Remnant-like lipoprotein particles as risk factors for coronary artery disease in elderly patients.

Although remnant-like lipoprotein particles (RLPs) are known to be atherogenic, the relationship between serum RLP-cholesterol (RLP-C) level and coronary artery disease (CAD) has not as yet been evaluated. This clinical study was aimed at investigating the pathological significance of serum RLP-C among several coronary risk factors with a clear focus on elderly patients. We took fasting venous blood samples to determine lipid profiles including RLP-C from 188 patients with angiographically identified CAD and 68 control patients. Overall analysis showed that the RLP-C/HDL-C ratio was higher in both single-vessel CAD group (n = 67; p < 0.01) and multi-vessel CAD group (n = 121; p < 0.001) compared to controls. Further, multiple logistic regression analysis indicated that the diabetes, HDL-C and the RLP-C/HDL-C ratio could discriminate CAD patients from controls. In patients younger than 65 years, diabetes, HDL-C, LDL-C and the LDL-C/HDL-C ratio as well as the RLP-C/HDL-C ratio could discriminate CAD. In patients 65 aged years or older, however, diabetes, triglyceride and RLP-C as well as the RLP-C/HDL-C ratio could discriminate CAD, whereas LDL-C and the LDL-C/HDL-C ratio could not. These results led us to believe that the contribution of a given risk factor to the development of CAD in elderly patients may be different from that in younger patients. In elderly patients, RLP-C rather than LDL-C was strongly associated with the development of CAD. Accordingly, serum RLP-C levels may serve as a convenient and reliable index for assessing CAD.

Acute myocardial infarction associated with myocardial bridge and coronary artery vasospasm.

A 65-year-old man was admitted to our hospital with acute myocardial infarction (MI). Emergency coronary angiography showed no significant organic lesions, but a myocardial bridge was found at the mid-left anterior descending artery An acetylcholine provocation test revealed 90% spastic stenosis just proximal to the myocardial bridge. His acute MI could have been caused by both a coronary spasm and the myocardial bridge.

Clinical significance of antibody against oxidized low density lipoprotein in patients with atherosclerotic coronary artery disease.

OBJECTIVES: This study was designed to establish the clinical significance of antibodies against oxidized low density lipoprotein (anti-Ox-LDL) titer in atherosclerotic coronary artery disease (CAD). BACKGROUND: Oxidative modification of LDL, which plays a key role in the development of atherosclerosis, induces immunogenic epitopes in the LDL molecule, and the presence of anti-Ox-LDL has been demonstrated in human sera. METHODS: Anti-Ox-LDL titer was measured by enzyme-linked immunosorbent assay in 108 patients who had angiographically verified CAD, and 31 patients who had chest pain but no significant CAD, as controls. RESULTS: The anti-Ox-LDL titer was higher (p < 0.01) in patients with multivessel CAD (19.4 +/- 10.1 AcU/ml, n = 68) than in the controls (9.8 +/- 4.1). However, no significant difference was shown between the single-vessel CAD group (15.1 +/- 6.4, n = 40) and the controls, or between the multivessel CAD group and the single-vessel CAD group. The titer was higher in patients with unstable angina (21.5 +/- 11.8 AcU/ml, n = 20, p < 0.01), or in patients with acute myocardial infarction (23.1 +/- 12.0, n = 20, p < 0.01) than in patients with stable-effort angina or old myocardial infarction (12.2 +/- 8.6, n = 68). Multiple logistic regression analysis indicated that the anti-Ox-LDL titer most powerfully discriminated CAD patients from controls (odds ratio [OR]: 1.20, 95% confidence interval [CI]: 1.07-1.33, p = 0.0006) and acute coronary syndrome from chronic CAD (OR: 1.09, 95% CI: 1.04-1.14, p = 0.0008). CONCLUSIONS: Serum anti-Ox-LDL titer not only can predict a presence of atherosclerotic CAD but also may be a marker of plaque instability. Low density lipoprotein oxidation may play an important role in the development of plaque instability.

