This study aimed to examine the characteristics and the clinical significance of atrio-ventricular (AV) junctional automaticity in sick sinus syndrome. Maximum sinus node recovery time (max SRT) or maximum junctional recovery time (max JRT). and AV nodal Wenckebach block rate were. evaluated before and after pharmacologic autonomic blockade (AB) in 43 patients with sick sinus syndrome. Max JRT shorter than 3000 msec was obtained after AB in 13 patients (group 1) and apparent enhancement of junctional automaticity after AB was observed in these patients. Thirty patients showed max JRT or max SRT longer than 3000 msec after AB (group 2). The Wenckebach block rate increased significantly after AB in group I but did not change significantly in group 2. The Wenckebach block rate after AB in group I was significantly higher than that in group 2. Max JRT was obtained only after AB in 8 patients in group I (subgroup 1). and in 9 in group 2 (subgroup 2). Max SRT before AB and the intrinsic heart rate were not significantly different between these subgroups. Only one of 8 patients in subgroup I had a history of near syncope. On the other had, syncope was observed in 5 patients. and near syncope in one, in group 2. In conclusion, intrinsic junctional automaticity is preserved in some patients with sick sinus syndrome, and might compensate for sinus node dysfunction to prevent clinical symptoms. Organic impairment should affect conductivity as well as automaticity in the AV junction.

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The characteristics of the coupling interval (CI) of ventricular premature con-traction (VPC) were studied in 100 patients with frequent VPCs using 24h ambulatory ECG recording. All R-R intervals were registered on computer to determine the mean value of CIs (Mean CI) and the standard deviation of CIs (SD-CI). We compared the Mean CI and the SD-CI between idiopathic VPCs and VPCs with organic heart disease (OHD). In addition, we evaluated the efficacy of disopyramide (DP) and mexiletine (MX) and we examined the relationship between the efficacy of these drugs and the characteristics of CI. The Mean CI of VPCs with OHD was longer than that of idiopathic VPCs (530 vs. 494 msec, p<0.05). The SD-CI of VPCs with OHD was larger than that of idiopathic VPCs (54.1 vs. 39.3 msec, p<0.01). In all treated cases. the drug efficacy was not different between DP (11/18, 61%) and MX (9/19, 47% ). However when we isolated cases of OHD, we found a tendency that DP (9/12, 75%) was more effective than MX (7/16, 44%). In cases where DP was administered. the Mean CI of VPCs was not different between effective and ineffective cases. while in cases where MX was administered, the Mean CI of ineffective cases had a tendency to be longer than that of effective cases (552 vs. 506 msec, p<0.1). In cases where DP was administered, the SD-CI of VPCs showed no difference between effective and ineffective cases, while in cases where MX was administered. the SD-CI of ineffective cases was larger than that of effective cases (66.9 vs 36.7 msec. p<0.05). These results suggest that DP seems to be superior to MX for VPCs with OHD, because of the fact that MX was not effective on VPCs with OHD in which the Mean CI was longer and the SD-CI was larger.

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The plasma concentration of atrial natriuretic peptide (pANP) was investigated at fixed times during 48h following the onset of an initial attack of mild acute myocardial infarction (AMI) in 11 patients. Six hours after onset, the mean pANP was elevated, but 6h later pANP had returned to the baseline level. Forty-eight hours after onset the mean pANP increased again. Thus, the curve of the time course of pANP consisted of 2 peaks separated by a dip. Six hours after onset, systemic hemodynamics and humoral factors were measured in 27 patients. At 48h they were measured in 14 patients. The late elevation of pANP correlated with mean pulmonary arterial wedge pressure (r=0.63, n=14, p<0.05), while the early elevation of pANP did not (r=0.31, n=27, n.s.). The early elevation of pANP correlated with plasma concentrations of both noradrenaline (r=0.55, n=27, p<0.01) and creatine phosphokinase (r=0.54, n=27, p<0.01). In addition, noradrenaline levels positively correlated with mean pulmonary arterial wedge pressure (r=0.38. n=27, p<0.05). The cause of the early elevation of pANP in AMI is unclear, but it is suggested that injury to myocardium and activated sympathetic nerve activity may be responsible in part.

