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Biomedical subjects

J Agmon

Publications and source records attributed to J Agmon.

At least 73 records · Page 4Linked to original sources
PubMed1987

Short- and long-term dobutamine treatment in chronic ischemic heart failure.

This study was undertaken in order to characterize the short-term (1 hour) and long-term (72 hours) effect of dobutamine on hemodynamic and regional ejection fraction parameters measured by radionuclear angiography in patients with chronic congestive heart failure due to coronary artery disease. Baseline hemodynamic and radionuclear parameters were measured and then intravenous dobutamine (8.5 mu/kg/min) was administered. The above parameters were determined again after 1 hour and 72 hours of continuous dobutamine administration. Sixty minutes (short-term) after dobutamine administration heart rate and cardiac index increased significantly (p less than 0.001 for both) and peripheral resistance decreased concomitantly (p less than 0.005). Global left ventricular ejection fraction (LVEF) as measured by multigated equilibrium nuclear angiography (MUGA) increased from 21.8 +/- 10.6% to 25 +/- 13.5 (p less than 0.02). Count-based mean regional ejection fraction in the septal, inferoapical, posterolateral (45 degrees left anterior oblique view) and inferior apical and anterolateral (30 degree right anterior oblique gated first pass) regions increased also. At 72 hours (long-term) after continuous dobutamine infusion, heart rate and cardiac index were still significantly higher and peripheral resistance lower than in the control study. However, global and count-based regional ejection fraction decreased to control values in the right anterior oblique view (first-pass analysis) and the left anterior oblique view (MUGA). Global LVEF measured in the right anterior oblique view by first-pass technique was significantly higher than control in the long-term study (23 +/- 9.7 vs. 27.8 +/- 2.4; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Ischemic ST segment depression in leads V2-V3 as the presenting electrocardiographic feature of posterolateral wall myocardial infarction.

In this study of 14 patients hospitalized with a first event of myocardial infarction, maximal ST segment depression in precordial leads V2 and V3 was the sole ECG finding during chest pain in the first 24 hours of evolving posterolateral infarction, based upon further two-dimensional echocardiographic examination and cardionuclear imaging. Other ECG findings compatible with posterolateral infarction such as the appearance of Q waves in leads V5 and V6, increased R/S ratio in leads V1 and V2, and a diminution of R wave amplitude in leads 1, aVL, V5, and V6 were relatively delayed manifestations in the majority of patients. The clinical course of all patients was benign. It therefore seems reasonable to conclude that ST segment depression in leads V2 and V3 in the absence of reciprocal ECG changes may represent the initial ECG finding of posterolateral infarction in the suitable clinical context of an acute coronary event.

Adult↗
PubMed1987

Natural course of electrocardiographic components and stages in the first twelve hours of acute myocardial infarction.

Time course evolution of R, Q, T and ST components of the electrocardiogram during the first 12 hours of an acute myocardial infarction was studied. A comparison between anterior-extensive and anteroseptal wall infarctions (anterior group), and inferior-extensive and inferior wall infarction (inferior group) showed appearance of significant Q waves within two hours in both groups. R wave loss was nearly a mirror image of Q wave development in both groups. T waves became negative and ST more isoelectric earlier in the inferior than in the anterior group. When combined variations of the four electrocardiographic components were analyzed, four stages of acute infarction were delineated. Stage I--tall R, no Q, ST elevation and positive T; Stage II--significant Q wave appearance; Stage III--negativity of T waves; and Stage IV--ST isoelectric. The inferior group reached stages III-IV within 12 hours; the anterior group remained mostly in stage II. An early appearance of Q waves correlated well with rapid progression to stages III-IV within 12 hours in both infarction groups.

Electrocardiography↗
PubMed1987

Effect of metaraminol during acute inferior wall myocardial infarction accompanied by hypotension: preliminary study.

