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4.
J Cardiovasc Electrophysiol ; 30(3): 299-307, 2019 03.
Article in English | MEDLINE | ID: mdl-30516299

ABSTRACT

INTRODUCTION: Cardiac perforation of the right ventricle associated with pacemaker or implantable cardioverter defibrillator (ICD) leads' implantation is uncommon, albeit potentially life-threatening, complication. The aim of this study is to further identify the optimal therapeutic strategy, especially when lead dislocation has occurred outside the pericardial sac. METHODS AND RESULTS: The study population included 10 consecutive patients (six female, mean age: 66.5 years old) diagnosed with early ventricular lead perforation following a pacemaker or ICD implantation, with significant protrusion inside the pericardial sac (n = 2) or migration of the lead at the pleural space ( n = 3), the diaphragm ( n = 1), or the abdominal cavity ( n = 4), during the period 2013-2017. All patients were symptomatic; however, individuals presenting with hemodynamic instability were excluded. The outcome of the percutaneous therapeutic approach was retrospectively assessed. All patients underwent a successful removal of the perforating lead percutaneously at the electrophysiology lab, by direct traction, and repositioning in another location of the right ventricle. The operation was performed by a multidisciplinary team, under continuous hemodynamic and transesophageal echocardiographic monitoring and cardiac surgical backup. The periprocedural period was uneventful. Subjects were followed up for at least 1 year. Interestingly, all patients developed a type of postcardiac injury syndrome, successfully treated with a 3-month regimen of ibuprofen and colchicine. CONCLUSION: Percutaneous traction and repositioning of the perforating ventricular lead are effective, safe, and less invasive compared with the thoracotomy method in hemodynamically stable patients when dislocation has occurred outside the pericardial sac provided that there is no visceral organs injury.


Subject(s)
Defibrillators, Implantable , Device Removal , Foreign-Body Migration/surgery , Heart Injuries/surgery , Heart Ventricles/surgery , Pacemaker, Artificial , Prosthesis Implantation/instrumentation , Aged , Aged, 80 and over , Device Removal/adverse effects , Female , Foreign-Body Migration/diagnostic imaging , Foreign-Body Migration/etiology , Heart Injuries/diagnostic imaging , Heart Injuries/etiology , Heart Ventricles/diagnostic imaging , Heart Ventricles/injuries , Humans , Male , Middle Aged , Prosthesis Design , Prosthesis Implantation/adverse effects , Reoperation , Retrospective Studies , Risk Factors , Time Factors , Treatment Outcome
6.
Recent Pat Cardiovasc Drug Discov ; 1(2): 185-91, 2006 Jun.
Article in English | MEDLINE | ID: mdl-18221085

ABSTRACT

Heart failure is characterised by decreased cardiac output, which results in the development of both peripheral hypoperfusion and pulmonary congestion and can lead to the development of acute pulmonary edema. The primary objective in treating a patient with decompensated heart failure is hemodynamic stabilization, which is usually achieved by inotropic support. Classic inotropic agents provide short-term hemodynamic improvement, but their use has been correlated with poor prognosis. Levosimendan, a new calcium sensitizer, offers hemodynamic and symptomatic improvement without increasing cAMP and intracellular calcium concentrations. This agent improves contractility without increasing the risk of cardiac events such as arrhythmias. By combining a positive inotropic action mediated via calcium sensitization and a vasodilatory effect via ATP-dependent potassium channels, it appears to be superior than classic positive inotropic agents. Furthermore, it seems to have prolonged benefit in heart failure patients, and it also has anti-inflammatory and antiapoptotic properties. In conclusion, levosimendan seems to be a particularly promising agent for the treatment of decompensated heart failure, as in addition to improving cardiac output, it has a more favorable side-effect profile than classic inotropic agents, and it affects multiple pathways with key role in the pathophysiology of heart failure.


Subject(s)
Cardiotonic Agents/therapeutic use , Heart Failure/drug therapy , Hydrazones/therapeutic use , Pyridazines/therapeutic use , Vasodilator Agents/therapeutic use , Animals , Apoptosis/drug effects , Hemodynamics/drug effects , Humans , Hydrazones/pharmacokinetics , Hydrazones/pharmacology , Pyridazines/pharmacokinetics , Pyridazines/pharmacology , Simendan
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