[Acute myocardial infarction during sport].

Thirty patients with acute myocardial infarction which occurred during sport were investigated to identify the type of sport, prodromata, situations at the onset of disease, habit of exercise, preceding medical evaluation, coronary risk factors, and coronary angiographic findings. Infarction occurred during golf in 12 patients, bowling in 4, gateball in 4, jogging or running in 5, baseball in 2, and tennis or table tennis in 3. The majority of the patients were playing ball games. Twenty-seven patients were men (90%) and 3 were women (10%). All patients had played the same kind of sport for several years. Twenty-four patients had one or more coronary risk factors, and especially 18 patients smoked cigarettes. Nine patients had experienced anterior chest pain but only two patients had received medical evaluation. Coronary angiography was performed in 25 patients (83.3%), revealing single-vessel disease in 14, two-vessel disease in 6, three-vessel disease in 4, and disease of all left main coronary trunks in 1. The acute episode of infarction occurred mainly in spring or fall. Many patients with acute myocardial infarction occurring during sport participate in sports of low or moderate dynamic and low static exercises which are generally regarded safe. Many patients had enjoyed their sports regularly for a long time. Though many patients had coronary risk factors, only a few had received a medical check before their heart attack.

The first report of a case with acute myocardial infarction showing familial deficiency of creatine kinase.

A 46-year-old male patient was diagnosed as suffering from acute myocardial infarction, but his serum creatine kinase (CK) level was extremely low and no CK isozymes were detected in the serum. The total CK activities in the skeletal muscle amounted to only 2% of that of the control. Electrophoresis of the CK isozymes in the skeletal muscle showed that CK-MM was absent but the CK-BB and abnormal isozyme bands were present. There was no evidence of myocardial ischemia, although the exercise treadmill test revealed ST segment depression in the chest leads. One of the patient's sisters had an extremely low serum CK level suggesting inheritance of this abnormality. This is the first report of a case showing familial deficiency of CK.

[Left ventricular wall motion mimicking stunned myocardium in hypertrophic obstructive cardiomyopathy with normal coronary arteries: a case report].

A 63-year-old woman was admitted to the coronary care unit of Hyogo College of Medicine because of cardiogenic shock. She previously had been hospitalized in the Gynecology Department for the treatment of recurrent uterine cancer. She had poor appetite due to chemotherapy which was given for 10 days prior to her admission. On admission, echocardiography and cardiac catheterization revealed hypertrophic obstructive cardiomyopathy and extensive left ventricular wall motion abnormalities. Coronary arteriography showed no coronary artery disease. Left ventriculography as well as echocardiography performed on the 21st post-admission day revealed that the wall motion abnormalities had completely resolved and the systolic anterior motion of the mitral valve (SAM) was no longer evident. The systolic pressure at the apex of the left ventricle was 200 mmHg on admission. The increased ventricular pressure and the simultaneous resolution of the wall motion abnormality and SAM suggest that marked obstruction of the left ventricular outflow tract is more likely to be involved in transient ventricular wall motion abnormality rather than acute myocardial ischemia. The mechanism of the SAM in the present case seemed to be related to a Venturi effect which was augmented by the decreased preload due to hypovolemia. In addition, papillary muscle contraction seemed to pull the mitral valve toward the interventricular septum during systole.

[Exercise tolerance in patients after successful percutaneous transluminal coronary angioplasty].

