Corin (an atrial natriuretic peptide converting enzyme) represents a potential biomarker for gestational hypertensive disorders; yet, its role in blood pressure regulation throughout pregnancy remains unclear. We investigated the time-course of change in blood corin content in relation to blood pressure and sympathetic nerve activity throughout pregnancy. Forty-four women (29±0.9 yrs) participated. Following-term, 23 had 'low-risk' (no personal history of gestational hypertensive disorders) normal pregnancies, 13 had 'high-risk' (personal history of gestational hypertensive disorders) normal pregnancies, and eight developed gestational hypertension. Blood pressure, heart rate, muscle sympathetic nerve activity, and serum corin were measured prior-to pregnancy, during early-(4-8 wks) and late-pregnancy (32-36 wks), and post-partum (6-10 wks). Overall, compared to pre-pregnancy, corin remained unchanged during early-pregnancy, increased markedly during late-pregnancy (P<0.001), and returned to pre-pregnancy levels post-partum. In women who developed gestational hypertension, the change in corin from early-to late-pregnancy was greater than those with 'low-risk' normal pregnancies (Δ971±134 vs. Δ486±79 pg/mL; P<0.05). Throughout pregnancy, blood pressure and muscle sympathetic nerve activity were augmented in women with gestational hypertension (all P<0.05). Finally, changes in corin from early-to late-pregnancy were related to all indices of blood pressure (R=0.454-0.551; all P<0.01) in late-pregnancy, whereas burst frequency, burst incidence, and total muscle sympathetic nerve activity (R=0.576-0.614; all P<0.001) in early-pregnancy were related to changes in corin from early-to late-pregnancy. Corin plays a unique role in blood pressure regulation throughout

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The effect of acute increases in cardiac contractility on cerebral blood flow (CBF) remains unknown. We hypothesized that the external carotid artery (ECA) downstream vasculature modifies the direct influence of acute increases in heart rate and cardiac function on CBF regulation. Twelve healthy subjects received two infusions of dobutamine [first a low dose (5 μg·kg·min) and then a high dose (15 μg·kg·min)] for 12 min each. Cardiac output, blood flow through the internal carotid artery (ICA) and ECA, and echocardiographic measurements were performed during dobutamine infusions. Despite increases in cardiac contractility, cardiac output, and arterial pressure with dobutamine, ICA blood flow and conductance slightly decreased from resting baseline during both low- and high-dose infusions. In contrast, ECA blood flow and conductance increased appreciably during both low- and high-dose infusions. Greater ECA vascular conductance and corresponding increases in blood flow may protect overperfusion of intracranial cerebral arteries during enhanced cardiac contractility and associated increases in cardiac output and perfusion pressure. Importantly, these findings suggest that the acute increase of blood perfusion attributable to dobutamine administration does not cause cerebral overperfusion or an associated risk of cerebral vascular damage. A dobutamine-induced increase in cardiac contractility did not increase internal carotid artery blood flow despite an increase in cardiac output and arterial blood pressure. In contrast, external carotid artery blood flow and conductance increased. This external cerebral blood flow response may assist with protecting from overperfusion of intracranial blood flow.

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.

Background Accurate assessment of cardiac output is critical to the diagnosis and management of various cardiac disease states; however, clinical standards of direct Fick and thermodilution are invasive. Noninvasive alternatives, such as closed‐circuit acetylene (C 2 H 2 ) rebreathing, warrant validation. Methods and Results We analyzed 10 clinical studies and all available cardiopulmonary stress tests performed in our laboratory that included a rebreathing method and direct Fick or thermodilution. Studies included healthy individuals and patients with clinical disease. Simultaneous cardiac output measurements were obtained under normovolemic, hypovolemic, and hypervolemic conditions, along with submaximal and maximal exercise. A total of 3198 measurements in 519 patients were analyzed (mean age, 59 years; 48% women). The C 2 H 2 method was more precise than thermodilution in healthy individuals with half the typical error (TE; 0.34 L/min [ r =0.92] and coefficient of variation, 7.2%) versus thermodilution (TE=0.67 [ r =0.70] and coefficient of variation, 13.2%). In healthy individuals during supine rest and upright exercise, C 2 H 2 correlated well with thermodilution (supine: r =0.84, TE=1.02; exercise: r =0.82, TE=2.36). In patients with clinical disease during supine rest, C 2 H 2 correlated with thermodilution ( r =0.85, TE=1.43). C 2 H 2 was similar to thermodilution and nitrous oxide (N 2 O) rebreathing technique compared with Fick in healthy adults (C 2 H 2 rest: r =0.85, TE=0.84; C 2 H 2 exercise: r =0.87, TE=2.39; thermodilution rest: r =0.72, TE=1.11; thermodilution exercise: r =0.73, TE=2.87; N 2 O rest: r =0.82, TE=0.94; N 2 O exercise: r =0.84, TE=2.18). The accuracy of the C 2 H 2 and N 2 O methods was excellent ( r =0.99, TE=0.58). Conclusions The C 2 H 2 rebreathing method is more precise than, and as accurate as, the thermodilution method in a variety of patients, with accuracy similar to an N 2 O rebreathing method approved by the US Food and Drug Administration.

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.

URL: https://www.clinicaltrials.gov. Unique Identifier: NCT02039154.

Conversion to EVL from MMF in maintenance periods after HTx may decrease the rate of CAV progression based on IVUS indices.