Previous studies have suggested that patients with acute myocardial infarction (AMI) who presented without chest pain had an unfavorable prognosis due to undertreatment. Despite this, few studies have been conducted on the topic, particularly in Japan. The present analysis aimed at determining whether Japanese AMI patients without chest pain are undertreated and experience higher mortality during hospitalization. Data from the Tokai Acute Myocardial Infarction Study II sample were used, which is a prospective study of all consecutive patients admitted to the 15 acute care hospitals in the Tokai region with the diagnosis of AMI from 2001 to 2003. Data on baseline and procedural characteristics and hospital outcome were collected. Differences in the baseline and procedural characteristics and clinical outcomes between patients presenting with and without chest pain were assessed. We evaluated a total of 1769 patients who presented with chest pain and 452 who did not. The patients with AMI in the absence of chest pain were older and were more likely to have worse clinical conditions than those with chest pain. They were more likely to be undertreated, although the probability of vasopressor use was higher. The patients without chest pain had a significantly higher in-hospital mortality rate than those with chest pain. According to multivariate analysis, however, chest pain was not identified as an independent predictor of in-hospital death. The results suggest that the higher in-hospital mortality rate among Japanese AMI patients without chest pain could be accounted for by differences in clinical conditions.

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The decision to admit a patient to a coronary care unit for acute coronary syndrome (ACS) has serious medical and financial consequences. In this study, we aimed to develop a computer program to predict the existence of ACS in patients with chest pain at home; it is intended that patients will be able to access the program via the website to test its validity.
This study proceeded in two phases. In the first phase, a computer-based decision protocol was developed using recursive-partitioning analysis to predict ACS in 250 patients with chest pain on the basis of their historical data. In the second phase, this protocol was tested in 115 patients for diagnosis of ACS prospectively. Thirty-two of the patients answered the algorithm questions on the website. All of the patients who visited the website of this study were advised to go to the emergency department.
Although the algorithm showed the presence of ACS in 82 of 115 patients, 60 of 115 patients were diagnosed as having ACS in the emergency department (n = 55) or at follow-up. The agreement between the diagnosis of the algorithm and the true diagnosis was moderate and statistically significant (Kappa coefficient 0.61, P < 0.001). The sensitivity of the algorithm was 100%, although its specificity was 60%. The accuracy of the algorithm in diagnosing ACS was 81%.
The algorithm diagnoses patients with ACS at a high ratio and decreases the number of patients being unnecessarily admitted to the emergency with non-ACS.

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Statins are known to reduce high-sensitivity C-reactive protein (hs-CRP) concentrations and improve endothelial function. However, whether statin withdrawal causes re-elevated concentrations of hs-CRP and von Willebrand Factor (vWF) (a marker of endothelial damage) remains unknown. We hypothesized that the concentrations of hs-CRP and vWF are substantially increased in patients with unstable angina pectoris (UAP) and noticeably decreased following coronary stenting along with atorvastatin therapy. However, re-elevations of these biomarker concentrations occurred once again after withdrawing atorvastatin therapy. We serially examined the plasma concentrations of hs-CRP and vWF in 51 patients with UAP before (day 0) and after (days 21, 90, 180, 270) performing coronary artery stenting. The concentrations of these 2 biomarkers were also measured in 30 healthy control subjects. Patients were treated with atorvastatin (40 mg/day orally) for 180 days, after which the therapy was withdrawn. The hs-CRP and vWF concentrations were significantly higher in the patients than in the healthy control subjects before the procedure (both P values < 0.001). The hs-CRP concentration decreased significantly on day 21 (P < 0.001), and further to a substantially lower level on day 180 (P < 0.0001). However, the hs-CRP level significantly increased again on day 270, as compared with that on day 180 (P < 0.001). The vWF plasma concentration decreased gradually to a significantly lower level on day 180. The concentration of this biomarker did not differ between days 180 and 270. In conclusion, although hs-CRP concentrations decreased markedly following combined stenting and atorvastatin therapy, re-elevation after atorvastatin therapy was withdrawn in UAP patients undergoing coronary stenting was not observed. Conversely, restoration of endothelial function was slow and persistent in these patients.