In 32 patients with successful percutaneous transluminal coronary angioplasty (PTCA), we performed treadmill exercise tests (TMET) before and about one month after PTCA to assess the correlation between the improvement in coronary artery lesions and exercise tolerance. Either the Bruce protocol (B: n = 12) or the modified Bruce protocol (MB: n = 20) was used; with the latter being applied to patients whose cardiac function seemed depressed. In 15 patients, oxygen consumption (VO2) was measured by analyzing the expired gases, 13 patients underwent exercise thallium-201 myocardial perfusion scintigraphy before and after PTCA, whose results were compared with those of TMET. In both B and MB protocols, the treadmill walking time was significantly prolonged after PTCA, compared to that before PTCA (B: 7.4 +/- 1.3 vs 9.5 +/- 1.9, MB: 11.4 +/- 3.5 vs 12.7 +/- 3.5 min). Heart rates (HR) and rate pressure products (RPP) were significantly increased after PTCA in both protocols (HR B: 139 +/- 18 vs 154 +/- 17, MB: 121 +/- 20 vs 137 +/- 19 bpm, RPP B: 26,500 +/- 5,600 vs 30,300 +/- 6,700, MB: 19,400 +/- 6,200 vs 22,700 +/- 6,600 mmHg.bpm), however, systolic blood pressure did not change significantly after PTCA in either protocol. While there was a significant improvement in VO2 after PTCA (21.6 +/- 6.3 vs 25.7 +/- 4.2 ml/kg/min), the O2-pulse remained unchanged. Thallium-201 myocardial scintigraphy revealed improvement of myocardial perfusion in 8 of the 13 cases examined.(ABSTRACT TRUNCATED AT 250 WORDS)

[Medical and surgical treatment for patients with dissecting aneurysms of the aorta].

The medical and surgical treatment of 96 patients of dissecting aneurysms was reviewed. There were 42 patients with Stanford type A dissecting aneurysms, 19 of whom received medical treatment and 23 of whom had surgical treatment. Among 54 patients with Stanford type B dissecting aneurysms, 24 had medical and 30 had surgical treatments. The treatment results and the long-term outcomes were studied using the Kaplan-Meier method, categorizing the subjects in non-survivor (in-hospital) and survivor groups. The results indicated that those with surgical treatment had a higher survival rate (75%) in the early post-operative course, for both type A and type B aneurysms. However, the long-term outcome of the survivor group was not different between type A and type B aneurysms regardless of type of treatment. Fifty-six percent of cases with type A aneurysms with serious complications survived by medical treatment alone, and no intimal tears were visualized on angiogram. Therefore, it was suggested that, in patients who had no angiographically defined intimal tears in the acute phase, medical treatment may be more effective, even for type A dissecting aneurysms.

[Precordial ST segment depression in acute inferior myocardial infarction: the importance of posterolateral wall infarction].

To determine whether precordial ST segment depression during acute inferior myocardial infarction indicates posterolateral wall ischemia, anatomical predominance of coronary circulation was examined by coronary angiography and evaluated in 43 patients who experienced first acute inferior myocardial infarction. Among patients who underwent intracoronary thrombolysis within six hours from the onset of symptoms, the infarct-related artery was the right coronary artery (RCA) in 35. In addition, their early 12-lead electrocardiographic features were compared with those in eight patients having the infarct-related left circumflex coronary artery (group Cx). Thirty-five patients with RCA obstruction were categorized in four groups: Four patients with left predominant type (group L), 10 with balanced type (group B), five with right super-predominant type (group SR), and 16 with right intermediate type (group RI). Seventeen of the 21 patients in groups SR and RI demonstrated precordial ST segment depression, whereas it was present in only six of the 14 patients in groups L and B (p less than 0.05). Of the 29 patients in groups SR, Cx and RI, total ST segment depression in leads V1 through V4 (sigma ST) was greater in the 14 patients in groups L and B (p less than 0.05) than in other groups. Furthermore, in these 29, all patients in groups SR and Cx had greater sigma ST than did the patients in group RI (p less than 0.05). There was no significant difference in sigma ST between groups SR and Cx. Precordial ST segment depression did not correlate with concomitant disease of the left anterior descending artery and was not a mirror image of ST segment elevation in inferior leads. On thallium-201 scintigraphy, additional perfusion defects of the posterolateral wall were present in all eight patients in group Cx and in ten of the 21 patients in groups SR and RI. Thus, precordial ST segment depression during acute inferior myocardial infarction seemed to be affected by the pattern of coronary circulation. It was concluded that this ST depression represents more extensive involvement of the posterolateral wall in patients with right predominant coronary circulation as well as in those with left circumflex artery obstruction.

[Clinical significance of precordial ST segment depression during acute inferior myocardial infarction].

