Since there is in sufficient evidence on patients with coronary artery disease in Japan, the Japanese Coronary Artery Disease (JCAD) Study, in which 217 institutions participate, was designed to collect basic data based on evidence-based medicine (EBM). In this study, cardiac catheterization is performed on all cases to select study subjects confirmed as having CAD diagnosed based on the criteria that he or she has stenosis in at least one branch of a coronary artery to the extent of 75% or higher according to the AHA classification. Data including background information, risk factors, clinical management, and medication are to be collected over the web. The follow-up arm of the study consists of following each subject for three years to obtain data on the long-term prognosis of patients with CAD while the other arm is for enrolling new subjects every six months who will be followed for six months only for the purpose of determining the latest trend in patients. The two arms of the study have been ongoing since April 2000. As of September 30, 2003, 15,506 subjects have been enrolled in the follow-up arm and the follow-up data have been entered in the database. The authors plan to report data showing any correlation between incidence rate, focusing mainly on cerebrocardiovascular events, and other factors such as the management of risk factors, and type and dosage of medications obtained in the largest cohort ever studied in Japan of patients with a coronary artery lesion confirmed by cardiac catheterization.
ST segment resolution in ST elevated myocardial infarction has independent predictive value for congestive heart failure and death at 30 days.1-2) ST segment depression in unstable angina pectoris (UAP) and non-ST elevated myocardial infarction (NSTEMI) predicts high risk of MI and death and may discriminate patients likely to have greater benefit from aggressive antithrombotic and interventional therapy.5-6) This study assessed the effect of tirofiban added to conventional treatment on ST segment resolution in NSTEMI patients. Sixty-four patients were randomized to one of the two groups: 32 patients received conventional treatment while tirofiban was added in the second group of 32 patients. In the first group, 6 patients refused to participate further after giving initial informed consent while 1 patient in the tirofiban group dropped out. We had 26 patients (mean age, 59 years) in the conventional treatment group and 31 patients (mean age, 59 years) received also tirofiban. Tirofiban was administered by intravenous infusion over a 72 hour period. More than 50% regression of depression was considered to be ST segment resolution. The characteristics of the two groups were comparable (Table I). The ST segment resolution evolution did not differ at the 4th and 24th hours between the two groups. Significant differences occurred in the 72nd hour ECG (Table III). ST resolution was present in 67.9% of the tirofiban patients and in 32.1% of the conventional treatment group (P < 0.05). Tirofiban treatment was not associated with an increase in major bleeding even though there was a trend toward an increase in minor bleeding cases and did not influence the occurrence of refractory angina pectoris.
We investigated whether plasma levels of adiponectin in patients with both coronary artery disease (CAD) and diabetes mellitus (DM) are lower than in patients with CAD alone. We examined plasma adiponectin levels in 113 patients, 82 with CAD (40 of whom had both CAD and type 2 DM) and 31 normal controls. We found differences in plasma adiponectin levels between CAD patients with and without DM (7.8 ± 4.75 versus 12.1 ± 6.87 μg/mL, P = 0.002), between patients with CAD and controls (10.0 ± 6.27 versus 15.3 ± 5.38 μg/mL, P < 0.0001), and between men and women (10.2 ± 6.41 versus 13.1 ± 6.22 μg/mL, P = 0.017). Plasma adiponectin levels were correlated negatively with body mass index, triglyceride, total cholesterol, hemoglobin A1c, and fibrinogen levels (r = -0.456, P < 0.0001 ; r = -0.355, P < 0.0001 ; r = -0.286, P = 0.002; r = -0.299, P < 0.0001 ; r = -0.400, P < 0.0001, respectively), but were not significantly correlated with high sensitivity C-reactive protein or low density lipoprotein levels (r = -0.088, P = 0.352; r = -0.167, P = 0.077, respectively). Plasma adiponectin levels correlated positively with high density lipoprotein levels (r = 0.410, P < 0.0001). Our study demonstrates that plasma adiponectin levels in patients with both CAD and DM are lower than in patients with CAD alone. We speculate that people who have very low plasma adiponectin levels may be at increased risk of developing both CAD and DM.
