The clinical implications of silent myocardial ischemic (SMI) episodes in patients with coronary artery disease were assessed in 253 patients whose angina symptoms were resolved by antianginal drugs. This population included 93 patients without a history of myocardial infarction (angina group) and 160 patients with myocardial infarction (infarction group). These patients were further divided into 2 subgroups according to whether or not SMI was detected by Holter monitoring immediately before discharge. The incidence of cardiac events was 19% for the angina group and 18% for the infarction group. The incidence of cardiac events did not differ between the 2 groups, but the cardiac event profile did. Briefly, 14 angina patients experiencing cardiac events needed coronary revascularization for worsening symptoms, while 18 myocardial infarction patients experiencing cardiac events had another infarction. In both angina and myocardial infarction patients, the cumulative rates of cardiac events were significantly higher in the subgroups with SMI (p<0.01 in either group). The significant prognostic factors as determined in the Cox regression model were multivessel disease, asynergy score, and SMI on Holter monitoring for angina patients, and SMI on Holter monitoring and multivessel disease for myocardial infarction patients. In conclusion, the cardiac event rate is significantly elevated in the subgroups with SMI, regardless of whether the patient had previous myocardial infarction; patients with SMI carry a poor prognosis, especially when they have a history of myocardial infarction.

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In order to compare the prognostic significance of late potentials (LPs) on signal-averaged electrocardiogram (SA-ECG), left ventricular ejection fraction (EF) and 24-hour Hotter monitoring (HM) following myocardial infarction, a prospective study on 60 patients (age 61.7±8.02 years old) just after acute myocardial infarction (AMI) was done. LPs, EF and HM were performed in all patients. Coronary arteriography had been done in 25 patients. The results showed that LPs were associated with a slightly higher incidence of life-threatening arrhythmia (34.8%) than HM (28.6%) and EF (25%). During the follow-up period (10±6 months), 9 patients had serious ventricular arrhythmic events, among whom 3 had sudden death due to ventricular fibrillation. The event rate in patients with abnormal LPs was higher than in patients with normal LPs (p=0.01, odds ratio=19.2). The study showed that there was no correlation between abnormal LPs and sex, age, number of narrowed coronary arteries, ventricular aneurysm, location of myocardial infarction, or EF alone. But there was a correlation between abnormal LPs and high grade ventricular ectopic activity detected by HM (r=0.62899, p=0.024). In addition, the combination of abnormal values of LPs, EF and HM could predict sustained ventricular tachycardia or sudden death in the first year after myocardial infarction with very high sensitivity (100%) as well as high specificity (p=0.0009, odds ratio =19).

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To investigate the significance of precordial ST-segment depression in acute inferior myocardial infarction, we compared the Gensini score of coronary artery stenosis between 2 groups of patients with and without precordial ST-segment depression. Group I consisted of 28 patients who showed ST-segment depression on admission (≥1mm in V2-V6) and Group II (n=16) those without ST-segment depression (<1mm). The Gensini score of the coronary arteries (56±29 vs. 28±18; p<0.001), the partial score of the infarction-related artery (29±16 vs. 17±11; p<0.01) and of the infarction-nonrelated artery (27±24 vs. 11±12; p<0.02) were significantly higher in Group I than in Group II. The Killip score (≥II) (34% vs. 6%; p<0.05), frequency of arrhythmias (75% vs. 38%; p<0.02) and peak CK value (3, 676±2, 290 vs. 1, 818±1, 153 IU/L; p<0.005) were higher in Group I than in Group II. Four patients in Group I died following admission, while no patient died in Group II (N.S.). Autopsy findings from the 4 Group I patients revealed fresh extensive inferior infarction and healed diffuse subendocardial infarction which could not be predicted from electrocardiograms.
All patients who survived the acute stage performed treadmill exercise testing and 22 patients underwent exercise thallium-201 single photon emission computer tomography (SPECT). On treadmill exercise test, there was no significant difference between the 2 groups in the frequency of angina pectoris and ST-segment depression. On SPECT, the perfusion defect area under 55% of maximum uptake at the redistribution phase was 45.8±19.6cm2 in Group I (n=14) and 34.7±21.3cm2 in Group II (n=8; N.S.).
In conclusion, precordial ST-segment depression in acute inferior myocardial infarction suggested advanced atherosclerosis in both the infarction-related and nonrelated coronary arteries, indicating a larger infarct size.