This study was designed to evaluate the effects of metaraminol (Aramine) in six patients with evolving acute inferior wall myocardial infarction accompanied by hypotension and warm limbs. There were 16 episodes of acute inferior wall ischemia, and the response to therapy was judged by evaluating blood pressure and ST segment and T wave abnormalities. Three patients received intravenous isosorbide dinitrate and two received streptokinase as the initial therapy. The mean ST segment elevation was significantly reduced (from 4.94 +/- 1 to 0.5 +/- 0.7 [p less than 0.0001]) after metaraminol infusion was initiated. The average T wave height also decreased (from 6.8 +/- 2 to -1.3 +/- 2.5 mm [p less than 0.0005]). The average heart rate decreased from 82 +/- 11 to 69 +/- 9 beats/min (p less than 0.05) and the mean arterial blood pressure increased from 81 +/- 12 mm Hg before metaraminol treatment to 126 +/- 8 mm Hg after treatment. All these changes occurred within a few minutes after metaraminol therapy was instituted. In 12 episodes, accelerated idioventricular rhythm appeared concomitantly with the resolution of ST segment elevation. Coronary angiography performed between 4 and 10 days after admission demonstrated significant obstruction in all infarct-related arteries, but none was totally occluded. Left ventricular function was normal in three patients and slightly hypokinetic in the inferior wall in two. These results indicate that in a selected group of patients with acute inferior myocardial infarction, metaraminol administration (in certain hemodynamic circumstances) can alleviate acute ischemia within a few minutes and thereby reduce ischemic injury.

Adult↗
PubMed1987

Positivization of T wave with or without ST segment elevation in patients with unstable angina. Coronary angiographic findings and in-hospital prognosis.

The coronary angiographic findings and the in-hospital prognosis of unstable angina pectoris presenting with T wave positivization only (group A: 32 patients) or with additional ST segment elevation (group B: 27 patients) were evaluated. Clinical data and haemodynamic parameters before and during unstable anginal events showed no significant statistical difference, indicating blood flow reduction as the probable mechanism of ischaemia in both groups. The incidence of hospital myocardial infarction was higher in patients of group B (group A 6.24% vs group B 31%; P less than 0.02). Death due to haemodynamic deterioration occurred in 2 patients of group B. This finding can be partially explained by more developed collateral circulation in patients with T wave changes only (25 of 65 obstructed arteries in group A vs 8 out of 48 obstructed arteries in group B; P less than 0.05). Left ventricular function was comparable between the two groups. The extent, severity and location of coronary artery disease was similar in the groups. Thus, the electrocardiographic pattern of T wave changes only, in patients with unstable angina pectoris (group A) define a subgroup who have a favourable prognosis and development similar to patients with chronic stable angina pectoris. Urgent measures may be delayed in this group.

Adult↗
PubMed1987

Plasma viscosity and haematocrit in the course of acute myocardial infarction.

Plasma viscosity and haematocrit were determined in 44 patients with acute myocardial infarction on the 1st, 2nd, 3rd and 10th day of hospitalization. The highest haematocrit value for the entire group was found on the 1st day of acute myocardial infarction--43.3 SD +/- 4.6% declining progressively to 38.8 SD +/- 3.5% on the 10th day (P less than 0.001). Plasma viscosity for the entire group was normal on the first day of acute myocardial infarction (1.44 SD +/- 0.10 cp) and started to increase on the second day (1.51 SD +/- 0.16 cp, P less than 0.001). A relationship was found between reinfarction or death (17 patients) occurring during hospitalization and changes in haematocrit and plasma viscosity. In this group plasma viscosity rose to 1.63 SD +/- 0.19 cp on the second day of acute myocardial infarction (P less than 0.001 vs plasma viscosity value on the first day). This elevation persisted on the third day. Haematocrit values in this group were 47.9 SD +/- 3.6% on the first day of acute myocardial infarction declining progressively and significantly afterwards. In the remaining patients both plasma viscosity and haematocrit were normal and did not change. No correlation of plasma viscosity and haematocrit were found when tested for other clinical complications, sex, age, maximal creatine phosphokinase values and coronary risk factors. We suggest that variations in haematocrit and plasma viscosity during acute myocardial infarction exist in a group of patients in whom reinfarction or death occurs. The changes in haematocrit and plasma viscosity precede the complications by 4-8 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Room temperature ADP induced first stage hyperaggregation of human blood platelets: a previously undescribed phenomenon and its relationship to spontaneous cold induced platelet aggregation.

