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Purpose: Coronavirus disease-2019 (COVID-19) affects the cardiovascular system even after the acute phase of the disease. Cardiopulmonary rehabilitation may improve post-COVID-19 symptoms. This study aims to evaluate the impact of a cardiopulmonary rehabilitation program after acute COVID-19 on arterial stiffness, left ventricular function, and ventriculoarterial coupling (VAC)., Methods: Forty-eight adults were examined 1 (T0) and 3-mo (T1) following recovery from COVID-19 and randomized 1:1 to participate or not in a 3-mo rehabilitation program. Matched subjects were enrolled as a non-COVID-19 group. Arterial stiffness was evaluated by carotid-femoral pulse wave velocity (PWV). Left ventricular (LV) systolic performance was evaluated with global longitudinal strain (GLS). The PWV/LV-GLS ratio was calculated as an index of VAC. High-sensitivity C reactive protein (hs-CRP) was measured., Results: At T0, convalescent patients with COVID-19 had impaired PWV ( P = .001) and reduced VAC ( P = .001) compared to non-COVID-19 subjects. PWV (8.15 ± 1.37 to 6.55 ± 0.98 m/sec, P < .001) and LV-GLS (-19.67 ± 1.98 to -21.3 ± 1.93%, P < .001) improved only in convalescent patients with COVID-19 undergoing rehabilitation. Similarly, VAC was only improved in the rehabilitation group (-0.42 ± 0.11 to -0.31 ± 0.06 m · sec -1  ·% -1 , P < .001). A significant improvement in VO 2max was noted after rehabilitation (15.70 [13.05, 21.45] to 18.30 [13.95, 23.75] ml · kg -1  · min -1 , P = .01). Finally, hs-CRP was improved in both groups with a significantly greater improvement in the rehabilitation group., Conclusion: A 3-mo rehabilitation program in convalesced patients with COVID-19 enhances the recovery of arterial stiffness, left ventricular function, and VAC, highlighting the beneficial mechanisms of rehabilitation in this patient population., Competing Interests: All authors declare no conflicts of interest., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Hypertension is a modifiable cardiovascular risk factor and displays a rapidly growing incidence due to aging and the acquisition of an unhealthy lifestyle. Hypertension is linked to the development of target organ damage in several vascular beds such as coronary arteries, peripheral, cerebral, and renal arteries. Besides, along with the presence of other cardiovascular risk factors, it aggravates vascular dysfunction due to the aging process. The mechanisms of vascular dysfunction in hypertension are complex and involve excessive salt intake and water retention, activation of neurohormonal systems, induction of endothelial dysfunction of large arteries and microcirculation, development of arterial stiffness, and complex interactions with cellular pathways of inflammation, oxidative stress, and thrombosis. The extent of vascular dysfunction in patients with hypertension can be assessed by evaluating endothelial function, measuring arterial stiffness, and testing the levels of circulating biomarkers of oxidative stress, pro-inflammatory cytokines, and thrombosis. Assessing these markers in subjects with and without hypertension could aid in identifying those at risk of vascular damage and improving risk prediction for future cardiovascular events. While several lifestyle and pharmacological therapies have shown promise in addressing vascular dysfunction in hypertension, none of these biomarkers have been established as an independent risk factor or treatment target. Therefore, in this article, we review the literature on the evidence that exists regarding the role of vascular dysfunction in the pathophysiology, diagnosis, progression, and treatment of hypertension, highlighting the lack of conclusive evidence in this field., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Coronary artery disease exhibits growing mortality and morbidity worldwide despite the advances in pharmacotherapy and coronary intervention. Coronary artery disease is classified in the acute coronary syndromes and chronic coronary syndromes according to the most recent guidelines of the European Society of Cardiology. Antithrombotic treatment is the cornerstone of therapy in coronary artery disease due to the involvement of atherothrombosis in the pathophysiology of the disease. Administration of antiplatelet agents, anticoagulants and fibrinolytics reduce ischemic risk, which is amplified early post-acute coronary syndromes or post percutaneous coronary intervention; though, antithrombotic treatment increases the risk for bleeding. The balance between ischemic and bleeding risk is difficult to achieve and is affected by patient characteristics, procedural parameters, concomitant medications and pharmacologic characteristics of the antithrombotic agents. Several pharmacological strategies have been evaluated in patients with coronary artery disease, such as the effectiveness and safety of antithrombotic agents, optimal dual antiplatelet treatment schemes and duration, aspirin de-escalation strategies of dual antiplatelet regimens, dual inhibition pathway strategies as well as triple antithrombotic therapy. Future studies are needed in order to investigate the gaps in our knowledge, including special populations., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)