Unusual coronary artery aneurysm and acute myocardial infarction in a middle-aged man with systemic lupus erythematosus.

A 55-year-old man developed acute myocardial infarction (AMI) related to a large coronary artery aneurysm and a distal coronary stenotic lesion after steroid therapy for systemic lupus erythematosus (SLE). Only 13 SLE patients with AMI caused by coronary artery aneurysms have been reported, 11 of whom were young or middle-aged women and the 2 remaining were young men. This is the first report of a middle-aged man with multiple coronary lesions.

Antibody against oxidized low density lipoprotein may predict progression or regression of atherosclerotic coronary artery disease.

OBJECTIVES: This study aimed to elucidate whether an antibody against oxidized low density lipoprotein (anti-Ox-LDL) could predict short-term coronary artery atherosclerotic lesion progression. BACKGROUND: It is still controversial whether higher levels of the anti-Ox-LDL titer are associated with atherosclerotic coronary artery disease. METHODS: In 52 patients undergoing coronary angioplasty and six-month follow-up angiography, we performed quantitative coronary angiographic analysis of a lesion on a branch away from the intervention site vessel and assessed lesion progression or regression using the Progression-Regression score calculated as the baseline minimal lumen diameter minus the follow-up minimal lumen diameter. The serum anti-Ox-LDL titer was measured using an enzyme-linked immunosorbent assay method just before the initial angiography in all patients. RESULTS: The anti-Ox-LDL titer was 16.6+/-1.5 AcU/ml in the progression group (Progression-Regression score >0.15 mm; n = 20), which was significantly higher (p < 0.001) than the value of 9.5+/-1.2 in the regression group (< or =-0.15 mm; n = 14) and also higher (p < 0.01) than the value of 11.4+/-1.3 in the no-change group (-0.15 to 0.15 mm; n = 18). The Progression-Regression score was correlated with the antibody titer in all patients (r = 0.56, p < 0.001). Multiple regression analysis showed that the Progression-Regression score was independently correlated with the antibody titer (r = 0.44, p < 0.01) as well as lipoprotein (a) (r = 0.33, p < 0.05). CONCLUSIONS: Anti-Ox-LDL may be an independent predictor of coronary atherosclerotic lesion progression in the short term.

Idiopathic adrenal hemorrhage.

A case of idiopathic adrenal hemorrhage is reported. A 76-year-old woman exhibited a left adrenal tumor, 3 cm in diameter, on abdominal computed tomography. The patient was receiving aspirin medication for atrial fibrillation. There was no evidence of increased adrenal hormones. The mass enlarged to 6 cm in diameter within 18 months, and malignancy was suspected. The mass was diagnosed as adrenal hematoma by operative findings.

Direct discrimination and full-day disclosure of ventricular parasystole on new heart rate tachograms.

INTRODUCTION: To discriminate ventricular parasystole from fixed coupling interval ventricular premature complexes (VPCs), we developed a new diagnostic method using a dot distribution pattern corresponding to VPCs recorded on a heart rate tachogram using ambulatory ECG monitoring data. We tested our hypothesis that widely scattered VPC dots on instantaneous heart rate tachograms indicate a constant VPC-VPC interval compatible with parasystole. METHODS AND RESULTS: Patients with frequent VPCs > 5,000/day) were divided into two groups depending on the tachogram dot distribution patterns: group S (n = 10, aged 61 +/- 16 years) showed widely scattered VPC dot distribution, whereas group F (n = 10, 60 +/- 17 years) showed fixed VPC dot distribution limited to a narrow zone. Using digitized R-R interval data, full-day heart rate tachograms and VPC-VPC intervals were depicted simultaneously. Group S demonstrated constant basic VPC-VPC intervals (1,285 to 2,052 msec, mean 1,738 +/- 219), with a coefficient of variation (CV) of 0.061 +/- 0.018. Their VPC coupling intervals were markedly variable (651 +/- 113 msec; CV = 0.193 +/- 0.034). Each patient's basic VPC-VPC intervals showed small diurnal alterations (minimum -13% +/- 3% to maximum +15% +/- 6%). VPC-VPC intervals in group F were not constant and showed marked variation. Group F VPC coupling intervals were shorter and constant (480 +/- 30 msec, P = 0.0002; with CV = 0.076 +/- 0.013, P < 0.0001). CONCLUSION: Ventricular parasystole with constant VPC-VPC intervals consistently became evident based on VPC dot patterns recorded on heart rate tachograms.

