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A 49-year-old woman presented with bilateral coronary fistulas with multiple sites of drainage. She had been referred to hospital for evaluation of a cardiac murmur, and a coronary arteriogram revealed multiple coronary fistulas. One fistula originated from the proximal part of the left anterior descending coronary artery and connected to the main pulmonary artery. Three coronary artery fistulas arised from a conal branch of the right coronary artery and drained into the main pulmonary artery, the right atrium and the great cardiac vein. This is the first reported case of bilateral coronary fistulas with multiple sites of drainage. (Jpn Circ J 1998; 62: 783 - 784)

Baroreflex control of heart rate, pressor responses to alpha agonist (phenylephrine) and isometric exercise before and during salt loading were compared between 13 normotensive subjects with hypertensive relatives (group A) and 9 normotensive subjects with no family history of hypertension (group B). Baroreflex slope was significantly lower in group A than in group B (9.6 +/- 1.6 vs 17.6 +/- 1.9 msec/mmHg; p less than 0.01), although blood pressure, heart rate and aortic distensibility were not different between two groups. Pressor responses to phenylephrine and isometric exercise were identical for both groups. During salt loading, pressor responses to phenylephrine and isometric exercise were significantly greater in group A than in group B. Baroreflex slope was not affected by salt loading in the two groups. These results suggest that baroreflex control of heart rate is impaired in normotensive young subjects with hypertensive relatives and this defect may be inherited rather than the result of elevated arterial pressure and decreased aortic distensibility. Pressor responses to alpha agonist and isometric exercise during high-sodium diet were augmented in subjects with a family history of hypertension.

The effects of insulin on pressor responsiveness to alpha agonist (phenylephrine) and angiotensin II, and baroreflex function were studied in fifteen diabetic patients without autonomic neuropathy. The dose of phenylephrine required to increase systolic pressure by 25 mmHg (PD25) was significantly increased from 38 +/- 7 to 62 +/- 9 micrograms (p less than 0.05) after IV injection of 4 U of Actrapid monocomponent insulin. The dose of angiotensin II required to increase systolic pressure by 30 mmHg (AD30) was also increased from 0.29 +/- 0.07 to 0.48 +/- 0.10 micrograms (p less than 0.01). Following insulin administration, the dose-response curves for phenylephrine and angiotensin II were shifted to the right. The baroreflex sensitivity was not affected by insulin. In contrast, there was no significant change in PD25, AD30 or baroreflex sensitivity after the injection of saline. These results suggest that insulin attenuates the pressor responsiveness to alpha agonist and angiotensin II, which may be one of the significant mechanisms in insulin-induced vasodilation.