Inferior ST segment changes during acute anterior myocardial infarction: a marker of the presence or absence of concomitant inferior wall ischemia.

The significance of inferior ST segment changes during acute anterior myocardial infarction was studied in 60 patients with acute anterior infarction who had angiographic visualization of the entire distribution of the left anterior descending artery after thrombolytic therapy with streptokinase. In 34 patients (Group 1) this artery supplied the anterior wall of the left ventricle up to or including the apex but did not reach the inferior wall; in 16 patients (Group 2) it continued beyond the apex onto the inferior wall of the left ventricle; and in 10 patients with prior inferior infarction (Group 3) it partially supplied the inferior wall of the left ventricle through collateral channels to an occluded right or dominant circumflex coronary artery. Consistent with this anatomy, evidence of inferior wall ischemia was significantly more frequent in Groups 2 and 3 than in Group 1 by thallium-201 scintigraphy (91 versus 7%) and by contrast left ventriculography (91 versus 13%). There was no difference in the magnitude of precordial ST segment elevation among the three groups but the inferior ST segment depression was significantly smaller in Groups 2 and 3 with concomitant inferior wall ischemia than in Group 1 (aVF: -0.5 +/- 0.7; -0.5 +/- 1.0; -1.8 +/- 0.8 mm, respectively; p less than 0.001) with 10 of the 26 patients in Groups 2 and 3 having an elevated or isoelectric ST segment in aVF compared with none of the 34 patients in Group 1 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiographic validation of bedside markers of reperfusion.

OBJECTIVES: We sought to validate with coronary angiography several primary and ancillary markers of reperfusion. BACKGROUND: The availability of bedside markers of reperfusion is of major importance in the thrombolytic therapy of acute myocardial infarction. However, the reliability of current markers is still controversial. METHODS: Changes in chest pain, ST segment elevation and heart rate and rhythm were assessed every 5 to 10 min for up to 3 h after initiation of recombinant tissue-type plasminogen activator therapy in 82 patients with acute myocardial infarction. Coronary angiography was performed within 24 h. RESULTS: At angiography, 69 of the 82 patients had a patent infarct-related artery with Thrombolysis in Myocardial Infarction trial (TIMI) grade 3 flow and a rapid and progressive decrease in chest pain and ST elevation. The pain resolved in 24 +/- 23 min (range 3 to 50). The ST elevation decreased by > or = 50% within 16 +/- 14 min (range 5 to 41). Accelerated idioventricular rhythm developed in 49% of patients and sinus bradycardia in 23%; conduction abnormalities and atrial fibrillation resolved. All markers appeared in close temporal proximity to the onset of an abrupt increase in plasma creatine kinase (CK) and CK-MB isoenzyme activity, a previously validated marker of the time of reperfusion. Before its final resolution, ST elevation transiently decreased and increased in 58% of patients. Comparison of one pretreatment and one posttreatment electrocardiogram significantly reduced the reliability of ST segment change as a marker of reperfusion. In 13 of 82 patients, the infarct-related artery demonstrated TIMI grade < or = 2 flow; in 9, pain and ST elevation did not lessen and CK and CK-MB activity showed no abrupt increase. The remaining four patients initially demonstrated a decrease in pain and ST elevation; however, within 3 h and before angiography, the recurrence of pain and ST elevation suggested reocclusion. CONCLUSIONS: A rapid and progressive decrease in pain and ST elevation is a reliable marker of reperfusion with TIMI grade 3 flow. Because ST elevation and pain often fluctuate before undergoing final resolution with reperfusion, frequent or continuous monitoring of ST elevation is essential for reliable recognition of the fact and time of reperfusion. Accelerated idioventricular rhythm and episodes of sudden sinus bradycardia, although specific to reperfusion, do not occur in all patients with reperfusion.

Clinical failure of streptokinase due to an unsuspected high titer of antistreptokinase antibody.

