These findings suggested that neither abnormalities in the coronary circulation nor acute myocarditis was related to the etiology. Although neurogenic stunned myocardium induced by emotional or physical stress was suggested as the etiology, further investigations are necessary.

Left ventriculography with simultaneous pressure micromanometry was performed in 11 normal control subjects and 17 patients with dilated cardiomyopathy (DCM). Left ventricular silhouettes in the right anterior oblique projection were divided into eight areas, and regional wall stress was computed by Janz's method in each area excluding the two most basal areas. Wall stress was higher in DCM patients than in control subjects (p<0.01). The percent area changes from end diastole to end systole in each area were lower in DCM patients than in control subjects (mean for six areas, 22+14% versus 54±9%o, respectively, p <0.01), but the coefficient of variation for the percent area changes in the six areas of the left ventricle in DCM patients was greater than that in control subjects (32±17% versus 15±4%, respectively, p<0.01), indicating regional differences in hypokinesis. There was a significant negative correlation between end-systolic regional wall stress and percent area change (r=-0.60 to -0.86, p<0.05) in each area. Thus, excessive regional afterload may play an important role in causing regional hypokinesis in DCM. (Circulation 1990;82:2075-2083 iffuse hypokinesis of the left ventricular wall D motion has been reported in patients with dilated cardiomyopathy (DCM).' However, recent studies on DCM with the use of left ventricular cineangiography2-5or radionuclide ventriculography6,7 suggest that left ventricular wall motion is not always diffusely hypokinetic and that regional differences in the degree of hypokinesis are frequently present. In clinical settings, patients with segmental wall motion abnormality may have better global left ventricular function and better prognosis than patients with diffuse wall motion abnormality.6 Thus, the importance of estimating left ventricular regional wall dynamics in patients with DCM has been emphasized.3-7

These data suggest that 1) ST re-elevation at reperfusion is a sign of limited myocardial salvage by thrombolysis, and 2) high ST elevation and TIMI grade 0 flow without good collateral flow before thrombolysis may be predictive variables for marked myocardial necrosis after reperfusion.

A 77-year-old Japanese female developed Churg-Strauss syndrome (CSS), showing fever and numbness in bilateral hands. She was being treated for bronchial asthma with combination inhalant of corticosteroid with beta(2)-agonist, and an oral leukotriene receptor antagonist (LTRA), montelukast, for 15 months. She presented fever up to 38°C with microscopic hematuria and proteinuria, serum creatinine level of 0.7 mg/dl, and C-reactive protein of 11 mg/dl. After referral to our hospital, eosinophilia and high myeloperoxidase (MPO)-antineutrophil cytoplasmic antibody (ANCA) level were observed together with hematuria and proteinuria; renal biopsy examination was performed to clarify the disorder. Renal biopsy specimens showed necrotizing crescent formation, severe granulomatous angiitis in an interlobular artery, and interstitial eosinophilic infiltration. It was noted that nearly intact glomeruli were infiltrated with eosinophils. After treatment with oral prednisolone at initial dose of 40 mg (1 mg/kg body weight), urinary findings rapidly became normal with mild elevation of serum creatinine to 1.5 mg/dl and trace level of serum C-reactive protein in 1 month. Because she was previously treated with montelukast without oral corticosteroid, linkage between CSS and LTRA was highly suspected.

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