To examine the incidence of arrhythmias in dipyridamole infusion and the relation between dipyridamole-induced arrhythmias and ST-segment depression, dipyridamole electrocardiography tests were performed on 100 patients with coronary artery disease. Dipyridamole was infused at a rate of 0.568mg/kg for 4min, and 87-lead body surface mapping was performed to determine ischemic ST-segment depression. Positive ischemic response was defined as ≥0.10mV horizontal or downsloping ST-segment depression below the baseline, lasting 80msec after the J point. Arrhythmias were observed by continuous electrocardiographic monitoring using a CM-5 lead electrocardiography. With respect to ventricular premature contractions (VPC), a group of patients with previous myocardial infarction (MI group) had a significantly higher incidence than a group of patients without previous myocardial infarction (non-MI group) before (16.7% vs. 1.7%, p<0.01) and after (38.1% vs. 3.4%, p<0.005) the dipyridamole infusion. The incidence of supraventricular premature contractions (SVPC), however, was not significantly different between the MI and non-MI groups. A group of patients with positive ischemic response had a significantly higher incidence of SVPC after the dipyridamole infusion than a group of patients with negative ischemic response (p<0.005). However, there was no significant difference in the incidence of VPC between the negative and positive ischemic response groups. These results suggest that dipyridamole-induced VPC is not always associated with ischemic ST-segment depression, but dipyridamole-induced SVPC is associated with dipyridamole-induced ischemic ST-segment depression in patients with coronary artery disease.

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To elucidate differences in conduction properties among the normal atrioventricular (AV) node and the antegrade fast and slow dual AV nodal pathways (DAVNPW), AV nodal conduction curves were analyzed quantitatively in 38 patients. Eighteen patients had antegrade DAVNPW with AV nodal reentrant tachycardia (AVNRT) (dual pathways group) and the remaining 20 had smooth AV nodal conduction curves, without evidence of AV nodal dysfunction (control group). The effective refractory period (ERP) of the antegrade fast pathway was longer than that of the normal AV node (at both basic cycle lengths of 700 and 500msec, p<0.01). Although the atrial premature beats were delayed by a longer ERP in the fast pathway, there was no significant difference in the degree of prolongation of AV nodal conduction time related to shortening of the coupling interval (i.e., ratio of A2H2 increment to A1A2 decrement) between these two pathways. On the other hand, the ERP of the antegrade slow pathway was similar to that of the normal AV node. The degree of prolongation of AV nodal conduction time (relative to the shortening of the coupling interval) was greater in the antegrade slow pathway than in the normal AV node. In conclusion, these findings suggest that in DAVNPW with AVNRT: (1) the antegrade fast pathway is similar to the AV node and its conduction properties are unlikely to be better than those of the normal AV node and (2) the antegrade slow pathway has quantitatively poorer conduction properties than the normal AV node, since it has a greater degree of decremental conduction.

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This study was conducted retrospectively to elucidate whether the long-term use of nifedipine is effective against the progression of coronary atherosclerosis in humans. Twenty-nine subjects with ischemic heart disease, on whom repeated coronary angiographic examinations (CAG) were performed, were randomly selected. Sixteen subjects were on nifedipine therapy (40mg/day; NIF group, age 53±2) and 13 subjects not on nifedipine therapy served as the control group (C group, age 58±3). No significant differences were observed in clinical backgrounds, including the interval between CAG, between the 2 groups. The lesions with 25 to 75% stenosis on the first CAG were defined as the regions of interest (ROI), and the magnitude of stenosis was quantitatively measured by videodensitometry for each ROI on the first and the second CAG. The magnitude of stenosis showed a small increase (54.1±2.6 to 58.6±3.3%: N.S.) for 37 ROIs in the C group. In contrast, it showed a significant decrease (52.5±3.8 to 46.2±4.3%: p<0.05) for 33 ROIs in the NIF group. The trend was more apparent in the left coronary artery. The change in the mean value for ROIs in each subject produced similar results. These results suggest that the long-term use of nifedipine might be effective in retarding the progression of coronary atherosclerosis in humans. However, a prospective study should be performed to confirm this.

