Left ventricular asynergy has been shown to occur commonly in patients with coronary artery disease (CAD) and to be induced or exaggerated by exercise. The purpose of this study is to report on a method to detect asynergy and estimate its severity by M-mode echocardiographic analysis of left ventricular wall motion at rest and during supine ergometric exercise. Sixteen patients with CAD underwent graded supine ergometric exercise until anginal pain occurred or apparent ischemic changes were noted on ECG.
This study was done using the following criteria:
1) Asynergy at rest was defined as occurring when the amplitudes of the interventricular septum and/or the posterior left ventricular wall were below normal values at rest.
2) Asynergy during exercise was defined as occurring when one or both of the two amplitudes were more than 2mm below the values at rest (severe) or were unchanged in spite of sufficient exercise load (mild).
The results were as follows:
1) In the normal subjects, the septal and posterior wall amplitudes increased during exercise (ranging from 7mm to 9mm for the septum, and from 13mm to 16mm for the posterior wall). In patients with CAD, asynergy at rest was demonstrated in only 3 cases (19%), whereas septal and/or posterior wall asynergy during exercise was noted in 75% of cases.
2) The location of exercise-induced asynergy detected by echocardiography showed a good correlation with that of coronary artery lesions (_??_75% stenosis) recognized by angiography.
3) Significant differences were observed between changes in left ventricular dimensions in patients with CAD and those of normals during exercise. In the normal subjects, left ventricular endsystolic dimension (ESD) decreased without significant change in end-diastolic dimension (EDD) during exercise. On the other hand, both ESD and EDD increased during exercise in patients with CAD. Although echocardiographic analysis of left ventricular wall motion during exercise has some limitations, this study suggests that asynergy induced or exaggerated by ergometric exercise can be successfully detected by M-mode echocardiography.

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Pulsed Doppler echocardiography (PDE) was performed on 67 patients with ventricular septal defect (VSD) using an ATL 500A pulsed Doppler system. The subjects were divided into 3 groups according to their clinical diagnosis.
Group 1 consisted of 39 patients with isolated VSD and 15 with associated cardiac malformations. The VSD jet was recognized through the interventricular septum (IVS) and was followed into the right ventricular cavity. These PDE findings were obtained in 52 of the 54 Group 1 cases. There was a false negative PDE diagnosis in 2 patients who showed a bidirectional communication at the ventricular level. Thus the sensitivity of PDE to this lesion was 94%. The disturbed systolic flow within the IVS was mainly detected below the aortic root, near the septal tricuspid leaflet (STL) and between them. In 23 patients, regurgitant flow was recognized only at the defect. In 12 of the 54 cases, PDE revealed the VSD jet from the defect to the distal right ventricular outflow tract (RVOT) toward the pulmonary valve. These PDE findings were frequently obtained from patients with supracristal VSD; 8 of the 12 had angiographically and/or surgically proven supracristal VSD, 3 had clinical signs and echocardiographic findings that implied this type of defect and the remaining one was a type II VSD (Kirklin) with hyperkinetic pulmonary hypertension.
Six patients showed a systolic flutter of the tricuspid valve and/or systolic anterior movement on M-mode echocardiogram. Five of them were shown to have aneurysms of the membranous septum and another one had a type III VSD at surgery. A disturbed systolic flow pattern was obtained when the sample volume was placed on the fluttered valve and also within the aneurysmal sac.
Group 2 was composed of 3 cases with Eisenmenger's complex and 7 with tetralogy of Fallot. PDE revealed no disturbed flow at the defect. In 2 patients with Eisenmenger's complex, systolic turbulence was seen within the left ventricular outflow tract, while in 8 cases, an early diastolic right-to-left communication was demonstrated as a laminar reversed flow, a finding consistent with an abrupt posterior movement of the remnant of the tricuspid leaflet into the left ventricle in one of this group.
Group 3 was comprised of 3 cases with left ventricular-right atrial communication. The regurgitant flow was detected as a systolic wide band pattern through the IVS near the STL and was followed into the right atrium. No patients in this group showed clinical signs or echocardiographic findings of this lesion.
Based upon our findings, PDE was thought to be useful for noninvasive identification of various types of VSD.

