Cardiac tamponade due to rupture of coronary artery fistula to the coronary sinus with giant aneurysm of coronary artery: usefulness of transthoracic echocardiography.

A 68-year-old woman was admitted to our hospital because of back pain and syncope. Transthoracic echocardiography revealed pericardial effusion, a collapsed right ventricle, a giant aneurysm connected to the coronary sinus, a dilated left main trunk coronary artery, and a dilated left circumflex artery (LCx). Furthermore, there was a coronary artery fistula arising from the LCx that drained into the coronary sinus. We diagnosed cardiac tamponade due to rupture of the coronary artery fistula or giant aneurysm, and successful emergency surgery was performed. Rupture of coronary artery aneurysm or coronary artery fistula is very rare. Transthoracic two-dimensional echocardiography was very useful in our case for the diagnosis of cardiac tamponade, giant coronary aneurysm, and coronary artery fistula.

Cardiotrophin-1 stimulates intercellular adhesion molecule-1 and monocyte chemoattractant protein-1 in human aortic endothelial cells.

Intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) play critical roles in mediating monocyte adhesion to the vascular endothelium and monocyte migration into the subendothelial regions of the vessels. Inasmuch as cardiotrophin-1 (CT-1), an IL-6-type cytokine, was expressed in human atherosclerotic plaque, we examined whether CT-1 induces monocyte adhesion and migration by stimulating gene and protein expressions of ICAM-1 and MCP-1 in human aortic endothelial cells (HAECs). Immunocytochemistry revealed that CT-1 increased intensity of ICAM-1 and MCP-1 immunoreactivity in HAECs. Adhesion assay and chemotaxis assay revealed that CT-1 increased human monocytic THP-1 cell adhesion to HAECs and promoted chemotaxis in THP-1 cells, which were attenuated by anti-ICAM-1 and anti-MCP-1 antibody, respectively. Western blot analysis showed that CT-1 increased phosphorylation of ERK1/2 MAP kinase, p38 MAP kinase, and Akt and that their inhibitors, PD-98059, SB-203580, and LY-294002, respectively, inhibited phosphorylation. RNase protection assay and ELISA demonstrated that CT-1 increased gene and protein expressions of ICAM-1 and MCP-1. EMSA revealed that CT-1 enhanced NF-kappaB DNA-binding activity. CT-1-mediated upregulation of ICAM-1 and MCP-1 was suppressed by PD-98059, SB-203580, LY-294002, and parthenolide. The present study demonstrates that CT-1 promotes monocyte adhesion and migration by stimulating ICAM-1 and MCP-1 through mechanisms that involve ERK1/2 MAP kinase, p38 MAP kinase, phosphatidylinositol 3-kinase, and NF-kappaB pathways and suggests that CT-1 plays an important role in the pathophysiology of vascular inflammation and atherosclerosis.

Plasma levels of soluble glycoprotein 130 in acute myocardial infarction.

OBJECTIVES: Soluble glycoprotein 130 (sgp130), a circulating form of receptor subunit for the interleukin (IL) -6 cytokine family, modulates the biological actions of its ligands as an inhibitory regulator. The role of sgpl30 in cardiovascular diseases such as acute coronary syndrome remains unknown. METHODS: Plasma levels of sgp130 were examined by enzyme-linked immunosorbent assay in 33 patients with acute myocardial infarction (AMI; mean age 67 +/- 2 years, 21 males and 12 females), who were admitted to our hospital within 24 hr of onset of AMI and survived for 4 weeks. RESULTS: Plasma sgp130 levels were significantly higher at admission (260.5 +/- 7.3 ng/ml), and were significantly lower from day 2 to day 5 (202.4 +/- 5.1 ng/ml at day 3) as compared with normal control subjects (n = 38, 227.1 +/- 5.6 ng/ml). The lowest sgp130 levels inversely correlated with white blood cell count at admission (r = -0.42, p < 0.05) and with peak C-reactive protein levels (r = -0.43, p < 0.05). Additional in vitro study revealed that incubation of AMI plasma with exogenous IL-6 plus soluble IL-6 receptor resulted in a decrease in plasma sgp130 levels, suggesting the possible reason for reduced plasma sgp130 levels in AMI. CONCLUSIONS: The present study indicates that plasma sgp130 levels were modulated during the time course of AMI and inversely associated with inflammation in AMI.