Cyclic bursts of ventricular premature contractions of more than one minute intervals.

Ventricular premature contractions (VPCs) occasionally appear successively in the form of bigeminy, trigeminy or quadrigeminy associated with quiescent periods. However, details of these rhythmic VPC bursts have not been well documented. We analyzed the incidence, periodicity and interval of VPC bursts exhibiting bigeminy or trigeminy using ambulatory ECG monitoring and computer analysis. We defined VPC bursts as more than 5 successive groups of VPCs each containing more than 20 VPCs in the form of bigeminy or trigeminy that were interrupted by normal sinus rhythm lasting for more than 60 seconds. Bursts thus defined were observed transiently or continuously in 78 out of 500 consecutive patients showing > 3000 VPCs a day. Their age ranged from 14 to 76 years (mean 48). Forty patients were men and 38 were women. We could discriminate between two types of bursts on the instantaneous heart rate tachograms. Dome type bursts (n = 48) showed gradual shortening of the VPC coupling intervals whereas horizontal type bursts (n = 30) demonstrated fixed coupling intervals during the bursts. Cycle length of the dome type burst was 185 +/- 40 seconds and regular, whereas it was 210 +/- 63 seconds and irregular in the horizontal type (NS). Duration of the VPC bursts was 101 +/- 31 seconds in the dome type and 98 +/- 41 seconds in the horizontal type. Both burst types were associated with transient increases in sinus rate and abbreviated VPC-VPC intervals. We suspect ventricular parasystole to be the mechanism of these bursts especially in the dome type. Recognition of these two burst types from heart rate tachograms may be of value in the suppression of VPCs.

[Evaluation of restenosis after percutaneous transluminal coronary angioplasty using a Doppler index, the Tei index].

Cardiac function and restenosis were evaluated after percutaneous transluminal coronary angioplasty (PTCA) using a Doppler index (the Tei index). Thirty-eight patients, 31 men and 7 women (mean age 57 years) with ischemic heart disease were studied. The underlying heart diseases were angina pectoris without left ventricular asynergy in 16 patients and old myocardial infarction (OMI) with left ventricular asynergy in 22 . Ejection fraction was measured by M-mode echocardiography and deceleration time, and the interval between cessation and onset of the mitral inflow velocity (a), ejection time at aortic valve (b), and the Tei index [(a-b)/b] were measured by M-mode echocardiography performed before and 6 months after PTCA. The ejection fraction, deceleration time and Tei index showed no changes after PTCA in patients with angina pectoris with or without restenosis. In patients with OMI with restenosis, the Tei index increased slightly after PTCA, from 0.56 +/- 0.15 to 0.61 +/- 0.13. The deceleration time changed from 0.23 +/- 0.03 to 0.24 +/- 0.02 msec, and the ejection fraction from 0.46 +/- 0.11 to 0.51 +/- 0.17, neither significantly. However, in patients with OMI without restenosis (15 out of 22 patients), the Tei index significantly improved after PTCA, from 0.55 +/- 0.13 to 0.48 +/- 0.12 (p < 0.05). In patients with left ventricular asynergy due to old myocardial infarction, without restenosis, the Tei index significantly improved after PTCA. The Tei index is useful for evaluating restenosis after PTCA in patients with OMI.

Six-year survival of unoperated ventricular septal rupture following myocardial infarction.

We present the case of a patient who survived for 6 years without surgical repair of a ventricular septal rupture that followed an acute myocardial infarction. To the best of our knowledge, only 3 other cases have been reported in which the patient survived for more than 5 years.

