Injecting a ventricular tachycardia into the heart-Α unique case report.

INTRODUCTION: A 52-year-old woman presented with a complex ventricular arrhythmia in an intraoperative context, during kyphoplasty for an osteoporotic fracture of a lumbar vertebra. The subject showed no indications of a previous cardiovascular condition. METHODS AND RESULTS: Causes of arrhythmias associated with the procedure were excluded. Due to her positive family history for dilated cardiomyopathy, upcoming thoughts were made for unmasking a previous asymptomatic cardiomyopathy. Nevertheless, an intracardiac cement embolism was diagnosed and, finally, the patient underwent an open-heart surgery with successful removal of the cardiac cement. Νo new arrhythmia recorded during follow up. CONCLUSION: To the best of our knowledge, this is the first reported case of ventricular arrhythmogenic presentation of a cardiac cement embolus after a KP procedure.

Miocardiopatías inducidas por arritmias: ¿el enigma del huevo o la gallina todavía sin resolver?

Resumen Especialmente en las últimas décadas varios estudios han intentado confirmar la hipótesis que sostiene que la contracción miocárdica inapropiadamente rápida, irregular, o asincrónica provoca miocardiopatía. Las frecuencias ventriculares rápidas resultantes de arritmias supraventriculares y fibrilación auricular (FA), la irregularidad del ritmo cardíaco -elemento básico de la FA- y la asincronía, determinada por estimulación ventricular derecha, bloqueo de rama, o complejos ventriculares prematuros frecuentes, han sido establecidas como las causas primarias de miocardiopatía inducida por arritmias. Se han aclarado las principales vías fisiopatológicas involucradas; éstas incluyen la activación neurohumoral, el agotamiento de los depósitos energéticos, y anomalías que ocurren durante el estrés y la sobrecarga. Desgraciadamente, desde un punto de vista clínico, los pacientes habitualmente consultan recién cuando aparecen síntomas, a pesar de que la arritmia causal pueda haber aparecido ya meses o años antes, llevando así a una remodelación del miocardio y disfunción diastólica y sistólica. En algunos casos, tratar de establecer un diagnóstico definitivo puede convertirse en un ejercicio agotador para el médico tratante, ya que la arritmia puede no estar siempre presente, y además, implica que primero tiene que indicar un tratamiento, para confirmar el diagnóstico recién retrospectivamente. Otra dificultad que plantea el proceso diagnóstico es que los criterios diagnósticos estrictos siguen siendo tema de controversia. Las opciones terapéuticas incluyen pruebas empíricas con agentes farmacológicos, terapias por catéter, y en el contexto de la estimulación ventricular crónica, la resincronización. Es de esperar que en la mayoría de los pacientes se logre una recuperación parcial o completa, pero aun así los pacientes tendrán que ser seguidos cuidadosamente debido al riesgo de recurrencia. Se hace entonces indispensable realizar ensayos aleatorizados controlados de gran tamaño que permitan optimizar la estratificación de los pacientes y definir la elección de estrategias terapéuticas

The hypothesis testing of inappropriate fast, irregular, or asynchronous myocardial contraction provoking cardiomyopathy has been the primary focus of numerous research efforts, especially during the last few decades. Rapid ventricular rates resulting from supraventricular arrhythmias and atrial fibrillation (AF), irregularity of heart rhythm-basic element of AF-and asynchrony, as a consequence of right ventricular pacing, bundle branch block, or frequent premature ventricular complexes, have been established as primary causes of arrhythmia-induced cardiomyopathy. The main pathophysiological pathways involved have been clarified, including neurohumoral activation, energy stores depletion, and abnormalities in stress and strain. Unfortunately, from a clinical point of view, patients usually seek medical advice only when symptoms develop, while the causative arrhythmia may be present for months or years, resulting in myocardial remodelling, diastolic, and systolic dysfunction. In some cases, making a definite diagnosis may become a strenuous exercise for the treating physician, as the arrhythmia may not be present and, additionally, therapy must be applied for the diagnosis to be confirmed retrospectively. The diagnostic process is also hardened due to the fact that strict diagnosing criteria are still a matter of discrepancy. Therapy options include pharmaceutical agents trials, catheter-based therapies and, in the context of chronic ventricular pacing, resynchronization. For the majority of patients, partial or complete recovery is expected, although they have to be followed up thoroughly due to the risk of recurrence. Large, randomized controlled trials are more than necessary to optimize patients’ stratification and therapeutic strategy choices

Arrhythmia-induced cardiomyopathies: the riddle of the chicken and the egg still unanswered?

The hypothesis testing of inappropriate fast, irregular, or asynchronous myocardial contraction provoking cardiomyopathy has been the primary focus of numerous research efforts, especially during the last few decades. Rapid ventricular rates resulting from supraventricular arrhythmias and atrial fibrillation (AF), irregularity of heart rhythm-basic element of AF-and asynchrony, as a consequence of right ventricular pacing, bundle branch block, or frequent premature ventricular complexes, have been established as primary causes of arrhythmia-induced cardiomyopathy. The main pathophysiological pathways involved have been clarified, including neurohumoral activation, energy stores depletion, and abnormalities in stress and strain. Unfortunately, from a clinical point of view, patients usually seek medical advice only when symptoms develop, while the causative arrhythmia may be present for months or years, resulting in myocardial remodelling, diastolic, and systolic dysfunction. In some cases, making a definite diagnosis may become a strenuous exercise for the treating physician, as the arrhythmia may not be present and, additionally, therapy must be applied for the diagnosis to be confirmed retrospectively. The diagnostic process is also hardened due to the fact that strict diagnosing criteria are still a matter of discrepancy. Therapy options include pharmaceutical agents trials, catheter-based therapies and, in the context of chronic ventricular pacing, resynchronization. For the majority of patients, partial or complete recovery is expected, although they have to be followed up thoroughly due to the risk of recurrence. Large, randomized controlled trials are more than necessary to optimize patients' stratification and therapeutic strategy choices.

Electrophysiological effects of carvedilol administration in patients with dilated cardiomyopathy.

PURPOSE: Several studies suggest the clinical efficacy of carvedilol in reducing atrial and ventricular arrhythmias in patients with left ventricular dysfunction (LVD) due to congestive heart failure (CHF) or following myocardial infarction. However, the mechanisms supporting its antiarrhythmic efficacy have been derived from experimental studies. In this prospective, placebo-controlled trial we examined the electrophysiological effects of a high oral dose of carvedilol in patients with CHF and LVD due to non-ischemic dilated cardiomyopathy. METHODS: Thirty-one patients with stable CHF underwent electrophysiological study and were randomly assigned to treatment with carvedilol or placebo. After 2 months of treatment the study was repeated. RESULTS: Carvedilol prolonged almost all conduction times. In the same group atrial and ventricular effective refractory periods were significantly prolonged, while the parameters of repolarization remained virtually unchanged. The prolongation of refractoriness was most pronounced in the atrium. The change in ventricular refractoriness was correlated with ejection fraction (r = 0.94, p < 0.01) suggesting that patients with more preserved left ventricular function responded to treatment with greater prolongation. CONCLUSION: Even after a short period of administration carvedilol has marked and diffused electrophysiological effects that would be beneficial for patients with CHF and may contribute to the positive outcome of clinical trials.