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In this study, 431 consecutive patients with mitral valve prolapse (MVP) diagnosed by two-dimensional echocardiography were employed to further investigate the site-related difference in the prevalence of MVP. Following echocardiographic determination of the site and severity of MVP, a pulsed-Doppler technique was further performed to assess the existence and severity of mitral regurgitation (MR) in all patients. These patients were then classified by age in 10-year groups with patients older than 60 years being enrolled in one group. The younger groups accounted for a large number of the patients with MVP in our study, with the number of patients being reduced with age. In addition, female patients tended to predominate up until the 50s, but not in the 50 and older groups. The prevalence of MVP at the centro-medial site of the anterior mitral leaflet (AML) predominated in all age groups, gradually decreasing with age, except for a peak in the 40s, before continuing to decline in the 50 and older groups. On the other hand, the prevalence of MVP at the lateral site of the AML and at the posterior mitral leaflet (PML) increased with age. In the 50 and older age groups, the prevalence of MVP at these sites increased steeply with age. However, the prevalence of MVP at both the lateral site of the AML and PML did not significantly increase with age. The trend shown above was not significantly different for gender. The number of patients with MR increased with age independent of the site of MVP. However, the prevalence and severity of MR associated with MVP at the lateral site of the AML and/or at the PML were significantly greater than at the other sites up until the 50s (p<0.05). When patients were older than 50 years, this significant site-related difference in the prevalence of MR was not observed because of the higher prevalence of MR in the older patients in this study. Forty-one patients could be followed for 2 to almost 5 years. Three of the 41 patients were observed to have MVP at the centro-medial site of the AML in the initial examination, but the site of MVP had extended to the lateral side of the AML in the final examination. Two patients with MVP at all 3 sites of the AML demonstrated an increase in the severity of MVP. However, there were no newly documented cases of MR among those patients. These findings suggested that 1) different causes relating to the site of the mitral valve are exerted to create MVP, 2) it is clinically important to consider the greater prevalence and severity of MR associated with MVP of the lateral site of the AML and/or the PML when MVP involves these sites even though minimum changes in the valvular lesions are observed, 3) it should be noted in the majority of MVPs at the centro-medial site of the AML, that follow-up patients will have the same site and severity of MVP at the final examination; however, for some patients where MVP initially appeared at the centro-medial site of the AML, there will be newly extended MVP to other sites, indicating deteriorating prognosis of MVP.

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Apical hypertrophic cardiomyopathy is characterized by a spade-like left ventricular cavity and by both giant negative T waves and tall R waves in the electrocardiogram. However, the mechanisms of these ECG abnormalities have not been satisfactorily clarified. We have recently developed a three-dimensional computer model of ventricular depolarization and repolarization processes. This model has successfully simulated normal QRST waves and changes characterizing some abnormal conditions. A model of apical hypertrophic cardiomyopathy was constructed by adding model units to the endocardium of the left ventricular apex. The surface ECG was then calculated by assuming different gradients of action potential durations and different proportions of the hypertrophic cells in the apical segment. A negative T wave of -1.45mV in lead V₄, similar to the clinically reported ECG, was obtained by assuming: (1) diffusely distributed hypertrophic cells at the apex and (2) uniform, long action potential durations of hypertrophic cells. It is suggested that these properties may account for the distinctive ECG abnormalities in apical hypertrophic cardiomyopathy.

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To study the effects of sympathetic stimulation (SS) and vagal stimulation (VS) on the induction of atrial flutter (AF) and its cycle length, aseptic pericarditis was produced surgically in 17 adult mongrel dogs. Programmed atrial stimulation was used to induce AF and to determine the effective refractory periods (ERP) and maximum conduction delay (maxCD) of the atrium. These tests were performed before and during stimulation of the right cervical vagus nerve and the right stellate ganglion. Results showed: (1) AF could be induced in animals with short ERP and large maxCD before SS; (2) ERP was significantly shortened, maxCD was significantly increased by VS; (3) During SS, ERP was slightly shortened, but there were no changes in maxCD and the induction rate of AF; (4) The cycle length of AF was shortened by SS, however, the cycle length of AF was shortened more notably by VS than by SS. From these findings, a shortening of the ERP and an increase in maxCD appear to be related to an increased AF induction rate by VS.