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The electrocardiographic effects of mental arithmetic stress were studied in 19 young, healthy male subjects. Blood pressure was measured by the cuff method before and during mental stress and electrocardiogram (V₅) was monitored and recorded continuously throughout the study using a computerized ECG monitoring system.
Heart rate increased from 65.8±7.0 (mean±standard deviation) to 76.7±9.9beats/min (p<0.001). Systolic blood pressure rose from 122.7±9.6 to 129.1±11.7mmHg (p<0.05), diastolic blood pressure from 76.2±8.8 to 83.0±11.0mmHg (p<0.001), and mean blood pressure from 91.7±7.9 to 98.5±10.1mmHg (p<0.001). These changes were all statistically significant. R wave amplitude decreased significantly from 18.6±6.9 to 17.0±6.5mm for the group (p<0.001). No changes in the ST segment were observed; ST depression decreased from 0.56±0.47 to 0.54±0.43mm (N.S.) and ST slope from 0.87±0.59 to 0.77±0.63mm/sec (N.S.).
Thus it is apparent that mental stress reduced R wave amplitude without causing ST segment changes in young, healthy subjects. The mechanism and clinical implications are discussed.

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This experimental and clinical study evaluates the degree of myocardial protection afforded by coronary perfusion with cold lactated Ringer's solution plus mannitol. In the experimental study, diluted blood at 30°C (Control G.), lactated Ringer's solution at 4°C (G.A), 1, 000ml lactated Ringer's solution plus 200ml of 20% mannitol at 4°C (G.B), and 1, 000ml lactated Ringer's soultion plus 500ml of 20% mannitol at 4°C (G.C) were used for coronary perfusion. The myocardial-protecting effect of each perfusate was evaluated by examining serum isoenzymes (CPK-MB, LDH1+2, ), left ventricular function (Vmax, LVEDP, CO), and the ultrastructure of myocardium. There were no significant differences in myocardial changes between the control group, G.A and G.B. Left ventricular enddiastolic pressure increased significantly in G.A and a significant increase in CPK-MB was seen in G.C. Mitochondrial scores for each group were 98 (Control G.), 86 (G.A), 93 (G.B), and 51 (G.C). Minimal myocardial change was seen in G.B.
In the clinical study aortic root perfusion with cold lactated Ringer's solution (400m Osm) under aortic cross clamping (27-144min) was employed in 25 patients. They all survived and CPK-MB returned to preoperative values within 49 hours after operation. In 6 cases, the ultrastructure of left ventricular papillary muscle was examined. It was confirmed that no significant mitochondrial changes developed during aortic cross-clamping.

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Phospholipid methylation of canine cardiac membranes was studied in vitro to determine its relationship to the regulation and function of β-adrenergic and digitalis receptors. Cardiac membranes were prepared from the left ventricle of mongrel dogs. Phospholipid methylation was assayed by measuring [³H] methyl incorporation after incubation with methyl donor S-adenosyl-L-[methyl-³H] methione at 37°C. The reaction of phospholipid methylation had an optimum pH around 9 and a linear time course of up to 60min. The reaction was inhibited by the addition of S-adenosyl-L-homocysteine, a known antagonist of biological transmethylation. L-isoproterenol enhanced phospholipid methylation markedly, but ouabain had no effect. On the other hand, after phospholipid methylation in cardiac membranes was stimulated by pre-incubation with S-adenosyl-L-methionine for 60min at 37°C, [125I] iodohydroxybenzylpindolol binding to the membranes was increased. The number of the β-adrenergic receptor binding sites (B_max), calculated from Scatchard analysis in cardiac membranes of 3 dogs significantly increased. On the other hand, [³H] ouabain binding and Na⁺, K⁺, Mg²⁺-ATPase activity were not increased. The increase in [¹²⁵I] iodohydroxybenzylpindolol binding was inhibited by the addition of S-adenosyl-L-homocysteine. These findings suggest that phospholipid methylation is closely related to β-adrenergic receptors, but not digitalis receptors in cardiac membranes.

