It has been suggested that oxidative stress may play a role in the pathophysiology of heart failure. However, little is known about the clinical relationship between oxidative stress and left ventricular dilatation after acute myocardial infarction (AMI). We prospectively studied 28 consecutive patients, successfully treated with primary coronary angioplasty, after their first AMI. To evaluate oxidative stress, plasma oxidized low-density LDL levels (U/mL) were measured serially 1 day, 7 days, 14 days, 30 days, and 90 days after the onset of AMI using a specific sandwich enzyme-linked immunosorbent assay. Left ventriculography and coronary angiography were obtained in all patients 3 months after the AMI and infarct-related arteries were all patent. Peak plasma oxidized LDL levels were seen 7 days after AMI (after 1 day: 14.71.5, 7 days: 21.02.8, 14 days: 20.22.8, 30 days: 18.32.5, 90 days: 16.52.3 U/mL). Plasma oxidized LDL levels 7 days after AMI were significantly correlated with left ventricular end-diastolic volume (1157 mL; r=0.54, P=0.0025) and end-systolic volume (585 mL; r=0.49, P=0.008) 3 months after the AMI. Moreover, they were also correlated with end-diastolic volume index (684 mL/m², r=0.40, P<0.05). However, no correlation was seen between peak plasma oxidized LDL levels and ejection fraction. These findings suggest that oxidative stress may play an important role in the development and progression of left ventricular remodeling after AMI.

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In this prospective study, we monitored two laboratory parameters, C-reactive protein (CRP) and fibronectin (FIN) levels, in 30 patients undergoing elective surgery for ischemic heart disease. These patients were divided into three groups according to the surgical procedure used: group A, approach through a median sternotomy with the use of extracorporeal circulation; group B, approach through a median sternotomy without the use of extracorporeal circulation; and group C, approach through a left anterior small thoracotomy (LAST) without the use of extracorporeal circulation. Peak CRP levels were found in all three groups on the second postoperative day, with the mean levels being statistically significantly higher in group C. This group also showed the highest mean CRP levels on the third and fourth postoperative days, with the difference being statistically nonsignificant. These findings can be explained by an enhanced production of cytokines, which in turn trigger CRP synthesis, induced by postoperative pain due to the LAST procedure. No statistically significant correlation between preoperative CRP levels and their postoperative development was found. None of the groups studied showed any statistically significant decrease in FIN plasma levels, either prior to adjustment for hemodilution or after adjustment for hematocrit and serum albumin.

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We hypothesized that the change in aortic elastic properties could directly be shown with color Doppler tissue imaging (CDTI), that these findings could be related to aortic stiffness and distensibility and that, through these, coronary artery disease (CAD) could be predicted.
One hundred and twenty six patients (group I: 83 with CAD, mean age 54±10 years, 18 female, 65 male; group II: 43 without CAD, mean age 53±10 years, 27 female, 16 male) having been evaluated for coronary artery disease by angiography were examined by echocardiography. Arterial pressure was measured immediately before echocardiographic evaluation. Internal aortic systolic and diastolic diameters by M-mode echocardiography and aortic upper wall tissue velocities (Aortic S, E, A, m/sec) by CDTI were measured 3 cm above the aortic valve. Lateral mitral annulus tissue velocities (Annulus S, E, A, m/sec) were also recorded. Aortic distensibility (cm²•dynes^-1) and aortic stiffness index were calculated using formulas. In the statistical analyses, CAD risk factors and left ventricular ejection fraction were used for adjustment.
Aortic stiffness (2.79±3.49 vs 1.62±1.31, P=0.03), distensibility (1.55±1.46 vs 2.37 ±3.08, P=0.04), and aortic S velocity (0.057 ±0.016 vs 0.064±0.015, P=0.02) differed significantly between groups I and II. After adjustment, while aortic stiffness and S velocity were still statistically different (P=0.04; P=0.03 respectively), the significance of the difference in aortic distensibility disappeared (P=0.051). Aortic stiffness and aortic S velocity (0.06 m/sec<) were important CAD determinants (Odds ratio=1.4 P=0.03; Odds ratio=3.6 P=0.01, respectively), but aortic distensibility was not. Aortic stiffness was correlated only with aortic S velocity (r=-0.28, P=0.01), and aortic distensibility had a significantly positive correlation with aortic S velocity (r= 0.20, P=0.02). The interobserver and intraobserver correlation coefficients for aortic S velocities were 0.65 and 0.71, respectively (P<0.05).
Elastic properties of the aorta can directly be assessed by reproducibly measuring the movements in the upper wall of the aorta by CDTI. Reduced aortic S velocity is associated with increased aortic stiffness. Increased aortic stiffness and reduced aortic S velocity are important predictors of CAD.

