Low-molecular-weight heparins (LMWH) of different types have yielded different results when used in the setting of unstable angina (UA) or non Q-wave myocardial in-farction (NQMI). We compared the safety and therapeutic efficacy of two different LMWHs, namely dalteparin (Dalt.) and enoxaparin (Enox.), in the acute phase (first 5 days) of UA or NQMI.
One hundred and forty-two patients with UA/NQMI were randomly assigned to treatment with either Dalt. [120 IU/kg twice daily by subcutaneous (SC) injection] or Enox. [1 mg/kg twice daily by SC injection]. The occurrence of any one of death, myocardial infarction, or angina recurrence within 5 days of the first LMWH injection was the endpoint of the study. There were 69 patients in the Enox. group (53 males, 16 females, mean age : 60.3±11.9) and 73 patients in the Dalt. group (54 males, 19 females, mean age : 59.6 ±10.3). The baseline characteristics of the patients in the two groups were similar. There were no deaths in either group. Myocardial infarction occurred in two patients in the Dalt. group (4%). Angina recurrence was seen in 11 patients in the Enox. group (16%) and in 11 patients in the Dalt. group (15%). Overall, any of the events that made up the endpoint occurred in 11 (16%) and 14 (19%) patients in the Enox. and Dalt. groups, respectively (P>0.05). The time to occurrence of the first event, however, was significantly longer in the Enox. group (82.3±33.2 versus 37.6±23.4 hours, P=0.007). Thrombocytopenia and allergic reactions were not detected in any patient. Major bleeding was seen in 1 patient in the Enox. group. Minor bleeding occurred in 17 (25%) and 21 (29%) patients in the Enox. and Dalt. groups, respectively (P>0.05).
Enoxaparin and dalteparin were found to be equally safe and effective for the early management of UA/NQMI, but enoxaparin appeared to delay the occurrence of MI or angina recurrence as compared to dalteparin in this setting.

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Nicorandil has been reported to have a preconditioning effect which suppresses the ST-segment shift or lactate production during coronary angioplasty in patients with stable angina pectoris. The present study investigated whether the preconditioning effect of ni-corandil affects troponin T (TnT) levels after coronary angioplasty. Twenty-four patients with stable angina pectoris were randomized to receive a 1-minute intravenous infusion of nicorandil (100 μg/kg) or normal saline. Five minutes later they underwent three 2-minute balloon inflations 5 minutes apart. The sum of ST-segment elevation in all leads (∑ST) was determined at the end of each balloon inflation. Serum levels of TnT were measured 6 and 18 hours after the procedure, and the higher value of the two measurements was compared between the groups. ∑ST decreased progressively during the three sequential balloon inflations in both groups and was less in the nicorandil group than in the control group. The TnT level after the procedure was significantly lower in the nicorandil group than in the control group (0.05±0.05 vs 0.11±0.10 ng/mL). In conclusion, pretreatment with intravenous nicorandil suppresses TnT release after coronary angioplasty as well as ST-segment elevation during coronary angioplasty, suggesting pharmacological preconditioning by nicorandil.

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The relationship between the location and size of an infarction and QT dispersion was investigated in 84 Japanese patients with chronic myocardial infarction (54 with anteroseptal infarction and 30 with inferior infarction). The control group consisted of 23 subjects without ischemic heart disease (13 normal subjects and 10 hypertensive patients). Corrected QT dispersion (maximum corrected QT interval minus minimum corrected QT interval: QTc dispersion), was significantly larger in the anterior infarction group than in the control group (69.9±21.5 msec vs 53.0±17.6 msec), while the inferior infarction group showed no significant difference from control subjects. QTc dispersion was significantly greater in the patients with large anterior infarcts than in those with small anterior infarcts (80.5±20.5 msec vs 61.9±18.8 msec). In patients with chronic myocardial infarction, QT dispersion is influenced by the infarct location and size. Accordingly, interpretation of QT dispersion data should take these factors into consideration.

