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Objectives: The exact role of pressure gradient across the prosthetic valve estimated from Doppler flow velocity remains controversial. This in-vivo study was designed to assess the actual discrepancy between Doppler and catheter measurements of the pressure gradients for small bileaflet prosthetic valves in the aortic position. Methods: Bileaflet prosthetic valves (19 mm-ATS) were implanted into the aortic position in pigs, and pressure gradients across the valves were examined by volume loading under right heart bypass. The pressure gradient obtained by catheter was defined as the conventional peak-to-peak gradient between the left ventricle and aorta. The peak Doppler gradients were calculated from the maximal instantaneous Doppler velocity with the ultrasound probe positioned on the diaphragm at the level of the cardiac apex. Results: There were strong correlations between pressure gradients and cardiac output. The Doppler gradient was constantly higher than the catheter values, and the resultant discrepancy between Doppler and catheter measurements was directly dependent on cardiac output (y=9.9x+0.6, r2=0.55). For cardiac output ≧5.0 L/min, the difference between Doppler and catheter gradients reached 40 mmHg, and maximum differences of up to 80 mmHg were observed. Conclusions: In view of the presence of striking overestimation of catheter gradient by Doppler measurement, Doppler ultrasound should be used cautiously to assess small-size bileaflet prosthetic valve function with consideration of the patient’s hemodynamic state.

To clarify whether inflammation is a cause or consequence of atrial fibrillation (AF), we measured high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) before and after pharmacological cardioversion in 15 patients with paroxysmal AF. Levels of hs-CRP, IL-6, and TNF-alpha after cardioversion were significantly higher than those in controls (P < 0.05). Furthermore, the levels of these indices did not differ significantly even at 24 hours and 2 weeks after cardioversion. These results suggest that inflammation is a causative agent of paroxymal AF.

Permanent pacemakers are commonly used in veterinary practice and can have a dramatic effect on the treatment of heart block. A Labrador Retriever dog suffering from exercise intolerance secondary to third degree atrioventricular block was treated with a new pacemaker system. A steroid-eluting screw-in type lead that has the advantage of being more fixed to the myocardial wall without increasing the pacing threshold was used. The heart rate was regulated with an acceleration sensing pacemaker generator that included several automatic modulation systems. Nineteen months after implantation, the dog has a normal level of activity. The present case suggests that this pacemaker design may offer important advantages for canine patients.

We performed a histopathological investigation on arteriosclerotic development in the influx and intravisceral arteries of the liver, kidney and lung of male WHHL rabbits. In the influx arteries of these organs, we observed severe atherosclerotic vascular lesions with high-grade luminal stenosis. In the intravisceral arteries of the liver and kidney, no arteriosclerotic lesions were observed. However, in the intrapulmonary arteries, we recognized severe atherosclerotic vascular changes with high-grade stenosis or total obstruction of the lumen in some middle to large sized pulmonary arteries. These observations indicate that the development of arteriosclerosis in parenchymatous organs differs, and that some organs are predisposed to arteriosclerosis formation.

We treated a case of ventricular septal perforation (VSP) who survived for 14 years after myocardial infarction. Nine years after the onset of myocardial infarction, an apparent cardiac murmur was discovered by chance, and following further examination, the patient was diagnosed as having VSP. The patient is still in the NYHA functional class I, and requiring no surgical treatment. In general, the prognosis of myocardial infarction complicated with VSP is so poor that there have only been 14 reported cases of long survival without surgical treatment. Among these patients, only 2 survived for more than 10 years. The present case is extremely rare, and evidently is the longest living survivor with this condition yet reported.

