Imaging myocardial carcinoid with T2-STIR CMR

We used T2-STIR (Short Tau Inversion Recovery) cardiovascular magnetic resonance to demonstrate carcinoid tumor metastases to the heart and liver in a 64-year-old woman with a biopsy-proven ileal carcinoid tumor who was referred because of an abnormal echocardiogram

Inhibition of renin-angiotensin system (RAS) reduces ventricular tachycardia risk by altering connexin43

Renin-angiotensin system (RAS) activation is associated with arrhythmias. We investigated the effects of RAS inhibition in cardiac-specific angiotensin-converting enzyme (ACE) overexpression (ACE 8/8) mice, which exhibit proclivity to ventricular tachycardia (VT) and sudden death because of reduced connexin43 (Cx43). ACE 8/8 mice were treated with an ACE inhibitor (captopril) or an angiotensin receptor type-1 blocker (losartan). Subsequently, electrophysiological studies were performed, and the hearts were extracted for Cx43 quantification using immunoblotting, immunohistochemistry, fluorescent dye spread method, and sodium current quantification using whole cell patch clamping. VT was induced in 12.5% of captopril-treated ACE 8/8 and in 28.6% of losartan-treated mice compared to 87.5% of untreated mice (P<0.01). Losartan and captopril treatment increased total Cx43 2.4-fold (P=0.01) and the Cx43 phosphorylation ratio 2.3-fold (P=0.005). Treatment was associated with a recovery of gap junctional conductance. Survival in treated mice improved to 0.78 at 10 weeks (95% confidence interval 0.64 to 0.92), compared to the expected survival of less than 0.50. In a model of RAS activation, arrhythmic risk was correlated with reduced Cx43 amount and phosphorylation. RAS inhibition resulted in increased total and phosphorylated Cx43, decreased VT inducibility, and improved survival

Optimising drug therapy for non-infectious uveitis

Introduction Uveitis encompasses a wide variety of sight-threatening diseases characterized by intraocular inflammation. It is often classified as infectious and non-infectious uveitis. Unlike infectious uveitis, a distinct infectious agent cannot be identified in non-infectious uveitis and disease origin is usually autoimmune, drug related, or idiopathic. The Issue at Hand Non-infectious uveitis can often have a relapsing-remitting course, making it difficult to treat, and poses a significant challenge to ophthalmologists. The autoimmune nature of non-infectious uveitis warrants the use of anti-inflammatory and immunomodulatory agents for disease control. However, a subset of patients has persistent or recurrent ocular inflammation despite appropriate treatment, stressing the need for newer therapies aimed at more specific inflammatory targets such as tumour necrosis factor (TNF) alpha agents, anti-interleukin agents, and anti-interleukin receptor agents. Objectives This article discusses the various medical options available for the treatment of non-infectious uveitis in the light of the most recent evidence. Conclusion Successful management of non-infectious uveitis requires the clinician carefully balance advantages and disadvantages of each new and old therapy while considering individual circumstances. Counselling regarding the benefits and complications of each therapy can help patients make an informed choice