Atherosclerotic changes in the coronary artery are exacerbated by the balance betweenLDL, which carries cholesterol into the arterial wall, and HDL, which carries it out from the wall. The molecular weight of LDL is about 2×10⁶ and that of HDL is about 4×10⁵, which is almost 1/5 of the molecular weight of LDL. For this reason, LDL/HDL×5 should be a good indicator of coronary heart disease. We evaluated this index in two subject groups. At first, we determined whether it could predict the incidence of effort angina in participants of a medical examination system. Most of the subjects were healthy and good candidates for primary prevention. LDL/HDL×5 was a more sensitive indcx predicdng effort angina than toal cholesterol, LDL or HDL.
The concentrations of HDL were significantly lower in myocardial infarction patients at all ages in both sexes. The average serum concentration of HDL was 56.6±15.0mg/dl in the medical examination group and 38.9±122 mg/dl in the AMI group.
We tested whether our new index, LDL/HDL×5, could predict the incidence of re-infarction in patients with myocardial infarction who were candidates for secondary prevention. LDL/HDL×5 was a more sensitive index predicting re-infarction than total cholesterol, LDL or HDL.

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Lysophosphatidylcholine (LPC) is an amphiphilic metabolite that can be produced from membrane-phospholipids by activation of phospholipase A₂ (PLA₂), and it accumulates in the heart during ischemia and reperfusion. It is known that LPC is an arrhythmogenic substance. Recent studies have revealed that LPC produces mechanical and metabolic derangements in perfused working rat hearts, and Ca²⁺-overload in isolated cardiac myocytes. Thus, LPC possesses an ischemia-like effect on the heart. LPC accumulated in the myocardium activates phospholipase A₂, establishing a vicious circle; i.e. LPC itself has an ability to produce another LPC. Therefore, a drug that has an anti-LPC effect would protect or improve ischemia/reperfusion damage. This article will review the effect of LPC in relation to ischemia, and consider a possibility of developing new anti-ischemic drugs on the basis of the anti-LPC action.

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We assessed the influence of residual antegrade coronary perfusion on long-term mortality and morbidity in 262 patients (256 men and 6 women, aged 52.3±9.8 years) with medically treated old myocardial infarction and single-vessel disease who were followed for 117.0±39.8 months. Partial or complete antegrade coronary perfusion of the infarct artery was present in 165 patients (group I); no or minimal antegrade perfusion of the infarct artery was present in 97 patients (group II). There was no significant difference in survival between group I (5-year survival rate, 96.9% and 10-year survival rate, 90.7%) and group II (93.8% and 92.7%, respectively). There was also no significant difference in the event free survival rate between group I (5-year, 92.6% and 10-year, 79.7%) and group II (89.5% and 74.8%, respectively). The extent of left ventricular dysfunction was an important determinant of prognosis: 10-year survival rates in patients with ejection fractions of >60%, 40-60% and <40% were 94.8%, 90.6% and 74.8%, respectively. In the majority of patients the subsequent cardiac events were related to the progression of atherosclerosis in previously nonstenotic coronary arteries. Thus, the presence or absence of residual antegrade coronary flow in the chronic phase of myocardial infarction did not significantly influence the long-term prognosis of patients with singlevessel disease.

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To assess the usefulness of adenosine triphosphate (ATP) as an alternative agent for functional determination of coronary circulation in children and to reveal the dose-response kinetics of intracoronary ATP, systemic hemodynamics and spectral coronary flow velocity dynamics using Doppler guide wire were measured during hyperemic responses to an intracoronary bolus injection of ATP (0.01μg/kg, 0.1μg/kg and 1.0μg/kg) in consecutive 40 Kawasaki disease patients (age: 8.4±5.1 years, 30 boys and 10 girls) without angiographic coronary lesions.
ATP did not produce any significant change in heart rate, systolic blood pressure and mean blood pressure, but mildly decreased diastolic blood pressure. The coronary flow reserve (CFR) calculated as a ratio of hyperemic to basal averaged peak velocity (APV) for ATP was 2.05±0.31, 2.26±0.38 and 2.50±0.51 in LAD, and 2.24±0.28, 2.44±0.41 and 2.60±0.47 in RCA, respectively, for each of the three doses. There was no statistical significance between the mean values of GFR in LAD with ATP (1.0μg/kg: 2.39±0.16) and papaverine (0.15μg/kg: 2.43±0.16) in six patients without angiographic coronary lesions. The maximal coronary hyperemia was reached rapidly after intracoronary bolus injection of ATP in all doses (10, 10-15 and 15-20 seconds in both LAD and RCA, respectively, for each of the three doses). The time required for APV to return to basal levels (<T 10%) increased with the dose of ATP (30, 55 and 110 seconds in LAD and 35, 45 and 100 seconds in RCA, respectively, for each of the three doses). Three patients (3/40: 7.5%) developed transient (<5 seconds) asymptomatic second degree atrioventricular block, but no patient had clinically significant arrhythmias. The change ratio in OTc interval after ATP injection was 1.96±1.87% (not significant). In addition, an intracoronary injection of ATP did not increase the absolute angiographic coronary luminal diameter.
This study indicates that ATP is a safe alternative agent for pharmacological induction of coronary hyperemia for evaluation of coronary stenotic lesions and for the study of coronary circulation and coronary flow reserve in children.