Washout rate of iodine-123 metaiodobenzylguanidine (MIBG) myocardial scintigraphy is correlated with the degree of myocardial damage. The aim of this study is to ascertain whether there is any relationship between QRS complex duration at right ventricle (RV) pacing and the degree of myocardial damage assessed by I-123 MIBG myocardial scintigraphy in normally functioning left ventricle. The study included 22 patients (10 men and 12 women, ranging in age from 48 to 89 years), with atrioventricular (AV) block (n = 15) and sick sinus syndrome (n = 7). All patients had baseline QRS duration of less than 120 ms and received implantation of a DDD-mode permanent pacemaker. Iodine-123 MIBG myocardial scintigraphy was performed before the pacemaker implantation, and QRS duration at RV pacing at a rate of 70 ppm was calculated immediately after the implantation. With the use of RV pacing, QRS duration was prolonged ranging from 122.4 to 185.6 ms with a mean of 153.2 ± 15.2 ms. Washout rate of I-123 MIBG myocardial scintigraphy (WR) was calculated as ranging from 5.0 to 83.0% with a mean of 44.2 ± 17.5%. There was a strong correlation between WR and QRS duration at RV pacing (r = 0.735, p

We present a case of a 61-year-old man who underwent aortic valve replacement for aortic regurgitation complicated with left ventricular noncompaction. The pathogenesis of this condition remains unknown. In advanced form, left ventricular noncompaction produces marked disability and carries a poor prognosis. We underscore that familiarity with this disease entity will help to stimulate early diagnosis and timely treatment when necessary.

His-bundle pacing gives a more physiological ventricular contraction in comparison to right ventricular apical pacing. However the problems of lead fixation and stability of long-term His-bundle pacing are yet unsolved. We used six adult beagles, in which a screw-in lead was anchored in the His-bundle region for observation of the pacing conditions and histopathologic changes of the conduction system over the course of 2 months. In the results, a satisfactory fixation was obtained using a conventional screw-in lead and no histological influence on the conduction system was observed. The pacing threshold at the time of implantation was 1.15 +/- 0.69 V (3.23 +/- 3.08 mA) in the pulse width of 0.5 ms. R wave amplitude, the impedance and slew rate were 7.28 +/- 2.04 mV, 409 +/- 102 Ohm, and 0.65 +/- 0.41 V/s, respectively. Two months later, these parameters changed to 2.83 +/- 1.06 V (10.4 +/- 5.71 mA), 5.63 +/- 1.62 mV, 310 +/- 71.3 Ohm, and 0.49 +/- 0.22 V/s, respectively. These results suggest the feasibility of clinical application of permanent His-bundle pacing.

We evaluated a 68-year-old male patient with isolated levocardia without intracardiac anomaly. The patient's condition was complicated by the absence of the inferior vena cava, a lobulated spleen and sick sinus syndrome. Isolated levocardia without intracardiac anomaly is very rare and only 25 cases of this disease have been reported, to our knowledge. In general, it is accepted that cardiac rhythm disorder is frequently observed in cases of isolated levocardia and/or absence of inferior vena cava. However, there are few cases of isolated levocardia without intracardiac anomaly complicated by the absence of the inferior vena cava, a lobulated spleen and apparent sick sinus syndrome.

Three months after implantation of endocardial pacing leads in 10 mongrel dogs, the tensile forces needed to remove 5 tined type and 5 screw-in type leads were compared experimentally. Mean maximum tensile force was 291 +/- 174 g with the screw-in type and 1174 +/- 369 g with the tined type (p < 0.01). Histopathologically, no changes suggesting any myocardial damage due to lead extraction were recognized in cases where screw-in type leads were used. These results support the clinical feasibility of safe and easy manual retraction of infected pacing leads of the screw-in type.

