Extensive myocardial salvage and reversal of cardiogenic shock after reperfusion of the left main coronary artery by intravenous streptokinase.
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Biomedical subjects
Publications and source records attributed to D S Berman.
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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.
In 5 of 69 patients (7%) undergoing intracoronary or intravenous streptokinase treatment, the ST-segment elevations in leads V1 to V5 were caused by occlusion of the right rather than the left anterior descending coronary artery and by myocardial infarction (MI) of the right ventricular (RV) wall rather than the anterior left ventricular (LV) wall or the ventricular septum. RV involvement was documented by technetium pyrophosphate uptake, hypokinesia, dilatation and depressed RV ejection fraction. The left anterior descending artery was patent and the anterior LV wall had normal thallium-201 uptake, no technetium uptake and normal wall motion. ST-segment elevation was highest in lead V1 or V2 and decreased toward lead V5; in patients with anterior LV MI, the ST-segment elevations are usually lowest in lead V1 and increase toward the V5 lead. In contrast to anterior LV infarcts, the R waves in leads V1 to V5 did not decrease and Q waves did not evolve with progression of the MI. The ST-segment elevations in leads V1 to V5 in our patients were associated with small or absent ST-segment elevations in leads, II, III and aVF, suggesting that in other cases of RV infarction, the appearance of ST-segment elevations in leads V1 to V5 is blocked by the dominant electrical forces of the LV inferior MI. This suggestion was confirmed in a canine model. Recognition of the presence of RV infarction may be therapeutically important.
Pericardial or mediastinal hemorrhage requiring reoperation occurs in 2% to 5% of patients, usually early (0 to 48 hours), after open-heart surgery. This hemorrhage may be occult, and resulting cardiac tamponade may easily be misinterpreted as ventricular dysfunction, common early postoperatively. In such cases, appropriate and timely intervention may not occur. Of 50 patients evaluated by technetium-99m red blood cell gated equilibrium radionuclide ventriculography (RNV) because of early postoperative cardiogenic shock of uncertain etiology, 17 had unique scintigraphic images suggestive of intrathoracic hemorrhage. Of these 17, 5 had a generalized "halo" of abnormal radioactivity surrounding small hyperdynamic right and left ventricles, 11 had localized regions of intense blood pool activity outside the cardiac chambers (two with compression of single chambers), and one demonstrated marked radionuclide activity in the right hemithorax (2000 ml of blood at reoperation). Twelve patients had exploratory reoperation for control of hemorrhage as a direct result of the scintigraphic findings, three were successfully treated with fresh frozen plasma and platelet infusions along with medical interventions to optimize cardiac performance, and two patients died in cardiogenic shock (presumed tamponade) without reoperation. In the 12 reoperated patients, all were confirmed to have active pericardial bleeding. Scintigraphic localization of abnormal blood pools within the pericardium corresponded to the sites at which active bleeding was witnessed at reoperation. The abnormal bleeding was etiologically related to the tamponade state, with marked improvement in hemodynamics after reoperation. Nine additional patients were reoperated for presumed tamponade after RNV revealed an exaggerated halo of photon deficiency surrounding the cardiac chambers.(ABSTRACT TRUNCATED AT 250 WORDS)
Twenty-five patients with septic shock underwent simultaneous radionuclide ventriculography and right heart catheterization to clarify the role of the right ventricle in this syndrome. A depressed right ventricular ejection fraction (less than 38%) was present in 13 patients and was found in patients with elevated cardiac output (4 of 6 patients) and with normal or low cardiac output (9 of 19 patients). Right ventricular dysfunction was seen with or without acute respiratory failure. In eight patients, a depressed right ventricular ejection fraction was seen in combination with an abnormal left ventricular ejection fraction (less than 48%), but in five patients, right ventricular ejection fraction impairment occurred with normal left ventricular ejection fraction. There was no significant correlation between abnormal right ventricular afterload and depressed right ventricular ejection fraction. No clinical or hemodynamic finding could be used to identify patients with diminished right ventricular ejection fraction. On follow-up study in 17 surviving patients, right ventricular ejection fraction improved in 6 and was unchanged in 11. Improvement in right ventricular ejection fraction occurred more frequently in patients without pulmonary hypertension or respiratory distress. The results suggest that right ventricular dysfunction in septic shock may be more common than previously suspected. It may be caused by abnormalities in right ventricular afterload in some patients and depressed myocardial contractility in others. The findings are of therapeutic importance since interventions that diminish right ventricular afterload and increase right ventricular contractility would be appropriate in patients with septic shock and right ventricular dysfunction.
