Evaluation of serum lipid profile and cardiac enzyme changes in cerebrovascular accidents

Serum lipid profile is, total cholesterol, high density lipoprotein (HDL), low density lipoprotein (LDL) and triglycerides and serum cardiac enzymes ie, creatinine phosphokinase (CPK), creatinine phosphokinase isoenzyme MB (CPK-MB), lactate dehydrogenase (LDH) and serum aspartate aminotransferase (AST/SGOT) levels were estimated in 50 cases of cerebrovascular accidents (CVA) consisting of 26 cases of cerebral haemorrhage and 24 cases of cerebral thrombosis. All analyses were made on day 1 and day 7. Serum cholesterol, LDL and triglycerides levels were significantly higher in CVA patients on day 1. Lipid level fell significantly on day 7 in respect to day 1. On comparing the lipid levels between cerebral haemorrhage and cerebral thrombosis, no significant difference was observed. Cardiac enzymes like CPK and CPK-MB were significantly raised whereas, AST/SGOT and LDH were marginally raised on day 1 in CVA patients. However, there was no change in cardiac enzyme levels between cerebral haemorrhage and cerebral thrombosis patients.     

An evaluation of serum troponin T and signal-averaged electrocardiography in predicting electrocardiographic abnormalities after blunt chest trauma

OBJECTIVE: Despite multiple inquiries, there are no available tests to definitively detect blunt myocardial injury. The evaluation of patients with chest wall injuries without other indications for intensive care unit (ICU) admission has ranged from a single emergency department electrocardiogram (ECG) to 72 hours of continuous electrocardiographic monitoring. Recently, signal-averaged ECG and serum cardiac troponin T have demonstrated clinical utility in the evaluation of ischemic heart disease. The purpose of this study is to determine the ability of these diagnostic tests to predict the occurrence of significant electrocardiographic rhythm disturbances for patients with chest wall injuries and no other indication for ICU admission. METHODS: We prospectively evaluated 71 consecutive adult patients admitted to a regional Level I trauma center with chest wall injuries not requiring ICU admission. We obtained admission signal-averaged ECG, serum troponin T level, standard ECG, and creatine phosphokinase (CPK-MB) level. Patients received continuous electrocardiographic monitoring, follow-up 12-lead electrocardiography, and serial monitoring of troponin and CPK-MB. Echocardiography was performed for patients with abnormal CPK-MB levels. Electrocardiographic events were graded as normal, abnormal but clinically insignificant, or clinically significant. Multiple stepwise logistic regression analysis was used to evaluate predictors for the development of clinically significant electrocardiographic events. RESULTS: On admission, 17 of 71 patients (23.9%) had normal sinus rhythm; 13 (18.3%) had a clinically significant finding. For 50 patients, follow-up ECG was abnormal; for 26, the findings were clinically significant. Of 17 patients with normal initial ECGs, 7 (41%) developed a clinically significant abnormality. Six patients received intervention for ECG findings. Eleven of 71 patients (16%) had positive troponin T; 5 of 71 (7%) had positive CPK-MB; 15 of 71 (21%) had positive signal-averaged ECG; and 4 of 13 had positive echocardiograms. Initial electrocardiographic abnormalities and a troponin T level > 0.20 microg/L were the only variables found to predict clinically significant electrocardiographic events. Sensitivity and specificity of troponin T in predicting clinically significant abnormalities were 27 and 91%, respectively. CONCLUSIONS: 1. The best predictors for the development of significant electrocardiographic changes are an admission ECG abnormality and an elevated serum troponin T level. 2. Both tests have high specificity with low to moderate sensitivity. 3. Patients with normal ECGs may develop clinically significant events. 4. CPK-MB and echocardiograms continue to be poor predictors of significant electrocardiographic events.     

