Background-Experimental studies suggest that low wall shear stress (WSS) promotes plaque development and high WSS is associated with plaque destabilization. We hypothesized that low-WSS segments in patients with coronary artery disease develop plaque progression and high-WSS segments develop necrotic core progression with fibrous tissue regression. Methods and Results-Twenty patients with coronary artery disease underwent baseline and 6-month radiofrequency intravascular ultrasound (virtual histology intravascular ultrasound) and computational fluid dynamics modeling for WSS calculation. For each virtual histology intravascular ultrasound segment (nϭ2249), changes in plaque area, virtual histology intravascular ultrasound-derived plaque composition, and remodeling were compared in low-, Key Words: atherosclerosis Ⅲ coronary artery disease Ⅲ hemodynamics Ⅲ intravascular ultrasonography, interventional Ⅲ wall shear stress A lthough cardiovascular risk factors lead to systemic inflammation, oxidative stress, and endothelial dysfunction, it is recognized that coronary atherosclerotic plaques are focally distributed with highly variable rates of progression. However, prediction of regional plaque progression in an individual coronary segment remains elusive. Editorial see p 763 Clinical Perspective on p 788Alterations in wall shear stress (WSS) have been implicated in the focal distribution and pathophysiology of coronary atherosclerosis. [1][2][3][4][5] Low WSS leads to a proatherogenic endothelial cell phenotype 1-3 and focal development of atherosclerosis and vascular remodeling in experimental models 6 -8 and pilot clinical studies. 9,10 Both low WSS and high WSS have been implicated in the production of matrix metalloproteinases and plasmin by endothelial cells that can destabilize plaque fibrous caps. [11][12][13] In addition, high WSS has been shown to induce apoptosis of smooth muscle cells, 14,15 which might enhance plaque vulnerability.To date, the role of both low WSS and high WSS in the development of plaque progression, change in plaque com- Received January 23, 2011; accepted May 9, 2011 Methods Study PopulationTwenty patients presenting to the cardiac catheterization laboratory at Emory University Hospital between December 2007 and January 2009 with an abnormal noninvasive stress test or stable anginal syndromes and found to have a nonobstructive lesion requiring invasive physiological evaluation were enrolled. Exclusion criteria included myocardial infarction, cardiogenic shock or hemodynamic instability, lesion requiring percutaneous or surgical revascularization, coronary artery bypass surgery, severe valvular heart disease, presence of visual coronary collaterals, inability to provide informed consent, serum creatinine Ͼ1.5 mg/dL, liver disease, or significant hematologic disease. All patients underwent baseline and 6-month follow-up radiofrequency backscatter IVUS (VH-IVUS) and baseline computational fluid dynamics (CFD) modeling for WSS calculation. All patients underwent lipid profile assessm...

Pulmonary embolism (PE) is a life-threatening condition and a leading cause of morbidity and mortality. There have been many advances in the field of PE in the last few years, requiring a careful assessment of their impact on patient care. However, variations

Structured Abstract Background Multiple scoring systems have been devised to quantify angiographic coronary artery disease (CAD) burden, but it is unclear how these scores relate to each other and which scores are most accurate. The aim of this study was to compare coronary angiographic scoring systems 1) with each other and 2) with intravascular ultrasound (IVUS) derived plaque burden in a population undergoing angiographic evaluation for CAD. Methods Coronary angiographic data from 3600 patients was scored using 10 commonly used angiographic scoring systems and inter-score correlations were calculated. In a subset of 50 patients, plaque burden and plaque area in the left anterior descending coronary artery was quantified using IVUS and correlated with angiographic scores. Results All angiographic scores correlated with each other (range for Spearman coefficient (ρ): 0.79-0.98, p<0.0001); the two most widely used scores, Gensini and CASS-70, had a ρ = 0.90, p<0.0001. All scores correlated significantly with average plaque burden and plaque area by IVUS (range ρ: 0.56-0.78, p<0.0001 and 0.43-0.62, p<0.01, respectively). The CASS-50 score had the strongest correlation (ρ: 0.78 and 0.62, p<0.0001) and the Duke Jeopardy score the weakest correlation (ρ: 0.56 and 0.43, p<0.01) with plaque burden and area, respectively. Conclusions Angiographic scoring systems are strongly correlated with each other and with atherosclerotic plaque burden. Scoring systems therefore appear to be a valid estimate of CAD plaque burden.

