Mortalidad en pacientes con dengue en la epidemia 2012-2013 / Mortality during an outbreak of dengue 2012 - 2013

Introducción: el dengue presenta diversas formas clínicas, desde asintomáticas hasta fatales. Existen diversos factores de riesgo asociados a la mortalidad por dengue. Objetivo: determinar los factores de riesgo asociados a la mortalidad por dengue. Metodología: estudio de casos (adultos fallecidos por dengue) y controles (adultos sobrevivientes al dengue), durante la epidemia verano 2012-2013 en Paraguay. Resultados: los factores de riesgo asociados significativamente a la mortalidad por dengue fueron: presencia de comorbilidades, hemorragias, hepatitis, hipoproteinemia e hipoalbuminemia. El choque por dengue fue la causa de óbito más frecuente (49%). Conclusiones: los factores asociados a la mortalidad por dengue son inherentes al paciente (comorbilidades) y a la gravedad de la infección, resultante de las manifestaciones hemorrágicas, afectación sistémica y fuga capilar.

Introduction: Dengue has several clinical forms, from asymptomatic to fatal. There are several risk factors associated with mortality from dengue. Objective: To determine the risk factors associated with mortality from dengue. Methodology: case studies (death of dengue adults) and controls (survivors dengue adults) during summer 2012-2013 epidemic in Paraguay. Results: Risk factors significantly associated with mortality from dengue were: presence of comorbidities, hemorrhage, hepatitis, hypoproteinemia and hypoalbuminemia. Dengue shock syndrome was the most common cause of death (49%). Conclusions: The mortality associated with dengue factors are inherent to the patient (comorbidities) and the severity of infection, resulting in hemorrhagic manifestations, systemic involvement and capillary leak.osus reaction.

Increased N-terminal-pro-B-type natriuretic peptide levels in patients with appropriate implantable defibrillator therapies.

BACKGROUND: The ability to better identify predictors of implantable defibrillator therapies in patients with heart failure would allow the optimization of patient selection. N-terminal-Pro-B-type natriuretic peptide (NT-ProBNP) is secreted by the ventricles in response to myocardial stretching and is a sensitive marker of left ventricular dysfunction and cardiac mortality in patients with heart failure. We assessed the relationship between NT-ProBNP and defibrillator therapies for primary or secondary prevention of arrhythmic death. METHODS: NT-ProBNP levels were analyzed in 45 patients with stable heart failure symptoms and defibrillator devices, with and without device therapies, and appropriate and inappropriate therapies. Univariate and multivariate analyses were used to identify predictors of appropriate defibrillator therapies. RESULTS: Device interventions occurred in 21 patients: 12 appropriate therapies and 9 inappropriate therapies. Patients with appropriate therapies had higher NT-ProBNP levels than patients with no device therapies (2469.1 +/- 2281.8 pg/mL vs 838.7 +/- 832 pg/mL; P = .0019), inappropriate therapies (730.4 +/- 503 pg/mL; P = .0046), and combined inappropriate plus no therapies (2469.1 +/- 2281.8 pg/mL vs 713.9 +/- 510.6 pg/mL; P = .0008). The NT-ProBNP level was the only independent predictor of appropriate device therapies during the observation period (P = .004). CONCLUSION: Elevated NT-ProBNP was an independent predictor of appropriate defibrillator therapies. Extensive myocardial remodeling may create the electrophysiologic conditions necessary to elicit ventricular tachyarrhythmias. Further research is necessary to clarify whether the identification of a subgroup of higher risk may benefit from a more aggressive defibrillator programming.

Hypothermia-induced J waves.

A 36 years old woman with acquired immunodeficiency syndrome was admitted to the hospital for pulmonary Mycobacterium Avis Complex infection. Seventy-two hours after the admission she became hypothermic and bradycardic. The ECG showed sinus bradycardia, J waves in leads II, III, aVF, aVR, aVL, V5 and V6 along with QT prolongation and T wave abnormalities. After rewarming the J waves and repolarization abnormalities disappeared. The proposed cellular basis of hypothermia-induced J waves is the accentuation of the spike-and-dome morphology of the action potential of M and epicardial cells.

Mechanism of atrial flutter occurring late after orthotopic heart transplantation with atrio-atrial anastomosis.

OBJECTIVE: We sought to better define the electrophysiologic mechanism of atrial flutter in patients after heart transplantation. BACKGROUND: Atrial flutter is a recognized problem in the post-cardiac transplant population. The electrophysiologic basis of atrial flutter in this patient population is not completely understood. METHODS: Six patients with cardiac allografts and symptoms related to recurrent atrial flutter underwent diagnostic electrophysiologic study with electroanatomic mapping and radiofrequency catheter ablation. Comparison was made with a control non-transplant population of 11 patients with typical counterclockwise right atrial flutter. RESULTS: In each case, mapping showed typical counterclockwise activation of the donor-derived portion of the right atrium, with concealed entrainment shown upon pacing in the cavotricuspid isthmus (CTI). The anastomotic suture line of the atrio-atrial anastomosis formed the posterior barrier of the reentrant circuit. Ablation of the electrically active, donor-derived portion of the CTI was sufficient to terminate atrial flutter and render it noninducible. Comparison with the control population showed that the electrically active portion of the CTI was significantly shorter in patients with transplant-associated flutter and that ablation was accomplished with the same or fewer radiofrequency lesions. CONCLUSIONS: Atrial flutter in cardiac transplant recipients is a form of typical counterclockwise, isthmus-dependent flutter in which the atrio-atrial anastomotic suture line forms the posterior barrier of the reentrant circuit. Ablation in the donor-derived portion of the CTI is sufficient to create bidirectional conduction block and eliminate this arrhythmia. Ablation or surgical division of the donor CTI at the time of transplantation could prevent this arrhythmia.