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Background: Despite advances in medical and cardiac resynchronization therapy (CRT), individuals with chronic congestive heart failure (CHF) have persistent symptoms, including exercise intolerance. Optimizing cardio-locomotor coupling may increase stroke volume and skeletal muscle perfusion as previously shown in healthy runners. Therefore, we tested the hypothesis that exercise stroke volume and cardiac output would be higher during fixed-paced walking when steps were synchronized with the diastolic compared with systolic portion of the cardiac cycle in patients with CHF and CRT., Methods: Ten participants (58±17 years of age; 40% female) with CHF and previously implanted CRT pacemakers completed 5-minute bouts of walking on a treadmill (range, 1.5-3 mph). Participants were randomly assigned to first walking to an auditory tone to synchronize their foot strike to either the systolic (0% or 100±15% of the R-R interval) or diastolic phase (45±15% of the R-R interval) of their cardiac cycle and underwent assessments of oxygen uptake (V̇o 2 ; indirect calorimetry) and cardiac output (acetylene rebreathing). Data were compared through paired-samples t tests., Results: V̇o 2 was similar between conditions (diastolic 1.02±0.44 versus systolic 1.05±0.42 L/min; P =0.299). Compared with systolic walking, stroke volume (diastolic 80±28 versus systolic 74±26 mL; P =0.003) and cardiac output (8.3±3.5 versus 7.9±3.4 L/min; P =0.004) were higher during diastolic walking; heart rate (paced) was not different between conditions. Mean arterial pressure was significantly lower during diastolic walking (85±12 versus 98±20 mm Hg; P =0.007)., Conclusions: In patients with CHF who have received CRT, diastolic stepping increases stroke volume and oxygen delivery and decreases afterload. We speculate that, if added to pacemakers, this cardio-locomotor coupling technology may maximize CRT efficiency and increase exercise participation and quality of life in patients with CHF., Competing Interests: Disclosures None.

Background: Individuals with left ventricular (LV) hypertrophy and elevated cardiac biomarkers in middle age are at increased risk for the development of heart failure with preserved ejection fraction. Prolonged exercise training reverses the LV stiffening associated with healthy but sedentary aging; however, whether it can also normalize LV myocardial stiffness in patients at high risk for heart failure with preserved ejection fraction is unknown. In a prospective, randomized controlled trial, we hypothesized that 1-year prolonged exercise training would reduce LV myocardial stiffness in patients with LV hypertrophy., Methods: Forty-six patients with LV hypertrophy (LV septum >11 mm) and elevated cardiac biomarkers (N-terminal pro-B-type natriuretic peptide [>40 pg/mL] or high-sensitivity troponin T [>0.6 pg/mL]) were randomly assigned to either 1 year of high-intensity exercise training (n=30) or attention control (n=16). Right-heart catheterization and 3-dimensional echocardiography were performed while preload was manipulated using both lower body negative pressure and rapid saline infusion to define the LV end-diastolic pressure-volume relationship. A constant representing LV myocardial stiffness was calculated from the following: P=S×[Exp {a (V-V 0 )}-1], where "P" is transmural pressure (pulmonary capillary wedge pressure - right atrial pressure), "S" is the pressure asymptote of the curve, "V" is the LV end-diastolic volume index, "V 0 " is equilibrium volume, and "a" is the constant that characterizes LV myocardial stiffness., Results: Thirty-one participants (exercise group [n=20]: 54±6 years, 65% male; and controls (n=11): 51±6 years, 55% male) completed the study. One year of exercise training increased max by 21% (baseline 26.0±5.3 to 1 year later 31.3±5.8 mL·min -1 ·kg -1 , P <0.0001, interaction P =0.0004), whereas there was no significant change in max in controls (baseline 24.6±3.4 to 1 year later 24.2±4.1 mL·min -1 ·kg -1 , P =0.986). LV myocardial stiffness was reduced (right and downward shift in the end-diastolic pressure-volume relationship; LV myocardial stiffness: baseline 0.062±0.020 to 1 year later 0.031±0.009), whereas there was no significant change in controls (baseline 0.061±0.033 to 1 year later 0.066±0.031, interaction P =0.001)., Conclusions: In patients with LV hypertrophy and elevated cardiac biomarkers (stage B heart failure with preserved ejection fraction), 1 year of exercise training reduced LV myocardial stiffness. Thus, exercise training may provide protection against the future risk of heart failure with preserved ejection fraction in such patients. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03476785.

