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Background: The cardioprotective effects of certain alcoholic beverages are partly related to their polyphenol content, which may improve the vasodilatory reactivity of arteries. Effect of cognac on coronary circulation, however, remains unknown. The purpose of this randomized controlled cross-over study was to determine whether moderate doses of cognac improve coronary reactivity as assessed with cold pressor testing (CPT) and coronary flow reserve (CFR) measurement., Methods: Study group consisted of 23 subjects. Coronary flow velocity and epicardial diameter was assessed using transthoracic echocardiography at rest, during CPT and adenosine infusion-derived CFR measurements before drinking, after a moderate (1.2 +/- 0.1 dl) and an escalating high dose (total amount 2.4 +/- 0.3 dl) of cognac. To explore the bioavailability of antioxidants, the antioxidant contents of cognac was measured and the absorption from the digestive tract was verified by plasma antioxidant capacity determination., Results: Serum alcohol levels increased to 1.2 +/- 0.2 per thousand and plasma antioxidant capacity from 301 +/- 43.9 micromol/l to 320 +/- 25.0 micromol/l by 7.6 +/- 11.8%, (p = 0.01) after high doses of cognac. There was no significant change in flow velocity during CPT after cognac ingestion compared to control day. CFR was 4.4 +/- 0.8, 4.1 +/- 0.9 (p = NS), and 4.5 +/- 1.2 (p = NS) before drinking and after moderate and high doses on cognac day, and 4.5 +/- 1.4, and 4.0 +/- 1.2 (p = NS) on control day., Conclusion: Cognac increased plasma antioxidant capacity, but it had no effect on coronary circulation in healthy young men., Trial Registration: NCT00330213.

Background: Red wine consumption is associated with reduced cardiovascular disease mortality. Its cardioprotective properties may be partly related to its ability to improve endothelial function. The purpose of this randomized controlled cross-over study was to determine whether moderate doses of red wine and de-alcoholized red wine improve coronary flow velocity reserve (CFR)., Methods: Using transthoracic Doppler echocardiography, 176 CFR measurements were made in 22 healthy men before and after ingestion of a moderate (4.0+/-0.4 dl) and an escalating high dose (total amount 8.1+/-0.9 dl) of alcohol-containing red wine and de-alcoholized red wine, which contained similar amounts of phenolic substances. The difference in plasma antioxidant capacity was determined by colorimetric assay kit., Results: Red wine increased CFR from 3.8+/-1.4 to 4.5+/-1.4 (p<0.01) and 4.0+/-1.2 (p=NS) after moderate and high doses, respectively; whereas de-alcoholized red wine had no significant effects on CFR (4.0+/-0.7, 4.3+/-1.3 and 4.5+/-1.4, respectively). Plasma antioxidant capacity increased significantly after high dose of red wine (27.5+/-14.7%, p<0.001), but not after de-alcoholized red wine (0.5+/-10.5%, p=NS) despite similar amounts of phenolic substances. Differences between CFR and plasma antioxidant capacities before and after drinking had no significant association., Conclusions: A moderate dose of red wine, but not de-alcoholized red wine increases CFR. The increase of CFR is probably mediated by other than direct antioxidant properties of polyphenols, because the simultaneous increase of CFR and plasma antioxidant capacity were not associated.

The objective of this study was to identify risk markers for attenuated coronary flow velocity reserve (CFVR) that exist in healthy young men without evident atherosclerotic risk factors. Coronary blood flow velocity was measured with transthoracic Doppler echocardiography at baseline and during adenosine infusion in 37 healthy nonsmoking men [mean age, 27 yr (SD 4.0)]. Body composition and distribution of fat tissue were assessed with anthropometric measures and regulation of fat metabolism by determination of adiponectin and leptin levels. Physical performance capacity was tested with ergospirometry. The mean body mass index was 23 kg/m2 (SD 1.9), waist-to-hip ratio was 0.84 (SD 0.04), and CFVR was 3.5 (SD 0.61). Obesity indexes at study outset, leptin, adiponectin, maximal load (Max load in W/kg) and maximal oxygen consumption (Vo2 peak in ml x kg(-1) x min(-1)) in ergospirometry, rate-pressure product, and heart rate at rest were significantly associated with CFVR. In multivariate analysis, Max load (in W/kg) and waist-to-hip ratio were the only independent predictors of CFVR. We found no relationship between CFVR and serum lipids or body mass index. We conclude that abdominal fat accumulation and low aerobic fitness are independently associated with CFVR in men.

Myocardial perfusion reserve (MPR, defined as the ratio of the maximum myocardial blood flow (MBF) to the baseline) is an indicator of coronary artery disease and myocardial microvascular abnormalities. First-pass contrast-enhanced magnetic resonance imaging (CE-MRI) using gadolinium (Gd)-DTPA as a contrast agent (CA) has been used to assess MPR. Tracer kinetic models based on compartmental analysis of the CA uptake have been developed to provide quantitative measures of MBF by MRI. To study the accuracy of Gd-DTPA first-pass MRI and kinetic modeling for quantitative analysis of myocardial perfusion and MPR during dipyridamole infusion, we conducted a comparison with positron emission tomography (PET) in 18 healthy males (age = 40 +/- 14 years). Five planes were acquired at every second heartbeat with a 1.5T scanner using a saturation recovery turboFLASH sequence. A perfusion-related parameter, the unidirectional influx constant (Ki), was computed in three coronary artery territories. There was a significant correlation for both dipyridamole-induced flow (0.70, P = 0.001) and MPR (0.48, P = 0.04) between MRI and PET. However, we noticed that MRI provided lower MPR values compared to PET (2.5 +/- 1.0 vs. 4.3 +/- 1.8). We conclude that MRI supplemented with tracer kinetic modeling can be used to quantify myocardial perfusion., ((c) 2006 Wiley-Liss, Inc.)

