The autonomic nervous system may play an important role in regulating coronary arterial tone. To evaluate the role of autonomic nervous activity in patients with vasospastic angina (VSA), we studied 10 VSA patients with patent coronary artery (mean; 56 yr, range; 44-66 yr) and 8 normal subjects (mean; 58 yr, range; 35-71 yr). ECG and arterial pressure were continuously recorded for 4 min in a supine position at 7:30 am, 10:30 am, and 4:30 pm. Low-frequency (LF; 0.04-0.15 Hz) and high-frequency (HF; 0.20 Hz) components of the beat-to-beat variabilities of the R-R interval (RRI) and systolic arterial pressure (SAP) were then estimated by autoregressive power spectral analysis. The LF-Normalized Power (LF-NP; [LF Power]/[Total Power]-[Direct Current Power]) of both the RRI and SAP variabilities were greater in VSA patients than in normal subjects (RRI: 0.51±0.07, 0.51±0.07, 0.53±0.06, vs 0.25±0.04, 0.31±0.05, 0.31±0.06, at 7:30 am, 10:30 am, and 4:30 pm respectively: p=0.010, 0.044, 0.018. SAP: 0.62±0.06, 0.53±0.06, 0.57±0.06 vs 0.37±0.04, 0.30±0.06, 0.26 ±0.07, respectively: p=0.006, 0.017, 0.003.). The LF-power of SAP variability also tended to be greater in VSA patients. There was no difference in the HF-component coefficient of variance (CCV (%)= 100× (component power) ^1/2/mean RR intervals) of the RRI variabilities between the 2 groups. These results indicate that increased sympathetic vasomotor tone and cardiac sympathetic predominance may play an important role in patients with VSA. (Jpn Circ J 1996; 60: 10 - 16)

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To clarify the significance of exercise BMIPP (β-methyl iodophenyl pentadecanoic acid) and resting Tl delayed single photon emission computed tomography (SPECT) in the assessment of ischemia and viability, we studied maximal exercise-loading BMIPP SPECT following rest-injected Tl 3 h SPECT in 11 control subjects, 20 patients with effort angina and 38 patients with old myocardial infarction. The left ventricular wall on ECT was divided into 9 segments. BMIPP and Tl uptake were scored as 0=normal, 1=reduced, 2=severely reduced, or 3=absent. Discordance was defined as when segments with a reduced BMIPP uptake had a better resting Tl uptake. Significant coronary artery stenosis was defined as stenosis of 75% or greater on coronary arteriogram. Left ventricular wall motion was assessed as either normokinesis, hypokinesis, severe hypokinesis, akinesis or dyskinesis on left ventriculogram. When discordance was considered to be a marker of ischemia, the sensitivity and specificity in effort angina and control subjects were 95.2% and 84.6% for patients and 83.9% and 94.4% for diseased vessels, respectively. There were no differences between the sensitivity and specificity in left anterior descending artery (LAD), Ieft circumflex artery (LCx) and right coronary artery (RCA) Iesions (83.3%, 95.5% in LAD, 83.3%, 95.5% in LCx, 85.7%, 92.6% in RCA, respectively). All of the patients with old myocardial infarction had reduced exercise BMIPP uptake in infarcted regions. In old myocardial infarction, 35 patients had segments with discordant uptake. Discordance was observed in 75 (91.5%) of 82 segments with hypokinesis, and in 24 (92.3%) of 26 segments with severe hypokinesis. Even among the 36 segments with akinesis or dyskinesis, 25 (69.0%) had discordant uptake. When discordance in the infarcted region was considered to be a marker of viability, regions with severe asynergy showed a high possibility of viability. Thus, discordant uptake on exercise BMIPP and resting Tl delayed SPECT may be a useful marker of ischemia in effort angina and of viability in old myocardial infarction. (Jpn Circ J 1996; 60: 17 - 26)

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To examine whether or not granulocyte activation is involved in restenosis after percutaneous transluminal coronary angioplasty (PTCA), we prospectively followed the time course of the plasma level of granulocyte elastase, which is an index of granulocyte activation, before and after successful angioplasty in 43 consecutive patients. Restenosis was defined as a more than 50% Ioss of the initial gain in the coronary diameter achieved by PTCA with more than a 50% resultant stenosis in the follow-up coronary arteriography performed 3 months after PTCA. There was no difference in the level of granulocyte elastase between the 2 groups with (n=15) and without (n=28) restenosis before, the day after and 1 month after PTCA. However, 3 months after PTCA, the level of granulocyte elastase was significantly higher in the group with restenosis than in that without restenosis (171±13 vs 147±6 mg/l, P<0.05). The level of granulocyte elastase at 3 months after PTCA also correlated significantly with the percent luminal stenosis at the angioplasty site (P<0.05). These results suggest that granulocyte activation may be involved in restenosis after PTCA. (Jpn Circ J 1996; 60: 27 - 34)