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Although an association between Chlamydia pneumoniae (Cpn) or Cytomegalovirus (CMV) infection and coronary atherosclerosis has been reported, such an association is less clear for acute coronary syndromes (ACS). The purpose of this study was to investigate the pathogenic roles of Cpn and CMV infection of coronary plaques in ACS. We divided 38 coronary plaque specimens obtained from 38 patients who underwent directional coronary atherectomy or thrombectomy into an ACS group (n = 21) and a non-ACS group (n = 17). Cpn and CMV in specimens were stained using immunohistochemical techniques and analyzed quantitatively. The detection rate for either Cpn- or CMV-positive cells in ACS patients was slightly higher compared with non-ACS patients. Detection rates for both Cpn- and CMV-positive cells were significantly higher in ACS patients than in non-ACS patients (P = 0.010). Furthermore, the density of Cpn- and CMV-positive cells in plaques was significantly higher in ACS patients than in non-ACS patients (P < 0.003). The results indicate that the presence and severity of Cpn and CMV infection in coronary plaques are greater in patients with ACS compared with non-ACS patients. We conclude that infection with Cpn and CMV in coronary plaques may be involved in the pathogenesis of ACS.

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The aim of the present study was to prospectively compare contrast-enhanced magnetic resonance imaging (CE-MRI) with single-photon emission tomography using ²⁰¹Thallium chloride (SPECT Tl) in the detection of myocardial viability. Patients with chronic coronary artery disease and systolic dysfunction defined by an ejection fraction (EF) ≤ 45% were included. CE-MRI was performed 10-15 minutes after the administration of a gadolinium-based contrast agent using an Inversion Recovery Turbo FLASH (fast low-angle shot) sequence. A 4-hour rest redistribution protocol was used for SPECT Tl. Radionuclide ventriculography was used for the assessment of EF. Forty patients with an EF of 33.1 ± 7.7% were included. Thirty-two underwent a follow-up examination after revascularization. Comparison of viability assessment was performed in 1360 segments. Agreement was noted in 1065 (78.3%) segments, resulting in a kappa value of 0.336. Discrepancies were observed in 96 SPECT Tl viable segments that were described as nonviable according to CE-MRI and in 199 SPECT Tl nonviable segments that were viable in the CE-MRI study.
In patients undergoing the follow-up examination, EF increased by 5.5 ± 7.3% (33.6 ± 8.6% to 39.2 ± 9.7%), but the relation between the amount of dysfunctional viable myocardium defined by both methods studied and the change in EF after revascularization was very weak and not statistically significant.
Moderate agreement in the myocardial viability assessment between CE-MRI and SPECT Tl was observed. CE-MRI seems to be more accurate in identifying myocardial viability in inferior and inferolateral segments. We were unable to verify if either of the methods studied is useful for the prediction of EF improvement after revascularization.

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The 6 minute walk test (6 MWT) has been shown to provide a clinically useful index of functional capacity in chronic heart failure. We hypothesized that similar results would be found in patients who had a recent (ie, within a week) myocardial infarction (MI). Twenty-five patients (23 males, aged 43 to 72 years) who had undertaken an exercise stress test without complications underwent 3 consecutive 6 MWTs (1 hour apart). Heart rate, systolic and diastolic blood pressure, the level of perceived exertion (Borg scale), and the walking distance were determined. In addition, chest pain was assessed by a 0 to 10 numerical rating scale (NRS) and the ECG was continuously monitored. All subjects were able to successfully complete the exercise tests without major cardiovascular complications: mild chest pain (NRS 1 to 3) was found in 3 patients. A Bland-Altman analysis revealed that the mean bias ± 95% confidence interval of the differences on distance walked between test 2 - test 1 were substantially higher than test 3 - test 2 differences (18 ± 66 m and 6 ± 41 m, respectively). The intraclass correlation coefficients were consistently high for all physiological and sensorial responses at the end of the 6 MWTs (range, 0.75 to 0.95). The 6 MWT is a safe and reproducible measurement of functional capacity in stable patients after a noncomplicated MI, even when performed within a week of the event. Therefore, this test might be useful for the evaluation of exercise tolerance in phases I and II of inpatient cardiovascular rehabilitation programs or to assess functional responses to selected interventions.

