Benjamin D Levine

University of Texas Southwestern Medical Center, Dallas, Texas, United States

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Publications (363)1414.18 Total impact

  • Benjamin D Levine, William K Cornwell, Mark H Drazner
    JACC. Heart failure. 07/2014;
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    ABSTRACT: Background: Exposure to microgravity causes functional and structural impairment of skeletal muscle. Current exercise regimens are time-consuming and insufficiently effective; an integrated countermeasure is needed that addresses musculoskeletal along with cardiovascular health. High-intensity, short-duration rowing ergometry and supplemental resistive strength exercise may achieve these goals. Methods: 27 healthy volunteers completed 5 weeks of head down tilt bed rest; 18 were randomized to exercise, 9 remained sedentary. Exercise consisted of rowing ergometry 6d/week including interval training, and supplemental strength training 2d/week. Measurements before and after bed rest, and following reambulation included assessment of strength, skeletal muscle volume (MRI), and muscle metabolism (MRS); quadriceps muscle biopsies were obtained to assess muscle fiber types, capillarization and oxidative capacity. Results: Sedentary bed rest (BR) led to decreased muscle volume (quadriceps: -9±4%, p<0.001; plantarflexors: -19±6%, p<0.001). Exercise (ExBR) reduced atrophy in the quadriceps (-5±4%, interaction p=0.018) and calf muscle, though to a lesser degree (-14±6%, interaction p=0.076). Knee extensor and plantarflexor strength was impaired by BR (-14±15%, p=0.014 and -22±7%, p=0.001) but preserved by ExBR (-4±13%, p=0.238 and +13±28%, p=0.011). Metabolic capacity as assessed by VO2max, (31)P-MRS and oxidative chain enzyme activity was impaired in BR but stable or improved in ExBR. Reambulation reversed the negative impact of bed rest. Conclusions: High-intensity, short-duration rowing and supplemental strength training effectively preserved skeletal muscle function and structure while partially preventing atrophy in key antigravity muscles. Due to its integrated cardiovascular benefits, rowing ergometry could be a primary component of exercise prescriptions for astronauts or patients suffering from severe deconditioning.
    Journal of Applied Physiology 05/2014; · 3.48 Impact Factor
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    ABSTRACT: This study sought to examine the frequency and hemodynamic correlates of shortness of breath when bending forward, a symptom we have termed "bendopnea." Many heart failure patients describe bendopnea such as when putting on their shoes. This symptom has not previously been characterized. We conducted a prospective study of 102 subjects with systolic heart failure referred for right-heart catheterization. Time to onset of bendopnea was measured prior to catheterization. Forty-six subjects also underwent hemodynamic assessment when sitting and bending. Hemodynamic profiles were assigned on the basis of whether pulmonary capillary wedge pressure (PCWP) was ≥22 mm Hg and cardiac index (CI) was ≤2.2 l/min/m(2). Bendopnea was present in 29 of 102 (28%) subjects with median (25th, 75th percentiles) time to onset of 8 (7, 11) seconds. Subjects with bendopnea had higher supine right atrial pressure (RAP) (p = 0.001) and PCWP (p = 0.0004) than those without bendopnea but similar CI (p = 0.2). RAP and PCWP increased comparably in subjects with and without bendopnea when bending, but CI did not change. In those with, versus without, bendopnea, there was more than a 3-fold higher frequency of a supine hemodynamic profile consisting of elevated PCWP with low CI (55% vs. 16%, respectively, p < 0.001) but no association with a profile of elevated PCWP with normal CI (p = 0.95). Bendopnea is mediated via a further increase in filling pressures during bending when filling pressures are already high, particularly if CI is reduced. Awareness of bendopnea should improve noninvasive assessment of hemodynamics in subjects with heart failure.
    JACC. Heart failure. 02/2014; 2(1):24-31.