Background: Ghrelin is an acylated peptide hormone mainly secreted from the stomach. When administrated externally it modulates vascular tone mainly through the regulation of autonomic nerve activity. However, the effects of blood pressure (BP) on the production and secretion of ghrelin remain to be clarified. Methods and Results: We examined the stomach and plasma levels of ghrelin in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats after a 4-week-intervention with antihypertensive agents (candesartan-cilexetil [ARB], doxazosin [DZN], metoprolol [MP], reserpine [RES]) to clarify the influence of BP on the secretion of ghrelin. The effect of these agents on ghrelin production and secretion were examined by comparing vehicle-treated controls (WKY-Intact, SHR-Intact). Treatment with the 4 antihypertensive drugs all yielded a significant decline in systolic BP in both SHR and WKY. Under these conditions, significantly lower levels of stomach and plasma ghrelin were detected in WKY treated with ARB (P

A case of infective endocarditis (IE) caused by a rare pathogen, Gemella morbillorum, is presented. Because of persistent low-grade fever after dental treatment, the patient was given oral antibiotics. Whereas he was diagnosed as having aortic regurgitation by a cardiologist, and IE was not suggested unfortunately. After long-term chemotherapy over five months, he was aware of nocturnal dyspnea and Gemella morbillorum was detected by blood culture. Then, he was treated with intravenous administration of Penicillin-G, and underwent surgical operation for valve replacement. No cases of IE due to this organism have been reported in Japan.

We examined serum lipids, lipoproteins, apolipoproteins (Apo), lipoprotein(a) (Lp(a)), C4b-binding protein (C4bp) and lathosterol in 22 normolipidemic (serum total cholesterol less than 220 mg/dl and serum triglycerides less than 150 mg/dl) male patients with coronary artery disease (CAD) and 33 normal male subjects. Many of the patients in the CAD group with normal total cholesterol (T-Ch) and triglycerides (TG) had higher TG, low-density lipoprotein (LDL)-Ch, beta-lipoprotein (Lipo) and Apo B values and lower high-density lipoprotein (HDL)-Ch, Apo A-I and Apo A-II values than those of the control group. Differences were also observed in the beta-Lipo/HDL-Ch, Apo B/Apo A-I, and HDL-Ch ratios and the atherogenic index [A.I. = (T-Ch--HDL-Ch)/HDL-Ch], all of which are generally accepted as indices for atherosclerosis. Even in CAD patients with normolipidemia, the HDL-Ch/T-Ch ratio and A.I. seemed to be important risk factors. In addition, Lp(a) and lathosterol, an accepted indicator of whole-body cholesterol synthesis, were higher in the CAD group. The CAD group also appeared to have a higher C4bp value, suggesting that this parameter is correlated with other lipids.

We report a 57-yr-old woman with severe cardiac failure secondary to postnephrectomy arteriovenous fistula which was successfully removed. A review of the literature shows the rarity of this complication; only 72 cases have been reported in the world literature including 6 cases (including the present case) from Japan. Surgical intervention is generally the treatment of choice from a fistula and provides satisfactory results for cardiac failure which is the major complication of this fistula. A characteristic bruit was observed in all reported cases. Therefore, nonsurgical closure by percutaneous embolization for a small sized shunt may be possible if early diagnosis is obtained by careful auscultation of the loin.

We experienced a rare case of a patient with acute myocardial infarction. It was rare in that a piece of tissue, probably a remnant valve of the inferior vena cava in the right atrium, was dislodged by the Swan-Ganz catheter during a right heart catheterization study in the chronic phase of the disease. As far as we know, no other such case has been reported. Such remnants are considered to be present in 2 to 3% of the general population. Therefore, it is necessary to determine the presence or absence of a remnant before cardiac catheterization and to modify the procedure, such as by changing the catheter's approach, when a remnant is present.

Arteriovenous shunt is one of the causes of heart failure, but heart failure caused by common iliac arteriovenous fistula is relatively rare. A 64-year-old man who developed acute heart failure due to venous perforation of a common iliac aneurysm and also had bilateral aneurysms (diameter 58 mm) was referred to our department. On admission, the patient complained of dyspnea and swollen left leg, so diuretic agent was administered to treat the heart failure. Cardiac catheterization showed a shunt rate of 80.6%, as well as 5.0 Qp/Qs and O2 step-up across perforation of the common iliac vein. Despite the therapy, pleural effusion and ascites exacerbated, and the heart failure became difficult to control, so surgical treatment was performed. The aneurysm was replaced with an artificial vessel, and the fistula was closed by direct suturing. Postoperatively, the symptoms disappeared, and the patient is in good health.