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Prostaglandin E1 is a potent vasodilator in severe chronic heart failure. To evaluate the time sequence and magnitude of prostaglandin E1's hemodynamic effects a dose finding study was performed in 24 patients. Right heart catheterization was performed and prostaglandin E1 was administered via a central venous line in incremental doses of 2.5, 10, 20, 30 and 40ng/kg/min, each dose, lasting 15min before hemodynamic evaluation. The first significant change was a∼20% decrease in systemic vascular resistance index accompanied by a∼18% increase in cardiac index at an infusion rate of 2.5ng/kg/min of prostaglandin E1, which was sustained at 5ng/kg/min in all patients. A dose response-curve with cumulative doses ranging from 2.5 to 25ng/kg/min of prostaglandin E1 was established in a subset of 14 patients due to 10 drop-outs at lower dosages. At 2.5 and 5ng/kg/min of prostaglandin E1, cardiac index increased by 18% (p<0.05) and peripheral resistance decreased by 18% (p<0.01). These changes were sustained up to a maximal dose of 25ng/kg/min, which was tolerated by all patients in this group. At 15 and 20ng/kg/min of prostaglandin E1 a significant decrease in blood pressure of -4mmHg (p<0.05) was observed which was reversed at the next dose step.
In a second analysis maximal tolerated dosages of prostaglandin E1 were evaluated in all 24 patients (group A, 26±2ng/kg/min), and in two subsets using a maximum tolerated dose of 20ng/kg/min as a cutpoint (B: 14 patients, 34±2ng/kg/min; C: 10 patients, 15±2ng/kg/min) Then the respective peak dosages were halved for continuous infusion through 12 hours. In the acute study pulmonary capillary wedge pressure (by A: -11%, p<0.01; B: -4%, p<0.01; C: -22%, p<0.01) and systemic vascular resistance (by A: -32%, p<0.0001; B: -25%, p<0.001; C: -43%, p<0.001) decreased significantly in all three groups and cardiac index increased (by A: +38%, p<0.0001; B: +33%, p<0.0001; C: +59%, p<0.0001). In the chronic study these changes were sustained. Furthermore, mean arterial pressure (by A: -14%, p<0.0001; B: -13%, p<0.001; C: -13%, p<0.05), right atrial pressure (by A: -36%, p<0.0001; B: -36%, p<0.01; C: -30%, p<0.01), pulmonary artery pressure (by A: -16%, p<0.0001; B: -16%, p<0.01; C: -19%, p<0.01) and pulmo-nary vascular resistance (by A: -28%, p<0.01; B: -31%, p<0.01; C: -25%, p<0.01) were significantly reduced after 12 hours.
Conclusion. These results demonstrate potent hemodynamic effects of low-dose prostaglandin E1 in severe heart failure. While systemic effects appear rapidly, a slow onset of the pulmonary effects was observed.

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From 1982 to 1994, 54 patients (47 men; mean age 72 years) were referred to the Hospital of Ferrara, Italy for spontaneous rupture of abdominal aortic aneurysm. Sixteen died in the emergency department and 38 underwent urgent surgery. Day and month of onset of acute symptoms leading to urgent surgery were recorded. A seasonal variation with significant peaks in spring and autumn was found.
These findings are likely influenced by local environmental, social and epidemiological factors, but may be relevant for the appropriate timing of the follow-up and therapeutic strategies for abdominal aortic aneurysms.