Atrial fibrillation (AF) has been treated with DC shocks delivered transthoracically, but in 5-30% of patients, the procedures fail to restore sinus rhythm (SR). We hypothesized that applying high energy shock waves to the chest may overcome the inadequate penetration of electrical shock to the atrium. The aim of this study was to evaluate the efficacy of higher energy external DC shock for the treatment of refractory AF coexisting with cardiovascular disease using a synchronized double external defibrillator. Fifteen patients (mean age 65 ± 8) with refractory AF to standard DC cardioversion (CV) underwent higher energy DC shock using a double external defibrillator. Concomitant heart disease was present in all patients. Warfarin and amiodarone (600 mg/day), were administered for at least three weeks duration before DC CV. Sedation was performed with IV midazolam. Two defibrillator paddles were positioned on the anterior and posterior chest wall in a right lateral decubitus position. Defibrillators were synchronized to the R waves and simultaneously 720 joules of energy was administered to the patients. Amiodarone (200 mg/day) was continuously administered after DC shock to maintain SR. Sinus rhythm was obtained in 13 patients. Sinus rhythm was persistent in 11 patients for six months duration. Creatine kinase MB fractions were normal at 4 (22 ± 4 IU/L) and 12 hours (18 ± 4 IU/L). None of the patients developed significant hemodynamic compromise or congestive heart failure, higher AV block, stroke, or transient ischemic cerebral events. The results indicate that higher energy DC shock application using a double external defibrillator is an effective and safe method for the cardioversion of refractory AF. We believe this procedure should be performed before internal atrial cardioversion.
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.
Scarring and collagen deposition in the valves and destruction of myocytes may result from the combined effects of a smoldering rheumatic process and a constant trauma to the mitral valve or aortic valve by the turbulent flow in rheumatic heart disease (RHD). It has been suggested that angiotensin I-converting enzyme (ACE) may be responsible for the increased valvular fibrosis and calcification in the pathogenesis of RHD. However, the role of ACE genetic variant in RHD has not been studied among the Chinese population in Taiwan. Hence, a case-controlled study was carried out to investigate the possible relationship between the ACE gene insertion/deletion (I/D) and G2350A polymorphisms and RHD. A group of 115 patients with RHD documented by echocardiography and 100 age- and sex-matched normal control subjects were studied. ACE gene I/D and G2350A polymorphisms were identified by polymerase chain reaction-based restriction analysis. There was a significant difference in the distribution of ACE I/D genotypes (P = 0.02) and allelic frequencies (P = 0.04) between RHD cases and normal controls. An odds ratio for the risk of RHD associated with the ACE I/D II genotype was 2.12 (95% CI, 1.21-3.71). An odds ratio for the risk of RHD associated with the ACE I allele was 1.50 (95% CI, 1.02-2.21). The ACE G2350A polymorphism showed no association with RHD (P = 0.90). Further categorization of RHD patients into mitral valve disease and combined valve disease subgroups revealed no statistical difference in these gene polymorphisms when compared between the two subgroups. This study shows that patients with RHD have a higher frequency of ACE II genotype and I allele, which supports a role for ACE I/D gene polymorphisms in determining the risk of RHD in Taiwan Chinese.
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.
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.
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.
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.
It remains controversial as to whether mitral annular calcification (MAC) is an independent predictor of stroke. The aim of this study was to investigate whether there is an association between the presence of MAC and stroke or whether MAC is one of the predictive factors of carotid atheroma and therefore is a secondary risk for stroke. Fifty-six patients who had MAC demonstrated by echocardiography underwent carotid artery duplex sonography and computed brain tomography with various causes were enrolled in the study. They were compared with 58 control patients without MAC. MAC was defined as a dense, localized, highly reflective area larger than 5 mm at the junction of the atrioventricular groove and posterior mitral valve leaflet. Carotid artery stenosis was defined as lumen diameter narrowing exceeding 60%. Cerebral ischemia was detected by spiral tomography and was classified as infarction and lacunae. A significant association was found between the presence of MAC and carotid atheroma (P = 0.011), MAC and hyperechogen plaque (P = 0.034), and MAC and stenosis (P = 0.008). There was an association between the presence of carotid atheroma and cerebral infarction (P = 0.007). Logistic regression analysis revealed hypertension and diabetes mellitus were independent risk factors (P = 0.030, P = 0.034, respectively) for developing carotid atheroma. MAC was an independent factor for carotid stenosis (P = 0.029). MAC may not be a significant causative factor for stroke, but may be a secondary risk factor. A significant association between the presence of MAC and carotid artery atherosclerotic disease may explain the high prevalence of stroke in patients with MAC.
