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BackgroundThe severity of epicardial coronary stenosis can be assessed by invasive measurements of trans-stenotic pressure drop and flow. A pressure or flow sensor-tipped guidewire inserted across the coronary stenosis causes an overestimation in true trans-stenotic pressure drop and reduction in coronary flow. This may mask the true severity of coronary stenosis. In order to unmask the true severity of epicardial stenosis, we evaluate a diagnostic parameter, which is obtained from fundamental fluid dynamics principles. This experimental and numerical study focuses on the characterization of the diagnostic parameter, pressure drop coefficient, and also evaluates the pressure recovery downstream of stenoses.MethodsThree models of coronary stenosis namely, moderate, intermediate and severe stenosis, were manufactured and tested in the in-vitro set-up simulating the epicardial coronary network. The trans-stenotic pressure drop and flow distal to stenosis models were measured by non-invasive method, using external pressure and flow sensors, and by invasive method, following guidewire insertion across the stenosis. The viscous and momentum-change components of the pressure drop for various flow rates were evaluated from quadratic relation between pressure drop and flow. Finally, the pressure drop coefficient (CDPe) was calculated as the ratio of pressure drop and distal dynamic pressure. The pressure recovery factor (η) was calculated as the ratio of pressure recovery coefficient and the area blockage.ResultsThe mean pressure drop-flow characteristics before and during guidewire insertion indicated that increasing stenosis causes a shift in dominance from viscous pressure to momentum forces. However, for intermediate (~80%) area stenosis, which is between moderate (~65%) and severe (~90%) area stenoses, both losses were similar in magnitude. Therefore, guidewire insertion plays a critical role in evaluating the hemodynamic severity of coronary stenosis. More importantly, mean CDPe increased (17 ± 3.3 to 287 ± 52, n = 3, p < 0.01) and mean η decreased (0.54 ± 0.04 to 0.37 ± 0.05, p < 0.01) from moderate to severe stenosis during guidewire insertion.ConclusionThe wide range of CDPe is not affected that much by the presence of guidewire. CDPe can be used in clinical practice to evaluate the true severity of coronary stenosis due to its significant difference between values measured at moderate and severe stenoses.

OBJECTIVE -Patients with the metabolic syndrome often have abnormal levels of proinflammatory and pro-oxidative mechanisms within their vasculature. We sought to determine whether the ACE inhibitor quinapril regulates markers of oxidative stress in the metabolic syndrome.RESEARCH DESIGN AND METHODS -Forty patients with the metabolic syndrome were randomized in a double-blind manner to either the ACE inhibitor quinapril (20 mg/day) or matching placebo for 4 weeks. Serum markers of vascular oxidative stress were measured.RESULTS -After 4 weeks of therapy, serum 8-isoprostane was reduced by 12% in the quinapril group when compared with placebo (quinapril, 46.7 Ϯ 1.0; placebo, 52.7 Ϯ 0.9 pg/ml; P ϭ 0.001). Erythrocyte superoxide dismutase activity increased 35% in the quinapril group when compared with placebo (quinapril, 826.3 Ϯ 17.1; placebo, 612.3 Ϯ 6.9 units/g Hb; P Ͻ 0.001). In addition, lag time to oxidation of LDL, a marker of oxidative stress, was increased by 48% in the quinapril group when compared with placebo (quinapril 89.2 Ϯ 9.2 vs. placebo 60.1 Ϯ 12.3 min; P Ͻ 0.001). Therapy with quinapril was well tolerated.CONCLUSIONS -The addition of the ACE inhibitor quinapril reduces markers of vascular oxidative stress and may attenuate the progression of the pathophysiology seen in the metabolic syndrome. Diabetes Care 27:1712-1715, 2004T he metabolic syndrome is a constellation of abnormal glucose and lipid metabolism that has reached epidemic proportions over the last decade (1). Patients with the metabolic syndrome are at considerable risk for developing atherosclerosis-related diseases, including a two-to fourfold increased risk of stroke and a three-to fourfold increased risk of myocardial infarction when compared with those without metabolic syndrome (2).Recent studies (3,4) suggest that prooxidative and proinflammatory processes play a significant role in the progression of atherosclerosis. In fact, inflammatory markers are predictors of cardiovascular events and progression to type 2 diabetes in healthy individuals as well as those with the metabolic syndrome, underscoring the link between inflammation, metabolic disorders, and cardiovascular disease (5,6). Chronic inflammation and an abnormal pro-oxidant state are both found in the metabolic syndrome and may play a role in its pathogenesis (7,8).The renin-angiotensin system (RAS) plays a central role in the pathogenesis of atherosclerosis-related diseases. Angiotensin II, the central molecule in the RAS, has multiple effects on inflammation, oxidation, atherosclerotic plaque initiation, and progression (9). In the present study, we determine potential mechanisms by which the administration of the ACE inhibitor quinapril regulates mechanisms of oxidative stress in subjects with the metabolic syndrome. RESEARCH DESIGN AND METHODS -Men and women agedՆ18 years and with the metabolic syndrome were enrolled in the study. The metabolic syndrome was defined using the National Cholesterol Education Program Adult Treatment Panel III criteria (Table 1), and elig...