Noninvasive prediction of complications with anteroseptal acute myocardial infarction by left ventricular Tei index.

BACKGROUND: Tei index has been proposed as a noninvasive and simple index that enables the evaluation of global left ventricular (LV) function and prediction of patient prognosis. However, its use to predict complications with acute myocardial infarction (AMI) is not fully investigated. Therefore, the purpose of this study was to investigate whether or not LV Tei index allows noninvasive prediction of complications with AMI. METHODS: In all, 80 consecutive patients with anteroseptal AMI were enrolled. LV Tei index was measured at the time of admission as (a - b)/ b , where a is the interval between cessation and onset of mitral filling flow and interval b is the aortic flow ejection time. Subsequent complications including cardiac death, shock, congestive heart failure, ventricular tachycardia/fibrillation, paroxysmal atrial fibrillation/flutter, advanced atrioventricular block requiring pacing, pericardial effusion, and LV aneurysm during the 30 days after the onset of AMI were prospectively evaluated and compared with the initial Tei index at admission. RESULTS: Complications developed in 31 of 80 (39%) patients with AMI. The Tei index was significantly increased for patients with complications compared with those without them (0.69 +/- 0.16 vs 0.50 +/- 0.11, P < .0001). When Tei index > or = 0.59 was used for the criteria, the sensitivity, specificity, and overall accuracy to predict subsequent complications were 77%, 86%, and 85%, respectively. CONCLUSION: In patients with anteroseptal AMI, LV Tei index at arrival to the hospital in the acute phase allows noninvasive prediction of subsequent complications.

R353Q polymorphism, activated factor VII, and risk of premature myocardial infarction in Japanese men.

BACKGROUND: The association between myocardial infarction (MI) and the R353Q polymorphism of the Factor VII (FVII) gene, which reportedly influences FVII concentrations, activated Factor VII (FVIIa), or FVII antigen (FVIIag), remains controversial. METHODS AND RESULTS: The present case - control study in 127 Japanese men with their first MI at or before 45 years of age and 150 matched healthy controls was designed to clarify this association in premature MI. R353Q polymorphism was determined by polymerase chain reaction, and plasma concentrations of FVIIa and FVIIag were assayed. The distribution of the RR, RQ, and QQ genotypes with respect to R353Q polymorphism was 117, 10, and 0 in the patients, and 131, 17, and 2 in the controls. The Q allele was negatively associated with premature MI (odds ratio =0.41, p=0.038). The plasma concentration of FVIIa was slightly higher in patients (55.1+/-40.9 U/L) than in controls (44.8+/-20.2 U/L), but not significantly (p=0.078); the plasma concentration of FVIIag did not differ between patients (88.7+/-15.7%) and controls (87.0+/-9.0%) (p=0.557). Plasma FVIIa concentrations were influenced by R353Q polymorphism (p<0.001). CONCLUSIONS: The Q allele may be protective against premature MI.

Rationale for the use of combination angiotensin-converting enzyme inhibitor and angiotensin II receptor blocker therapy in heart failure.

BACKGROUND: The present multicenter study investigated whether the combination of angiotensin-converting enzyme inhibitor (ACEI) and angiotensin II receptor blocker (ARB) is more beneficial for preventing left ventricular remodeling and suppressing neurohumoral factors than either ACEI or ARB alone. METHODS AND RESULTS: One hundred and six patients with mild-to-moderate congestive heart failure treated in 26 Japanese institutes were randomly assigned to the combination therapy or monotherapy. Changes in physical activity (New York Heart Association functional classes, Specific Activity Scale (SAS)), concentrations of neurohumoral factors (plasma renin activity, angiotensin II, aldosterone, and brain natriuretic peptide (BNP)), and cardiac function for 6 months were compared between the 2 groups. It was found that the combination therapy, which was administered at doses standard in Japan, increased the SAS score (4.5 +/- 1.5 to 4.9 +/- 1.5, p<0.05) and decreased the plasma BNP concentration (183 +/- 163 to 135 +/- 118 pg/ml, p<0.05). In contrast, there were no changes in SAS score (4.5 +/- 1.4 to 4.6 +/- 1.4, NS) or BNP concentration (156 +/- 157 to 151 +/- 185 pg/ml, NS) in the patients receiving monotherapy. CONCLUSIONS: The results of the study demonstrate that the combination therapy, even at the standard doses for Japan, improves physical activity and plasma BNP concentration more than the monotherapy. A larger study is required to assess the effects of the combination therapy on major clinical outcomes.

