Comparative diagnostic yield and 3-month outcomes of "triple rule-out" and standard protocol coronary CT angiography in the evaluation of acute chest pain.

BACKGROUND: "Triple rule-out" CT angiography simultaneously evaluates coronary artery disease, pulmonary embolism, and aortic dissection in a single imaging examination. However, the clinical outcomes of this approach are unknown. OBJECTIVE: Using standard cardiac CT angiography as a reference, this study was performed to describe the diagnostic yield and clinical outcomes of patients undergoing triple rule-out in clinical practice. METHODS: We identified consecutive patients at 2 institutions undergoing triple rule-out or cardiac CT angiography for acute chest pain. The primary outcome was a composite diagnostic yield consisting of coronary artery diameter stenosis >50%, pulmonary embolism, and aortic dissection. Other reported outcomes included radiation dose, downstream resource use, and 90-day clinical outcomes. RESULTS: Among 2068 patients (272 triple rule-out and 1796 cardiac CT angiograms), the composite diagnostic yield was 14.3% with triple rule-out and 16.3% with cardiac CT (P = 0.41) and was driven by the diagnosis of obstructive coronary artery disease (13.2% triple rule-out versus 16.1% cardiac CT, P = 0.22). The diagnostic yield for pulmonary embolism was low (1.1% triple rule-out and 0.2% cardiac CT, P = 0.052) and no aortic dissections were found in either group. Compared with cardiac CT, the triple rule-out approach was associated with higher radiation exposure (12.0 ± 5.6 mSv versus 8.2 ± 4.0 mSv, P < 0.0001), a greater incidence of subsequent emergency center cardiac evaluations (5.9% versus 2.5%, P = 0.0017), and more downstream pulmonary embolism-protocol CT angiography (3.3% versus 0.9%, P = 0.0034). CONCLUSIONS: Among patients with acute chest pain, a triple rule-out approach resulted in higher radiation exposure compared with cardiac CT, but was not associated with improved diagnostic yield, reduced clinical events, or diminished downstream resource use.

The antiarrhythmic effects of ranolazine.

The genesis of cardiac arrhythmia can be grouped into 3 common mechanisms: abnormal automaticity, triggered activity, and re-entry. Alteration of automaticity, triggered activity, conduction, and/or refractoriness of myocardial tissue by drugs will perturb and often prevent the occurrence of arrhythmias. Ranolazine is a novel agent approved in the United States for antianginal therapy. The potential of ranolazine as an antiarrhythmic drug stems from observation of its ability to modify multiple ionic currents in cardiac cells responsible for generation of the action potential. In contrast to currently available antiarrhythmic drugs, ranolazine is well tolerated and has few side effects. Small clinical trials suggest that ranolazine may have a role in the treatment of patients with non-ST-elevation acute coronary syndrome, atrial fibrillation, long QT syndromes, and sinus node dysfunction.