One of the most intriguing developments in recent years towards prevention of restenosis after angioplasty is the use of ionizing radiation. The background for the use of radiation treatment for this application is sound, since radiation is used not only to treat malignant cancerous growths but also is used for treatment of benign hyperplastic disorders such as post-surgical keloid formation and recurrence of pterygium after surgical removal. Restenosis can be considered a form of overexuberant wound healing triggered by angioplasty. Ionizing radiation inhibits serum-stimulated proliferation of many cell types including fibroblasts and smooth muscle cells in vitro and also suppresses the synthesis of collagen by cultured fibroblasts. Liermann who showed inhibition of post-stent restenosis first used ionizing radiation for restenosis prevention clinically in iliac and iliofemoral arteries. Subsequently, extensive animal studies in various restenosis models have shown a profound inhibitory effect of catheter-based radiation (endovascular brachytherapy) on neointima formation and overall vessel shrinkage (negative remodeling). Based on these results clinical trials have been initiated with several types of devices and isotopes. Among these are ¹⁹²Ir, ³²P, ⁹⁰Y, ⁹⁰Sr / Y and ¹⁸⁸Re. Additionally, radioactive stents have been developed; devices for clinical use are made radioactive at the μ Ci level by surface implantation of 32P ions. Results from early clinical trials are encouraging and brachytherapy appears safe for clinical use and at an appropriate dose, may be highly effective for restenosis prevention.

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Acute left main coronary artery obstruction is rare and most patients in this clinical setting die of sudden death or cardiogenic shock. During the past 8 years, we encountered 13 patients with acute myocardial infarction caused by total occlusion of the left main coronary artery (LMCA-AMI). Thus, we surveyed these patients, and attempted to elucidate helpful predictors related to the prognosis. Six of 13 patients with LMCA-AMI survived. Successful left coronary artery dilatation was achieved in all survivors (group S), and in 5 (71%) non-survivors (group non-S). The age was not different between the two groups. A past history of angina was confirmed in 83% of group S, while only in 29% of group non-S. Clinical findings such as time of onset of AMI, interval from the AMI onset to admission, elapsed period from the AMI onset to recanalization of LMCA and the value of CK on admission were not different between the two groups. However, cardiogenic shock occurred in only 1 patient (17%) in group S compared with 5 patients (71%) in group non-S. As emphasized in the literature, good collateral circulation to the left anterior descending artery was observed in 5 patients (83%) in group S, while not observed in group non-S. Electro cardiographically, ST elevation in the aVR lead was very characteristic. This finding was confirmed in 69% of the total patients. Noticeably, 5 out of 6 non-survivors (83%) showed ST elevation not only in leads aVR but also in the aVL lead. In addition to the absence of collateral circulation, this electrocardiographic finding, which obviously indicates the presence of extensive myocardial ischemia in the diseased heart, is a simple and important predictor suggesting a poor prognosis in LMCA-AMI patients.

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The aim of this study was to investigate the role of nitric oxide (NO) in the coronary circulation and its relation to basal coronary artery tone in patients with vasospastic angina (VSA). We evaluated the level of nitric oxide end-products (NOx; nitrite + nitrate) in coronary circulation blood using an HPLC-Griess system for nine patients with VSA and nine control patients. All of the patients with VSA experienced focal spasm in the proximal to middle segments of the left anterior descending coronary artery (LAD) in response to intracoronary injection of ergonovine maleate. The luminal diameter of the coronary artery was measured in each patient by quantitative coronary arteriography. Blood samples for NOx measurement were obtained from the coronary sinus (NOx^V) and the ostium of the left coronary artery (NOx^A). The NOx difference, calculated from the coronary venous-arterial difference in NOx, was close to zero for the control patients whereas it was clearly negative for the patients with VSA. In addition, the NOx difference in the patients with VSA showed a negative correlation with basal coronary artery tone (r = - 0.91, p < 0.01) and a positive correlation with the dose of ergonovine required for spasm provocation (r = 0.77, p < 0.05). These results indicate that increased basal coronary artery tone and higher susceptibility to ergonovine in patients with VSA would be a consequence of coronary endothelial dysfunction as is indicated by NOx.

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Prognostic assessment of unstable angina pectoris is a common clinical problem for physicians. Markers of myocardial cell injury, serial electrocardiographic findings and ST segment monitoring are mainly studied for prognosis.
We investigated the relation between myocardial injury and the value of cardiac troponin T and QT interval dispersion in hospitalized unstable angina patients.
This is a prospective study that includes adult patients admitted to an emergency department with Braunwald class IIIB unstable angina pectoris. Eighty-six patients were enrolled in the study (mean age of 57 ± 12 years, 63 males and 23 females). Cardiac troponin T was assayed and QT dispersion calculated from surface ECG. Fifty-eight patients with troponin T < 0.1 ng / ml and 28 patients with troponin T levels ≥ 0.1 formed group 1 and group 2, respectively.
There were no significant differences in sex, age, history of coronary revascularization or ECG findings such as ST depression and T inversions between the two groups. The QT dispersion was significantly greater in patients with elevated cardiac troponin T levels (77 ± 18 msec vs 38 ± 13 msec; p < 0.014).
Because QT interval dispersion exhibited an association with cardiac troponin T levels, it may be used as a non-invasive marker of ischemic injury in patients with unstable angina.

