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The present study investigated whether the exercise-induced ST-segment elevation can predict the prognosis for patients with myocardial infarction. Among 529 patients with myocardial infarction, 411 underwent treadmill exercise testing about 5 weeks after the onset. All patients were followed up (mean [+/-SD] 54 +/- 41 months) to compare the incidence of cardiac events. One hundred and eighteen patients (22%) could not perform the exercise test due to cardiac or noncardiac limitation. Ineligibility for exercise test was most useful for risk stratification. Multivariate analysis showed that elimination from the stress test with cardiac limitation was the most significant predictor for cardiac death. Excluding the 16 patients with bundle branch block, the 395 patients were classified into four groups of ST-segment elevation (107 cases, 27%), ST-segment elevation combined with depression (22 cases, 6%), ST-segment depression (106 cases, 27%), ST-segment unchanged (160 cases, 40%). Among the various stress test abnormalities, only low exercise duration was a predictor for cardiac death. ST-depression and ST-elevation combined with depression were independent risk predictors for all cardiac events. Most patients with ST-elevation had single-vessel disease with excellent exercise capacity and low incidence of cardiac events. ST-segment elevation during exercise 5 weeks after myocardial infarction is not associated with a poor prognosis.

A 58-year-old man was involved in an automobile accident and suffered remittent fever, leukocytosis and high C-reactive protein level. He developed a diastolic murmur 2 months after the accident. Transesophageal echocardiography showed severe aortic regurgitation with a vegetation-like echo image attached to the right coronary cusp leaflet, suggesting infective endocarditis. Intensive medical treatment for 11 months did not improve the vegetation-like echo-image, so aortic valve replacement was performed. Disruption of the right coronary cusp leaflet was confirmed surgically. Prolapse had occurred as a result of disruption during diastole. The vegetation-like echo-image was considered to be the tip of this leaflet.

The prevention of left ventricular aneurysm formation and left ventricular remodeling by percutaneous transluminal coronary angioplasty (PTCA) performed 24 to 48 hours after onset of acute myocardial infarction was investigated. Left ventriculography and coronary angiography were performed in 25 patients within 24 hours of onset of acute myocardial infarction. The patients were divided into two groups; reperfusion group (n = 17) and successful PTCA group (n = 8). The reperfusion group and the PTCA group included patients whose infarct-related coronary arteries were successfully reperfused to 99%, Thrombolysis in Myocardial Infarction (TIMI) grade II or III, immediately after coronary thrombolysis. However, the reperfusion group did not include the patients with spontaneous reperfusion or reperfusion after PTCA. The PTCA group consisted of patients who underwent successful PTCA performed within 24 to 48 hours after onset of infarction (mean 28.4 +/- 6.0 hours). Non-reperfusion in the acute phase was defined as TIMI grade 0-I. The size of the ventricular aneurysm in the PTCA group was significantly reduced compared with the reperfusion group (PTCA group 4.2 +/- 8.7%, reperfusion group 27.2 +/- 6.6%; p < 0.01). The increase of left ventricular end-diastolic volume (delta LVEDVI) from the acute to chronic phases was calculated to estimate left ventricular remodeling. There was a significant difference between the two groups in delta LVEDVI (PTCA group 4 +/- 19 ml/m2, reperfusion group 19 +/- 17 ml/m2; p < 0.05). PTCA performed within 24 to 48 hours after onset in patients with acute myocardial infarction and infarct-related coronary arteries, resulting in reperfusion to 99% TIMI grade II or III immediately after coronary thrombolysis, prevents left ventricular aneurysm formation and remodeling.

Two-dimensional echocardiography was used for diagnosing coronary vasospasm during the cold pressor stress test immediately after hyperventilation in five patients with suspected vasospastic angina. The test consisted of hyperventilation for 6 min and cold water pressor for 2 min under continuous electrocardiographic and echocardiographic monitoring. Coronary angiography with intracoronary injection of acetylcholine was performed in all patients within 1 month after the stress test. During the stress test, new asynergies of both the anterior and inferior walls were seen in three of the five patients, and new asynergy of the anterior wall in the other two patients. All acetylcholine induced coronary artery spasms occurred at the same locations as the new asynergies provoked by the stress test. In three patients, wall motion abnormality occurred earlier than ST segment elevation, and the other two patients had no ST changes. Chest pain was induced in three patients and delayed in comparison to electrocardiographic and echocardiographic changes. Echocardiographic monitoring during the stress test could detect spasms unaccompanied by either ST segment changes or chest pain, and could detect multivessel coronary spasms. Hyperventilation and cold pressor stress echocardiography may be used for the diagnosis of vasospastic angina.