Patients with myocardial bridges are often asymptomatic but this anomaly may be associated with exertional angina, acute coronary syndromes, cardiac arrhythmias, syncope or even sudden cardiac death. This review presents our understanding of the pathophysiology of myocardial bridging and describes prevailing diagnostic modalities and therapeutic options for this challenging clinical entity.

Although traditional cardiovascular risk factors ‘prime the soil’ for atherogenesis systemically, atherosclerosis primarily occurs in a site-specific manner with a predilection towards the inner wall of curvatures and outer wall of bifurcations with sparing of flow-dividers. Wall shear stress is a frictional force exerted parallel to the vessel wall that leads to alteration of the endothelial phenotype, endothelial cell signaling, gene and protein expression leading to a proinflammatory phenotype, reduced nitric oxide availability and disruption of the extracellular matrix, which in turn leads to plaque development. Clinical and experimental data are emerging that suggest the pathobiology associated with abnormal wall shear stress results in atherosclerotic plaque development and progression.

No abstract

BackgroundExtremes of wall shear stress (WSS) have been associated with plaque progression and transformation, which has raised interest in the clinical assessment of WSS. We hypothesized that calculated coronary WSS is predicted only partially by luminal geometry and that WSS is related to plaque composition.Methods and ResultsTwenty‐seven patients with coronary artery disease underwent virtual histology intravascular ultrasound and Doppler velocity measurement for computational fluid dynamics modeling for WSS calculation in each virtual histology intravascular ultrasound segment (N=3581 segments). We assessed the association of WSS with plaque burden and distribution and with plaque composition. WSS remained relatively constant across the lower 3 quartiles of plaque burden (P=0.08) but increased in the highest quartile of plaque burden (P<0.001). Segments distal to lesions or within bifurcations were more likely to have low WSS (P<0.001). However, the majority of segments distal to lesions (80%) and within bifurcations (89%) did not exhibit low WSS. After adjustment for plaque burden, there was a negative association between WSS and percent necrotic core and calcium. For every 10 dynes/cm2 increase in WSS, percent necrotic core decreased by 17% (P=0.01), and percent dense calcium decreased by 17% (P<0.001). There was no significant association between WSS and percent of fibrous or fibrofatty plaque components (P=NS).ConclusionsIn patients with coronary artery disease: (1) Luminal geometry predicts calculated WSS only partially, which suggests that detailed computational techniques must be used to calculate WSS. (2) Low WSS is associated with plaque necrotic core and calcium, independent of plaque burden, which suggests a link between WSS and coronary plaque phenotype. (J Am Heart Assoc. 2012;1:e002543 doi: 10.1161/JAHA.112.002543.)

Intravascular ultrasound (IVUS) provides valuable information on the coronary vascular lumen and wall and has been an important tool in the cardiac catheterization laboratory for over 2 decades. The major utility of IVUS relates to optimizing stent deployment, particularly in complex lesions. In percutaneous coronary intervention with bare-metal stents, IVUS guidance reduces restenosis. In percutaneous coronary intervention with drug-eluting stents, IVUS guidance may reduce rates of stent thrombosis with little affect on restenosis. The benefit of IVUS guidance is most important in complex lesion subsets, such as left main and bifurcation lesions, where studies suggest that IVUS guidance may reduce mortality. Whereas IVUS luminal area measurements have been used to assess intermediate lesion severity, recent studies have demonstrated that IVUS accurately identifies nonischemic lesions for which percutaneous coronary intervention can be safely deferred, but cannot accurately predict hemodynamically significant lesions and should not solely be used to justify revascularization. In the current review, we focus on clinical applications of IVUS in interventional cardiology.