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Background and Methods. In order to assess the effects of testosterone undecanoate (TU; 120mg/d orally for 2 months) on serum lipid, lipoprotein, and apolipoprotein levels in healthy elderly men, the placebo (PL) controlled study was performed on 37 elderly men, aged between 53 and 89 years. In all subjects venous blood samples were taken after an overnight (10 hours) fast and sera were stored -70°C until analysis.
Results. In PL group, neither hormonal data nor lipid, lipoprotein, and apolipoprotein levels showed significant changes. After TU supplementation, serum total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and estradiol (E2) levels decreased from 198±30.7mg/dl to 174±41.9mg/dl (p<0.05), from 111±18.14mg/dl to 87.9±29.4mg/dl (p<0.01), and from 862±16.9pmol/l to 70.5±18pmol/l (p<0.01), respectively. Statistically significant differences were not observed in the serum triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and apolipoprotein (apo) A-1 and apo B levels after TU treatment. The mean ratios TC/HDL-C and LDL-C/HDL-C as coronary risk factor criteria decreased significantly in the TU but not in the PL group. No obvious side effect was observed in those who took TU except for reported pyrosis in 2 of 17 elderly men.
Conclusions. These data indicate that the increased serum levels of total testosterone (TT) produced by administration of TU, 120mg/d orally for 2 months lead to supressed levels of TC and LDL-C and E2 but not significantly changed levels of TG, HDL-C, apo A-1 and apo B. Thus, we conclude that TU may be an effective drug for protecting coronary heart disease in healthy elderly men with lowered TT and FT levels. It may also have beneficial effects for sexual function and behavior.

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Background. Studies have shown that patients with chronic renal failure have a high frequency of cardiocascular atheromatous disease.
Methods. We examined serum lipoprotein (a) [Lp(a)], very-low density lipoprotein cholesterol (VLDL-C), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C), apolipoprotein A1 (apo A1) and B (apo B), triglyceride (TG) and total cholesterol (TC) levels as possible risk factors for atherosclerosis in 45 patients with chronic renal failure (CRF) treated by hemodialysis (HD) and in 15 CRF patients who were not on HD. A control group of 20 healthy subjects was also studied.
Results. The proportion of smokers and body mass indexes were similar between the groups. In both patient groups, higher TG, TC and Lp(a) and lower apo A1 and HDL-C levels in serum were found than in those of controls. Serum apo B and LDL-C were similar in the patients treated by HD and the controls. Serum VLDL-C and LDL-C were similar in the CRF patients who were not on HD and the controls. The highest ratios of apo B/apo A1 and LDL-C/HDL-C were found in HD patients. The highest ratio of TC/HDL-C was found in the other patient group.
We found significant correlations between Lp(a) and other parameters of lipoprotein metabolism in CRF patients, both those who were and those who were not on HD.
Conclusions. Our results indicate that CRF patients who both were and were not on HD show atherogenic changes in the lipoprotein pattern, and that the increase in Lp(a) during the CRF phase is basically related to the loss of renal function and may also depend on the resultant alterations which are produced in other lipoprotein variables.

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In order to clarify the time course of superoxide generation in situ duringischemia and reperfusion in the rabbit heart, we used a method of enhanced chemiluminescence (CL) with 2-methyl-6-[p-methoxyphenyl]-3, 7-dihydroimidazo[1, 2-α]pyrazin-3-one (MCLA) as a specific probe for detecting superoxide radicals. The surface of the rabbit heart was exposed to a photomultiplier tube in a light-proof box. We introduced a reversible snare occluder into the box to continuously observc thelight emission.An ischemia-reperfusion group (I/R, n=7)was subjected to 30mins of coronary occlusion, followed by 90mins of reperfusion. We performed the same procedure (except for coronary occlusion) in the sham-operated group (n=4). Another group of rabbits(n=4) subjected to I/R received superaxide dismutase (SOD: 20mg/kg, iv)during reperfusion to observe the CL response.
In the I/R-group, the increase in CL began at 13±2 (mean±SEM) mins and peaked at 52±12mins of reperfusion. GL in the I/R-group gradually increased from 818±350counts/10 secs in the preischemic period to 1077±401counts/10 secs during reperfusion (p<0.01). In contrast, there was no increase in CL in the sham-operated group. The administration of SOD briefly attenuated CL by 24.1±6.8% for a period of 24.3±6.8mins.
The superoxide generation in situ in the ischemic rabbit heart appears to increase gradually and persists for a period following reperfusion.

