Japanese heart journal最新文献

Embryogenesis of the inferior vena cava (IVC) is a complex process involving the formation and regression of several anastomoses, thus, various anomalies may occur. We report a case of deep venous thrombosis (DVT) accompanied by a double inferior vena cava (DIVC). A 76-year-old-man was admitted because of right leg edema and pain. Venography revealed two IVC and massive venous thrombus. To avoid massive pulmonary embolism (PE), it was necessary to block both the right and the left IVC. However, the right IVC was too small to implant the filter, so we placed a temporary IVC filter (Antheor filter) in the suprarenal portion of the IVC, after the confluence of the two IVC, and started thrombolytic and anticoagulant therapy. Venography, performed 6 days after filter implantation, showed a considerable amount of remaining thrombus. We replaced the Antheor filter with a Gunther retrievable filter because the former has a catheter and is not suited for long-term use, whereas the latter can be used permanently. Two weeks after filter exchange, thrombus had decreased but remained. We therefore did not remove the Gunther filter. The patient's symptoms gradually improved in response to anticoagulant therapy, and he was discharged with no complications. The present case illustrates the importance of a correct understanding of anatomy and demonstrates the effectiveness of using a suprarenal IVC filter in DVT.

Unlabelled: Recently, it has been reported that circulating oxidized low-density lipoprotein (Ox-LDL) might be a pivotal indicator for coronary artery disease and the severity of acute coronary syndromes. The purpose of this study was to investigate the effects of statins on Ox-LDL in patients with hypercholesterolemia. Sixteen patients with hypercholesterolemia were randomly assigned to 2 groups, one received 10 mg of pravastatin (n = 8) and the other received 20 mg of fluvastatin (n = 8). The plasma level of Ox-LDL was measured using a newly developed sandwich enzyme-linked immunosorbent assay (ELISA) method. There were no differences between the two groups in Ox-LDL, total cholesterol (TC), or LDL cholesterol (LDL-C) at the baseline. The reduction in Ox-LDL in the fluvastatin group was significantly higher than that in the pravastatin group (47.5% versus 25.2%, P = 0.033). The reductions in TC and LDL-C did not differ between the two groups.

Conclusion: The present study has shown for the first time that the level of circulating Ox-LDL was significantly decreased by treatment with statins. In addition, the lowering effect of statins on the circulating Ox-LDL was independent of their lipid-lowering effect. Fluvastatin was more effective than pravastatin with regard to decreasing the circulating Ox-LDL.

Coronary artery disease is the most important cause of morbidity and mortality in patients with end-stage renal failure (RF). Hypercholesterolemia is an important risk factor for coronary heart disease. Patients with chronic renal failure (CRF) have difficulties in compliance with their care and treatment. Intermittent simvastatin treatment may help to increase compliance and can be a treatment alternative in patients with CRF at risk of coronary artery disease. We investigated the effects of simvastatin and compared intermittent with continuous simvastatin treatment in hypercholesterolamic patients with CRF. The study group included 40 of 422 CRF patients on dialysis in our clinic. The inclusion criterion was low density lipoprotein cholesterol (LDL-C) of 130 mg/dL or more. Twenty patients received simvastatin 10 mg/day (continuous group) and 20 patients received simvastatin 20 mg three times a week (only dialysis days- intermittent group) for four months. Nineteen patients served as controls and they were given a prescribed diet only. Total cholesterol (TC) and LDL-C decreased markedly in patients receiving intermittent and continuous simvastatin compared to controls. Continuous simvastatin decreased TC by 23% (P < 0.001) and LDL-C by 39% (P < 0.001). Intermittent simvastatin decreased TC by 26% (P < 0.001) and LDL-C by 40% (P < 0.001). The atherogenic index ratios in both the continuous and intermittent groups (TC/High density lipoprotein-cholesterol (HDL-C) and LDL-C/HDL-C) decreased significantly. There was no significant difference in patient compliance between the two groups. Intermittent simvastatin is as effective and reliable as continuous simvastatin treatment and can be an alternative treatment in hypercholesterolemic patients on dialysis.

Some angiogenic factors, including hepatocyte growth factor (HGF), basic fibroblast growth factor (bFGF), and vascular endothelial growth factor (VEGF), have been reported to promote angiogenesis and improve myocardial perfusion in experimental models of ischemic heart disease. These factors are produced in various tissues, including myocardium. We measured the concentrations of HGF, bFGF, and VEGF by enzyme-linked immunosorbent assay in plasma and in pericardial fluid sampled during open heart surgery (12 patients with ischemic heart disease and 17 with nonischemic heart disease). HGF levels were significantly higher in plasma than in pericardial fluid (12.0 +/- 1.8 versus 0.26 +/- 0.04 ng/mL, P < 0.0001). On the other hand, bFGF levels were significantly higher in pericardial fluid than in plasma (243.5 +/- 50.9 versus 49.6 +/- 7.8 pg/mL, P = 0.009). VEGF levels were not significantly different between pericardial fluid and plasma (47.2 +/- 17.6 versus 24.5 +/- 3.6 pg/mL, P = 0.23). Concentrations of angiogenic factors in pericardial fluid and in plasma were not significantly different between patients with ischemic and nonischemic heart disease. These results suggest that the production, secretion, and kinetics of HGF, bFGF, and VEGF are different. These angiogenic factors may have different pathophysiologic roles.

