A recent study investigated the association of gender with the growth rate of AAAs and found a significant increase in the growth rate of AAAs in women than in men. On the basis of these observations, we hypothesize that there are gender-associated differences in AAA wall integrity and mechanical strength. The purpose of this study was to explore this hypothesis by comparing the tensile strength of freshly resected AAA tissue specimens between women and men. Seventy-six rectangular specimens (20 mm long x 5 mm wide) from 34 patients (24 male, 10 female) were excised from the anterior wall of patients undergoing open repair of their abdominal aortic aneurysm and tested in a uniaxial tensile tester. Ultimate tensile strength (UTS) was taken as the peak stress obtained before specimen failure. While there were no statistical differences in strength between specimens taken from male and female patients, there was a trend toward a decrease in strength in females as compared to males (87.6 +/- 6.7 N/cm(2) vs. 67.6 +/- 8.1 N/cm(2), p = 0.09). To the authors knowledge this work represents the first report of differences in biomechanical properties as a function of gender. The nearly significant decrease in UTS in women versus men reported here may be important in assessing the risk of rupture in AAA. Further testing is warranted to confirm the current trends.

BackgroundLower muscle mitochondrial energy production may contribute to impaired walking endurance in patients with peripheral arterial disease. A borderline ankle‐brachial index (ABI) of 0.91 to 1.10 is associated with poorer walking endurance compared with higher ABI. We hypothesized that in the absence of peripheral arterial disease, lower ABI is associated with lower mitochondrial energy production.Methods and ResultsWe examined 363 men and women participating in the Baltimore Longitudinal Study of Aging with an ABI between 0.90 and 1.40. Muscle mitochondrial energy production was assessed by post‐exercise phosphocreatine recovery rate constant (kPCr) measured by phosphorus magnetic resonance spectroscopy of the left thigh. A lower post‐exercise phosphocreatine recovery rate constant reflects decreased mitochondria energy production.The mean age of the participants was 71±12 years. A total of 18.4% had diabetes mellitus and 4% were current and 40% were former smokers. Compared with participants with an ABI of 1.11 to 1.40, those with an ABI of 0.90 to 1.10 had significantly lower post‐exercise phosphocreatine recovery rate constant (19.3 versus 20.8 ms−1, P=0.015). This difference remained significant after adjusting for age, sex, race, smoking status, diabetes mellitus, body mass index, and cholesterol levels (P=0.028). Similarly, post‐exercise phosphocreatine recovery rate constant was linearly associated with ABI as a continuous variable, both in the ABI ranges of 0.90 to 1.40 (standardized coefficient=0.15, P=0.003) and 1.1 to 1.4 (standardized coefficient=0.12, P=0.0405).ConclusionsAn ABI of 0.90 to 1.10 is associated with lower mitochondrial energy production compared with an ABI of 1.11 to 1.40. These data demonstrate adverse associations of lower ABI values with impaired mitochondrial activity even within the range of a clinically accepted definition of a normal ABI. Further study is needed to determine whether interventions in persons with ABIs of 0.90 to 1.10 can prevent subsequent functional decline.

Out-of-hospital cardiac arrest is a leading cause of death in the US, with a mortality rate over 90%. Preclinical studies demonstrate that cooling during cardiopulmonary resuscitation (CPR) is highly beneficial, but can be challenging to implement clinically. No medications exist for improving long-term cardiac arrest survival. We have developed a 20–amino acid peptide, TAT-PHLPP9c, that mimics cooling protection by enhancing AKT activation via PH domain leucine-rich repeat phosphatase 1 (PHLPP1) inhibition. Complementary studies were conducted in mouse and swine. C57BL/6 mice were randomized into blinded saline control and peptide-treatment groups. Following a 12-minute asystolic arrest, TAT-PHLPP9c was administered intravenously during CPR and significantly improved the return of spontaneous circulation, mean arterial blood pressure and cerebral blood flow, cardiac and neurological function, and survival (4 hour and 5 day). It inhibited PHLPP-NHERF1 binding, enhanced AKT but not PKC phosphorylation, decreased pyruvate dehydrogenase phosphorylation and sorbitol production, and increased ATP generation in heart and brain. TAT-PHLPP9c treatment also reduced plasma taurine and glutamate concentrations after resuscitation. The protective benefit of TAT-PHLPP9c was validated in a swine cardiac arrest model of ventricular fibrillation. In conclusion, TAT-PHLPP9c may improve neurologically intact cardiac arrest survival without the need for physical cooling.