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Arching and barotrauma, seen with high energy DC catheter ablation, are responsible for diffuse cardiac damage and coronary sinus rupture. In six anesthetized dogs, we investigated the effects of an increasing number of short time-constant capacitive shocks on the volume of myocardial damage. Each dog received capacitive shocks of 2J/kg at 3 sites in the left ventricle. One shock was delivered in 2 dogs, 2 shocks were delivered in 2 dogs and 3 shocks were delivered in 2 dogs. Shock delivery was not accompanied by hemodynamic collapse, sustained ventricular tachycardia or ventricular fibrillation. The dogs were sacrificed at 60 minutes. Mean (SEM) lesion volumes were 195(39)mm³, 480(41)mm³, and 595(110)mm³, respectively. Despite variability in individual volume of damage, there was a significant increase in lesion volume with an increasing number of shocks. There was no evidence of perforation or tamponade. Increasing myocardial damage can be produced using repetitive capacitive shocks. Delivery of 2 shocks produces clinically useful lesions without the adverse effects associated with single high energy shocks. Repetitive capacitive shocks offer a method of increasing lesion volume without increasing energy and thereby without compromising safety.

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A case of development of monomorphic sustained ventricular tachycardia in the prehospital phase of acute myocardial infarction is reported. By performing pacing from the right ventricular outflow tract during ventricular tachycardia, constant fusion and progressive fusion were documented without constant and progressive fusion from the right ventricular apex pacing, and it was terminated by pacing from the right ventricular outflow tract. Thus, reentry was considered to be the mechanism of this ventricular tachycardia occurring in the prehospital phase. Direct angioplasty successfully recanalized the totally occluded coronary artery, but late potential was present probably because of late reperfusion. In an electrophysiologic study in the chronic phase, slow conduction areas were found at the interventricular septum and the exit of this ventricular tachycardia was at the mid-septum of the right ventricle. A review of the literature failed to reveal any report of a similar case.

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In this report, we describe a case of sustained ventricular tachycardia of right ventricular outflow tract origin, induced by dobutamine infusion in a patient with symptomatic, frequent ventricular premature depolarizations but no documented clinical ventricular tachycardia. Radiofrequency catheter ablation abolished not only the ventricular tachycardia itself, but also the frequent ventricular premature depolarizations responsible for all the symptomatology. In conclusion, provocation by catecholamine infusion may have a place in the search for an alternative to antiarrhythmic therapy in patients with isolated, frequent and symptomatic ventricular premature depolarizations.

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A case of fetal tuberous sclerosis with multiple intracardiac rhabdomyomas exhibited persistent supraventricular tachycardia. The tachycardia was terminated by the use of cardiac version. The largest tumor almost occluded the right ventricular inlet portion. The obstruction was relieved after surgical removal of the largest tumor. No arrhythmia was noted after 3 months of follow-up.

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We report a patient in whom hypertrophic cardiomyopathy, with both left ventricular hypertrophy and diastolic dysfunction, was masked by acute severe aortic regurgitation and marked left ventricular dilation. Upon admission, 1) two-dimensional echocardiogram of the left ventricle revealed a dynamic and flail vegetation on the aortic right coronary cusp and marked left ventricular dilation, 2) a massive aortic regurgitant signal was recorded by color Doppler flow imaging, and 3) transmitral flow velocity by pulsed Doppler echocardiogram revealed a pseudonormalization. However, symmetric hypertrophy of the left ventricular wall, a decrease in early diastolic wave and a compensatory increase in atrial systolic wave of the transmitral flow velocity appeared after successful aortic valve replacement.

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A 58-year-old man with idiopathic dilated cardiomyopathy was treated with incremental administration of a β-blocker (metoprolol) and an angiotensin converting enzyme inhibitor (enarapril). The left ventricular end-diastolic dimension and ejection fraction improved in 8 months from 83.3mm and 17.3% to 46mm and 69%, respectively. The washout ratio and heart-to-mediastinum ratio depicted on the delayed image for iodine-123 metaiodobenzylguanidine (¹²³I-MIBG) uptake improved from 61.7% and 1.34 to 23.1% and 1.85, respectively, in association with improvement of left ventricular indices. Successive endomyocardial biopsy specimens disclosed reduction of the degrees of vacuolation, staining irregularity, and deformity of myocyte cytoplasm and nucleus compared to the findings before therapy. In this patient with dilated cardiomyopathy ¹²³I-MIBG scintigraphy was useful for the evaluation of the effects of therapy. We conclude that it may be informative in the estimation of the histopathological abnormalities of the myocardium.

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