Antonio B Fernandez1,2,3, Waseem Chaudhry4,5, Paul D Thompson4,5. 1. Division of Cardiology, Hartford Hospital, Hartford, CT, USA. antonio.fernandez@hhchealth.org. 2. University of Connecticut School of Medicine, Farmington, CT, USA. antonio.fernandez@hhchealth.org. 3. Athletes' Heart Program, Hartford Hospital, 80 Seymour Street, Hartford, CT, 06102, USA. antonio.fernandez@hhchealth.org. 4. Division of Cardiology, Hartford Hospital, Hartford, CT, USA. 5. University of Connecticut School of Medicine, Farmington, CT, USA.
Abstract
PURPOSE OF REVIEW: This manuscript reviews the data on the mechanisms and significance of atherosclerotic cardiovascular disease (ASCVD) in masters athletes. It describes recent advances in understanding the biological pathway for the development and progression of ASCVD in athletes. It also reviews salient clinical trials, guidelines on managing ASCVD in masters athletes, and future research directions. RECENT FINDINGS: Recent data have produced controversy as to whether high levels of physical activity and endurance training can promote ASCVD. Longstanding, vigorous endurance exercise may increase the development of calcified and non-calcified coronary plaques. There are no clinical trials to inform clinicians on how to manage masters athletes with occult ASCVD. We provide a review of the data on ASCVD in older athletes, the risks and benefits of exercise in active individuals with ASCVD, and our approach to evaluating and managing these patients. Vigorous physical exertion transiently increases the risk of acute coronary syndrome (ACS) and sudden cardiac death in patients with ASCVD. New research has demonstrated increases in both calcified and non-calcified plaque in athletes, although the dominant plaque type is usually calcific. The mechanisms mediating this possible increase in atherosclerosis in active individuals is uncertain, as is the prognostic implications of the increased atherosclerosis. The predominance of calcified plaque may indicate that coronary plaques in athletes are less prone to rupture and to produce acute coronary events. Some guidelines offer recommendations on the management of non-athletic patients with elevated CAC but data on athletes is scarce. Until additional studies are available, we suggest that athletes with CAC values > 100 Agatston units be managed as if they have preclinical ASCVD. They should be informed of the symptoms of angina and ACS and the importance of prompt medical attention should such symptoms occur. Serum calcium and parathyroid hormones levels should be measured to exclude hyperparathyroidism. Patients should undergo symptom-limited maximal exercise stress testing and aggressive lipid treatment to achieve low-density lipoprotein cholesterol (LDL-C) values < 70 mg/dl.
PURPOSE OF REVIEW: This manuscript reviews the data on the mechanisms and significance of atherosclerotic cardiovascular disease (ASCVD) in masters athletes. It describes recent advances in understanding the biological pathway for the development and progression of ASCVD in athletes. It also reviews salient clinical trials, guidelines on managing ASCVD in masters athletes, and future research directions. RECENT FINDINGS: Recent data have produced controversy as to whether high levels of physical activity and endurance training can promote ASCVD. Longstanding, vigorous endurance exercise may increase the development of calcified and non-calcified coronary plaques. There are no clinical trials to inform clinicians on how to manage masters athletes with occult ASCVD. We provide a review of the data on ASCVD in older athletes, the risks and benefits of exercise in active individuals with ASCVD, and our approach to evaluating and managing these patients. Vigorous physical exertion transiently increases the risk of acute coronary syndrome (ACS) and sudden cardiac death in patients with ASCVD. New research has demonstrated increases in both calcified and non-calcified plaque in athletes, although the dominant plaque type is usually calcific. The mechanisms mediating this possible increase in atherosclerosis in active individuals is uncertain, as is the prognostic implications of the increased atherosclerosis. The predominance of calcified plaque may indicate that coronary plaques in athletes are less prone to rupture and to produce acute coronary events. Some guidelines offer recommendations on the management of non-athletic patients with elevated CAC but data on athletes is scarce. Until additional studies are available, we suggest that athletes with CAC values > 100 Agatston units be managed as if they have preclinical ASCVD. They should be informed of the symptoms of angina and ACS and the importance of prompt medical attention should such symptoms occur. Serum calcium and parathyroid hormones levels should be measured to exclude hyperparathyroidism. Patients should undergo symptom-limited maximal exercise stress testing and aggressive lipid treatment to achieve low-density lipoprotein cholesterol (LDL-C) values < 70 mg/dl.
Authors: Adam Hartley; Matthew Shun-Shin; Mikhail Caga-Anan; Christopher Rajkumar; Alexandra N Nowbar; Michael Foley; Darrel P Francis; Dorian O Haskard; Ramzi Y Khamis; Rasha K Al-Lamee Journal: Front Cardiovasc Med Date: 2021-10-11