RESUMEN
PURPOSE: The frequent occurrence of ventricular tachycardia can create a serious problem in patients with an implantable cardioverter defibrillator. We assessed the long-term efficacy of catheter-based substrate modification using the voltage mapping technique of infarct-related ventricular tachycardia and recurrent device therapy. METHODS: The study population consisted of 27 consecutive patients (age 68 ± 8 years, 25 men, mean left ventricular ejection fraction 31 ± 9%) with an old myocardial infarction and multiple and/or hemodynamically not tolerated ventricular tachycardia necessitating repeated device therapy. A total of 31 substrate modification procedures were performed using the three-dimensional electroanatomical mapping system. Patients were followed up for a median of 23.5 (interquartile range 6.5-53.2) months before and 37.8 (interquartile range 11.7-71.8) months after ablation. Antiarrhythmic drugs were not changed after the procedure, and were stopped 6 to 9 months after the procedure in patients who did not show ventricular tachycardia recurrence. RESULTS: Median ventricular tachycardias were 1.6 (interquartile range 0.7-6.7) per month before and 0.2 (interquartile range 0.00-1.3) per month after ablation (P = 0.006). Nine ventricular fibrillation episodes were registered in seven patients before and two after ablation (P = 0.025). Median antitachycardia pacing decreased from 1.6 (interquartile range 0.01-5.5) per month before to 0.18 (interquartile range 0.00-1.6) per month after ablation (P = 0.069). Median number of shocks decreased from 0.19 (interquartile range 0.04-0.81) per month before to 0.00 (interquartile range 0.00-0.09) per month after ablation (P = 0.001). One patient had a transient ischemic attack during the procedure, and another developed pericarditis. Nine patients died during follow-up, eight patients due to heart failure and one patient during valve surgery. CONCLUSION: Catheter-based substrate modification using voltage mapping results in a long-lasting reduction of cardioverter defibrillator therapy in patients with multiple and/or hemodynamically not tolerated infarct-related ventricular tachyarrhythmia.
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Ablación por Catéter/métodos , Desfibriladores Implantables , Infarto del Miocardio/complicaciones , Taquicardia Ventricular/diagnóstico , Taquicardia Ventricular/terapia , Centros Médicos Académicos , Anciano , Mapeo del Potencial de Superficie Corporal/métodos , Estudios de Cohortes , Terapia Combinada , Electrocardiografía , Femenino , Estudios de Seguimiento , Humanos , Estimación de Kaplan-Meier , Masculino , Persona de Mediana Edad , Infarto del Miocardio/diagnóstico , Recurrencia , Estudios Retrospectivos , Medición de Riesgo , Estadísticas no Paramétricas , Taquicardia Ventricular/etiología , Factores de Tiempo , Resultado del TratamientoRESUMEN
AIMS: To assess procedural characteristics and adjudicated procedure-related (
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Estimulación Cardíaca Artificial , Desfibriladores Implantables , Anciano , Estimulación Cardíaca Artificial/efectos adversos , Estimulación Cardíaca Artificial/mortalidad , Femenino , Insuficiencia Cardíaca/mortalidad , Insuficiencia Cardíaca/terapia , Humanos , Masculino , Persona de Mediana Edad , Marcapaso Artificial , Complicaciones Posoperatorias , Análisis de Supervivencia , Resultado del TratamientoRESUMEN
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is a heart muscle disorder of unknown course that is characterised pathologically by fatty or fibrofatty replacement of the right ventricular myocardium and electrical instability. Clinical manifestations include structural and functional malformations of the right ventricle, electrocardiographic abnormalities, and presentation of ventricular tachycardias with left bundle branch pattern or sudden death. The disease is often familial with an autosomal inheritance. In addition to right ventricular dilatation, right ventricular aneurysms are typical deformities of ARVD/C and they are distributed in the so-called 'triangle of dysplasia', i.e. the right ventricular outflow tract, apex and infundibulum. Ventricular aneurysms at these sites can be considered highly suggestive for ARVD/C. Another typical hallmark of ARVD/C is fatty or fibrofatty infiltration of the right ventricular free wall with potential extension to the left ventricle. These functional and morphological characteristics are relevant to clinical imaging investigations such as contrast angiography, echocardiography, radionuclide angiography, ultrafast-computed tomography and magnetic resonance (MR) imaging. Among these techniques, MR imaging allows the most comprehensive assessment of the heart, in particular because it provides functional and flow-dynamic information in addition to anatomic images. Furthermore, MR imaging offers the specific advantage of visualising adipose infiltration as a bright signal of the right ventricular myocardium. Non-pharmacological treatment by radio-frequency ablation and implantable defibrillators will play an increasing role in the treatment of patients with ARVD/C, especially in case of drug ineffectivity. Despite new diagnostic and therapeutic approaches in ARVD/C, there remain many unanswered issues since the current guidelines present criteria that are highly specific but lack sensitivity. Therefore, optimal assessment of diagnostic criteria would require a prospective evaluation from a large population obtained by an international registry.
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OBJECTIVE: To detect possible cardiological risk factors in the acute phase of MI for developing depressive symptoms after first MI. DESIGN: Retrospective analysis of cardiac and psychiatric data of 111 consecutive patients admitted with a first MI. METHODS: During one year, all consecutive patients with a first MI, less than 12 hours chest pain and a maximal aspartate aminotransferase (ASAT) value of at least 80 U/l, admitted to the University Hospital of Maastricht, were screened for the presence of depressive symptoms using the 90-item 'Symptom checklist' (SCL-90) questionnaire at one month post-MI. Inclusion criteria were fulfilled by 111 patients; 28 patients refused to participate in the study. RESULTS: No correlation was found between LVEF, peak ASAT, peak CK value and characteristics, location or mode of treatment of the MI and depressive symptoms post-MI. A statistically significant negative correlation was found between SCL-90 depression score and cardiac tissue loss as defined by cumulative ASAT release at 24, 48 and 72 hours after the acute event (p values 0.029, 0.028 and <0.009, respectively) at the one month post-MI screening. CONCLUSIONS: No cardiological parameters were correlated to depressive symptoms post-MI. If there was a connection at all, this appeared to be a negative correlation between infarct size as measured by ASAT release and the occurrence of depressive symptoms at one month post-MI.
