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Biomedical subjects

W J Rowe

Publications and source records attributed to W J Rowe.

9 recordsLinked to original sources
PubMed1997

Interplanetary travel and permanent injury to normal heart.

This hypothesis is that some crewmen on prolonged space flights may develop permanent myocardial injury despite the absence of coronary atherosclerosis and even without the hazards of radiation beyond orbit. This may resuIt from atrophy of skeletal muscle and bone resulting in magnesium ion deficiency predisposing to a vicious cycle with catecholamine elevations, with the latter aggravated by stress, dehydration-provoked angiotensin elevations, unremitting endurance exercise, and in turn a second vicious cycle with severe ischemia. Toxic free radicals can develop complicating ischemia and potential high radiation, with magnesium ion deficiency and high vascular catecholamines playing contributing roles. These free radicals may lead to inactivation of endothelium-derived relaxing factor (EDRF) causing coronary endothelial injury by a third vicious cycle, increased peripheral resistance and coronary vasospasm intensifying ischemia. Local and systemic thrombogenesis could contribute ultimately to focal fibrosis of the myocardium, if the ischemia is not recognized. Sufficient magnesium and time for repair are vital.

Aerospace Medicine↗
PubMed1997

Transient right but not left ventricular dysfunction after strenuous exercise at high altitude.

OBJECTIVES: We sought to evaluate whether prolonged exercise in ultramarathon runners results in left ventricular (LV) damage. BACKGROUND: Strenuous exercise has been reported to cause LV damage. METHODS: Fourteen runners who completed an ultramarathon at high altitude underwent echocardiography, finger-tip oximetry and blood measurements of cardiac troponin I (cTnI) and creatine kinase, MB fraction (CK-MB) levels before, immediately after and 1 day after the race. RESULTS: At baseline, the echocardiograms showed normal LV and right ventricular (RV) size and function in all subjects, as well as mild tricuspid regurgitation in nine subjects, with normal estimated pulmonary artery systolic pressure (mean 28 mm Hg). At baseline, all oxymetric readings and CK-MB measurements were normal, and cTnI was undetectable. Immediately after the race, the echocardiograms showed the expected augmentation of global and segmental LV function in all subjects. Although the RV was normal in nine subjects, five developed marked RV dilation and hypokinesia, paradoxic septal motion, pulmonary hypertension and wheezing. CK-MB values were elevated in all subjects. In all but one subject cTnI was undetectable. In that subject there was a small elevation in cTnI accompanied by severe RV dysfunction and pulmonary hypertension. At the 1-day follow-up study, the echocardiographic measurements had normalized in all subjects. CONCLUSIONS: In trained athletes, strenuous exercise at high altitude did not result in LV damage. However, wheezing, reversible pulmonary hypertension and RV dysfunction occurred in a third of those completing the race. The incidence and pathogenesis of these findings remain to be determined.

Adult↗
PubMed1992

Extraordinary unremitting endurance exercise and permanent injury to normal heart.

This hypothesis is that permanent cardiac injury could develop in some endurance athletes despite the absence of coronary atherosclerosis and ventricular hypertrophy. The proposed mechanism by which this injury could arise involves two physiological "vicious cycles". The first vicious cycle would occur between severe ischaemia and high catecholamines, the second would be between coronary vasospasm (induced by high catecholamines) and endothelial injury. The likelihood of the injury becoming permanent might increase if there is insufficient time between bouts of endurance exercise for regression of ischaemia and endothelial repair. Furthermore, magnesium ion deficiency, which can be induced by exercise, could exacerbate these vicious cycles and also contribute to catecholamine-induced thrombogenesis. In addition to ischaemia, there are several mechanisms, including the effect of free fatty acids liberated by the lipolytic effect of high catecholamines, that could cause direct myocardial injury.

Catecholamines↗
PubMed1991

A world record marathon runner with silent ischemia without coronary atherosclerosis.

A 62-year-old world record marathon runner was found to have silent ischemia manifested by a very abnormal stress test, whereas at autopsy nine months later, there was virtually no coronary atherosclerosis nor other disease of the coronary microvasculature. However, there was focal fibrosis of the papillary muscles consistent with remote ischemia secondary to possible CV. It is postulated that endurance-related high catecholamine levels might have been responsible.

Catecholamines↗