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    ABSTRACT: An increased "dose" of endurance exercise training is associated with a greater maximal oxygen uptake (VO2max), a larger left ventricular (LV) mass, and improved heart rate and blood pressure control. However, the effect of lifelong exercise dose on metabolic and hemodynamic response during exercise has not been previously examined. Methods and Results: We performed a cross-sectional study on 101 (69 men) seniors (60 yr and older) focusing on lifelong exercise frequency as an index of exercise dose. These included 27 who had performed ≤2 exercise sessions/wk (sedentary), 25 who performed 2-3 sessions/wk (casual), 24 who performed 4-5 sessions/wk (committed) and 25 who performed ≥6 sessions/wk plus regular competitions (Masters athletes) over at least the last 25 yr. Oxygen uptake and hemodynamics (cardiac output [Qc], stroke volume [SV]) were collected at rest, two levels of steady-state submaximal exercise and maximal exercise. Doppler ultrasound measures of LV diastolic filling were assessed at rest and during LV loading (saline infusion) to simulate increased LV filling. Body composition, total blood volume, and heart-rate recovery after maximal exercise were also examined. VO2max increased in a dose-dependent manner (P<0.05). At maximal exercise, Qc and SV were largest in committed exercisers and Masters athletes (P<0.05), while arteriovenous oxygen difference was greater in all trained groups (P<0.05). At maximal exercise, effective arterial elastance, an index of ventricular-arterial coupling, was lower in committed exercisers and Masters athletes (P<0.05). Doppler measures of LV filling were not enhanced at any condition irrespective of lifelong exercise frequency. Conclusion: These data suggest that performing 4 or more weekly endurance exercise sessions over a lifetime results in significant gains in VO2max, SV and heart rate regulation during exercise; however, improved SV regulation during exercise is not coupled with favorable effects on LV filling, even when the heart is fully loaded.
    Journal of Applied Physiology 01/2014; · 3.48 Impact Factor
  • Qi Fu, Benjamin D. Levine
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    ABSTRACT: Syncope is a common clinical condition occurring even in otherwise healthy people without underlying cardiovascular disease. Neurally mediated syncope is by far the the most common cause of syncope in individuals without any structural heart disease. Based on traditional wisdom, loss of sympathetic tone with relaxation of vascular smooth muscle is the key mechanism underlying the pathophysiology of syncope, especially in patients without an acute decrease in heart rate. However, this concept has recently been challenged. Some microneurographic studies indicate that sympathetic withdrawal may not always be a prerequisite even for the development of classic “vasodepressor” forms of syncope. Conversely, a decrease in cardiac output appears to be a determinant factor for syncope in most circumstances. This article reviews the relative contribution of cardiac output versus sympathetic vasoconstriction in neurally mediated syncope in otherwise healthy individuals. It is suggested that a moderate to severe fall in cardiac output with or without vasodilatation may contribute to syncope.
    Autonomic Neuroscience. 01/2014;
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    ABSTRACT: Young black women have higher prevalence of hypertension during pregnancy compared to white women, which may be attributable to differences in blood pressure (BP) regulation. We hypothesized that young normotensive black women would demonstrate augmented muscle sympathetic nerve activity (MSNA) and renal-adrenal responses to orthostasis. Fifteen white and ten black women (30 ± 4 vs. 32 ± 6 years; means ± SD) had haemodynamics and MSNA measured during baseline (BL), 30 and 60° head-up tilt (HUT), and recovery. Blood was drawn for catecholamines, direct renin, vasopressin, and aldosterone. BL brachial systolic BP (SBP: 107 ± 6 vs. 101 ± 9 mmHg) and diastolic BP (DBP: 62 ± 4 vs. 56 ± 7 mmHg) were higher in white women (both p < 0.05). Δ DBP (60° HUT-BL) was greater in black women compared to white (p < 0.05). Cardiac output and total peripheral resistance were similar between groups. MSNA burst frequency was higher in whites (BL: 16 ± 10 vs. 14 ± 9 bursts/min, main effect p < 0.05) and increased in both groups during HUT (60°: 39 ± 8 vs. 34 ± 13 bursts/min, p < 0.05 from BL). Noradrenaline was higher in white women during 60° HUT (60° HUT: 364 ± 102 vs. 267 ± 89 pg/ml, p < 0.05). Direct renin was higher and vasopressin and Δ aldosterone tended to be higher in blacks (BL, direct renin: 12.1 ± 5.0 vs. 14.4 ± 3.7 pg/ml, p < 0.05; BL, vasopressin: 0.4 ± 0.0 vs. 1.6 ± 3.6 pg/ml, p = 0.065; Δ aldosterone: -0.9 ± 5.1 vs. 3.8 ± 7.5 ng/ml; p = 0.069). These results suggest that young normotensive white women may rely on sympathetic neural activity more so than black women who have a tendency to rely on the renal-adrenal system to regulate BP during an orthostatic stress.