Connexin 43 (Cx43), a primary component of gap junctions, contributes to intercellular electrochemical communication. Cx43 undergoes dephosphorylation in early ischemia. We examined whether Cx43 is degraded in association with dephosphorylation during early myocardial ischemia and whether ischemic preconditioning (IP) affects the degradation after rat coronary artery occlusion. Male Sprague-Dawley rats underwent coronary artery occlusion for 1, 2, or 3 hours, or for 1 hour following treatment either with a calcineurin inhibitor (cyclosporine A), proteasome inhibitor (PSI), or lysosomal inhibitor (E64c), or following IP alone or after protein kinase C (PKC) inhibitor (chelerythrine) pretreatment. The IP was afforded by three cycles of 3 minute ischemia and 5 minute reperfusion. A large portion of the phosphorylated Cx43 (pCx43) in the membrane fraction was dephosphorylated, while a small portion was degraded at 1 hour of ischemia. The effects of the inhibitors were dephosphorylation and degradation by calcineurin and proteasome/lysosome, respectively. IP suppressed the decrease in pCx43 and increase in dCx43, while only the former was inhibited by the PKC inhibitor chelerythrine. The Cx43 mRNA level was reduced at 3 hours, but not at 1 hour of ischemia, irrespective of IP. We believe that Cx43 is dephosphorylated and degraded in early ischemia, whereas Cx43 transcription was suppressed at a later phase of ischemia.
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.
Premature coronary artery disease is very rare and complication with thrombus formation in the left ventricle is rarer still. A 23-year-old man was admitted to hospital for recent acute myocardial infarction after being struck by a basketball eight days previously. Echocardiography identified two peduncle thrombi at the apex of the left ventricle, which were confirmed with computed tomography. The proximal left anterior descending coronary artery was totally occluded. Following two weeks of treatment with heparin and warfarin, the patient agreed to undergo a coronary artery bypass graft and thrombectomy. The ecchymosed tissue around the coronary artery implied that a trauma injury might have been the cause of the coronary artery disease in this case. This work reviews the pathophysiology and natural history of coronary artery disease in a case of very young myocardial infarction.
Twiddler's syndrome is characterized by coiling of the pacemaker lead due to the rotation of the pacemaker generator on its long axis. Reel syndrome is another form of Twiddler's syndrome. It occurs due to the rotation of the pacemaker generator on its transverse axis with subsequent coiling of the pacemaker leads around the pulse generator. In this article we describe a patient with a two-chamber pacemaker who presented with sudden onset of abdominal pulsation and was subsequently diagnosed as Reel syndrome. To the best of our knowledge, this case is the first case of Reel syndrome that developed in a patient with a two-chamber pacemaker.
Wolff-Parkinson-White syndrome with manifest preexcitation is a common cause of false-positive exercise test results. However, false-positive results are extremely rare without manifest preexcitation. We report a case with intermittent Wolff-Parkinson-White syndrome and exercise-induced marked ST depressions in the absence of preexcitation of the QRS complexes. His coronary arteries were normal on angiography and no ST changes were observed in the control exercise test after ablation of the accessory pathway.
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 μg/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.
Pulmonary and aortic valve endocarditis are uncommon especially in an adult patient with patent ductus arteriosus. A 27-year-old woman diagnosed with pulmonary and aortic valve endocarditis underwent surgical treatment. Here, we report our clinical and surgical experience in treating a case of double valve endocarditis with clinically silent patent ductus arteriosus.
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 Günther 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 Günther 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.
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, aVF, and V3 through V6 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.
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