This is the first comprehensive volumetric IVUS analysis of CBL, to our knowledge, demonstrating that KBI restores the MV stent volume, area, and symmetry loss after SB dilation in the bifurcation segment, and induces asymmetric stent expansion in the proximal segment.

Gottliebson WM, Effat MA. Influence of heart rate on fractional flow reserve, pressure drop coefficient, and lesion flow coefficient for epicardial coronary stenosis in a porcine model. Am J Physiol Heart Circ Physiol 300: H382-H387, 2011. First published October 8, 2010 doi:10.1152/ajpheart.00412.2010.-A limitation in the use of invasive coronary diagnostic indexes is that fluctuations in hemodynamic factors such as heart rate (HR), blood pressure, and contractility may alter resting or hyperemic flow measurements and may introduce uncertainties in the interpretation of these indexes. In this study, we focused on the effect of fluctuations in HR and area stenosis (AS) on diagnostic indexes. We hypothesized that the pressure drop coefficient (CDPe, ratio of transstenotic pressure drop and distal dynamic pressure), lesion flow coefficient (LFC, square root of ratio of limiting value CDP and CDP at site of stenosis) derived from fluid dynamics principles, and fractional flow reserve (FFR, ratio of average distal and proximal pressures) are independent of HR and can significantly differentiate between the severity of stenosis. Cardiac catheterization was performed on 11 Yorkshire pigs. Simultaneous measurements of distal coronary arterial pressure and flow were performed using a dual sensor-tipped guidewire for HR Ͻ 120 and HR Ͼ 120 beats/min, in the presence of epicardial coronary lesions of Ͻ50% AS and Ͼ50% AS. The mean values of FFR, CDPe, and LFC were significantly different (P Ͻ 0.05) for lesions of Ͻ50% AS and Ͼ50% AS (0.88 Ϯ 0.04, 0.76 Ϯ 0.04; 62 Ϯ 30, 151 Ϯ 35, and 0.10 Ϯ 0.02 and 0.16 Ϯ 0.01, respectively). The mean values of FFR and CDPe were not significantly different (P Ͼ 0.05) for variable HR conditions of HR Ͻ 120 and HR Ͼ 120 beats/min (FFR, 0.81 Ϯ 0.04 and 0.82 Ϯ 0.04; and CDPe, 95 Ϯ 33 and 118 Ϯ 36). The mean values of LFC do somewhat vary with HR (0.14 Ϯ 0.01 and 0.12 Ϯ 0.02). In conclusion, fluctuations in HR have no significant influence on the measured values of CDP e and FFR but have a marginal influence on the measured values of LFC. However, all three parameters can significantly differentiate between stenosis severities. These results suggest that the diagnostic parameters can be potentially used in a better assessment of coronary stenosis severity under a clinical setting. coronary disease; hemodynamics; catheterization CORONARY ANGIOGRAPHY is the current gold standard for detecting epicardial coronary artery disease. Augmenting this anatomical data with coronary functional parameters (pressure, flow, and/or velocity) provides unique information that facilitates fully informed therapeutic decision making in the catheterization laboratory. Several invasive functional approaches have been used for the past several years within the cardiac catheterization laboratory that allow for a determination of the functional significance of epicardial coronary stenoses. These methods include measurement of coronary flow reserve [CFR, the ratio of hyperemic flow to basal flow (10) (9), an advanced func...