[Echocardiographic observation of appearance and progression of mitral annular calcification in a patient with familial obstructive hypertrophic cardiomyopathy].

A 37-year-old man with familial hypertrophic obstructive cardiomyopathy (HOCM) developed mitral annular calcification (MAC) during the follow-up period. At the age of 23 years, a systolic murmur and electrocardiographic abnormality including giant T wave inversion were detected incidentally. His elder brother also had HOCM. Catheterization disclosed a left ventricular outflow pressure gradient of 25 mmHg and thickened interventricular septum. Echocardiography showed asymmetric septal hypertrophy and systolic anterior motion of the mitral valve. The patient was followed up by repeated echocardiography from age 37 years and the onset of MAC (2 mm in thickness) was found at age 48 years. One year later, the MAC had progressed markedly (5 mm) without other remarkable changes in the M-mode echocardiogram, except mitral regurgitation (at age 41 years), left ventricular apical as well as posterior wall hypertrophy (age 43 years) and left atrial enlargement (age 46 years). The left ventricular inflow velocity at the atrial contraction period decreased significantly concomitantly with MAC. MAC is a rare complication in young and middle aged patients. The onset and progression of MAC is still obscure in HOCM. This patient showed that sudden onset and rapid progression of MAC can occur in young patients with HOCM.

Ischemic change on electrocardiogram induced by hypoglycemia in a diabetic patient.

A 34-year-old female patient who presented to our hospital had been treated with insulin for diabetes since she was 25 year old. For the previous year she had experienced chest pain on exertion and during hypoglycemia. During both chest pain and exercise tests, ST depression and flattening of the T wave were recognized in leads II, III, aVF, and V2-V6 on the electrocardiogram, and thus ischemic heart disease was suspected. Cardiac catheterization was performed, but no organic stenosis or spasms were found. Hypoglycemia (41 mg/dl) was induced by intravenous injection of rapid insulin (total 18 U, 0.4 U/kg). However, no coronary change was seen, although she felt chest pain and the same ischemic electrocardiographic changes occurred. We hypothesized the causes of the ischemic change to be both the effects of insulin on the cardiovascular system and the physiologic stress induced by the existence of microvascular abnormality. Special care should therefore be taken with diabetic patients being treated with insulin or hypoglycemic agents.

Effect of enalapril maleate on cerebral blood flow in patients with chronic heart failure.

The effect of enalapril on cerebral blood flow (CBF) was studied in 11 patients with chronic heart failure (NYHA II or III, dilated cardiomyopathy in 6 and old myocardial infarction in 5). CBF was evaluated by analyzing the Patlak-Plot curve obtained from radionuclide angiography with technetium-99m hexamethylpropylene amine oxime (99mTC-HM-PAO). Cardiac index (CI) and stroke volume (SV) were simultaneously measured by impedance cardiography. These measurements were performed before and at four weeks after daily administration of 5 mg enalapril. The stroke volume, cardiac index, and heart rate were not significantly changed after four weeks of enalapril administration. However, CBF was increased by 6.5% from 36.72 +/- 4.66 to 39.13 +/- 5.65 mL/100g/min (P < 0.05). These results suggest that enalapril increased cerebral blood flow, which was not related to increased cardiac output in congestive heart failure. Patlak-Plot analysis of radionuclide angiography using 99mTC-HM-PAO may be available for quantitative assessment of brain perfusion.

[Successful surgical treatment of aortic regurgitation due to annuloaortic ectasia and mitral regurgitation caused by tendon rupture in a case of osteogenesis imperfecta].

A 54-year-old man presented with osteogenesis imperfecta complicated with both aortic regurgitation due to annuloaortic ectasia and mitral regurgitation secondary to tendon rupture. He had spinal and carpal deformities in his childhood, and heart murmurs were identified at the age of 25. He was admitted complaining of dyspnea on effort. His height was 142 cm and his weight was 46 kg. He had kyphosis, scoliosis and carpal deformity. Blue sclera was not observed. Chest radiography showed cardiomegaly and lung congestion. Echocardiography showed annuloaortic ectasia, mild aortic regurgitation, and serious mitral regurgitation due to postero-apical tendon rupture. Bone deformity and his statues were indicative of osteogenesis imperfecta. He received modified Bentall and mitral valve replacements.