Neutralization of streptokinase by an unsuspected high titer of antistreptokinase antibody prevented activation of the fibrinolytic system and induction of a lytic state in a 62 year old man with an acute inferior myocardial infarction. There was no decrease in serum fibrinogen, minimal decrease in serum plasminogen and only a small increase in serum fibrin degradation products after intravenous administration of 1.5 million units of streptokinase. A high titer of antistreptokinase antibody, sufficient to neutralize 1.5 million units of streptokinase, was demonstrated by semiquantitative counterelectrophoresis . There was no clinical evidence of coronary artery reperfusion, and coronary angiography confirmed complete occlusion of the left circumflex artery.

Elevated serum D dimer: a degradation product of cross-linked fibrin (XDP) after intravenous streptokinase during acute myocardial infarction.

D dimer, a degradation product of cross-linked fibrin, is generated by lysis of fibrin but not by lysis of fibrinogen and can be reliably detected by specific monoclonal antibody techniques. The generation of D dimer after intravenous streptokinase in acute myocardial infarction was studied with the use of a semiquantitative latex agglutination immunoassay. This assay utilizes the monoclonal antibody DD-3B6/22, raised by conventional hybridoma technology, against a highly purified preparation of human D dimer and is adjusted to give a positive agglutination at a D dimer serum concentration of greater than 200 ng/ml (upper limit of normal). Twenty-one patients with acute transmural myocardial infarction of less than 3 hours' duration were studied. Fifteen patients received 0.75 to 1.5 million U intravenous streptokinase and 6 patients were treated conventionally without thrombolytic therapy. An elevated serum level of D dimer was detected before treatment in only 1 of 15 patients receiving intravenous streptokinase and within 2 hours of treatment in the remaining 14 patients who received streptokinase. In contrast, an elevated serum D dimer level was not detected during the first 24 hours in any of the six conventionally treated patients, including two patients who manifested the clinical syndrome of spontaneous reperfusion. The data suggest that in patients with acute myocardial infarction, an elevated serum level of D dimer, a cross-linked fibrin degradation product occurs early after administration of a large dose of streptokinase, but is infrequent during the first 24 hours in conventionally treated patients with acute infarction. Measurement of D dimer may be potentially useful for monitoring thrombolysis in patients with acute myocardial infarction.

Precordial ST segment depression during acute inferior myocardial infarction: early thallium-201 scintigraphic evidence of adjacent posterolateral or inferoseptal involvement.

To investigate the myocardial perfusion correlates of precordial ST segment depression during acute inferior myocardial infarction, a rest thallium-201 scintigram and a closely timed 12 lead electrocardiogram were obtained within 6 hours of the onset of infarction in 44 patients admitted with their first acute inferior myocardial infarction. Thirty-six patients demonstrated precordial ST segment depression (group 1) and eight did not (group 2). A perfusion defect involving the inferior wall was present in all 44 patients. Additional perfusion defects of the adjacent posterolateral wall (n = 20), the ventricular septum (n = 9) or both (n = 6) were present in 35 of 36 patients from group 1 compared with only 1 of 8 patients from group 2 (p less than 0.001). There was no significant difference in the frequency of multivessel coronary artery disease or disease of the left anterior descending artery between group 1 and group 2 or between patients with and those without a thallium-201 perfusion defect involving the ventricular septum. Thus, precordial ST segment depression during an acute inferior myocardial infarction is associated with thallium-201 scintigraphic evidence of more extensive involvement of the adjacent posterolateral or inferoseptal myocardial segments, which probably reflects the extent and pattern of distribution of the artery of infarction, rather than the presence of coexistent multivessel coronary artery disease or disease of the left anterior descending artery.

Transient ischemic dilation of the left ventricle on stress thallium-201 scintigraphy: a marker of severe and extensive coronary artery disease.