We investigated the effect of olprinone on canine myocardial pump function and myocardial damage after ischemia-reperfusion injury. Three dogs of the experimental group were given olprinone (Olprinone group) and another 3 dogs were served as control (Intact group). All animals were occluded left anterior descending artery for 60 min, followed by 6 hr of reperfusion. In the experiment, hemodynamics, infarct area, creatine kinase and troponin-I were measured. Olprinone infusion induced significantly high cardiac output value and significantly low values in left ventricular end diastolic pressure and systemic vascular resistance index after reperfusion. Also, olprinone tend to attenuate the infarct area, creatine kinase and troponin-I.

冠動脈造影の際, 偶然発見された右腎動脈瘤を切除し, 切除断端は直接縫合して動脈再建した. 内臓動脈瘤のうち, 腎動脈瘤は脾動脈瘤に次ぐ頻度とされるが本邦での報告例は少ない. 同時に胆石症を合併しており, 胆嚢摘出術を行った.

To clarify whether inflammation is a cause or consequence of atrial fibrillation (AF), we measured high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) before and after pharmacological cardioversion in 15 patients with paroxysmal AF. Levels of hs-CRP, IL-6, and TNF-alpha after cardioversion were significantly higher than those in controls (P0.05). Furthermore, the levels of these indices did not differ significantly even at 24 hours and 2 weeks after cardioversion. These results suggest that inflammation is a causative agent of paroxymal AF.

The aim of this study was to evaluate the effectiveness of an angiotensin-converting enzyne inhibitor (ACEI, quinapril) or angiotensin II receptor blocker (ARB, candesartan) on atrial natriuretic peptide (ANP) activity in rats with hypertension induced by nitric oxide (NO) inhibition. ACEI and ARB have a number of pharmacologic effects, including blood pressure reduction, myocardial preservation, and an unknown effect in the circulation. The changes in ANP in NO inhibitor-induced hypertensive rats were evaluated in order to elucidate the interaction between ANP and NO in the regulation of blood pressure. Thirty-six rats were divided into 4 groups and administered the experimental agents for 8 weeks: group CONTROL was given regular food (n=9), group N(G)-nitro-L-arginine (L-NNA) was administered L-NNA (25 mg. kg(-1). day(-1), n=9), group ACEI was administered L-NNA and quinapril (10 mg. kg(-1). day(-1), n=9), and group ARB was administered L-NNA and candesartan (10 mg. kg(-1). day(-1), n=9). Blood pressure, plasma ANP, atrial ANP, ANP mRNA, and ANP granules were measured. A significant elevation in blood pressure was observed in group L-NNA. However, there were no increases in plasma ANP (L-NNA: 138.8+/-64.4, CONTROL: 86.7+/-36.4), ANP mRNA (L-NNA: 2.2+/-1.0, CONTROL: 1.7+/-0.5) or ANP granules (L-NNA: 61.1+/-10.2, CONTROL: 64.5+/-8.5). No increase in blood pressure was seen in groups ACEI and ARB. However, plasma ANP (ACEI: 1,392.3+/-1,034.4, ARB: 1,142.8+/-667.3), ANP mRNA (ACEI: 52.8+/-29.1, ARB: 42.9+/-21.2), and ANP granules (ACEI: 122.5+/-23.4, ARB: 136.3+/-33.2) increased significantly. NO inhibitor-induced hypertension caused no changes in ANP concentrations. However, the ACEI and ARB had a direct effect on the induction of ANP secretion. The findings suggest that ANP secretion is directly effected by ACEI and ARB, which seems to play a key role in lowering blood pressure, relieving heart failure symptoms, and preserving the myocardium.

