It is well known that the incidence of left ventricular (LV) thrombosis is high in patients with acute myocardial infarction (AMI). Due to the high degree of structural homology with plasminogen, lipoprotein(a) may produce thrombogenic effects by modulating the fibrinolytic system. However, the role of Lp(a) level in the formation of LV thrombus has not been studied. This study sought to determine whether Lp(a) is a risk factor for LV thrombus in patients with AMI.
We have analyzed clinical, echocardiographic and biochemical data in 102 consecutive patients (aged 58 ± 12 years; 92 men / 10 women) with first anterior AMI. Two-dimensional examination was performed on days 1, 3, 7, 15, and 30. Blood samples were obtained within 12 h after the onset of symptoms and before beginning the therapy. Plasma levels of fibrinogen and Lp(a) were measured using enzyme-linked immunosorbent assay and immunonephelometric methods, respectively. LV thrombus was detected in 20 (20.3 %) patients. No significant difference was found for admission Lp(a) levels between patients with or without thrombus (30.5 ± 17.2 vs 32.3 ± 22.4 mg / dl, p = 0.7). Univariate analysis showed that patients with LV thrombus had a higher wall motion score index (1.8 ± 0.3 vs 1.4 ± 0.3, p = 0.002), a higher peak creatine kinase level (2945 ± 898 vs 1805 ± 1336, I / U p = 0.004), a larger end-diastolic volume (139.7 ± 38.6 vs 114.1 ± 41.8 ml, p = 0.04), a larger end-systolic volume (83.1 ± 34.3 vs 59.2 ± 30.6 ml, p = 0.02 ), and a lower ejection fraction (38 ± 12 vs 47 ± 11, p = 0.04). In multivariate analyses, only peak creatine kinase level (p = 0.04) and LV wall motion score index (p = 0.002) were independent predictors of left ventricular thrombus formation.
These results suggest that Lp (a) is not a risk factor for LV thrombus in patients with AMI. Our data demonstrate that the best predictors of LV thrombus formation after AMI are a high peak creatine kinase level and a high LV wall motion score index.

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The renin-angiotensin system is believed to play important roles in the development of acute myocardial infarction, and gene polymorphisms may also be involved. To investigate the genetic background in patients with acute myocardial infarction, we performed a case control study in a Japanese population.
The study included 150 patients with acute myocardial infarction and 150 healthy, age- and sex-matched controls. We examined polymorphisms of angiotensin II type 1 receptor (1166 A / C), type 2 receptor (3123 C / A), and bradykinin B2 receptor (-58 T /C) in these subjects.
The allelic frequencies of angiotensin II type 1 receptor C and angiotensin II type 2 receptor A were significantly higher in the acute myocardial infarction subjects than in the control subjects, and this tendency was more significant in the younger patients. The combined ratios of angiotensin II type 1 receptor C and type 2 receptor A alleles in patients under 64 years old were significantly higher than in their older counterparts. However the total numbers of conventional coronary risk factors (hypertension, hypercholesterolemia, diabetes mellitus, and smoking) in individual subjects were not significantly different between younger and older patients.
These polymorphisms were found to be involved in the development of acute myocardial infarction, particularly in the younger patients, and it was concluded that the incidence of acute myocardial infarction might be reduced by management from the genotypes.

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Despite the diagnostic efficacy of stress myocardial perfusion imaging, the correlation between the actual perfusion tracer activity and diseased state of a coronary artery has not been studied in detail. We estimated exercise-related perfusion augmentation in relation to disease states of a coronary artery in diabetic and non-diabetic patients by a newly developed quantitative technetium (Tc)-99m-tetrofosmin myocardial imaging technique. Tc-99m-tetrofosmin tomographic imaging with an exercise-rest protocol was performed in 26 stable coronary patients and in 8 age-matched controls. Percent increase (%IR) in myocardial count during symptom-limited submaximal exercise-stress was calculated in 16 non-infarcted polar map segments and in each coronary territory by a subtraction technique with corrections for physical decay and injected tracer doses, and the results were compared with those of angiographically quantified coronary diameter stenosis (%DS). Percent IR and peak heart rate during exercise showed a positive linear correlation both in coronary territories with significant stenosis (%DS ≥ 75%) and in control or non-stenotic (%DS < 75%) territories. The regression line in stenotic regions was, however, significantly (p < 0.01) shifted downward compared to that in non-stenotic regions. Percent IR in stenotic regions showed a significant inverse correlation with %DS. Coronary stenosis of 75% or more was identified by a %IR cutoff value of 40% with 77% sensitivity, 70% specificity, and an accuracy of 72%. In coronary territories with a %DS of less than 75%, %IR in diabetic patients was significantly lower (46 ± 15%) than that in non-diabetic patients (61 ± 25%). Thus, blunted exercise-related augmentation of myocardial uptake of Tc-99m-tetrofosmin correlates with the severity of coronary narrowing and diabetic state.