On exercise thallium-201 scintigraphy, it has been noted that the size of the left ventricle is sometimes larger on the immediate poststress image than on the 4 hour redistribution image; this phenomenon has been termed transient ischemic dilation of the left ventricle. The angiographic correlates of this finding were assessed in 89 consecutive patients who underwent both stress-redistribution thallium-201 scintigraphy and coronary arteriography. A transient dilation ratio was determined by dividing the computer-derived left ventricular area of the immediate postexercise anterior image by the area of the 4 hour redistribution image. In patients with a normal coronary arteriogram or nonsignificant coronary stenoses (less than 50%), the transient dilation ratio was 1.02 +/- 0.05 and, therefore, an abnormal transient dilation ratio was defined as greater than 1.12 (mean + 2SD). The transient dilation ratio was insignificantly elevated in patients with noncritical coronary artery disease (50 to 89% stenosis) (1.05 +/- 0.05) and in patients with critical stenosis (greater than or equal to 90%) of only one coronary artery (1.05 +/- 0.05). In contrast, in patients with critical stenoses in two or three vessels, the transient dilation ratio was significantly elevated (1.12 +/- 0.08 and 1.17 +/- 0.09, respectively; p less than 0.05 compared with all other patient groups). An abnormal transient dilation ratio had a sensitivity of 60% and a specificity of 95% for identifying patients with multivessel critical stenosis and was more specific (p less than 0.05) than were other known markers of severe and extensive coronary artery disease, such as the presence of multiple perfusion defects or washout abnormalities, or both.(ABSTRACT TRUNCATED AT 250 WORDS)

Reverse redistribution of thallium-201: a sign of nontransmural myocardial infarction with patency of the infarct-related coronary artery.

The pattern of reverse redistribution on the day 10 poststreptokinase resting thallium-201 myocardial scintigrams is a common finding in patients who have undergone streptokinase therapy in evolving myocardial infarction. To investigate this phenomenon, 67 patients who underwent streptokinase therapy were studied pre- and 10 days poststreptokinase therapy resting thallium-201 studies, poststreptokinase therapy resting radionuclide ventriculography and coronary arteriography (60 of the 67 patients). Of the 67 patients, 50 (75%) showed the reverse redistribution pattern on the day 10 thallium-201 study (Group I), 9 (13%) had a nonreversible defect (Group II) and the remaining 8 (12%) had a normal study or showed a reversible defect (Group III). The reverse redistribution pattern was associated with patency of the infarct-related artery (100%), quantitative improvement in resting thallium-201 defect size from day 1 to day 10 study (94%) and normal or near normal wall motion on day 10 radionuclide ventriculography (80% of segments with marked and 54% of those with mild reverse redistribution). In contrast, nonreversible defects were associated with significantly less frequent patency of the infarct-related artery (67%, p = 0.01), improvement in defect size (11%, p less than 0.001) and normal or near normal wall motion (21%, p less than 0.05). Group III patients were similar to Group I with respect to these variables. The quantitated thallium-201 percent washout was higher in the regions with the reverse redistribution pattern (49 +/- 15%) compared with the contralateral normal zone (24 +/- 15%, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Comparative methods for quantifying myocardial infarct size by thallium-201 SPECT.

Maximum-count circumferential profile analysis of 201TI single photon emission computed tomograms (SPECT) was employed to quantify infarct size (15) in ten dogs with acute closed chest coronary occlusion (seven left anterior descending coronary artery and three left circumflex coronary artery) who underwent rest-redistribution 201TI SPECT. The extent of hypoperfused myocardium was calculated as a percentage of slice mass on rest-redistribution 201TI SPECT. Pathologic IS was determined by triphenyl tetrazolium chloride (TTC) staining. On each tomogram, SPECT IS was defined as the % of the maximum-count circumferential profile points falling below normal. To calculate total LV infarct size, slice ISs were added to one another after each was multiplied by a coefficient K that reflected the contribution of that slice to the total left ventricular mass. K was derived from an observed relationship in normal dogs between slice fractional distance from the apex and either its actual weight, its geometric SPECT area, or its count-based SPECT area, the assessment of which was independent of edge detection. Using any of these algorithms, there was a high linear correlation between the tomographic and TTC IS. A similar algorithm was also developed from tomograms of eight normal patients. These data offer promise for the clinical noninvasive assessment of the extent of hypoperfused myocardium.

Electrocardiographic differentiation of occlusion of the left circumflex versus the right coronary artery as a cause of inferior acute myocardial infarction.

