As compared with echocardiographic parameters of LA size and LA function, AEMI appears to be more useful for identifying PAF patients. AEMI may enable to detect high risk PAF patients, especially those categorized into low risk by CHADS2 score.
A 47-year-old woman with normotensive primary aldosteronism is reported. In this case, hypopotassemia was found, but the patient's blood pressure was within the normal range. Her condition was diagnosed as primary aldosteronism without hypertension, which is very rare, based on an increased level of plasma aldosterone concentration, low plasma renin activity, and a typical finding of aldosterone-producing adenoma by adrenal scintigraphy. In the present case, similar values for urinary volume, renal function, plasma aldosterone concentration, plasma renin activity, plasma volume, total exchangeable sodium, urinary kallikrein excretion and a similar weight of the resected adenoma, but a shorter duration between the onset of symptom and hospital admission were observed as compared with those in 13 previously experienced cases of primary aldosteronism with hypertension. Thus, a shorter duration of primary aldosteronism appears to be an important factor in explaining the mechanism of normotension. However, we were unable to reach a definite conclusion and this is only a hypothesis. Further investigation will be required to clarify the mechanism of normotension in primary aldosteronism.
In both low and normal renin essential hypertensive groups, urinary excretion of kallikrein quantity by direct radioimmunoassay and activity by kininogenase assay were significantly lower than those in normal subjects. In comparing between normal and low renin groups, no difference was found in kallikrein quantity, while kallikrein activity tended to be lower in the low renin group than in the normal renin group. A significant positive correlation was observed between kallikrein quantity and activity in the normal subjects, the normal renin group and the low renin group. However, the slope of the regression line in the low renin group was significantly more moderate than that in the normal renin group, and tended to be more moderate than that in normal subjects. The addition of kallikrein inhibitors (aprotinin and gabexate mesilate) resulted in a significant suppression of enzymatic activity but not of enzyme quantity. These findings suggest that suppression of the renal kallikrein system in both groups of essential hypertension was confirmed by the decreased excretion of kallikrein both as enzyme quantity and activity, and that in the mechanism of the suppression of urinary kallikrein activity in the low renin group, the renal kallikrein inhibitors may play some role.
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