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Isolated coronary ostial stenosis (OS) is a rare disease of unknown etiology. Five cases of OS were observed amongst 700 elective coronary bypass patients and were compared with 111 cases of atherosclerotic left main trunk disease (LMTD) to clarify clinical characteristics. Mean age for LMTD patients was 61.2 years, while, it was 43.0 years for OS patients. 4 patients out of the 5 cases (80%) in the OS group were female, but there were only 10 females (9%) in the LMTD group. 60% of the OS group presented unstable angina without any episodes of myocardial infarction. 69.4% of the LMTD group presented stable angina, and 42% had a previous myocardial infarction. Left ventricular function was well preserved in the OS group compared to the LMTD group. Aorto-coronary bypass grafting was the only surgical method of our choice in both groups. The average number of grafts were 2.2 for the OS group, and 2.4 for LMTD group. Operative mortality was 0% for the OS group and 0.9% for the LMTD group. Clinical and angiographic profiles of ostial stenosis suggest that this group may represent a distinct entity, different from the more common atherosclerotic left main trunk stenosis. Coronary bypass grafting can provide good operative prognosis in ostial stenosis as well as in left main trunk stenosis.

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First-pass radionuclide ventriculography followed by myocardial SPECT with technetium-99m methoxy isobutyl isonitrile (Tc-99m MIBI) was performed on 12 patients with suspected coronary artery disease at rest and during exercise. Left ventricular wall motion and myocardial perfusion were assessed simultaneously and compared on a segment-by-segment basis. Segmental agreement between Tc-99m MIBI and Tl-201 with regard to the presence of perfusion defects was 95% (57/60) at rest and 93% (37/40) during exercise. With respect to the assessment of myocardial ischemia and/or infarction, abnormalities in regional wall motion agreed with the presence of myocardial perfusion defects in 18 out of 21 segments (86%). SimuJtaneous evaluation of regional wall motion and myocardial perfusion by Tc-99m MIBI may provide useful information for the assessment of myocardial ischemia.

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We described a 37-year-old man with a subaortic "fibrous sac", admitted for congestive heart failure. On 2-dimensional echocardiography a saccular structure was seen to extend from the left coronary cusp of the aortic valve to the outflow tract of the left ventricle. By color Doppler imaging. a grade 3 aortic regurgitation was recognized. Aortic regurgitant flow was recorded from the left coronary cusp to the saccular lesion. When congestive heart failure became exacerbated, the repeat examination showed the regurgitant flow passing through the perforated bottom of this lesion and reaching the left ventricular cavity. On microscopic examination of the excised valve, capillary proliferation and inflammatory changes were recognized near the annular region of the left coronary cusp. The edge of the valve leaflet and the other 2 cusps were intact. It is likely that our patient had a mycotic aneurysm near the aortic ring. We speculate that aortic regurgitation followed inflammation. It dilated the left ventricular cavity and contributed to congestive heart failure. Inflammation also weakened the tissue near the annulus, causing it to protrude into the subaortic region thus forming a small aneurysm. It may have grown to become a large saccular structure under high aortic pressure. That is, it became a "giant endocardial pocket with inflammatory process. Finally, the rupture of this sac caused a massive aortic regurgitation, exacerbating congestive heart failure.

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A 53-year-old woman presented with symptoms of dyspnea on exertion and edema of lower extremities. Chronic cardiac tamponade caused by the rupture of the right atrial wall was diagnosed by two-dimensional contrast echocardiography. Autopsy findings revealed primary cardiac hemangiopericytoma.

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The functional response of the left ventricle with scar to increased afterload. was examined in 15 patients with old myocardial infarction and left ventricular aneurysm (OMI). Interventional cine left ventriculography during elevating left ventricular pressure with methoxtimine. Wall motion was assessed by the radial and the centerline method. Augmented afterload didn't change ejection fraction in patients with OMI, but normalized wall motion (Z) increased in the aneurysmall region and decreased in the remote region in both methods. In the remote region in patients with OMI, afterload stress shortened left ventricular pressure-radial length (P-L) loops along length axis, and reduced percent systolic radial shortening (SS). In the aneurysmal region. P-L loops showed systolic elongation of length at rest and the slope of end-diastolic point to end-systolic point became steeper with increased afterload, resulting in a decrease of aneurysmal expansion. In summary, with increasing afterload, wall motion decreased in non-infarcted regions and increased in anertysmal regions, in left ventricles with aneurysm. This mechanism may be interpreted as afterload-induced shifts of P-L loops in each region.