To determine whether the admission electrocardiogram can identify left circumflex or right coronary artery occlusion as the cause of an inferior acute myocardial infarction (AMI), findings from electrocardiography and coronary angiography performed within 12 hours of each other were retrospectively assessed in 41 consecutive patients with inferior AMI. All patients had ST-segment elevation in 1 or more inferior leads (II, III or aVF). Of the 12 patients with circumflex coronary artery occlusion, 10 (83%) had ST-segment elevation in 1 or more lateral leads (aVL, V5 or V6) without ST-segment depression in lead I. Similar electrocardiographic findings were noted in only 1 of 29 patients (4%) with right coronary occlusion (p less than 0.001). ST-segment depression in precordial leads V1-V3 was equally prevalent in both groups. Thus, the presence of both ST-segment elevation in 2 or more inferior leads and ST-segment elevation in 1 or more lateral leads with an isoelectric or elevated ST segment in lead I identified circumflex coronary occlusion with a sensitivity of 83%, specificity of 96%, positive predictive accuracy of 91% and negative predictive accuracy of 93%. When these criteria were prospectively applied to an additional cohort of 19 consecutive patients with inferior AMI (5 with left circumflex and 14 with right coronary artery occlusion), presence of left circumflex coronary artery occlusion was predicted with a sensitivity of 80%, specificity of 93%, positive predictive accuracy of 100% and negative predictive accuracy of 93%. Thus, the admission 12-lead electrocardiogram can assist in differentiating left circumflex from right coronary artery occlusion in patients with inferior AMI.

Mortality and morbidity rates of patients older and younger than 75 years with acute myocardial infarction treated with intravenous streptokinase.

The influence of patient age on mortality risk and on the incidence of serious hemorrhagic complications after treatment of acute myocardial infarction (AMI) with intravenous streptokinase (SK) and heparin was examined in 120 consecutive patients. No upper age limit was set for patient inclusion. The mortality rate increased abruptly in patients aged 75 years or older such that the 24 patients in that age group had a 10-fold higher in-hospital mortality rate (33% vs 3%) and 1-year mortality rate (42% vs 4%) than the 96 patients younger than 75 years. This increased mortality rate in the elderly patients was related to a 2-fold higher incidence of major hemorrhagic complications (24% vs 11%) and an increased incidence of anterior AMI, healed prior AMI, multiple-vessel coronary artery disease and extensive myocardial necrosis estimated by peak creatine kinase-MB. Hemorrhagic complications were more frequent in women than in men and in patients with diabetes mellitus or systemic hypertension; all of these conditions were more prevalent in patients aged 75 years and older than in those younger than 75 years. In contrast, the incidence of hemorrhagic complications in nondiabetic elderly men (1 of 12) was similar to the incidence of bleeding in the patients younger than 75 years. Based on our data and those from other studies reporting no reduction in mortality in elderly patients with AMI who are treated with intravenous SK, it is recommended that patients aged 75 years or older should not be routinely treated with intravenous SK.(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of residual plasma fibrinogen after intravenous streptokinase for predicting delay or failure of reperfusion in acute myocardial infarction.

The relation between the level of residual plasma fibrinogen and coronary artery reperfusion after 750,000 IU of intravenous (i.v.) streptokinase (SK) was examined in 76 patients with acute myocardial infarction. Both the frequency and rapidity of reperfusion were greater in the 53 patients in whom the residual fibrinogen level was 50 mg/dl or less (low fibrinogen) than in the 23 patients in whom it was more than 50 mg/dl (high fibrinogen). Reperfusion occurred in all 53 patients in the low-fibrinogen group, compared with only 15 patients in the high-fibrinogen group (p less than 0.001). The interval from initiation of SK to clinical signs of reperfusion was 50 +/- 34 minutes in the low-fibrinogen group and 110 +/- 54 minutes in the high-fibrinogen group (p less than 0.001). A high fibrinogen level occurred in 58% of patients who weighed more than 85 kg and in 25% of patients who weighed 85 kg or less (p less than 0.05). No patient who weighed 60 kg or less had a high fibrinogen level. The high-fibrinogen group also had a greater incidence of a high anti-SK antibody titer: 8 of 13 patients (62%) tested, compared with none of the 8 patients tested in the low-fibrinogen group (p less than 0.01). Our data indicate that a high residual fibrinogen level after administration of i.v. SK identifies patients in whom SK is relatively ineffective, probably because of inadequate dosage of inactivation of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Ratio of ST-segment depression in lead V2 to ST-segment elevation in lead aVF in evolving inferior acute myocardial infarction: an aid to the early recognition of right ventricular ischemia.