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The frequency of Brugada sign was found to differ among ethnic groups. Yet, there is no data regarding the prevalence of Brugada syndrome and sign in our country. The aim of this study was to determine the frequency of a Brugada-type electrocardiogram (ECG) pattern in southern Turkey.
A total of 1238 subjects (males, 671, females, 567) were included in the study. The previously archived ECGs of 807 subjects without any evidence of structural heart disease were chosen randomly and evaluated. In addition, prospective analysis of the ECGs of 431 subjects (males, 293, females, 138) randomly chosen from healthy university students were also included. The mean age was 38.9 ± 17.6 years. Six subjects (0.48%) had a Brugada-type ECG pattern. One (0.08%) of them had the coved-type and 5 (0.40%) had the saddleback-type. All subjects were asymptomatic.
A Brugada-type ECG pattern was obtained in 1 (0.17%) female and in 5 (0.74%) males (OR: 4.2 CI: 0.5-36.4, P = 0.2). The Brugada-type ECG pattern frequency was 0.12% in subjects ≥ 25 years old and 1.16% in subjects between 17-24 years old (OR: 9.4 CI: 1.1-81.2, P = 0.02). Young males between 17-24 years had the highest (1.70%) frequency.
The results indicate that the frequency of the Brugada-type ECG pattern was 0.48% in the general population, being more prevalent in young males in our region. These results are similar to the findings of studies performed in other countries.

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The aim of this study was to conduct a longitudinal follow-up on age-related changes in 24-hour total heart beats (THBs) and total premature beats and their correlations in healthy elderly subjects. In 15 healthy elderly subjects (mean age, 70.0 ± 4.1, age range at 1st recording, 64 to 80 years, 10 females, 5 males), we conducted Holter monitoring twice at an interval of 15 years and analysed age-related changes in THBs, atrial premature beats (APBs), and ventricular premature beats (VPBs), as well as their correlations.
The results indicated that THBs, APBs, and VPBs all significantly increased with age in the healthy elderly subjects at a mean age of 70.0 ± 4.1 (THB: 91074.1 ± 11515.3 versus 99457.5 ± 12131.0; P = 0.0004, APB:119.2 ± 97.8 versus 884.4 ± 1193.8; P = 0.0008, VPB: 15.2 ± 53.6 versus 140.7 ± 228.9; P = 0.0328). Moreover, we divided the subjects into increase and nonincrease groups based on the age-related changes in APB and VPB for 15 years ([n]; Inc-APB: Noninc-APB = 6 : 9, Inc-VPB: Noninc-VPB = 5 : 10). In the increase groups, premature beats tended to increase in proportion to changes in THBs with age (APB: Y = 207.488 + 0.136 * X, r = 0.848, P = 0.0303; VPB: Y = -27.594 + 0.028 * X, r = 0.727, P = 0.1921).
In conclusion, this 15-year follow-up of Holter recordings in healthy elderly subjects revealed that THBs, APBs, and VPBs increased with age, and that the increases in premature beats, especially APBs, were in proportion to those in THBs.

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The aim of this study was investigate the effects of carvedilol therapy on ventricular repolarization characteristics as assessed by QT dispersion (QTd) and heart rate variability (HRV) in patients with heart failure.
Thirty-one patients with heart failure (mean age, 63.9 years) were included in the study. Carvedilol was administered in addition to standard therapy for CHF at a dose of 6.25 mg/day and uptitrated to the maximum tolerated dose. Control group consisted of 14 patients with heart failure (mean age, 69.4 years) who could not take carvedilol due to several reasons. All patients were followed-up 6 months. QT dispersion (QTd), and corrected QTd (QTcd) values were calculated at baseline and at the end of follow-up. Time domain and frequency domain heart rate variability analysis were performed with ambulatory Holter ECG.
Mean carvedilol dose was 23.9 ± 13.9 mg. Significant reductions were observed in the QTd (P = 0.016) and QTcd (P = 0.001) with carvedilol therapy, whereas QTd (P = 0.47) and QTcd (P = 0.43) did not change significantly in the control group. The QT maximum value did not change significantly but the QT minimum value (P = 0.03) was significantly increased after carvedilol therapy. Although the mean SDANN value was improved (P = 0.039), other HRV parameters such as mean SDNN (P = 0.32), rMSSD (P = 0.74), and the LF/HF ratio (P = 0.35) did not change significantly after carvedilol therapy.
This prospective controlled study shows that carvedilol therapy decreased QT dispersion and improved ventricular repolarization characteristics but did not change autonomic dysfunction in patients with heart failure.

