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Biomedical subjects

A T Weiss

Publications and source records attributed to A T Weiss.

At least 19 recordsLinked to original sources
PubMed1991

Clinical, psychological and thallium stress studies in patients with chest pain and normal coronary arteries.

The clinical and psychological profiles of 36 consecutive patients with chest pain and normal coronary arteries (study group) were compared to those of 34 patients with chest pain and significant coronary arterial disease (control group). All 70 patients were hospitalized for chest pain at least once prior to coronary angiography. The features of a typical episode of chest pain were similar in the normal coronary arteries and coronary arterial disease groups, but the female patients with normal coronary arteries had a shorter duration of a typical episode of chest pain, and the male patients with normal coronary arteries had a lower frequency of positive effort tests. Psychological testing showed the women with normal coronary arteries to have a tendency to increased somatization, anxiety, and a lower ability to identify origin of difficulties. The patients in the normal coronary and coronary arterial disease groups had psychological profiles typical of patients with chronic somatic disease. A psychiatric interview demonstrated an increased frequency of depressive trait (score 0-2) in the normal women (0.6 +/- 0.8 vs 0, P less than 0.05), and a tendency to increased somatization, anxiety, and sleeping disorders. Increased somatization was found in the normal coronary men (1.1 +/- 0.7 vs 0.5 +/- 0.7, P less than 0.05). Twenty-five patients of the normal coronary group underwent quantitative thallium stress studies, and 13 patients (52%) had evidence of stress-induced myocardial perfusion defect. There were no differences in the clinical and psychological profiles of the patients with normal and those with pathological thallium stress tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Chest Pain↗
PubMed1990

Partial resistance to anticoagulation after streptokinase treatment for acute myocardial infarction.

This study examines the response of 3 different groups of patients to anticoagulants: 50 patients previously treated with streptokinase for acute myocardial infarction (AMI) (group 1), 24 patients with AMI who had received anticoagulants without prior thrombolysis (group 2) and 11 subjects who received anticoagulants for noncoronary indications (group 3). No significant differences were detected between groups 2 and 3; therefore, they were combined for analysis. After streptokinase, patients required 37,755 +/- 1,516 (mean +/- standard error of the mean) U of heparin per day to achieve the desired activated partial thromboplastin time (APTT). The dosage was 30,294 +/- 1,089 U/day in patients without antecedent thrombolysis (p less than 0.001). Group 1 patients required 5 +/- 0.4 days until adequate anticoagulation was achieved, compared with 3 +/- 0.2 days in the control group (p = 0.01). Despite higher heparin requirements, group 1 patients had a lower APTT value than the other subjects (87 +/- 5 vs 101 +/- 6 seconds, p = 0.08). Group 1 patients required 5 +/- 0.3 days to reach anticoagulation with warfarin versus 4 +/- 0.2 days in groups 2 + 3 (p = 0.05). Comparison of groups 1 and 2 yielded similar, although smaller, differences. Patients treated with streptokinase for AMI seem to be partially resistant to anticoagulation, which may increase the risk of reocclusion.

Anticoagulants↗
PubMed1990

Systemic embolization following thrombolytic therapy for acute myocardial infarction.

We describe a patient with acute inferior myocardial infarction who developed a "saddle" aortic embolus during streptokinase infusion. Three months previously, this patient had sustained an anterior infarction, and an apical aneurysm was found. This patient's embolus had most probably originated from a left ventricular mural thrombus that had been dislodged by streptokinase. As fibrinolytic treatment is gaining wide acceptance, physicians should be aware of this rare, but possible, complication.

Aged↗
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↗
PubMed1989

Evidence of prolonged myocardial dysfunction in heat stroke.

Heat stroke is a life-threatening syndrome of multi-organ dysfunction caused by elevated body temperature. It may result from failure of the thermoregulatory mechanisms or from inadequate heat dissipation and affects members of several risk groups. A number of authors reported cardiac involvement in heat stroke, but heart failure rarely has been documented. We report the cases of two heat stroke victims, one of whom developed pulmonary edema and the other, peripheral edema. In both, RVG demonstrated dilatation and diffuse hypokinesis of the right ventricle, which persisted for several weeks. We conclude that the heart may be involved in heat stroke and that heart failure is a potential complication of the syndrome that can have a prolonged subclinical course. Fluid replacement in heat stroke should be done under careful observation, which may be facilitated by noninvasive assessment of cardiac function.

Adolescent↗
PubMed1988

Early prediction of left ventricular function in streptokinase-treated acute myocardial infarction.

