To demonstrate innervation in human atrioventricular valves, we examined the tricuspid and mitral valves of apparently normal autopsied hearts of four men (ages ranging from 50 to 74 years). Whole valve tissues were stained for acetyl-cholinesterase by a histochemical method. Acetylcholinesterase-positive nerve fibers with a diameter of 2 to 5 μm were distributed widely in the deep atrialis of the atrioventricular valves and partly in the fibrosa. The nerve fibers formed a network or plexus from the base to the anatomical edge of the valves. Meshes of the nerve fiber network were more dense towards the base and at the commissure than either towards the edge or at the body. Thicker nerve fibers, which were interspersed coarsely in the leaflets, were intercalated by special varicose apparatuses at a few sites in their long running course. On the contrary, thinner nerve fibers which were distributed abundantly, ended, as a rule, in small dotor brush-like formations. Approximately half of the chordae tendineae were innervated by the nerve fibers. The mode of vagal innervation suggests that the nerve system may assist valve movement by moderating myocyte contraction in the valve base and change valve structure by sensing a stress in the valves.

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To assess the relationship between aging and autonomic regulation of sinus node function, 56 subjects of various ages (range 14-75 years, mean 43±19 years) without sinus node disease were studied. Heart rate, corrected sinus node recovery time and sinoatrial conduction time were measured before (basic) and after (intrinsic) pharmacologic autonomic blockade (propranolol+ atropine i.v.). Percent chronotropies of the above parameters were calculated by a modified Jordan's method. Basic heart rate and basic corrected sinus node recovery time did not vary with age (r= -0.15, r=0.08, respectively), while basic sinoatrial conduction time tended to increase with age (r=0.32, p<0.05). Intrinsic heart rate decreased (r=-0.76, p<0.001), and intrinsic corrected sinus node recovery time and intrinsic sinoatrial conduction time both increased with age (r=0.55, p<0.001; r=0.56, p<0.001, respectively). The younger the subject, the more negative the percent chronotropies of the above parameters were, and the percent chronotropies correlated positively with age (r=0.68, p<0.001; r=0 52 p<0.001 and r=0.34, p<0.05, respectively). In conclusion, ' intrinsic sinus node functions deteriorated with age. Furthermore, parasympathetic tone on the sinus node functions decreased with age, which may compensate for age-related deterioration of intrinsic sinus node function.

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The purpose of the present study was to evaluate the factors which influence the effect of heparin exercise treatment on treadmill capacity, and to examine the long-term efficacy of the treatment in 16 patients with chronic effort angina. Treadmill exercise was performed 20 times for 2 to 3 weeks according to standard Bruce protocol. A single intravenous dose of heparin (5, 000 IU) was given 10min before each exercise period. Exercise with heparin pretreatment in-creased the total exercise duration from 6.6±1.6 (SD) to 9.4±1.9min (p<0.05) and the maximal rate-pressure product from 19, 200±4, 700 to 24, 700±5, 900 mmHg·beats/min (p<0.05). The rate-pressure product at the onset of angina was also increased by 32% (p<0.05). The ST segment depression at the same exercise time as in control exercise was ameliorated from 0.16±0.05 to 0.12±0.06 mV (p<0.05). Multivariate analysis of the determinants of the effect of the treatment on treadmill capacity indicated that the treatment is more effective in patients without previous myocardial infarction. A11 of the above-mentioned variables of treadmill capacity did not change significantly during a follow-up period of 13±7 months (range; 4-24 months). These findings lend further support to heparin exercise treatment as a possible therapeutic approach in patients with chronic stable effort angina, and particularly in those without previous infarction.

