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Biomedical subjects

A S Lew

Publications and source records attributed to A S Lew.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1986

Utility of echocardiography for the early assessment of patients with nondiagnostic chest pain.

A two-dimensional (2D) echocardiogram was recorded shortly after admission in 46 patients with nondiagnostic chest pain. Eighteen patients were studied during chest pain and 28 were studied following the resolution of chest pain. Of the 18 patients studied during chest pain, six of the eight patients who had a regional wall motion abnormality (RWMA) evolved an acute infarction and the remaining two patients had evidence of significant coronary artery disease. Only 1 of 10 patients without a RWMA evolved an infarction and none had significant coronary artery disease. Of the 28 patients studied following the resolution of chest pain, 8 of the 10 patients with a RWMA evolved an acute infarction and one patient had evidence of significant coronary artery disease, whereas of 18 patients without a RWMA, none evolved an acute infarction and five had evidence of significant coronary artery disease. These data suggest that in patients presenting with nondiagnostic chest pain, an early assessment of regional wall motion by 2D echocardiography can reliably differentiate patients with myocardial ischemia or early infarction from patients with nonischemic chest pain when performed during an episode of chest pain; can also identify those patients with early acute myocardial infarction, even when performed following the resolution of chest pain; but is not useful for the detection of patients with significant coronary artery disease without infarction when performed following the resolution of chest pain.

Adult↗
PubMed1986

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.

Aged↗
PubMed1986

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)

Adult↗
PubMed1986

Enhancement of thrombolysis with tissue-type plasminogen activator by pretreatment with heparin.

The effect of pretreatment with heparin on lysis of arterial thrombi by tissue-type plasminogen activator (rt-PA) was studied in 19 dogs. Copper coil-induced carotid artery thrombi were weighed, inserted into the femoral arteries, and exposed to a 15 min infusion of rt-PA at 10 micrograms/kg/min either with (n = 6 thrombi) or without pretreatment with a 200 unit/kg bolus of heparin (n = 6 thrombi). The infusion of rt-PA without pretreatment reduced the thrombus weight by 27.6 +/- 7.4%, while infusion of rt-PA with pretreatment reduced it by 79.1 +/- 12.3% (p less than .0001). To test the hypothesis that heparin enhanced thrombolysis by preventing continued incorporation of new fibrin into the thrombus during thrombolysis we repeated the experiments using pretreatment with 8 U/kg of ancrod, which rapidly depletes fibrinogen. Pretreatment with ancrod (n = 6 thrombi) depleted fibrinogen and enhanced the lytic effect of rt-PA to a similar degree as pretreatment with heparin, resulting in a 67.6 +/- 12.3% (NS) decrease in thrombus weight. We conclude that heparin significantly enhances the thrombolytic effect of rt-PA, probably by preventing new fibrin formation and its incorporation into the thrombus during lysis.

Ancrod↗
PubMed1985

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.

Aged↗
PubMed1985

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.

Aged↗
PubMed1985

The effects of the rate of intravenous infusion of streptokinase and the duration of symptoms on the time interval to reperfusion in patients with acute myocardial infarction.

We studied the influence of the following variables on the time interval from initiation of an intravenous infusion of 750,000 U of streptokinase until reperfusion (reperfusion time) in 140 consecutive patients with an evolving acute myocardial infarction: (1) the rate of infusion of streptokinase, (2) the duration of chest pain before initiation of treatment, (3) patient age, (4) patient sex, (5) location of infarction, (6) history of previous myocardial infarction, and (7) pretreatment pathologic Q waves. The time of reperfusion was recognized by clinical criteria that were completely concordant with the anatomic findings in all 119 patients in whom patency or occlusion of the artery of infarction was established at delayed angiography (n = 116) or at postmortem examination (n = 3). The mean reperfusion time for the 129 patients for whom data were available was 49 +/- 36 min. The reperfusion time was inversely related to the rate of infusion of streptokinase (r = .41, p less than .001), but this effect of infusion rate appeared to plateau at rates of greater than 500 U/kg/min. In the 64 patients receiving infusions at rates of 500 U/kg/min or less, the mean reperfusion time was 60 +/- 40 min, whereas in the 58 patients receiving the drug at rates greater than 500 U/kg/min it was 35 +/- 22 min (p less than .001). The duration of chest pain before treatment was the only other studied variable found to influence the reperfusion time, but only at infusion rates of less than 250 U/kg/min (r = .6, p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1985

The hypotensive effect of intravenous streptokinase in patients with acute myocardial infarction.

We studied the hypotensive effect of a rapid intravenous infusion of high-dose streptokinase in 98 patients with an acute myocardial infarction. The systolic blood pressure fell from 132 +/- 20 (range 90 to 174) to 97 +/- 21 mm Hg (range 58 to 152) at 15 +/- 8 min (range 4 to 40) after the commencement of the streptokinase infusion (p less than .001). A fall in diastolic blood pressure from 80 +/- 16 (range 51 to 105) to 61 +/- 15 mm Hg (range 32 to 92) accompanied the fall in systolic pressure (p less than .001). The fall in blood pressure was associated with an increase in heart rate (73 +/- 14 to 78 +/- 17 beats/min, p less than .001), preceded the appearance of clinical signs of reperfusion by 37 +/- 38 min and was similar in magnitude and timing in patients with anterior and inferior infarction. There were direct relationships between the rate of infusion of streptokinase and both the magnitude (r = .49, p less than .001) and the rate of fall of systolic blood pressure (r = .67, p less than .001) as well as both the magnitude and rate of fall of diastolic blood pressure. In most patients, the fall in blood pressure was transient (9 +/- 6 min, range = 2 to 30) and easily managed by slowing or stopping the infusion, placing the patient in the Trendelenburg position, or by administering an infusion of low-dose norepinephrine or dopamine. However, in four patients with severe left ventricular dysfunction, severe hypotension persisted for more than 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