Introduction:The standard treatment of sinus node dysfunction (SND) is the pacemaker implantation, and the ideal methodology for the management of atrial fibrillation (AF) is rhythm control, but this is sometimes very hard to accomplish. For such actions, complete isolation of all pulmonary veins (PVI) is currently widely accepted as the best endpoint.Case Presentation:In this case, we report a female patient, 81 years old, with controlled hypertension, without coronary artery disease, bearer of bilateral knee replacement, and dual chamber pacemaker implanted 1.5 years ago owing to sinus node disease, presenting the following symptoms: presyncope episodes associated with sustained irregular palpitation tachycardia. The evaluation of the pacemaker-recorded episodes of atrial fibrillation, the echocardiogram-presented normal systolic function and measurements, as well as the resting myocardial scintigraphy and with drug use did not demonstrate ischemia and/or fibrosis. The patient was in use of valsartan 320 mg daily, amlodipine 10 mg daily, sotalol hydrochloride 120 mg 2 times daily, and dabigatran 110 mg 2 times daily. At the end of the PVI, the patient presented hemodynamic instability, with a decrease in heart rate to 30 bpm and invasive arterial blood pressure to 60/30 mmHg. The pericardial puncture was quickly carried out with the possibility of cardiac tamponade as the first hypothesis, but no pericardial effusion was found. Next, we detected acute capture loss from the ventricular pacemaker lead, unvarying with high voltage and pulse width, even with stable impedance, sense and keeping the same position visualized by fluoroscopy. And there was soon afterwards induction of sustained ventricular tachycardia degenerating to spontaneous ventricular fibrillation. Electrical cardioversion-defibrillation was performed with 200J, and the sinus rhythm was reestablished, but there was a dead short, and the pacemaker generator was burned and disabled.Conclusions:So, we can speculate that application of atrial radiofrequency for PVI diffused through the tissues, affecting in some way the tip of the ventricular electrode, causing a microlesion in this structure and making it impossible to capture the right ventricle by the pacemaker. As we cannot see it, we can call it of phantom injury of the ventricular lead.
A persistent left-superior vena cava (PLSVC) is an uncommon identification with a form of 0.3% to 0.5% of persons in the common population [1][2][3][4][5]. Nevertheless, it is the most common thoracic venous anomaly [6][7][8][9][10]. Typically, the left superior vena cava fades post embryological developement. The identification can be missed by the manifestation of a standard right superior vena cava. This subject did not have an ordinary or rest of a right superior vena cava. Furthermost of the individuals do not present the symptoms, and the presence of the persistent left superior vena cava is by the way found during or after insertion of a central venous catheter (CVC) or pacemaker electrodes. The correct report of a PLSVC and lack of a right superior vena cava has significant clinical repercussions in definite circumstances, such as oncological therapy, totally implantable vessels catheters, hemodynamic checking in intenive care unit (ICU) or the correct location of pacemakers [1][2][3][4][5][6][7][8][9][10]. The further clinical relevance of the described anomaly could be due to common tachyarrhythmia and conduction disturbances [11][12][13][14][15]. The PLSVC usually descends vertically, anterior, and to the left of the aortic arch and main pulmonary artery. It runs adjacent to the left atrium (LA) before turning medially, piercing the pericardium to run in the posterior atrioventricular (AV) groove [16]. In about 90% of cases, it drains into the coronary sinus (CS); alternative sites include the inferior vena cava, hepatic vein, and LA. The entry into LA is invariably associated with an atrial septal defect ASD [17,18].In this case, we describe a female patient, 63 years old, with hypertension and dilated cardiomyopathy, without coronary artery disease. She was recovered from sudden cardiac death, with previous events of syncope, dyspnea on habitual exertion, and pre-syncope that began 6 months ago. She also was in use of acetylsalicylic acid 100 daily, carvedilol 25 twice a day, digoxin 0.25 mg per day, furosemide 40 mg daily, atorvastatin 40 mg daily, spironolactone 50 mg daily. The basal eletrocardiogram (ECG) presented sinus rhythm and QRS complex duration 170 ms. The 24-hour Holter monitoring showed sinus rhythm, with minimum -average -maximum heart rate (HR) of 39, 56 and 93 bpm, respectively, as well as, 6737 polymorphic ventricular ectopic beats and 5 episodes of non-sustained ventricular tachycardya, being the highest composed 16 beats at 180 bpm. The transthoracic echocardiogram showed: LA 4,3 cm, LVED 6,3 cm, LVES 5,8 cm, LVEF 17,2%, left ventricular mass index 139,3 g/m 2 , andd diffuse hypokinesia of the left ventricle. The coronary angiography did not present any new obstruction.The patient was submitted to general anesthesia by an anesthesiologist, and 2 g of cefazolin was administered intravenously. During the surery, a persistent left superior vena cava (PLSVC) was perceived. The left venography revealed a lack of contrast filling in an innominate vein (IV) and a quadripolar diagnostic ...
Introduction:We started this research line since October 2002 with nuchal translucency. We initiated the investigation with nasal bone and ductus venosus in a first trimester screening in September 2003. These studies examines: 1) the association between absent nasal bone (NB) at the 11-14 weeks scan and chromosomal anomalies in Brazilian pregnant women sample. 2) The association between ductus venosus abnormal wave form at the 11-14 weeks Doppler and chromosomal anomalies in Brazilian pregnant women sample Methods: Since September 2003, 35 patients have been included in this study. Ultrasound and Doppler examination of fetal profile was carried out between 11 and 14 weeks of gestation. All data was obtained with a Voluson 730 GE and Toshiba SSH 140 A. All patients referred to our department have accepted fetal karyotyping. Results: A total of 35 fetuses were included in this study. When we analyzed the NB, the sensitivity was 50%, specificity was 96.8%, positive predictive value (PPV) was 50% and negative predictive value (NPV) was 96.8%. The association was not statistically significant (P = 0.11 -Fisher). When we analyzed the ductus venosus, the sensitivity was 50%, specificity was 100%, positive predictive value (PPV) was 100% and negative predictive value (NPV) was 97.1%. The association was statistically significant (P = 0.05 -Fisher). Conclusions: This is only a first view of our research (previous note). Based on the small sample, conclusions at this time cannot be used for clinical purpose.
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