The influence of different concentrations of flavanol chocolate bars under acute supplement conditions on exercise and performance

The purpose of this study was to assess the effects and acute dosage of different flavanol concentrations in a dark chocolate bar on physiological parameters during steady state (SS) and incremental exercise. In a double-blind, randomised, crossover study, 15 healthy participants with a mean ± SD age of 30 ± 7 years; stature 176.8 ± 8.6 cm and body mass 80.3 ± 8.4 kg supplemented with high flavanol (HF) (1060 mg), moderate flavanol (MF) (746 mg), low flavanol (LF) (406 mg), or a control (CON) (88 mg) chocolate bar (~ 34 g), 2 h prior to 40 min of SS cycling (80% gas-exchange threshold) followed by an incremental test to volitional fatigue. During the SS cycle oxygen consumption ([Formula: see text]), respiratory exchange ratio (RER) and heart rate (HR) were continuously monitored. Plasma samples were collected prior to commencing exercise to determine nitrate (NO ) and nitrite (NO ) levels under each condition. There was no observed effect between flavanol concentrations on [Formula: see text], RER, and HR during SS cycling (P > 0.05). [Formula: see text], peak power, HR peak, and RER peak also did not significantly differ between conditions (P > 0.05). There was a small trend for higher plasma NO levels following higher flavanol concentration; however, this did not reach statistical significance (P > 0.05). Acute supplementation with cocoa of differing flavanol concentrations does not appear to have any effect on exercise and performance. It is plausible that longer flavanol supplementation periods might have greater accumulative effects and thus may potentially elicit a larger effect

Regulation of Coronary Blood Flow

The heart is uniquely responsible for providing its own blood supply through the coronary circulation. Regulation of coronary blood flow is quite complex and, after over 100 years of dedicated research, is understood to be dictated through multiple mechanisms that include extravascular compressive forces (tissue pressure), coronary perfusion pressure, myogenic, local metabolic, endothelial as well as neural and hormonal influences. While each of these determinants can have profound influence over myocardial perfusion, largely through effects on end-effector ion channels, these mechanisms collectively modulate coronary vascular resistance and act to ensure that the myocardial requirements for oxygen and substrates are adequately provided by the coronary circulation. The purpose of this series of Comprehensive Physiology is to highlight current knowledge regarding the physiologic regulation of coronary blood flow, with emphasis on functional anatomy and the interplay between the physical and biological determinants of myocardial oxygen delivery. © 2017 American Physiological Society. Compr Physiol 7:321-382, 2017

Effect of ATP-sensitive potassium channel inhibition on coronary metabolic vasodilation in humans

© 2004 American Heart Association. All rights reserved.ObjectiveExperimental evidence indicates that ATP-sensitive potassium (K(ATP)) channels regulate coronary blood flow (CBF). However, their contribution to human coronary metabolic vasodilation is unknown.Methods and resultsSeventeen patients (12 male, age 58+/-10 years) were studied. Coronary hemodynamics were assessed before and after K(ATP) channel inhibition with subselective intracoronary glibenclamide infused at 40 microg/min in an angiographically smooth coronary artery after successful percutaneous coronary intervention to another vessel. Metabolic vasodilation was induced by 2 minutes of rapid right ventricular pacing. Coronary blood velocity was measured with a Doppler guidewire and CBF calculated. The time course of hyperemia was recorded for 2 minutes after pacing, and hyperemic volume was estimated from the area under the flow-versus-time curve (AUC). Compared with vehicle infusion (0.9% saline), glibenclamide reduced resting CBF by 9% (P=0.04) and increased resting coronary vascular resistance (CVR) by 15% (P=0.03). Glibenclamide reduced pacing-induced peak CBF (50.8+/-6.8 versus 42.0+/-5.4 mL/min, P=0.001), peak CBF corrected for baseline flow (25.1+/-4.6 versus 17.6+/-3.1 mL/min, P=0.01), and increased minimum CVR (2.6+/-0.3 versus 3.1+/-0.3 mm Hg/mL per minute, P=0.002). Compared with vehicle, glibenclamide reduced total AUC at 2 minutes (3535+/-397 versus 3027+/-326 mL, P=0.001).ConclusionsVascular K(ATP) channels appear to be involved in functional coronary hyperemia after metabolic stimulation.H. M. Omar Farouque, Stephen G. Worthley and Ian T. Meredit

An unusual cause of arrhythmic syncope: the Brugada syndrome

P. Sanders, O. Farouque, D. A. Cehic, G. D. Youn

Effect of anticoagulation on the occurrence of deep venous thrombosis associated with temporary transvenous femoral pacemakers

© 2001 Excerpta Medica Inc. All rights reserved.Prashanthan Sanders, Omar Farouque, Dale T. Ashby, Leo J. Mahar, and Glenn D. Youn

Elevated plasma angiotensin converting enzyme 2 activity is an independent predictor of major adverse cardiac events in patients with obstructive coronary artery disease