When coronary artery disease is extensive and of relatively uniform severity, regional myocardial hypoperfusion may be balanced during stress, precluding development of spatially relative perfusion defects. Assessment of the washout of thallium-201 from myocardial regions may provide diagnostic assistance in these cases because washout analysis is spatially nonrelative and hypoperfused myocardial regions manifest a slow thallium-201 washout rate. In 1,265 consecutive patients having quantitatively analyzed stress-redistribution scintigraphy, 46 had a diffuse slow washout pattern with no or a maximum of one regional perfusion defect. Thirty-two underwent clinically indicated coronary angiography, and 23 (72%) of these were found to have three vessel or left main disease. Of 30 similar patients without a diffuse slow washout pattern and with no or a maximum of one perfusion defect, only 5 (17%) had extensive coronary disease. An independent relation between diffuse slow washout and extensive coronary disease was demonstrated by a Mantel- Haentzel chi-square analysis of a wide variety of other indexes of extensive disease. A diffuse washout abnormality, even in the absence of other scintigraphic, clinical or electrocardiographic indicators, carries a high predictive value for three vessel or left main coronary artery disease. The predictive value is maintained when the exercise level achieved is submaximal. Although an infrequent occurrence (3.6% of tested patients), a diffuse slow washout pattern without other scintigraphic indications of extensive coronary disease should lead to further diagnostic testing.
To assess alternative criteria for the prediction of multivessel coronary artery disease after myocardial infarction, we compared the clinical, bicycle electrocardiographic, and radionuclide ventriculographic (ejection fraction and wall motion) responses in 110 patients undergoing coronary angiography after myocardial infarction. Ninety-seven of the 110 patients had multivessel coronary artery disease (two or more diseased vessels). Clinical or electrocardiographic abnormalities were observed in 41 of 97 (sensitivity = 43%) patients with multivessel disease, and in only two of 13 (specificity = 85%) patients without multivessel disease. The average information content of these combined clinical and electrocardiographic variables relative to perfect discrimination was 5%. Among the scintigraphic parameters, the conventional criterion for ejection fraction abnormality, a rise of less than 5% had a sensitivity of 72% and a specificity of 62% for multivessel coronary artery disease, while a fall in ejection fraction of 5% or more had a sensitivity of 39% and specificity of 92% for multivessel coronary artery disease. The presence of an exercise wall motion abnormality in the nonadjacent noninfarcted (remote) region had a sensitivity of 82% and specificity of 55% for multivessel coronary artery disease. A more stringent criterion, worsening of remote wall motion with exercise, had a sensitivity of 52% and specificity of 75%. When this latter criterion was combined with a fall in ejection fraction, the sensitivity for multivessel coronary artery disease increased to 62%, specificity remained 75%, and information content increased from 5% to 10%. We conclude that conventional diagnostic criteria for abnormal clinical, bicycle electrocardiographic, or scintigraphic results do not identify patients with additional coronary artery disease after infarction with high accuracy. Two alternative ventriculographic parameters--a fall in ejection fraction and wall motion worsening--are similar to clinical parameters in specificity, but have a higher sensitivity and information content.
Fifty-one patients with primary lung cancer were evaluated using 67Ga citrate scintigraphy with respect to detection of peripheral primary, hilar metastasis, and mediastinal metastasis. The results demonstrated the necessity for an understanding of the criteria used in considering the gallium scintigram as either positive or negative, as well as the instrumentation employed in performing the test before any meaningful sensitivity and specificity figures can be derived within a given institution. Only with this understanding can actual strategy for instituting invasive procedures be achieved.