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Changes in potassium (K) concentration in erythrocytes (RBC) were investigated during the early developing stage (1 and 2 weeks after) and the chronic established stage (12 to 16 weeks after the renal artery constriction) in two-kidney (group 2H) and one-kidney Goldblatt hypertension (group 1H) of the rabbit. In both group 2H and group 1H, blood pressure was already elevated significantly during week 1, and reached a level about 70mmHg higher than the pre-constriction level at the chronic stage. It did not change in the control group (group C). During week 2, the change in RBC K concentration showed a significant negative correlation with the change in blood pressure in group 2H (r=-0.529, n=26, p<0.01). During the chronic stage, the RBC K concentration was lower in group 2H (103.5±1.7mEq/1 RBC, n=10, p<0.01 com-pared with group C) and in group 1H (102.1±1.6, n=7, p<0.001) than in group C (111.6±2.2, n=9). The change in this parameter from the pre-constriction value was -11.9±2.1mEq/l RBC (p<0.001) in group 2H, -13.0±1.8 (p<0.001) in group 1H, and -2.4±2.6 (not significant) in group C. The results suggest that the intracellular electrolyte metabolism is altered in both types of chronic Goldblatt hypertension.

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The effects of large doses of angiotensin II on the rabbit kidney and heart and or the ability of perfused canine kidney to inactivate angiotensin II were examined to clarify the role of angiotensin II in the low cardiac output syndrome after open-heart surgery. Intravenous infusion of angiotensin II at a rate of 1.1 to 1.4μg/Kg/min for 48 hours caused multifocal myocardial necrosis and renal mononuclear cell infiltration and necrosis. Isolated canine kidney preparations inactivated 76% of angiotensin I and 79% of angiotensin II. The results indicates that the kidney can inactivate angiotensin and that high doses of angiotensin II can produce myocardial and renal lesions. It is suggested that an increased concentration of angiotensin II may result in the low cardiac output syndrome through myocardial damage, and that decreased inactivation of angiotensin II by the kidney accelerates the myocardial damage.

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An extracorporeal bypass was performed in mongrel dogs for 2 hours with or without hypertonic mannitol infusions. In animals given mannitol, the plasma osmolality was elevated maximally to 344±7.1mOsm/L and the urine volume was maintained well during bypass. A hypertonic mannitol solution was effective in maintaining the C_PAH during and after bypass, but was not effective in minimizing the reduction in Ccr. When the mean arterial pressure during bypass was kept at 60mmHg, the carbon filling rates in glomeruli showed the favorable effects of mannitol upon renal function, but no effects were observed at a mean arterial pressure of 80mmHg.
In 11 patients who had undergone a bypass lasting more than 2hrs with mannitol infusions, the plasma osmolality reflected the serum mannitol level and reached 320±11.0mOsm/L at 150min of bypass. The mean urine volume was 5.0±3.3ml/min/M² during the bypass, which was about 7 times as great as before the bypass. The Ccr increased during the first 30min of the bypass, but it fell to about one half of the initial value after 90min of the bypass. It was concluded that a hypertonic mannitol solution is effective in maintaining the RPF and urine volume during and after the bypass and that it also preserved the glomerular perfusion even at a low arterial pressure.

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To evaluate the role of the central nervous system on the furosemide-induced increases in plasma noradrenaline (PNA), renin activity (PRA), and aldosterone concenrtation (PAC), central vasoactive sympathetic structures were inhibited by intravertebral artery infusion of colnidine. Intravertebral artery infusion of clonidine (0.06μg/Kg/min) significantly reduced basal PNA, heart rate, and arterial pressure, while both PRA and PAC were increased. Intravenous infusion of the same dose of clonidine caused no significant changes in PNA, PRA, and PAC. Intravertebral artery infusion of clonidine (0.02 or 0.1μg/Kg/min) significantly suppressed the furosemide-induced increases in PNA and heart rate, and induced a drop in arterial pressure. Although the furosemide-induced increase in PRA was suppressed by intravertebral artery infusion of clonidine, the furosemide-induced increase in PAC was not affected. These results suggest that the furosemide-induced increase in PNA may be mediated by the central sympathetic nervous system and that some of the furosemide-induced increase in PRA may be mediated by central sympathetic neural activation.