The potential value of the ratio of precordial ST-segment depression to inferior ST-segment elevation as a sign of concomitant right ventricular (RV) ischemia was examined. The study group consisted of 68 patients, admitted within 3 hours of the onset of inferior acute myocardial infarction (AMI), in whom there was no evidence of prior AMI. In 27 of the 34 patients in whom inferior AMI was the result of right coronary artery occlusion proximal to the RV branch, the magnitude of ST-segment depression in lead V2 was 50% or less of the magnitude of ST-segment elevation in lead aVF, whereas in only 3 of the 34 patients in whom the site of occlusion was either distal to the RV branch (n = 23) or in the left circumflex artery (n = 11) was this ratio 50%; in no patient was it less than 50% (p less than 0.001). All 34 patients with occlusion of the right coronary artery proximal to the RV branch also had regional or global ischemic RV dysfunction by radionuclide ventriculography, with a mean RV ejection fraction of 30 +/- 10% compared with 42 +/- 6% in patients with occlusion distal to the RV branch or in the left circumflex artery (p less than 0.001). In conclusion, in patients with evolving inferior AMI, ST-segment depression in lead V2 of 50% or less of the magnitude of ST-segment elevation in lead aVF may be a useful sign (sensitivity 79%, specificity 91%, positive predictive value 90% and negative predictive value 82%) for identifying patients with concomitant RV ischemia.

Time course and characteristics of ventricular arrhythmias after reperfusion in acute myocardial infarction.

The time course and characteristics of ventricular arrhythmias were studied in 45 consecutive patients with acute myocardial infarction who received intravenous streptokinase and underwent 24-hour Holter monitoring both after admission and before discharge 8 +/- 3 days later. In 41 of the 45 patients, thrombolytic treatment resulted in reperfusion as determined by characteristic clinical signs, i.e., rapid relief of pain associated with rapid resolution of ST-segment elevation and simultaneous abrupt increase in serum creatine kinase-MB activity. During the first 24 hours after reperfusion, the prevalence of ventricular premature complexes (VPCs) and couplets was nearly 100%, with an average frequency of 67 VPCs (range 1 to 1,336, median 44) and 6 couplets per hour per patient (range 1 to 97, median 4). Ninety percent of patients had an average of 8 runs of accelerated idioventricular rhythm per hour per patient (range 1 to 226, median 5) and 23% of the patients had an average of 2 runs of ventricular tachycardia per hour per patient (range 1 to 22, median 2) during the first 24 hours after reperfusion. The frequency of arrhythmias began to decrease 8 to 12 hours after reperfusion. Except for VPCs, ventricular arrhythmias were rare during the predischarge Holter study. Arrhythmias after reperfusion did not produce clinical symptoms and did not degenerate into ventricular fibrillation even though the patients were not receiving antiarrhythmic therapy. In the 4 patients without signs of reperfusion, the prevalence and frequency of all ventricular arrhythmias during the 24 hours after treatment was lower than in patients with reperfusion, and none had an accelerated idioventricular rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)

Efficacy of a two-hour infusion of 150-mg tissue plasminogen activator in acute myocardial infarction.

Forty-two patients with acute myocardial infarction received 150-mg recombinant human tissue-type plasminogen activator (rt-PA) at 2.3 +/- 1.2 hours after the onset of chest pain. After a 40 U/kg bolus of heparin, rt-PA was given as a 10-mg bolus followed by a 2-hour continuous infusion of 90 mg in the first hour and 50 mg in the second hour. Nonangiographic signs of reperfusion occurred during treatment (41 +/- 21 minutes) in 35 patients and in 1 other patient about 30 minutes after rt-PA. Three patients had discordant nonangiographic signs of reperfusion, 2 patients had no evidence of reperfusion and 1 patient in cardiogenic shock died before completion of the rt-PA infusion and before reperfusion status could be ascertained. Clinical signs of early reocclusion occurred in 4 of the 36 patients with evidence of reperfusion, 3 of whom were retreated with rt-PA with clinical success in 2. Coronary angiography 10 +/- 8 hours later revealed a patent artery of infarction in 35 patients: 32 with nonangiographic signs of sustained reperfusion, both patients with successfully treated reocclusion and 1 of 3 patients with discordant signs of reperfusion. Angiography revealed evidence of partial reperfusion in the remaining 2 patients with discordant signs, and an occluded artery was found in both patients without any evidence of reperfusion and in both patients with clinical signs of persistent reocclusion. Hemorrhagic complications occurred in 9 patients, 7 were related to procedural trauma and 2 patients required a blood transfusion. Four patients died, each of a cardiac cause: 3 in hospital and 1 at home.(ABSTRACT TRUNCATED AT 250 WORDS)