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Prevention of restenosis after percutaneous transluminal coronary angioplasty (PTCA) continues to be a significant problem. Recent controlled studies have demonstrated that cilostazol suppresses restenosis after PTCA. The effects of ticlopidine, another antiplatelet agent, were compared in terms of outcomes of patients randomized for treatment with the two drugs after PTCA. A total of 35 patients (47 lesions) were assigned prospectively and randomly to ticlopidine (17 patients, 24 lesions) and cilostazol (18 patients, 23 lesions) groups. Minimal luminal diameter (MLD) and percentage of stenosis to reference diameter were estimated before PTCA, just after the procedure and after 4 months follow-up. All patients underwent 4 months angiographic follow-up, at the end of which MLD was 2.03 ± 0.71 mm in the ticlopidine group and 2.05 ± 0.68 mm in the cilostazol group (p = 0.95), and the percentage of stenosis to reference diameter was 31.4 ± 16.7% and 30.0 17.0%, respectively (p = 0.78). The restenosis rate was 12.5% in the ticlopidine group and 17.4% in the cilostazol group (p = 0.69), relatively low as compared to the 20% to 30% reported in previous studies. Adverse drug reactions during the follow-up period were observed in two of the ticlopidine group and none of the cilostazol group. We conclude that both ticlopidine and cilostazol are effective for the prevention of restenosis after PTCA, however the former may be associated with slight side effects.

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Atrial fibrillation, the most common chronic arrhythmia, results in an increased risk of stroke. Anticoagulation therapy can reduce this risk, but appears to be underused. The objective of this study was to examine the use of warfarin and prevalence of stroke in patients with rheumatic, nonrheumatic valvular and nonvalvular atrial fibrillation.
Between January 1993 and December 1998, 457 chronic atrial fibrillation patients with continuous follow-up in our hospital were identified as having rheumatic heart disease (n = 114); nonrheumatic valvular disease (n = 65); or nonvalvular disease (n = 278). Warfarin was used less often in patients with nonrheumatic valvular (16.7%) and nonval-vular diseases (20.1%) than in those with rheumatic heart disease (81.6%, p < 0.001). In contrast, the prevalence of stroke among patients with nonvalvular disease was 40.3% which was similar to the 33.3% found in patients with rheumatic heart disease but significantly higher than the 24.6% found in patients with nonrheumatic valvular disease (p < 0.05). A history of stroke did not alter the trend of use of warfarin among the three groups of patients. Only 20.6% of patients on warfarin received monthly monitoring of prothrombin time.
In conclusion, the anticoagulation therapy in our patients with chronic atrial fibrillation, regardless of their associated valvular diseases, is significantly underutilized. This underuse could account for a high prevalence of stroke. This risk of stroke, however, is less in patients with nonrheumatic valvular disease than in those with nonvalvular atrial fibrillation.

