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Background: Engaging in habitual resistance exercise training (RET; also known as strength training) causes systemic health effects beyond those caused by aerobic/endurance exercise training alone. Despite the resoundingly favorable effect of habitual RET on measures of cardiovascular disease risk, controversy still exists regarding the vascular health effects of this exercise modality largely because some studies find increases in large artery stiffness and central pulsatile hemodynamics with RET. In this two-part series, we examine the effect of acute resistance exercise (RE) and RET on large artery stiffness and pulsatile hemodynamics. We perform a historical overview of seminal/classic studies and report on key findings that have shaped the field. We provide personal commentary on the studies and potential implications of findings related to the acute effects of RE on large artery stiffness and central pulsatile hemodynamics. For part one of this two-part series, we perform a detailed analysis of the hemodynamic signature produced during RE and discuss the sub-acute effects on short-term modulation of large artery stiffness and central pulsatile hemodynamics.

Summary: Acute RE elicits marked ("extreme") elevations in arterial pressure, mediated primarily by increases in vascular resistance and intrathoracic pressure (ITP). Vascular compression from muscular contraction contributes to increases in afterload via increased vascular resistance and pressure from wave reflections. However, as a result of the higher ITP associated with breath holds (Valsalva maneuver) during high relative efforts (>80%), the change in pressure across the aortic wall (transmural pressure) is less than the change in intra-arterial pressure.

Key messages: The high arterial pressures during some heavy weight lifting exercises are associated with positive swings with ITP related to the Valsalva maneuver and elevations in vascular resistance. The pressure oscillations lead to marked stress within the vascular wall and likely contribute to elevations in large artery stiffness over the subsequent hour.

Introduction: Cardio-ankle vascular index (CAVI), a blood pressure-independent measure of heart-ankle pulse wave velocity, is a relatively new indicator of arterial stiffness. The absolute value of the difference in right CAVI and left CAVI (diff-CAVI) has been proposed as a new indicator of leg ischemia in patients with lower extremity arterial disease (LEAD). The aim of this study was to elucidate the relationships between diff-CAVI and peptides related to hypertensive disorders of pregnancy (HDP), which have been proposed as biomarkers for leg ischemia in patients with LEAD.

Methods: The participants were 165 outpatients with LEAD who had already received medication therapy for LEAD. The relationships between diff-CAVI and serum levels of the seven HDP-related peptides, which were measured by mass spectrometry, were investigated.

Results: HDP-related peptides with m/z 2091 (P-2091) and m/z 2378 (P-2378) showed significant positive correlations with diff-CAVI, and odds ratios (ORs) for large diff-CAVI (≥1.05) of the 3rd vs. 1st tertile groups of P-2091 (OR [99.3% confidence interval]: 3.71 [1.24-11.15]) and P-2378 (OR: 4.46 [1.39-14.30]) were significantly higher (p < 0.01) than the reference level. The associations of P-2091 and P-2378 with diff-CAVI were shown to be independent of age, gender, habit of smoking, history of diabetes, BMI, and blood pressure in multivariate analyses. The other peptides with m/z 2081, 2127, 2209, 2858, and 3156 did not show significant associations with diff-CAVI.

Conclusion: P-2091 and P-2378 were associated with diff-CAVI and are thought to be useful indicators of leg ischemia in patients with LEAD.

Introduction: Aortic structure impacts cardiovascular health through multiple mechanisms. Aortic structural degeneration occurs with aging, increasing left ventricular afterload and promoting increased arterial pulsatility and target organ damage. Despite the impact of aortic structure on cardiovascular health, three-dimensional (3D) aortic geometry has not been comprehensively characterized in large populations.

Methods: We segmented the complete thoracic aorta using a deep learning architecture and used morphological image operations to extract multiple aortic geometric phenotypes (AGPs, including diameter, length, curvature, and tortuosity) across various subsegments of the thoracic aorta. We deployed our segmentation approach on imaging scans from 54,241 participants in the UK Biobank and 8,456 participants in the Penn Medicine Biobank.

