Congenital giant aneurysm of the left atrial appendage mimicking pericardial absence case report.

A 25-year-old man was found to have an abnormal cardiac contour on a chest radiograph, and was referred. Transesophageal echocardiography suggested herniation of the left atrial appendage (LAA) through a gap in the pericardium, and magnetic resonance imaging indicated congenital partial absence of the pericardium. Cardiac dysfunction was caused by compression from the enlarged left atrium and thrombi were thought to be present in the appendage, so surgery was performed. The intraoperative diagnosis was congenital LAA aneurysm. Although distinguishing between congenital LAA aneurysm and congenital absence of the pericardium is reported to be possible with magnetic resonance imaging, we were unable to so in this case.

Effect of angiotensin-converting enzyme gene polymorphism on left ventricular remodeling after anteroseptal infarction.

BACKGROUND AND HYPOTHESIS: Genetic influence on cardiac remodeling is uncertain. The purpose of this study is to determine the effects of polymorphism of the angiotensin-converting enzyme (ACE) gene on cardiac remodeling after myocardial infarction. METHODS: The subjects were 43 patients with old anteroseptal myocardial infarction. Based on the polymorphism of the ACE gene, they were classified into a deletion group of 25 patients (D/D genotype in 4 and D/I genotype in 21) and an insertion group of 18 patients (all I/I genotype). Echocardiograms were used to determine left ventricular end-diastolic and end-systolic diameters, interventricular septal and posterior wall thicknesses, left ventricular mass, left atrial diameter, and left ventricular ejection fraction. Blood concentrations of atrial and brain natriuretic peptide were also measured. RESULTS: Left ventricular end-systolic and end-diastolic dimensions, left ventricular mass, and levels of both atrial and brain natriuretic peptide were significantly higher in the deletion group. In contrast, septal thickness, posterior wall thickness, and ejection fraction showed no differences between the two groups. CONCLUSIONS: In patients with old anteroseptal infarction, ACE gene polymorphism of the D/D and D/I genotypes has a stronger influence on left ventricular remodeling than polymorphism of the I/I genotype.

Dynamic changes of QT dispersion as a predictor of myocardial ischemia on exercise testing in patients with angina pectoris.

The difference between the maximum and minimum QT intervals on the standard 12-lead ECG (QT dispersion) may be a significant predictor of serious arrhythmias. Dynamic changes in QTd were determined during exercise-induced ischemia in 15 patients with effort angina (> or = 75% coronary stenosis) and 10 normal individuals. Treadmill exercise testing was performed according to Bruce's protocol and the rate-corrected QT dispersion (QTcd) was calculated using Bazett's formula. The resting QTcd before exercise was similar in the angina patients and the controls. After the first stage of exercise, QTcd was significantly increased in the angina patients (p = 0.035), while it remained near baseline in the controls. Five minutes after completing exercise, QTcd was significantly greater in the angina patients than in the controls (p = 0.011). Furthermore, QTcd values after the first stage of exercise were significantly correlated with the maximum ST depression observed on completing exercise in the angina patients (r = 0.714, p = 0.0028). Because QTd may represent the heterogeneity of ventricular repolarization, its significant exercise-induced increase in the angina patients suggests that myocardial ischemia caused repolarization disorders. The significant correlation between QTcd values after the first stage of exercise (before significant ST depression) and the maximum ST depression on completing exercise suggests that an increase in QTcd preceding ischemic ST depression may predict myocardial ischemia. In addition, even daily activities not causing significant ST changes may increase QTcd and the risk of serious arrhythmia in angina patients.

Beneficial effects of mechanical reperfusion therapy on left ventricular remodeling and late outcome following myocardial infarction.

The long-term relative benefits of thrombolysis and mechanical reperfusion therapy following acute myocardial infarction (AMI) have not been established. The purpose of this study was to compare left ventricular function, left ventricular remodeling and late outcome after AMI for different reperfusion therapies. Thirty consecutive patients suffering their first anterior wall myocardial infarction with coronary stenoses limited to the left anterior descending coronary artery were studied. They included 10 patients who underwent intracoronary thrombolysis (ICT), 10 who underwent PTCA and 10 who underwent noninterventional medical treatment. All patients underwent coronary angiography (CAG) during the acute phase of AMI and also during the follow-up period, and left ventriculography during the follow-up period and clinical follow-up was performed (mean clinical follow-up period: 53 +/- 31 months). No significant difference in global ejection fraction was noted among the groups, although the end-diastolic volume index (EDVI) in the PTCA group (79.4 +/- 17.5 ml/m2) was significantly smaller than in the noninterventional (106.1 +/- 25.1 ml/m2) and ICT (107.9 +/- 28.3 ml/m2) group (p < 0.05). The regional wall motion index (RWMI) for the anterior region in the PTCA group (-2.7 +/- 0.8) was greater (p < 0.05) than in the noninterventional (-3.4 +/- 0.6) and ICT (-3.3 +/- 0.6) groups. A significant linear correlation was found between EDVI and % diameter stenosis and also between RWMI and % diameter stenosis following reperfusion (p = 0.01). There was no difference in the incidence of cardiac death, nonfatal reinfarction, bypass surgery or congestive heart failure among the groups. Disturbed left ventricular regional wall motion and remodeling benefit most from angioplasty because of prompt restoration of adequate blood flow. However, there was no difference in late outcomes following AMI among the three groups.