Hyperbaric oxygen therapy (HBOT) is a well-established treatment for a variety of conditions. Hyperbaric oxygen therapy is the administration of 100% oxygen breathing in a pressure vessel at higher than atmospheric pressure (1 atmosphere absolute = 101 kPa). Typically, treatment is given daily for between 1 and 2 h at pressures of 2.0 to 2.8 ATA, depending on the indication. Sporting injuries are often treated over 3 to 10 sessions. Hyperbaric oxygen therapy has been documented to be effective and is approved in 14 medical indications by the Undersea and Hyperbaric Medical Society, including, but not limited to, carbon monoxide poisoning, compromised skin grafts and flaps, crush injuries, necrotizing soft tissue infections, and nonhealing ulcers with arterial insufficiencies. Recently, HBOT for sports musculoskeletal injuries is receiving increased attention. Hyperbaric oxygen therapy may allow injured athletes to recover faster than normal rehabilitation methods. Any reduction in collegiate and professional athletes' rehabilitation period can be financially significant for top-level sports teams; however, further research is required to confirm HBOT's benefits on sports musculoskeletal injuries. The purpose of this review to discuss the current understanding of HBOT as a treatment modality for common musculoskeletal injuries in sport medicine. Moreover, we will highlight the advantages and disadvantages of this modality, as well as relevant clinical and research applications.

Background: Individuals with left ventricular hypertrophy (LVH) and elevated cardiac biomarkers in middle age are at high risk for the development of heart failure with preserved ejection fraction (HFpEF). However, it is unknown what the pathophysiological underpinnings of this high-risk state may be. We tested the hypothesis that patients with LVH and elevated cardiac biomarkers would demonstrate elevated left ventricular (LV) myocardial stiffness in comparison with healthy controls as a key marker for future HFpEF., Methods: Forty-six patients with LVH (LV septum >11 mm) and elevated cardiac biomarkers (N-terminal pro-B-type natriuretic peptide [>40 pg/mL] or troponin T [>0.6 pg/mL]) were recruited, along with 61 age- and sex-matched (by cohort) healthy controls. To define LV pressure-volume relationships, right heart catheterization and 3-dimensional echocardiography were performed while preload was manipulated using lower body negative pressure and rapid saline infusion., Results: There were significant differences in body size, blood pressure, and baseline pulmonary capillary wedge pressure between groups (eg, pulmonary capillary wedge pressure: LVH, 13.4±2.7 versus control, 11.7±1.7 mm Hg, P <0.0001). The LV was less distensible in LVH than in controls (smaller volume for the same filling pressure). When preload was expressed as transmural filling pressure (pulmonary capillary wedge pressure - right atrial pressure), LV myocardial stiffness was nearly 30% greater in LVH than in controls (LVH stiffness constant, 0.053±0.027 versus controls, 0.042±0.020, P =0.028)., Conclusions: LV myocardial stiffness in patients with LVH and elevated biomarkers (stage-B HFpEF) is greater than in age- and sex-matched controls and thus appears to represent a transitional state from a normal healthy heart to HFpEF. Although the LV myocardial stiffness of patients with LVH is greater than that of healthy controls at this early stage, further studies are required to clarify whether interventions such as exercise training to improve LV compliance may prevent the full manifestation of the HFpEF syndrome in these high-risk individuals., Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifiers: NCT03476785 and NCT02039154.

