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Biomedical subjects

J Agmon

Publications and source records attributed to J Agmon.

At least 55 records · Page 3Linked to original sources
PubMed1988

The natural course of electrocardiographic stages of acute inferior myocardial infarction in regard to R/Q ratio group classification.

Forty-three patients with their first acute inferior wall myocardial infarction (IWMI) were divided into three groups according to the R/Q ratio in standard lead II. This was done to correlate these groups with the characteristic course of electrocardiographic stages. The R/Q ratio was measured on the ninth day of follow-up study, and the electrocardiographic stages were followed from the onset of the IWMI up until the ninth day. Patients with R/Q greater than 2 (group I) had a more rapid progression through the electrocardiographic stages, along with a better clinical course than patients with a lower R/Q ratio. Patients in group III, with R/Q less than 1, had a slower electrocardiographic stage progression, which correlates well with a more complicated clinical course. Group II was an intermediate group in both the electrocardiographic and clinical course. Rapid stage evolution in the first 12 hours of the IWMI was followed by a more rapid progression through stages during the rest of the follow-up period. It is suggested that the R/Q ratio in lead II can be used as a marker of the severity of IWMI, since it correlates well with the course of electrocardiographic stages. The greater the R/Q ratio, the more rapid the progression of electrocardiographic stages, and the better the clinical course. This may be an additional simple and inexpensive electrocardiographic tool for following the natural course of IWMI.

Adult↗
PubMed1988

Ventricular fibrillation in a patient with 'silent' mitral valve prolapse.

A patient with clinically silent mitral valve prolapse experienced an episode of out-of-hospital cardiac arrest due to ventricular fibrillation. This arrhythmia was easily replicated in the electrophysiology laboratory and despite treatment with amiodarone alone and amiodarone in combination with propranolol. Amiodarone in combination with quinidine prevented the induction of ventricular fibrillation and proved effective during a 3-year follow-up period. Even though a clear-cut relationship between the arrhythmias and mitral valve prolapse cannot be established, this case suggests that sudden death can occur in patients with mitral valve prolapse but without the known risk factors for the development of sudden death.

Adult↗
PubMed1988

Ventricular fibrillation complicating acute myocardial infarction. Two distinct clinical and electrocardiographic features.

Two distinct electrocardiographic patterns of ventricular fibrillation (VF) complicating acute myocardial infarction (AMI) were observed in 34 patients during the first 24 hours from initial symptoms. Type 1 (seven patients) was characterized by fast disorganized ventricular activity, small voltage, and no clear identifiable QRS complexes (fine VF). Type 2 (27 patients) was defined as multiform QRS configuration (greater than 300/min) with marked changes in the amplitude (polymorphous VF). Type 1 rhythm was seen mostly during the hyperacute ischemic phase, probably associated with total coronary vessel occlusion; type 2 was observed when Q waves were already present in the electrocardiogram.

Adult↗
PubMed1988

Acute myocardial ischemia with prolonged left ventricular dyskinesia and mural thrombus formation in asymmetric septal hypertrophy.

A 52-year-old man had longstanding hypertension and asymemtric septal hypertrophy and normal major coronary arteries. His acute anterior wall ischemia gave rise to transient Q waves and septoapical dyskinesia, complicated by mural thrombus formation. Follow-up revealed a gradual and complete recovery of echocardiographic left ventricular function with total disappearance of mural thrombi and of electrocardiographic Q waves. Acute myocardial ischemia can cause prolonged electrical and mechanical stunning which can lead to mural thrombus formation.

Cardiomyopathy, Hypertrophic↗
PubMed1988

The effect of intravenous amiodarone on heart rate in patients with acute myocardial infarction or ischemia and sinus tachycardia.

The effect of intravenous (IV) amiodarone (300 mg) on heart rate was investigated in 22 patients with acute myocardial infarction (18) or ischemia (4) and sinus tachycardia. There were 11 men and 11 women (age range, 48 to 83 years; mean, 63.5). Amiodarone IV slowed the mean heart rate from 109 +/- 14 beats/min to 94 +/- 15 beats/min (p less than 0.0005). There was a linear correlation between the initial heart rate (preamiodarone) and the final heart rate (postamiodarone), (r = 0.6930, p less than 0.0005). Most of the patients with initial heart rates higher than the mean maintained relatively high heart rates (above the mean), while most patients with lower initial heart rates showed low heart rates (below the mean) after amiodarone administration. Patients in Killip class 1 showed a significant reduction in heart rate after receiving amiodarone, from a mean of 105 +/- 10 to 88 +/- 11 beats/min (p less than 0.01). Patients in Killip class 2 also had reduced heart rates (118 +/- 14 to 81 +/- 39 beats/min), but these changes were not statistically significant. Of the three patients in Killip class 3 to 4, the heart rate slowed by 10 beats/min in one, while in the remaining two no changes were observed. There were no significant side effects from the administration of amiodarone.

