To test the hypothesis that syndrome X is a systemic vascular disorder, technetium-99m ethyl cysteinate dimer (Tc-99m ECD) brain single photon emission computed tomography (SPECT) was used to detect abnormal regional cerebral blood flow (rCBF) in 30 patients with syndrome X.
These patients were separated into group 1, 20 patients with definite myocardial perfusion defects diagnosed by thallium-201 (Tl-201) myocardial perfusion SPECT; and group 2, 10 patients without any myocardial perfusion defects.
Tc-99m ECD brain SPECT demonstrated hypoperfusion brain lesions in 95% (19/20) and 20% (2/10) of patients in groups 1 and 2, respectively. This difference in the cidence between the two groups was significant. In group 1 and 2 patients, parietal lobes were the most common hypoperfusion areas, while the cerebellum was the least common hypoperfusion area of the brain.
Syndrome X is a systemic vascular disorder with a high incidence of hypoperfusion lesions of the brain based on the findings of Tc-99m ECD brain SPECT, and is usually coincident with myocardial defects based on the Tl-201 myocardial perfusion SPECT findings.

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Syndrome X is used to describe patients with chest pain and a normal coronary angiogram. We reviewed technetium-99m tetrofosmin (Tc-99m TF) myocardial perfusion single photon emission computed tomography (SPECT) results and clinical data of 43 syndrome X patients and 30 healthy controls with normal left ventricular ejection fraction and no cardiac abnormalities. The Tc-99m TF myocardial perfusion SPECT results showed 12 (27.9%) syndrome X patients had normal myocardial perfusion and 31 (72.1%) had abnormal myocardial perfusion, including 6 (14.0%) patients with fixed defects, 20 (46.5%) patients with transient defects, and 5 (11.6%) patients with reverse defects. The results of exercise ECG were not related to perfusion defects in Tc-99m TF myocardial perfusion SPECT. In contrast, all of the 30 (100.0%) healthy controls had normal myocardial perfusion SPECT results. We conclude that abnormal Tc-99m TF myocardial perfusion SPECT is common in syndrome X and does not correlate well with the exercise ECG. However, further studies with larger case numbers and long term follow up in patients with myocardial events are necessary to support our findings.

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In an attempt to determine the early and late outcomes of small vessel stenting, we retrospectively evaluated our database on 51 consecutive patients (41 males, mean age, 57.1 ± 10.1 years) who underwent stenting of at least one significant lesion in a coronary artery with a reference vessel diameter (RVD) < 2.8 mm between March 1999 and March 2001.
Sixty balloon expandable tubular stents were implanted in 57 lesions (29 Type B2/C, mean RVD: 2.54 ± 0.16 mm) without intravascular ultrasound guidance under a heparin-aspirin-ticlopidine regimen. The mean diameter stenosis (DS) decreased from 75.8 ± 13.6% to 4.2 ± 1.9% (P < 0.0001) with stenting at a mean deployment pressure of 13.6 ± 1.7 atm and a final balloon to RVD ratio (FB/RVD) of 1.08 ± 0.03. All stents were deployed successfully. Acute stent thrombosis occurred in 3 patients (6%), one died, and 2 developed non-Q-wave myocardial infarction (procedural success 94%). Clinical follow-up, available in 48 patients, revealed a 29% target lesion revascularization rate, a 2% myocardial infarction rate, and a 71% event-free survival at a mean of 11.6 months. Angiographic follow-up, available in 40 patients, showed a DS of 48.8 ± 31.3% and a binary restenosis rate of 50% at a mean of 7.7 months. The FB/RVD ratio was significantly lower in the group with restenosis than in the group without (1.06 ± 0.02 vs 1.1 ± 0.05, P = 0.04). Subgroup analysis yielded a significantly greater rate of restenosis in diabetics with complex (Type B2/C) lesion morphology compared to nondiabetics with simple (Type A/B1) lesions (75% vs 21%, P < 0.05).
In conclusion, stenting in vessels < 2.8 mm was found to be associated with a high rate of acute stent thrombosis and in-stent restenosis. Further analysis detected a subgroup of patients without diabetes or complex lesions who could be stented with an acceptable in-stent restenosis rate.

