Pentoxifylline influences acute-phase response in acute myocardial infarction.
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Biomedical subjects
Publications and source records attributed to F Dienstl.
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Endothelin-1 concentrations were measured in peripheral venous blood samples from 42 patients with acute myocardial infarction. In patients with ischemic or hemodynamic complications (n = 11), endothelin-1 concentrations were significantly higher already on admission (P = 0.008) and remained significantly higher until day 6 after admission compared to patients with uncomplicated infarctions (n = 31; P = 0.035). There were no close correlations between peak concentrations of endothelin-1 and creatine kinase or creatine kinase isoenzyme MB mass in either group. Only in complicated patients did left ventricular ejection fraction correlate closely and inversely with peak endothelin-1 concentrations (r = -0.71; P = 0.03). Therefore, plasma endothelin-1 concentrations in patients with acute myocardial infarction patients may reflect states of markedly depressed cardiac performance and recurrent myocardial ischemia.
Plasma concentrations of calcitonin gene-related peptide (CGRP), a potent regulator of vascular tone, creatine kinase, myoglobin, and cardiac troponin T were assessed in 31 patients with acute myocardial infarction. In patients who had sustained acute myocardial infarctions, maximum CGRP concentrations (median, 3.2 pmol/L; interquartile range, 1.5 to 4.8 pmol/L) were markedly elevated as compared with healthy control subjects (n = 23; median, 1.02 pmol/L; p = 0.02). However, no marked differences in CGRP levels were observed between patients with early reperfusion (n = 19; median, 3.5 pmol/L) and patients without early reperfusion (n = 12; median, 2.6 pmol/L; p = 0.96), as well as between those with congestive heart failure (n = 8; median, 3.9 pmol/L) and those without congestive heart failure (n = 23; median, 3.2 pmol/L; p = 0.62). CGRP did not correlate closely with myocardial protein release or hemodynamic parameters (heart rate and blood pressure) or the occurrence of arrhythmias. Therefore we conclude that elevated peripheral venous CGRP concentrations in patients who have sustained an acute myocardial infarction are independent of successful reperfusion and hemodynamic state. Although the cause of CGRP increase is not yet identified, CGRP may play a role in the regulation of coronary vascular tone in patients after acute myocardial infarction.
OBJECTIVE: To evaluate a rapid immunoturbidimetric assay for myoglobin and to investigate its clinical usefulness in the early detection of acute myocardial infarction. DESIGN: Prospective study. Immunoturbidimetrically determined myoglobin concentrations were compared with radioimmunoassay results obtained with the same blood samples. The diagnostic performance of myoglobin determination was compared with creatine kinase and creatine kinase MB activity (current standard of routine diagnosis). SETTINGS: Part 1: coronary care unit. Part 2: emergency room in a university hospital. PATIENTS: Part 1:30 patients with acute myocardial infarction admitted not later than four hours (median two hours) after the onset of symptoms. Part 2: 126 patients admitted to the emergency room with chest pain not caused by trauma (51 cases of acute myocardial infarction, 51 cases of angina pectoris, and 24 cases of chest pain not related to coronary artery disease). INTERVENTIONS: Part 1: routine treatment including intravenous thrombolytic treatment (28 patients). Part 2: routine emergency treatment without thrombolytic treatment. MAIN OUTCOME MEASURES: The analytical quality of the immunoturbidimetric myoglobin assay and a comparison between the myoglobin assay and creatine kinase and creatine kinase MB for diagnostic sensitivity and performance. RESULTS: The immunoturbidimetric myoglobin assay was fast and convenient and gave myoglobin determinations of high analytical quality. The concentration of myoglobin increased, peaked, and returned to the reference range significantly earlier than creatine kinase (p < or = 0.0001) and creatine kinase MB (p < or = 0.0002). Before thrombolytic therapy was started the diagnostic sensitivity of myoglobin was significantly higher than that of creatine kinase MB activity 0-6 h after the onset of chest pain and significantly higher (0.82 v 0.29) than creatine kinase 2-4 h after the onset of chest pain. In almost all patients (92%) plasma myoglobin concentrations were increased 4-6 h after the onset of chest pain. CONCLUSION: Myoglobin was more sensitive in detecting early myocardial infarction than creatine kinase and creatine kinase MB activity. Immunoturbidimetric myoglobin measurements could be useful in the early evaluation of patients with suspected myocardial infarction because this assay takes less than two minutes.
In the last several decades serum levels of cardiac enzymes and isoenzymes have become the final arbiters by which myocardial damage is diagnosed or excluded. Because conventionally used enzymes are neither perfectly sensitive nor specific, there is need for a new sensitive and cardiospecific marker of myocardial damage. Cardiac troponin T (TnT) is a contractile protein unique to cardiac muscle and can be differentiated by immunologic methods from its skeletal-muscle isoform. An enzyme immunoassay specific for cardiac TnT is now available in a commercial kit for routine use. The biggest advantage of this assay is its cardiospecificity. TnT measurements, however, are also highly sensitive in diagnosis of myocardial injury and accurately discern even small amounts of myocardial necrosis. TnT measurements are, therefore, particularly useful in patients with borderline CK-MB and in clinical settings in which traditional enzymes fail to diagnose myocardial damage efficiently because of lack of specificity--for example, perioperative myocardial infarction or blunt heart trauma. TnT release kinetics reveal characteristics of both soluble, cytoplasmic, and structurally bound molecules. It starts to increase a few hours after the onset of myocardial damage and remains increased for several days. TnT allows late diagnosis of myocardial infarction. The diagnostic efficiency remains at 98% until 6 d after the onset of infarct-related symptoms. TnT is also useful in monitoring the effectiveness of thrombolytic therapy in myocardial infarction patients. The ratio of peak TnT concentration on day 1 to TnT concentration at day 4 discriminates between patients with successful (greater than 1) and failed (less than or equal to 1) reperfusion. TnT measurements are very sensitive and specific for the early and late diagnosis of myocardial damage and could, therefore, provide a new criterion in laboratory diagnosis of the occurrence of myocardial damage.