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The percutaneous cardiopulmonary support system (PCPS) has been widely accepted for the treatment of patients with severe cardiac failure. This system, which uses Seldinger's method through a percutaneous approach, enables rapid application in emergency situations. However, the indication for deployment and discontinuation of PCPS has not yet been established. We evaluated the results of PCPS use for the treatment of patients with severe cardiac failure and investigated factors that would predict successful weaning from PCPS.
A total of 32 patients (23 men and 9 women) who had PCPS for the treatment of severe cardiac failure between January 1997 and October 2004 were retrospectively reviewed. The mean age of the patients was 57 ± 17 years (range, 14 to 78 years). PCPS was necessary for severe cardiac failure after cardiac surgery in 15 patients, pulmonary infarction in 4, acute myocardial infarction in 3, acute myocarditis in 3, and other causes in 7.
The mean duration of PCPS support in all 32 patients was 134 ± 117 hours (range, 8 to 532). Twelve patients (38%) could be weaned from PCPS (group A), while the remaining 20 patients (62%) could not (group B). The incidence of cardiac arrest prior to PCPS use (n = 10, 31%) was significantly (P < 0.05) lower in group A (1/12, 8%) than in group B (9/20, 45%). There were significant differences in the APACHE II scores, urine output, serum lactate levels, and epinephrine and dopamine dose received from PCPS induction to 72 hours after PCPS use between the 2 groups (P < 0.05). Multivariate logistic regression analysis showed that an episode of cardiac arrest prior to PCPS induction was the only significant predictor for the unsuitability for discontinuation of PCPS.
This retrospective study showed the limitation of PCPS therapy for patients with an episode of cardiac arrest who did not show improvement in their APACHE II score, urine output, serum lactate levels, and catecholamine dose received within 72 hours after PCPS induction. These results may help formulate criteria for indication and discontinuation of PCPS for patients with severe cardiac failure.

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There have only been a few studies of the chronobiological occurrence of acute aortic dissection (AAD), and most were international and multicentered. The aim of the present study, conducted at only one center, was to determine the most frequent daily, monthly, and seasonal occurrences of AAD.
The study population included 204 patients (66.5% male) treated at our institute between January 1, 1998 and January 1, 2004. A significantly higher frequency of AAD occurred from 6:00 AM to 12:00 noon, compared with other time periods (P < 0.001). The results showed a significant circadian variation in AAD (P < 0.001) with a peak between 9:00 AM and 10:00 AM. No significant variation was found for the day of the week; however, AAD occurred most frequently on Wednesday and Monday. The frequency of AAD was found to be significantly higher during winter versus other seasons (P < 0.001). The analysis of monthly variations of the onset of AAD confirmed a peak in February (12.9%) and in January (12.3%).
Similar to other cardiovascular diseases, AAD exhibits significant circadian and seasonal/monthly variations. Our findings indicate that the prevention of AAD, especially during the aforementioned vulnerable periods, is possible by adequate tailoring of the treatment of hypertension, which is the main AAD predisposing factor.

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The aim of the present study was to evaluate the effects of IV lidocaine on autonomic cardiac function changes in tracheal intubation (TI) during sevoflurane anaesthesia by using more reliable parameters, namely, the analysis of QT dispersion and heart rate variability (HRV) from Holter monitoring. In this prospective, double-blind study, 44 American Society of Anaesthesiologists class I-II patients scheduled for hysterectomy were randomly and equally divided into 2 groups; a control sevoflurane group (group S, n = 22) and a lidocaine sevoflurane group (group LS, n = 22).
Before the induction of anaesthesia, the electrocardiograms (ECG) of all patients were recorded for 3 minutes as baseline parameters. In both groups, the anaesthesia was induced with 7% sevoflurane in O₂ at 6L min^-1 via a facemask for 2 minutes. However, before the induction of sevoflurane anaesthesia in group LS, 1 mg kg^-1 of lidocaine was given intravenously (IV). For muscle relaxation during TI, vecuronium was given to all participants. Three minutes after administration of vecuronium, TI was performed and an ECG was recorded synchronously for another 3 minutes. The results from the later records were used as postintubation parameters.
Baseline and postintubation data were analysed. When compared to baseline values, postintubation LF/HF and SDNN values were increased in group S (P = 0.005, P = 0.001, respectively), whereas postintubation LF and HF values were decreased in group LS (P = 0.014, P = 0.041, respectively). Under the influence of sevoflurane anaesthesia, TI resulted in sympathetic activation. However, this activation was attenuated by the administration of IV 1 mg kg^-1 lidocaine 5 minutes prior to TI.