Statins have pleiotrophic effects related to the pathogenesis of atherosclerosis and thrombogenicity of the vessel wall beyond lipid lowering. The aim of the present study was to examine the effect of atorvastatin treatment on the fibrinolytic system in patients with dyslipidemia. The investigation was carried out on 41 dyslipidemic patients (21 males and 20 females) with a mean age of 53.8 years (range, 30-76). The patients were divided into subgroups according to their cholesterol and triglyceride levels as hypercholesterolemic (n = 26) and mixed-type hyperlipidemic (n = 15) and their risk factors for coronary heart disease including age, sex, hypertension, obesity, smoking, and family history. The patients were started on atorvastatin 10 mg/day, and evaluated within 6-12 weeks to assess the changes in fibrinolytic parameters including global fibrinolytic capacity, plasminogen activator inhibitor type-1 and tissue plasminogen activator, and lipids. After successful lipid-lowering therapy, global fibrinolytic capacity (P = 0.003) and tissue plasminogen activator levels (P = 0.04) were found to be increased and plasminogen activator inhibitor type-1 levels (P = 0.02) decreased in dyslipidemic patients. Global fibrinolytic capacity levels increased (P < 0.001) and plasminogen activator inhibitor type-1 levels decreased (P = 0.01) in patients with hypercholesterolemia (n = 26). However, no significant changes were observed in fibrinolytic parameters in patients with mixed-type hyperlipidemia (n = 15). When the patients were separately evaluated according to risk factors, significant beneficial effects on the fibrinolytic system were observed, especially in patients without obesity and hypertension as well as in older patients and males. These findings suggest that atorvastatin treatment has a beneficial effect on the fibrinolytic system in patients with hypercholesterolemia, but not in patients with mixed-type hyperlipidemia. Further studies are needed to show whether higher doses and longer periods of lipid lowering treatment have beneficial effects in patients with mixed type hyperlipidemia and some risk factors.

We treated an 88-year-old man with aortic valvular stenosis/insufficiency and paroxysmal atrial fibrillation, who developed ventricular tachycardia due to pilsicainide toxicity. He was treated at the outpatient clinic of his local hospital, and was administered pilsicainide (100 mg/day) for atrial fibrillation. The electrocardiographic findings on admission to our hospital indicated wide QRS with frequent episodes of ventricular tachycardia. We diagnosed him as having pilsicainide toxicity because of a low cardiac output and renal dysfunction. His creatinine level was 2.4 mg/dL and the serum pilsicainide level was 2.42 microg/mL on admission. Fluid infusion and continuous hemodiafiltration were performed to achieve an early reduction in the serum pilsicainide level. His serum pilsicainide concentration was significantly decreased by these treatments, and the prolongation of the QTc and ventricular tachycardia improved in parallel to the decrease in the serum pilsicainide level. The changes in the serum pilsicainide level showed a significant positive correlation with the changes in the electrocardiographic findings (PQ, QRS, ST intervals, and QTc). Pilsicainide should be administered with great care to elderly patients, especially patients with cardiac dysfunction and renal dysfunction. Estimation of the serum level may be possible from the electrocardiographic findings if the pilsicainide toxicity occurs.

A 74-year-old woman, with a history of hypertension and hyperlipidemia, was admitted to our hospital. She was found to have a sinus tachycardia with ST-segment elevations in leads II, III, (a)V(F), and V(3) through V(6) in electrocardiography, hypokinesis of the left ventricular apex by echocardiography, and normal findings on coronary angiography. Blood analysis revealed an increase in the creatine kinase MB fraction, a significant positive detection in troponin T, and transient elevations in the concentrations of free triiodothyronine, free thyroxine, thyroid globulin antibody, and thyroid peroxidase antibody. Defects in myocardial perfusion and fatty acid metabolism in the apical area were also demonstrated by myocardial scintigraphy. These data suggest that tako-tsubo syndrome or myocardial infarction may be induced in patients with mild and transient hyperthyroidism.

The purpose of this study was to validate whether dipyridamole stress ultrasonic tissue characterization with cyclic variation of integrated backscatter (CVIBS) compared with dipyridamole stress echocardiography and dipyridamole stress Tc99m-MIBI SPECT myocardial perfusion scintigraphy could predict myocardial ischemia in patients with chronic coronary artery disease. Twenty patients (16 M, 4 F) who had coronary angiography for stable angina pectoris were included in the study. Mean age was 62 +/- 8 years. The left ventricle was divided into 16 segments. Regional wall motion analysis and CVIBS measurements were obtained from 16 myocardial segments at rest and after dipyridamole (0.84 mg/kg) infusion. After 10 minutes, Tc-99m MIBI (10 mCi) was injected and SPECT myocardial imaging was performed. After 3 hours, 25 mCi Tc-99m MIBI was reinjected and rest images were obtained. A total of 320 ventricular wall segments were evaluated. Two hundred and six ventricular wall segments were supplied by stenotic coronary arteries and 114 segments were supplied by normal coronary arteries. Dipyridamole stress Tc-99m MIBI SPECT studies showed abnormal myocardial perfusion in 176 segments and normal perfusion in 144 segments. Transient regional wall motion abnormality was detected in 116 segments. A significant decrease in CVIBS after dipyridamole stress was detected in 184 segments. The sensitivity and specificity of dipyridamole stress echocardiography, Tc-99m MIBI SPECT, and CVIBS were 56% and 100%, 85% and 92%, and 89% and 100%, respectively, compared with the results from coronary angiography. Dipyridamole stress ultrasonic tissue characterization with CVIBS may provide more sensitive detection of myocardial ischemia than dipyridamole stress echocardiography and may be as valuable as dipyridamole stress myocardial perfusion scintigraphy.

Information concerning acute myocardial infarctions (AMI) after heroin injection is limited. Only one report has described the association between heroin injections and AMI in a young woman. AMI after heroin injection in a patient with a normal coronary angiogram has not been reported. We report a 38-year-old man who developed AMI after heroin injection. He is probably the first case of AMI with normal coronary artery angiograms associated with heroin abuse. The heroin-induced toxic effect and/or coronary spasm are highly suspected to be the causes of the infarction episode.