Japanese heart journal最新文献

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.

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.

ST segment resolution in ST elevated myocardial infarction has independent predictive value for congestive heart failure and death at 30 days. 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. 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.

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.

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.

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 microg/mL, P = 0.002), between patients with CAD and controls (10.0 +/- 6.27 versus 15.3 +/- 5.38 microg/mL, P < 0.0001), and between men and women (10.2 +/- 6.41 versus 13.1 +/- 6.22 microg/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.

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.

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.

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.