Measurement of cardiac troponin T is an effective method for predicting complications among emergency department patients with chest pain

STUDY OBJECTIVES: To determine the test performance characteristics of serum cardiac troponin T (cTnT) measurement for diagnosis of acute myocardial infarction (AMI), and to determine the ability of cTnT to stratify emergency department patients with chest pain into high- and low-risk groups for cardiac complications. METHODS: We conducted a prospective observational cohort study with convenience sampling in a tertiary care, urban ED. The study sample comprised 667 patients presenting to the ED with a complaint of chest pain or other symptoms suggesting acute ischemic coronary syndrome (AICS). Patients were assigned to different blood sampling protocols for cTnT therapy on the basis of their ECG at presentation: nondiagnostic for AMI at 0, 3, 6, 9, 12, and 24 hours after ED presentation; or ECG diagnostic for AMI at 0, 1, 2, 3, 4, 5, 6, 7, 8, 9, 12, 18, and 24 hours after ED presentation. RESULTS: Of 667 patients, 34 had AMI diagnosed within 24 hours of ED arrival. Using a .2 microgram/L discrimination level for cTnT, sensitivity for AMI within 24 hours of ED arrival was 97% (95% confidence interval, 91.4% to 99.9%), and specificity was 92% (89.8%-94.1%). When the effects of age, race, sex, and creatine kinase-MB isoenzyme subunit test results were controlled, a patient with cTnT of .2 microgram/L or greater was 3.5 (1.4 to 9.1) times more likely to have a cardiac complication within 60 days of ED arrival than a patient with a cTnT value below .2 microgram/L. CONCLUSION: Measurement of cTnT will accurately identify myocardial necrosis in patients presenting to the ED with possible AICS. Elevated cTnT values identify patients at increased risk of cardiac complications.     

Diagnostic difficulties of myocardial infarct in an admissions and emergency service: influence of age

OBJECTIVE: To analyze the clinical signs and electrocardiographic and enzyme data in patients admitted to an emergency ward for myocardial infarction in order to highlight diagnostic pitfalls. PATIENTS AND METHODS: All patients admitted to our emergency ward between October 1995 and October 1996 with elevated myoglobulin or creatinine phosphokinase (CPK) levels (n = 457 patients) were included in the study series. Patient files were randomly selected (n = 257 files) for review by an emergency ward specialist and a cardiologist to identify cases of myocardial infarction (n = 88 patients, mean age 73.4 +/- 15.2 years). Clinical, electrical and enzyme data (including CPK-MB) were analyzed. RESULTS: The patients had been referred for chest pain (69%), dyspnea (24%) or another disorder (7%). Pain was located in the retrosternal area in 51%, in the lower chest in 19% and elsewhere in 30%. Delay between onset of pain and transfer to the emergency ward was 5 h 20 min +/- 6 h. Signs of left heart failure were observed in 50% of the patients. The admission electrocardiogram showed complete criteria for myocardial infarction in 43% of the cases, incomplete criteria in 21% and was non-contributive in 36%. Enzyme results were elevated in 78% of the cases at the first assay and in 98.2% at the second assay. Both typical chest pain and ECG were observed in only 30% of the cases. Chest pain was present in 55% of the patients over 75 years of age and in 81% of those under 75 years (p = 0.007). CONCLUSION: A typical syndrome is observed in less than one-third of all patients with myocardial infarction admitted to emergency wards. The frequency of atypical presentations increases with age.     

Effects of short-term supplementation with coenzyme Q10 on myocardial protection during cardiac operations

BACKGROUND: Coenzyme Q10 (CoQ10) is a naturally occurring vitamin-like substance that may have a beneficial role in ischemia-reperfusion injury. Coenzyme Q10 administered either as an additive to cardioplegia or as long-term preoperative oral supplementation has been reported to ameliorate myocardial injury after cardiac operations. METHODS: To determine whether short-term supplementation with large doses of CoQ10 (600 mg in divided doses 12 hours before operation) was effective in myocardial protection, 20 patients with well-preserved left ventricular function (ejection fraction greater than 0.50) undergoing elective coronary revascularization were enrolled in a prospective, double-blind, placebo-controlled randomized trial. Serial concentrations of CoQ10, myoglobin, creatine kinase MD fraction, and cardiac troponin T were measured preoperatively and 1, 6, 24, 72, and 120 hours postoperatively. Efficacy of myocardial protection was also assessed by clinical outcome and serial changes in electrocardiographic indices. RESULTS: The patient groups were similar with respect to preoperative and intraoperative characteristics. There was no significant difference in the preoperative plasma levels of CoQ10. These levels fell significantly in both groups after operation, although the magnitude of the decrease was less in the CoQ10-supplemented group (43% versus 60%). In both groups, there were significant postoperative increases in myoglobin, creatine kinase MB fraction, and cardiac troponin T. The magnitude of increases in cardiac troponin T was greater in the CoQ10-supplemented group, reaching marginal overall statistical significance (p = 0.06). CONCLUSIONS: Short-term supplementation with large doses of CoQ10 does not lead to improved myocardial protection in patients undergoing coronary revascularization with well-preserved ventricular function and relatively short ischemic times.     