    Frontiers in Physiology 01/2014; 5:86.
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    ABSTRACT: While a number of published studies exist to guide endurance athletes with the best practices regarding implementation of altitude training, a key unanswered question concerns the proper timing of return to sea level prior to major competitions. Evidence reviewed herein suggests that the combination of the de-acclimatization response of hematological, ventilatory, and biomechanical factors with return to sea level likely interact to determine the best timing for competitive performance.
    Journal of Applied Physiology 12/2013; · 3.48 Impact Factor
  • Robert F Chapman, Abigail S Laymon, Benjamin D Levine
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    ABSTRACT: Abstract Chapman, Robert F., Abigail S. Laymon, and Benjamin D. Levine. Timing of arrival and pre-acclimatization strategies for the endurance athlete competing at moderate to high altitudes. High Alt Med Biol 14:319-324, 2013.-With the wide array of endurance sport competition offerings at moderate and high altitudes, clinicians are frequently asked about best practice recommendations regarding arrival times prior to the event and acclimatization guidelines. This brief review will offer data and current advice on when to arrive at altitude and various potential sea level-based pre-acclimatization strategies in an effort to maximize performance and minimize the risk of altitude sickness.
    High altitude medicine & biology 12/2013; 14(4):319-24. · 1.58 Impact Factor
  • Clinical Autonomic Research 11/2013; · 1.48 Impact Factor
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    ABSTRACT: This study assessed effects of head-down-tilt (HDT) bed rest on dynamic cerebral autoregulation (CA) in 21 healthy young adults with volume loading and exercise countermeasures. Of them, 7 underwent an 18 day bed rest without exercise countermeasures (sedentary group). Volume loading with Dextran infusion was performed after bed rest to restore the reduced plasma volume to pre-bed rest level. In the other 14 subjects, supine cycling during bed rest was performed to preserve pre-bed rest cardiac work (exercise group). Volume loading was also performed in a subgroup of these subjects (Ex+Dex, n=7). Dynamic CA was estimated by transfer function analysis of changes in arterial pressure and cerebral blood flow (CBF) velocity in the very low (VLF, 0.02 - 0.07 Hz), low (LF, 0.07 - 0.20 Hz) and high frequency ranges (HF, 0.20 - 0.35 Hz). After bed rest, transfer function gain was reduced in the sedentary group (VLF, 0.93 ± 0.23 to 0.61 ± 0.23 cm/s/mmHg, p=0.007) and in the exercise group (LF, 1.22 ± 0.43 to 0.94 ± 0.26 cm/s/mmHg, p=0.005, HF, 1.32 ± 0.55 to 1.00 ± 0.32 cm/s/mmHg, p = 0.010). After volume loading, transfer function gain increased in the sedentary group, but not in the Ex+Dex group. Taken together, these findings suggest that dynamic CA was preserved or improved after HDT bed rest in both the sedentary and exercise subjects. Furthermore, increases of transfer function gain with volume loading suggest that changes in plasma volume may play an important role in CBF regulation.