Homocysteine and hemostatic disorder as a risk factor for myocardial infarction at a young age.

INTRODUCTION: Hyperhomocysteinemia is a coronary risk factor, but its pathophysiologic mechanism remains unclear. MATERIALS AND METHODS: The importance of hyperhomocysteinemia in the pathogenesis of early myocardial infarction, was determined in case-control study of 127 men with a first early myocardial infarction

[Usefulness of rapid quantitative cardiac troponin T and myoglobin assays for the diagnosis of acute myocardial infarction].

BACKGROUND AND OBJECTIVES: The rapid cardiac troponin T (cTnT) test is widely used to detect myocardial necrosis in the emergency setting. This assay system is rapid and myocardial-specific, but the plasma cTnT concentration is difficult to determine quantitatively. A recently developed bedside cTnT and myoglobin (Mb) analyzer (CARDIAC system) was evaluated. METHODS: The new CARDIAC system was used to measure plasma cTnT and Mb levels, and serum levels of creatine kinase MB isoenzyme (CK-MB), cTnT and Mb were measured by conventional assays in 160 consecutive emergency patients with suspected acute myocardial infarction. RESULTS: The sensitivity of cTnT for identifying acute myocardial infarction was 76%, significantly higher than that of Mb (67%, p < 0.01) and CK-MB (54%, p < 0.05). The diagnostic sensitivities in patients admitted < or = 3 hr and 3-6 hr after onset were 52% and 65% for cTnT, 60% and 90% for Mb, and 36% and 50% for CK-MB, respectively. These sensitivities of Mb were significantly higher than those of CK-MB but not cTnT. However, the sensitivity of cTnT (100%) was significantly higher than that of Mb (58%, p < 0.01) and CK-MB (70%, p < 0.001) in patients admitted > 6 hr after onset. The specificities of cTnT, Mb and CK-MB were 96%, 76% (p < 0.001 vs cTnT and CK-MB) and 95%, respectively. Therefore, cTnT (86%) had significantly (p < 0.001) higher diagnostic accuracy compared with Mb (71%) and CK-MB (75%). Combination diagnosis using cTnT and Mb showed the highest sensitivity (86%) compared with cTnT (p < 0.05) and Mb (p < 0.001). The correlation coefficients between the levels measured by CARDIAC system and those by ordinary assays were 0.98 in cTnT and 0.97 in Mb. CONCLUSIONS: Bedside rapid quantitative assays of cTnT and Mb are useful as a point of care test for the diagnosis of acute myocardial infarction.

Transesophageal echocardiographic diagnosis of left atrial mass as thrombus by demonstrating its attachment to the patch closing atrial septal defect: a case report.

A 65-year-old-man was referred for echocardiographic examination because of palpitations. He had a history of an atrial septal defect surgically treated with an artificial synthetic polyester textile fiber patch. TTE showed a large, mobile mass in a dilated left atrium. The attachment site of the mass was not clear by transthoracic approach, and it was difficult to diagnose the mass as a thrombus or a myxoma from the nature of the echocardiographic findings. Transesophageal echocardiography clearly demonstrated that the mass was attached to the patch closing the atrial septal defect and the mass was confirmed as thrombus at surgery. A patient with left atrial thrombus in whom transesophageal echocardiographic demonstration of the attachment of the left atrial mass to a patch closing an atrial septal defect served as an essential clue leading to accurate diagnosis is reported. Transesophageal echocardiography is feasible to evaluate the attachment site of a left atrial mass and to lead to an accurate diagnosis.