Kára, Tomáš

Introduction: The popularity of energy drinks among young adults is rising. Warnings have been issued regarding potential health risks including adverse cardiovascular complications. We and others have previously shown that energy drink consumption increases blood pressure. The mechanisms are not fully understood. Hypothesis: We hypothesized that increase in blood pressure after drinking a commercially available energy drink, compared to a placebo, is secondary to increased sympathetic activation. Methods: In a randomized, double-blind, placebo-controlled, cross-over study, we studied 25 healthy subjects, age 29±1 years, who were free of known disease, had no known cardiovascular risk factors, and were not on any medications. Each subject consumed a can, 16-fluid ounces, of Rockstar energy drink or a placebo drink in random order on two separate days. Blood pressure (n=25) and plasma norepinephrine levels (n=23) were measured before and 30-minutes after drink consumption. Results: Despite the increase in blood pressure after drinking Rockstar energy drink, which would be expected to elicit reflex reductions in central sympathetic outflow, plasma norepinephrine levels increased markedly after energy drink consumption vs placebo (73.6±9.7% vs 30.9±9.7%, respectively, P=0.003; Figure). Specifically, plasma norepinephrine levels increased from 149.8±11.7pg/ml to 249.8±17.3pg/ml after the energy drink consumption and from 139.9±11.7pg/ml to 178.6±17.3pg/ml after placebo (P=0.0007 for timeхtreatment comparison). Conclusions: Increased blood pressure after consumption of commercially available energy drink is associated with significantly increased catecholamine levels in young healthy adults. These acute hemodynamic and adrenergic changes may predispose to increased cardiovascular risk by triggering arrhythmias or ischemia, particularly in individuals with a vulnerable cardiovascular substrate.

Tomas Konecny, 2012 Finalist and Presenting Author

Background: Left ventricle assist device (LVAD) support, a well established therapy in advanced CHF, improves renal function assessed by creatinine. While renal function in large numbers of continuous flow (CF) LVADs vs pulsatile flow (PF) LVADs has been evaluated at 3 mo., long term studies are needed with large numbers of CF vs PF devices. To date longer term analysis comparing renal function in CF vs PF devices have relied on a small number of CF devices. We evaluated renal function assessed by creatinine in a large number of CF (HM II) (n=119) devices and compared this to renal function in a group of subjects treated with PF devices (HM XVE) (n=8) at 6 mo. post implant. Our aim was to evaluate change in creatinine between 3 and 6 months in these groups. Methods and Results: Plasma creatinine was evaluated at 3 and 6 months in two groups: subjects with CF HM II (n=119) and PF LVAD (HM XVE, n=8). The data were collected from two centers in patients undergoing implant for destination or bridge to transplant therapy. Baseline creatinine was higher in the HM XVE group at baseline (BL), and decreased at 3 mo. (1.7 [1.1-2.1] vs 1.1 [0.8-1.5] mg/dL, p<0.05). BL creatine in the HM II group decreased at 3 mo as well (1.2 [1-1.5] vs 1.1 [0.9-1.3] mg/dL, p,0.05). Between 3 and 6 months there was no difference in degree of creatinine change in CF vs PF, however both groups had an increase in Creatinine in this time frame: PF (1.1 [0.8-1.5] vs 1.35 [1.05-1.9] mg/dL, p<0.05); CF (1.1 [0.9-1.3] vs 1.2 [0.92-1.4] mg/dL, p<0.05). Conclusion: This is the first study to demonstrate with large numbers of CF LVAD that creatinine does not incrementally increase between 3 and 6 mo. in comparison to PF LVAD. Further studies are required with large numbers of continuos flow LVADs evaluating the comparative effect of long term continuous flow vs pulsatile flow. Additionally, it remains important to identify surrogates of pulsatility in subjects with continuous flow devices and evaluate prognostic impact on renal function long term.

Background: The epicardial adipose tissue (EAT) has been identified as a sensitive marker of cardiometabolic risk. Recent evidence suggests efficacy of long-term statin therapy in reducing the EAT in patients with coronary artery disease. Whether the volume of EAT changes in patients with atrial fibrillation (AF) treated with a statin for a short time period is currently unknown. Methods: A population of AF patients undergoing pulmonary vein isolation was randomized to receive either 80 mg/day of atorvastatin (n=51, 44 males, age 55±10 years) or placebo (n=51, 41 males, age 56±10) for a 3 month period. EAT volume was assessed by cardiac computed tomography at baseline and after 3-month follow-up. Results: Patients randomized to statin treatment exhibited significant decreases in EAT volume (baseline vs follow-up: 105.8 ± 52.95 vs 103.05 ± 52.55 cm3, p = 0.05), C-reactive protein (2.97 ± 4.3 mg/L vs 2.03 ± 2.2 mg/L, p < 0.05), total cholesterol (182.5 ± 36.9 vs 129.3 ± 40.6 mg/dL, p < 0.001), and low density lipoprotein-cholesterol (111.88 ± 28 vs 61 ± 32.6 mg/dL, p < 0.001) at follow-up, while the body mass index did not vary (29.42 ± 5.2 vs 29.11 ± 4.8 kg/m2, p = 0.28). No changes were seen in the placebo group. Conclusions: Short-term high-dose statin therapy significantly reduced the volume of EAT in AF patients. EAT volume modulation might be an important mechanism by which statins may influence cardiovascular risk.

