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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.

Introduction: Central aortic pressure waveform analyses can provide clinically relevant information beyond conventional brachial blood pressure (BP) assessment. This waveform can be reproduced noninvasively through application of a generalized transfer function (GTF) on a peripheral waveform, as conventionally performed by applanation tonometry. Photoplethysmography (PPG) is an alternate approach; however, differences in measurement site and modality demand the use of a transfer function (TF) specific for those differences. This study aimed to compare central aortic waveform features generated from radial tonometry (reference) using a proprietary GTF with a central aortic waveform and its features generated from a simultaneous fingertip PPG measurement using a selective method where one of three different TFs is chosen based on the input signal harmonic profile.

Methods: Brachial BP was measured in triplicate under resting conditions and was used for subsequent calibration. Multiple simultaneous radial tonometry (SphygmoCor CVMS) and fingertip PPG measurements were then performed in individual participants (n = 21, 10 females, age: 39 ± 16 years). Measurements were converted into central aortic waveforms with their respective TFs. Twenty central aortic pressure waveform parameters were compared through correlation analysis, Bland-Altman plots, and a repeated measure mixed-effects ANOVA model. Central aortic waveform shape was compared using the root-mean-squared error (RMSE).

Results: Correlation (r) of PPG-derived parameters with radially tonometry-derived central aortic parameters was high ranging from 0.79 to 0.99. Mean differences of pressure-related parameters were within 1.3 mm Hg, and differences of time-related parameters ranged from -2.2 to 3.4%. While some parameters were statistically different, these differences are not physiologically meaningful. Central aortic waveform shape had an average RMSE of 1.8 ± 0.9%.

Conclusion: Fingertip PPG-derived central aortic waveform parameters using a novel selective TF were comparable to central aortic waveform features derived from radial tonometry using a previously validated GTF.

Background: Enhanced regenerative therapeutic strategies are required to treat intractable ischemic heart disease.

Summary: Since the discovery of putative endothelial progenitor cells (EPCs) in 1997, many studies have focused on their extraction, ex vivo processing, and autotransplantation under ischemic conditions. Nonetheless, numerous randomized clinical trials involving thousands of patients have yielded only marginal treatment effects, highlighting the need for advances regarding insufficient dosage and complex ex vivo processing. The prevailing paradigm of cellular differentiation highlights the potential of direct cellular reprogramming, which paves the way for in situ reprogramming. In situ reprogramming holds the promise of significantly enhancing current therapeutic strategies, yet its success hinges on the precise targeting of candidate cells for reprogramming. In this context, the spleen emerges as a pivotal "in situ reprogramming hub," owing to its dual function as both a principal site for nanoparticle distribution and a significant reservoir of putative EPCs. The in situ reprogramming of splenic EPCs offers a potential solution to overcome critical challenges, including the aforementioned insufficient dosage and complex ex vivo processing.

Key messages: This review explores the latest advancements in EPC therapy and in situ reprogramming, spotlighting a pioneering study that integrates those two strategies with a specific focus on the spleen. Such an innovative approach will potentially herald a new era of regenerative therapy for ischemic heart disease.

Background: Despite advancements in coronary artery disease (CAD) treatment with drug-eluting stent, its morbidity and mortality remain high. In context, intravascular imaging-guided percutaneous coronary intervention (PCI) is increasingly recommended for better clinical outcomes in patient with CAD. Near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS), as one of the intravascular imaging methods, is effective in detecting lipid-rich plaques, which is crucial for identifying high-risk or vulnerable plaques employing near-infrared light. High lipid core burden, as identified by NIRS-IVUS, correlates with an increased risk of adverse cardiac events and shows varying degrees of efficacy in plaque management and event prevention.

Summary: This article addresses about how NIRS-IVUS can be used to predict event of CAD. The study highlights the crucial role of NIRS-IVUS in predicting future cardiovascular events. Findings indicate that the presence of high lipid core burden is related to increased risks of periprocedural myocardial infarction and reduced coronary flow during PCI. The study also outlines the predictive value of NIRS-IVUS in non-culprit lesions, where plaques with high lipid core burden significantly increase the occurrence of major adverse cardiac events as demonstrated in the PROSPECT II trial. In terms of therapeutic strategies, the study reviews the effectiveness of high-intensity lipid-lowering strategies in stabilizing vulnerable plaques, as evidenced in trials such as the YELLOW and PACMAN AMI trials.

Key messages: NIRS-IVUS emerges as a valuable diagnostic tool in treating CAD. It effectively identifies vulnerable plaques and aids in predicting and preventing future adverse cardiac events. However, to enhance its practicality and promote widespread adoption in clinical settings, further long-term outcome research of NIRS-IVUS-guided PCI is necessary. These efforts can potentially make NIRS-IVUS a more accessible and indispensable tool in cardiovascular disease management.

Background: Genetic variants causing diseases with hypertension as a secondary feature have previously been identified. Studies focussing on primary hypertension have utilised common and latterly rare genetic variants in attempts to elucidate the genetic contribution to the risk of primary hypertension.

Summary: Using genome-wide association studies (GWASs), associations of hypertension with hundreds of common genetic variants have been reported, implicating thousands of genes. Individual variants have small effect sizes and cumulatively account for around 6% of genetic risk. The common variant signal is enriched for relevant tissues and physiological processes, while some variants are associated with traits expected to have secondary impacts on hypertension risk, such as fruit intake, BMI, or time watching television. Studies using rare variants obtained from exome sequence data have implicated a small number of genes for which impaired function has moderate effects on blood pressure and/or hypertension risk. Notably, genetic variants which impair elements of guanylate cyclase activation, stimulated by either natriuretic hormones or nitric oxide, increase hypertension risk. Conversely, variants impairing dopamine beta-hydroxylase or renin production are associated with lower blood pressure. Variants for which a definite effect can be designated remain cumulatively extremely rare and again make only a small contribution to overall genetic risk. Although these results are of interest, it is not clear that they provide radical new insights or identify drug targets which were not previously known. Nor does it seem that genetic testing could be useful in terms of quantifying disease risk or guiding treatment.

Key messages: Research has increased our knowledge about the relationship between naturally occurring genetic variation and risk of hypertension. Although some results serve to confirm our understanding of underlying physiology, their value in terms of potentially leading to practical advances in the management of hypertension appears questionable.