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It has long been established that advanced age is not only associated with greater myocardial infarction frequency but also greater mortality and morbidity. The treatment of acute myocardial infarction (AMI) in 80 year old patients remains problematic with conflicting results; in these patients, the risks of conservative treatment are high and the risks and benefits of thrombolytic therapy are still controversial. The purpose of this study was to evaluate whether primary angioplasty can offer an important alternative method to improve short- and long-term outcomes in octogenarian or older patients who experience AMI.
Between May 1986 and March 2000, 171 consecutive 80 year old patients hospitalized for AMI were not randomized to be registered and divided into a medical therapy group (group 1: an historical control group, n=111) and a primary angioplasty group (group 2, n=60). In-hospital mortality was markedly increased with advanced Killip scores (Killip 3 or 4) in both groups. Twenty-four hours after admission, group 1 patients had a significantly higher incidence of progression to higher Killip scores than did group 2 patients (P=0.006). The 30-day overall mortality of group 2 patients was significantly lower than in group 1 patients (30.0% vs 54.1%, P=0.003). Patients without cardiogenic shock treated by primary angioplasty had a significantly lower incidence of overall mortality at 30 days than patients without cardiogenic shock treated conservatively [3.1% vs 24.3%, P=0.016 (Killip 1 and 2); 18.2% vs 52.6%, P=0.044 (Killip 3)]. However, the mortality rate of cardiogenic shock was extremely high and did not differ significantly between groups 1 and 2 (86.1% vs 88.2%, P=0.99). The 3-year cumulative survival rate was significantly higher in group 2 than in group 1 patients (P=0.0009).
In conclusion, primary angioplasty is feasible and effective, and can improve short- and long-term mortalities in octogenarian or older patients with AMI but without cardiogenic shock.

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Vegetative electrode infection following permanent pacemaker implantation is a rare and serious complication. Among 1920 patients who underwent permanent pacemaker implantation in our institute between 1980 and 2000, 7 patients aged 65 to 78 years were diagnosed to have pacemaker related endocarditis. In this study, the clinical course and management strategies for these patients are reviewed. The most frequently encountered factors contributing to development of pacemaker infection were local complications such as postoperative hematoma and inflammation, and recurrent surgical interventions on the pacemaker system. In blood cultures S. aureus was the most common causative microorganism. Echocardiography could be performed in 5 patients. Three patients were referred to open-heart surgery for total removal of the pacemaker system, and one patient had his pacemaker system removed percutaneously. The remaining 3 patients did not agree to either surgical or percutaneous removal. These patients have been under antibiotic therapy for approximately 3 years and they still do not have any signs of a serious infection. Consequently, in patients with permanent pacemakers, infective endocarditis should be considered in the presence of fever and local symptoms. Blood cultures should be obtained and echocardiography should be performed. Complete removal of the pacemaker system with intensive antibiotic treatment is necessary for complete eradication of the infection. However, if percutaneous or surgical removal of the electrodes cannot be done because of high perioperative risk or the patient does not agree to undergo either method, medical treatment with long term antibiotic use may be considered as an alternative.

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Cardiac risk factors are observed more frequently in patients with polycystic ovary syndrome (PCOS). On the other hand, increased QT dispersion, which is a risk factor for cardiac arrhythmias and sudden death, has not been investigated in this syndrome. In this study, we evaluated QT dispersion in PCOS patients without overt heart disease. Thirty-six consecutive women with PCOS (mean age 24 ±5 years) and 36 healthy women of similar ages (mean age 24±4 years) participated in this study. PCOS was diagnosed if there were polycystic ovaries by ultrasound (enlarged ovaries with ≥8 cysts 2-8 mm in diameter), oligoamenorrhea (intermenstrual interval >35 days), hirsutism (Ferriman-Gallwey score, ≥7) and elevated serum levels of testosterone (≥2.7 nmol/L). Electrocardiograms were recorded at a paper speed of 50 mm/s. QT intervals were manually measured by a cardiologist. All intervals were corrected for heart rate according to Bazett's formula: QTc interval=QT interval/square root of the RR interval. Mean values of body mass index, heart rate, and blood pressure were not significantly different between the two groups (P>0.05). No significant differences in QT intervals (maximum QT, minimum QT, QT dispersion, minimum corrected QT, maximum corrected QT, and corrected QT dispersion) were observed between the two groups (P>0.05). Our results suggest that the risk of ventricular arrhythmias or sudden cardiac death is not increased in PCOS patients.