We encountered a 72-year-old woman with a left atrial hemangioma arising in the appendage and growing like an extracardiac mass. Life-threatening cardiac tamponade, recurrent over a 5-year clinical course, was the only sign of this rare tumor. The extraatrial growth pattern of the tumor made it difficult to distinguish the cardiac origin from a paracardiac mass. With the aid of cardiopulmonary bypass, the tumor was removed from the left atrium at the base of the appendage. Pathologic diagnosis was a combination of cavernous- and venous-type hemangioma. The postoperative course was uneventful, and the patient was doing well with no pericardial effusion at the 10-month follow-up.

To examine acute effects of olprinone hydrochloride (CAS 106730-54-0, Coretec) on pulmonary hypertension, hypoxic pulmonary hypertension was produced in 6 adult Beagle dogs. Using this pulmonary hypertension model, single intravenous bolus injections of olprinone at doses of 10, 30 and 100 micrograms/kg were administered at 5-min intervals and hemodynamic parameters were evaluated. Heart rate increased at doses of 30 and 100 micrograms/kg, but did not change at a dose of 10 micrograms/kg. Mean aortic pressure, mean pulmonary arterial pressure, pulmonary vascular resistance and systemic vascular resistance and right ventricular stroke work index did not change at doses of 10 and 30 micrograms/kg, but they decreased significantly at a dose of 100 micrograms/kg. On the other hand, cardiac index and the first derivative value of the left ventricular pressure did not show significant change at all doses. These results indicate the vasodilating effects on peripheral and pulmonary vessels in hypoxic model at high doses of olprinone. Its application in right heart failure accompanied by pulmonary hypertension therefore is expected to yield promising results.

To examine both of the target vessels and the optimal time of their endothelial denudation to study vascular restenosis after balloon injury in cholesterol-loaded rabbits, we made 36 atherosclerotic rabbits by feeding a hypercholesterol diet, and histologically examined the onset time and the development of atherosclerosis. Atheromatous changes were observed first after the 5th week in the thoracic aorta from the start of the diet, and then extended to the abdominal aorta, coronary artery with time. The atherosclerotic lesions in the thoracic aorta and the proximal portion of the coronary artery showed high-grade concentric intimal thickening with luminal stenosis. The abdominal aortic lesion mildly progressed. In the renal, carotid and femoral arteries, in contrast, slight atheroscleromatous changes developed during the diet period. These results suggest that the thoracic and abdominal aortas and the coronary artery would be suitable as target vessels to study vascular restenosis after balloon injury, and the endothelial denudation of these vessels should be performed between the 8th and 15th week in this diet protocol for an accurate analysis.

Blunt traumatic cardiac rupture is associated with a high mortality rate. Motor vehicle accidents account for most cardiac ruptures, but crush injury is relatively rare. We describe a case of a 77-year-old man who had the left atrial 'basal' appendage ruptured through blunt trauma due to a fall. He was surgically treated and recovered without complication.

We report an interesting case of aortic regurgitation. Phonocardiographically, the shape of the diastolic musical murmur in this case changed in each cardiac cycle despite being in sinus rhythm, in the same posture and in the same breathing phase. Experimentally, we were able to obtain a similar noise pattern using an artificial respirator and a hemispherical silicone membrane. We concluded that the irregular and chaotic change in the shape of the diastolic musical murmur in the present case occurred due to irregular swaying of the non-coronary cusp under the influence of the Venturi effect owing to a regurgitant jet stream. (Jpn Circ J 1996; 60: 993 - 997)

We report a case of sudden death due to variant angina during Holter electrocardiogram (ECG) monitoring. The patient, a 60-year-old man, had been aware of chest discomfort lasting less than one minute at midnight 2 days earlier. Because variant angina or arrhythmia was suspected, Holter ECG monitoring was performed. The patient spent a whole day without a recurrence of chest pain before going to bed, but at midnight he developed sudden chest pain, and died immediately after taking a sublingual tablet of isosorbide-dinitrite. Analysis of the Holter ECG revealed ventricular fibrillation after several ventricular premature beats following ST-segment elevation in both the CM5 and NASA leads. This case shows that sudden death from variant angina may occur within a few days after the first onset, and also highlights whether priority should be given to making a definite diagnosis or giving treatment when variant angina is strongly suspected.