Fulminant hepatic failure due to cardiac tamponade associated with mixed connective tissue disease.

We describe a 42-year old Japanese woman with mixed connective tissue disease (MCTD) who developed fulminant hepatic failure and hepatic encephalopathy. Massive pericardial effusion accompanying cardiac tamponade was shown by echocardiography. The hepatic failure was considered to be caused by a low cardiac output state because of cardiac tamponade, which might be due to cardiac involvement of MCTD. This is a rare case, showing an unusual progressive course in MCTD.

Tricuspid valve infectious endocarditis associated with dental treatment.

A 52-year-old man with neither congenital heart disease nor history of drug abuse had a spiking fever after dental treatment and was diagnosed with pneumonia at a local clinic. He was treated with antibiotics and his fever went down. Ten months later, he had again pyrexia and suffered from congestive heart failure. He admitted to our hospital and tricuspid valve endocarditis was proved by echocardiography. He was treated with penicillin. However, during the treatment, he developed a pulmonary embolism. So he underwent surgical treatment. We should take dental treatment into account one of predisposing causes of tricuspid endocarditis.

Systemic amyloidosis following ankylosing spondylitis associated with congestive heart failure. A case report.

We report the case of a 38-year-old man who developed fatal, systemic amyloidosis following ankylosing spondylitis. He was admitted for symptoms of congestive heart failure. Based on parotid gland biopsy and echocardiography, he was diagnosed as having systemic amyloidosis following active ankylosing spondylitis. However, the clinical course was rapidly progressive and eventually the patient died of acute necrotizing pancreatitis. The association has been reported thus far in a limited number of cases worldwide. The literature has featured localized lesions and a benign clinical course of the amyloidosis. This case, the first report from Japan, indicates that the amyloidosis associated with ankylosing spondylitis might exhibit a rapidly progressive clinical course, thereby suggesting that in such a case, meticulous treatment is required.

[A case of coronary artery embolism associated with combined valvular heart disease].

A 53-year-old-man afflicted with combined valvular heart disease and atrial fibrillation was admitted to our department complaining of chest pain. ST elevation on ECG (II, III, aVF) and elevated CPK value were recognized. He was diagnosed as having acute myocardial infarction, and percutaneous transluminal coronary recanalization was performed immediately. The coronary angiogram showed occlusions at the proximal left branch (#12). But these lesions could not be recanalized by 960000 IU urokinase administration. The cineangiogram after one month revealed perfect recanalization of these occlusions. Mitral stenosis with neovascularity to the left atrium and aortic regurgitation were recognized. We supposed this infarction caused by coronary embolism originated from left atrial thrombi. Acute myocardial infarction associated with mitral stenosis has been reported in fifteen cases previously in Japan, but only three cases revealed coronary occlusion in the acute phase with normal coronary artery in the chronic stage. However, there has been no report, except for this case, demonstrating occlusion in two coronary arteries at the same time. So, our case is the first report of the involvement of two coronary artery occlusions.

[A case of angina pectoris with cardiac arrest at treadmill stress test].

We reported a case of angina pectoris with cardiac arrest immediately after treadmill exercise test, and the effect of PTCA in the same case. A 69-year-old Japanese male had chest oppression on exertion. Initial treadmill test showed 2 mm ST-segment depression in leads V4-6. Two minutes after exercise, he had atrio-ventricular (A-V) block and cardiac arrest with episodes of fainting. He was resuscitated by chest thump. Coronary angiography showed 90% stenosis in the right coronary artery (RCA). PTCA for RCA was able to dilate the stenotic lesion. The second treadmill test after PTCA did not induce bradycardia nor A-V block. It was suggested that the RCA lesion may play a critical role.