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The authors report the increased incidence of patients with deep negative T waves without Q wave after the Great Hanshin Earthquake of 1995. Subjects underwent cardiac metaiodobenzyl guanidine (123I-MIBG) imaging, 201Tl scintigraphy, and coronary angiography. Among 2,756 inpatients of the preceding 5-year period, 33 (1.2%) showed the deep negative T waves, whereas 6 of 94 (6.4%; P < 0.001) showed it after the earthquake. Four of six patients had an episode of chest pain. Cardiac metaiodobenzyl guanidine imaging revealed the extent defects in all six patients despite a minimal change of 201Tl image. In addition, cardiac metaiodobenzyl guanidine imaging washout rate was hastened not only in the defect area but also in the nondefect area, which suggested augmented sympathetic activation. Natural disasters can affect the frequency of deep negative T waves, which relate abnormal cardiac sympathetic imaging.

itric oxide (NO) is an important modulator of biological function in physiologic and pathologic states. It exerts blood flow regulation, blood pressure control, platelet aggregation and vascular remodeling. 1-3 Congestive heart failure (CHF) is characterized by peripheral circulatory failure caused by cardiac pump dysfunction and/or excessive vasoconstrictive stimuli despite augmented vasodilating factors. 4 It is well known that the vasodilation to endothelium-dependent vasodilating stimuli is blunted in CHF. Insufficient endotheliumderived vasodilating reserve, however, can be caused by diminished NO release or increased basal NO production, which is an issue in CHF. [5][6][7][8][9] A recent study demonstrated that endogenous NO is detectable in the range of parts per billion (ppb) in the exhaled air of animals and humans. 10 Exercise enhances exhaled NO output in healthy subjects [11][12][13][14][15][16] and it is suspected that this exercise-induced elevation in exhaled NO is linked to cardiovascular activation during exercise. Oxygen kinetics determined at the onset of exercise (ie, oxygen deficit and time constant for oxygen uptake (V • O2) increment) are a marker of cardiac output response 17 and are characteristically impaired in patients with CHF. [17][18][19][20] One can hypothesize that abnormal endothelial function may be linked to abnormal blood flow response and abnor-

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