Background: Moderate intensity exercise is associated with a decreased incidence of atrial fibrillation. However, extensive training in competitive athletes is associated with an increased atrial fibrillation risk. We evaluated the effects of 24 months of high intensity exercise training on left atrial (LA) mechanical and electric remodeling in sedentary, healthy middle-aged adults., Methods: Sixty-one participants (53±5 years) were randomized to 10 months of exercise training followed by 14 months of maintenance exercise or stretching/balance control. Fourteen Masters athletes were added for comparison. Left ventricular (LV) and LA volumes underwent 3D echocardiographic assessment, and signal-averaged electrocardiographs for filtered P-wave duration and atrial late potentials were completed at 0, 10, and 24 months. Extended ambulatory monitoring was performed at 0 and 24 months. Within and between group differences from baseline were compared using mixed-effects model repeated-measures analysis., Results: Fifty-three participants completed the study (25 control, 28 exercise) with 88±11% adherence to assigned exercise sessions. In the exercise group, both LA and LV end diastolic volumes increased proportionately (19% and 17%, respectively) after 10 months of training (peak training load). However, only LA volumes continued to increase with an additional 14 months of exercise training (LA volumes 55%; LV end diastolic volumes 15% at 24 months versus baseline; P<0.0001 for all). The LA:LV end diastolic volumes ratio did not change from baseline to 10 months, but increased 31% from baseline in the Ex group ( P<0.0001) at 24 months, without a change in controls. There were no between group differences in the LA ejection fraction, filtered P-wave duration, atrial late potentials, and premature atrial contraction burden at 24 months and no atrial fibrillation was detected. Compared with Masters athletes, the exercise group demonstrated lower absolute LA and LV volumes, but had a similar LA:LV ratio after 24 months of training., Conclusions: Twenty-four months of high intensity exercise training resulted in LA greater than LV mechanical remodeling with no observed electric remodeling. Together, these data suggest different thresholds for electrophysiological and mechanical changes may exist in response to exercise training, and provide evidence supporting a potential mechanism by which high intensity exercise training leads to atrial fibrillation., Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT02039154.

Background: The dynamic Starling mechanism, as assessed by beat-by-beat changes in stroke volume and left ventricular end-diastolic pressure, reflects ventricular-arterial coupling. It deteriorates with age, and is preserved in highly trained masters athletes. Currently, it remains unclear how much exercise over a lifetime is necessary to preserve efficient ventricular-arterial coupling. The purpose of this study was to assess the dose-dependent relationship between lifelong exercise training and the dynamic Starling mechanism in healthy seniors., Methods: One hundred two seniors were recruited and stratified into 4 groups based on 25 years of exercise training history: sedentary subjects (n=27, <2 sessions/week), casual exercisers (n=25, 2-3 sessions/week), committed exercisers (n=25, 4-5 sessions/week), and competitive Masters Athletes (n=25, 6-7 sessions/week). The dynamic Starling mechanism was estimated by transfer function gain between beat-by-beat changes in diastolic pulmonary artery pressure, a surrogate for left ventricular end-diastolic pressure, and stroke volume index., Results: The transfer function gain of pulmonary artery pressure-stroke volume index was markedly enhanced in committed and competitive exercisers compared with more sedentary seniors and correlated with higher peak oxygen uptake (Vo 2 ) and lower left ventricular stiffness. The power spectral density of pulmonary artery pressure was greater in sedentary adults than in committed and competitive exercisers, whereas the power spectral density of stroke volume index was greater in competitive exercisers than in the other groups., Conclusions: There is a graded, dose-dependent improvement in ventricular-arterial coupling with increasing amounts of lifelong regular exercise in healthy older individuals. Our data suggest that the optimal dose of lifelong endurance exercise to preserve ventricular-arterial coupling with age appears to be at least 4 to 5 sessions per week.