ADP induced human platelet aggregation was shown to be accentuated when tested at 20-30 degrees C as increased sensitivity and as a greater change of optical density although second stage aggregation and the release reaction did not occur. This previously undescribed phenomenon is defined as room temperature ADP induced first stage hyperaggregation. Aggregation, which occurs under the above mentioned conditions with a quantity of ADP insufficient to maintain the aggregation (usually less than 1.5 micron), is reversible when the temperature is raised to 37 degrees C. After rewarming to these temperatures, second stage aggregation appeared in the presence of larger quantities of ADP (usually more than 2 microns) and could be blocked by aspirin. The absence of the release reaction was demonstrated with a lumi-aggregometer. Spontaneous cold induced platelet aggregation seen after chilling platelets to 0-4 degrees C is shown to be a distinct phenomenon.

Adenosine Diphosphate↗
PubMed1987

Acute transmural myocardial infarction in elderly patients hospitalized in the coronary care unit versus the general medical ward.

The hospital records of 126 patients over 75 years of age with transmural myocardial infarction initially treated in the coronary care unit were compared with a concurrent similar group of 94 patients admitted directly to the general medical wards. The in-hospital mortality rate for both groups together was 40%. The mortality rate within the coronary care unit was 24% as compared with 46% in the ward group (P less than 0.005). However, the mortality rate for the coronary care unit group as a whole (including those patients later transferred to the general ward) was 35 versus 46% in the ward group. Congestive heart failure and cardiogenic shock were the most frequent complications in both groups (47 and 30%, respectively), and they were the main cause of death. Patients with these complications were less likely to be successfully resuscitated, even in the coronary care unit. The overall incidence of serious ventricular arrhythmias and complete heart block was similar to that reported for younger patients. Eleven patients in the coronary care unit group were successfully resuscitated from these arrhythmias and eight survived to be discharged from hospital. In contrast, only two patients in the ward group were successfully resuscitated and eight (9%) patients died suddenly and the fatal event could not be diagnosed. We concluded that elderly patients with an acute myocardial infarction can benefit from early admission to a coronary care unit.

Aged↗
PubMed1987

Prosthetic valve endocarditis caused by Acinetobacter calcoaceticus subsp. lwoffi.

Acinetobacter spp. are uncommon etiologic agents of prosthetic valve endocarditis. Two patients with Acinetobacter calcoaceticus subsp. lwoffi prosthetic valve endocarditis are described. The patients were successfully treated with antibiotics (cefotaxime sodium and gentamicin sulfate); thus, we suggest medical treatment rather than early valve replacement in this particular type of infection.

Acinetobacter Infections↗
PubMed1987

Lactate dehydrogenase isoenzymes in serum during recent acute myocardial infarction.

Lactate dehydrogenase (LD, EC 1.1.1.27) isoenzymes 1 and 2 and the LD 1:2 ratio were determined in 62 patients with recent myocardial infarction 24, 48, and 72 h after total serum LD activity had returned to normal values. From the results we could define two groups of patients. The first, 40 patients in whom proportions of LD-1 and LD-2 isoenzymes in serum and the LD 1:2 ratio were all within the normal reference interval, all had an uncomplicated course of recovery from myocardial infarction. In the remaining 22 patients, LD-1 still exceeded LD-2 24 to 72 h after total LD activity returned to normal values; i.e., the ratio was similar to that in patients with myocardial infarction. Seven of these 22 patients (32%) had a complicated course, with re-infarction in all seven. Thus, even in the presence of normal total LD activity, a high LD 1:2 ratio may reflect a consistent focal myocardial necrosis in some patients with recent myocardial infarction and may serve as an early marker for further re-infarction.