Conclusion: Our method provides a fully automated approach toward quantifying the three-dimensional structural parameters of the aorta. This approach expands the available phenotypes in two large representative biobanks and will allow large-scale studies to elucidate the biology and clinical consequences of aortic degeneration related to aging and disease states.

Introduction: Aortic stiffness, assessed through carotid-femoral pulse wave velocity (PWV), has been associated with an increased risk of cardiovascular events and mortality. Measurements of PWV are based on the proper identification of the foot of the pulse waveform by either the maximum of the second-derivative method (as used in Complior) or the intersecting tangents algorithms (as used in SphygmoCor). These approaches can give different results, especially at higher PWV ranges. However, these devices also differ by signal acquisition technology, signal filtering, and quality control algorithms, making the true contribution of analytical algorithms uncertain. The aim of the present study was to identify the differences in pulse transit time (PTT) and PWV calculated by these two algorithms when provided with the same input signal.

Methods: In 113 subjects, 346 recordings of 10 s were obtained using the Complior Analyse system (PWV_Comp-2nd). The pulse waves were imported into MATLAB and filtered (n = 4,102 pairs of pulse waves), where after inspection 3,770 pairs were available for determination of PTT using second-derivative and intersecting tangents algorithms (PTT_Mat-2nd and PTT_Mat-IT) and the respective PWV_Mat-2nd and PWV_Mat-IT for each pair. Additionally, the same pulse wave recordings were analyzed using the SphygmoCor system in simulation mode, employing the intersecting tangents algorithm (PWV_Sphyg-IT).

Results: The mean beat-by-beat PTT_Mat-2nd and PTT_Mat-IT were 54.55 ± 18.55 ms (range 15.00-129.00) and 54.61 ± 18.61 ms (range 15.00-126.00) (p = 0.09), respectively. The mean per participant PWV_Mat-2nd and PWV_Mat-IT were 9.67 ± 3.46 m/s and 9.66 ± 3.4 m/s with a mean difference of 0.01 ± 0.32 m/s (p = 0.35). The PWV_Comp-2nd and PWV_Sphyg-IT were 9.48 ± 3.25 m/s and 9.59 ± 3.25 m/s with a mean difference of 0.11 ± 0.66 m/s (p = 0.04).

Conclusion: The present study shows that the difference between the two algorithms is negligible across a wide range of PTT and hence does not support the need for adjusting PWV according to the algorithm used for determining PTT.

Background: Aortic stiffness, quantified by carotid-femoral pulse wave velocity (PWV), is a strong predictor of cardiovascular disease events. In general, dynamic "aerobic" exercise training performed regularly for many years in middle and older age is associated with an attenuated or absence of an age-related increase in aortic stiffness without hypertension. However, cross-sectional studies can be confounded by physiological or lifestyle factors that may contribute in part to the lower aortic stiffness observed, and prospective interventions are often limited by short duration and inadequate exercise frequency to have clinical benefit. Therefore, this review will discuss the evidence for the de-stiffening effects of regular, dynamic aerobic exercise training on aortic stiffness in the presence or absence of hypertension with some discussion on high-intensity interval training (HIIT).

Summary: Short-term (3-12 months) aerobic exercise interventions, 2-3 days per week initiated in middle age or older age without hypertension, result in small decreases in carotid-femoral PWV that is likely the result of reductions in distending pressure (i.e., mean arterial pressure) rather than an alteration in structural wall properties. However, cross-sectional data indicate that 4-5 days/week appears to be the minimal frequency that is obligatory for de-stiffening of the aorta among adults who perform regular exercise in middle age and continue into older age. Despite greater improvements in aerobic fitness by high-intensity interval training (HIIT), short-term HIIT 4 days/week does not provide any benefit over moderate-intensity continuous training for de-stiffening the aorta among older adults with or without hypertension.