    Journal of Applied Physiology 10/2013; · 3.48 Impact Factor
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    ABSTRACT: Chronic living at altitudes ~2500m causes consistent hematological acclimatization in most, but not all, groups of athletes; however, responses of erythropoietin (EPO) and red cell mass to a given altitude show substantial individual variability. We hypothesized that athletes living at higher altitudes would experience greater improvements in sea level performance, secondary to greater hematological acclimatization, compared to athletes living at lower altitudes. After 4 weeks of group sea level training and testing, 48 collegiate distance runners (32M, 16W) were randomly assigned to one of four living altitudes (1780m, 2085m, 2454m, or 2800m). All athletes trained together daily at a common altitude from 1250m - 3000m following a modified Live High - Train Low model. Subjects completed hematological, metabolic, and performance measures at sea level, before and after altitude training; EPO was assessed at various time points while at altitude. Upon return from altitude, 3000m time trial performance was significantly improved in groups living at the middle two altitudes (2085m and 2454m) but not in groups living at 1780m and 2800m. EPO was significantly higher in all groups at 24h and 48h, but returned to sea level baseline after 72h in the 1780m group. Erythrocyte volume was significantly higher within all groups after return from altitude, and was not different between groups. These data suggest that when completing a 4 week altitude camp following the Live High - Train Low model, there is a target altitude between 2000m and 2500m that produces an optimal acclimatization response for sea level performance.
    Journal of Applied Physiology 10/2013; · 3.48 Impact Factor
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    ABSTRACT: -Lifelong exercise training maintains a youthful compliance of the left ventricle (LV), while a year of exercise training started later in life fails to reverse LV stiffening, possibly because of accumulation of irreversible advanced glycation end-products (AGE). Alagebrium breaks AGE crosslinks and improves LV stiffness in aged animals. However, it is unclear whether a strategy of exercise combined with alagebrium would improve LV stiffness in sedentary older humans. -62 healthy subjects were randomized into 4 groups: Sedentary+placebo; Sedentary+Alagebrium (200mg/day); Exercise+placebo; and Exercise+Alagebrium. Subjects underwent right heart catheterization to define LV pressure-volume curves; secondary functional outcomes included cardiopulmonary exercise testing and arterial compliance. Fifty seven/62 subjects (67±6 yrs; 37f/20m) completed one year of intervention followed by repeat measurements. Pulmonary capillary wedge pressure and LV end-diastolic volume were measured at baseline, during decreased and increased cardiac filling. LV stiffness was assessed by the slope of LV pressure-volume curve. After intervention, LV mass and end-diastolic volume increased and exercise capacity improved (by ~8 %) only in the exercise groups. Neither LV mass nor exercise capacity was affected by Alagebrium. Exercise training had little impact on LV stiffness (Training×Time effect p=0.46), while Alagebrium showed a modest improvement in LV stiffness compared to placebo (Medication×Time effect p=0.04). -Alagebrium had no effect on hemodynamics, LV geometry, or exercise capacity in healthy, previously sedentary seniors. However it did show a modestly favorable effect on age-associated LV stiffening. Clinical Trial Registration-URL: Unique identifier: NCT01014572.