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The effects of captopril, an inhibitor of angiotensin-converting enzyme, on sinus rate and atrial contraction were investigated in 10 isolated dog atria and in 3 intact anesthetized donor dogs. Captopril (10-1, 000μg) caused an increase in heart rate and the development of atrial contractile tension when injected into the sinus node artery of the isolated atrium perfused with arterial blood of the anesthetized dog. At extremely high doses (1-3mg), captopril produced brief negative effects followed by positive ones. The positive effects were completely blocked by 10μg of propranolol, after which the negative ones became more evident. The positive effects were also significantly suppressed by 30μg of imipramine, whereas the negative ones were not influenced by treatment with atropine.
In all 3 cases when captopril (0.3mg/Kg) was administered intravenously to donor dogs, the blood pressure decreased and a slight tachycardia usually appeared. In contrast, no significant change was observed in sinus rate and contractile tension of isolated atria. Thus, it is concluded that only at extremely high doses does captopril cause a release of catecholamine by a tyramine-like action which may have a slight depressive action on the sinus node and contractility.

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Characteristics of the temporal elevation of diastolic tension, produced by ischemia-reperfusion in isolated and paced Langendorff's hearts of guinea pigs, were studied. The elevation of diastolic tension corresponded with an elevation of left ventricular end diastolic pressure after a short ischemic period in the isovolumic heart. These phenomena were thought to be a result of incomplete relaxation. The degree of the elevation of diastolic tension depended upon the duration of ischemic period (3-10min). This elevation was reproducible in one preparation; nearly the same changes were obtained in a second trial after 35min of reperfusion when the ischemic period was within 5min. An increment in the pacing rate to 150% of the first trial value doubled the elevation of diastolic tension by the second 5min ischemia. Inhibition of glycolytic flux by iode acetic acid augmented the elevation after 3min of ischemia. In addition, 5min of ischemia with iode acetic acid caused contracture and recovery was slight. On the other hand, either lowering the Ca²⁺ concentration in the perfusing solution to a half the normal value, or treatment with Ca²⁺ antagonists (such as diltiazem), reduced the elevation of diastolic tension significantly. Diltiazem also suppressed the increment in elevation produced by a high pacing rate.
It can be concluded that the temporal elevation of diastolic tension during reperfusion reflects the ischemic failure of the heart. This change is presumably due to intracellular Ca²⁺ overload or accumulation. In addition, since ischemic changes were reproducible in this preparation, it is a useful model for estimating the effects of drugs on the ischemic heart.

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Effects of 2-nicotinamidoethyl nitrate (SG-75) on contractile responses of dog coronary arteries to indomethacin were investigated in vitro. Indomethacin (3×10^-8and 3×10^-7Gm/ml) produced contractions of isolated coronary arterial strips, which were reproduced by successive administration of the drug. SG-75 (10^-5Gm/ml) administered 5min prior to indomethacin, significantly depressed indomethacin-induced contractions of the strips. In coronary arterial strips under potassium-contracture, SG-75 10^-8-10^-4Gm/ml) produced concentration-dependent relaxations, which were not affected by prior administration of indomethacin (3×10^-6Gm/ml). Tranylcypromine (10^-4Gm/ml) did not influence the relaxant responses of the strips to SG-75 (10^-8-10^-5Gm/ml) but significantly depressed them to SG-75 (10^-4Gm/ml). Results indicate that large doses of SG-75 will induce a relaxant effect on isolated dog coronary arteries through activation of intravascular biosynthesis or release of prostacyclin from vascular tissues.

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We present a case of massive calcification of the right ventricular wall and cavity, which extended from the base of the tricuspid valve to the pulmonary valve, and caused pulmonic stenosis and incompetence with a valve deformity. To our knowledge, this is the first description of this condition.

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Myocardial infarction in the presence of coronary arteriovenous fistula (CAVF) has rarely been reported. Two young male patients with dual abnormalities, an organic stenosis and a CAVF in the left anterior descending artery, were reported. Each fistula originated closely proximal to the stenotic lesion and drained into the main pulmonary artery. It was thought that the coronary steal phenomenon through the fistula further reduced the coronary blood flow distal to the stenosis. Thus, both the stenotic lesion and the fistula possibly contributed to the occurrence of the myocardial infarction. Since angiographic details of myocardial infarction with CAVF have rarely been reported these findings may be important in clarifying the mechanism of myocardial infarction with CAVF.

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