Key messages: Short-term aerobic exercise interventions 2-3 days/week at moderate intensity initiated in middle age or older age have small or no favorable blood pressure-independent effect on aortic wall stiffness. In contrast, 4-5 days/week appears to be the minimal obligatory dose of aerobic exercise to have some de-stiffening effects if performed during middle age and continuing into older age. Short-term HIIT provides no greater de-stiffening effects on the aged aorta than continuous aerobic exercise training.

Introduction: It is not well-known which indicator, central blood pressure (CBP) or arterial stiffness, has a greater impact on carotid atherosclerosis. This study aimed to assess the associations of carotid atherosclerosis with arterial stiffness and CBP in the same individuals.

Methods: A total of 142 patients (mean age: 69 years; 43% female) with documented atherosclerotic cardiovascular disease or multiple risk factors were analyzed. Brachial-ankle pulse wave velocity (baPWV) and CBP measurements, along with carotid ultrasound, were performed on the same day. CBP was assessed using radial artery tonometry.

Results: In simple linear regression analysis, only baPWV exhibited a significant correlation with carotid intima-media thickness (CIMT) (r = 0.272; p = 0.001), whereas none of the CBP parameters (systolic, diastolic, pulse pressures, and augmentation index) correlated with CIMT (p > 0.05 for each). Multiple linear regression analysis indicated that baPWV had no significant association with CIMT after adjusting for age (p = 0.264). A higher baPWV (≥1,656 cm/s) was significantly associated with carotid plaque presence, even after accounting for potential confounders (odds ratio: 3.66; 95% confidence interval: 1.65-8.12; p = 0.001). Moreover, as the number of carotid plaques increased, there was a linear rise in baPWV (p < 0.001). None of CBP parameters were associated with the presence of carotid plaque (p > 0.05 for each).

Conclusions: Among a high-risk Korean population, baPWV demonstrated a stronger association with carotid plaque presence and extent compared to CBP parameters. Thus, baPWV may serve as a valuable marker for identifying carotid plaque.

Introduction: Arterial stiffening is a hallmark of vascular ageing, and unravelling its underlying mechanisms has become a central theme in the field of cardiovascular disease. While various techniques and experimental setups are accessible for investigating biomechanics of blood vessels both in vivo and ex vivo, comparing findings across diverse methodologies is challenging.

Methods: Arterial stiffness in the aorta of adult (5 months) and aged (24 months) wild-type C57Bl/6J mice was measured in vivo, after which ex vivo biomechanical evaluation was performed using the Rodent Oscillatory Tension Setup to study Arterial Compliance (ROTSAC; University of Antwerp, Belgium) and the DynamX setup (Maastricht University, The Netherlands). Stiffness of aortic tissue was measured in both absence and presence of activated smooth muscle cells (i.e., contraction). Measurements in both setups were conducted in parallel with matched protocols and identical buffers and chemicals.

Results: Overall, both methods revealed age-related increased aortic stiffness, although parameters of aortic mechanics showed different numerical values, suggesting that results are not directly interchangeable between methods. Surprisingly, smooth muscle cell contraction had opposing effects between the setups. Indeed, smooth muscle cell contraction increased arterial stiffness in the ROTSAC but decreased stiffness in the DynamX. These opposing effects could be attributed to how the two setups differentially load the collagen fibres in the arterial wall, ex vivo.

Conclusion: Overall, this study provided critical insights into how different experimental setups can influence the interpretation of aortic biomechanics, emphasizing the need for careful consideration and contextualization of results based on the methodology used.

Background: In this second section of our 2-part review on the role of physical activity (PA) and cardiorespiratory fitness (CRF) in preventing and treating atherosclerotic cardiovascular disease (CVD), we expand on topics covered in part 1, including a comparison of moderate-intensity continuous training versus high-intensity interval training, the beneficial role of PA and CRF in heart failure, potential mal-adaptations that may result from extreme endurance exercise regimens, and the incidence of cardiac arrest and sudden cardiac death during marathon running and triathlon participation. Further, we review the principles of exercise prescription for patients with known or suspected CVD, with specific reference to exercise modalities, contemporary guidelines, the minimum exercise training intensity to promote survival benefits, and long-term goal training intensities, based on age-, sex-, and fitness-adjusted targets. Finally, we provide practical "prescription pearls" for the clinician, including a simple rule to estimate metabolic equivalents (METs) during level and graded treadmill walking, research-based exercise training recommendations, using steps per day, MET-minutes per week, and personal activity intelligence to achieve beneficial treatment outcomes, as well as the heart rate index equation to estimate energy expenditure, expressed as METs, during recreational and leisure-time PA.

