Myocardial bridges: A meta-analysis.

Myocardial bridges are anatomical entities characterized by myocardium covering segments of coronary arteries. In some patients, the presence of a myocardial bridge is benign and is only incidentally found on autopsy. In other patients, however, myocardial bridges can lead to compression of the coronary artery during systolic contraction and delayed diastolic relaxation, resulting in myocardial ischemia. This ischemia in turn can lead to myocardial infarction, ventricular arrhythmias and sudden cardiac death. Myocardial bridges have also been linked to an increased incidence of atherosclerosis, which has been attributed to increased shear stress and the presence of vasoactive factors. Other studies however, demonstrated the protective roles of myocardial bridges. In this study, using systematic review and a meta-analytical approach we investigate the prevalence and morphology of myocardial bridges in both clinical imaging and cadaveric dissections. We also discuss the pathophysiology, clinical significance, and management of these anatomical entities.

Small molecules and Alzheimer's disease: misfolding, metabolism and imaging.

Small molecule interactions with amyloid proteins have had a huge impact in Alzheimer's disease (AD), especially in three specific areas: amyloid folding, metabolism and brain imaging. Amyloid plaque amelioration or prevention have, until recently, driven drug development, and only a few drugs have been advanced for use in AD. Amyloid proteins undergo misfolding and oligomerization via intermediates, eventually forming protease resistant amyloid fibrils. These fibrils accumulate to form the hallmark amyloid plaques and tangles of AD. Amyloid binding compounds can be grouped into three categories, those that: i) prevent or reverse misfolding, ii) halt misfolding or trap intermediates, and iii) accelerate the formation of stable and inert amyloid fibrils. Such compounds include hydralazine, glycosaminoglycans, curcumin, beta sheet breakers, catecholamines, and ATP. The versatility of amyloid binding compounds suggests that the amyloid structure may serve as a scaffold for the future development of sensors to detect such compounds. Metabolic dysfunction is one of the earliest pathological features of AD. In fact, AD is often referred to as type 3 diabetes due to the presence of insulin resistance in the brain. A recent study indicates that altering metabolism improves cognitive function. While metabolic reprogramming is one therapeutic avenue for AD, it is more widely used in some cancer therapies. FDA approved drugs such as metformin, dichloroacetic acid (DCA), and methylene blue can alter metabolism. These drugs can therefore be potentially applied in alleviating metabolic dysfunction in AD. Brain imaging has made enormous strides over the past decade, offering a new window to the mind. Recently, there has been remarkable development of compounds that have the ability to image both types of pathological amyloids: tau and amyloid beta. We have focused on the low cost, simple to use, near infrared fluorescence (NIRF) imaging probes for amyloid beta (Aß), with specific attention on recent developments to further improve contrast, specificity, and sensitivity. With advances in imaging technologies, such fluorescent imaging probes will open new diagnostic avenues.