To investigate the mechanisms and clinical significance of precordial (V1-V4) ST segment depression during acute inferior myocardial infarction, stress thallium-201 scintigrams and coronary angiograms were obtained within four to eight weeks after the onset of myocardial infarction in 37 patients experiencing their first acute inferior myocardial infarction. Among 18 patients with precordial ST depression (group 1), 11 with concomitant disease of the left anterior descending artery (LAD) had positive results on exercise test, whereas in seven patients without LAD lesion, only two had positive exercise test (p less than 0.01). In 19 patients without precordial ST depression (group 2), 11 had severe stenosis in the LAD. However, among these 11 patients, only two had positive exercise tests. Patients with precordial ST depression demonstrated a higher frequency of positive exercise tests than those without it (p less than 0.01). On stress thallium-201 scintigraphy, a perfusion defect involving the inferior wall was present in all patients, but additional anterior wall ischemia was present in only five of the 18 patients in group 1. These five patients had chest pain on exercise tests and a severe stenosis greater than 90% in the LAD. There was no significant difference in the frequency of additional posterolateral wall infarction between groups 1 and 2. In 18 patients in group 1, sigma ST (total degrees of ST segment depression in leads V1, V2, V3, and V4 in the acute stage) was significantly greater in 11 patients with LAD lesion than in seven without (p less than 0.05), and sigma ST greater than five mm was observed in 12 of 13 patients who had additional anterior wall ischemia and posterolateral wall infarction on stress thallium-201 scintigraphy (p less than 0.05). Myocardial revascularization, such as aortocoronary bypass surgery or percutaneous transluminal coronary angioplasty (PTCA), was performed in six of the 18 patients in group 1 in the chronic stage, but in only one of the 19 patients in group 2. Thus, in patients with initial acute inferior myocardial infarction, those with precordial ST depression seemed to be a high-risk group. It was suggested that, during the early stage of myocardial infarction, this abnormality on electrocardiograms is related to the summation of effects of anterior wall ischemia and posterolateral wall infarction. Furthermore, the sigma ST evaluation is useful in differentiating a mirror image of inferior wall infarction from anterior wall ischemia and posterolateral wall infarction as the mechanism of precordial ST depression.

[Indications for coronary revascularization and the postoperative evaluations using Tl-201 exercise myocardial scintigraphy and a bull's eye display].

Tl-201 exercise myocardial scintigraphy and quantitative analysis using bull's eye display were performed in 31 cases (18 bypass cases, 13 PTCA cases) to determine the indications for coronary artery bypass surgery and PTCA, and to evaluate postoperative improvement. Regions of interest (ROI) corresponding to each revascularized area were created on a bull's eye display. Then the washout rates (WR) and % uptakes were expressed as percentages. Improvement was judged to have occurred if the revascularized coronary artery was patent and both the WR and % uptake returned to the normal range as determined from the examinations of 20 normal cases. The results were as follows: 1. The preoperative mean WR of the improved areas (30 vessels) was 19 +- 15%, while that of the unimproved areas (15 vessels) was 35 +- 7%. We assumed that the area was suitable for revascularization when the preoperative WR was less than 25% which was in the lower limit of the normal range. Then, 18 vessels were judged to be suitable for surgery, and subsequent postoperative improvement was obtained in the 17 areas. 2. In 32 scintigraphically-improved areas, 30 vessels were angiographically patent, while five vessels were obliterated angiographically in 13 scintigraphically-unimproved areas (diagnostic validity was 76% of all 45 vessels). 3. The exercise tolerance increased significantly (p less than 0.01) from 8.7 +- 2.0 min to 11.6 +- 2.5 min in the improved cases in which all the revascularized areas were improved after revascularization. There was no change of the exercise tolerance (before: 9.4 +- 3.4 min, after: 9.4 +- 2.5 min) in the unimproved cases in which all the revascularized areas were unimproved. 4. Quantitative analysis was useful for objective evaluation, because the visual evaluations did not always agree with the quantitative evaluation. We concluded that the area with the preoperative WR less than the normal range is suitable for revascularization. As the scintigraphic evaluation was in accord with improved exercise tolerance and with patency as observed by coronary angiography, our method seems useful for postoperative follow-up.