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Coronary sinus (CS) pacing has been shown to prevent induction of atrial fibrillation (AF) by suppression of the propensity of atrial premature beats at high right atrium (HRA) to induce local conduction delay at the posterior triangle of Koch. However, other mechanisms of CS pacing in preventing induction of AF have not been explored. This study investigated whether a differential conduction delay exists between the HRA and distal CS pacing in patients with paroxysmal AF but not in patients without AF. Nine patients with atrioventricular reentrant tachycardia utilizing a left accessory pathway undergoing catheter ablation were included in this study. Group 1 consisted of 5 patients with clinically documented paroxysmal AF and group 2 4 patients without a history of AF. The effective refractory periods (ERPs) of HRA, distal CS, and four different left atrial sites were determined. The interatrial conduction time and conduction delay between the HRA and distal CS during HRA or distal CS pacing were measured. The interatrial conduction delay (ICD) from the HRA to the distal CS during HRA pacing was significantly longer than that from the distal CS to the HRA during distal CS pacing in patients of group 1. However, the ICD from the HRA to the distal CS during HRA pacing was not significantly longer than that from the distal CS to the HRA during distal CS pacing in group 2 patients. A differential conduction delay between the HRA and the distal CS pacing is present in this specific population of patients with paroxysmal AF but not in patients without AF. The shorter conduction delay during DCS pacing may contribute to the prevention of induction of AF.

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Predictors of recurrence in lone atrial fibrillation have not been clearly identified. Acoustic quantification (AQ) is a promising method in the assessment of left atrial (LA) volumes. The purpose of the present study was to investigate the potential of LA volumes obtained by standard manual tracing and AQ methods in predicting AF-recurrence after restoring the sinus rhythm in patients with lone AF, and to test the agreement between the two approaches. Standard echocardiography combined with AQ was performed in 28 patients with lone AF one hour after the sinus rhythm was regained, and in 10 controls. LA volumes were determined by conventional manual tracing and AQ methods. AQ waveforms of LA were obtained by drawing a region of interest around the LA border. The agreement of the two methods was tested by Bland-Altman analysis. Patients were followed up for 6 months for the occurrence of AF recurrence. A good correlation was observed between AQ and manual tracing methods in determining both minimal (r=0.59) and maximal (r=0.88) LA volumes. Patients with AF recurrence had a significantly larger maximum LA volume as assessed with both methods (P<0.05 for both). M-mode derived LA dimension and isovolumic relaxation time were additional predictors of recurrence in patients with lone AF. In lone AF, patients prone to recurrence could be predicted by determining LA maximum volume assessed either by AQ or manual tracing methods. AQ provides on-line, accurate estimation of LA volumes.

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Cardiac complications are major limiting factors regarding the success of high-dose chemotherapy supported by blood stem cell transplantation (BSCT). The cardiotoxicity of cyclophosphamide remains obscure relative to that of anthracyclines. The aim of this study was to estimate noninvasively the cardiotoxicity of cyclophosphamide administered during the pretransplant conditioning of BSCT for patients with various hematological diseases. A total of 27 consecutive patients were divided into two groups depending on the conditioning regimen, ie, group A (n=15) which received cyclophosphamide (median dose of 120 mg/kg; range 100 to 200 mg/kg) and group B (n=12) which did not. Ultrasound cardiograms (UCG) and signal-averaged electrocardiograms (SAECG) were recorded in the two groups both preceding and following the BSCT. There were no statistical intergroup or intragroup differences in left ventricular (LV) dimensions or contractile function. Significant (P<0.01) posttransplant increases in interventricular septal wall thickness and Ap/Ep ratio were noted in group A. Moreover, the filtered QRS duration as estimated by SAECG was prolonged (P<0.05) whereas the summated LV voltage (S_V1+R_V5) was reduced in the posttransplant period only in group A. These results suggest that early cyclophosphamide cardiotoxicity was characterized by LV diastolic rather than systolic dysfunction. These findings may contribute to acute hemodynamic deterioration observed after cyclophosphamide-containing conditioning chemotherapy.