Background: Exercise mitigates many cardiovascular risk factors associated with atrial fibrillation. Endurance training has been associated with atrial structural changes which can increase the risk for atrial fibrillation. The dose of exercise training required for these changes is uncertain. We sought to evaluate the impact of exercise on left atrial (LA) mechanical and electrical function in healthy, sedentary, middle-aged adults., Methods: Sixty-one adults (52±5 years) were randomized to either 10 months of high-intensity exercise training or yoga. At baseline and post-training, all participants underwent maximal exercise stress testing to assess cardiorespiratory fitness, P-wave signal-averaged electrocardiography for filtered P-wave duration and atrial late potentials (root mean square voltage of the last 20 ms), and echocardiography for LA volume, left ventricular end-diastolic volume, and mitral inflow for assessment of LA active emptying. Post-training data were compared with 14 healthy age-matched Masters athletes., Results: LA volume, Vo 2 max, and left ventricular end-diastolic volume increased in the exercise group (15%, 17%, and 16%, respectively) with no change in control ( P <0.0001). LA active emptying decreased post-exercise versus controls (5%; P =0.03). No significant changes in filtered P-wave duration or root mean square voltage of the last 20 ms occurred after exercise training. LA and left ventricular volumes remained below Masters athletes. The athletes had longer filtered P-wave duration but no difference in the frequency of atrial arrhythmia., Conclusions: Changes in LA structure, LA mechanical function, and left ventricular remodeling occurred after 10 months of exercise but without significant change in atrial electrical activity. A longer duration of training may be required to induce electrical changes thought to cause atrial fibrillation in middle-aged endurance athletes., Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique Identifier: NCT02039154., (© 2018 American Heart Association, Inc.)

Purpose: The current study examined whether age-related changes in left ventricular (LV) longitudinal systolic function is an adaptation to a more sedentary lifestyle and can be preserved by lifelong exercise training., Methods: A cross-sectional examination of 18 sedentary young (37 ± 6 yr), 29 sedentary seniors (71 ± 5 yr, 0-3 exercise sessions per week), and 26 seniors (68 ± 5 yr) who had performed a committed level (four to seven exercise sessions per week) of lifelong (>25 yr) exercise. Invasive right heart catheterization (pulmonary capillary wedge pressure) and noninvasive measures of LV function were collected at the following conditions: 1) supine rest, 2) during LV unloading (lower body negative pressure), and 3) LV loading (saline infusion). Ejection fraction and preload-recruitable stroke work (PRSW) were used to describe global LV systolic function, while peak systolic tissue velocity and longitudinal strain (LS) indicate LV longitudinal systolic function. To adjust LS for aging and training-related differences in LV preload and afterload, LV end-diastolic volume and end-systolic pressure (ESP) were included as covariates in ANCOVA models., Results: Ejection fraction and PRSW were unaffected by aging or lifelong exercise (P = 0.22, P = 0.08, respectively). Peak systolic tissue velocities decreased with aging (P < 0.001) and sedentary seniors had a smaller LS compared with young (P = 0.023) and lifelong exercisers (P = 0.046). Preload-recruitable stroke work, ESP as a covariate did not alter group differences; however, LV end-diastolic volume eliminated group differences between senior groups. Longitudinal strain was preload dependent (P < 0.001), which was independent of aging and lifelong exercise., Conclusions: Sedentary aging leads to a reduction in systolic LS, which is attenuated by committed lifelong exercise due to improved LV diastolic filling.