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In cardiac muscle and the heart, the maximum mechanical efficiency is relatively constant (15-25%) under various acute and chronic inotropic interventions, whereas the economy of isometric force development varies by 2-4 times with these interventions. We speculated about this discrepancy using Huxley's 1957 crossbridge model. Our theoretical derivation showed that the economy is proportional to the product of the thermodynamic efficiency (w/e in Huxley's notation) and the reciprocal of the rate constant of crossbridge detachment in the forward position (g₁ in Huxley's notation): (w/e) (l/g₁). The w/e value is the maximum limit of the mechanical efficiency. This w/e value has been assumed to be 0.75 for fast contracting skeletal muscle and 0.95 for slow contracting skeletal muscle; a 1.3-fold difference. Representative g₁ values are 6/s for the fast skeletal muscle and 0.12/s for the slow skeletal muscle; a 50-fold difference. These differences in w/e and g₁ between the fast and slow skeletal muscles predict that the economy would change by 65 (=1.3×50) times while the efficiency changes by only 1.3 times. Extrapolation of this relation to fast and slow contracting cardiac muscles suggests that only a 4-fold change in the economy, which is the observed maximum difference between the rat or rabbit hypo- and hyperthyroid myocardium, would be associated with only a less than 10% change in the maximum mechanical efficiency.

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We have previously shown that Ca-antagonists and a-blockers substantially inhibit the cellular proliferation of cultured rat vascular smooth muscle cells (VSMC). This study explored whether these inhibitory effects on cellular proliferation differ between cultured VSMC from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY).
SHR VSMC proliferated much faster than WKY VSMC in 10% FCS. Cellular proliferation, determined by both cell number count and ³H-thymidine incorporation, was significantly blunted in the presence of either nifedipine (Nif) or bunazosin (Bun). The magnitude of these inhibitory effects was more pronounced for SHR cells than WKY cells (% reduction of ³H-thymidine uptake with Nif: 62.1±7.8% for SHR vs 75.3±10.2% for WKY, n=6, p<0.05, and with Bun: 70.2±7.8% for SHR vs 82.1±9.9% for WKY, n=6, p<0.05). In contrast, the intracellular water volume was unaffected by these antihypertensive agents based on equilibrium distribution of 3-O-methyl-D-glucose¹⁴C.
It is concluded that SHR VSMC grow much faster than WKY VSMC and that this abnormality is innate to the SHR cells. It is also concluded that both Ca-antagonists and α-blockers exerted a substantial inhibitory effect on cellular proliferation of the cultured VSMC of either SHR or WKY. Furthermore, the greater inhibition of proliferation in the SHR VSMC suggests that Ca mediated- and/or α-receptor mediated processes of cellular proliferation of SHR could differ from that of WKY and that these abnormalities may contribute to the hyperproliferative changes of VSMC in this model.

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A patient with severe hypertension, hypokalemia and marked T-U wave alternans on electrocardiogram is reported for its rarity. Relevant literature is reviewed. Recent data indicate that electric alternans is related to changes in action potential configuration, and that it may be a marker of cardiac electrical instability.

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We describe a patient whose electrocardiograms showed ventricular tachycardia and atrial flutter which could be reproduced by arm movements. Careful review of the initiation and termination of the arrhythmia, the relation of the arrhythmia to body motion, and the associated symptoms and signs may be helpful to differentiate artifact from true arrhythmia.

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Symptomatic infants with congenital absence of pulmonary valve leaflets suffer primarily from respiratory insufficiency caused by bronchial compression by the dilated pulmonary arteries, and have a high mortality rate. We report the successful treatment of absent pulmonary valve syndrome with intact ventricular septum in a neonate. The treatment consisted of resection of the pulmonary artery aneurysm and enlargement of the pulmonary annulus.

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The case of a 1-year-old cyanotic boy diagnosed with asplenia syndrome has been reported. By physical and laboratory examinations, levocardia, atrial inversion, primum ASD, single atrioventricular valve, single ventricle (left-hand morphology), rudimentary right ventricle (anterior, left-sided), pulmonary stenosis, left-sided vena cava, single vena cava superior were established and the case was diagnosed with asplenia syndrome. The patient has concordance between tracheo-bronchial situs and lung anatomy and inverted atrial and visceral situs, but without atrial isomerism that makes his case an unusual variation of asplenia syndrome.

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A 50-year-old woman with aortitis syndrome complicated by aortic dissection, is reported. The dissection was observed at the level of the descending thoracic aorta by aortography and at the intimal side of the dilated aorta on CT. An aneurysm of the right subclavian artery and a diffusely thick wall of the abdominal aorta were also observed. This case suggests that the uneven wall of the aorta in aortitis syndrome might be dissected at the intimal side by dilatation.

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