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Monitoring the current smoking status by an objective method may augment the effects of smoking cessation instruction. To quantitatively evaluate smoking status and its modification by smoking cessation instruction, urinary cotinine, a major metabolite of nicotine, was measured by radioimmunoassay in 64 patients with a smoking habit before and during smoking cessation instruction. Urinary cotinine levels were used to discriminate between smokers and nonsmokers (with 50 ng/ml used as a threshold). In 49 patients who clairned to have stopped smoking, urinary cotinine concentrations I month after instruction indicated that only 30 (61%) of them had actually stopped (before: 243±104, after: 1±3 ng/ml) (mean±standard deviation). In the remaining 15 patients who failed to stop smoking while reporting a reduction of cigarette consumption (before: 27±12, after: 7±5/day), there was no appreciable reduction in urinary cotinine levels (before: 298±140, after: 229±171 ng/ml). When the patients who had failed to stop smoking again received intensive smoking cessation instruction, the success rate increased from 47% (30/64) to 69% (44/64) (p<0.05). Thus, urinary cotinine measurement may provide a useful and quantitative method for monitoring actual smoking habits and thus augment the efficacy of smoking cessation educational programs.

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Background: The coupling interval of ventricular premature contraction is relatively constant in some patients, while it varies in others. The clinical implications of this variability in the coupling intervals of ventricular premature contractions remains to be clarified. Methods: Ambulatory electrocardiograms were recorded in 48 patients who had 2000 or more ventricular premature contractions per day. In each subject, 24h ambulatory electrocardiograms were recorded in the absence of anti-arrhythmic drug (control), and during treatment with various antiarrhythmic drugs. Data on R-R intervals were obtained using a Marquette 8000T, and transmitted to a personal computer. For each of the control recording, an R-R interval scatterplot was constructed by plotting the coupling intervals of ventricular premature contractions as a function of the preceding R-R intervals of normal sinus beats. The standard deviation of the coupling intervals (SD_NV), that of the preceding R-R intervals (SD_NN), and their ratio (SD_NV/ SD_NN) were calculated. Results: At control recording, two primary R-R scatterplot patterns were recog-niged; 1) Fixed, where the coupling intervals remained constant at various pre-ceding R-R intervals (SD_NV/ SD_NN<0.5 and SD_NV<50 msec) (n=29), and 2) Variable, where the coupling intervals showed a much greater (n=19). The prevalence of organic heart disease was higher in the Variable group than in the Fixed group (47% vs 14%, p<0.05). SD_NV/SD_NN Was higher in patients with organic heart disease than in those without (0.62±0.34 vs 0.44±0.23, p<0.05). The efficacy of antiarrhythmic drugs was compared between the two groups. A reduction of 80% or more in the total number of ventricular premature contractions was considered effective. Class Ia, Ib, and Ic drugs had almost the same efficacy in the Fixed and Variable groups (Ia, 43% and 41%; Ib, 36% and 22% ; Ic, 64% and 63%, respectively). Class II drugs (beta-blockers) were more effective in the Fixed group than in the Variable group (50% vs 0%, p<0.05). Conclusion: The R-R interval scatterplot of ambulatory electrocardiograms was useful in exploring the variability in the coupling intervals of ventricular premature contractions, and may help to predict the efficacy of antiarrhythmic drugs.

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The purpose of this study was to elucidate the possible link between lipoprotein(a) (Lp(a)) and the occurrence of restenosis after initial elective percutaneous transluminal coronary angiopasty (PTCA). Serum lipids, including Lp(a), total cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol, apolipoprotein A-I (Apo A-I), and apolipoprotein B (Apo B), and the Apo B/Apo A-I ratio were examined in 63 consecutive patients (41 men and 22 women, average age 63±8 years) who underwent initial elective PTCA in our department. Forty two target lesions were in left anterior descending, 10 were in left circumflex and 11 were in right coronary branches. Restenosis was observed in 22 patients (35%) 6.4±2.6 months after PTCA. The serum Lp(a) level was significantly higher in the restenosis group than in the non-restenosis group (38.0 vs 19.9 mg/dl, p<0.05). A significant correlation was observed between serum Lp(a) levels and the degree of % restenosis after PTCA (r=0.557, p<0.001). However, other lipids showed no significant relationship to restenosis. In addition, the % stenosis before PTCA was found to be related to the occurrence of restenosis after successful PTCA. We conclude that the serum Lp(a) level has a close correlation with the degree of % restenosis after PTCA, and may be a useful index for predicting the possibility of restenosis after PTCA, especially in patients with an Lp(a) level above 30 mg/dl.