[Blood flow patterns in the left ventricle in patients with myocardial infarction and ventricular aneurysm: evaluation using real-time two-dimensional Doppler echocardiography].

To evaluate how the intraventricular blood flow is affected by the size of a left ventricular aneurysm and ventricular dysfunction, systolic left ventricular blood flow patterns were evaluated using two-dimensional Doppler flow images (real-time 2-D Doppler echo). The subjects consisted of 10 normal controls, 35 patients with anteroseptal infarction, two patients with inferior infarction and five patients with anteroseptal-inferior infarctions. The systolic period was divided into three subsets; early, mid- and end-systole. Forty-two patients with myocardial infarction were classified into three groups according to the left ventricular inflow patterns on real-time 2-D Doppler echo using the apical left ventricular long-axis approach; i.e., inflow signals confined to early systole (Group I), visualized up to mid-systole (Group II) and end-systole (Group III). Left ventricular end-diastolic dimension (LVDd), left ventricular end-systolic dimension (LVDs), and % non-contractile circumference (delta L) were calculated by the same echocardiographic approach. Ejection fraction (EF) was calculated by left ventricular cineangiography using the Simpson's method. The left ventricular inflow Doppler signals in the normal controls and Group I turned in the apex and then directed toward the left ventricular outflow tract during late diastole and early systole. Significant differences in EF were observed among the three groups. EF in Group I, II and III was 53 +/- 9%, 41 +/- 8% and 29 +/- 7%, respectively. However, LVDd, LVDs and delta L had the largest values in Group III and the smallest values in Group I. LVDd, LVDs and delta L were smallest in Group I and largest in Group III. In the normal controls, the left ventricular inflow signals proceeded to the apex and directed toward the left ventricular outflow tract in the early systolic period. Various changes in the inflow pattern were observed in patients with myocardial infarction and severe wall motion abnormalities, including delayed timing in proceeding from the apex to the left ventricular outflow tract, stagnant blood at the apex and further inflow of blood toward the apex even during end-systole. The patients with sustained inflow during late systole had hypofunction of the left ventricle as demonstrated by smaller EF and larger LVDd, LVDs, and delta L. In conclusion, the observation of intracardiac blood flows by real-time 2-D Doppler echo is of help in evaluating the severity of myocardial infarction.

[Comparison of two-dimensional echocardiography with 201T1-single photon emission computed tomography for evaluating the myocardial infarct zone].

The reliability of measuring the myocardial infarct zone by two-dimensional echocardiography (2 DE) was compared with that by regional myocardial blood flow as evaluated by single photon emission computed tomography (SPECT) in 47 patients with old myocardial infarction, with ventricular aneurysm (An group; n = 15), and without ventricular aneurysm (Non-An group; n = 32). Short-axis images of the left ventricle at the level of the mitral valve, the papillary muscles, and the apex were obtained both by 2DE and SPECT. The left ventricular wall was divided into 36 segments in 2DE and 40 segments in SPECT with reference points at the posterior end of the right side of the interventricular septum. The segments in which the radial shortening on 2DE and the 201Tl uptake index on SPECT were below one standard deviation from the means of 10 normal subjects were defined as those with abnormal wall motion and hypoperfused areas, respectively. The relationships between these findings were studied. The extent of apical movement was measured by left ventricular cineangiography in each case, and was compared between the An and Non-An groups. 1. Wall motion abnormalities on 2DE and hypoperfusion on SPECT showed a correspondence of 81% in the An group and 78% in the Non-An group at the level of the mitral valve, and 78% in the An group and 76% in the Non-An group at the papillary muscle level. However, a better correspondence was observed in the An group (84%) as compared to the Non-An group (64%) at the level of the apex. 2. Apical movement assessed by cineangiography showed more extensive changes in the Non-An group than in the An group (2.3 +/- 0.9 mm vs 4.1 +/- 1.7 mm in the RAO view, 2.4 +/- 1.9 mm vs 5.3 +/- 2.1 mm in the LAO view). From these observations, it was suspected that the cause of disparity between radial shortening and the 201Tl uptake index at the level of the apex is related to the cardiac movement of the apex toward the base during systole. 3. Since wall motion abnormalities demonstrated by radial shortening (2DE) and hypoperfusion indicated by the 201Tl uptake index (SPECT) generally corresponded well, 2DE was thought to be a useful method for evaluating myocardial infarct zone.

