Since its introduction, the TIMI frame count method has contributed to the understanding of the pathophysiology of coronary artery disease. In this article, the evolution of the TFC method and its applicability in the assessment of various therapeutic modalities are described.

Although percutaneous coronary intervention restores optimal epicardial blood flow in most cases, abnormal myocardial perfusion may still persist. This might be as a result of macro and microembolization, neutrophil plugging, vasoconstriction, myocyte contracture, local intracellular and interstitial edema, intramural haemorrhage, and endothelial blistering. Local delivery of intracoronary pharmacotherapy via the coronary arteries may increase local drug concentration several fold, and may improve drug efficacy. Several pharmacological agents such as adenosine, calcium channel blockers, alpha blockers, beta2 receptor activators, vasodilators, antithrombotics, and antiplatelet agents have been used to treat coronary microvascular dysfunction. This article reviews the results of trials of intracoronary pharmacotherapy to date.

Potent antiplatelet and antithrombotic agents have significantly reduced mortality in the setting of acute coronary syndromes and percutaneous coronary intervention. However these agents are associated with increased bleeding which is in turn associated with adverse clinical outcomes. In many centers, transfusion is often used to correct for blood loss. Blood transfusion in the setting of acute coronary syndrome has been associated with adverse clinical outcomes including increased mortality. Transfusion associated microchimerism (TA-MC) is a newly recognized complication of blood transfusion. There is engraftment of the donor's hematopoietic stem cells in patients who then develop microchimerism. This article discusses the association of bleeding/blood transfusion with adverse outcomes and the potential role of TA-MC in clinical outcomes.

SVG patency is lower with smaller recipient vessel size (<2mm). However, the relationship between the presence of an over-sized or under-sized SVG relative to the native artery (NA) diameter at follow-up has not been fully explored. It was hypothesized that the presence of a larger SVG to NA diameter at 1 year follow-up would be associated with inferior antegrade flow in SVG and NA. Methods : Data were drawn from the PREVENT IV trial, a phase III, multicenter, randomized, double-blind, placebo-controlled trial in which autologous SVGs were treated ex vivo with edifoligide for patients undergoing CABG with repeat angiography within 18 months post CABG and films were evaluated by a core laboratory for SVG diameter, TIMI flow grade (TFG), TIMI frame counts (TFCs) and TIMI myocardial perfusion grade (TMPG). Results: The average ratio of SVG to NA diameter was 1.71±0.45 (n=1,945 in 1,203 patients). As the ratio of the SVG to NA diameter increased, the occurrence of optimal TFG 3 in the SVG was lower (Figure A ) and TFCs were higher (p=0.0001). The frequency of TFG 3 in the NA artery was also lower as the degree of mismatch between SVG and NA diameter increased (p=0.028). Conversely, as the SVG to NA mean diameter ratio increased, the occurrence of TMPG 3 was higher (Figure B ). Conclusion: Larger SVGs in relation to NA at 1 year follow-up were associated with slower flow but improved myocardial perfusion. Greater SVG diameter may be reflective of a larger SVG volume and may explain in part the longer time to fill the SVG; likewise the larger volume of the SVG may explain the apparent improved perfusion of the myocardium. Slower dye transit in large SVGs does not necessarily imply poor perfusion.

No abstract

The Texas A&M Transportation Institute's Urban Mobility Report (UMR) is acknowledged to be the most authoritative source of information about traffic congestion and its possible solutions. As policy makers from the local to national levels devise strategies to reduce greenhouse gas (GHG) emissions, the level of interest in the environmental impact of urban congestion has increased. To this end, the researchers developed and applied a methodology to determine carbon dioxide (CO2) emissions caused by congestion for inclusion in the UMR. The methodology also estimated fuel consumption on the basis of the CO2 emissions estimates. The researchers developed a five-step methodology with data from three primary data sources: (a) FHWA's Highway Performance Monitoring System, (b) INRIX traffic speed data, and (c) the U.S. Environmental Protection Agency's Motor Vehicle Emissions Simulator model. Results were intuitive and reasonable when emission rates (pounds of CO2 per mile) were compared with the emissions inventories in selected cities. The researchers incorporated the new methodology for all urban areas into the 2012 UMR and plan to include the same measures in future releases of the report. The researchers reported that, in 2011, 56 billion pounds of additional CO2 were produced in all 498 urban areas during congestion only; this amount equated to 2.9 billion gallons of wasted fuel. The amount of CO2 produced under free-flow conditions (i.e., absent congestion) was 1.8 trillion pounds in 2011 in all 498 urban areas.

No abstract

No abstract