We administered 750,000 units of intravenous streptokinase to 121 consecutive patients experiencing their first acute myocardial infarction within 4 h of pain onset. The following information was collected: hours between pain onset and streptokinase administration (TS), hours of pain after streptokinase administration (DP), initial and peak creatine phosphokinase levels (ICK and PCK), time to peak creatine phosphokinase, time to electrocardiographic ST segment resolution. Six days after the infarction, catheterization was performed to calculate ejection fraction, infarct-related regional ejection fraction, and dysfunction index. Data was analyzed using stepwise multiple regression. In patients experiencing anterior infarctions, the following equation was obtained predicting the ejection fraction (EF) with a correlation coefficient of 0.86: EF = 69 - 0.0050(PCK) - 3.7(TS) - 1.8(DP). In anterior infarctions the infarct-related ejection fraction and dysfunction index were similarly predictable. We were slightly less accurate in forecasting the outcome of inferior infarctions. The outcome of intravenous streptokinase therapy can be predicted early in the evolution of acute myocardial infarction using routinely available information.

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

Prehospital coronary thrombolysis. A new strategy in acute myocardial infarction.

Thirty-four patients with acute myocardial infarction were treated prospectively using a new strategy of prehospital intravenous streptokinase given by a physician-operated mobile intensive care unit. The 29 prehospital-treated patients who had experienced no previous myocardial infarction were compared to a similar group treated with streptokinase inhospital. Patients receiving streptokinase in the prehospital phase of acute myocardial infarction had smaller infarcts and better residual myocardial function than the group given streptokinase inhospital in terms of peak creatinine phosphokinase, ejection fraction, computer-derived dysfunction index, and electrocardiographic QRS score. The only difference between these groups at baseline was the duration of pain prior to initiation of streptokinase therapy. There were no major complications related to prehospital administration of streptokinase.

Aged↗
PubMed1987

Influence of vessel involvement and early streptokinase therapy on regional and global left ventricular function in acute myocardial infarction.

150 consecutive patients with acute myocardial infarction received 750,000 units of intravenous streptokinase within four hours of pain onset. Angiography was performed on day 6, from which ejection fraction (EF), infarct-related ejection fraction (IREF), and non-infarct related ejection fraction (NREF) were calculated. 50% stenosis was considered to be significant. The streptokinase patients with patent infarct-related arteries who had no evidence of previous myocardial infarction were compared with 82 conventionally treated (without streptokinase) patients who had no evidence of previous myocardial infarction. Sub-group analysis based on vessel involvement, usage and timing of streptokinase was done. Streptokinase was associated with better left ventricular function in all sub-groups if given less than 2 hours after pain onset. In inferior myocardial infarction, streptokinase patients with single-vessel disease had normal EF (67 +/- 8), compared to significantly depressed EF in multi-vessel disease (56 +/- 12, p less than 0.05). This difference is accounted for more by the NREF than the IREF. In anterior infarction, patients with single-vessel disease did only slightly better than multi-vessel disease. In multi- and single-vessel anterior infarction, preservation of function by streptokinase appears to be due to the compensatory ability of the non-infarcted region as well as the residual function of the infarct-related region. region.

Cardiac Output↗
PubMed1987

Early treatment of acute myocardial infarction with intravenous streptokinase. A high-risk syndrome.

Fifty-one successive patients treated with intravenous streptokinase 1.7 +/- 0.8 (mean +/- SD) hours after onset of symptoms of acute myocardial infarction were evaluated during a three-month posthospital follow-up period. Coronary angiography was performed four to nine days after the initial hospital admission. Twenty-eight patients had a second late angiogram. Forty-one patients had successful reperfusion but only 25% of all patients were without significant clinical cardiovascular manifestations during this period. Postmyocardial infarction angina pectoris occurred in 21 patients, an abnormal stress test result was present in 28 patients, eight patients developed congestive heart failure, and five patients had reinfarction. An intervention with percutaneous transluminal coronary angioplasty or coronary artery bypass graft was performed in 15 (37%) of 41 reperfused patients. A significantly higher intervention rate was present in patients treated with streptokinase within one hour following the onset of symptoms. Early reocclusion (within three months of the infarct) was noted in patients with 60% or more residual stenosis in their infarct-related coronary artery. These patients also had a significantly greater incidence of angina pectoris. Our findings indicate that early thrombolytic therapy of acute myocardial infarction preserves myocardium, and since the infarct-related artery is patent, but narrowed, the jeopardized area is responsible for a high-risk syndrome with an increased likelihood of ischemic symptoms. An early aggressive approach may be indicated, especially for patients with greater than 60% residual stenosis in their infarct-related coronary artery.