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The effect of nifedipine on ventriculoarterial coupling was examined in 8 patients with old myocardial infarction who showed a depressed ejection fraction (37±7%). Left ventricular (LV) pressure and LV volume were determined simultaneously by micromanometer and conductance catheter, respectively. We measured the slope (Ees) of the end-systolic pressure-volume relation during transient inferior vena caval occlusion, the slope (Ea) of the end-systolic pressure-stroke volume relation, the ratio of Ea to Ees (Ea/Ees), and the work efficiency (the ratio of external work to the systolic pressure-volume area) at baseline and after the sublingual administration of nifedipine (10 mg). Nifedipine slightly increased the heart rate from 71±14 to 78±17 beats/min. Although nifedipine had little effect on Ees (2.54±0.68 vs 2.47±0.62 mmHg/ml/m², ns), it significantly decreased Ea from 3.47±1.16 to 2.37 ±0.54 mmHg/ml/m². Consequently, Ea/Ees decreased from 1.42±0.47 to 0.97±0.31 and work efficiency increased from 48±12 to 59±13% after nifedipine administration. These data suggest that nifedipine reduces afterload (Ea) and improves left ventriculoarterial coupling without depressing left ventricular contractility in patients with failing hearts due to old myocardial infarction. (Jpn Circ J 1996; 60: 35 - 42)

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It is believed that reciprocating tachycardia and accessory pathways play important roles in atrial fibrillation (AF) in patients with Wolff-Parkinson-White (WPW) syndrome. However, the mechanism by which AF occurs is not yet fully understood. This study was performed to evaluate the contribution of sympathoadrenal activity to the onset of AF in patients with WPW syndrome. Symptom-limited treadmill exercise testing was performed and plasma norepinephrine and epinephrine concentrations were measured simultaneously in 27 patients with WPW syndrome and 20 control subjects. In 13 patients with WPW syndrome and AF, plasma norepinephrine and epinephrine concentrations increased to 3.69±2.44 and 0.76±0.69 ng/ml at maximum exercise, respectively. These values were significantly higher (p<0.001) than those in control subjects and in patients without AF. Pretreatment with 0.2 mg/kg of propranolol significantly reduced the incidence of exercise-induced atrial premature complexes (χ²=7.33, p<0.05). With oral β-blockade for an average of 22.8 months, the incidence of AF decreased significantly from 1.77±0.53/patient per year to 0.33±0.57/patient per year (p<0.001). Augmented sympathoadrenal activity in patients with WPW syndrome may contribute to AF. (Jpn Circ J 1996; 60: 43 - 49)

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The hereditary cardiomyopathic strain of Syrian hamster has been extensively studied as a model of cardiomyopathy and heart failure. We attempted to determine whether an angiotensin converting enzyme (ACE) inhibitor, enalapril, prevents the increase in extracellular collagen matrix which connects the myocytes in cardiomyopathy. Enalapril was administered at an average dosage of 10 mg/kg per day to 10- to 20-week-old hamsters with hypertrophic (Bio 14.6) and dilated (Bio 53.58) cardiomyopathy, as well as to control Syrian hamsters (F1β). Collagen concentration estimated by hydroxyproline concentration and the collagen type III:I ratio significantly increased in the hearts of the Bio 14.6 and Bio 53.58 strains at 20 and 40 weeks of age as, compared with those in age-matched F1β hamsters. When Bio 14.6 hamsters were given enalapril for 10 weeks from 10 to 20 weeks of age, the collagen concentration, the collagen type III:I ratio and type III collagen mRNA expression were significantly decreased, compared with those in untreated animals of the same strain. After the administration of enalapril, scanning electron microscopic examination also revealed a decrease in fibrillar collagen accumulation in the interstitium and the network surrounding the cardiac myocytes. These prophylactic effects were not observed in the Bio 53.58 strain. These results indicate that the administration of ACE inhibitor prevents type III collagen production in the Bio 14.6 strain but not in the Bio 53.58 strain of Syrian hamster. (Jpn Circ J 1996; 60: 50 - 61)

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To determine the innervation of human semilunar valves, we examined the pulmonary and aortic valves of the normal autopsied hearts of 3 men (53 to 71 years old). Whole valve tissues with the aorta or pulmonary trunk were stained for acetylcholinesterase by a histochemical method. Acetylcholinesterase-positive nerve fibers with a diameter of 2 to 20 mm were located on the ventricular side of the semilunar valves. Innervation of the semilunar valves was extremely sparse compared with that of the atrioventricular valves and that of the aortic or pulmonary arterial wall. The nerves originated from the subendocardium of the ventricles and the adventitia of the arterial walls. The nerves were more distributed in the basal site than in the marginal site of the semilunar valve. The nerve fibers formed a network in the basal two-thirds of the leaflet. Thick nerves ramified in the thin nerve plexus. The thick nerves had a varicose-like structure. Thin nerves had a dot- and brush-like ending. The nerves in human semilunar valves may play a role in valve motion. (Jpn Circ J 1996; 60: 62 - 66)

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Paroxysmal atrial flutter is a drug-resistant supraventricular tachyarrhythmia that is often accompanied by hemodynamic instability due to an excessive ventricular response. We report here a case of atrial flutter with 1:1 atrioventricular conduction, in which we were able to rescue the patient from a state of cardiogenic shock by using intravenous dofetilide, a new class III antiarrhythmic agent. Dofetilide was suitable for the treatment because it immediately increased atrioventricular nodal refractoriness without any negative inotropic action. (Jpn Circ J 1996; 60: 67 - 69)

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Two cases in which a right-to-left shunt appeared across a patent foramen ovale after mitral valve surgery were clinically and echocardiographically followed for a long period of time. The right-to-left shunt markedly decreased in the supine position on transesophageal Doppler echocardiography in both cases within 2 years after the cardiac surgery, which presumably corresponds to a decreased risk of paradoxical embolism. (Jpn Circ J 1996; 60: 70 - 74)

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