Dobutamine stress echocardiography was used in the diagnosis of myocardial ischemia in patients with implanted VVI pacemakers. A 69-year-old woman received a pacemaker for Mobitz II type AV block in October 1992. She had suffered from chest pain during effort since January 1993 and underwent dobutamine stress echocardiography in April 1993. Although the electrocardiogram failed to identify ischemia because of the pacemaker rhythm, ischemia of the anterior wall was revealed as a worsening of the wall motion on the echocardiogram. The coronary angiogram showed 99% stenosis of the left descending artery. A direct coronary atherectomy was performed on the lesion. A 68-year-old man received a pacemaker for sick sinus syndrome in August 1993. He had suffered from chest oppression during effort since May 1992 and underwent dobutamine stress echocardiography in October 1993. Spontaneous rhythm appeared with dobutamine infusion, but the electrocardiogram could not demonstrate ischemia because of incomparability with the rhythm at rest. Echocardiography detected a new wall motion abnormality of the inferior wall caused by dobutamine. The coronary angiogram showed 90% stenosis of the right coronary artery. PTCA was performed on the lesion. Dobutamine stress echocardiography is useful for the diagnosis of myocardial ischemia in patients with implanted pacemakers.

The mechanism of exercise-induced ST-segment elevation in previous myocardial infarction was investigated using isoproterenol infusion with atrial pacing to simulate exercise hemodynamics in seven closed chest dogs with myocardial infarction. The myocardial infarction was induced by cellulose embolization of the left anterior descending artery. One week after infarction, 1) isoproterenol 0.3 microgram/min infusion, 2) right atrial pacing alone, and 3) isoproterenol infusion after the injection of propranolol 0.5 mg/kg were performed. The heart rate was kept constant by atrial pacing during the examination. Precordial ST-segment deviation, left ventricular global and regional wall motions, lactate extraction ratio, and regional myocardial blood flow were measured. Isoproterenol induced a significant elevation of the ST-segment, i.e., the sum of ST-segment elevation at chest leads V2, V3 and V4, sigma STV234, increased from 0.32 +/- 0.11 (mean +/- SEM) to 0.82 +/- 0.22 mV (p < 0.01). However, pacing alone and isoproterenol with pretreated propranolol did not. During isoproterenol-induced ST-segment elevation, left ventricular ejection fraction increased (29.2 +/- 3.3 to 39.1 +/- 3.9%, p < 0.01), lactate extraction ratio decreased but within the normal range for lactate metabolism (30.2 +/- 7.0 to 16.7 +/- 4.2%, p < 0.01), and the inner/outer ratio of regional blood flow did not change significantly (0.81 +/- 0.18 to 0.97 +/- 0.13 in the non-infarct border area, NS; 0.37 +/- 0.04 to 0.42 +/- 0.07 in the infarct border area, NS). Isoproterenol enhanced ventricular wall motion in the border and non-infarct areas, but did not induce aggravation in the infarct area.(ABSTRACT TRUNCATED AT 250 WORDS)

Left isomerism with critical arrhythmia in a 34-year-old housewife is reported. Left isomerism is rare among adult congenital disorders. The prognosis in childhood depends on intractable heart failure, but is unclear in adulthood. We describe an adult patient with left isomerism who recovered from life-threatening arrhythmias. Transesophageal echocardiography was especially useful to identify the morphology of both atrial appendages.