Aged↗
PubMed1988

Significance of the magnitude of a QS wave deflection in evaluating the uninvolved muscle in anterior wall myocardial infarction.

The significance of dynamic changes of the QS wave magnitude, as demonstrated in the precordial leads, within the natural evolution of acute anterior wall myocardial infarction (AAMI) was assessed in 25 patients within two weeks of their admission to the intensive cardiac care unit. Two sets of tests, including 12-lead electrocardiogram and a full radionuclear study, were performed in two time periods: (1) within the first 48 hours of admission; and (2) between the 12th and 15th day after admission. Comparison and correlation between the electrocardiographic data, QS waves in leads V2 and V3 and in V1 to V6 (sigma QV2-3 and sigma QV1-6), and radionuclear regional ejection fractions of the noninfarcted posterior muscle (inferior, infero-apical, and posterolateral regions and posterior index) were done. Significant linear correlations were demonstrated between the electrocardiographic variant differences in percentages (sigma QV2-3 and sigma QV1-6) and the radionuclear variant differences, especially the posterolateral and the infero-apical regions, as well as the posterior radionuclear index (r between 0.5 and 0.75; p less than 0.01). In addition, almost all of the patients who showed deepening of QS waves in the precordial leads also showed an increase in regional ejection fractions in uninvolved myocardium, and vice versa. It is concluded that the dynamic changes of the QS wave magnitude in the precordial leads within the evolution of acute anterior myocardial infarction well reflect the changes of the posterior noninfarcted muscle contraction and therefore offers a simple, inexpensive, and indirect electrocardiographic method for evaluating changes in contraction patterns of noninfarcted myocardium.

Electrocardiography↗
PubMed1988

Total lactate dehydrogenase and its isoenzymes in serum of patients with non-small-cell lung cancer.

Values for total lactate dehydrogenase (LD, EC 1.1.1.27) activity in serum and LD isoenzymes were determined at diagnosis in 273 patients with non-small-cell lung cancer, 85 of whom were in stage 1, 92 in stage 2, and 96 in stage 3. We divided the patients into three groups, based on their total serum LD values: less than 225 U/L (normal reference range), 226-500 U/L, and greater than 500 U/L. Overall values for LD were above normal at diagnosis for 69% of the patients, being moderately increased in 63 patients and highly increased in 125. Eighty percent of the patients in stage 1 had normal values for LD at diagnosis, but 88% of the patients in stage 2 and 94% of the patients in stage 3 had above-normal LD values at diagnosis. In 55% of the patients in stage 2 and 73% of the patients in stage 3, LD activity was highly increased. In the patients with normal values for total LD, the proportions of the LD isoenzymes were normal. In the patients with increased LD, the isoenzyme proportions were increased for LD-4 and LD-5, up to twice the normal values. The sensitivity of LD in detection of lung cancer was 60% for LD at the cutoff point of 250 U/L in comparison with normal controls, and 47% for LD at the cutoff point of 310 U/L in comparison with the benign lung disease group of patients (95% specificity). We conclude that total LD in serum may be a direct indicator of clinical stage and tumor burden in patients with non-small-cell lung cancer.

Adenocarcinoma↗
PubMed1988

Atypical patterns of lactate dehydrogenase isoenzymes in acute myocardial infarction.