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Sustained monomorphic ventricular tachycardia (VT) can be frequently entrained and interrupted with rapid pacing and the mechanism of the pacing-induced interruption is considered to be due to orthodromic block.
This study focused on the incidence of VT which was interrupted at a critical cycle length and was characterized by an abrupt loss of constant fusion in the surface electrocardiogram (ECG), and the role of orthodromic block as the cause of such characteristic change and interruption of VT was analyzed.
Among 45 consecutive patients with symptomatic VT, rapid pacing was performed in 43 VTs of 39 patients. The exit was mapped as the earliest site of the activation during VT and an electrode catheter was located at the site. Rapid pacing was performed at progressively shorter cycle lengths in steps of 10 msec until VT was interrupted and the timing of the orthodromic and direct capture was compared at the exit.
Abrupt loss of constant fusion was observed in 25 of 39 patients (64.1%): and the loss was invariably associated with interruption of VT. When the timings of the activation of the exit were compared, which were measured from the preceding (n-1) stimulus as the time reference, the direct capture was relatively delayed compared to that of the orthodromic capture. This finding suggests that orthodromic block is the cause of the direct capture as well as the pacing-induced interruption of VT.
In the remaining 13 patients (35.9%), the surface ECG showed a gradual transition into the fully paced QRS morphology. The direct capture was confirmed in the non-fused beats, but it was not necessarily associated with interruption of VT. The interval from the stimulus to the entrained electrogram at the exit showed a gradual prolongation until the exit was finally captured directly from the pacing site.
The confirmation of constant fusion followed by abrupt loss in ECG can be a reliable hallmark of orthodromic block as the cause of the interruption of VT during transient entrainment at a critical paced cycle length.

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It has been demonstrated that successful cavotricuspid isthmus ablation of typical atrial flutter combined with atrial fibrillation (AF) sometimes influences the preablation history of paroxysmal AF. However, the effectiveness of only isthmus ablation on AF itself is unclear.
Endocardial catheter mapping during induced AF was performed around the tricuspid annulus using duodecapolar electrode catheters in 39 patients with drug-refractory paroxysmal AF. Isthmus ablation was performed in 16 patients (41%) in whom catheter mapping during AF showed an organized activation pattern around the tricuspid annulus.
During a mean follow-up of 12.3 months, isthmus ablation was successful in preventing AF in 12 (75%) patients, 8 without medication and 4 with a previously ineffective drug. This success group had a significantly higher F wave amplitude in lead V1 (0.29 ± 0.10 vs 0.15 ± 0.04 mV, p < 0.01), a higher left ventricular ejection fraction (74 ± 9 vs 58 ± 2%, p < 0.05), and a smaller left atrial dimension (35 ± 6 vs 43 ± 4mm, p < 0.05) than the failure group.
Isthmus ablation may be effective in preventing paroxysmal AF with an organized activation pattern around the tricuspid annulus. F wave amplitude, left ventricular ejection fraction, and left atrial dimension were significant predictors of success.

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The clinical manifestations and natural history of acute aortic intramural hemorrhage are not well characterized. Therefore, we have evaluated the differences in the clinical features and prognosis between acute intramural hemorrhage and acute classic aortic dissection.
One hundred two consecutive patients with acute aortic syndrome were diagnosed between November 1994 and May 1999. The clinical features, treatment modalities and survival of these patients were analyzed.
Thirty one of the 102 patients (30%) had intramural hemorrhage and 71 (70%) had aortic dissection. Patients with intramural hemorrhage were older than those with aortic dissection (mean ages 67 and 55 years, respectively) (p < 0.001), and intramural hemorrhage showed a lower proportion of type A than did aortic dissection (32% and 58%, respectively) (p = 0.018). The incidence of severe complications was significantly lower in patients with intramural hemorrhage than in those with aortic dissection (19% and 27%, respectively) (p < 0.001). Mean follow-up duration was 23.1 ± 16.0 months.
The overall death rate for patients with intramural hemorrhage (2 / 31; 6%) tended to be lower than those with aortic dissection (14 / 71; 20%) (p = 0.104). The Stanford classification and treatment modalities were not correlated with death. Late follow-up imaging studies in intramural hemorrhage showed partial to complete resolution of intramural hematoma (9/15; 60%).
In this study, intramural hemorrhage was fairly common, more frequent among older patients, had a lower proportion of type A, and showed a lower incidence of severe complications and a more favorable prognosis in terms of mortality, than aortic dissection.