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The protective effect of severe mitral regurgitation (MR) against left atrial thrombus formation has been well documented. It was also proposed that severe MR may prevent thrombus formation within the left ventricle (LV) with systolic dysfunction. Therefore, we investigated whether ischemic MR prevents thrombus formation within the LV in patients with systolic dysfunction. The study population was comprised of 1313 patients (1133 males, 180 females, age 56±18) with ischaemic LV dysfunction documented by coronary angiography and left ventriculography. None of the patients had a history of chronic anticoagulation. Epicardial coronary arteries were normal in 91 patients, and single-vessel, two-vessel, and triple-vessel disease were detected in 328, 330, and 564 patients, respectively. Left ventricular thrombus and severe MR were detected in 191 (14.5%) and 125 (9.5%) patients, respectively. Overall incidence of LV thrombus was lower in patients with severe MR than in patients without severe MR (4% vs 15.6%, OR: 0.2, P<0.001). Severe MR compared with absence of severe MR was associated with a lower incidence of LV thrombus both in patients with ischemic dilated cardiomyopathy (6.8% vs 34.2%, OR: 0.19, P<0.001), and in patients with aneurysm (3% vs 18%, OR: 0.14, P<0.0001) involving anterolateral, septal and/or apical LV segments. A similar trend without statistical significance was also observed in patients with dyskinesia (4.7% vs 16%, OR: 0.26, P=0.1) related to anterolateral, septal and/or apical LV segments. However, MR had no impact on the incidence of LV thrombus in patients with aneurysm or dyskinesia related to posterior and/or inferior segments (3.7% vs 3%, OR: 1.2, P>0.05).
In conclusion, severe MR seems to prevent LV mural thrombus formation in patients with ischemic dilated cardiomyopathy, and in patients with aneurysm related to anterolateral, septal, and/or apical LV segments. This relative risk reduction may be associated with diastolic volume overloading due to severe MR which may overcome stagnation and a procoagulant state within the LV with severe systolic dysfunction.

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The aim of this study was to assess the value of the left ventricular cavity-to-myocardium count ratio (C / M ratio) of technetium-99m (Tc-99m) tetrofosmin single photon emission computed tomography (SPECT) to identify abnormal left ventricular ejection fraction (LVEF) responses after exercise in patients with coronary artery diseases (CAD). We studied 50 patients with recent CAD undergoing rest and exercise first-pass ventriculography to calculate LVEF and rest and exercise Tc-99m tetrofosmin myocardial perfusion SPECT to calculate left ventricular C / M ratios. Group A, consisting of 25 CAD patients with normal responses (increased LVEF ≥ 5% after exercise), had significantly higher rest and exercise C / M ratios than those of the group B, consisting of 25 CAD patients with abnormal responses (increased LVEF <5% after exercise) after exercise. However, the C / M ratios between exercise and rest did not differ significantly between groups A and B. In addition, there was significant correlation between LVEF and C / M ratios in all of the patients. C / M ratios of Tc-99m tetrofosmin myocardial perfusion SPECT are useful parameters for identifying patients with abnormal LVEF responses among patients with CAD.