Total lactate dehydrogenase (LD; EC 1.1.1.27) activity in serum and LD isoenzymes were quantified in 190 patients with acute myocardial infarction (AMI) 24, 48, and 72 h after admission. In 90% of the 570 blood specimens an LD isoenzyme pattern typical of AMI (LD-1/LD-2 greater than 0.76) was found. The other 56 blood specimens showed an LD isoenzyme pattern atypical of AMI (LD-1/LD-2 less than 0.76). They were divided into three groups: 28 specimens with isomorphic pattern (relative increase in all five LD isoenzymes); 18 with relatively increased LD-3 proportion (greater than 35%); and 10 specimens with increased LD-5 proportion (greater than 10%). No difference was found in mean total LD activity in serum between the typical isoenzyme group and the three atypical groups. The LD isomorphic pattern was found in 60% of AMI patients complicated by cardiogenic shock. Fifty percent of AMI patients admitted with pulmonary edema showed increased LD-3 proportion and half of the patients with AMI and congestive heart failure, predominant right, demonstrated increased LD-5 proportion. We conclude that although most patients with AMI present at diagnosis with a typical LD isoenzyme pattern, it is important to recognize that some may present with atypical LD isoenzyme patterns, which may be associated with specific AMI complications.

Adult↗
PubMed1988

Significance of isolated increases in total lactate dehydrogenase and its isoenzymes in serum of patients with bacterial pneumonia.

Total lactate dehydrogenase (LD, EC 1.1.1.27) activity in serum and LD isoenzymes were quantified at the time of diagnosis in 320 patients with bacterial pneumonia. In eighty, LD activity was increased, but this was accompanied by either other pathological results for liver-function tests or associated diseases that could explain it. The remaining 240 patients were divided into four groups, based on their total serum LD values: group A, less than 225 U/L (normal limit); group B, 226-350 U/L; group C, 351-499 U/L; and group D, greater than 500 U/L. Total LD was above normal at diagnosis in 40% of the patients. Recovery time was twice as long in group D as in groups A, B, and C. In five patients from group D, the pneumonia reflected underlying lung cancer. In groups B and C, the LD-3 ratio was increased in comparison with group A; in group D, LD-4 and LD-5 were increased up to twice the normal limit. Evidently nearly half of patients with bacterial pneumonia may show isolated increases in total LD activity (mostly LD-3) in serum. In cases with high activity, prolonged recovery time is expected. Intensive follow-up and extensive investigation are warranted in these patients, because some may have underlying lung cancer.

Aged↗
PubMed1988

The efficiency of lactate dehydrogenase isoenzyme determination for the diagnosis of acute myocardial infarction.

Values for total lactate dehydrogenase (LDH; EC 1.1.1.27) activity and LDH isoenzymes 1 and 2 were determined in 80 patients with acute myocardial infarction (AMI) and in 40 without AMI every 24 hours up to 15 days after admission, when total serum LDH level returned to normal. The sensitivity, specificity, and efficiency of three LDH isoenzyme factors (LDH-1, greater than 90 U/L; LDH-1 greater than LDH-2; LDH-1/LDH ratio, greater than 0.4) for diagnosing AMI were assessed in three groups of patients according to total serum LDH values--group A, LDH level over 600 U/L; group B, 400 to 599 U/L; group C, 225 to 399 U/L--and in five groups of patients according to the time after admission--(1) first 48 hours; (2) three to five days; (3) six to eight days; (4) nine to 11 days; (5) 12 to 15 days. All three factors were found to be highly efficient for diagnosing AMI (91.5% to 97.5%) in groups A and B, but the most efficient factor in each group was LDH-1 value above 90 U/L. In group C, the only efficient factor was the LDH-1 value over 90 U/L (96%). The most efficient factor for diagnosing AMI in relation to time after admission up to 15 days after AMI was the LDH-1 value over 90 U/L (96% to 97.5%). The factors LDH-1 greater than LDH-2 and LDH-1/LDH above 0.4 were more efficient in patients up to five days after AMI (91.5% to 97.5%) than in patients six to 15 days after admission. We conclude that the most efficient LDH value for diagnosing AMI is the absolute value of LDH-1 above 90 U/L. Its superiority over other LDH isoenzyme values is best documented in a group of patients six to 15 days after admission and with only slight to moderate elevation of total serum LDH values (225 to 399 U/L).

Adult↗
PubMed1988

Patterns of lactate dehydrogenase isoenzymes in serum of patients with acute pulmonary edema.

