Outflow tract ventricular tachycardia mapped to the coronary arteries: anatomical correlates and management strategies.

BACKGROUND: The coronary cusps have been well described as a successful site for ablation in patients with symptomatic outflow tract ventricular tachycardia. The earliest site of activation is rarely found at the ostia or into the main coronary arteries. The exact anatomic substrate, diagnostic characteristics, and therapeutic approaches for such instances are poorly understood. METHODS: We retrospectively reviewed outflow tract ventricular arrhythmia (OTVA) ablations done at Mayo Clinic Rochester from 2003 to 2011 (total VT: 414; outflow tract VT: 106). Three cases were identified where the earliest site of activation was not within the cusp but rather at or within the coronary ostia (3/414 for all VT: 0.7%; 3/106 for all OTVT: 2.8%). RESULTS: In 1 patient, the left main coronary artery (LMCA) was found to have electrograms (EGMs) recorded with bipolar mapping that preceded activation in the cusps or the left ventricular outflow tract. In 2 cases, the right coronary ostium and proximal right coronary artery recorded the earliest signals. Intracardiac echocardiographic guidance was used to successfully ablate these arrhythmias targeting the aortic route (1 patient) or the right coronary cusp (2 patients), and essentially isolated the focus of origin from the ventricular outflow tracts. Detailed mapping of surrounding structures, including the atrial appendages, the contralateral outflow tract, and the coronary venous system excluded far-field mapping in the artery as a cause for early activation at the ostial location. Local EGM characteristics suggested an unusually lengthy supravalvar myocardial extension as the likely arrhythmogenic substrate. Ablation was successful without coronary arterial or valvular injury and without valvular or root stenosis. CONCLUSIONS: Endocardial ablation isolating foci of origin in the vicinity of the coronary ostia is a challenging procedure but can be performed safely with appropriate visualization and is effective in the treatment of OTVA.

Stroke or transient ischemic attack in patients with transvenous pacemaker or defibrillator and echocardiographically detected patent foramen ovale.

BACKGROUND: A patent foramen ovale (PFO) may permit arterial embolization of thrombi that accumulate on the leads of cardiac implantable electronic devices in the right-sided cardiac chambers. We sought to determine whether a PFO increases the risk of stroke/transient ischemic attack (TIA) in patients with endocardial leads. METHODS AND RESULTS: We retrospectively evaluated all patients who had endocardial leads implanted between January 1, 2000, and October 25, 2010, at Mayo Clinic Rochester. Echocardiography was used to establish definite PFO and non-PFO cohorts. The primary end point of stroke/TIA consistent with a cardioembolic etiology and the secondary end point of mortality during postimplantation follow-up were compared in PFO versus non-PFO patients with the use of Cox proportional hazards models. We analyzed 6075 patients (364 with PFO) followed for a mean 4.7 ± 3.1 years. The primary end point of stroke/TIA was met in 30/364 (8.2%) PFO versus 117/5711 (2.0%) non-PFO patients (hazard ratio, 3.49; 95% confidence interval, 2.33-5.25; P<0.0001). The association of PFO with stroke/TIA remained significant after multivariable adjustment for age, sex, history of stroke/TIA, atrial fibrillation, and baseline aspirin/warfarin use (hazard ratio, 3.30; 95% confidence interval, 2.19-4.96; P<0.0001). There was no significant difference in all-cause mortality between PFO and non-PFO patients (hazard ratio, 0.91; 95% confidence interval, 0.77-1.07; P=0.25). CONCLUSIONS: In patients with endocardial leads, the presence of a PFO on routine echocardiography is associated with a substantially increased risk of embolic stroke/TIA. This finding suggests a role of screening for PFOs in patients who require cardiac implantable electronic devices; if a PFO is detected, PFO closure, anticoagulation, or nonvascular lead placement may be considered.

Acute decrease in serum magnesium level after ischemic stroke may not predict decrease in neurologic function.

BACKGROUND: Higher serum levels of magnesium (Mg2+) may contribute to improved outcome following ischemic stroke, and this may be related to vessel recanalization. Patients with low or normal serum magnesium levels during the acute phase of ischemic stroke may be more susceptible to neurologic deterioration (ND) and worse outcomes. METHODS: All patients who presented to our center within 48 hours of acute ischemic stroke (July 2008 to December 2010) were retrospectively identified. Patient demographics, laboratory values, and multiple outcome measures, including ND, were compared across admission serum Mg2+ groups and change in Mg2+ from baseline to 24-hour groups. RESULTS: Three hundred thirteen patients met inclusion criteria (mean age: 64.8 years, 42.2% female, 64.0% black). Mg2+ groups at baseline were not predictive of poor functional outcome, death, or discharge disposition. Patients whose serum Mg2+ decreased during the first 24 hours of admission were also not at greater odds of ND or poor outcome measures compared with patients with unchanging or increasing Mg2+ levels. CONCLUSIONS: Our results suggest that patients who have low Mg2+ at baseline or a reduction in Mg2+ 24 hours after admission are not at a higher risk of experiencing ND or poor short-term outcome. Ongoing prospective interventional trials will determine if hyperacute aggressive magnesium replacement affords neuroprotection in stroke.