Sam Hanon

Ventricular arrhythmias in patients treated with methadone for opioid dependence

PurposeOver the last decade, there has been a significant rise in reported cases of methadone induced QT prolongation (QTP) and Torsades de Pointes (TdP) in patients treated for opioid dependence. Optimal management of these patients is challenging.MethodsWe report a case series of 12 consecutive patients admitted to our institution with methadone-induced QTP and ventricular arrhythmias.ResultsAll patients survived the presenting arrhythmia. Successful transition to buprenorphine was accomplished in three patients. QT interval normalized and none of these patients had recurrent arrhythmias. Methadone dose was reduced in five patients with improvement of QT interval and resolution of arrhythmia. Four patients, including two with ICDs, refused or did not tolerate a reduction in their methadone dose.ConclusionVentricular arrhythmias in patients on methadone are an uncommon but important problem. Buprenorphine, a partial µ-opiate–receptor agonist and a κ-opiate–receptor antagonist does not cause QTP or TdP. Buprenorphine is a useful and effective alternative to methadone in a select group of patients, including those with documented ventricular arrhythmias on methadone. Pacemakers or defibrillators should be reserved for patients who have failed buprenorphine or a reduced methadone dose.

Persistent formation of angiotensin II despite treatment with maximally recommended doses of angiotensin converting enzyme inhibitors in patients with chronic heart failure

JRAAS 2000;1:147-50 Introduction Decreasing activation of the renin-angiotensinaldosterone system (RAAS) is an essential target of the pharmacological treatment of patients with congestive heart failure (CHF). Several large, randomised, placebo-controlled trials have shown that angiotensin converting enzyme (ACE) inhibition enhances life expectancy and alleviates symptoms in patients with CHF and with acute myocardial infarction and left ventricular (LV) systolic dysfunction. The exact mechanisms that mediate the clinical benefits of ACE inhibitors are still poorly understood, although it is generally assumed that the benefits are somehow related to decreased activity of the RAAS and thereby reduced levels of tissue and plasma angiotensin II (Ang II).

The Canadian Durata Experience: Grounds for cautious optimism?

Implantable cardioverter-defibrillator (ICD) therapy by any measure is an enormous success. Thousands of sudden deaths are prevented each year in populations at risk. The Achilles heel of ICD therapy, the transvenous ICD lead, has tempered the celebration of this success. Significant advances made in lead design in the first decade of transvenous implants improved lead handling, durability, and finally size. Yet leads remain prone to early and late failure, with lead malfunction reaching 40% at 8 years postimplant. Although there are varied mechanisms for lead dysfunction, insulation defects make up the majority of lead failures at any point in a lead’s service. In contrast to the early advances in ICDs, the last several years have been marred by the unfortunate experience with the Medtronic Sprint Fidelis and St. Jude Riata leads. The highly public failures of these leads have inhibited penetration of this lifesaving therapy, impaired new technology adoption, and substantially slowed the pace of innovation in this field. The Riata lead manifests a unique mechanism of failure wherein the conductor cables erode through the silicone insulation, resulting in “inside–out” abrasion of lead components. Externalization has been described in up to 25% to 30% of Riata leads at 5-year follow up. The frequency and extent of externalization increase with lead age. Ethylenetetrafluoroethylene (ETFE) coating, still present around the externalized cables and lead components, delays or prevents electrical dysfunction. For the vast majority of these leads, the defect is electrically silent. Mid-term data for Riata leads indicate that electrical abnormalities are in the range of other ICD leads, but recent reports suggest that electrical failure may be higher in externalized leads. Thus, long-term (45 year) data are essential. Management of the externalized leads presents a tremendous hazard for patients and physicians because there are no guidelines based on data around these compromised leads.

Wide QRS tachycardia: what is the rhythm?

We report a case of an elderly man who presented to the emergency room complaining of palpitations. Electrocardiogram revealed wide QRS tachycardia with a narrow beat within the tachycardia. Most commonly, a narrow complex beat during a wide complex tachycardia suggests a capture or fusion beat in the setting of ventricular tachycardia. However, there are situations where supraventricular tachycardia can also manifest this way. In our patient a pacemaker interrogation clarified the diagnosis.