Massive endobronchial hemorrhage is a lethal complication in pulmonary embolectomy. We report a case of massive endobronchial hemorrhage occurring after successful restoration of pulmonary blood flow using cardiopulmonary bypass in a patient with pulmonary embolism. Two possible causative factors of this complication are described.

To clarify the relationship between the results of intracoronary thrombolytic therapy (ICT) and fibrino-coagulation in patients with acute myocardial infarction (AMI), the thrombin-antithrombin III complex (TAT) and fibrinopeptide A (FPA), as indices of accelerated coagulation, and the plasmin- alpha 2-plasmin inhibitor complex (PIC), as an index of accelerated fibrinolysis in peripheral blood, were measured just before and after heparin injection (5,000 U), and immediately after ICT. Twenty-four patients with AMI were divided into 2 groups according to the results of ICT; successful ICT (group S) and unsuccessful ICT (group F). As a control group (group C), 14 age-matched normal volunteers were also studied. The levels of TAT and FPA before ICT were significantly higher in groups S and F than in group C (p < 0.01). The TAT level before ICT in group F was higher than that in group S (p = 0.07), however, the TAT, FPA and PIC levels showed no significant differences between groups S and F at each sampling time. TAT/PIC before ICT was significantly higher in group F than in group S (F: 0.026 +/- 0.020 vs S: 0.008 +/- 0.004, p < 0.05), whereas there was no remarkable difference in FPA/PIC between groups S and F. These results indicate that hyper-coagulation had occurred in the AMI cases and that coagulation had been more accelerated in group F. TAT/PIC might be an index of the equilibrium of the fibrino-coagulating system. Therefore, TAT/PIC measurement before thrombolytic therapy may be more useful than TAT measurement alone for evaluating recanalization in ICT.

We examined histologically whether the severity of arterial stretch injury is related to the degree of subsequent intimal hyperplasia. In six male New Zealand White rabbits, the common carotid artery was hyperextended with a 3F Fogarty balloon catheter. Two weeks later, no proliferative change was evident in the intima in the most hyperextended portion. Paradoxically, however, intimal hyperplasia due to smooth muscle cell proliferation was observed in the moderately extended portions. The intimal hyperplasia appeared to be exacerbated where the arterial stretching was more severe. It is concluded that the severity of arterial stretch injury is closely related to the intimal proliferation of smooth muscle cells.

We observed a case of acute myocardial infarction induced by second diagonal branch occlusion. Electrocardiogram (ECG) on admission showed ST elevation in leads I, aVL and V2-6. Since emergency coronary angiography disclosed complete occlusion of the second diagonal branch, intra-coronary thrombolysis (ICT) was performed, superselectively. Transient coronary reperfusion was obtained, however, reocclusion occurred after several minutes. Rescue percutaneous transluminal coronary angioplasty (PTCA) was then performed immediately and blood flow was improved to TIMI grade 2. During these processes, the ST-segment on the ECG changed in leads I, aVL and V2-6 always corresponding to the blood flow of the second diagonal branch. We have not seen a report hitherto in which occlusion of only the second diagonal branch could be a cause of extensive anterior infarction-like ECG changes. Although the mechanism of ECG changes in this patient cannot be clearly explained by conventional concepts, we report this case because it is considered to be very rare.

