Drug-Coated Balloon Angioplasty for Axillary Artery Stenosis.

We present a case report of a patient with symptomatic bilateral severe axillary artery stenosis who underwent drug-coated balloon angioplasty. A 59-year-old female with a past medical history of peripheral artery disease presented with bilateral upper extremity claudication on exertion and episodes of syncope. Peripheral angiography showed significant bilateral upper extremity peripheral artery disease (PAD) including bilateral severe axillary artery stenosis. The patient underwent endovascular management with drug-coated balloon angioplasty of the axillary artery bilaterally. Symptoms completely resolved and the patient continues to be on follow-up. Arterial duplex studies on both upper extremities showed no evidence of high-grade stenosis six years after intervention. Drug coated balloon angioplasty can be a successful modality of endovascular management for patients with symptomatic severe axillary artery stenosis. However, more randomized controlled data is required before making any conclusion.

Clot in Transit: Therapy via Peripherally Inserted Central Catheter Line.

There are currently no definitive guidelines for the optimal management of clots in transit (CIT) due to a distinct lack of quality research to suggest a recommended therapy. The three main treatment modalities that are commonly utilized for pulmonary emboli (PE) (a sequela of CIT) are thrombolysis, pulmonary embolectomy, and anticoagulation alone. The current recommendation for severe PE with hemodynamic collapse is to consult cardiothoracic surgery for clot retrieval. One ongoing area of research involves the use of catheter-directed application of thrombolytic agents as it may have similar outcomes to the systemic application while minimizing the risk of bleeding events due to a lower dose of medication used. We report the case of a patient in whom, by taking advantage of an already placed peripherally inserted central catheter (PICC) line, tissue plasminogen activator (tPA) was successfully delivered at a localized site near the clot for active thrombolysis while only causing minimal adverse effects related to recent laminectomy/fasciectomy and foraminotomy compared to what may have been observed with systemic tPA administration.

Increased susceptibility of spontaneously hypertensive rats to ventricular tachyarrhythmias in early hypertension.

Hypertension is a risk factor for sudden cardiac death caused by ventricular tachycardia and fibrillation (VT/VF). We hypothesized that, in early hypertension, the susceptibility to stress-induced VT/VF increases. We compared the susceptibility of 5- to 6-month-old male spontaneously hypertensive rats (SHR) and age/sex-matched normotensive rats (NR) to VT/VF during challenge with oxidative stress (H2 O2 ; 0.15 mmol l(-1) ). We found that only SHR hearts exhibited left ventricular fibrosis and hypertrophy. H2 O2 promoted VT in all 30 SHR but none of the NR hearts. In 33% of SHR cases, focal VT degenerated to VF within 3 s. Simultaneous voltage-calcium optical mapping of Langendorff-perfused SHR hearts revealed that H2 O2 -induced VT/VF arose spontaneously from focal activations at the base and mid left ventricular epicardium. Microelectrode recording of SHR hearts showed that VT was initiated by early afterdepolarization (EAD)-mediated triggered activity. However, despite the increased susceptibility of SHR hearts to VT/VF, patch clamped isolated SHR ventricular myocytes developed EADs and triggered activity to the same extent as NR ventricular myocytes, except with larger EAD amplitude. During the early stages of hypertension, when challenged with oxidative stress, SHR hearts showed an increased ventricular arrhythmogenicity that stems primarily from tissue remodelling (hypertrophy, fibrosis) rather than cellular electrophysiological changes. Our findings highlight the need for early hypertension treatment to minimize myocardial fibrosis, ventricular hypertrophy, and arrhythmias.