Adult↗
PubMed1986

Importance of early initiation of intravenous streptokinase therapy for acute myocardial infarction.

The importance of timing of intravenous streptokinase (SK) administration in patients with acute myocardial infarction (AMI) was evaluated. Intravenous SK, 750,000 U, was administered within 4 hours of the onset of ischemic chest pain to 72 consecutive patients having their first AMI. Six days later, cardiac catheterization was performed to calculate global ejection fraction (EF), and computer-derived infarct-related regional EF and dysfunction index were also determined; electrocardiograms were recorded, from which QRS scores could be calculated to estimate infarct size. Of 19 patients who had an anterior AMI, 12 (63%) who received intravenous SK within 2 hours after onset of pain sustained only minimal damage in terms of global EF, infarct-related EF, dysfunction index and QRS score. All 10 patients who received SK 2 to 4 hours after pain onset had large infarcts (p less than 0.001). Of the former group, 11 of 12 patients (91%) whose pain was relieved within 1.5 hours of intravenous SK administration (presumably due to successful reperfusion) had a good outcome, whereas all 7 whose pain lasted longer did poorly (p less than 0.001). Furthermore, among patients with anterior AMI, 11 of 14 (79%) whose pain was relieved within 3.5 hours of onset had small infarcts, compared with none of the 12 patients whose pain lasted longer (p less than 0.0001). In inferior AMI, the critical time between onset of pain and initiation of intravenous SK was 1.5 hours (p less than 0.05). The timing of initiation of thrombolytic therapy and the total pain duration are critical in determining outcome in AMI, and time intervals vary depending on infarct localization.

Aged↗
PubMed1986

Radionuclide left ventricular function curve during atrial pacing in normal subjects and in patients with coronary artery disease.

We used radionuclide angiography during right atrial pacing to assess left ventricular function in 7 normal subjects and 20 patients with coronary artery disease. A left ventricular function curve relating stroke volume to end-diastolic volume was plotted for each patient. The normal pacing ventricular function curve was a straight line passing through the origin of axes. The pacing ventricular function curve was abnormal in 18 of the 20 patients with coronary artery disease, and three different shaped curves were obtained, reflecting decreased contractile force for the same end-diastolic volume during ischemia. Cardiac output and blood pressure do not change during atrial pacing, thus the Frank-Starling relationship is evaluated by this method during almost experimentally controlled conditions. Relating stroke volume to end-diastolic volume, and not end-diastolic pressure, distinguishes between overall left ventricular systolic function and left ventricular compliance.

Adult↗
PubMed1986

Pneumoperitoneum as the presenting sign of pulmonary barotrauma during artificial ventilation.

Massive pneumoperitoneum developing immediately following initiation of artificial ventilation is an unusual sign of pulmonary barotrauma, and must be distinguished from pneumoperitoneum following rupture of a hollow abdominal viscus. We present a case of massive pneumoperitoneum and scrotal pneumatocele which we attributed to pulmonary barotrauma after excluding other causes. Awareness of this entity will enable early diagnosis and avoid unnecessary laparotomy.

Barotrauma↗
PubMed1986

Bradycardia and hypotension following reperfusion with streptokinase (Bezold-Jarisch reflex): a sign of coronary thrombolysis and myocardial salvage.

Acute myocardial infarction, particularly of the inferior wall, is frequently associated with bradycardia and hypotension. This study reports the occurrence of transient bradycardia hypotension (TBH) (Bezold-Jarisch reflex) following thrombolytic therapy with intravenous streptokinase. Of the 52 patients, 42 had successful reperfusion, and 12 of the latter developed reflex TBH. The Bezold-Jarisch reflex occurred in 10 of 24 patients with inferior wall acute myocardial infarction and in 2 of 28 patients with anterior wall infarction (p less than 0.05). The reflex was associated with significantly more non-Q wave infarctions (p less than 0.05) and also with reduction of left ventricular damage, as evidenced by a lower QRS score (4 +/- 3.8 vs 8.9 +/- 5.6, p less than 0.01) and a higher ejection fraction (61 +/- 13% vs 49 +/- 16%, p less than 0.05). Patients with inferior wall acute myocardial infarction were divided into those with TBH (10 patients) and those without TBH (14 patients). TBH was associated with a significantly higher infarct-related regional ejection fraction (60 +/- 19% vs 35 +/- 18%, p less than 0.05). The results of this study confirm previous findings that reperfusion of the inferoposterior myocardium is capable of stimulating reflex TBH. Furthermore, TBH is associated with patency of infarct-related coronary arteries and myocardial salvage.

Adult↗