Objective: Diabetes has been associated with increased oxidative stress and impaired vascular function. Statins have been shown to reduce low-density lipoprotein (LDL) oxidizability and improve myocardial perfusion in hypercholesterolemic nondiabetic subjects. We studied whether pravastatin decreases LDL oxidation and improves myocardial perfusion in normocholesterolemic subjects with type 1 diabetes., Methods and Results: In this randomized, double-blind study, myocardial perfusion was measured at rest and during dipyridamole stimulation with positron emission tomography and [15O]H2O during hyperinsulinemic euglycemia in 42 patients (age 30+/-6 years; LDL cholesterol 2.48+/-0.57 mmol/L) before and after 4-month treatment with pravastatin 40 mg/d or placebo. In addition, 12 healthy nondiabetic subjects were studied. LDL oxidation was measured by determining the level of baseline diene conjugation in lipids extracted from LDL. The level of LDL oxidation was similar in the pravastatin and placebo groups before treatment (23.9+/-4.6 versus 25.6+/-9.5 micromol/L, respectively) and decreased significantly during pravastatin treatment to 19.5+/-5.0 micromol/L (P<0.005). Myocardial perfusion reserve was significantly lower in diabetic patients compared with controls (4.15+/-1.29 versus 5.31+/-1.86, P<0.05) and did not change after treatment. Glycemic control and insulin sensitivity remained unchanged during treatment., Conclusions: Pravastatin treatment, resulting in decreased LDL oxidation, did not improve myocardial perfusion reserve in subjects with type 1 diabetes.

Abstract: Transthoracic Doppler echocardiography (TTE) has been introduced as a noninvasive tool to measure coronary flow velocity reserve (CFVR). Velocity measurement, however, fails to take into account epicardial coronary artery vasodilation during hyperemia and this may cause underestimation of CFVR measurements. Therefore, we sought to determine whether the vasodilation of epicardial coronary artery can be measured during cold pressor test (CPT) and adenosine infusion simultaneously with the flow velocity measurement using TTE. We studied 41 healthy nonsmoking men with a linear high-frequency 8.0-MHz transducer. The CPT and adenosine infusion dilated the diameter of the distal left anterior descending coronary artery (LAD) from 1.4 ± 0.4 mm to 1.5 ± 0.4 mm (14 ± 13%, p < 0.01) and from 1.4 ± 0.4 mm to 1.8 ± 0.5 mm (31 ± 19%, p < 0.01), respectively. The CPT increased flow velocity and calculated coronary blood flow rate (velocity time integral × cross-sectional area) from 0.23 ± 0.05 m/s to 0.36 ± 0.13 m/s (31 ± 34%, p < 0.01) and from 8.1 ± 4.2 mL/min to 11.4 ± 6.0 mL/min (47 ± 51%, p < 0.01). CFVR and calculated coronary blood flow rate reserve were 3.9 ± 1.0 and 6.0 ± 1.9, respectively. In Bland-Altman analysis, velocity measurements underestimated the vasodilation response of the CPT and adenosine compared with the measurements where epicardial diameter dilation was taken into account. Intra- and interobserver variability of diameter measurements was low (coefficient of variation [CV] 2.6 to 6.5%). Day-to-day, within-day and intersonographer variabilities were of similar magnitude (CV 4.6 to 8.2%), suggesting good reproducibility. This study demonstrates that TTE can be used to assess changes in both epicardial coronary artery diameter and flow velocity simultaneously in the distal LAD artery. (E-mail: tuoski@utu.fi) [Copyright &y& Elsevier]

We studied whether diameters of coronary arteries can be measured accurately with the use of transthoracic echocardiography (TTE). By knowing the anatomic diameter of the coronary artery together with coronary flow velocity it is possible to measure coronary flow volume more precisely by TTE. However, the suitability of TTE for measurement of diameters of all main epicardial coronary arteries has not been systematically validated. We measured the diameters of the left main (LM), left anterior descending (LAD), left circumflex (LCX), and right coronary arteries (RCA) with the use of TTE [manual twodimensional (2D), color-Doppler, and automated 2D analysis] in 30 patients who had normal coronary anatomy. We compared these diameters to those measured with quantitative coronary angiography (QCA). We could measure diameters of LM, LAD, LCX, and RCA by TTE in up to 37%, 63%, 7%, and 60% of patients, respectively. The overall correlation coefficients between TTE and QCA measurements were 0.83 (P < 0.01) with manual 2D analysis, 0.82 (P < 0.01) with automated 2D analysis, and 0.94 (P < 0.01) with a color-Dopplerbased analysis. Interobserver variability of TTE measurements was low (coefficient of variation 5.4 ± 4.6–7.5 ± 8.8%). TTE is an accurate method to evaluate coronary artery diameter in patients with healthy coronary arteries. [ABSTRACT FROM AUTHOR]