[Left ventricular asynergy detected by cardiac blood pool emission computed tomography using the subtraction method].

To evaluate left ventricular regional wall motion, ECG dual-gated cardiac blood pool ECT was performed for 25 patients with ischemic heart disease, including 19 cases of myocardial infarction, five cases of angina pectoris, and one case of post A-C bypass surgery. There were six normal controls. Following SPECT obtained using 32 views (180 degrees), the vertical and horizontal long axes were reconstructed from transaxial images. Then, regional wall motion was evaluated from subtraction images; (end-diastolic)-(end-systolic) and (end-systolic)-(end-diastolic) images. SPECT images were compared with left ventriculography (LVG); vertical long-axial ECT images with segments 1-5 of LVG by the AHA classification, and horizontal ECT long-axial images with segments 6 and 7 of LVG, respectively. The subtraction images from ECG dual-gated cardiac blood pool ECT corresponded with left ventriculography in 79.4% of 175 segments in 25 patients with ischemic heart disease (sensitivity 92.6%, specificity 68.0%, and accuracy 79.4%). When wall motion was classified as normal, hypokinesis, akinesis, and aneurysmal, good agreement was observed between the two methods in 68% of these segments. The locations of asynergy as obtained by this method were closely in accord with those of perfusion defects by Tl-201 myocardial SPECT in 74.4% of segments. Left ventricular aneurysms were detected using subtraction image; (end-systolic)-(end-diastolic). We conclude that this subtraction method is useful for evaluating left ventricular asynergy.

[Two-dimensional echocardiography in ventricular septal rupture after acute myocardial infarction].

We studied the echocardiographic findings of 11 patients with proven ventricular septal defect following acute myocardial infarction. There were seven men and four women whose ages ranged from 48 to 77 years, with an average of 66 years. Nine patients had acute anterior and two acute inferior myocardial infarctions. Two-dimensional echocardiography (2DE) was performed for eight patients and M-mode echocardiography for all 11 patients. In all eight patients with apical four-chamber view, in whom four had additional apical short-axis view, the septal defect was directly visualized, but it was not detected by M-mode echocardiography. The defect was visualized in the apical region of the septum in all eight patients by the apical four-chamber view. The anteroapical region of the septum was the site in three with anterior infarction and the inferoapical region in one with inferior infarction by the apical short-axis view. In five of the eight patients who underwent 2DE, surgical or autopsy confirmation of the defects was obtained, with a complete agreement with the echocardiographic findings. In two patients with echocardiographic findings of septal defects, the perforations were confirmed at surgery. Two cases with aneurysmal bulges of thin septum into the right ventricle had the thin necrotic muscle in the anteroapical regions. One patient with a cystic bulge into the septum showed an irregular tear in the inferoapical region of the septum at surgery. In eight patients, the left ventricular wall motion was assessed by 2DE. Six patients revealed hyperkinetic motion in the non-infarcted areas of the basal septum or posterior wall, and these cases had good prognosis. We concluded that 2DE is a sensitive, prompt and safe technique for diagnosing and observing the risk of complicating septal defects in acute myocardial infarction. In this respect, both the apical four-chamber and short-axis views should be utilized for the topographic diagnosis of the defect.

[Two-dimensional echo-Doppler technic for evaluating dissecting aneurysms using the paravertebral approach].