Adult↗
PubMed1987

Amiodarone-induced thrombocytopenia.

Amiodarone hydrochloride-induced thrombocytopenia seems to be an additional side effect in the course of amiodarone treatment. Two patients with thrombocytopenia during amiodarone treatment are described, in whom the diagnosis of amiodarone-induced thrombocytopenia was made by the fact that thrombocytopenia developed during amiodarone treatment and by rechallenge with the drug. Amiodarone-induced thrombocytopenia is probably due to delayed hypersensitivity reaction as indicated by the strongly positive lymphocyte stimulation test results using amiodarone. According to our results, platelet counts should be included in the routine follow-up of patients within the first two weeks after initiation of amiodarone treatment.

Aged↗
PubMed1986

Beta-endorphins in acute myocardial infarction.

The endogenous peptide B-endorphin (B-EP) is closely connected with different aspects of homeostasis, behavior, and in particular with the perception of pain. The purpose of this study was to investigate the correlation between: the level of plasma B-EP and the intensity of pain in acute myocardial infarction (AMI); and the B-EP and specific enzymes for AMI serum glutamic oxolo-acetic transferase, lactate dehydrogenase, and creatine phosphokinase and some stress hormones (cortisol, growth hormone). Twenty-six patients hospitalized in the CCU for acute MI were studied during the first 72 hours from the onset of symptoms. Seven normal subjects served as controls. Blood was taken for hormone and B-EP evaluation before treating the patients by opiates. Plasma B-EP levels were determined using the protocol of the Immunonuclear Corporation (Stillwater, MN). Statistical analysis of the results showed: Nonsignificant differences between B-EP levels of all MI patients and control group. Unaltered B-EP levels in patients with acute MI suffering from moderate pain. Significant differences in drop of B-EP in the group with most severe pain (p less than 0.025). A tendency toward decreased B-EP in patients suffering from more prolonged pain (greater than 6 hours). Significant negative correlation was shown between B-EP and chest pain intensity (0-4 graduation) (r = 0.8, p less than 0.01); lactate dehydrogenase (r = 0.7, p less than 0.01); serum glutamic oxolo-acetic transferase (r = 0.6, p less than 0.01); creatine phosphokinase (r = 0.6, p less than 0.05; plasma cortisol level (r = 0.5, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aspartate Aminotransferases↗
PubMed1986

The acute effect of sublingual nifedipine and isosorbide dinitrate on plasma viscosity in patients with acute myocardial infarction.

The effect of sublingual nifedipine 10 mg (pierced capsule) and isosorbide dinitrate (ISDN) 5 mg on plasma viscosity (Pl.V) was investigated in 60 consecutive patients 7-10 days after hospitalization for acute myocardial infarction (AMI), who were randomized for either nifedipine (30 patients) or ISDN (30 patients). Pl.V, hematocrit (Htc), and erythrocyte sedimentation rate (ESR) were measured 20 minutes before and thereafter at 5, 10, and 30 min after drug administration while in the recumbent position. Blood pressure (BP) and heart rate (HR) were determined before each blood sample. In 18 patients (60%) Pl.V decreased by greater than 0.05 centipoise (Cp) after nifedipine (0.0953 +/- 0.033 Cp p less than 0.001 vs. initial values). After ISDN, Pl.V decreased by greater than 0.05 Cp (0.0933 +/- 0.036 Cp) in only 7 patients (23%). Systolic blood pressure (SBP) fell by 11.7 +/- 14.6 mmHg after nifedipine and by 16 +/- 14 mmHg after ISDN (nifedipine vs. ISDN = NS). Diastolic blood pressure (DBP) fell by 8 +/- 9.6 mmHg after ISDN and by 6.6 +/- 19.3 mmHg after nifedipine (nifedipine vs ISDN = NS). HR, ESR, and Htc did not change after drug administration. It is thus concluded from our study that nifedipine 10 mg sublingual has a significant Pl.V-lowering activity compared to sublingual ISDN 5 mg in patients with AMI.

