No abstract

This report describes a novel approach of accessing the superficial veins of the upper extremity for the treatment of pulmonary emboli (PE) with an ultrasound enhanced thrombolytic infusion catheter. In a patient suffering from saddle PE and impending right heart failure, separate basilic and cephalic venous access sites in the right arm were utilized to insert EKOS EndoWave Infusion Catheter (EKOS Corporation, Bothell, WA) insertion in each pulmonary artery (PA). This technique could be advantageous, particularly for patients at high risk for access site complications and those unable to lie supine for prolonged duration of infusion therapy.

Spontaneous coronary dissection is more commonly reported in females and is an important differential diagnosis for acute coronary syndrome. Accelerated idioventricular rhythm has been reported before with reperfusion post myocardial ischemia. We report a case of accelerated idioventricular rhythm in a patient with spontaneous coronary artery dissection. A 45-yearold Caucasian female presented with left sided chest pain radiating to the neck and palpitations. Admission ECG showed accelerated idioventricular rhythm. Troponin I peaked at 0.5 ng/ml. Coronary angiography showed mid to distal left anterior descending artery dissection with adequate distal flow. Patient was initially medically managed with aspirin, metoprolol, intravenous heparin and eptifibatide infusions but continued to have symptoms of unstable angina. She underwent successful percutaneous coronary intervention with 2 drug eluting stents and was discharged back home symptom free on dual platelet therapy. Spontaneous coronary artery dissection is an important differential diagnosis for acute coronary syndrome especially in younger females. Accelerated idioventricular rhythm can be a presentation of coronary dissection and may indicate instability. Early percutaneous coronary intervention should be considered in such patients.

For nearly half a century, the therapeutic options for the risk reduction of stroke in atrial fibrillation have been stagnant with vitamin K antagonists, such as warfarin, being the primary therapy. Although antiplatelet agents have been investigated over this time, they were never shown to reduce the risk of stroke at the level warfarin has. Considering the limited therapeutic options, the main decision facing clinicians was not determining which agent to use, but whether a patient was at high enough risk of stroke to benefit from anticoagulation. The CHADS2 and, more recently, the CHADSVASC risk assessment schemes have been shown to be a simple and predicable tool in determining an individual's risk for stroke. Now, after nearly 50 years with limited alternatives, there has been a surge in therapies in the form of dabigatran, rivaroxaban and apixaban, which have been shown to be non-inferior and in some cases, superior to warfarin in their respective randomized controlled trials. This increase in available options is exciting but at the same time adds another layer of confusion to the process of selecting the appropriate agent for individual patients.