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Increased lung uptake of thallium-201 (Tl-201) and technetium-99m (Tc-99m) MIBI in myocardial perfusion imaging is a reliable marker of left ventricular dysfunction. The goal of our study was to establish whether the lung-to-heart (L/H) uptake ratio with a newer cardiac imaging agent, Tc-99m tetrofosmin, can also provide valuable information about left ventricular function.
We studied 60 patients with recent coronary artery diseases (CAD) undergoing first-pass radionuclide ventriculography to calculate left ventricular ejection fraction (LVEF) and myocardial perfusion imaging to calculate the L/H ratio. Group A consisting of 30 CAD patients with higher LVEF (≥40%) had a significanly lower L/H ratio than group B consisting of 30 CAD patients with abnormal LVEF (<40%) during exercise and rest. In groups A and B, the exercise and rest L/H ratios did not differ significantly. However, a statistically significant inverse correlation was found between the L/H ratio and LVEF during exercise and rest among the 60 patients.
L/H ratios, measured by 99mTc-tetrofosmin imaging, provide clinically useful information with which to predict left ventricular dysfunction in CAD patients.

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The objective of the present study was to compare pre- and postoperative pulmonary function tests in adult patients who had intubation periods greater and less than 24 hours following elective open heart surgery.
Group l consisted of 91 patients (18 females and 73 males) gr, whose intubation periods were more than 24 hours (mean: 8.1±18.6 hours); and group 2 75 patients (13 females and 62 males) who had intubation periods less than 24 hours (mean: 13.25±3.60 hours). The pulmonary function test measurements were obtained from a vitalograph before and after the operation (just before being discharged from the hospital), All patients underwent cardiopulmonary physiotherapy and a rehabilitation programme during their hospital stay.
The patients were similar in height and weight. The duration of hospitalization of the patients who had a prolonged intubation period was 17.26±9.7 days, while that of the control group was 10.64±2.04 days (P<0.0001).
When the preoperative pulmonary function test values of each patient were compared with the expected values, the percent values of forced expiratory volume for one second, flow velocity of the mid-forced expiration and forced expiratory flow which were achieved by group 2 were significantly high compared to those of group 1 (P=0.014, P= 0.03 and P<0.0001, respectively). However, the percent values of forced vital capacity were similar.
When the percent variations of the differences between the pre-and postoperative pulmonary function test values of the groups were compared, all values except the flow velocity of the mid-forced expiration, and forced vital capacity, were found to be significantly lower statistically in the group having a prolonged intubation period.
As a result, it was determined that the patients whose preoperative pulmonary function test values were poor, had longer intubation periods and similarly, they continued to be worse after the operation. We believe that it is advantageous to apply more intensive pulmonary rehabilitation for prolonged periods to these patients in the postoperative period.

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The efficacy of ACE inhibitors (ACEIs) in the treatment of chronic heart failures is well documented. However, ACEIs may provide incomplete blockade of the renin-angiotensin system (RAS) because of the alternative pathways for angiotensin II (AII) production. We hypothesized that more complete blockade of RAS by adding an AT1 receptor blocker (ARB) may have greater potential to decrease mortality associated with heart failure and improve cardiac function than monotherapy with ACEIs.
The objective of this study was to evaluate the effect of combined therapy on cardiac functions and survival in cardiomyopathic hamsters.
Male cardiomyopathic hamsters (BIO TO2) were administered either placebo (group C), enalapril (30 mg/kg/day) (group E), or enalapril (30 mg/kg/day) + valsartan (500 mg/kg/day) (groupEV), starting at the age of 6 weeks. Kaplan-Meier analysis was performed to assess the differences in survival. Cardiac functions were evaluated by echocardiogram and cardiac catheterization.
Group EV showed significant increases in fractional shortening, LV dP / dTmax, and deceleration time, and showed significant decreases in left ventricular diastolic dimension, LV dP / dTmin, and early diastolic mitral velocity / atrial systolic velocity. Treatment with enalapril resulted in longer survival compared with placebo. Moreover, life expectancy (median probability of survival: 433 days) increased significantly in group EV compared with group E (P<0.05) as well as group C (P<0.001).
It is concluded that combined therapy improved cardiac function and survival compared to placebo or enalapril monotherapy.