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The objective of the present study was to determine if carvedilol protects against myocardial degeneration and fibrotic change, and reduces mortality in TO2 hamsters.
Carvedilol was administered intraperitoneally to 8 week-old TO2 hamsters for 21 weeks at a dose of 11 mg/kg/day. There were 15 TO2 hamsters in the carvedilol group (group C) and 10 in the untreated group (group N). The control group consisted of 11 Fb hamsters (group F). The mortality rate was determined from the number of surviving hamsters after 29 weeks. Myocardial fibrosis was evaluated by MRI and histopathological examination. EF and LVDd were determined by echocardiography at 8 and 29 weeks, while the MRI score was calculated at 29 weeks.
Mortality, histopathological fibrosis, and MRI score were all lower in group C than in group N. Carvedilol had a protective effect against myocardial fibrosis and decreased the mortality rate in TO2 hamsters.

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The objective of the present stndy was to elucidate the mechanisms underlying the so-called injury potentials, including the origin of monophasic action potentials and the role of recording electrodes.
Two-dimensional computer simulation was performed for cardiac tissue containing an inactivated region due to high extracellular K concentration. Myocardial activation was reproduced using a membrane model. The bidomain model was utilized for the calculation of intra-and extracellular potentials.
A bipolar lead from electrodes at injured and intact regions showed a monophasic curve corresponding to the transmembrane potential of the fiber under the electrode of the intact region. Unipolar leads from injured and intact regions showed monophasic and biphasic curves, respectively. Lowering the extracellular conductivity was associated with an increase in the wave amplitude.
The injured region of myocardium was associated with monophasic potential variations. A bipolar lead with electrodes at injured and intact regions reflected the activity of the intact region.

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Pulmonary hypertensive model rats were prepared by treating them with monochrotaline (MCT). Using these model rats, we examined myocyte remodeling in the right ventricle in response to increased right ventricular pressure.
Male Sprague-Dawley rats were divided into 2 groups. Group M received MCT and group C received physiological saline. The 2 groups were examined at weeks 2, 5, and 7 after MCT or saline injection, respectively. At week 2, a significant difference in cell form was not observed in either group. At week 5, cell volume and myocyte cross-sectional area (CSA) of the right ventricle in group M were significantly greater than those in group C. At week 7, cell volume, CSA, and cell length of the right ventricle in group M were all significantly greater than those in group C. These results suggest that pulmonary hypertension causes hypertrophy, accompanying the enlargement of CSA in the right ventricle, and that cells lengthen in the phase of right ventricular failure.
These results are similar to the changes observed in left ventricular myocytes due to overload pressure. Both right and left ventricular myocytes may share a common mechanism for myocyte remodeling as an adaptive and maladaptive response to increased ventricular pressure.

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Blunt chest trauma rarely induces acute myocardial infarction. We report a 36-year-old man who suffered from blunt trauma to the anterior chest wall while operating a punching machine. This case is the first report of simultaneous blunt chest trauma to the left anterior descending artery and left circumflex artery. The patient was treated surgically and discharged without any serious sequela. Early detection of the lesion site is important with regard to selecting the appropriate treatment strategy in patients with coronary injury caused by blunt chest trauma. Routine 12-lead electrocardiography and serial cardiac enzyme evaluation are necessary in every patient with chest trauma because they supply crucial information about the extent of cardiac damage. Treatment with primary angioplasty or bypass surgery should be based on the characteristics of the lesion and the associated problem.

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A patient with recurrent abdominal pain was admitted to our hospital. Computed tomography showed a soft dense mass surrounding the abdominal aorta at the infrarenal level, which was compatible with retroperitoneal fibrosis. ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) positron emission tomography showed abnormal uptake of ¹⁸F-FDG into these lesions. Two months after the initiation of corticosteroid therapy, the abnormal uptake of ¹⁸F-FDG had ceased along with a reduction in the fibrous mass surrounding the abdominal aorta.

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