Perindopril postmarketing surveillance: a 12 month study in 47,351 hypertensive patients

We investigated the effect of electrical cardioversion of atrial fibrillation in patients with heart failure. The study group consisted of 24 patients with mild to moderate heart failure [13 men, mean age 67+/-7 years, mean peak oxygen consumption (peak VO2) 16.3+/-2.8 ml/min/kg] and chronic atrial fibrillation (median duration 19 (1-228) months). Patients were stable on digoxin, diuretics, nitrates and angiotensin converting enzyme inhibitors; no prophylaxis with antiarrhythmics was started after cardioversion. Cardioversion was unsuccessful in 6 patients; of the 18 patients in whom sinus rhythm was obtained 9 had a relapse of atrial fibrillation within 6 weeks after cardioversion. The remaining 9 patients with maintenance of sinus rhythm and the 15 (6+9) patients with atrial fibrillation at follow-up after 6 weeks did not differ with respect to any baseline characteristic, including age, peak VO2, duration of atrial fibrillation, echocardiographic left ventricular and left atrial dimensions, plasma atrial natriuretic peptide and norepinephrine. In the patients with maintenance of sinus rhythm, baseline measurements were repeated at follow-up. Peak VO2 did not change significantly (16.7+/-2.8 to 17.6+/-3.3 ml/min/kg, P=0.29); also, echo parameters, atrial natriuretic peptide and norepinephrine were not significantly affected. These results indicate that it is difficult to achieve lasting sinus rhythm through electrical cardioversion in patients with atrial fibrillation and mild to moderate heart failure. Moreover, in patients with maintenance of sinus rhythm after cardioversion no significant benefit in terms of peak VO2, cardiac dimensions, and neurohumoral status is to be expected. Hence, indiscriminate cardioversion of atrial fibrillation in the setting of heart failure does not appear to be useful.     

Comparison of myoglobin, creatine kinase-MB, and cardiac troponin I for diagnosis of acute myocardial infarction

Serial plasma concentrations of myoglobin, creatine kinase MB (CK-MB) isoenzyme, and cardiac troponin I (cTnI) were measured in 25 patients with a confirmed diagnosis of acute myocardial infarction (AMI), and 74 patients who were suspected of AMI but were subsequently ruled out for this diagnosis. The cutoff concentration for the cTnI assay was optimally determined to be 2.5 ng/mL. Of the three markers, myoglobin had the highest clinical sensitivity (50 percent) when blood was collected between 0 to 6 h after the onset of chest pain. Assays for all serum markers used had high clinical sensitivity (> 93 percent) 6 to 24 h after onset. The CK-MB remained highly sensitive for 48 h, while cTnI was sensitive for up to 72 h. Between 72 and 150 h, cTnI had a clinical sensitivity of 70 percent as compared to 21 percent and 18 percent for myoglobin and CK-MB, respectively. The clinical specificity of cTnI for non-AMI patients was equivalent to CK-MB and significantly higher than for myoglobin. The clinical efficiency of cTnI for all samples was better than either CK-MB or myoglobin, owing mainly to the wider diagnostic window. The specificity of cTnI for 59 patients with chronic renal failure, skeletal muscle trauma and disease was better than all of these markers including cardiac troponin T (cTnT). Results of this study show that cTnI is an effective marker for the retrospective diagnosis of AMI, and consideration should be given to its use in place of CK-MB.     