Cross-sectional echocardiography facilitates recognizing dissecting aortic aneurysms, but the diagnosis of abnormalities of the descending aorta in the retrocardiac portion is difficult. We prospectively designed to assess the usefulness of a new echocardiographic technique in defining the retrocardiac descending thoracic aorta in its long and short axes. Two patients with dissecting aneurysms involving the retrocardiac descending aorta were studied in the 90 degrees right lateral position using a Toshiba SSH-11A or SSH-40A cross-sectional echocardiographic apparatus. The transducer was positioned in the third or fourth intercostal space closely to the left of the thoracic vertebrae, and the ultrasonic beam was directed toward the retrocardiac descending aorta from the patient's back. The descending thoracic aorta was identified in its long axis as a straight tubular structure with parallel walls. The transducer was then rotated approximately 90 degrees, to visualize the descending aorta in its short axis as a circular structure. This "paravertebral approach" has not previously been reported. In both patients, the retrocardiac descending thoracic aorta was clearly visualized in its long and short axes, and the oscillating intimal flap was visualized within the descending aorta in the paravertebral approach. Pulsed Doppler echocardiography (PDE) using the long-axis paravertebral approach identified the flow in the false and true lumens of the descending thoracic aorta. Flow patterns including the peak flow velocity and the velocity profile obviously varied between the true and false lumens. The peak flow velocities in the former were extremely high compared to those in the latter. The former exhibited laminar profiles, but the latter showed some spectral broadening. By the same approach, the entrance tear was explored and the jet flow through the tear was detected in Case 1 by PDE, which had high flow velocity with wide spectral broadening and aliasing in systole and also had relatively low flow velocity with some spectral broadening in diastole. To our knowledge, there has been no previous report of detecting flow at the entrance tear by PDE. These cross-sectional echocardiographic studies suggest that the paravertebral approach may prove helpful in initially evaluating patients with symptoms or signs suggestive of acute dissecting aneurysms. However, comprehensive studies are necessary to define the sensitivity and specificity of these echocardiographic techniques in recognizing all types of dissecting aneurysms.

[Scintigraphic detection of thrombi using indium-111-labeled autologous platelets].

Intracardiac and arterial thrombi were examined by scintigraphy using In-111-oxine labeled autologous platelets. In 22 cases of myocardial infarction including six with ventricular aneurysms, four had positive findings of thrombi on imaging and detected also by echocardiography. All four had ventricular aneurysms. The so-called "moya-moya" echoes (fuzzy echoes) were demonstrated in two of these four cases. We encountered two cases with positive findings on imaging in 13 with mitral valve disease. These two had systemic embolic episodes after scintigraphic examination. "Moya-moya" echoes were detected in the left atrial cavity in four with negative findings on imaging. Positive images were obtained in two of three with acute arterial occlusive disease, and in both cases platelet deposition was observed in the proximal site of obstruction. Though thrombectomy was performed for one of these two cases, no thrombus was detected at the site of platelet deposition. After one month, re-examination revealed only negative findings in all sites in both these patients. In the six cases of aortic aneurysm, three had platelet deposition within their aneurysms, and surgery was performed for these positive cases, but one of them had no thrombus. Positive images were obtained in only one of seven patients with chronic arterial occlusive disease. Coagulation tests and platelet studies were investigated for patients with positive or negative platelet scans. Only the data of the thrombo-test showed a significant difference (97 +/- 9% vs 23 +/- 7%, p less than 0.001). Three cases of positive imaging became negative after anticoagulant therapy. We tried ECT for eight cases 24 hours after injection of In-111-oxine labeled platelets. Three cases showed clear images of thrombi, while the planar images could not detect them at an early stage. Therefore, we propose that ECT can be a useful technique for diagnosing intracardiac thrombi in early stage.

[Pulsed Doppler echocardiographic evaluation of so-called "moyamoya" echoes in left ventricular aneurysms].

