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• W2413049892 abstract "Various physiologic (1–3) and pharmacologic (4–6) interventions that produce changes in coronary blood flow are used in the detection of coronary artery disease (CAD), often in conjunction with myocardial perfusion imaging. Many of these techniques were devised to help provide objective evaluations of patients who are unable to complete a full exercise test. When pharmacologic agents such as dipyridamole (4,5) and adenosine (6) became routinely available, other forms of nonexercise stress testing became less popular. Although pharmacologic stress testing with myocardial perfusion imaging was primarily developed to detect regional disparities in coronary blood flow, stressinduced perfusion defects have prognostic value as well (7,8). CAD patients with pharmacologically induced perfusion defects have an increased incidence of cardiac events, including nonfatal myocardial infarction and death, that is independent of other symptoms or signs of myocardial ischemia. Given this background, the article by Giannetti et al (9) in this issue of The Green Journal that examines myocardial perfusion imaging in conjunction with sauna bathing presents some novel information. Although it is highly unlikely that these authors would recommend sauna bathing stress testing as an alternative to traditional nonexercise testing, the physiologic concept of this protocol is similar to the physiologic or pharmacologic agents (vasodilators or catecholamine analogs) that have been used. The authors evaluated the potential risk of sauna bathing in a group of patients with mild to moderate CAD. They began with the hypothesis that the thermal exposure involved with the sauna would provoke myocardial ischemia in a fashion similar to standard exercise testing. Previous reports (10 –12) of the physiologic effects of sauna bathing have reported a rise in heart rate, catecholamine levels, and occasionally blood pressure that could lead to an increase in myocardial oxygen demand. This would be a stimulant to increasing coronary blood flow, which in the presence of significant coronary stenoses could result in stress-induced myocardial perfusion defects analogous to those associated with exercise. It is also pertinent to know what, if any, medical risk might apply to CAD patients who undergo such recreational activity. The limitation in patient selection to those with mild to moderate anginal symptoms—excluding those with more severe symptoms of heart failure, unstable angina or class III angina, or recent myocardial infarction—was appropriately prudent. The question is how to advise patients with chronic stable CAD about the risk of sauna bathing. The clinical protocol that randomly assigned the order of testing and objectively quantitated the perfusion scan results was admirable. This design results in a study that is as unbiased and objective as possible. In addition, because the study was limited to patients with exerciseinduced transient perfusion defects, we can directly compare the sauna bathing perfusion results with those of the more familiar standard treadmill testing. Given this design, we can conclude that sauna bathing produces a disparity in regional myocardial blood flow that is similar in anatomic location to that associated with dynamic exercise testing, but that is smaller and less severe. In addition, there were no symptoms of angina or diagnostic S-T segment changes during sauna bathing, in contrast to the signs and symptoms of ischemia during routine exercise testing. What does this mean? We know that increased demand for myocardial oxygen consumption is a strong stimulus for increasing coronary blood flow. Increases in heart rate, blood pressure, and myocardial contractility all result in greater demand for myocardial oxygen. During sauna bathing, there was a significant increase in heart rate of 132% 6 20% and a relatively small decrease of 13% 6 67% in systolic blood pressure. Thus, the rate-pressure product increased by 14% 6 21%, which was in the same direction as the ratepressure change noted during exercise (1190% 6 40%), but much less intense. The hemodynamic changes associated with sauna bathing are similar to changes during pharmacologic stress testing utilizing dipyridamole (13) or adenosine (14). Both vasodilation and exercise testing typically result in tachycardia, but systolic blood pressure usually increases during exercise and decreases during vasodilation. Therefore, these hemodynamic changes during sauna bathing can be physiologically explained by the peripheral vasodilation of thermal stress and the endogenous release of catecholamines (10 –12). Given these types of physiologic and hemodynamic changes, it is understandable that myocardial perfusion studies during a sauna bath would be similar to full exercise testing, but not as severely abnormal. The increase in oxygen demand as evaluated by the double product is much greater with treadmill testing, and the vasodilaAm J Med. 1999;107:290 –292. From the Department of Radiology, Division of Nuclear Medicine, University of Massachusetts Memorial Medical Center, Worcester, Massachusetts. Requests for reprints should be addressed to Jeffrey A. Leppo, MD, Division of Nuclear Medicine, Department of Radiology, University of Massachusetts Memorial Medical Center, 55 Lake Avenue North, Worcester, Massachusetts 01655-0243." @default.
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• W2413049892 date "1999-09-01" @default.
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• W2413049892 doi "https://doi.org/10.1016/s0002-9343(99)00230-2" @default.
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