Diastolic mitral regurgitation (MR) is known to be induced by prolonging atrioventricular (AV) delay in patients implanted with a DDD pacemaker. We studied the relationship between diastolic MR and PQ intervals on cardiac function in 50 patients (71.3 +/- 11.3 years old: mean +/- SD), who had been implanted with DDD pacemakers. In 19 patients, prior to pacemaker implantation, pulmonary capillary wedge pressure (PCWP) was measured using a Swan-Ganz catheter during AV sequential pacing with an AV delay of 0.165 seconds. Transmitral blood flow was measured with pulsed Doppler echocardiography, while prolonging AV delay stepwise by 0.025 seconds from 0.065 seconds for about 5 minutes each. In nine patients, AV delay could not be prolonged enough due to occurrence of intrinsic AV conduction. In the other 41 patients, diastolic MR was induced by prolonging AV delay. The critical PQ intervals that induced diastolic MR ranged from 0.14 to 0.26 (0.23 +/- 0.03) seconds. Four of five patients whose critical PQ intervals were 0.20 seconds or shorter had heart failure, while 36 patients whose critical PQ intervals were greater than 0.20 seconds were free from signs and symptoms of heart failure. Their PCWPs were 2-27 (7.5 +/- 5.1) mmHg. There was a significant negative correlation between the critical PQ intervals for the appearance of diastolic MR and PCWP during AV sequential pacing, which was performed prior to pacemaker implantation (r = -0.85, P less than 0.001). It is suggested that the appearance of diastolic MR is determined mainly by PQ intervals and cardiac function.(ABSTRACT TRUNCATED AT 250 WORDS)

A 24-year-old woman with Takayasu's disease developed unstable angina pectoris. Angiographic studies demonstrated an isolated left coronary ostial stenosis without any other systemic arterial involvement. She is unique in that the coronary lesion, which is rarely the major manifestation of Takayasu's disease, is the sole arterial involvement of the disease.

Female adult rabbits with coaxial bipolar electrodes chronically implanted in the brain were used. Evoked potentials (EVPs) were recorded in the medial basal hypothalamus (MBH) including the median eminence and the arcuate nucleus in response to stimulation of the dorsal hippocampus, medial amygdala and preoptic area. In the present experiment, the influence of ovulation-blocking drugs (pentobarbital, atropine and chlorpromazine) upon those EVPs was investigated. Since short-latency responses (less than 4.5 msec), which were not consistently observed in those EVPs, were resistent to pentobarbital, they may be considered to be involved in the direct or pauci-neuronal pathways. These pathways were also not depressed in the excitability by atropine and chlorpromazine. The efferent multi-neuronal pathways from the hippocampus to the MBH were influenced in different ways by pentobarbital, atropine and chlorpromazine, but the efferent multi-neuronal pathways from the amygdala to the MBH were depressed in the excitability by them. On the other hand, the EVPs elicited by preoptic stimulation was hardly affected by those drugs. These findings may suggest that the excitability of the neuronal pathways from the preoptic area to the MBH may be maintained against those agents. In other words, pentobarbital, atropine and chlorpromazine differ in the manner of action upon the neural mechanism, in spite of their inhibitory effect upon ovulation. The peak-latency of EVPs was scarcely influenced by those ovulation-blocking agents. Finally, it is discussed that the multi-neuronal pathways could be concerned with the neural mechanism of copulatory ovulation and that the direct or pauci-neuronal pathways concerned with the electrically stimulated ovulation.

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