BACKGROUND: Angiotensin converting enzyme 2 (ACE2) is an endogenous regulator of the renin angiotensin system. Increased circulating ACE2 predicts adverse outcomes in patients with heart failure (HF), but it is unknown if elevated plasma ACE2 activity predicts major adverse cardiovascular events (MACE) in patients with obstructive coronary artery disease (CAD). METHODS: We prospectively recruited patients with obstructive CAD (defined as ≥50% stenosis of the left main coronary artery and/or ≥70% stenosis in ≥ 1 other major epicardial vessel on invasive coronary angiography) and measured plasma ACE2 activity. Patients were followed up to determine if circulating ACE2 activity levels predicted the primary endpoint of MACE (cardiovascular mortality, HF or myocardial infarction). RESULTS: We recruited 79 patients with obstructive coronary artery disease. The median (IQR) plasma ACE2 activity was 29.3 pmol/ml/min [21.2-41.2]. Over a median follow up of 10.5 years [9.6-10.8years], MACE occurred in 46% of patients (36 events). On Kaplan-Meier analysis, above-median plasma ACE2 activity was associated with MACE (log-rank test, p = 0.035) and HF hospitalisation (p = 0.01). After Cox multivariable adjustment, log ACE2 activity remained an independent predictor of MACE (hazard ratio (HR) 2.4, 95% confidence interval (CI) 1.24-4.72, p = 0.009) and HF hospitalisation (HR: 4.03, 95% CI: 1.42-11.5, p = 0.009). CONCLUSIONS: Plasma ACE2 activity independently increased the hazard of adverse long-term cardiovascular outcomes in patients with obstructive CAD

Radiation Dose Optimization in Interventional Cardiology: A Teaching Hospital Experience

Radiological interventions play an increasingly relevant role in cardiology. Due to the inherent risks of ionizing radiation, proper care must be taken with monitoring and optimizing the dose delivered in angiograms to pose as low risk as possible to staff and patients. Dose optimization is particularly pertinent in teaching hospitals, where longer procedure times are at times necessary to accommodate the teaching needs of junior staff, and thus impart a more significant radiation dose. This study aims to analyze the effects of different protocol settings in routine coronary angiograms, from the perspective of a large tertiary center implementing a rapid dose reduction program. Routine coronary angiograms were chosen to compare baseline levels of radiation, and the dose imparted before and after dose optimization techniques was measured. Such methods included lowering dose per pulse, fluoroscopic pulse rates, and cine acquisition frame rates. The results showed up to 63% reduction in radiation dose without adverse impact on clinical or teaching outcomes. A 10 fps/low and 5 pps/low setting was found to achieve maximum dose optimization, with the caveat that settings require incremental changes to accommodate for patient complexities

Effect of ATP-sensitive potassium channel inhibition on resting coronary vascular responses in humans

© 2002 American Heart Association, Inc.Experimental data suggest that vascular ATP-sensitive potassium (K(ATP)) channels regulate coronary blood flow (CBF), but their role in regulating human CBF is unclear. We sought to determine the contribution of K(ATP) channels to resting conduit vessel and microvascular function in the human coronary circulation. Twenty-five patients (19 male/6 female, aged 56 +/- 12 years) were recruited. Systemic and coronary hemodynamics were assessed in 20 patients before and after K(ATP) channel inhibition with graded intracoronary glibenclamide infusions (4, 16, and 40 microg/min), in an angiographically smooth or mildly stenosed coronary artery following successful elective percutaneous coronary intervention to another vessel. Coronary blood velocity was measured with a Doppler guidewire and CBF calculated. Adenosine-induced hyperemia was determined following bolus intracoronary adenosine injection (24 microg). Time control studies were undertaken in 5 patients. Compared with vehicle infusion (0.9% saline), glibenclamide reduced resting conduit vessel diameter from 2.5 +/- 0.1 to 2.3 +/- 0.1 mm (P<0.01), resting CBF by 17% (P=0.05), and resting CBF corrected for rate pressure-product by 18% (P=0.01) in a dose-dependent manner. A corresponding 24% increase in coronary vascular resistance was noted at the highest dose (P<0.01). No alteration to resting CBF was noted in the time control studies. Glibenclamide reduced peak adenosine-induced hyperemia (P=0.01) but did not alter coronary flow reserve. Plasma insulin increased from 5.6 +/- 1.2 to 7.6 +/- 1.3 mU/L (P=0.02); however, plasma glucose was unchanged. Vascular K(ATP) channels are involved in the maintenance of basal coronary tone but may not be essential to adenosine-induced coronary hyperemia in humans.H.M. Omar Farouque, Stephen G. Worthley, Ian T. Meredith, R. Andrew P. Skyrme-Jones, Michael J. Zhan

Cardiorespiratory fitness and physical activityafter stroke: A longitudinal study

Current understanding of cardiorespiratory fitness (CRF)and physical activity (PA) change over time post-stroke is limited.Establishing this time course may help identify a target window forintervention