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We investigated atrial natriuretic peptide (ANP) and cyclic guanosine monophosphate (cGMP) in patients undergoing elective direct current cardioversion (CV group) due to atrial fibrillation (n = 9) or atrial flutter (n = 3). Anesthesia for cardioversion (CV) was induced with propofol 1.5 mg/kg. Conversion was achieved in all patients. Before CV all patients had elevated ANP and cGMP plasma levels. After CV the concentrations of ANP and cGMP decreased significantly within 15 and 30 minutes (p less than 0.01), respectively. Only one patient in the CV group showed increasing ANP and cGMP levels although his heart rate had decreased after CV and his blood pressure remained stable. High concentrations of ANP and cGMP might possibly be a compensatory mechanism of cardiac dysfunction. To study the influence the anesthetic agent on plasma levels of ANP and cGMP, we investigated six patients anesthetized with propofol for high-density radiation (HDR group). The data from this control group showed that propofol did not influence the plasma levels of ANP and cGMP. ANP correlated statistically significantly (p less than 0.05) with cGMP in both groups (r = 0.88 and 0.76 in the HDR and CV groups, respectively). In addition, we found a cGMP release of 149.6 +/- 17.6 per mol ANP in the HDR group, in the CV group the release was 109 +/- 54.2 cGMP per mol ANP. This phenomenon could be due to minor response of target cells to ANP stimulation (receptor down-regulation) in patients with heart disease. In conclusion, ANP and cGMP levels decreased after successful cardioversion.(ABSTRACT TRUNCATED AT 250 WORDS)
We investigated 69 patients (most belonging to NYHA classes II and III) undergoing elective direct current cardioversion of atrial fibrillation (46 patients) and atrial flutter (23 patients), respectively. Without premedication anaesthesia was induced with the new soya bean emulsion of propofol ('Diprivan') 1.2 mg.kg-1 over 45 s. Recovery time was measured from the start of the anaesthetic injection to the moment at which the patients regained consciousness. Completeness of recovery was assessed with two methods: opening eyes on command and time orientation. Good amnesia was observed in all patients. Conversion was achieved in all but seven patients (90%). After injection of propofol, the mean arterial pressure decreased slightly (2% below baseline). Induction of anaesthesia and successful DCC effected a statistically significant decrease in both the heart rate and the rate pressure product. Eleven patients required assisted ventilation for 2 min due to respiratory depression. Fifteen patients developed arrhythmias. Side-effects, such as myocloni, recall or vomiting, were not observed. In conclusion, propofol may well prove to be the anaesthetic of choice for DCC in cardiac patients because of good amnesia, low incidence of side-effects and short recovery time (mean 5.3 min).
Troponin T is a structurally bound protein found in striated muscle cells. We tested concentrations of its cardiac-specific isotype in peripheral venous blood samples serially drawn from 72 patients with confirmed myocardial infarction. Fifty-nine patients received thrombolytic treatment with intravenous streptokinase, urokinase, or recombinant tissue-type plasminogen activator; because of contraindications, the remaining 13 patients did not. Concentrations of troponin T in plasma, measured by an enzyme-linked immunosorbent assay, started increasing within a few hours after the onset of symptoms (median, 4 h; range, 1-10 h). The sensitivity of troponin T for detecting myocardial infarction was 100% from 10 to 120 h after the onset of symptoms; sensitivity on the seventh day after admission was 84%. Concentrations were increased for up to three weeks in some patients with late or high peak values. Successful reperfusion in Q-wave infarction obviously influences the release of troponin T into plasma, with all such cases showing peak values less than or equal to 26 h (median, 14 h) after the onset of symptoms. Troponin T concentrations in these patients returned to within the reference interval more rapidly than in nonreperfused subjects. In the 13 patients without fibrinolytic therapy, troponin T tended to peak approximately 48 h (median) after the onset of chest pain. Troponin T concentrations in patients for whom thrombolysis was unsuccessful resembled those in patients without fibrinolytic therapy. The specificity of the assay was 96% as tested in samples of 96 emergency-room patients. The reference interval (less than 0.5 micrograms/L) was established from samples of 100 healthy blood donors. Troponin T measurements are a specific and sensitive method for the early and late diagnosis of acute myocardial infarction and could, therefore, provide a new criterion in laboratory diagnosis of its occurrence.
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Antiplatelet therapy to prevent occlusion of coronary bypass grafts is widely used. Though the value of this therapy after bypass surgery is not yet settled, some favourable results have been achieved. Many physicians continue to use the Mayo Clinic recommendations (peri- and postoperative administration of aspirin and dipyridamole) while others used dipyridamole and aspirin after surgery, and others use aspirin alone. It is now well established that pretreatment with platelet inhibitors is effective in lowering the incidence of acute vessel closure after angioplasty: Numerous drugs, including warfarin, aspirin and dipyridamole, aspirin and heparin, nifedipine, diltiazem and the experimental antiplatelet agent ticlopidine have proved ineffective in reducing the rate of restenosis after coronary angioplasty. Only high dose administration of an omega-3 fatty acid dietary supplement for 1 week before angioplasty lowers patients' risk for restenosis, but this therapy does not appear effective if begun the night before the procedure or done with somewhat lower dose. Until additional results are available, clinicians must treat patients on extrapolation from the published trials. Low-dose aspirin should be used for several weeks after the procedure. Careful attention to risk factor modification, especially smoking, lipid profile and diabetes control, seems essential in any long-term plan of management in the patient with coronary disease.
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