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Evidence suggesting the involvement of activated monocytes and T-lymphocytes in the acute phase of coronary artery disease (CAD) has been increasing. But a detailed analysis of a correlation between monocyte and T-lymphocyte activation markers in CAD has not yet been done. We analyzed plasma C-reactive protein (CRP) levels and the expression levels of CD14 and CD11b on monocytes and the percentage of HLA-DR⁺ T-lymphocytes in 25 patients with acute coronary syndrome (ACS), 12 stable angina (SA) patients, and 23 control subjects using flow-cytometry. The expression of CD14 by monocytes was increased significantly in ACS patients (activation index = 38.7 ± 2.5, mean ± SEM) in comparison to the control subjects (8.0 ± 1.9) and the SA patients (16.9 ± 3.9) (p < 0.001 and p < 0.01, respectively). The expression of CD11b by monocytes of ACS patients (4.6 ± 0.6) was also increased significantly in comparison to control subjects (2.2 ± 0.1) and the SA patients (2.2 ± 0.3) (p < 0.001 for both). Also, a significantly higher percentage of HLA-DR positive T-lymphocytes (19.2 ± 1.8 vs 13.5 ± 1.2%, p < 0.05) was observed among ACS patients in comparison to control subjects. Significant increases in plasma CRP levels were also detected in ACS patients. Furthermore, there were statistically significant correlations among these activation markers. These results indicate that activation of inflammatory cells may play a role in the pathogenesis of ACS. The correlation between the activation status of monocytes and T-lymphocytes indicates that the activation of these immune cells is linked in such a way that activation of one type of cell may lead to the activation of another type of cell.

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In a previous study we found that hemoconcentration, which was identified by an increase in hematocrit, occured during a paroxysm of atrial fibrillation. In the present study we investigated the changes in hematocrit from sinus rhythm to paroxysm in 10 patients who had multiple paroxysms of atrial fibrillation in order to assess the ranges of the changes in hematocrit among the paroxysms. In these patients hematocrit was measured simultaneously with electrocardiographic recording during 3 or more paroxysms and sinus rhythm just before each paroxysm. The changes in hematocrit varied among the paroxysms. The maximum increase in hematocrit in each patient ranged from 3.5 to 8.0 points with an average of 5.1 points. Such a distinct increase in hematocrit which abruptly develops with a paroxysm of atrial fibrillation may be a potential risk for thrombus formation.

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This study included 87 consecutive patients with unexplained syncope or pre-syncope who had undergone the head-up tilt (HUT) test with concomitant isoproterenol infusion. A positive response was defined as development of syncope or pre-syncope in association with substantial hypotension (decline of systolic blood pressure > 20 mmHg). Coronary artery spasm was suggested from the clinical symptoms and electrocardiographic findings in 1 patient (1 / 87 = 1.1%). Intolerance to isoproterenol infusion was noted in 8 cases (8 / 87 = 9%). Of the 78 patients who completed the study, 73 showed positive responses (73 / 78 = 94%). (baseline systolic blood pressure = 125 ± 23 mmHg vs endpoint systolic blood pressure = 76 ± 11 mmHg, p < 0.05; baseline heart rate = 73 ± 14 beats per minute vs endpoint HR = 80 ± 24 beats per minute, p < 0.05). In 73 patients who showed positive responses, the systolic blood pressure (SBP) and heart rate (HR) returned to a safe level at 2 minutes when the patients were returned to a supine position (post-study 2 minutes SBP = 124 ± 18 mmHg vs baseline SBP = 125 ± 23 mmHg, p = NS; post-study 2 minutes HR = 82 ± 18 beats per minute vs baseline HR = 73 ± 14 beats per minute, p < 0.05). All 73 patients with a positive HUT test received Atenolol therapy (50 mg daily). Only 35 of these 73 patients took Atenolol regularly and had a repeat HUT test. After atenolol therapy, persistent positive responses were observed in 19 cases (19 / 35 = 54%) and negative responses were noted in 16 cases (16 / 35 = 46%). The mean dosage of isoproterenol needed to provoke a positive HUT test in 19 patients who had received Atenolol therapy and had a positive repeat HUT test was 2.3 ± 1.2 mg / min at baseline and 3.5 ± 0.9 mg / min for post-Atenolol therapy (p < 0.001). Sixteen patients with a negative repeat HUT test were treated continuously with Atenolol and followed for a mean period of 13 ± 11 months (range, 1-34 months). All 16 patients were free of syncope or pre-syncope during the period of follow up. In conclusion, the HUT test is mostly well tolerated and safe, even though the test has a low rate of adverse effects. Atenolol is effective for the prevention of provoked or spontaneous recurrent syncope or pre-syncope.