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Diffuse in-stent restenosis remains an important problem in percutaneous transluminal coronary angioplasty (PTCA). In this trial, we studied the early and mid-term outcomes of excimer laser coronary angioplasty (ELCA) on diffuse in-stent restenosis.
ELCA was performed in 23 patients (19 males). The mean length of the lesions was 14.3 ±3 mm and the mean age was 58 ±7 years. The minimal lumen diameter (MLD) was measured by on-line quantitative coronary angiography. Before the procedure, MLD was 0.9 ±0.4. The Q/non-Q-wave myocardial infarction (MI), coronary artery bypass graft (CABG), PTCA, and mortality were recorded during the procedure and at 6 months follow up.
The fluence of laser emission was 45 mj/m² and the repetition rate was 25 pulses per second. Adjunctive balloon angioplasty was performed in all of the cases at a mean 7 ±2 atm pressure. The procedure was successfully performed in all of the cases. Type-B dissection developed. after ELCA in 1 patient (4%). Perforation, death, cerebrovascular accidents, emergency CABG, PTCA or Q/non-Q wave myocardial infarction were not observed. MLD was 0.9 ±0.4 mm before ELCA, 1.8 ±0.9 mm (P < 0.05) after ELCA, and 3.1 ±0.7mm after PTCA.
At 6months follow up, there were 2 (8.7%) Q-wave myocardial infarctions and 2 (8.7%) recurrent anginal pain cases. Control angiography was obtained in 20 cases (87%). Control angiography was not accepted by 3 patients. Their maximal exercise test was negative. Angiographic restenosis was observed in 6 cases (30%). The rate of target lesion revascularization (TLR) was 5 of 23 (22%) in the patients treated with ELCA.
It is concluded, ELCA is a safe and efficient debulking technology for treating diffuse in-stent restenosis.

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This study was undertaken in acute myocardial infarction (AMI) patients with non-insulin-dependent diabetes mellitus (type 2 DM) to investigate their impaired chronotropic response to exercise. Seventy-one AMI subjects entered the study, 30 with type 2 DM and 41 age- and body mass index-matched non-DM (control) patients. One month after the onset of AMI, these patients underwent cardiopulmonary exercise testing on a treadmill under a ramp protocol. Anaerobic threshold (AT) and peak oxygen uptake (peak VO₂) were determined as indicators of exercise capacity. Plasma norepinephrine (NE) concentration was measured in blood samples obtained at 2 time points: during pre-exercise rest and immediately after peak exercise. The change in NE concentration during exercise, as an index of sympathetic nervous activity, was calculated as a percentage: ΔNE = [(NE during exercise) - (resting value)]/(resting value) × 100. The change in heart rate (HR) during exercise was calculated as a simple difference: ΔHR = [(peak HR) - (rest HR)]. Index of chronotropic response to exercise was then quantified as the ΔHR/ ΔNE during exercise. No significant intergroup differences in ejection fraction at rest or HR at peak exercise were observed. However, VO₂ at AT, peak VO₂, ΔHR, and ΔHR/ΔNE were significantly lower in the type 2 DM group than in the non-DM group. ΔHR correlated with VO₂ at AT (r = 0.49, P < 0.001) and with peak VO₂ (r = 0.53, P < 0.001) in all subjects. Also, ΔHR/ ΔNE correlated with VO₂ at AT (r = 0.42, P < 0.001) and with peak VO₂ (r = 0.44, P < 0.001) in all subjects. AMI patients with type 2 DM had impaired cardiopulmonary responses to maximal and submaximal exercise testing and impaired chronotropic response to exercise, even though their cardiac function at rest was similar to that of non-DM AMI patients. The data suggest that one mechanism of impaired cardiopulmonary response to exercise in AMI patients with type 2 DM groups is an impaired chronotropic response.

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White blood cells (WBC) destabilize coronary artery plaques and an elevated WBC count is a risk factor of coronary artery disease (CAD). Nevertheless, the differences between the forms of CAD in the relationship with WBC count remain to be elucidated. To study these differences, we reviewed the health-checkup records from 1994 to 1999 for 6021 Japanese post office workers without any cardiovascular abnormalities. Baseline WBC counts of patients with acute coronary syndrome (ACS) were significantly higher than those of subjects free from coronary artery disease (mean ±SD = 9210 ±2703/μL vs 6205 ±1635/μL, P < 0.001), while the patients with stable angina pectoris (sAP) (6233 ±1528/ μL) were similar to subjects without coronary artery disease in baseline WBC counts. Hypertension at the baseline was related to sAP (relative risk [95% CI] = 61.78 [17.29 to 78.66]) but not to ACS. Conversely, hypercholesterolemia and cigarette smoking were risk factors for ACS (relative risk [95% CI] = 11.48 [2.39 to 18.03] and 10.04 [3.00 to 12.12], respectively) but not for sAP. Multivariate logistic regression analysis found only WBC count (1000/μL) discriminated between ACS and sAP (P = 0.038, odds ratio 2.049 [1.042-4.016]). We conclude that an elevated WBC count may be a risk factor of ACS but not sAP, and this finding is consistent with previous reports demonstrating the effects of WBCs in the destabilization of coronary artery plaques.