    Circulation Heart Failure 10/2013; · 6.68 Impact Factor
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    ABSTRACT: The Fick principle (cardiac output (Qc) = oxygen uptake (VO2) / systemic arterio-venous oxygen difference) is used to determine Qc in numerous clinical situations. However, estimated rather than measured V•O2 is commonly used due to complexities of the measurement, though the accuracy of estimation remains uncertain in contemporary clinical practice. From 1996 to 2005, resting VO2 was measured via the Douglas bag technique in adult patients undergoing right heart catheterization. Resting VO2 was estimated by each of 3 published formulae. Agreement between measured and estimated VO2 was assessed overall, and across strata of body mass index, sex, and age. The study included 535 patients, with mean age 55 yrs, mean BMI 28.4 kg/m(2); 53% women; 64% non-white. Mean (+ standard deviation) measured VO2 was 241 ± 57 ml/min. Measured VO2 differed significantly from values derived from all 3 formulae, with median (interquartile range) absolute differences of 28.4 (13.1, 50.2) ml/min, 37.7 (19.4, 63.3) ml/min, and 31.7 (14.4, 54.5) ml/min, for the formulae of Dehmer, LaFarge and Bergstra, respectively; (p<0.0001 for each). The measured and estimated values differed by >25% in 17% to 25% of patients depending on the formula used. Median absolute differences were greater in severely obese patients (BMI > 40 kg/m(2)), but were not affected by sex or age. Estimates of resting VO2 derived from conventional formulae are inaccurate, especially in severely obese individuals. When accurate hemodynamic assessment is important for clinical decision-making, VO2 should be directly measured.
    Circulation 09/2013; · 15.20 Impact Factor
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    ABSTRACT: Hypertension is associated with cardiovascular stiffening and left ventricular diastolic dysfunction, leading to comorbidities such as heart failure with preserved ejection fraction (HFpEF). It is unknown whether sex and hypertension subtype affect haemodynamics and left ventricular function in older individuals. Ninety-five older patients with Stage 1 hypertension (ambulatory awake SBP135-159 mmHg) and 56 normotensive controls were enrolled. Patients were stratified prospectively into isolated systolic hypertension (ISH, DBP <85 mmHg) or systolic-diastolic hypertension (SDH, DBP ≥85 mmHg). Haemodynamics and Doppler variables including early filling (E) and averaged mitral annular (E'mean) velocities were measured during supine rest. Ambulatory awake blood pressures (BPs) were the highest in SDH, whereas supine SBP was similar in both hypertensive groups. No sex difference was observed in supine or ambulatory awake BPs in all groups. Stroke volume was similar among groups within the same sex, but smaller in women. Women exhibited faster E, slower E'mean and greater E/E'mean, whereas no group difference was observed in E within the same sex. In women, E'mean was significantly slower in SDH (5.9 ± 1.6 vs. 7.4 ± 1.1 cm/s, P < 0.01) and ISH (6.6 ± 1.6 cm/s, P = 0.07) than controls, resulting in the highest E/E'mean in SDH. In men, E'mean and E/E'mean were similar among the three groups. These results suggest that elderly hypertensive women may have left ventricular early diastolic dysfunction and higher estimated filling pressure, consistent with their susceptibility to HFpEF. Women with SDH seemed to have more left ventricular diastolic dysfunction, which might be explained by the greater cumulative afterload when ambulatory.
    Journal of hypertension 09/2013; · 4.02 Impact Factor
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    ABSTRACT: Cardiovascular risk remains high in patients with hypertension even with adequate blood pressure (BP) control. One possible mechanism may be sympathetic activation via the baroreflex. We tested the hypothesis that chronic inhibition of renin reduces BP without sympathetic activation, but diuresis augments sympathetic activity in elderly hypertensives. Fourteen patients with stage-I hypertension [66±5 (SD) years] were treated with a direct renin inhibitor, aliskiren, (n=7) or a diuretic, hydrochlorothiazide, (n=7) for 6 months. Muscle sympathetic nerve activity (MSNA), BP, direct renin and aldosterone were measured during supine and a graded head-up tilt (HUT; 5-min 30° and 20-min 60°), before and after treatment. Sympathetic baroreflex sensitivity (BRS) was assessed. Both groups had similar BP reductions after treatment (all P<0.01), while MSNA responses were different between hydrochlorothiazide and aliskiren (P=0.006 pre/post x drug). Both supine and upright MSNA became greater after hydrochlorothiazide treatment (supine, 72±18 post vs. 64±15 pre; 60° HUT, 83±10 vs. 78±13 bursts 100beats-1; P=0.002). After aliskiren treatment, supine MSNA remained unchanged (69±13 vs. 64±8 bursts 100beats-1), but upright MSNA was lower (74±15 vs. 85±10 bursts 100beats-1; P=0.012 for pre/post x posture). Direct renin was greater after both treatments (both P<0.05), while upright aldosterone was greater after hydrochlorothiazide only (P=0.002). The change in upright MSNA by the treatment was correlated with the change of aldosterone (r=0.74, P=0.002). Upright sympathetic BRS remained unchanged after either treatment. Thus, chronic renin inhibition may reduce upright MSNA through suppressed renin activity, while diuresis may evoke sympathetic activation via the upregulated renin-angiotensin-aldosterone system, without changing intrinsic sympathetic baroreflex function in elderly hypertensive patients.