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Muerte Súbita Cardíaca , Adulto , Anciano , Estenosis de la Válvula Aórtica/mortalidad , Cardiomiopatía Dilatada/mortalidad , Cardiomiopatía Hipertrófica/mortalidad , Anomalías de los Vasos Coronarios/mortalidad , Muerte Súbita Cardíaca/epidemiología , Muerte Súbita Cardíaca/prevención & control , Desfibriladores Implantables , Femenino , Insuficiencia Cardíaca/mortalidad , Humanos , Síndrome de QT Prolongado/mortalidad , Masculino , Persona de Mediana Edad , Prolapso de la Válvula Mitral/mortalidad , Infarto del Miocardio/mortalidad , Medición de Riesgo , Factores de Riesgo , Síndrome de Wolff-Parkinson-White/mortalidadRESUMEN
AIMS: Complement inhibition by C1-inhibitor has been shown to reduce myocardial ischaemia-reperfusion injury in animal models. We therefore studied the effects of intravenous C1-inhibitor, following reperfusion therapy, in patients with acute myocardial infarction. METHODS AND RESULTS: C1-inhibitor therapy was started not earlier than 6h after acute myocardial infarction, in order to prevent interference with thrombolytic therapy. A loading dose of C1-inhibitor was followed by a continuous infusion for 48 h, using three escalating dosage schemes. Efficacy of complement inhibition was estimated from C4 activation fragments. Plasma concentrations of myocardial proteins were compared to values measured in matched control patients. In 22 patients, C1-inhibitor was well tolerated and drug-related adverse events were not observed. Target plasma levels of C1-inhibitor were reached, with values of 48.2 ml.kg(-1) for distribution space and 35.5h for the half-life time of C1-inhibitor. A dose-dependent reduction of C4 fragments was found P=0.005). In 13 patients who received early thrombolytic therapy, release of troponin T and creatine kinase-MB(mass) was reduced by 36% and 57%P =0.001), compared to 18 controls. CONCLUSION: Continuous 48-h treatment with C1-inhibitor provides safe and effective inhibition of complement activation after reperfused acute myocardial infarction and may reduce myocardial injury.
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Proteínas Inactivadoras del Complemento 1/administración & dosificación , Infarto del Miocardio/tratamiento farmacológico , Reperfusión Miocárdica/métodos , Adulto , Anciano , Anciano de 80 o más Años , Angioplastia Coronaria con Balón/métodos , Activación de Complemento , Complemento C4 , Relación Dosis-Respuesta a Droga , Femenino , Fibrinolíticos/uso terapéutico , Humanos , Masculino , Persona de Mediana Edad , Infarto del Miocardio/cirugía , Cuidados Posoperatorios/métodos , Estudios Prospectivos , Factores de TiempoRESUMEN
Anxiety and depression are common in patients receiving an implantable cardioverter defibrillator (ICD). An association between the number of ICD discharges and mood disturbances has been found. We performed a pilot study in ICD patients with frequent ICD shocks having a comorbid diagnosis of panic disorder with agoraphobia and depression, in which we treated them with a combination of a selective serotonin reuptake inhibitor (SSRI) and a behavior program. We hypothesized that this intervention would result in a decrease of ventricular premature beats or arrhythmias and possibly in a reduction of number of shocks. Four of 5 patients treated with such a combination therapy experienced no discharge of the ICD during a 6 month follow-up. The total number of ventricular premature beats decreased significantly after treatment. There was also clear psychiatric improvement. These results warrant larger scale studies on the pathophysiological mechanisms as well as treatment issues.
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Arritmias Cardíacas/terapia , Desfibriladores Implantables/estadística & datos numéricos , Trastorno de Pánico/tratamiento farmacológico , Inhibidores Selectivos de la Recaptación de Serotonina/uso terapéutico , Complejos Prematuros Ventriculares/terapia , Anciano , Arritmias Cardíacas/epidemiología , Femenino , Humanos , Incidencia , Masculino , Persona de Mediana Edad , Periodicidad , Proyectos Piloto , Complejos Prematuros Ventriculares/epidemiologíaAsunto(s)
Fibrilación Atrial/etiología , Ablación por Catéter , Taquicardia Atrial Ectópica/cirugía , Anciano , Fibrilación Atrial/diagnóstico , Aleteo Atrial/complicaciones , Mapeo del Potencial de Superficie Corporal , Técnicas Electrofisiológicas Cardíacas , Femenino , Humanos , Ligamentos , Taquicardia Atrial Ectópica/diagnósticoRESUMEN
The European Society of Cardiology has convened a Task Force on Sudden Cardiac Death in order to provide a comprehensive, educational document on this important topic. The main document has been published in the European Heart Journal in August 2001. The Task Force has now summarized the most important clinical issues on sudden cardiac death and provided tables with recommendations for risk stratification and for prophylaxis of sudden cardiac death. The present recommendations are specifically intended to encourage the development and revision of national guidelines on prevention of sudden cardiac death. The common challenge for cardiologists, physicians of other medical specialties and health professionals throughout Europe is to realize the potential for sudden cardiac death prevention and to contribute to public health efforts to reduce its burden.