To investigate the relationships between coronary artery size, left ventricular (LV) mass, and LV stroke work in aortic regurgitation (AR), these values were measured in 19 patients with severe AR. Twenty normal subjects and 15 patients with mitral regurgitation (MR) were used as control groups. The coronary area index, i.e., the coronary cross-sectional area divided by body surface area (BSA), was larger in the AR group than in the control groups in all measured sites except for the peripheral left anterior descending coronary artery (LAD) and right coronary artery (RCA). However, the coronary area index divided by the LV mass was significantly smaller in AR and MR patients than in normal subjects. Furthermore, the coronary area index divided by LV stroke work was smaller in AR patients than in MR patients and normal subjects. These results suggest that the coronary blood flow associated with the increased LV mass and stroke work caused by regurgitation was insufficient in patients with severe AR, especially in the area of the LAD. Therefore, the occurrence of myocardial ischemia in patients with severe AR may involve inadequate enlargement of the coronary artery which perfuses the LV, in addition to factors such as decreased coronary perfusion pressure, increased coronary artery resistance and decreased coronary flow reserve.

In order to elucidate the immunological aspects of acute myocardial infarction (AMI), we studied lymphocyte subpopulations, immunoglobulin levels, and natural killer (NK) cell activity in 21 patients serially after admission within 24 h of AMI onset. The percent T cells, T cell count, and percent CD4-positive cells were significantly decreased on the 1st hospital day, compared to days 7 and 28. The CD4/CD8 ratio on the 1st day was also significantly lower than on day 7, and was significantly lower than that of normal subjects. Natural killer (NK) cell activity and serum immunoglobulin G (IgG) levels showed substantial decreases each test day, compared with those in normal subjects. However, there were no significant serial changes in the percent B cells, the B cell count, or in the serum IgG, IgA, or IgM levels. Thus, not only T cell function, but also immunoglobulin levels and NK cell activity were depressed in the acute stage of myocardial infarction. Therefore, active measures should be taken to prevent infection in the acute stage of myocardial infarction in which invasive procedures such as insertion of indwelling catheters are often necessary.

We investigated changes in serum lipoprotein(a) (Lp(a)) and C4b-binding protein (C4bp) levels following acute myocardial infarction (AMI). Serum lipids, apolipoproteins, C-reactive protein (CRP), sialic acid and haptoglobin (Hp) were also measured and evaluated. The study involved 16 patients (11 men, 5 women, mean age 68.2 +/- 8.4 years) with AMI admitted within 12 h after the onset of illness. CRP rose sharply and immediately after the onset of AMI, reaching its maximum level on the 3rd day of illness. This was followed by temporary increases in sialic acid and Hp, both of which peaked on the 7th day of illness. The Apo A-I level was significantly lower on the 14th day, while the Apo B level was significantly lower on the 3rd day. Serum total cholesterol (T-Ch), HDL-Ch and LDL-Ch showed temporary decreases after the onset of illness. Serial examination of the serum of patients with AMI yielded the following findings; 1) Both Lp(a) and C4bp levels rose temporarily with similar patterns of variation, and 2) they took longer time to peak (around the 14th day) and lasted longer than the increases in the other acute reactive proteins.

We read with great interest the article by Seko, et al.1) on serum vascular endothelial growth factor (VEGF) and transforming growth factor (TGF) -β1 levels in patients with atrial fibrillation. However, some aspects of their methodology and discussion seem questionable. First, because of low serum VEGF levels, they eliminated 7 cases from an initial 20 patients with atrial fibrillation and thus only discussed the remaining 13 cases. It is reasonable to select the population on the basis of a factor which might influence the results. However, it is not reasonable from a validity standpoint to select the population on the basis of the results. Secondly, they reported that the serum VEGF levels were undetectable in normal control subjects.2) On the contrary, their results indicated that the serum VEGF levels after defibrillation were still higher than those in control subjects, and they did not explain the reason. If the study subjects had other underlying heart diseases, they should have been discussed. In addition, they stated that VEGF levels in patients with acute myocardial infarction returned rapidly to the normal range after reperfusion therapy.2) If atrial fibrillation was directly involved in VEGF secretion and the half life of VEGF was so short, then the serum VEGF levels might have returned rapidly to the normal range after defibrillation therapy. However, although the second blood sampling was done between 24 hours to 57 days after defibrillation, the serum VEGF levels were still higher than those in normal control subjects. Thus, we are obliged to question whether only atrial fibrillation really influenced the VEGF secretion.