    The Journal of Physiology 09/2013; · 4.38 Impact Factor
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    ABSTRACT: -Aging and sedentary lifestyles lead to cardiac atrophy, stiffening and impaired diastolic function. Both conditions are marked by increased adiposity which can lead to ectopic fat deposition in non-adipocyte tissues including the myocardium. The effect of excess intra-myocardial fat on cardiac function in non-obese individuals is unknown. -Cardiac lipid content was measured by magnetic resonance spectroscopy in 153 healthy non-obese subjects with varying fitness levels quantified by peak oxygen uptake (VO2peak) during treadmill exercise. Cardiac function (echo) and left ventricular (LV) filling pressures (right heart catheterization) were measured under varying preloads. LV stiffness was calculated from acurve fit of the diastolic portion of the pressure-volume (PV) curve. The strongest clinical predictors of lipid content were body mass index (BMI) (β, 95% CI: +0.03, 0.001 to 0.06) and VO2peak (-0.02, -0.03 to -0.009) (R(2)=0.14; p<0.001). Subjects in the highest quintile had smaller LV end-diastolic volumes (68±13 vs. 58±12 ml/m(2), p<0.01), decreased peak early mitral annular and increased peak late mitral inflow velocities. There were no differences in LV stiffness but a leftward shift in the PV curve suggested a less distensible ventricle with increasing myocardial lipid levels. After adjusting for age, fitness and BMI, echocardiographic and morphometric differences amongst groups were attenuated and no longer significant. -BMI and fitness levels are the strongest predictors of myocardial lipid content in non-obese humans. Cardiac lipid content is associated with decreased ventricular distensibility and may provide a causal mechanism linking changes in LV function related to age and fitness.
    Circulation Cardiovascular Imaging 09/2013; · 5.80 Impact Factor
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    ABSTRACT: Pneumatic anti shock garments (PASG) have been proposed to exert their blood pressure-raising effect mechanically, i.e., by increasing venous return and vascular resistance of the lower body. Alternatively, we tested whether PASG inflation activates the sympathetic nervous system. Five men and four women wore PASG while mean arterial pressure (MAP), muscle sympathetic nerve activity (MSNA), heart rate (HR), and stroke volume (SV) were measured. One leg bladder (LEG) and the abdominal bladder of the pants were inflated individually (ABD), and in combination (ABD+LEG), at 60 or 90 mmHg for 3 min. By the end of 3 minutes of inflation, conditions that included the ABD region caused significant increases in MAP in a dose dependent fashion (7±2, 8±3, 14±4, and 13±5 mmHg for ABD60, ABD+LEG60, ABD90, and ABD+LEG90, respectively, p<0.05). Similarly, inflation that included ABD caused significant increases in total MSNA compared to control (306±70, 426±98, and 247±79 units for ABD60, ABD90, and ABD+LEG90, respectively, p<0.05 and units = burst frequency x burst amplitude). There were no changes in MAP or MSNA in the LEG alone conditions. ABD inflation also caused a significant decrease in stroke volume (-11±3 and -10±3 ml/beat in ABD90 and ABD+LEG90, respectively, p<0.05) with no change in cardiac output. Neither cardiopulmonary receptor deactivation nor mechanical effects can account for a slowly-developing rise in both sympathetic activity and blood pressure during ABD inflation. Rather, these data provide direct evidence that PASG inflation activates the sympathetic nervous system secondary to abdominal, but not leg, compression.