Intravenous streptokinase in evolving acute myocardial infarction.

Eighty-one consecutive patients presenting within 3 hours of the onset of acute myocardial infarction (AMI) and without contraindications to thrombolytic or anticoagulant therapy received a 15- to 30-minute intravenous infusion of 750,000 or 1.5 million units of streptokinase (STK) followed by anticoagulation. Treatment was instituted 130 +/- 41 minutes after the onset of symptoms and reperfusion was achieved 36 +/- 26 minutes later. Reperfusion of the "infarct artery" was recognized by indirect clinical criteria in 78 patients (96%). In all 66 patients who underwent coronary angiography 3 to 7 days later, there was complete concordance between indirect and angiographic evidence of reperfusion. In 6 patients there was early reocclusion within 24 hours of treatment; in 4 of these patients, the artery was reopened with an additional dose of STK. Two elderly patients suffered an intracranial hemorrhage and there were 8 other major hemorrhagic complications, of which 7 were related to procedural trauma. Five patients (6.2%) died in the hospital. The results of intravenous STK thrombolytic therapy are compared with those of our previous study using intracoronary STK.

Usefulness of a rapid initial increase in plasma creatine kinase activity as a marker of reperfusion during thrombolytic therapy for acute myocardial infarction.

This study evaluates a new nonangiographic marker of reperfusion--a rapid initial increase in plasma creatine kinase (CK) and CK-MB activity--in 50 patients receiving intracoronary streptokinase. Blood for CK and CK-MB activity was sampled at 30-minute intervals and angiography performed at 15-minute intervals or earlier if there were clinical signs suggestive of reperfusion. An absolute first-hour increase in CK activity of 480 +/- 345 IU/liter (range 54 to 1,440 IU/liter), or a relative first-hour increase of 34 +/- 18% (range 13 to 67% of the peak rise), or an absolute first-hour increase in CK-MB activity of 48 +/- 36 IU/liter (range 10 to 144 IU/liter) or a relative first-hour increase of 27 +/- 13% (range 13 to 57%) was found in patients immediately after reperfusion with Thrombolysis In Myocardial Infarction (TIMI) grade 3 perfusion of the artery of infarction. The onset of rapid increase in CK and CK-MB activity closely reflected the time of angiographic documentation of reperfusion. In contrast, in the absence of reperfusion, the absolute rate of increase in CK activity measured in the last hour of the 2 1/2-hour period beginning with the start of treatment was only 15 +/- 9 IU/liter on the average (range 2 to 30 IU/liter) and the relative rate of rise was 3 +/- 2% on the average (range 1 to 6%).(ABSTRACT TRUNCATED AT 250 WORDS)

Factors that determine the direction and magnitude of precordial ST-segment deviations during inferior wall acute myocardial infarction.

Sixty-one patients with inferior acute myocardial infarction (AMI) and no evidence of prior AMI were studied to determine which factors influence the magnitude of precordial ST-segment depression. In the total study group, there was a significant but weak correlation between the magnitude of precordial ST-segment depression and the magnitude of inferior ST-segment elevation (r = -0.46, p less than 0.001). In the 29 patients with evidence of concomitant right ventricular (RV) involvement, precordial ST-segment depression was significantly smaller both in absolute terms (-1.3 +/- 1.8 vs -2.8 +/- 1.9 mm, p less than 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of -0.2 +/- 1.0 vs -1.1 +/- 0.5, p less than 0.01), whereas in the 15 patients with lateral ST-segment elevation (greater than or equal to 1 mm in lead V6), precordial ST-segment depression was significantly greater both in absolute terms (-3.5 +/- 2.3 vs -1.6 +/- 1.7 mm, p less than 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of -1.1 +/- 0.8 vs -0.5 +/- 0.9, p less than 0.02). Consistent with these findings, the correlation between the magnitudes of precordial and inferior ST-segment deviations was considerably improved when only the 24 patients with neither evidence of RV involvement nor lateral ST-segment elevation were analyzed (r = 0.89, p less than 0.001, n = 24). These data suggest that in patients with inferior AMI, there is a reciprocal relation between precordial and inferior ST-segment deviations, which is distorted by concomitant RV involvement and by concomitant lateral left ventricular wall involvement.