Troponin T in patients with low grade or atypical angina. Identification of a high risk group for short- and long-term cardiovascular events

AIMS: Cardiac troponin T is an established marker of cardiovascular risk in patients with severe angina pectoris. Data are scarce on patients admitted to a coronary care unit with low grade or atypical angina pectoris to rule out myocardial infarction. METHODS AND RESULTS: We investigated 106 patients (57.4 SD 11.6 years) with low grade (Braunwald class I) or atypical symptoms out of 702 patients admitted to the coronary care unit with suspected acute myocardial infarction. Serum concentrations of troponin T were measured at admission and 4 h later. In hospital cardiovascular events including acute myocardial infarction, life threatening cardiac arrhythmias, congestive heart failure, and death were recorded. Patients were additionally observed after 3 and 6 months post-discharge regarding acute myocardial infarction, unstable angina, rehospitalization for cardiac causes and death. The patients were divided into a troponin T positive (> or =0.2 microg x 1(-1) at admission or 4 h later; n=11) and a troponin T negative group. The mean value of troponin T 4 h after admission in the positive group was 0.58 microg x 1(-1). Of the troponin T positive patients, 0.82 (0.95 CI: 0.48-0.98) had a cardiovascular event during their stay in hospital vs 0.41 (0.95 CI: 0.31-0.52) of troponin T negative patients (P<0.05). In the troponin T positive group 0.64 (0.95 CI: 0.31-0.89) developed myocardial infarction in hospital vs 0.07 (0.95 CI: 0.03-0.15) in the troponin T negative group (P<0.001). Troponin T predicts outcome after 3 and 6 months significantly (P<0.05). CONCLUSION: Troponin T identifies patients with low grade or atypical angina at risk of severe short- and long-term cardiovascular events. Therefore, troponin T adds substantial information in patients with ruled out acute myocardial infarction. Troponin T positive patients have to be observed carefully regardless of their symptom intensity and may have to receive early cardiac catheterization; troponin T negative patients could be released safely from the coronary care unit early.     

Incidence of myocardial lesions after vascular surgery: diagnosis by troponin Ic

OBJECTIVE: To compare the incidence of myocardial damages diagnosed following vascular surgery using the cardiac troponin I measurement technique and conventional methods. STUDY DESIGN: Prospective epidemiological study. PATIENTS: Fifty-four patients who underwent surgery for either aneurysmal disease in 28 cases or occlusive aortic disease in 26 cases. METHODS: Plasma concentration of cardiac troponin I (significant at a concentration > 1.5 ng.mL-1) was measured by immunoenzymofluorimetry on the second and fifth postoperative days. Conventional monitoring methods included daily electrocardiogram (ECG), enzymatic assay of total-PCK, and measurement of plasma levels of the MB isoenzyme of phosphokinase creatine (MB-PCK) (significant at > 1 ng.mL-1 and RI > 1.5). RESULTS: The cardiac troponin I measurement technique allowed the diagnosis of minor myocardial damages during the postoperative period in five patients, whereas with the conventional methods (clinical signs. ECG, and MB-PCK) only three myocardial lesions were diagnosed. CONCLUSION: The cardiac troponin I measurement technique allows diagnosis of minor myocardial damages following vascular surgery. Conventional methods underestimate the incidence of these damages.     

Prognostic role of troponin T versus troponin I in unstable angina pectoris for cardiac events with meta-analysis comparing published studies

Controversy exists as to the clinical roles and relative specificities of cardiac troponin T or I in patients with unstable angina pectoris (UAP). We measured troponin T and I levels on admission in 123 patients with UAP. Of the 107 patients with normal creatine kinase during the first 24 hours, troponin T and I were elevated in 14 and 13 patients, respectively. At 30 days, 5 of 14 patients (36%) with elevated troponin T and 3 of 93 patients (3.2%) with normal troponin T had acute myocardial infarction (odds ratio [OR], 16.7; 95% confidence interval [CI] 3.4 to 81.5; p <0.001). Of 13 patients with elevated troponin I, 5 patients (39%) and 3 of 94 patients (3.2%) with normal troponin I had acute myocardial infarction (odds ratio, 21.7; 95% CI 4.3 to 110; p <0.001). No deaths occurred within 30 days. Both markers demonstrated equivalent sensitivity (63%) and specificities (troponin T: 91%; troponin I: 92%) for myocardial infarction. Meta-analysis of 12 published troponin T and 9 troponin I studies in patients with UAP produced risk ratios of 4.2 (95% CI 2.7 to 6.4, p <0.001) for troponin I compared with 2.7 (95% CI 2.1 to 3.4, p <0.001) for troponin T. Comparison of the sensitivities and specificities of both markers using summary receiver operating characteristic curves showed no significant difference in their abilities to predict acute myocardial infarction and cardiac death. Troponin T and I show similar prognostic significance for acute myocardial infarction or death in the same patients with UAP. The 2 markers are equally sensitive and specific, as confirmed by meta-analysis, and this supports a role in risk stratification.     