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Three patients showed ST elevation on precordial electrocardiogram and ST depression on intracoronary electrocardiogram during angioplasty of the left anterior descending coronary arteries (LAD). While none of the patients had spontaneously visible collaterals, all showed transient recruitable collaterals to the LAD. No evident collaterals into the diagonal branches were observed. Possibly, if the intracoronary electrocardiogram represents the potential changes of the epicardial surface in the vicinity of the guidewire tip, then endocardial ischemia may have developed even though epicardial ischemia was not observed, due to relatively sufficient blood flow through the recruitable collaterals to the LAD. ST elevation on the precordial electrocardiogram may have represented epicardial and endocardial ischemia of the diagonal branches, where the recruitable collaterals could not protect against transmural ischemia. These phenomena suggest that the recruitable collaterals are functionally limited during acute coronary occlusion, even though the collaterals are well developed.

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To determine the cause of precordial ST depression in acute inferior myocardial infarction, we evaluated the relationship between precordial ST deviation and ventricular involvement. Forty-nine patients who were admitted to the hospital with an acute inferior myocardial infarction, and 60 patients who were treated with elective angioplasty to the right coronary artery, were analyzed. All patients had single vessel disease and were divided into 2 groups (A and B) according to the site of the lesion. Patients in group A had a lesion proximal to the largest right ventricular branch, while in group B the lesion was distal to that branch. There were no differences in inferior ST elevation between the 2 groups, but precordial ST segments were more depressed in group B than in group A. A significant correlation was observed between inferior and precordial ST deviation in group B, but not in group A. These results were similar in patients with myocardial infarction and in those treated by angioplasty. These results suggest that precordial ST depression in an evolving inferior infarction is due to reciprocal ST deviation which reflects inferoposterior involvernent. In addition, when inferior infarction is accompanied by right ventricular involvement the precordial ST depression is lessened.

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The effect of 5'-nucleotidase inhibitor (AMP-C) and xanthine oxidase inhibitor (Allopurinol: ALLO) on myocardial functional recovery and the restoration of myocardial high energy phosphates after 15 min of normothermic global ischemic insult, was studied in the isolated isovolemic Langendorff rat heart model. Fifty nine rats were divided into 4 groups: Group I; saline. Group II; AMP-C plus ALLO, Group III; AMP-C, Group IV; ALLO. Intermittent infusion of drugs was delivered in 3 ml of solution at 5 min intervals during ischemia. Percent recovery of left ventricular systolic function was as follows: Group I; 74.2±3.6%, Group II; 87.7±1.7%. Group III; 83.5±3.1%, Group IV; 86.4±2.6%. Improved recovery was statistically significant only in Group II (p<0.05 vs Group I). Suppression of reactive hyperemia was seen with re-perfusion in the groups which had been treated with AMP-C (i.e., Groups II and III). Myocardial adenine nucleotides and purines were measured in 6 hearts in each group using high performance liquid chromatography. Myocardial ATP levels was 0.89±0. 16 nmol/mg left ventricular wet weight in Group I, 1.370.12 in Group 11 (p<0.05 vs Group I), 1.42±0.17 in Group 111 (p<0.05) and 1.17±0.15 in Group IV. This study demonstrates that intermittent infusion of AMP-C plus ALLO during global myocardial ischemia results in improved myocardial functional recovery and improved preservation of high energy phosphates.