Total lactate dehydrogenase (LD; EC 1.1.1.27) activity in serum and proportions of LD isoenzymes were quantified on admission and discharge in 170 selected (from 240) patients with acute pulmonary edema (APE). The patients were divided into group A, 75 patients with normal LD values (less than 225 U/L); and groups B-E, with increased LD activity in serum: group B, 40 patients with increase in the proportion of LD-3 (greater than 38%); group C, 12 patients with increased LD-5; group D, 36 patients with an isomorphic pattern of LD isoenzymes; and group E, seven patients with LD-1/LD-2 greater than 0.75. Nine patients in group C (75%) had also signs of right-sided congestive heart failure, 30 in group D (83%) had hypotension on admission, and six in group E (86%) had signs of recent myocardial infarction. Evidently, half of patients with APE may show increased total LD activity in serum at the time of admission. LD isoenzyme proportions should be determined in such patients, because there is no one typical pattern of LD isoenzymes and some LD isoenzyme patterns may be associated with specific clinical situations.

Acute Disease↗
PubMed1987

Circulating aggregated platelets in coronary artery disease.

Circulating aggregated platelets were assessed in 30 patients with stable angina, 22 with unstable angina and 50 with acute myocardial infarction (AMI). Fifty healthy volunteers and 20 noncardiac patients served as controls. One milliliter of venous blood was separated into 2 solutions: 1 composed of ethylenediamine tetraacetic acid (EDTA) and formalin containing reversible and aggregates and 1 composed of EDTA alone containing irreversible aggregates only. By direct microscopic readings the percentage of platelets forming aggregates/1,000 counted platelets was determined in the 2 solutions. The number of reversibly aggregated platelets was estimated by subtracting the percentage of aggregated platelets in the second solution from that in the first solution. In patients with stable angina the percentage of aggregated platelets was higher than in control subjects (15 +/- 4% vs 7 +/- 2%, p less than 0.001). Most aggregated platelets (72% and 76%, respectively) were irreversibly aggregated. In the unstable angina group the percentage of aggregated platelets was similar to that of the AMI group (24 +/- 13% and 24 +/- 10%) and significantly higher than in the stable angina group. Only 11% and 17% of aggregated platelets in patients with stable angina and AMI were irreversibly aggregated and 89% and 83% of them were reversibly aggregated. Participation of platelets in the pathogenesis of unstable angina and AMI may be related to the early reversible phase of platelet activation.

Angina Pectoris↗
PubMed1987

Possible role of fibrinogen in the aggregation of white blood cells.

In order to verify whether leukocyte aggregation correlated with aggregation of other cellular elements during inflammation, we examined the state of leukocyte adhesiveness/aggregation (LAA) in the peripheral blood and red cell aggregation. Correlation was found to be significant as was the correlation between LAA and fibrinogen, and with the fibrin/fibrinogen degradation products concentration during various inflammatory states. In vitro leukocyte aggregation was decreased when the cells were suspended in autologous heat defibrinogenated plasma as compared to cells suspended in autologous native plasma. Heat aggregated fibrinogen but not native fibrinogen caused leukocyte aggregation in vitro. Finally, Arvin defibrinogenation in rabbits reduced the state of LAA in endotoxinemic rabbits. Integrating all this information, we assume that fibrinogen participates not only in the aggregation phenomena of red cells and platelets, but also in those of leukocytes.

Animals↗
PubMed1987

Myocardial infarction in young adults under 30 years: risk factors and clinical course.

The clinical features and course of 30 patients (26 men and 4 women) under 30 years of age (mean age 27.3 years) with an acute myocardial infarction (MI) are described. The most common risk factor among this group of patients was smoking in 20 patients (66%). The prevalence of the other risk factors was low: hyperlipidemia in four patients and family history of ischemic disease in another four patients, diabetes mellitus, hypertension, and obesity each in one patient. Seven patients (23%) had none of the conventional risk factors. Three patients were exerting themselves prior to the onset of their MI pain; all of them had normal coronaries. Five patients experienced chest pain prior to MI, among them only two experienced classical angina pectoris. Eighteen patients underwent uncomplicated MI. The complications in the other 12 during the acute MI were rhythm disturbances in eight and congestive heart failure in four. Cardiac catheterization was performed in 25 patients. The occurrence of zero, one, or multivessel disease was equal. The 30 patients were followed up from six months to 15 years (mean 7 years). In 18 patients circulating aggregated platelets were measured one year after the MI. Elevated values were found in all of them (mean +/- SD 34.9 +/- 9.1%). In 6 of the 18, all heavy smokers, extreme values were found in the range of 39-55%. Three out of the 30 patients died within five years after their first MI. The other 15 patients developed complications, most of them angina pectoris. Five patients were hospitalized for reinfarction. None of the 30 underwent aortocoronary bypass operation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