Knowledge and perceptions of medical abortion among potential users

Great advances in surgical techniques, perfusion technology and cardiac anesthesia have made heart surgery safer. However, the mayor advance over the past 15 years has been in the field of myocardial protection. Much remains to be done in this field and there is not complete agreement about the different methods of myocardial protection. At the Institute of Cardiac Surgery of Parma a research is developing to concern three different cardioprotective strategies, of which preliminary results are showing. Three groups of patients with the same clinical, surgical, anesthesiological features, who underwent cardiac surgery have been selected. In patients of group A intermittent cold hyperkalemic crystalloid cardioplegia has been used, in those of group B intermittent cold blood cardioplegia and in those of group C intermittent cold blood cardiolegia associated a warm glucose blood cardioplegic reperfusion before aortic unclamping. In all patients enzyme levels (CPK; CPK-MB; LHD; SGOT; SGPT) were measured 12, 24, 72, 120 hours postoperatively; data were collected, also, on spontaneous return to sinus rhythm, perioperative myocardial infarction and the need or not for inotropic agents. All data at first and then those of patients who underwent only coronary rivascularization (75% of patients) were statistically analyzed (one-way Fischer's test). It appears that the use of antegrade cold intermittent blood cardioplegia with reperfusion is more optimal for myocardial protection, how show lower levels of CPK-MB especially in the first postoperative period. In group C remains greater spontaneous resumption of normal sinus rhythm compare to group A and this suggests a best preservation of cellula-integrity and function with use of blood cardioplegia.     

Elevated serum cardiac markers in asymptomatic marathon runners after competition: is the myocardium stunned?

Prolonged strenuous exercise may trigger acute myocardial infarction (AMI), as exemplified by the occurrence of sudden cardiac death during marathon running. Serum creatine kinase MB (CK-MB) may be elevated in asymptomatic marathon runners after competition from exertional rhabdomyolysis of skeletal muscle altered by training, limiting its utility for evaluating acute cardiac injury in such athletes. Myoglobin and CK-MB2 isoform levels are emerging as earlier markers of AMI and troponin subunits as more specific than serum CK-MB mass. We tested runners before and sequentially after the 1995 Boston Marathon for conventional and newer markers including myoglobin, CK-MB mass and isoforms, cardiac troponin T, and cardiac troponin I using standard laboratory methods and rapid format assays if available. The mean serum values for myoglobin, CK-MB mass, CK-MB/myoglobin rapid panel tests, and CK-MB2 isoforms were normal or negative pre-race and elevated or positive 4 and 24 h after competition. These markers lack specificity for acute cardiac injury in trained runners. While the mean serum values for cardiac troponins T and I remained normal, 9 of 45 runners (20%) showed an increase in subunits by first-generation assays. All runners remained asymptomatic for cardiac disease and completed subsequent marathons 1 year later, making reversible myocardial injury or stunning unlikely. Elevated values of serum markers for AMI, including first-generation assays for both troponin subunits should be interpreted with caution in trained runners.     

Inducing effect of dimethy-4, 4''-dimethoxy-5, 6,5'',6-dimethylenedioxybipheny-2, 2''-dicarboxylate (DDB) on differentiation of leukemia HL-60 cells