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The TIMI frame count (TFC) is an index of coronary blood flow, and a correction in TFC (CTFC) for left anterior descending artery (LAD) has also been proposed. However, the relationship between TFC and intravascular ultrasound (IVUS) parameters of culprit coronary arteries has not been reported. The aim of this study was to investigate IVUS-derived correlates of TFC before and after stenting, and to assess the validation of its correction for LAD. The study population was comprised of 38 patients with acute coronary syndrome or stable coronary artery disease studied by IVUS before and after stenting (LAD 21, circumflex 8, right coronary artery 9). For LAD, CTFC was calculated by dividing the TFC by 1.7. Preintervention luminal % area stenosis was 82 ±12.3%. Pre-and postintervention target lesion lumen areas were 1.8 ± 0.5 mm² and 8.5 ± 0.5 mm² (P < 0.0001), and CTFC were 35.3 ±16.8 and 16.9 ± 4.3 (P < 0.0001), respectively. In the 76 IVUS studies, CTFC showed a good correlation to luminal % area stenosis (r = 0.69, P < 0.001), and a good and negative correlation to target lesion lumen area (r = −0.70, P < 0.001). Postprocedural improvement in CTFC showed a modest correlation to acute lumen gain (r = 0.5, P < 0.05). With respect to culprit arteries, pre and postintervention IVUS parameters and CTFC, and net CTFC change after stenting were not different (P > 0.05). However, uncorrected TFC of LAD was significantly higher than both the CTFC of LAD and TFC of the other two coronary arteries (P < 0.05).
We conclude that CTFC is closely correlated to target lesion luminal area and luminal % area stenosis whereas a modest correlation is present between improvement in CTFC and acute luminal gain due to stenting. Results from different coronary arteries with comparable IVUS parameters seem to support the validity of a correction in TFC.

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QT prolongation and torsades de pointes have been documented in patients administered cisapride and its blocking of potassium channels in myocytes has been suggested as the mechanism. An interaction with cytochrome P450 CYP3A4 inhibitor drugs like macrolide and azole antifungals is also thought to be a possible mechanism. Since mosapride has characteristics similar to cisapride, we examined the effects of mosapride on the electrocardiogram and pharmacokinetics before and after its coadministration with erythromycin. Ten healthy male volunteers were repeatedly administered mosapride 15 mg/day for 7 days followed by coadministration with erythromycin 1200 mg/day for 7 days. Coadministration with erythromycin resulted in a 1.6-fold increase in the C_max of mosapride and prolongation of t_1/2 from 1.6 to 2.4 hours, indicating the inhibition of mosapride metabolism. However, there were no significant differences in the QT interval and QTc between mosapride alone and concomitant use with erythromycin. There was no correlation between the electrocardiographic parameters and plasma mosapride concentrations, and no case exceeded the upper limit of the normal range of QTc. Although there was a certain pharmacokinetic interaction between mosapride and erythromycin, their coadministration did not affect the electrocardiogram at all, indicating a reduced likelihood of severe clinical adverse events like QT prolongation and torsades de pointes.

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“Standards on the Implementation of Clinical Trials on Drugs (New GCP)” is a Japanese government policy established in April 1998 with the aim of satisfying scientific and ethical requirements for industry-sponsored research, i.e., registration-directed clinical trials and clinical trials intended to support reexamination or reevaluation applications. Since then, efforts for more effective implementation of clinical trials have been promoted, including establishment of a system to invite more active participation of subjects in clinical trials and improvement of a network of medical institutions conducting clinical trials. These efforts should help to reactivate clinical trials in Japan, which reportedly have become stagnant. Although the New GCP addresses the quality of industry-sponsored clinical trials, investigators also construct study protocols without industry involvement. We reviewed clinical trials submitted by investigators at Gunma University Hospital to institutional review boards (IRBs) from June 1999 to February 2002. Ten clinical research coordinators contributed to the present survey. A total of 151 investigator-initiated clinical trials reviewed included a wide variety of content; and investigators from many institutions and organizations conducted trials. Most of the ethical guidelines for approving proposed trials represented the provisions of the Declaration of Helsinki. However, additional guidelines prepared by the Japanese Ministry of Health, Labour and Welfare were also helpful. Development of a support system for clinical trails requires the contribution of clinical research coordinators. Flexible management and careful attention to both the protocol and its execution by the investigators were also important for promoting clinical trials on the basis of meticulous patient care.