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The effects of L-arginine administration on systemic hemodynamics and plasma concentrations of neuro-endocrine hormones and amino acids were investigated in 10 normotensive healthy volunteers. Nitrite/nitrate in urine and cyclic guanosine monophosphate (c-GMP) in plasma were also measured as indicators of release of nitric oxide (NO).
L-arginine administration (30g/300ml/30min) caused hypotension (mean arterial pressure; 79.3±3.9mmHg fell to 68.8±2.2mmHg) with tachycardia (62.3±2.3 beats/min increased to 67.5±1.9 beats/min). The plasma concentration of L-arginine before administration was 98.8±8.2μmol/l and increased to 7263±567 μmol/l 20min after administra-tion. Cardiac output also increased to 127.2±3.9% by L-arginine administration. Total peripheral resistance was calculated to fall to 65.9±2.0%. L-arginine administration slightly changed several hormones, but all values were within normal ranges. Nitrite/nitrate in urine increased 142.1±12.4% compared to the values before L-arginine administration. Plasma concentrations of c-GMP and L-citrulline, the by-product of NO from L-arginine, were also significantly increased by L-arginine administration.
All our results provide evidence for the first time that systemically administered L-arginine releases NO in man.

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Conventional His-bundle ablation, performed at the site with the largest His-bundle potential, displays a high incidence of a new right bundle branch block with loss of pacemaker escape. Damage to the perinodal atrial area may decrease the injury to the His-bundle, such that the escape pacemaker activity with a narrow QRS complex is produced. This study reports data from 25 patients with drug-refractory atrial tachyarrhythmias. Nine patients (group I) received radiofrequency (RF) ablation of the atrioventricular junction (AVJ). General anesthesia was not necessary in group I patients. During a mean follow-up period of 10 months, a complete AV block persisted in 5 patients, and a first degree AV block persisted in 2 patients; these patients were asymptomatic and did not require treatment with antiarrhythmic agents. A successful direct-current (DC) ablation was performed in one of the patients with an unsuccessful RF lesion, producing a new right bundle branch block (RBBB). Sixteen patients (group II) received DC ablation of the AVJ. During a mean follow-up period of 20 months, a complete AV block persisted in 9 patients, a first degree AV block was produced in 7 patients, and a new RBBB occurred in 2 patients. Fifteen patients (94%) were asymptomatic without administration of antiarrhythmic agents. Complications, including nonsustained ventricular tachycardia (1 patient) and pericarditis (1 patient), occurred immediately after ablation in group II. Myocardial injury, reflected by creatine kinase-MB isoenzyme, was higher in group II than in group I (25±2 vs 10±1 IU/l). We conclude that (1) catheter-mediated RF ablation of the AV junction is safer than DC ablation, (2) a majority of patients with drug-refractory atrial tachyarrhythmias can be successfully treated with RF ablation and (3) failure to achieve AV junction ablation with RF does not mitigate against successful application of DC ablation.

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Continuous intravenous infusion of chlorpromazine (CPZ) was used for both sedation and after-load reduction in 13 Japanese patients (Group 1) supported by an intraaortic balloon pump (IABP) after open-heart surgery. CPZ was initiated at a dose of 0.05mg/kg/hr and was maintained in an approximate dose range of 0.1-0.3mg/kg/hr depending on individual patient needs. The drug was administered until the IABP was removed and the blood gases were normalized. During this period, the patients slept well and the trigger lines for the IABP were sufficiently secured. In order to evaluate the hemodynamic changes in these patients, the 10 patients who were supported by the IABP and given continuous intravenous sodium thiamylal (ST) for sedation in an approximate dose range of 1-2mg/kg/hr (Group 2) were employed as controls. After administration of CPZ, the systemic vascular resistance, central venous pressure, and left atrial pressure decreased, while the cardiac output increased. The predicted untoward effects of CPZ, such as tachycardia and hypotension, were minimal. In the ST group, by contrast, the cardiac output decreased somewhat in association with the increase in systemic vascular resistance. From these results, we conclude that constant intravenous CPZ is beneficial for postcardiotomy patients who have severe low cardiac output syndrome and are supported with IABP, by both successfully sedating the patients and reducing ventricular afterload.

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We studied the effects of hypoxia and reoxygenation on steady-state contractions and potentiated contractions of papillary muscles of guinea pigs. Isometric tension was measured while 120min periods of hypoxia and reoxygenation were repeated twice. Reoxygenation after the first period of hypoxia induced a gradual recovery in steady-state contractions and a rapid recovery in potentiated contractions from the first hypoxia-induced contractile depression. After the second period of hypoxia, steady-state and potentiated contractions decreased progressively. During the second period of reoxygenation, the recovery of steady-state and potentiated contractions was very poor and the marked elevation of diastolic tension did not decrease. There were no good correlations between hypoxic depression just before reoxygenation and the recovery of both potentiated contraction and steady-state contraction at 120min of reoxygenation. The recovery from the hypoxia-induced depression was poor in the preparations with marked elevation in diastolic tension.
From these findings, we conclude that hypoxia-induced depression is progressively worsened by an additional episode of hypoxia and that diastolic tension is one of the determinants of the low contractile level achieved by steady-state and potentiated contractions in the severely hypoxic state. The degree of hypoxia-induced depression does not determine redevelopment of force with reoxygenation.