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Seven patients with malignant cardiac tumors were treated surgically in the Department of Cardiothoracic Surgery of the University of Tokyo between 1981 and 2000. Their treatments and outcomes are summarized and discussed. The ages of the patients ranged from 21 to 70 years old (mean: 49.5±15) and there were three males and four females. The histopathological diagnoses were hepatocellular carcinoma (HCC), spindle cell sarcoma, round cell sarcoma, osteosarcoma, renal cell carcinoma, and leiomyosarcoma. In four of the cases, the tumor extended or metastasized from other organs, while in the other three cases it originated in the heart. Before the cardiac operation, an above-knee amputation, left nephrectomy, transarterial embolization, or extended right hepatic lobectomy had been performed to treat the primary site of the tumor. Tumor resection using cardio-pulmonary bypass was performed in every case. The NYHA classification of heart failure was significantly improved (preop: 3.3±0.8, postop: 1.9±0.7 [P<0.001]). The mean survival period of the patients who died was 8.8±7.0 months. A patient with renal cell carcinoma is still alive after 87 months of follow-up.
In summary, surgical treatment of malignant tumors of the right heart can improve the QOL in patients with cardiac failure. However, its effectiveness was temporary in all cases except one case of renal cell carcinoma.

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Although cardiac NHE1 is activated during myocardial ischemia and reperfusion injury, little is known about changes in expression in non-infarcted myocardium after acute myocardial infarction (AMI). The purpose of this study was to examine left ventricular function and region dependent NHE1 expression after myocardial infarction. Therefore, we produced two AMI models in rats, a small infarction model which was continuously ligated at the branches of the left coronary artery, and an extensive infarction model continuously ligated at the root of the artery. We examined NHE1 mRNA expression using RNase protection assay and protein levels using Western blot analysis in non-infarcted myocardium during the 24 hour period after AMI. The level of NHE1 mRNA and protein expression in the whole heart including the infarcted myocardium did not change after a small infarction. On the other hand, in the case of an extensive infarction, the levels of NHE1 mRNA and protein expression decreased significantly by 21.5% (P<0.05) and by 22.0% (P<0.05), respectively, in non-infarcted myocardium. Left ventricular systolic pressure (LVSP) decreased significantly by 13% and 38% with the branch and root ligation, respectively. However, left ventricular end-diastolic pressure (LVEDP) only increased with the root ligation. These results indicate that NHE1 expression decreased in response to extensive myocardial infarction only in non-infarcted myocardium. The present study may be important in furthering the understanding of NHE1 in myocardial infarction and suggests that decreased expression of NHE1 in non-infarcted myocardium may decrease the extent of cardiac cell injury.

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Ventricular fibrillation in a patient with ventricular preexcitation is usually due to atrial fibrillation with an extremely rapid ventricular rate from which it degenerates. We present a case with Wolff-Parkinson-White syndrome and coexistent idiopathic ventricular fibrillation. The patient, a 23-year-old male, had had a cardiac arrest four years earlier. In electrophysiological study, the accessory pathway was located in the left posteroseptal region and successfully eliminated with radiofrequency catheter ablation. After the ablation procedure, ventricular fibrillation was induced with programmed ventricular stimulation. A dual chamber implantable cardioverter defibrillator was implanted in the patient.

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Subacute left ventricular free wall rupture is a rare complication in acute myocardial infarction. With the increasing use of thrombolytic agents and glycoprotein IIb/IIIa inhibitors, this complication has been increasing recently. We report a case of subacute cardiac rupture with frank pericardial effusion receiving thrombolytic and glycoprotein IIb/IIIa inhibitor therapies.

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A total of 110 central venous access procedures using Port-A catheters were performed in our center for pediatric patients with oncologic or hematologic diseases over a period of 6 years from November 1994 to June 2000. Spontaneous dislodgement of the outlet catheters was noted in two cases. Both dislodged catheters were located in the left pulmonary artery and were successfully retrieved via the right femoral vein by nonsurgical transvenous snares. Awareness of the possibility of spontaneous catheter dislodgement and embolization of Port-A catheters is important as prompt retrieval will prevent further serious complications. When the procedure is performed by an open surgical method, to reduce the possibility of spontaneous catheter dislodgement, the use of a guidewire is recommended while a Port-A catheter is being inserted into the subclavian vein.

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Fibromuscular dysplasia (FMD) is a nonatherosclerotic, noninflammatory segmental arterial occlusive disorder that involves primarily the renal and carotid arteries, and less often the coronary, iliac, and visceral arteries. We report the case of 78-year-old Japanese woman who presented with acute abdomen complicated by shock. Autopsy revealed hemorrhagic necrosis of the small intestine due to severe narrowing of the mesenteric arteries. Histologically, smooth muscles showed in-bundle hyperplasia surrounding the adventitia together with medial and perimedial fibrodysplasia of these arteries, forming the characteristic petal-like appearance of FMD. No occlusive thrombus was observed. Further, another medial fibrodysplasia type of FMD was also seen in the renal and left circumflex coronary arteries. Unusual proliferation of smooth muscles resulted in the petal-like atypical FMD at the superior mesenteric artery.

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