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Three patients are presented in whom a false aneurysm of the left ventricle was surgically treated. False aneurysm of the left Ventricle is an unusual consequence of ventricular wall rupture with containment of the resulting hematoma. Most false aneurysms of the left ventricle develop following myocardial infarction. The false aneurysm wall contains no myocardium. The false aneurysm has a great tendency to rupture, regardless of its size. One patient developed progressive congestive heart failure following a myocardial infarction. The other two patients were asymptomatic following myocardial infarction. Preoperative magnetic resonance imaging showed characteristics of a false aneurysm. These included a distinct discontinuance of the myocardium at the neck of the aneurysm and a narrow neck relative to the diameter of the aneurysm. Two patients underwent successful closure of the orifice of the false aneurysms. One patient undewent emergency surgery because of acute rupture while awaiting surgery hut died of cerebral damage. Surgical correction of a false aneurysm is clearly advisable even in the absence of symptoms.

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An extremely unusual case of myocardial infarction associated with infective endocarditis (IE) is described. A 38-year old male with a high fever was transfer-red to our hospital for further treatment of IE. Two-dimensional echocardiogram showed a large mycotic aneurysm of the sinus of Valsalva in contact with neighbouring structures. The patient had a rapid recovery within several days after administration of antibiotic agents. However, he then developed abrupt onset of severe precordial pain. From the echocardiogram images and biochemical evaluation he was diagnosed as having an acute subendocardial infarction. Serial echocardiograms revealed expansion of the aneurysm, extending from the myocardium of the anterolateral free wall to the lower margin of the proximal left coronary artery. The cause of acute myocardial infarction was thought to be incomplete occlusion of the coronary artery through compression by the enlarging mycotic aneurysm of the sinus of Valsalva. Urgent surgery confirmed compression of the left coronary artery by the large mycotic aneurysm as the cause of acute myocardial infarction.

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The effects of regression of left ventricular hypertrophy following atenolol and bunazosin therapy on ischemic cardiac function and myocardial metabolism in spontaneously hypertensive rats (SHR) were studied. Atenolol (50mg/kg/day) and bunazosin (5mg/kg/day) were administered to SHR from 19 to 26 weeks of age, whereas tap water was given to control SHR and normotensive Wistar-Kyoto rats (WKY). Both atenolol and bunazosin significantly decreased arterial blood pressure and significantly decelerated the increase in left ventricular weight in SHR. At the end of the long-term treatment, hearts were removed and perfused by the working heart technique for 15 min. and then global ischemia was induced for either 10 or 30 min. The ischemic heart was reperfused for 30 min. The pressure-rate product and the extent of recovery of the coronary flow after reperfusion following 30 min of ischemia in the bunazosin-treated SHR were significantly higher than those in the control SHR and the atenolol-treated SHR. The levels of adenosine triphosphate (ATP). creatine phosphate (CrP). and energy charge potential in the SHR heart reperfused after 30 min of ischemia were significantly lower than those in the reperfused WKY. Both atenolol and bunazosin improved the restoration of ATP and CrP in SHR after reperfusion following 30min of ischemia. In conclusion. antihypertensive therapy with either atenolol or bunazosin was effective in preventing cardiac hypertrophy and ischemic damage caused by different mechanisms. Factors resulting from stimulation of the cardiac alpha₁ adrenoceptor may play an important role in the development of hypertensive cardiac hypertrophy, just as factors resulting from stimulation of the β₁-adrenoceptor do.

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We examined the effects of a new hyperosmotic agent (NIK-242inj.) on brain edema, energy metabolites and regional cerebral blood flow (r-CBF) during acute cerebral ischemia. Cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) using spontaneously hypertensive rats (SHR). The experimental animals were divided into 4 groups. A:20% NIK-242inj., B:20% mannitol, C:10% glycerol in 5% fructose. D:normal saline. All the animals were administered the agent or saline intravenously beginning at 1h after BLCL and continuing for 2h for a total dose of 6.8ml/kg body weight. Brain water content and metabolites (ATP, lactate. pyruvate) were determined 3h after BLCL. Regional cerebral blood flow (r-CBF) in thalamus was also measured by the hydrogen clearance technique. The brain water content in the NIK-242inj. group was significantly lower than that of saline group. The concentration of brain ATP in the NIK-242inj. group remained higher than those of saline group. Accumulation of lactate in the NIK-242inj. group was less than in the mannitol and saline groups. The lactate/pyruvate ratio of the NIK-242inj. group was significantly lower than that of the saline and mannitol groups. At 3h after BLCL. the reduction of r-CBF in the NIK-242inj. group was smaller than that of saline group. The present study suggests that NIK-242inj. as well as glycerol could ameliorate brain edema, disruption of brain energy metabolism and reduction of r-CBF in acutely induced cerebral ischemia.

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