Lyne Charbonneau

Usefulness of fluorine-18 positron emission tomography/computed tomography for identification of cardiovascular implantable electronic device infections.

OBJECTIVES This study evaluated the usefulness of fluorodesoxyglucose marked by fluorine-18 ((18)F-FDG) positron emission tomography (PET) and computed tomography (CT) in patients with suspected cardiovascular implantable electronic device (CIED) infection. BACKGROUND CIED infection is sometimes challenging to diagnose. Because extraction is associated with significant morbidity/mortality, new imaging modalities to confirm the infection and its dissemination would be of clinical value. METHODS Three groups were compared. In Group A, 42 patients with suspected CIED infection underwent (18)F-FDG PET/CT. Positive PET/CT was defined as abnormal uptake along cardiac devices. Group B included 12 patients without infection who underwent PET/CT 4 to 8 weeks post-implant. Group C included 12 patients implanted for >6 months without infection who underwent PET/CT for another indication. Semi-quantitative ratio (SQR) was obtained from the ratio between maximal uptake and lung parenchyma uptake. RESULTS In Group A, 32 of 42 patients with suspected CIED infection had positive PET/CT. Twenty-four patients with positive PET/CT underwent extraction with excellent correlation. In 7 patients with positive PET/CT, 6 were treated as superficial infection with clinical resolution. One patient with positive PET/CT but negative leukocyte scan was considered false positive due to Dacron pouch. Ten patients with negative-PET/CT were treated with antibiotics and none has relapsed at 12.9 ± 1.9 months. In Group B, patients had mild uptake seen at the level of the connector. There was no abnormal uptake in Group C patients. Median SQR was significantly higher in Group A (A = 2.02 vs. B = 1.08 vs. C = 0.57; p < 0.001). CONCLUSIONS PET/CT is useful in differentiating between CIED infection and recent post-implant changes. It may guide appropriate therapy.

Myocardial perfusion imaging findings and the role of adenosine in the warm-up angina phenomenon

OBJECTIVES This study examined the roles of myocardial perfusion and adenosine in warm-up angina. BACKGROUND In warm-up angina, neither the role of an adenosine-mediated mechanism, as is found in experimental ischemic preconditioning, nor of increased myocardial perfusion is well defined. METHODS In substudy A, a single-photon emission computed tomography (SPECT)-thallium-201 exercise test was performed by 12 subjects with ischemic heart disease on three occasions one week apart. The third test was preceded by a warm-up test. The extent of the thallium deficit and its intensity on the third test were compared with the baseline tests controlling for the heart rate-systolic blood pressure product (RPP) at thallium injection. In substudy B, 12 similar subjects did two successive exercise tests at two separate sessions and received the adenosine antagonist, aminophylline (intravenous 5 mg/kg bolus and 0.9 mg/kg/h infusion) at one session, and equivalent saline at the other session. Change in ischemic threshold (RPP at 1 mm ST segment depression) and in maximum ST depression adjusted for RPP were analyzed. RESULTS In substudy A, despite a significant attenuation of electrocardiogram indexes of myocardial ischemia between the baseline and third (warmed-up) tests, the thallium extent deficits (20.8 +/- 15.1% and 16.8 +/- 12.4%) and intensity deficits (41.2 +/- 12.6% and 39.3 +/- 12.6%) did not differ significantly. In substudy B, the increase in ischemic threshold on re-exercise was unaffected by aminophylline. Adjusted maximum ST depression even decreased to a greater extent on re-exercise with aminophylline (by 51 +/- 21%) than with saline (by 32 +/- 19%) (p = 0.012). CONCLUSIONS While warm-up angina is associated with a significant attenuation of exercise electrocardiogram indexes of ischemia, it is unaccompanied by significant changes in SPECT perfusion and does not appear to be mediated by an adenosine-dependent mechanism since it is not blocked by aminophylline. Thus, its mechanism, which appears distinct from experimental ischemic preconditioning, remains unidentified.

The Brugada syndrome in Canada: A unique French-Canadian experience

UNLABELLED The Brugada syndrome (BS) is a clinical entity involving cardiac sodium channelopathy, typical electrocardiogram (ECG) changes and predisposition to ventricular arrhythmia. This syndrome is mainly recognized by specialized cardiologists and electrophysiologists. Data regarding BS largely come from multicentre registries or Asian countries. The present report describes the Quebec Heart Institute experience, including the clinical characteristics and prognosis of native French-Canadian subjects with the Brugada-type ECG pattern. METHODS AND RESULTS BS has been diagnosed in 35 patients (mean age 51 +/- 12 years) at the Quebec Heart Institute since 2001. Patients were referred from primary care physicians for ECG abnormalities, syncope or ventricular arrhythmia, or were diagnosed incidentally on an ECG obtained for other purposes. The abnormal ECG was recognized after a syncopal spell in four patients and during family screening in four patients. All of the others were incidental findings following a routine ECG. No patient had a family history of sudden cardiac death at younger than 45 years of age. In this population, right bundle branch block pattern with more than 2 mm ST segment elevation in leads V1 to V3 was recorded spontaneously in 25 patients and was induced by sodium blockers in 10 patients. The sodium channel blocker test was performed in 21 patients and was positive in 18 patients (86%). An electrophysiological study was performed in 20 of 35 patients, during which ventricular fibrillation was induced in five patients; three of the five patients were previously asymptomatic. An implantable cardioverter-defibrillator was implanted in six of 35 patients (17%), including three of four patients with a history of syncope. A loop recorder was implanted in three patients. After a mean follow-up of 36 +/- 18 months, one patient died from a noncardiac cause and one patient (with a history of syncope) received an appropriate shock from his implantable cardioverter-defibrillator. No event occurred in the asymptomatic population. CONCLUSIONS BS is present in the French-Canadian population and is probably under-recognized. Long-term prognosis of individuals with BS, especially in sporadic, asymptomatic cases, needs to be clarified.

Combined Administration of Quinidine and Propafenone for Atrial Fibrillation: The CAQ‐PAF Study

Propafenone and its 5‐hydroxy metabolite exhibit different electrophysiological properties. Objectives of the CAQ‐PAF study were (1) to develop a strategy favoring propafenone instead of 5‐hydroxypropafenone in plasma following oral administration of propafenone and (2) to evaluate the potential of low‐dose quinidine to chronically inhibit CYP2D6. Patients (n = 102) with atrial fibrillation received propafenone 150 mg 3 times daily with either quinidine 100 mg twice daily or placebo. Throughout the study (follow‐up, 199 ± 155 days), quinidine successfully inhibited CYP2D6: propafenone concentrations were 3 times higher in patients receiving quinidine (1033 ± 611 ng/mL vs 328 ± 229 ng/mL; P < .001). Moreover, 80% (n = 10) of patients with propafenone levels greater than 1500 ng/mL were in sinus rhythm at 1 year. In contrast, recurrence of atrial fibrillation occurred in 22 of 23 patients with propafenone levels less than 1000 ng/mL (P < .0001). Thus, chronic inhibition of CYP2D6 is achievable with low‐dose quinidine in humans. Increased plasma levels of propafenone may be highly beneficial to prevent recurrence of atrial fibrillation.