Neurally mediated syncope and cardiac beta-adrenergic receptor function.

To evaluate the mechanism of neurally mediated syncope (NMS), we investigated basal autonomic nerve function using a conventional pharmacological method and [123I]-metaiodobenzyl-guanidine (MIBG) single photon emission computed tomography (SPECT). Nine patients with NMS, whose syncope was induced by head-up tilt test with or without isoproterenol, underwent [123I]-MIBG SPECT. Eight of nine NMS patients showed reduced myocardial uptake (two patients, diffuse; four patients, anteroseptal and inferior; one patient, anteroseptal; one patient, inferior). In the study of pharmacological autonomic nervous function test, atropine sulfate (atr.) (0.04 mg/kg), isoproterenol (isp.) (5 x 10(-3) microg/kg/min), propranolol (prop.) (0.2 mg/kg), phenylephrine (phenyl.) (0.4 microg/kg/min), and phentolamine (phent.) (0.2 mg/kg) were successively administered to patients with NMS (n = 5) and control subjects (n = 5). The heart rate (HR) after atr. and prop., and systolic blood pressure (SBP) after phent. were defined as intrinsic HR (IHR) and intrinsic SBP (ISBP). Parasympathetic activity (increase in HR by atr.), beta-sympathetic tone (HR after atr. minus IHR), beta-sensitivity (change in HR by 1 microg isp./kg/min), beta-secretion (beta-tone/beta-sensitivity), alpha-sympathetic tone (SBP before phenyl. minus ISBP), alpha-sensitivity (change in SBP by 1 microg phenyl./kg/min) and alpha-secretion (alpha-tone/alpha-sensitivity) were also calculated. The beta-secretion was decreased (0.0027+/-0.0008 versus 0.0060+/-0.0004 microg/kg/min/isp.; p < 0.05), while the beta-sensitivity was increased (5850+/-947 versus 3150+/-292 beats/microg/kg/min isp.; p < 0.05) in NMS compared with control subjects. In the other indexes, there were no significant differences between two groups. The results of the present study suggest that increased beta-sensitivity may contribute hypercontraction of left ventricles, which might partially explain the mechanism of NMS.

Walking 10,000 steps/day or more reduces blood pressure and sympathetic nerve activity in mild essential hypertension.

We investigated the effects of walking 10,000 steps/day or more on blood pressure and cardiac autonomic nerve activity in mild essential hypertensive patients. All subjects were males aged 47.0+/-1.0 (mean+/-SEM) years old. The original cohort consisted of 730 people in a manufacturing industry who measured the number of steps they walked each day using a pedometer. Eighty-three of these subjects walked 10,000 steps/day or more for 12 weeks. Thirty-two of these were hypertensives with systolic blood pressure (SBP) greater than 140 mmHg and/or diastolic blood pressure (DBP) greater than 90 mmHg. Thirty of these hypertensive subjects (HT) were examined twice, once during the pre- and once during the post-study period, for body mass index (BMI), maximal oxygen intake (Vo2max), blood pressure, heart rate (HR), and autonomic nerve activity by power spectral analysis of SBP and HR variability. In the HT group, walking 13,510+/-837 steps/day for 12 weeks lowered blood pressure (from 149.3+/-2.7/98.5+/-1.4 to 139.1+/-2.9/90.1+/-1.9 mmHg; p<0.01, respectively). In both the 34 normotensive controls and 17 hypertensive sedentary controls, blood pressure did not change. Walking also significantly lowered low-frequency fluctuations in SBP as an index of sympathetic nerve activity, from 1.324+/-0.192 to 0.738+/-0.154 mmHg2/Hz (p<0.05). VO2max rose significantly from 26.1+/-2.4 to 29.5+/-2.5 ml/kg/min (p<0.05). There were no changes in parasympathetic nerve activity, baroreceptor reflex sensitivity, or BMI. Our results indicate that walking 10,000 steps/days or more, irrespective of exercise intensity or duration, is effective in lowering blood pressure, increasing exercise capacity, and reducing sympathetic nerve activity in hypertensive patients.

Enhanced efficacy of nilvadipine in hypertensives whose raised ambulatory blood pressure is sustained during sleep.

This study was designed to clarify the relationship between the antihypertensive effects of the calcium antagonist nilvadipine, and circadian changes in blood pressure. Based on measurements using an ambulatory blood pressure monitoring system (ABPM), 17 outpatients with untreated essential hypertension were divided into two groups: a sustained hypertensive group (with a fall in blood pressure during sleep < 10%, n = 7) and a waking time hypertensive group (with a fall in blood pressure during sleep > or = 10%, n = 10). During treatment with nilvadipine (8 mg/day, > or = 2 weeks), patients were reexamined by ABPM. The antihypertensive effect of nilvadipine was significantly and negatively correlated with the night time fall in blood pressure: this effect was significantly greater in the sustained hypertensive group than in the waking time hypertensive group. These data suggest that the long acting calcium antagonist nilvadipine has more potent antihypertensive effects in patients with sustained hypertension ("nondippers") than in those whose hypertension lessens during sleep ("dippers").

[Management of permanent pacemaker implantation in elderly patients].

We evaluated the clinical characteristics of 297 consecutive patients who underwent permanent pacemaker implantation. Their mean age was 67 +/- 13 years; those at least 75 years old accounted for 30.9%. The underlying diseases were sick sinus syndrome in 36.7%, atrioventricular block in 58.9%, and atrial fibrillation with bradycardia in 4.4%. There was no association between age and either the voltage threshold or the R wave amplitude at the time of implantation. When pacemakers were exchanged, only patients aged 75 years or less had voltage thresholds that were higher and lead resistances that were lower than those measured at the time of initial implantation. No clear differences were observed in the R wave amplitude, regardless of age. With careful long-term management, permanent pacemaker implantation and follow-up clinical care can be safe, even in aged patients.

Pheochromocytoma-related myocardial damage following delivery.

We present the case of a 35-year-old woman whose pregnancy was complicated by the rare condition of transient pheochromocytoma-related myocardial damage. Short-duration left ventricular dysfunction was apparently caused by acute non-transmural myocardial infarction provoked by coronary artery vasospasm rather than catecholamine-induced cardiomyopathy. Forty-eight days after onset, a 50 x 55 x 35 mm tumor was excised and histologically confirmed to be a pheochromocytoma.