Exercise Physiology in the Cath Lab: Still Alive and Well!
Mount Sinai Medical Center, New York, NY.Circulation (Impact Factor: 14.43). 11/2012; 126(22). DOI: 10.1161/CIRCULATIONAHA.112.146662
Writing on the topic of 'pectoris dolor': "With respect to the treatment of this complaint, I have little or nothing to advance: nor indeed is it to be expected we should have made much progress in the cure of a disease, which has hitherto hardly had a place, or a name in medical books... Opium taken at bed-time will prevent the attacks at night. I know one who set himself a task of sawing wood for half an hour every day, and was nearly cured."(1) The salient observation defining the clinical syndrome of 'warm-up' angina, namely that anginal symptoms may be reduced with repeated episodes of work, was initially made over 200 years ago by the London physician William Heberden. Consistent with his original description, contemporary demonstrations of warm-up angina either involves greater time to ischemic signs or symptoms (i.e. ST segment depression or chest pain) or a reduction in ischemic manifestations at equivalent work load in patients with coronary artery disease (CAD) undergoing repeated bouts of exercise. Multiple theories have been advanced to explain this physiologic phenomenon, ranging from changes in myocardial signaling to increased collateral recruitment and ischemic preconditioning.(2-4) Greater appreciation of physiologic adaptations occurring with exercise vis a vis ventricular vascular coupling combined with novel methodologic approaches have provided fresh mechanistic insight and advanced our understanding of this clinical entity.(5-7).
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