Repeated sauna treatment improves impaired vascular endothelial function in the setting of coronary risk factors, suggesting a therapeutic role for sauna treatment in patients with risk factors for atherosclerosis.
actor VII (FVII) is the first enzyme in the extrinsic pathway of the blood coagulation system. Activation of the extrinsic coagulation pathway plays a key role in hemostasis, 1 and thus FVII contributes to the occurrence of thrombotic events. Although most FVII circulates in plasma in the zymogen form, small but significant amounts of activated FVII (FVIIa) also are present, and appear to serve as a primer for triggering the extrinsic cascade. [2][3][4][5] The Northwick Park Heart Study suggested that FVII coagulant activity is independently associated with risk of coronary events in middle-aged men, 6,7 and several additional studies have linked elevated concentrations of FVII in plasma to coronary heart disease. [8][9][10][11][12][13][14] Thus, FVII has become recognized as a hemostatic coronary risk factor.Plasma FVII concentrations are influenced by both genetic and environmental factors. Green et al reported a strong association between a common polymorphism in exon 8 of the FVII gene (R353Q polymorphism) and plasma FVII, 15 which has been confirmed by several other studies, 8,9,[16][17][18][19][20][21][22][23] especially with respect to FVIIa. 24 However, the association between R353Q polymorphism of the FVII gene and myocardial infarction (MI) remains controversial. The contribution of the coagulation system to the pathogenesis of MI can be studied most readily in patients with premature MI, who have less atherosclerotic coronary stenosis than elderly patients. [25][26][27][28] We performed a case -control study to determine whether plasma FVIIa concentrations and R353Q polymorphism are associated with risk of premature MI.
Methods
Study PopulationWe investigated 129 consecutive Japanese male patients treated as outpatients at Kagoshima Coronary Care Unit Network (2000)(2001)(2002)(2003), with a first MI occurring before the age of 45 years (mean ± SD, 40.4±4.5 years old) and giving informed consent. We angiographically confirmed occlusion or significant stenosis of a coronary artery in all patients. Of the 129 patients, 2 patients, one had Kawasaki disease and another had a coronary artery anomaly, were excluded. The remaining 127 patients (premature MI patients) had a mean age of 43.9±5.1 years at study entry, 3.3±3.8 years after initial MI. Coronary angiography showed single-vessel disease in 93 (73.2%), and multivessel disease in 34 (26.8%). Oral anticoagulant agents were administered to 33 patients. Control subjects were 150 consecutive age-matched healthy Japanese men (43.8±5.1 years old at entry), who underwent a medical checkup at Kagoshima Prefectural Comprehensive Health Center and
Prinzmetal's variant of angina occurred in a 48-year-old man who sustained two attacks of subarachnoid hemorrhage within 10 days. The first anginal pain started at the same time that the second cerebrovascular accident developed, but subsequent anginal episodes were not accompanied by other symptoms or signs that indicated new development of subarachnoid hemorrhage. Twelve days later, when nuchal rigidity was fairly improved, the episodes of chest pain ended. A vasospasm of the large coronary arteries--probably due to the derangement of the autonomic nervous system caused by subarachnoid hemorrhage--was presumed to contribute to the occurrence of the variant angina. Based on this case and on review of the literature, we propose that coronary arterial spasm is one of several causes of the cardiac changes seen in subarachnoid hemorrhage.
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