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A triple wavelength spectrophotometric method was developed to monitor changes in the concentrations of oxygenated and deoxygenated hemoglobin, and in the redox state of cytochrome oxidase in living tissue. Three wave-lengths of an NIR (near-infrared) laser beam were used to monitor hemoglobin (780, 805 and 830 nm) and cytochrome (cyt.) oxidase (780, 790 and 830 nm). Algorithms for calculating changes in the concentrations of oxidized cyt. oxidase (aa₃), and oxygenated and deoxygenated hemoglobin were developed using NIR spectral analysis of these chromatophores. To assess the ability of these algorithms to measure independent changes in the concentration of oxy-, deoxyhemoglobin and oxidized cyt. oxidase in tissue, experiments involving a fluorocarbon (FC-43) exchange transfusion at very low hematocrits were conducted in anesthetized rats. The observed data indicate that FC-43 circulation at FiO₂ 1.0 can supply sufficient oxygen to the rat brain to maintain the oxidation state of mitochondrial oxidase (cyt.aa₃) near pre-exchange levels. The relationships between changes in oxidized cyt. oxidase and oxyhemoglobin content in response to variations in FiO₂ of inspired gas were then examined in the rat brain. These results also confirmed the ability of the triple wavelength algorithms to distinguish changes in the oxidized copper band of cyt.aa₃ from those in absorption by oxy- and deoxyhemoglobin. NIR monitoring of skeletal muscle to determine the redox state of cyt. oxidase was performed in a few human cases and the results indicated that these observations can increase our understanding of the process of oxygen transport to tissues.

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Excessive vascular damage causes excessive vascular repair, which results in re-stenosis. To limit the thickness of the coagulation layer in laser balloon angioplasty, we used a carbon monoxide (CO) laser, which has high tissue absorption, as a therapy laser source instead of a Nd: YAG laser. To investigate the benefit of short-penetration CO laser light to vascular tissue, excised human abdominal aorta was irradiated with a CO laser through a 30μm polyethylene membrane. The temperature of the vascular tissue was continuously monitored during irradiation. CO laser irradiation of 20 W/cm² was performed in either a continuous mode or an intermittent mode with various duty ratios (exposure/interval duration). With a total fluence of 200 J/cm², the adventitial temperature decreased as the duty ratio was reduced. The adventitial temperature at a duty ratio of 1 : 2 was 43°C. Microscopic examination of aorta which had been intermittently irradiated duty ratio of 1 : 2 showed thermal coagulation localized within the intima and a flattened intimal surface. These results suggest that intermittent laser irradiation with a CO laser can be used to limit the depth of thermal coagulation, and can selectively weld the intima without excessive thermal damage. Laser balloon angioplasty using a CO laser may help to prevent restenosis.

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We report 2 patients with Wolff-parkinson-White Syndrome, who underwent radiofrequency (RF) catheter ablation under observation by biplane trans-esophageal echocardiography. One of the patients had Kent bundle in the lateral wall of the left ventricle, and the tip of the catheter could be easily con-firmed with transverse views. Since perforation was observed where the valve was attached to the posterior leaflet of the mitral valve during the 39th administration of RF energy, ablation was discontinued. The other patient had Kent bundle in the posterior septum of the left ventricle. The tip of the catheter could be easily confirmed with sagittal views. Ablation was successful after the 4th administration of RF energy, but particulate contrast echoes appeared from the site of the tip of the electrode which had been used for ablation during the 4th RF delivery. When the delivery of RF energy was discontinued, the contrast echo disappeared, and a thrombus was found at the tip of the removed catheter. TEE in RF catheter ablation was helpful for confirming the site of the tip of the catheter and for early detection of complications.

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We report a 54-year-old female with anomalous origin of the left coronary artery from the pulmonary artery who came to our hospital complaining of dizziness presumably due to ventricular tachycardia. Electrocardiography, echocardiography and myocardial scintigraphy were indistinguishable from anteroseptal myocardial infarction. Only coronary angiography enabled us to differentiate between atherosclerotic ischemic heart disease and anomalous origin of left coronary artery from the pulmonary artery.

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