In a previous study, we proved experimentally that transmural infarction was produced in the area of the left anterior descending artery (LAD) by coronary sinus occlusion attributable to thrombus formation. In an attempt to produce infarction due to thrombus formation and to investigate the influence of thrombosis. the anterior interventricular vein (AIV) was occluded in this study. In each of 6 adult mongrel dogs, a balloon-tipped catheter was wedged in the AIV via the jugular vein. After the occlusion of blood flow by inflation of the balloon. thrombin (30-50 IU) was injected into the AIV to produce thrombi and the balloon was removed 60 min later. As a result, ischemic changes of ST and T in an ECG were clearly observed in all 6 dogs, and serum levels of myocardial enzymes supported the development of myocardial necrosis. Coronary arteriography performed 48 hours after the occlusion of the AIV showed normal findings in all 6 dogs, and residual thrombi in the AIV were observed in 5 dogs by coronary venography. In these 5 dogs. very local contranction band necrosis (CBN) was noted in the epicardium surrounding the AIV. These experimental findings indicate the following: 1) CBN can also be induced by corocary venous occlusion. 2) once the occlusive mechanism acts on the coronary venous system. the changes which are clinically similar to myocardial infarction can be induced regardless of its causes. 3) ischemic changes in myocardium can be localized in the epicardium irrespective of its causes. Therefore, these findings are considered to be important in the investigation of the clinical onset mechanism of myocardial infarction.

The concentration of plasma antithrombin III (AT III) and the biological activity of plasma alpha2-plasmin inhibitor (alpha 2-PI) were measured in cases of mitral stenosis (MS) and rheumatic heart disease (RHD) without MS. Cases of MS showed the findings of the low levels of plasma AT III and normal or a little higher levels of plasma alpha 2-PI, that was not recognized in RHD without MS. This finding was interpreted to be hypercoagulable because of the acceleration of coagulation and of little or slight retardation of fibrinolysis. Besides, the influence of atrial fibrillation and chronic congestive heart failure on hypercoagulability in cases of MS was detected clearly, but the influence of them in cases of non-RHD was obscure. As the results, the severer the degree of MS, the clearer the hypercoagulable state. Therefore, the prethrombotic state existed in cases of MS, combined with blood flow disturbance due to atrial fibrillation or chronic congestive heart failure, endocardial damage resulted from rheumatic fever in an early stage and hypercoagulable state mentioned above in the present study. There was no significant difference between cases with and without thrombi in the degree of hypercoagulability in subjects with MS shown in the present work. It was concluded that the consumption of AT III caused the low levels of it in cases of MS, and that the low production of AT III in the liver rather than consumption caused the low levels of it in cases of non-RHD.

An attempt was made to evaluate a thrombotic tendency in cases of infective endocarditis (IE) from the viewpoint of the changes of platelets and coagulo-fibrinolysis. Qualitative changes of platelets by thrombi formation were detected by showing activated responses of platelets to adenosine diphosphate or collagen and by showing a high level of plasma beta-thromboglobulin which is released by platelets during aggregation. A mild hypercoagulable state without acceleration of fibrinolysis was also detected by showing low levels of plasma antithrombin III which is the most potent antithrombin in the blood and normal levels of plasma alpha 2-plasmin inhibitor in the blood. From above findings, it was concluded that a thrombotic tendency in cases of IE was clearly detected by qualitative changes of platelets by thrombi formation and by mild hypercoagulability without acceleration of fibrinolysis.