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Biomedical subjects

A S Lew

Publications and source records attributed to A S Lew.

At least 19 recordsLinked to original sources
PubMed1990

Critically ischemic myocardium in clinically stable patients following thrombolytic therapy for acute myocardial infarction: potential implications for early coronary angioplasty in selected patients.

The utility of post-thrombolysis, rest-redistribution thallium (TI)-201 scintigraphy was studied in 32 patients with a first myocardial infarction who were clinically stable following reperfusion. Day 1 scintigraphy obtained 5 +/- 4 hours (range 1 to 16) after thrombolysis revealed an average perfusion defect of 6.5 +/- 2.6 segments (range 1 to 11). There was a total of 208 abnormal segments, 137 of which were nonreversible at 4 hours, 50 of which were fully or partially reversible, and 21 of which had a reverse redistribution pattern. Repeat TI-201 scintigraphy on day 10 revealed significantly smaller perfusion defects of 4.9 +/- 2.4 segments (range 0 to 9) with improvement predominantly of the day 1 reversible segments, and the improvement in segmental perfusion correlated with better regional left ventricular function. Twenty-nine (58%) of the 50 reversible segments normalized by day 10, and 11 (22%) improved, whereas only 16 (12%) of 137 nonreversible segments had normalized by day 10, only 9 had (6%) improved and 112 (82%) were unchanged (p less than 0.001 reversible versus nonreversible). There was no significant change in segments with a pattern of reverse redistribution. The improvement of reversible segments was greater in the 16 patients who underwent coronary angioplasty (PTCA) during the interval between the two scintigrams than in the 16 who did not. All 24 reversible segments in the PTCA group improved or normalized by day 10 compared with 16 (62%) of 26 reversible segments in the No PTCA group (p less than 0.001). Furthermore, 8 of the 10 reversible segments in the No PTCA group that did not improve actually deteriorated and became nonreversible by day 10. The minor improvement of nonreversible segments was not related to PTCA. Consistent with the findings in individual segments, the 19 patients with a reversible component on the day 1 TI-201 scintigram had significantly greater improvement in perfusion defect by day 10 than the 13 patients without a reversible component (37 +/- 33% versus 7 +/- 22% decrease in perfusion defect severity, p less than 0.05), and this improvement was greatest in the 10 patients with a reversible component who underwent PTCA. In contrast, PTCA had no impact on the perfusion defect in the 13 patients without a reversible component. Our data suggest that following thrombolytic therapy for acute myocardial infarction, viable myocardium in the reperfused zone may remain ischemic, as manifested by a reversible pattern of TI-201 redistribution at rest, and thus may be in jeopardy of gradual progression to necrosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Decreased incidence of ventricular late potentials after successful thrombolytic therapy for acute myocardial infarction.

In some patients with acute myocardial infarction, low-amplitude potentials that prolong the QRS complex, termed "late potentials," can be recorded on a signal-averaged electrocardiogram. The presence of these late potentials is known to be associated with an increase in the risk of ventricular tachycardia and sudden death. Because patients with acute myocardial infarction who receive thrombolytic therapy have a reduced incidence of ventricular tachyarrhythmia and sudden death, we sought to determine whether such patients also have a decreased incidence of late potentials. We studied 106 patients less than 75 years of age who were admitted with a first myocardial infarction and in whom a signal-averaged electrocardiogram was recorded within 48 hours of admission. Within four hours of the onset of chest pain, tissue plasminogen activator (t-PA) was given to 44 patients, and 62 were treated conventionally. In the t-PA group, late potentials were recorded in 2 of 44 patients (5 percent), as compared with 14 of 62 (23 percent) in the conventionally treated group (P = 0.01). Furthermore, among the patients treated with t-PA, continued occlusion of the infarct-related artery was related to the presence of late potentials. In the t-PA group, late potentials were recorded within 24 hours of angiography in 2 of the 6 patients with an occluded infarct-related artery, as compared with none of the 38 patients with a patient infarct-related artery. Our data suggest that successful thrombolytic therapy is associated with a marked reduction in the incidence of late potentials on the signal-averaged electrocardiogram. Long-term follow-up will be required to determine whether this finding predicts a reduced incidence of subsequent ventricular tachyarrhythmia and sudden death.