    Experimental physiology 09/2013; · 3.17 Impact Factor
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    ABSTRACT: To determine if global brain hypoperfusion and oxygen hypometabolism occur in patients with amnestic mild cognitive impairment (aMCI). Thirty-two aMCI and 21 normal subjects participated. Total cerebral blood flow (TCBF), cerebral metabolic rate of oxygen (CMRO2), and brain tissue volume were measured using color-coded duplex ultrasonography (CDUS), near-infrared spectroscopy (NIRS), and MRI. TCBF was normalized by total brain tissue volume (TBV) for group comparisons (nTCBF). Cerebrovascular resistance (CVR) was calculated as mean arterial pressure divided by TCBF. Reductions in nTCBF by 9%, CMRO2 by 11%, and an increase in CVR by 13% were observed in aMCI relative to normal subjects. No group differences in TBV were observed. nTCBF was correlated with CMRO2 in normal controls, but not in aMCI. Global brain hypoperfusion, oxygen hypometabolism, and neurovascular decoupling observed in aMCI suggest that changes in cerebral hemodynamics occur early at a prodromal stage of Alzheimer's disease, which can be assessed using low-cost and bedside-available CDUS and NIRS technology.
    Alzheimer's & dementia: the journal of the Alzheimer's Association 07/2013; · 14.48 Impact Factor
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    ABSTRACT: Morning blood pressure (BP) surge is considered to be an independent risk factor for cardiovascular diseases. We tested the hypothesis that increased large-artery stiffness and impaired sympathetic baroreflex sensitivity (BRS) contribute to augmented morning surge in elderly hypertensives. Morning surge was assessed as morning systolic BP averaged for 2 hours just after waking up minus minimal sleeping systolic BP by using ambulatory BP monitoring (ABPM) in 40 untreated hypertensives [68±1 (SE) yrs] and 30 normotensives (68±1 yrs). Beat-by-beat finger BP and muscle sympathetic nerve activity (MSNA) were recorded in the supine position and at 60° upright tilt. We assessed arterial stiffness with carotid-to-femoral pulse wave velocity (cfPWV) and sympathetic BRS during spontaneous breathing. Awake and asleep ABPM-BPs and morning surge were higher in hypertensives than normotensives (all P<0.001). cfPWV was higher (P=0.002) and sympathetic BRS was lower (P=0.096) in hypertensives than normotensives. Hypertensives with morning surge ≥35 mmHg (median value) had higher cfPWV (11.9±0.5 vs 9.9±0.4 m•s(-1), P=0.002) and lower sympathetic BRS (supine: -2.71±0.25 vs -3.73±0.29, P=0.011; upright: -2.62±0.22 vs -3.51±0.35 bursts•100 beats(-1)•mmHg(-1), P=0.052) than those with morning surge <35 mmHg. MSNA indices were similar between groups (all P>0.05), while upright total peripheral resistance was higher in hypertensives with greater morning surge than those with lesser morning surge (P=0.050). Morning surge was correlated positively with cfPWV (r=0.59, P<0.001) and negatively with sympathetic BRS (r=0.51, P<0.001) in hypertensives only. Thus, morning BP surge is associated with arterial stiffness and sympathetic baroreflex sensitivity, as well as vasoreactivity during orthostasis in hypertensive seniors.