The radionuclide ventriculographic exercise response was evaluated in three patient populations representing alternative referent standards for cardiac normality: patients with normal coronary arteriograms, healthy volunteers, and uncatheterized patients with a low probability of coronary artery disease. Disease probability was determined by Bayesian analysis of age, sex, symptoms, and the results of cardiac fluoroscopy, exercise electrocardiography, or thallium scintigraphy. A wide range of ventriculographic responses was noted in the 62 catheterized normal patients; 21 (34%) had an abnormal ejection fraction response and 22 (35%) had an abnormal wall motion response. In contrast, the ejection fraction and wall motion responses were normal in the 9 volunteers. In 90 patients (18 catheterized and 72 uncatheterized) who had low disease probability (less than 1%), abnormal responses were rare; the ejection fraction response was abnormal in only 7% and the wall motion response was abnormal in 8%. Thus, these three populations are not equivalent referent standards of normality. Volunteers and patients with low disease probability provide too strict a standard, and their use can overestimate test specificity; catheterized normal patients, on the other hand, provide too lenient a standard, and their use can underestimate test specificity.
Acute acalculous cholecystitis is a relatively rare but potentially lethal condition if not treated promptly. Since stones are not present, diagnostic procedures such as ultrasound or other radiological procedures are frequently not helpful. Tc-99m iminodiacetic acid scan results were analyzed in 11 proven cases of acute acalculous cholecystitis. All had positive tests with nonvisualization of the gallbladder giving a sensitivity of 100%. Tc-99m iminodiacetic acid cholescintigraphy is a highly reliable test and is easily performed even in acutely ill patients and should be the test of choice in all patients predisposed to and suspected of acute acalculous cholecystitis.
The value of right ventricular thallium-201 analysis in detecting proximal right coronary artery stenosis in exercise myocardial scintigraphy was analyzed in 52 patients, 27 with and 25 without proximal right coronary artery stenosis. For the detection of proximal right coronary artery stenosis, the sensitivity and specificity of thallium scintigraphic analysis were 59 and 88% for a right ventricular abnormality, 67 and 68% for a left ventricular inferior wall abnormality, and 93 and 56% for an abnormality of either. When both right and left ventricular thallium images were abnormal, all 9 patients had proximal right coronary artery stenoses, and when both were normal, 26 of 28 patients had a normal proximal right coronary artery. The sensitivity and specificity of blood pool scintigraphic variables during exercise (right ventricular ejection fraction and left ventricular inferior wall motion) were not significantly different for detection of proximal right coronary artery stenosis. Thus, the additional analysis of the right ventricle on thallium-201 stress scintigrams can improve the detection of proximal right coronary artery stenosis. When both right ventricular and left ventricular thallium scintigrams are abnormal (or normal), the ability to predict the presence (or absence) of proximal right coronary artery stenosis is very high.
Progressive redistribution of pulmonary blood flow to the lung apices occurs with increasing degrees of left ventricular failure, and correlates with increasing pulmonary capillary wedge pressure (PCWP). If similar changes in pulmonary blood volume (PBV) occur, then technetium-99m equilibrium blood pool scintigraphy, by assessing relative distribution of PBV, may allow prediction of PCWP. Therefore 30 patients being monitored with pulmonary artery balloon flotation catheters underwent imaging. PCWP was compared with the average radioactive count density arising from apical (A) and basal (B) regions of interest within the right lung, expressed as an A/B ratio. Correlation was strong for patients imaged erect, either posteriorly (r = 0.864, p = 0.001) or in the 45 degrees left anterior oblique position (r = 0.842, p = 0.001), and only slightly less impressive for patients imaged supine (r = 0.678, p = 0.001). Especially when imaging was performed with patients erect, an A/B ratio greater than unity identified with high sensitivity (100%) and specificity (83 to 88%) an abnormally elevated PCWP (greater than 12 mm Hg). Moreover, directional changes in the A/B ratio reflected concomitant changes in PCWP after intervention. Thus, analysis of lung A/B radioactive count ratios obtained by equilibrium blood pool scintigraphy may be used to evaluate PCWP.