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Using a high frequency ultrasonic transducer, intramyocardial coronary blood flow (IM-CBF) can be visualized and evaluated during hemodynamic changes in the anterior wall and septum of the left ventricle (LV). We tested the hypothesis that detection and quantitative measurement of IM-CBF of entire LV segments are feasible using a high frequency ultrasonic transducer in conjunction with intravenous contrast injection in vivo.
A 3 - 8 MHz transducer was used to image and measure IM-CBF in 10 anesthetized dogs. We obtained a color Doppler image of IM-CBF in the LV short-axis view after intravenous Levovist(TM) injection (25 mg / ml). The IM-CBF velocity was recorded using spectral Doppler in the antero-septal and infero-posterior wall of closed chest dogs and in the entire LV after opening the chest. A significant increase in IM-CBF velocity was observed in all LV regions after adenosine 5'- triphosphate (ATP) administration. After Levovist(TM) injection, the visualization of IM-CBF was improved and the spectral Doppler pattern of coronary flow velocity was clarified compared to baseline. IM-CBF was assessed in the antero-septal region of the LV before and after left anterior descending coronary artery occlusion.
A high frequency ultrasonic transducer in conjunction with intravenous contrast injection improved IM-CBF visualization, enabling quantitative evaluation of the intramyocardial coronary circulation in the entire LV after coronary occlusion and hyperemia. This study may represent a step towards noninvasive assessment of myocardial perfusion before and after coronary reperfusion.

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Intravascular radiographic contrast media used in angiography, particularly nonionic contrast media, may cause activation of platelets. This study was designed to determine which properties of nonionic contrast media were potentially responsible for this action. Platelet aggregation after adenosine diphosphate stimulation was studied in the platelet rich plasma obtained from 37 patients who underwent left ventriculography using the highly sensitive method of particle counting with laser-light scattering. Platelet activation by contrast media was studied in the platelet rich plasma from healthy volunteers using flow cytometric analysis to detect platelet degranulation as P-selectin expression. There was a significant decrease in platelet aggregation in patients injected with ioxilan or iomeprol compared with patients injected with iohexol. There was a significant increase in P-selectin expression with the three groups of contrast media compared to control. The platelet activation with ioxilan or iomeprol was significantly less compared to the activation with iohexol. The comparison showed that previous generalization regarding platelet activation by nonionic contrast media might not be valid. It is presumed that the higher osmolality of iohexol may contribute to the increase in platelet aggregation and activation.

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Fibrillar collagen plays an essential role in ventricular remodeling, which is a major prognostic factor in various heart diseases. Inflammatory cytokines, including tumor necrosis factor α (TNFα), have been reported to play a role in various heart diseases and OPC-8212, a quinolinone derivative, has been demonstrated to reduce TNFα production. No studies have examined the effects of OPC-8212 on collagen metabolism in connection with inflammatory cytokine and growth factors. Using lipopolysaccharides as a tool to enhance TNFα, we examined the effects of OPC-8212 on the expression of type III collagen mRNA [α1(III)] in cultured neonatal rat cardiac fibroblasts. We also measured the concentration of TNFα and transforming growth factor β (TGFβ) in the cultured medium. Northern blot analysis revealed that LPS reduced the expression of α1(III) mRNA, and OPC-8212 counteracted this reduction (on average 25% above the reduced level by LPS stimulation). LPS enhanced the TNFα concentration in the medium, and OPC-8212 inhibited this enhancement. LPS increased the TGF-β1 concentration in the cultured medium, while OPC-8212 did not affect this increase. In summary, OPC-8212 counteracted the reduction in type III collagen mRNA expression by LPS accompanied by suppression of the increase in TNFα.

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Coronary artery aneurysm (CAA) is defined as coronary dilatation which exceeds the diameter of a normal adjacent segment or the diameter of the patients's largest coronary vessel by as much as 1.5 times. It is an uncommon pathology with a frequency of 1-4% in routine autopsies or coronary angiographies. Atherosclerosis plays an important role in the development of CAA, and it may be a predominant cause in the majority of patients. However, the timing of surgical intervention and the treatment options for CAA are still controversial. In this report, we present a patient who had multiple CAAs of all main coronary arteries and abdominal aortic aneurysm. Different treatment modalities and indications are also discussed.

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