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The interactive effects of verapamil and sympathetic nerve stimulation on the sinus and atrioventricular (AV) nodes were studied in 33 bilaterally stellectomized and vagotomized dogs. Sinus cycle length (SCL) and AV nodal conduction time (AH) at a constant drive cycle length (600 msec) were recorded. Sympathetic nerve stimulation (SNS) was performed for 40 sec by electrical stimulation of the right stellate ganglion. Several doses of verapamil (0.5-2.0μg/ml, 1.0ml) were injected directly into the sinus and AV node arteries at 20 sec of SNS. In addition, SNS was repeated at two different intensities after verapamil administration. Verapamil significantly increased the SCL and the AH in a dose dependent fashion, which was reduced by SNS. The reductions of SCL and AH by the SNS were attenuated in the presence of verapamil when the stimulation intensity was weak, but not when the stimulation intensity was strong. It is concluded that verapamil and sympathetic nerve activity interact antagonistically on the sinus node automaticity and AV nodal conduction.

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For a better understanding of the characteristics of blood flow in the pulmonary artery, we constructed three-dimensional images of velocity profiles of blood flow in the pulmonary artery from pulsed Doppler ultrasound recordings in 14 lambs aged 28-40 days. In 8 lambs, pulmonary hypertension was created by the central venous injection of monocrotaline pyrrole. Six lambs served as unaltered controls. The velocity data were sampled in 2mm increments along both an anterior-posterior axis and a right-left orthogonal axis in the main pulmonary artery. Using a computer-generated cross-sectional velocity matrix consisting of 0.25mm square grids, the velocity of blood flow was estimated at each intersection. The cross-sectional velocity matrices were generated at 5 msec intervals during the entire cardiac cycle. In all animals, significant velocity reversal was detected near the posterior wall. In 7 of 14 animals, the peak forward velocity was located near the posterior wall. Three of 8 hypertensive models showed reacceleration during the mid-systolic phase at the center of the velocity waveform, but one reacceleration disappeared at a point only 2mm away from the center of the vessel toward the posterior wall. Acceleration time correlated well with the mean pulmonary arterial pressure (PAP) (r=-0.85) and the log10 PAP (r=-0.86). Corrected acceleration time (acceleration time divided by the square root of the cardiac cycle length) also correlated with PAP (r=-0.78) and the log₁₀ PAP (r=-0.81).

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Angiotensinogen is a precursor of the multifunctional octapeptide hormone, angiotensin II. We have isolated the overlapping clones containing angiotensinogen gene locus from C57BL/6 mouse genomic DNA library and analyzed them by restriction enzyme mapping. The gene exhibited a structural organization similar to those of the human, rat and balb/c mouse angiotensinogen genes. Using a genomic DNA fragment of the mouse angiotensinogen gene as a probe, we have investigated the tissue distribution of angiotensinogen messenger RNA (mRNA) in C57BL/6 mouse. The angiotensinogen mRNA was highest in the liver and detectable in such tissues as brain, kidney, submandibular gland, ovary and heart. However, it was undetectable in lung and spleen under the condition used. Optimal alignments of the 5'-flanking regions among the human, rat and mouse angiotensinogen genes disclosed several deletions in the mouse sequence. To assay the promoter activity, the 5'-flanking region of the mouse angiotensinogen gene was ligated to the bacterial chloramphenicol acetyltransferase (CAT) gene, then transfected into different cultured cells. The angiotensinogen gene sequences elicited preferential expression of CAT activity when introduced into HepG2 cells derived from liver and 293 cells from kidney but not in HeLa cells from uterus, suggesting the presence of a cell type-specific promoter within the sequences. These findings on the structure and expression of the mouse angiotensinogen gene should prove useful in studying the function and control of the angiotensin.

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We report the case of a neonate with a rare association of tetralogy of Fallot and aortic valve stenosis, who died following percutaneous balloon valvuloplasty. Postmortem examination confirmed a tetralogy of Fallot morphology with a markedly hypoplastic pulmonary tree, hypertrophy of both ventricles, and a thickened and dysplastic aortic valve. Valvuloplasty was not effective despite the presence of a fissure in the cusp. The findings suggest that the left ventricular impairment and associated anomalies, with or without a dysplastic valve may contribute to the failure of balloon valvuloplasty in neonates with critical aortic valve stenosis.

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The development of atrial fibrillation in 2 patients, following an electrical shock is reported. One patient, with an underlying pre-excitation syndrome, had to be cardioverted due to rapid ventricular rate and hypotension. The other, with normal conduction, tolerated the arrhythmia well and atrial fibrillation reverted spontaneously after 24 hours.

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