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The aim of this research was to evaluate the possible protective effect of pravastatin on ultrastructural alterations induced by cold stress in the myocardium of rats.
Sixteen EPM-Wistar rats (Rattus norvegicus albinus) were used and distributed into four groups: 1) control; 2) pravastatin; 3) cold stress, and 4) pravastatin + cold stress. A daily oral dose of 10 mg/kg of weight of pravastatin was administered to each rat in groups 2 and 4 for 15 days. The stress induced by cold was obtained by keeping the group 3 and 4 rats in a freezer at -8°C for 4 hours. The animals were killed and the heart and fragments of the left ventricles (LV) were removed and processed prior to conducting electron microscopic analysis.
The ultrastructural alterations in cardiomyocytes were quantified through the number of mitochondrial cristae pattern (cristalysis). The group subjected only to cold stress showed a significant increase in cristalysis (391.9) when compared with control group (42.0). In the cold stress and pravastatin pretreatment group, a statistically significant (96.9)^*, P < 0.05 cristalysis reduction was observed when compared with cold stress group. The mitochondrial cristalysis profiles of the control and pravastatin groups were 42.0 and 65.7, respectively.
Cold stress induced a significant increase in the rate of mitochondrial cristalysis. In the group that received pravastatin and was exposed to cold stress, the drug protected the LV cardiomyocytes. This fact was confirmed by a reduction mitochondrial cristalysis pattern.

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There is still controversy with respect to how an increase in vagal tone changes left ventricular (LV) contractility. It is possible that a difference in LV vagal innervation density may affect the inotropic effect. To test this, we examined the effects of vagal stimulation and acetylcholine (ACh) infusion on the rat ventricle, in which LV vagal innervation density is sparse and a negative force-frequency relationship is uniquely observed. To evaluate LV contractility, we developed an in situ Langendorff preparation, in which the effects of changes in afterload, preload, and coronary flow during an intervention were minimized. Both vagal stimulation and ACh infusion significantly increased LV systolic pressure (34 ± 16%; 36 ± 22%, respectively) and its maximum positive first derivative with slowing of heart rate (51 ± 17%; 46 ± 18%). These effects of vagal stimulation were abolished by pretreatment with atropine. During a fixed heart rate, LV systolic pressure was not changed by vagal stimulation, however, it was decreased slightly but significantly (11 ± 8%) by ACh infusion. In conclusion, LV contractility changes due to ACh release during vagal stimulation were negligibly small, presumably due to a sparse vagal innervation density in rats, and therefore, a bradycardia-dependent indirect positive inotropic effect may be dominant compared to a direct negative inotropic action during vagal stimulation. Thus, the integrated effect of vagal nerve stimulation on LV contractility is different among species, because it is determined by a direct negative inotropic effect, which depends on the vagal innervation density in the left ventricle, as well as by bradycardia-dependent indirect inotropic changes.

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We report an acute myocardial infarction in a patient with a single coronary artery. The right coronary artery arose from the middle portion in the left anterior descending artery through the transverse branch. This type of single coronary artery has not been previously reported. Moreover, this is the first report in which the culprit lesion in a patient with a single coronary artery was observed by intravascular ultrasound and coronary angioscopy. The patient underwent successful coronary stent deployment.

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A 71-year-old Japanese woman presented with a chief complaint of throbbing sensations in the abdomen. When she was 16 years old, she was exposed to atomic radiation since she was 1.2 km away from the drop zone of the Nagasaki atomic bomb. Abdominal CT performed at the age of 61 revealed the presence of localized calcification below the renal artery, together with abdominal aortic aneurysms measuring 4.9 cm in maximum diameter. Since the abdominal aortic aneurysms enlarged in May 2000, the patient was admitted to our department for further examinations and treatment on July 7. Although the patient did not complain of thoracic symptoms, cardiac catheterization revealed the presence of multiple coronary artery aneurysms and severe stenosis in the main trunk of the left coronary artery and proximal regions of the right coronary artery, together with a complicated collateral circulation course. Coronary artery aneurysms were localized similar to the abdominal aortic aneurysms, and were complicated by severe calcification and obstructive lesions. Coronary arterial bypass grafting was performed after the severity of the coronary artery aneurysms was morphologically evaluated. The course of the abdominal aortic aneurysms was followed without surgical treatment. Although the etiology of the aneurysm formation in this patient was investigated, it remained unclear.

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A 66-year-old Turkish male patient admitted to our emergency department with a transient ischemic attack (TIA) is described. Transthoracic echocardiography revealed apical hypertrophic cardiomyopathy (HCM) and an ECG sinus rhythm. Transesophageal echocardiography detected severe spontaneous echocontrast (SEC) in the left atrial (LA) cavity with apical hypertrophy.

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Though acute rheumatic fever (RF) is now rare in Japan, it continues to be an important disease condition that physicians should be prepared to diagnose and treat. We describe a patient with acute RF accompanied by transient aortic regurgitation (AR). The AR was detected only by echocardiography. There were no other indications, and it disappeared after treatment with prednisolone. The changes in cardiac valves in the early phase of RF have been the subject of only a few case studies. Echocardiography is quite valuable in the workup of patients with acute RF and should be performed even if there are no signs of cardiac involvement.

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