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      Exercise Training and Interventions for Coronary Artery Disease

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          Abstract

          Coronary artery disease (CAD) may be considered a main cause of mortality and the prevalence of CAD is increasing nowadays, leading to high health costs in many countries. Despite the fact of the regression of the atherosclerotic plaque, the decrease in blood viscosity and the growth of collateral vessels have been proposed as improvements that CAD patients may obtain under exercise performance. Thus, the present narrative review aimed to carry out a brief specific analysis of the results achieved when performing endurance, strength or inspiratory muscle training. Exercise attenuates certain pathophysiological processes of this disease, such as endothelial dysfunction or the vulnerability of atherosclerotic plaques, and produces improvements in functional capacity and muscle strength, among others. Within the different exercise modalities, the most important parameter to be considered seems to be the total caloric expenditure, and not so much the modality itself. As such, in cardiac rehabilitation, when prescribing exercise, we should possibly focus on the modality that obtains more adherence in patients. To conclude, it must be highlighted that total caloric expenditure is not being taken into account when comparing interventions and this relevant information should be considered in future studies.

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          Most cited references76

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          Pathophysiology of coronary artery disease.

          During the past decade, our understanding of the pathophysiology of coronary artery disease (CAD) has undergone a remarkable evolution. We review here how these advances have altered our concepts of and clinical approaches to both the chronic and acute phases of CAD. Previously considered a cholesterol storage disease, we currently view atherosclerosis as an inflammatory disorder. The appreciation of arterial remodeling (compensatory enlargement) has expanded attention beyond stenoses evident by angiography to encompass the biology of nonstenotic plaques. Revascularization effectively relieves ischemia, but we now recognize the need to attend to nonobstructive lesions as well. Aggressive management of modifiable risk factors reduces cardiovascular events and should accompany appropriate revascularization. We now recognize that disruption of plaques that may not produce critical stenoses causes many acute coronary syndromes (ACS). The disrupted plaque represents a "solid-state" stimulus to thrombosis. Alterations in circulating prothrombotic or antifibrinolytic mediators in the "fluid phase" of the blood can also predispose toward ACS. Recent results have established the multiplicity of "high-risk" plaques and the widespread nature of inflammation in patients prone to develop ACS. These findings challenge our traditional view of coronary atherosclerosis as a segmental or localized disease. Thus, treatment of ACS should involve 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid "stabilization" of other plaques that may produce recurrent events. The concept of "interventional cardiology" must expand beyond mechanical revascularization to embrace preventive interventions that forestall future events.
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            Exercise capacity and mortality among men referred for exercise testing.

            Exercise capacity is known to be an important prognostic factor in patients with cardiovascular disease, but it is uncertain whether it predicts mortality equally well among healthy persons. There is also uncertainty regarding the predictive power of exercise capacity relative to other clinical and exercise-test variables. We studied a total of 6213 consecutive men referred for treadmill exercise testing for clinical reasons during a mean (+/-SD) of 6.2+/-3.7 years of follow-up. Subjects were classified into two groups: 3679 had an abnormal exercise-test result or a history of cardiovascular disease, or both, and 2534 had a normal exercise-test result and no history of cardiovascular disease. Overall mortality was the end point. There were a total of 1256 deaths during the follow-up period, resulting in an average annual mortality of 2.6 percent. Men who died were older than those who survived and had a lower maximal heart rate, lower maximal systolic and diastolic blood pressure, and lower exercise capacity. After adjustment for age, the peak exercise capacity measured in metabolic equivalents (MET) was the strongest predictor of the risk of death among both normal subjects and those with cardiovascular disease. Absolute peak exercise capacity was a stronger predictor of the risk of death than the percentage of the age-predicted value achieved, and there was no interaction between the use or nonuse of beta-blockade and the predictive power of exercise capacity. Each 1-MET increase in exercise capacity conferred a 12 percent improvement in survival. Exercise capacity is a more powerful predictor of mortality among men than other established risk factors for cardiovascular disease.
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              Exercise standards for testing and training: a scientific statement from the American Heart Association.

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                Author and article information

                Contributors
                (View ORCID Profile)
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                Journal
                JCDDB4
                Journal of Cardiovascular Development and Disease
                JCDD
                MDPI AG
                2308-3425
                May 2022
                April 25 2022
                : 9
                : 5
                : 131
                Article
                10.3390/jcdd9050131
                35621842
                6d8a42cb-8684-4b51-b300-5bf853bcc708
                © 2022

                https://creativecommons.org/licenses/by/4.0/

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