Cardiac Pacing, Artificial↗
PubMed1989

Exercise-induced ischemia in the streptokinase-reperfused myocardium: relationship to extent of salvaged myocardium and degree of residual coronary stenosis.

To assess the functional significance of residual stenosis at the site of the thrombolysed infarct-related coronary artery, 37 patients underwent exercise radionuclide ventriculography or stress-redistribution thallium-201 scintigraphy at an average of 7 weeks following streptokinase therapy during evolving myocardial infarction. The size of the initially jeopardized myocardium and the salvaged myocardium were quantitated on thallium-201 studies obtained immediately before and 10 days after streptokinase infusion. Exercise-induced ischemia (defined by reversible thallium-201 perfusion defects or stress-induced deterioration of regional wall motion) in the reperfused myocardium was absent in 46% of patients and was present in different degrees in the remaining 54%. A significantly lower proportion of patients, however, showed exercise-induced chest pain and/or ST segment depression (10% and 20%, respectively). By stepwise multiple logistic regression analysis, the quantitatively determined size of the salvaged myocardium (398 units versus 65 units, p less than 0.01) and the ratio of the salvaged myocardium/extent of initially jeopardized myocardium (70% versus 28%, p less than 0.01) were both independent predictors of stress-induced ischemia, whereas the extent of initially jeopardized myocardium (585 units versus 407 units, p = NS), incidence of greater than or equal to 99% coronary stenosis (37% versus 46%, p = NS), and ischemic time (160 versus 196 minutes, p = NS) did not provide additional predictive information. We conclude that exercise-induced ischemia, which is frequently present in the streptokinase-reperfused myocardium, cannot be detected accurately by exercise-induced chest pain or ST segment depression, nor can it be predicted by the severity of residual coronary stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

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)

Coronary Circulation↗
PubMed1987

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)

Adult↗
PubMed1987

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.

Arterial Occlusive Diseases↗
PubMed1987

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.

Ancrod↗
PubMed1987

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)

Cardiac Complexes, Premature↗
PubMed1987

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)

Acute Disease↗
PubMed1987

Acute myocardial infarction during streptokinase therapy.

A 45-year-old man developed sequential inferolateral and anterior myocardial infarctions within 10 hours of a possible allergic reaction to oral penicillin. The anterior myocardial infarction occurred during apparently successful streptokinase therapy for the initial inferolateral infarction. Subsequent coronary arteriography confirmed a subtotal stenosis of the left circumflex coronary artery and a complete thrombotic occlusion of the left anterior descending artery. This case documents the occurrence of three rare clinical phenomena; first, the occurrence of sequential acute myocardial infarctions in close temporal proximity; second, the occurrence of myocardial infarction during thrombolytic therapy; and third, the association of myocardial infarction with a possible allergic reaction.

Anaphylaxis↗
PubMed1987

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)

Adult↗
PubMed1987

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)

Adult↗
PubMed1987

Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion.

Seven of 214 patients (3%) with acute myocardial infarction (120 inferior and 94 anterior) developed atrial fibrillation within 3 hr of the onset of chest pain. All seven patients had an inferior infarction and in all seven the left circumflex artery was occluded proximal to the origin of its left atrial circumflex branch. In five patients this occlusion was acute and was the cause of inferior infarction and in the remaining two patients the occlusion was old and the inferior infarction was due to an acute occlusion of the right coronary artery that also supplied extensive collaterals to the previously occluded left circumflex artery. All seven patients also had impaired perfusion to the atrioventricular nodal artery, as evidenced by total occlusion proximal to its origin or by stenosis proximal to its origin associated with second- or third-degree atrioventricular block. In contrast, early atrial fibrillation did not occur in any of the 18 patients with inferior myocardial infarction due to acute occlusion of the distal left circumflex artery or in any of the five patients with inferior infarction due to acute occlusion of the proximal left circumflex artery if perfusion to the atrioventricular nodal artery was not impaired. Early atrial fibrillation did not occur in any of the 90 patients with inferior infarction due to acute occlusion of the right coronary artery, including 12 patients with occlusion proximal to the sinus nodal artery, but without coexistent occlusion of the left circumflex artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

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.

Algorithms↗
PubMed1986

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)

Coronary Circulation↗
PubMed1986

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.

Adult↗
PubMed1986

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.

Animals↗