Adult↗
PubMed1986

"Flipped" lactic dehydrogenase pattern in acute coronary insufficiency.

Serum lactic dehydrogenase (LDH) isoenzymes were measured 24, 48, and 72 hours after administration in 85 patients with acute coronary insufficiency (ACI) and 10 patients with stable angina pectoris who served as controls. The above patients did not develop myocardial infarction according to the criteria of development of new Q waves or elevation of cardiac enzymes. In 15 patients with ACI a "flipped" LDH pattern (LDH1 greater than LDH2) was found in the presence of normal total LDH activity and normal creatine kinase-MB. The values of LDH 1:2 ratio ranged between 1.02 and 1.13 (normal values 0.45-0.75). In the 10 control patients, normal levels of total LDH and normal LDH enzyme distribution and creatine kinase-MB were found. A possible explanation for the flipped LDH pattern in the ACI patients (indicating some myocardial damage) could be myocytolysis and coagulation necrosis found on postmortem examinations. The conclusion of our study is that LDH isoenzymes should be measured in patients with ACI to determine the LDH 1:2 ratio. The finding of a "flipped" LDH pattern demonstrating myocardial damage, lacking in stable angina, may also be helpful in patients who developed the clinical picture of ACI more than 24 hours before arrival at the hospital, since by that time the creatine kinase-MB may have already returned to normal. An additional advantage of measuring LDH isoenzymes in these patients may be that patients with "flipped" LDH pattern may need a longer rest and earlier coronary angiographic evaluation.

Acute Disease↗
PubMed1986

Unstable angina pectoris evolving to acute myocardial infarction: significance of ECG changes during chest pain.

We retrospectively evaluated 32 patients with unstable angina (UA) and no evidence of increased oxygen demand during episodes of chest pain (no significant changes in heart rate and blood pressure), who developed an acute myocardial infarction (AMI) during the same hospitalization. Based on the type of ST changes during anginal pain, two groups were defined: Group A included 19 patients who developed ST elevation during AMI; 15 of these 19 patients (79%) were in Killip class I, two were in class II, and there was one patient each in classes III and IV, respectively. Only one of the 19 patients died. Group B included 13 patients who developed ST depression during AMI; nine of these 13 patients were in Killip class IV and the remaining four patients died before they could be evaluated. Ten patients died (77%) (p less than 0.01), seven in electromechanical dissociation and three in cardiogenic shock. Postmortem examination, performed in four patients, revealed total obstruction of the left main coronary artery. It is concluded that patients with UA who, during attacks of chest pain, develop ST depression and no evidence of increased oxygen demand may have a poor prognosis when they develop an AMI. This selected group of high-risk patients appears to need immediate intensive medical care and most probably early surgical treatment.

Adolescent↗
PubMed1986

Unstable angina: the significance of ST segment elevation or depression in patients without evidence of increased myocardial oxygen demand.

We evaluated 46 patients with unstable angina (UA), who showed no significant changes in heart rate, blood pressure, and double product (as evidence of increased oxygen demand) during episodes of chest pain. Coronary angiography was performed in all patients during the same hospitalization. Of 26 patients with UA and ST depression (group A), 10 had left main coronary artery disease (CAD) and eight had left main equivalent CAD. Of 20 patients with UA and ST elevation (group B), only one had left main CAD and one had left main equivalent CAD. All patients in group A had ST depression in leads V4 and V5, and all patients in group B had ST elevation in leads V2 and V3. The presence of ST depression in leads V4 and V5 in UA patients without evidence of increased oxygen demand may be suggestive of significant left main or left main equivalent CAD. Therefore, coronary angiography is recommended during the same hospitalization.

Adult↗