Citations

In patients with aortic stenosis (AS) and eccentric transaortic flow, greater pressure loss occurs as the jet collides with the aortic wall together with delayed and diminished pressure recovery. This leads to the elevated transaortic valve pressure gradients noted on both Doppler and cardiac catheterization. Such situations may present a diagnostic dilemma where traditional measures of stenosis severity indicate severe AS, while imaging modalities of the aortic valve geometric aortic valve area (GOA) suggest less than severe stenosis. In this study, we present a series of cases exemplifying this clinical dilemma and demonstrate how color M‐mode, 2D and 3D transthoracic (TTE) and transesophageal (TEE) echocardiography, cardiac computed tomography angiography (CTA), and magnetic resonance imaging (MRI), may be used to resolve such discrepancies.

Abstract Migraine is increasingly understood to be a disorder of the brain. In susceptible individuals, a variety of ?triggers? may influence altered central excitability, resulting in the activation and sensitization of trigeminal nociceptive afferents surrounding blood vessels (i.e., the trigeminovascular system), leading to migraine pain. Transient receptor potential (TRP) channels are expressed in a subset of dural afferents, including those containing calcitonin gene related peptide (CGRP). Activation of TRP channels promotes excitation of nociceptive afferent fibers and potentially lead to pain. In addition to pain, allodynia to mechanical and cold stimuli can result from sensitization of both peripheral afferents and of central pain pathways. TRP channels respond to a variety of endogenous conditions including chemical mediators and low pH. These channels can be activated by exogenous stimuli including a wide range of chemical and environmental irritants, some of which have been demonstrated to trigger migraine in humans. Activation of TRP channels can elicit CGRP release, and blocking the effects of CGRP through receptor antagonism or antibody strategies has been demonstrated to be effective in the treatment of migraine. Identification of approaches that can prevent activation of TRP channels provides an additional novel strategy for discovery of migraine therapeutics.

Background— Spontaneous coronary artery dissection (SCAD) is an increasingly recognized nonatherosclerotic cause of acute coronary syndrome. The angiographic characteristics of SCAD are largely undetermined. The goal of this study was to determine the prevalence of coronary tortuosity in SCAD and whether it may be implicated in the disease. Methods and Results— Patients with confirmed SCAD (n=246; 45.3±8.9 years; 96% women) and 313 control patients without SCAD or coronary artery disease who underwent coronary angiography were included in this case–control study. Angiograms were reviewed for coronary tortuosity and assigned a tortuosity score. Tortuosity was common in patients presenting with their first SCAD event (78% versus 17% in controls; P <0.0001; tortuosity score, 4.41±1.73 versus 2.33±1.49 in controls; P <0.0001) despite a low prevalence of hypertension (34%). Recurrent SCAD (n=40) occurred within segments of tortuosity in 80% of cases. Severe tortuosity (≥2 consecutive curvatures ≥180°) was associated with a higher risk of recurrent SCAD (hazard ratio, 3.29; 95% confidence interval, 0.99–8.29; P =0.05). Tortuosity score >5 was associated with a trend toward higher risk of recurrent SCAD ( P =0.16). Prespecified angiographic markers of tortuosity including corkscrew appearance and multivessel symmetrical tortuosity were associated with extracoronary vasculopathy including fibromuscular dysplasia ( P <0.05 for both). Conclusions— Coronary artery tortuosity is highly prevalent in the SCAD population and is associated with recurrent SCAD. Recurrent SCAD most often occurs within segments of tortuosity. Angiographic features of SCAD are associated with extracoronary vasculopathy, including fibromuscular dysplasia. These findings suggest that coronary tortuosity may serve as a marker or potential mechanism for SCAD.