Introduction: An increasing number of healthy adults consume energy drinks to enhance their physical and mental performance. Energy drinks contain caffeine and multiple other “natural” stimulants and their combined effects on cardiac hemodynamics in healthy individuals are unclear. Hypothesis: We hypothesized that drinking a commercially available energy drink, Rockstar , compared to a placebo drink, increases resting blood pressure and heart rate in healthy adults, and these increases would be further accentuated by stress conditions. Methods: We enrolled 25 healthy, normotensive subjects (14 males), aged 29±1 years, with body mass index 24.5±1 kg/m 2 , in a randomized, double-blind, placebo-controlled, crossover study. Each subject consumed a placebo drink and a commercially available Rockstar energy drink (473 ml), in random order on two separate study days. Blood pressure and heart rate responses were recorded and compared before and 30 minutes after drink consumption, both at rest and then in response to physical, mental and cold stressors. Results: The Rockstar energy drink induced a 6±1% increase in resting systolic blood pressure, compared to 3±1% with the placebo drink (P=0.0078). Diastolic blood pressure increased by 7±1% vs 0±1% with the placebo drink (P=0.0007; Figure 1). Heart rate increased similarly in both groups, by 5±2% in the energy drink group vs. 7±2% in the placebo group. Blood pressure and heart rate increases during the stress stimuli (sustained handgrip, mental stress and cold stress) did not differ between energy drink and placebo. Conclusions: Drinking a commercially available Rockstar energy drink significantly increases resting blood pressure in young healthy adults. Blood pressure increases are not further accentuated by exercise, mental or cold pressor stress stimuli. These hemodynamic changes induced by energy drink consumption could predispose to cardiovascular events.

ObjectivesWe set to measure the interatrial pressure gradient during simulated obstructive sleep apnea (OSA).BackgroundOSA occurs when a sleeping patient attempts to inhale against an obstructed airway. How this event affects the interatrial pressure gradient has not been defined. We hypothesized that simulated OSA in a conscious subject (Mueller maneuver [MM], inspiration against obstruction) would promote increased right‐to‐left pressure gradient, and then the substrate for right‐to‐left atrial shunting.MethodsSelected patients underwent simultaneous measurement of airway and atrial pressures (both left and right atrium [LA, RA]) using high‐fidelity micromanometry at rest, during MM, and during VM, during right heart catheterization.ResultsTen patients (age 55 ± 11 years, two women) were successfully studied. During the onset of MM, RA pressure transiently but consistently exceeded LA pressure in response to the steep decline in intrathoracic pressure (maximum RA‐LA pressure gradient increased from 0.1 ± 1.4 mm Hg at baseline to 7.0 ± 4.3 mm Hg during MM, P < 0.001). The maximum right‐to‐left atrial pressure gradient during Mueller maneuver was higher than that achieved during the Valsalva maneuver release (P < 0.007).ConclusionsThe onset of MM increased right‐to‐left pressure gradient across the atrial septum, likely as a result of greater blood return to the RA from extrathoracic veins. The RA‐LA pressure gradient achieved during MM was greater than that observed during VM. These findings delineate the hemodynamic substrate for right to left shunting during OSA. © 2014 Wiley Periodicals, Inc.

Background— Obstructive sleep apnea is highly prevalent in patients with cardiovascular disease and has detrimental effects on systolic and diastolic function of the ventricles. In this research, the changes in strain (S) and strain rate (SR) during the performance of the Mueller maneuver (MM) in an effort to better understand how negative intrathoracic pressures affect ventricular mechanics. Methods and Results— The MM was performed to maintain a target intrathoracic pressure of −40 mm Hg. Echocardiography was used to measure various parameters of cardiac structure and function. Myocardial deformation measurements were performed using tissue speckle tracking. Twenty-four healthy subjects (9 women; mean age, 30�6 years) were studied. Global left ventricular longitudinal S in systole and SR in early filling were significantly decreased during the MM (S: baseline, −17.0�1.6%; MM, −14.5�2.2%; P <0.0001, SR: baseline, 1.09�0.20 s −1 ; MM, 0.92�0.21 s −1 ; P =0.01). Global right ventricular longitudinal S was also significantly decreased during the MM (baseline, −22.0�3.1%; MM, −17.2�2.5%; P <0.0001), as was global right ventricular longitudinal systolic SR (baseline, −1.34�0.35 s −1 ; MM, −1.02�0.21 s −1 ; P =0.0006). Conclusions— Left ventricular and right ventricular longitudinal deformation are significantly reduced during the MM. These results suggest that negative intrathoracic pressure during apnea may contribute to changes in myocardial mechanics. These results could help explain the observed changes in left ventricular and right ventricular mechanics in patients with obstructive sleep apnea.