Summary: This review compares moderate-intensity continuous training and high-intensity interval training, examines the role of PA and CRF in managing heart failure, and discusses the cardiovascular risks associated with extreme endurance exercise. It also provides practical guidelines for exercise prescription tailored to patients with CVD, highlighting advanced exercise prescription strategies to optimize cardiovascular health.

Key messages: Physicians and healthcare providers should prioritize referring patients to home-based or medically supervised exercise programs to leverage the cardioprotective benefits of regular PA. For most inactive patients, an exercise prescription is essential for improving overall health.

Background: The cardioprotective benefits and prognostic significance of regular moderate-to-vigorous physical activity (PA), increased cardiorespiratory fitness (CRF), or both are often underappreciated by the medical community and the patients they serve. Individuals with low CRF are two to three times more likely to die prematurely from atherosclerotic cardiovascular disease (CVD), than their fitter counterparts when matched for risk factor profile or coronary artery calcium (CAC) score. Accordingly, part 1 of this 2-part review examines these relations and the potential underlying mechanisms of benefit (e.g., exercise preconditioning) on atherosclerotic CVD, with specific reference to gait speed and mortality, CRF and PA as separate risk factors, and the relation between CRF and/or PA on attenuating the adverse impact of an elevated CAC score, as well as potentially favorably modifying CAC morphology, and on incident atrial fibrillation, all-cause and cardiovascular mortality, and on sudden cardiac death (SCD).

Summary: We explore the underappreciated cardioprotective effects of regular PA and CRF. Part 1 examines how CRF and PA reduce the risk of premature death from atherosclerotic CVD by investigating their roles as separate risk factors, the potential underlying mechanisms of benefit, and their impact on gait speed, mortality, and atrial fibrillation. The review also addresses how CRF and PA may mitigate the adverse impact of an elevated CAC score, potentially modifying CAC morphology, and reduce the risk of SCD.

Key messages: Regular PA and high CRF are essential for reducing the risk of premature death from CVD and mitigating the negative impact of elevated CAC scores. Additionally, they provide significant protection against SCD and atrial fibrillation, emphasizing their broad cardioprotective effects.

Background: Hypereosinophilic syndrome is characterized by a peripheral blood eosinophil count >1.5 × 10³/μL on two different examinations within a month of each other and/or a 20% or higher percentage of eosinophils in a bone marrow section, associated with organ damage. Rarely, neurological manifestations may occur, even in the early stages. We report a case of idiopathic hypereosinophilic syndrome with Loeffler endocarditis presenting with multiple bilateral strokes and encephalopathy as the first clinical manifestations.

Summary: Hypereosinophilia and echocardiographic findings suggested a Loeffler's endocarditis. Blood hyperviscosity and small vessels inflammation induced by the hypereosinophilia itself, the embolization of intracardiac thrombus, along with the impaired clearance of microthrombi in the watershed areas, are the main mechanisms involved in the pathophysiology of stroke in the hypereosinophilic syndrome. Additionally, encephalopathy could be considered as a consequence of multiple cerebral infarcts and neurotoxicity induced by hypereosinophilia since our patient's confusion and aggressive behavior gradually remitted after steroid therapy was started.

Key messages: To the best of our knowledge, our case report is a rare instance highlighting neurological involvement as the earliest manifestation of hypereosinophilia. We aimed to elucidate the central nervous system involvement in this intriguing disorder, with the goal of encouraging clinicians to consider hypereosinophilic syndrome in the diagnostic assessment of rare stroke etiologies.