The diagnostic usefulness of dipyridamole-stress two-dimensional echocardiography was assessed in 82 patients consisting of 27 patients with angina pectoris, 42 with myocardial infarction, and 13 control subjects. Two-dimensional echocardiographic monitoring was performed during dipyridamole infusion: 0.56 mg/kg for 4 minutes, then discontinuation for 4 minutes, followed by a final infusion of 0.28 mg/kg for 2 minutes. The cumulative dose was 0.84 mg/kg. Worsening or fixed wall motion abnormality with unaffected baseline indicated a positive finding. All patients underwent coronary angiography. The sensitivity and specificity of dipyridamole-stress two-dimensional echocardiography for diagnosis of significant coronary artery stenosis (> or = 75%) were 84% (58/69) and 92% (12/13), respectively. The sensitivity of this method for the branches of the coronary artery was 85% for the left anterior descending artery, 80% for the right coronary artery, and 75% for the left circumflex artery. The sensitivity for single-, double-, triple-vessel disease was 75%, 81% and 100%, respectively. The sensitivity and specificity of the dipyridamole electrocardiogram (ST depression more than 0.1 mV) were 33% (23/69) and 77% (10/13), respectively. The appearance of dipyridamole-stress induced wall motion abnormality was significantly earlier than those of chest pain and ST segment depression. Side effects were observed in 43% (35/82) of patients, but were only mild and transient. Dipyridamole-stress two-dimensional echocardiography is the best method for detecting coronary artery stenosis and predicting the localization of lesion sites.

Assessments of the significance of precordial ST segment depression in acute inferior myocardial infarction (AIMI) have yielded conflicting results. Among 92 AIMI patients admitted within 6 hrs after the onset, 65 showed ST depression, and the remaining 27 showed no ST depression. These depressions were present in all of V1-4 (right type; 17), V2-5 (middle type; 10), V3-6 (left type; 13) and V1-6 (broad type; 25). The clinical severity was Forrester subset I in the majority (89%) of patients without ST change, while complications were prevalent in patients with ST depression, especially in the right type (44% were Forrester subset II-IV). Peak CK was 2,150 +/- 399 U/L in patients without ST depression, but it was elevated to 3,172 +/- 811 in patients with ST depression, especially in the right type (4,506 +/- 499). Wall motion evaluated by echocardiography and QRS scores on ECG also revealed greater abnormality in patients with ST change. The initial right coronary angiogram on admission revealed complete occlusion in 76% of these patients with ST depression of whom all of the right type had completely occluded artery. Abnormal motion of the anterior wall, which suggests remote ischemia associated with AIMI was proved neither by left ventriculography nor echocardiography. Hospital mortality in patients with ST depression (9.2%) was as twice as high as that in those without ST depression (4.6%). We concluded that ST depression in patients with acute inferior infarction may not be indicative of remote ischemia but manifests as a mirror image of a large infarction with a complicated clinical course.

The left ventricular diastolic properties of patients with hypertrophic cardiomyopathy are impaired. Since there is degeneration or disarray of myocardial fibers in patients with hypertrophic cardiomyopathy (HCM), the rate of expansion in diastole may become asynchronous. Biplane coronary cineangiograms were performed in eight normal subjects and nine patients with HCM. The coordinates (x,y,z) of the ramifying points of the left coronary artery were measured, and the distance between any two of the points of the coronary artery was calculated (segment length). Fifteen segment lengths were calculated for each subject. Since the onsets of expansion of these 15 segment lengths were not simultaneous, they expanded at different times and the onsets of expansion occurred within a very short period of time, nearly at end-diastole. The variance (standard deviation) of the timing of expansions of these 15 segments and the rate of expansion within the late 40 msec of the isovolumic relaxation period (% delta L) were calculated. The time constant of the left ventricular pressure fall (T) in normal subjects was 41.3 +/- 7.7 (SD) msec, T in HCM was prolonged to 52.7 +/- 11.1 msec. The variance was 47 +/- 17 msec in normal subjects, but it increased to 99 +/- 26 msec in HCM. The rate of expansion again decreased in HCM (Normal 2.24 +/- 0.60 vs HCM 1.40 +/- 0.96%). The conspicuous diastolic asynchrony in the onset of expansion and the reduced rate of diastolic expansion in HCM may be the mechanism of impairing the diastolic properties of the left ventricle.