Influence of exercise on QT dispersion in ischemic heart disease.

UNLABELLED: QT dispersion (QTd: maximum QT interval-minimum QT interval) is associated with severe cardiac arrhythmia and with abnormal ventricular repolarization. We investigated the influence of exercise on QTd in patients with ischemic heart disease. On standard 12-lead electrocardiograms, QTd was measured before and after treadmill exercise in 7 normal subjects, 17 patients with effort angina pectoris (and > or = 75% stenosis on coronary arteriography), and 33 patients with old myocardial infarction. Bazett's formula was used to obtain the corrected QTd (QTcd). The pre-exercise resting QTcd was 45.9 +/- 10.6, 44.3 +/- 15.2, and 74.8 +/- 28.1 msec in the respective groups, being significantly greater in the infarct group (p < 0.05). The QTcd at 5 min after exercise was respectively 49.3 +/- 9.0, 58.8 +/- 19.9, and 75.4 +/- 30.9 msec (p = 0.0347, infarct vs. controls). The difference in QTcd was significant for the angina group before and after physical exercise (p = 0.0003). There was a significant increase of QTcd after exercise in the angina group whether or not the patients were receiving beta-blockers. The infarct patients without beta-blocker therapy showed an increase of QTcd after exercise, while those receiving beta-blockers showed a decrease. The post-exercise difference between these subgroups was significant (p = 0.0351). CONCLUSIONS: QTcd was significantly increased by exercise in the angina group, possibly reflecting impaired repolarization due to ischemia. Inhibition of the increase in QTd by beta-blockers suggested a possible preventive effect on severe arrhythmias due to nonhomogeneous ventricular repolarization.

A randomized trial of aspirin versus cilostazol therapy after successful coronary stent implantation.

Percutaneous transluminal coronary angioplasty (PTCA) is widely used to treat patients with ischemic heart disease, but the procedure involves a number of problems, including acute coronary occlusion and restenosis. Although stents have proved useful for preventing post-PTCA restenosis, especially elastic recoil during the acute phase, no method has yet been established to prevent restenosis caused by vascular smooth muscle cell proliferation in the late phase. Cilostazol selectively inhibits the 3'5'-cyclic-nucleotide phosphodiesterase (PDE) III (cyclic guanosine monophosphate-inhibited PDE) of the cyclic adenosine monophosphate PDE family; it also has antithrombotic and vasodilating effects, as well as an inhibitory effect on vascular smooth muscle cell proliferation through PDE III inhibition. From November 1995 to March 1997, the usefulness of cilostazol versus aspirin in preventing subacute thrombosis and restenosis was studied in 70 patients (55 men and 15 women; 82 total lesions) who had undergone successful elective Palmaz-Schatz stent implantation. Patients were randomly allocated to receive aspirin 81 mg/d (40 patients with 45 lesions) or cilostazol 200 mg/d (30 patients with 37 lesions) alone. There was no difference in patients or angiographic characteristics between these groups. No subacute thrombosis, acute complications (ie, death, emergent coronary artery bypass grafting, or hemorrhagic complications), or drug side effects were found in the cilostazol group. The minimal lumen diameter (mean +/- SD) at follow-up was 1.89 +/- 1.08 mm in the aspirin group (41 lesions, 5.63 +/- 1.74 months after stent implantation) and 2.34 +/- 0.74 mm in the cilostazol group (35 lesions, 5.14 +/- 1.91 months after stent implantation), revealing statistically significant dilatation in the cilostazol group. The restenosis rate was 26.8% in the aspirin group, compared with 8.6% in the cilostazol group; this difference was statistically significant. Administration of cilostazol alone after the implantation of intracoronary Palmaz-Schatz stents was useful for the prevention of subacute thrombosis and restenosis.

[Ultrastructural and biochemical enzymatic properties of right ventricular muscles during hindlimb suspension in rats].

As a result of exposure to microgravitational forces, the body fluids are shifted from lower part of the body to upper part with a volume of about 2 liters. Many reports on the hemodynamic, humoral, and other biomedical aspects of the body exposed by weightlessness have been reported. A 45 degree head-down tail suspension was introduced to examine ultrastructure and biochemical analyses on the right and left ventricles in rats. Increases in oxydative enzyme activities and relatively increase in m-CK(mitochondrial creatine kinase) were recognized in the right ventricle after suspension for 2 weeks. Mitochondrial volume and density of mitochondrial cristae were also increased. Direct measurement of right ventricular systolic pressure of suspended rats were significantly higher (28.99 +/- 3.11 mmHg) than that of control rats (20.99 +/- 2.94 mmHg), (p < 0.01).