So-called "moyamoya" echoes identified by two-dimensional echocardiography (2 DE) in two cases with ventricular aneurysm were studied by pulsed Doppler echocardiography. The results were as follows: The flow velocity patterns in the left ventricle obtained by pulsed Doppler method were consistent with those observed by the real time 2DE method; the moyamoya echoes moved in a slow, circular fashion, and only a flow with slow velocity toward the transducer was recorded in the posterior area, whereas only a flow with slow velocity away from the transducer was recorded along the interventricular septum during cardiac cycle. The ejection flow velocity at the left ventricular outflow tract was markedly diminished. The flow velocity of the moyamoya echoes was extremely decreased and ranged between 50 and 135 mm/sec. The velocity measurements by M-mode and pulsed Doppler echocardiography gave almost the same values. Thus, the results of the present report suggest that the moyamoya echoes behave like moving blood cells, and that the source of these echoes is the sludging in the stasis of blood.

[Echocardiographic study of right ventricular performance by acute and chronic pressure overloadings].

Echocardiographic analysis of right ventricular ejection time (RVET), pre-ejection time (RVPEP), RVPEP/ET and isovolumic relaxation time (RVIRT) was performed in patients with acute or chronic right ventricular pressure overloading. Fifty-five patients undergoing right ventricular cardiac catheterization, were categorized into seven groups; 11 patients with atrial septal defect (ASD) without pulmonary hypertension (PH) (group 1), 12 with ASD with PH (group 2), six with mitral stenosis (MS) without PH (group 3), nine with MS with PH (group 4), seven with primary pulmonary hypertension (PPH) (group 5), seven with acute pulmonary embolism (PE) (group 6), and three patients with convalescence of PE (group 7). Corrected RVIRT (RVIRTc) and RVET (RVETc) were calculated by regression analysis correlating with heart rate in normal subjects. RVIRTc, RVETc, RVPEP and RVPEP/ET in seven groups were significantly correlated with systolic pulmonary artery pressure (SPAP) (r = 0.62, p less than 0.001; r = -0.41, p less than 0.01; r = 0.61, p less than 0.001; r = 0.65, p less than 0.001, respectively), but RVDd did not correlate with SPAP (r = 0.370, p less than 0.05). Comparing acute right ventricular pressure overloading group (group 6) with each of chronic right ventricular pressure overloading groups (groups 2, 4, 5, and 7), RVIRTc and RVDd were significantly increased in the former than the latter, but RVETc, RVPEP and RVPEP/ET were not significantly different in both groups. There was a significant correlation between RVIRTc and RVPEP/ET in chronic pressure overloading, but not in acute pressure overloading. We concluded that early diastolic RV relaxation and systolic performance were both impaired by increased afterload in chronic pressure overloading. In acute pressure overloading, however, early diastolic RV relaxation was more significantly impaired possibly because of acute changes of muscle architectures due to acute right ventricular expansion and anoxia.

[Echocardiography in superacute phase of myocardial infarction: an experimental study].

The significance and usefulness of two-dimensional echocardiography (2DE) in the evaluation of superacute phase of myocardial infarction were studied in 13 dogs with coronary occlusion, and 2DE findings were compared with the hemodynamic indices. Myocardial infarction was produced by the occlusion of anterior descending branch of the left coronary artery in 13 anesthetized adult mongrel dogs. In 6 dogs, the end-diastolic area and percent fractional shortening (%FS) in each short-axis view of the left ventricle at the level of the mitral valve, chordae tendineae, papillary muscles, low papillary muscles and apex were measured during 60 minutes, and end-diastolic wall thickness of infarct area situated in the transitional zone between the septum and the anterior wall were compared with that of non-infarct area immediately and subsequent 60 minutes after occlusion. Positive dP/dt/P, time constant T and cardiac output were measured simultaneously with an echocardiographic study. Severe enlargement and expansion of the left ventricular cavity (ballooning) and a decrease of %FS and thinning of the left ventricular wall perfused by the occluded artery occurred immediately after occlusion and persisted during subsequent 60 minutes. Time constant T was significantly prolonged, while positive dP/dt/P and cardiac output were decreased immediately and continued up to 60 minutes after occlusion. 2DE findings corresponded well with the changes of cardiac function and hemodynamics determined simultaneously. We concluded that the detection of the left ventricular ballooning is important in the diagnosis of superacute phase of myocardial infarction in dogs.