestion of the lungs and cardiomegaly. Echocardiography showed severely chk1 inhibitor impaired LV wall motion compared to the results before DFT testing (Fig. 3). One day after DFT testing, laboratory data confirmed multiple organ failure (Table 1). Brain, chest, and abdominal CTs were obtained, but there was no evidence of cerebral infarction, hemorrhage, or aortic dissection. The hemodynamic status and clinical condition of the patient did not improve, and he died after 2 days.