    AJP Heart and Circulatory Physiology 07/2013; · 3.63 Impact Factor
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    ABSTRACT: Mountain activities characterized by strenuous exercise in a hypoxic setting place unique demands on the body. The mortality rate associated with mountain activities is high, with sudden cardiac death (SCD) representing the most frequent of all nontraumatic deaths. We evaluated the possible effect of acclimatization in reduction of SCD during high-altitude sojourns. This was a retrospective cohort study involving all deaths (N = 559) that occurred during mountain activities in Austria from 1985 through 1993. Baseline patient demographics, cardiovascular comorbidities, smoking history, family history of SCD, sleeping altitude, annual mountaineering frequency, and physical activity on the day of SCD were included in a questionnaire previously used in a pilot study. Data from 301 of 599 individuals without prespecified exclusions were available for analysis (79% of eligible cohort). Sudden cardiac deaths happened mostly around noon (29%), and mean altitude at which SCDs occurred was 1,710 ± 501 m. When sleeping altitude was divided into quartiles (<700 m, 700-999 m, 1,000-1,299 m, and >1,299 m), the odds ratio for SCD on the first day at altitude when sleeping below 700 m was 5.7 (95% CI 2.8-11.6) as compared with sleeping above 1,299 m. For males >34 years, those with history of coronary artery disease and/or prior infarction, and those unaccustomed to physical activity at altitude, sleeping at moderate altitude before exercising at altitude may reduce the risk of SCD.
    American heart journal 07/2013; 166(1):71-5. · 4.65 Impact Factor

Publication Stats

6k Citations
1,414.18 Total Impact Points


  • 1991–2014
    • University of Texas Southwestern Medical Center
      • • Division of Cardiology
      • • Institute for Exercise and Environmental Medicine
      • • Department of Internal Medicine
      Dallas, Texas, United States
  • 2013
    • Brigham and Women's Hospital
      • Division of Sleep Medicine
      Boston, MA, United States
    • Asan Medical Center
      Sŏul, Seoul, South Korea
    • Fourth Military Medical University
      Xi’an, Liaoning, China
  • 2007–2012
    • Texas Health Resources
      Southlake, Texas, United States
    • University of Michigan
      Ann Arbor, Michigan, United States
  • 2004–2012
    • Radboud University Medical Centre (Radboudumc)
      • • Department of Neurology
      • • Department of Human Genetics
      Nymegen, Gelderland, Netherlands
  • 2011
    • John Peter Smith Hospital
      Fort Worth, Texas, United States
  • 2006–2011
    • Qinghai University
      Hsi-ning-shih, Qinghai Sheng, China
    • Australian Institute of Sport (AIS)
      Canberra, Australian Capital Territory, Australia
  • 2010
    • Fort Belvoir Community Hospital
      Fort Belvoir, Virginia, United States
    • University of Cyprus
      • Department of Electrical and Computer Engineering
      Lefkoşa, Lefkosia, Cyprus
  • 2007–2010
    • Indiana University Bloomington
      • Department of Kinesiology
      Bloomington, IN, United States
  • 2008
    • VU University Amsterdam
      • Faculty of Human Movement Sciences
      Amsterdam, North Holland, Netherlands
  • 1999–2008
    • New York Presbyterian Hospital
      New York City, New York, United States
    • Uniformed Services University of the Health Sciences
      • Department of Family Medicine
      Maryland, United States
    • United States Army
      Washington, West Virginia, United States
  • 2002–2003
    • University of Southern California
      • Department of Biomedical Engineering
      Los Angeles, CA, United States
    • Michigan Technological University
      • Department of Biomedical Engineering
      Houghton, MI, United States
  • 2001–2002
    • Pennsylvania State University
      • Department of Kinesiology
      University Park, MD, United States
    • University of Oslo
      Kristiania (historical), Oslo County, Norway
    • Cleveland Clinic
      • Department of Cardiology
      Cleveland, Ohio, United States
  • 1994
    • Rigshospitalet
      København, Capital Region, Denmark
  • 1992–1994
    • IT University of Copenhagen
      København, Capital Region, Denmark