The diagnosis of active pericardial bleeding has traditionally depended on an invasive documentation by needle aspiration, angiography, or direct inspection. Blood pool scintigraphy performed in 2 patients just before and after the development of hemopericardium revealed unique images in which acute pericardial bleeding manifested itself by an additional blood pool adjacent to the cardiac chambers. With appropriate attention to technical factors, such distinctive images should be highly specific for active bleeding into the pericardial sac.
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The relationship between the severity of coronary artery stenosis and the time to completed redistribution of thallium 201 (TI-201) defects following maximal exercise was investigated in 59 patients undergoing stress-redistribution TI-201 scintigraphy, coronary angiography, and contrast ventriculography. Multiple view TI-201 scintigrams were obtained, beginning 6 minutes (immediately post stress), less than 1 hour (early), 3 to 5 hours (average), and 18 to 24 hours (late) following intravenous TI-201 injection at peak exercise. Angiographic lesions were grouped into five levels of severity by percent stenosis. In the 107 defects which were seen on the immediate post stress images, early redistribution was noted in 15 (14%) and late redistribution was found in 23 (21%). In addition, there was a correlation (r = 0.56) between the time to completed redistribution and the severity of the coronary artery stenosis (p = 0.001). In comparison to defects with early and average redistribution, the segments contralateral to those with defects showing late redistribution more often had a critical stenosis supplying that segment. The frequency of myocardial infarction on ECG and the number of segments with akinetic and dyskinetic wall motion were less in defects undergoing late rather than no redistribution. Thus the time to completed TI-201 redistribution following stress appears to be related to the severity of stenosis in the coronary artery supplying the defect. Also, late redistribution is associated with the presence and early redistribution with the absence of a significant stenosis in the coronary artery to the contralateral segment.
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ST-segment depression in the anterior precordial leads is seen in roughly one-half of patients with first acute inferior myocardial infarction. Concomitant stenosis of the left anterior descending artery can be detected angiographically in approximately 50% of all patients with inferior infarction whether or not precordial ST-segment depression is present. The presence of precordial ST-segment depression identifies a subgroup of patients with inferior myocardial infarction who have a lower left ventricular ejection fraction and quantitatively more severe abnormalities involving the posterolateral and inferoseptal segments. The contribution of anterior wall ischemia to the genesis of the precordial pattern remains problematic; although most studies to date have not supported this viewpoint, careful quantitative thallium perfusion studies have not been done. Short-term mortality and morbidity seem less favorable in the presence of precordial ST-segment depression, but this has not been substantiated by all authors.
An abnormal increase in pulmonary thallium activity may be visualized on post-stress thallium images in patients with coronary artery disease. Because this increased pulmonary thallium activity usually disappears by the time of redistribution imaging, this study was designed to assess whether measurement of the degree of pulmonary thallium washout between stress and redistribution might improve the detection of increased pulmonary thallium activity in patients with coronary artery disease. Quantitative analysis revealed abnormal (that is, greater than 2 standard deviations of normal values) pulmonary thallium washouts in 59 (64%) of 92 patients with coronary artery disease, but in only 2 (25%) of 8 subjects with angiographically normal arteries (p less than 0.06). By comparison, the visual analysis of pulmonary thallium washout and use of initial pulmonary to myocardial thallium ratio were significantly (p less than 0.05) less sensitive in detecting abnormality in patients with coronary artery disease. Abnormal pulmonary thallium washout was related to both the anatomic extent and functional severity of disease: it occurred with greatest frequency in patients with multivessel disease and in those with exercise-induced left ventricular dysfunction (p less than 0.005). When added to the quantitative analysis of myocardial scintigraphy, the analysis of pulmonary thallium washout increased the detection of coronary artery disease from 84 to 93% (p less than 0.05), but the sample size was too small to assess specificity. Thus, the analysis of pulmonary thallium washout is a useful diagnostic variable because it: 1) provides an objective measurement of abnormal pulmonary thallium activity and is more sensitive than other methods; 2) correlates with both the extent of coronary artery disease and the degree of exercise-induced left ventricular dysfunction, and 3) improves the sensitivity of quantitative myocardial thallium scintigraphy to detect the presence of coronary artery disease.