Objective: The aim of this study was to evaluate the prevention of liver ischemic injury by preoperative coil embolization in patients with a replaced hepatic artery scheduled for pancreatectomy with splanchnic artery resection., Methods: Between July 2009 and May 2012, 4 patients with replaced hepatic artery underwent pancreatectomy plus splanchnic artery resection. The replaced right hepatic artery was preoperatively embolized in 2 patients. In the other 2 patients, the common hepatic artery was embolized preoperatively. We evaluated the complications encountered in the perioperative period., Results: There were no embolization-related complications. Although 2 patients presented with small liver infarcts, the aspartate aminotransferase and alanine aminotransferase levels did not exceed 1000 IU/L in any of the patients, and none experienced severe liver injury., Conclusions: Coil embolization before pancreatectomy with splanchnic artery resection in patients with a replaced hepatic artery may help to prevent severe ischemic liver injury in the perioperative period.

Mechanical circulatory support by a left ventricular assist device (LVAD) is used to bridge patients with advanced heart failure to transplant or as a definitive treatment. We retrospectively sought predictors of long-term outcome in a cohort of 83 patients who had undergone LVAD treatment. We subjected perioperative clinical data of patients to statistical analysis to establish parameters associated with all-cause mortality, and the cutoff values, sensitivity, and specificity of those that had a statistically significant relation with survival. Mean follow-up was 717 days (standard deviation, 334 days; range, 17-1,592 days). Fourteen patients (16.8%) died, but nine (10.8%) were weaned from support. Serum brain natriuretic peptide (BNP) concentration measured 60 days after implantation was significantly associated with all-cause mortality. The optimal BNP cutoff value to predict death during LVAD support was 322 pg/ml, with a sensitivity of 71.4% and specificity of 79.8%. Two-year survival was 92.0% in those with 60 days serum BNP concentration <322 pg/ml compared with 70.5% in those in whom it was ≥322 pg/ml (p = 0.003). The relation between BNP and survival likely reflects recovery of native myocardial function and improvements in global health and should assist clinicians in the on-going management of long-term LVAD therapy.

Objectives: Recurrent hepatocellular carcinoma (HCC) often occurs with extrahepatic supply because of various factors. The right inferior phrenic artery (RIPA) is the most frequent extrahepatic feeding artery, however, it is rarely found that the RIPA supplies the tumor in patients with HCC at initial treatment. The purpose of this study is to evaluate the radiological findings of untreated cases of HCC fed by the RIPA., Materials and Methods: Medical records, computed tomography scans, and angiograms in 14 patients with HCC fed by the RIPA at initial therapy were reviewed. We evaluated growth pattern, size, location of tumors, and patency of the hepatic artery., Results: In all cases, tumors showed exophytic growth. Eleven cases (79%) were massive type. Tumor size ranged from 4.5 cm to 16.8 cm (mean, 11.1 cm). In 11 cases (79%), tumors were mainly located in liver segment 7. The patency of the hepatic arteries was intact in all cases., Conclusions: Regardless of initial therapy, HCC with exophytic growth pattern, especially located in the hepatic areas directly beneath the diaphragm and of massive type, can be supplied by the RIPA.

The utility of computed tomography pulmonary angiography (CTPA) for coil embolization therapy of pulmonary arteriovenous malformations (PAVMs) was considered. Three consecutive patients (group A) with PAVMs underwent CTPA and coil embolization. The CTPA was performed using a 16-detector-row computed tomography scanner. After careful selection of pulmonary vessel trees, each feeding artery, nidus, and drainage vein was colored using different codes. By using the colored images, a 5-French catheter was shaped to fit to each feeding artery, the best fluoroscopic angle to select each feeding artery was chosen, and interlocking detachable coils (IDCs) were used in embolization. The procedure time and contrast material dose of group A were compared with those of the previous 3 patients (group B) who were treated by the conventional method. All PAVMs of both groups were completely embolized without coil migration. The average procedure time per lesion was 48.4 minutes for group A and 124.0 minutes for group B (P < 0.05). The average contrast material dose per lesion was 37.5 mL in group A and 76.0 mL in group B (P < 0.05). Using CTPA and IDCs, procedure time and contrast material dose were statistically significantly reduced. This combination therapy is useful in treating PAVMs less invasively.