Interaction of SK-human plasmin, SK-dog plasmin complexes with alpha 2-antiplasmin and alpha 2-macroglobulin.

In patients treated with streptokinase there is a rapid and significant decrease in the level of fibrinogen in the circulation. In dogs given streptokinase there is no such change in circulating fibrinogen. To find an explanation for this species difference in response to streptokinase, the inhibition of SK-human plasmin and SK-dog plasmin by soybean trypsin inhibitor, alpha 2-antiplasmin and alpha2-macroglobulin were compared in this study. Soybean trypsin inhibitor completely blocked the hydrolysis of S-2251 substrate (D-val-L-leu-lys-p-nitroanilide) by SK-dog plasmin and had no effect on SK-human plasmin. Alpha 2-Antiplasmin, the physiologically important regulator of fibrinolysis, inhibited S-2251 hydrolysis by SK-dog plasmin but not the activity of SK-human plasmin. alpha 2-Macroglobulin showed 100% inhibition of proteolytic activity and 50% inhibition of S-2251 activity of SK-dog plasmin, and had no effect on SK-human plasmin. Studies with fresh human and dog plasma also showed that the SK-dog plasmin is rapidly inactivated by the alpha 2-antiplasmin present in the plasma. The inactivation of SK-dog plasmin and not SK-human plasmin by plasma inhibitors explains the differences in the response of dog and humans to the administration of streptokinase.

Ancrod enhances the thrombolytic effect of streptokinase and urokinase.

Since thrombi continue to incorporate fibrin during lysis we tested the effect of pretreatment with ancrod, a defibrinating agent from Malaysian pit viper venom, on thrombolysis with urokinase and streptokinase. Thrombi were induced by copper-coils in the carotid arteries of the dogs, weighed after 1 hour and inserted into the femoral arteries of the same animals. They were then exposed for 15 min to iv boluses of streptokinase 10,000 U/kg, urokinase 10,000 U/kg and urokinase 25,000 U/kg with or without pretreatment with ancrod. Ancrod depleted fibrinogen within 5 min and enhanced the lytic effect of streptokinase from 25 +/- 8% to 59 +/- 13% (p less than .05), urokinase 10,000 U/kg from 16 +/- 11% to 66 +/- 18% (p less than .01) and urokinase 25,000 U/kg from 27 +/- 17% to 85 +/- 8% (p less than .001) of the initial thrombus weight. Ancrod itself did not activate plasminogen to plasmin. We conclude that ancrod enhances thrombolysis probably by depleting fibrinogen and preventing new fibrin incorporation into the thrombus during lysis.

Self-verification and depression among youth psychiatric inpatients.

According to self-verification theory (e.g., W.B. Swann, 1983), people are motivated to preserve stable self-concepts by seeking self-confirming interpersonal responses, even if the responses are negative. In the current study of 72 youth psychiatric inpatients (36 boys; 36 girls; ages 7-17, M = 13.18; SD = 2.59), the authors provide the 1st test of self-verification theory among a youth sample. Participants completed self-report questionnaires on depression, self-esteem, anxiety, negative and positive affect, and interest in negative feedback from others. The authors made chart diagnoses available, and they collected peer rejection ratings. Consistent with hypotheses, the authors found that interest in negative feedback was associated with depression, was predictive of peer rejection (but only within relatively longer peer relationships), was more highly related to cognitive than emotional aspects of depression, and was specifically associated with depression, rather than being generally associated with emotional distress. The authors discuss implications for self-verification theory and for the phenomenology of youth depression.