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We compared the efficacy of four different in vivo hemagglutinating virus of Japan (HVJ)-liposome gene transfer methods, i.e., direct myocardial injection (IM), injection into the left ventricular cavity (LV), infusion at the level of the coronary cusps (CI), or injection into the left ventricular cavity with a balloon catheter blocking aortic flow (LV+B) to transfer β - galactosidase, FITC-labeled oligodeoxynucleotide (ODN), and / or luciferase genes into the rat heart. IM caused highly efficient gene transfer in the limited area around the injection site, which suggests that IM may be a suitable method for targeted treatment of focal lesion. In the LV+B group, all rats had myocardial β -galactosidase staining and fluorescence of FITC-labeled ODN in the nuclei of cardiac myocytes around the coronary arteries and the vasa vasorum, and some transfected myocytes were observed in the middle of the myocardium without any evidence of injury. In contrast, in the CI group, only half of the animals had myocardial expression of β - galactosidase. In contrast, fluorescence or luciferase activity was present throughout the left ventricle in the LV+B group. However, the percentage of myocytes that exhibited fluorescence was less than 1% of the total ventricular myocyte population and luciferase activity in the LV+B group was 1.6% of that in the IM group. No evidence of luciferase expression was observed in brain, lung, liver, kidney, or testis in either the IM or LV+B group. These results suggest that HVJ-liposome gene transfer into the myocardium through the coronary arteries using a balloon-catheter technique is safe and has the potential for causing widespread transgene expression with organ-specificity, although the efficiency of gene transfer should be improved.

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We report two cases in which the tips of guide catheters were damaged by rotational burrs during rotational coronary atherectomy of aorto-ostial lesions. There were no signs of embolization caused by the material of the guide catheters during and after the interventions.

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A 58-year-old Japanese woman was admitted to our hospital because of chest pain. A continuous murmur was detected at the left parasternal area. Electrocardiogram showed ST elevation in leads V₂, V₃ and V₄. Chest computed tomography and echocardiography demonstrated pericardial effusion and a large mass which was adjacent to the pulmonary artery. An abnormal blood flow was detected in the mass by Doppler echocardiography. Coronary angiography confirmed that the mass was a giant aneurysm of coronary arteriovenous fistula arising from both the left and right coronary arteries. This patient had no symptoms until rupture of the fistula. Rupture of a coronary arteriovenous fistula is very rare but can be a cause of chest pain and pericardial effusion.

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We report two unique cases of persistent fifth aortic arch with a systemic-to-pulmonary connection. All previously reported cases with such a connection in the literature have either been cases of pulmonary atresia or an aortic arch anomaly, and the existence of a fifth aortic arch was a benefit to the underlying great vessel anomaly. However, our two cases did not have this associated great vessel anomaly, and the fifth arch resulted in a large left-to-right shunt with severe pulmonary hypertension and heart failure. The first case was misdiagnosed preoperatively; an accurate diagnosis was made after cardiac surgery. Because of its rerity and complexity, a persistent fifth aortic arch is often ignored and misdiagnosed.

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We experienced a case of T-cell lymphoma demonstrating diastolic heart failure as an initial manifestation. An 81-year-old Japanese male was admitted to the University of Tokyo Hospital because of progressive dyspnea and general fatigue. Clinical presentation was congestive heart failure and cervical lymphadenopathy. Right heart catheterization revealed “dip and plateau” waveforms in right ventricular pressure, which suggested a constrictive nature of heart failure. Gallium scintigram showed marked uptake in the heart. Biopsy from a cervical lymph node confirmed the diagnosis of malignant lymphoma of T-cell origin. Diastolic heart failure remained after successful chemotherapy. Autopsy revealed pericarditis with severe adhesion of the pericardium and the epicardium.

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We read with great interest the article by Seko, et al.¹⁾ on serum vascular endothelial growth factor (VEGF) and transforming growth factor (TGF) -β1 levels in patients with atrial fibrillation. However, some aspects of their methodology and discussion seem questionable.
First, because of low serum VEGF levels, they eliminated 7 cases from an initial 20 patients with atrial fibrillation and thus only discussed the remaining 13 cases. It is reasonable to select the population on the basis of a factor which might influence the results. However, it is not reasonable from a validity standpoint to select the population on the basis of the results.
Secondly, they reported that the serum VEGF levels were undetectable in normal control subjects.²⁾ On the contrary, their results indicated that the serum VEGF levels after defibrillation were still higher than those in control subjects, and they did not explain the reason. If the study subjects had other underlying heart diseases, they should have been discussed.
In addition, they stated that VEGF levels in patients with acute myocardial infarction returned rapidly to the normal range after reperfusion therapy.²⁾ If atrial fibrillation was directly involved in VEGF secretion and the half life of VEGF was so short, then the serum VEGF levels might have returned rapidly to the normal range after defibrillation therapy. However, although the second blood sampling was done between 24 hours to 57 days after defibrillation, the serum VEGF levels were still higher than those in normal control subjects. Thus, we are obliged to question whether only atrial fibrillation really influenced the VEGF secretion.

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