Worldwide, population aging and unhealthy lifestyles have increased the incidence of high-risk health conditions such as cardiovascular diseases, sleep apnea, and other conditions. Recently, to facilitate early identification and diagnosis, efforts have been made in the research and development of new wearable devices to make them smaller, more comfortable, more accurate, and increasingly compatible with artificial intelligence technologies. These efforts can pave the way to the longer and continuous health monitoring of different biosignals, including the real-time detection of diseases, thus providing more timely and accurate predictions of health events that can drastically improve the healthcare management of patients. Most recent reviews focus on a specific category of disease, the use of artificial intelligence in 12-lead electrocardiograms, or on wearable technology. However, we present recent advances in the use of electrocardiogram signals acquired with wearable devices or from publicly available databases and the analysis of such signals with artificial intelligence methods to detect and predict diseases. As expected, most of the available research focuses on heart diseases, sleep apnea, and other emerging areas, such as mental stress. From a methodological point of view, although traditional statistical methods and machine learning are still widely used, we observe an increasing use of more advanced deep learning methods, specifically architectures that can handle the complexity of biosignal data. These deep learning methods typically include convolutional and recurrent neural networks. Moreover, when proposing new artificial intelligence methods, we observe that the prevalent choice is to use publicly available databases rather than collecting new data.

Due to the relatively limited amount of work done to date on developing prosthetic vein (as opposed to cardiac) valves, advances in this topic require progress in three distinct areas: 1) improved device design, 2) relevant device testing conditions, and, 3) appropriate parameters for evaluation of results. It is the purpose of this paper to address two of these issues (#2 and #3) by: 1) performing a study of normal volunteers to quantify the anatomy and hemodynamic features of healthy venous valves, 2) construction of a 2-step, in vitro testing procedure, which simulates both physiologic and postural conditions seen in the lower extremity venous system, and, 3) defining several modified and new parameters which quantify dynamic valve characteristics.

Background Common carotid intima medial thickness (IMT) increases with aging. However, the longitudinal association between IMT and other age‐associated hemodynamic alterations in men and in women are not fully explored. Methods and Results We analyzed repeated measures of IMT, blood pressure, and carotid‐femoral pulse wave velocity over a 20‐year period in 1067 men and women of the Baltimore Longitudinal Study on Aging; participants were ages 20 to 92 years at entry and free of overt cardiovascular disease. Linear mixed‐effects models were used to calculate the individual rates of change ( Change ) of IMT, pulse pressure, mean arterial pressure, and pulse wave velocity, among other covariates. Multivariate regression analysis was used to examine the association of IMT Change with baseline and rates of change of hemodynamic parameters and cardiovascular risk factors. IMT increased at accelerating rates from 0.02 mm/decade at age 50 years to 0.05 mm/decade at age 80 years greater rates in men than in women. IMT Change was positively associated with baseline low‐density lipoprotein, low‐density lipoprotein Change , and baseline systolic blood pressure and systolic blood pressure Change , but inversely with baseline diastolic blood pressure and diastolic blood pressure Change . When blood pressure was expressed as pulse pressure and MAP, IMT Change was positively associated with baseline pulse pressure and pulse pressure Change and inversely with baseline mean arterial pressure and mean arterial pressure Change . In sex‐specific analysis, these associations were observed in women, but not in men. Conclusions In summary, our analyses showed that IMT increases at accelerating rates with aging. Age‐associated changes in IMT were modulated by concurrent changes of low‐density lipoprotein in both sexes, and of pulsatile and mean blood pressure in women but not men.

Cardiopulmonary resuscitation (CPR) is a first-line therapy for sudden cardiac arrest, while extracorporeal membrane oxygenation (ECMO) has traditionally been used as a means of countering circulatory failure. However, new advances dictate that CPR and ECMO could be complementary for support after cardiac arrest. This review details the emerging science, technology, and clinical application that are enabling the new paradigm of these iconic circulatory support modalities in the setting of cardiac arrest.

BackgroundAging is associated with a modest decline in ankle‐brachial index (ABI); however, the underpinnings of this decline are not fully understood. The greater systolic ankle than brachial blood pressure, a normal ABI implies, is partially attributed to lower central than peripheral arterial stiffness. Hence, we examined the hypothesis that the age‐associated decline in ABI is associated with central arterial stiffening with aging, assessed by pulse wave velocity.Methods and ResultsWe analyzed longitudinal data from 974 participants aged 27 to 95 years from the Baltimore Longitudinal Study of Aging who were free of clinically significant cardiovascular disease. Participants had an average of 4 visits with a 6.8‐year average follow‐up time. Linear mixed‐effects models showed that the average ABI decline beyond the age of 70 years was 0.03 per decade. In multiple regression analysis, the ABI rate of change was inversely associated with initial age (standardized β=−0.0711, P=0.0282), independent of peripheral disease factors and baseline ABI. After adjustment, the pulse wave velocity rate of change was inversely associated with ABI rate of change (standardized β=−0.0993, P=0.0040), rendering the association of the latter with initial age nonsignificant (standardized β=−0.0265, P=0.5418).ConclusionsA modest longitudinal decline in ABI beyond the age of 70 years was shown to be independent of traditional risk factors for peripheral arterial disease but was accounted for by an increase in pulse wave velocity. A modest decline in ABI with aging might be a manifestation of changes in central hemodynamics and not necessarily attributable to peripheral flow–limiting factors.