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It has been indicated that the anti-estrogen agent, tamoxifen, developed for the treatment of breast cancer, may act on the vascular system as an estrogen agonist. However, to our knowledge few reports suggest that tamoxifen exerts anti-atherogenic actions. In the present study, we evaluated the anti-atherosclerotic effects of tamoxifen in ovariectomized cholesterol-fed rabbits. Ovariectomized rabbits were fed a 1% cholesterol diet and divided into 4 groups: control group (C, n=5); estrogen treatment (E, n=6); low-dose tamoxifen treatment (0.5 mg/kg) (LT, n=6); and high-dose tamoxifen (1.0 mg/kg) (HT, n=7). After 6 weeks, both Oil red O-positive areas on the intimal surfaces of aortae and the ratios of intimal to medial areas (I/M ratios) measured from cross-sections of aortae were significantly lower in groups E, LT and HT compared with group C. Although there were no significant differences in serum NOx (NO₂ and NO₃) levels among the 4 groups, NOx levels were slightly higher in groups E, LT and HT than group C. Acetylcholine (ACh) was administered to all animals, and the responses of ear arteriole diameters were compared among the 4 groups. While ear arteriole diameters were significantly decreased in group C, no significant changes were observed in groups E, LT or HT following ACh administration. Ratios of ear arteriole diameters after to before ACh administration were significantly greater in groups E, LT and HT compared to group C. These findings suggest that tamoxifen exerts anti-atherosclerotic effects, and that these effects are attributed to the maintenance of vascular endothelial function.

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Fibrinogen secretion is mediated by prostaglandin biosynthesis and is considered a risk factor for cardiovascular disease. Since meloxicam produces inhibition of prostaglandin biosynthesis it may help to normalize hyperfibrinogenemia.
We investigated the pharmacological effect of meloxicam on fibrinogen levels and the possible regression of histopathological lesions of thoracic aorta. Rats were subjected to multiple injuries (MI) in the form of laparotomies (Lx) during a 30 day period (1/week). Meloxicam 0.065 mg/kg/day (per rat) was administered orally immediately after the third Lx in multiple injury animals during a ten day period. Blood was obtained 72 hours after the last injury in all groups. Fibrinogen was measured by spectrophotometry and the values were expressed in mg/dL. A statistically significant increment of fibrinogen was observed when comparing uninjured animals (control) (208.7±6.0) with the multiple injury group (336.6±7.5) (P<0.001). Fibrinogen decreased to the control value in the meloxicam group (198±8.7). Histopathological lesions were similar in the MI and meloxicam groups, showing endothelial denudation and intima enlargement from the thoracic aorta in 96% of the slices studied. The decrease in fibrinogen in the meloxicam group would be due to cyclooxygenase-2 (Cox-2) selective inhibition, even though the histopathological lesions did not regress.

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The case of a 27-year-old Japanese woman with type A acute aortic dissection who had been diagnosed with systemic lupus erythematosus (SLE) is presented. The patient also had aortic regurgitation due to non-infective endocarditis and systemic hypertension, and had been maintained on steroid therapy for 15 years. Her twin sister was also diagnosed with SLE. The patient was admitted to emergency due to severe back pain. A chest x-ray showed enlargement of the upper mediastinum. Echocardiography revealed a thickened and deformed aortic valve with aortic regurgitation and dissection of the ascending aorta, but pericardial effusion was not found. Computed tomography demonstrated aortic dissection extending from the ascending aorta to the abdominal aorta. Graft replacement of the ascending aorta and proximal aortic arch was performed under hypothermic circulatory arrest with retrograde cerebral perfusion. The patient recovered uneventfully. Aortic dissection complicated with SLE is extremely rare, and this is only the 15th case reported in the English or Japanese literature.

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