OBJECTIVE: Myocardial injury is an important cause of mortality and morbidity after paediatric cardiac surgery. Data obtained from studies in animals imply that juvenile myocardium is more resistant to the effects of ischaemia and reperfusion than adult myocardium but there is little confirmatory evidence in the clinical setting. DESIGN: Prospective observational study of biochemical markers of myocardial injury in a paediatric population undergoing cardiac surgery. SETTING: Tertiary referral centre for paediatric cardiac surgery. PATIENTS: Forty patients undergoing paediatric cardiac surgery of varying complexity including closure of atrial and ventricular septal defects and arterial switch for simple transposition. A control group included patients undergoing thoracotomy for closure of a patent ductus arteriosus or repair of a coarctation. INTERVENTIONS: Serial measurements of myoglobin, the MB isoenzyme of creatine kinase (CK-MB), and the highly specific markers of myocardial damage cardiac troponin T (cTnT) and I (cTnI) were made before and 1, 6, 24, and 48 to 72 hours after operation. RESULTS: There were significant increases in myoglobin and CK-MB, but not cTnT or cTnI, in the control group. There were significant increases in the four biochemical markers in all the cardiac operations but especially in the ventricular septal defect and transposition group. Increases in CK-MB and cTnT were about five times greater than those previously reported in adult patients. CONCLUSIONS: (i) Cardiac troponins are more specific markers of myocardial injury in paediatric cardiac surgery than myoglobin and CK-MB. (ii) Paediatric myocardium seems to be more vulnerable to injury during cardiac surgery than adult myocardium.     

Subcortical vascular dementia: survey of treatment patterns and research considerations

OBJECTIVE: The purpose of this study was to evaluate retrospectively the efficacy of a proposed panel of three cardiac markers (myoglobin, creatine kinase-MB mass [CK-MB], and cardiac troponin I) in the diagnosis of acute myocardial infarction (AMI) in patients with atraumatic chest pain. DESIGN: A total of 110 patients admitted for the evaluation of atraumatic chest pain were examined. Forty-one of these patients were diagnosed with AMI. RESULTS: Five of the 41 patients with AMI had abnormally elevated myoglobin levels, whereas values of CK-MB and/or cardiac troponin I remained negative. Creatine kinase-MB mass alone had a sensitivity of 92.7%, a specificity of 89.9%, a positive predictive value of 84.4%, and a negative predictive value of 95.0% for the diagnosis of AMI. Cardiac troponin I alone had a sensitivity of 90.2%, a specificity of 95.7%, a positive predictive value of 92.5%, and a negative predictive value of 94.3% for the diagnosis of AMI. Cardiac troponin I is a more specific marker for the diagnosis of AMI than CK-MB, particularly in patients with chronic renal failure who are evaluated for chest pain. The combination of CK-MB and cardiac troponin I increased the sensitivity to 100% and the negative predictive value to 100% and had a specificity of 88.4% and a positive predictive value of 83.7%. The panel was diagnostic for all patients with AMI within 12 hours after admission. CONCLUSIONS: Our preliminary results indicate that this panel is highly effective for evaluation of AMI in patients with atraumatic chest pain. Elevated myoglobin levels were useful in detecting patients at high risk for AMI who initially were not detected with other markers. The combination of CK-MB and cardiac troponin I provided much higher sensitivity and had a much higher negative predictive value for the evaluation of AMI than cardiac troponin I or CK-MB alone. The 100% negative predictive value is particularly important because it indicates that patients with negative CK-MB and cardiac troponin I values 12 hours after admission have a negligible likelihood of AMI.     

Different intracellular compartmentations of cardiac troponins and myosin heavy chains: a causal connection to their different early release after myocardial damage

We investigated the net myocardial release of creatine kinase isoenzyme MB (CKMB), myoglobin, cardiac troponin T (cTnT), cardiac troponin I (cTnI), and cardiac beta-type myosin heavy chain (beta-MHC) into the coronary circulation after cardioplegic cardiac arrest in humans. Cardiac markers were measured in paired arterial, central venous, and coronary sinus blood in 19 patients undergoing elective coronary artery bypass grafting (CABG) before aortic cross-clamping and 1, 5, 10, and 20 min after aortic declamping. cTnT and cTnI were released into the coronary sinus in parallel to each other and almost simultaneously to myoglobin and CKMB within 20 min of reperfusion. In contrast, no beta-MHC was released in the same patients during the study period. The average soluble cTnT and cTnI pools in right atrial appendages of 11 patients with right atrial and right ventricular pressures within reference values were comparable and were approximately 8% of total myocardial troponin content. The soluble beta-MHC pool was <0.1% in all patients. Our results demonstrate the impact of the different intracellular compartmention of regulatory and contractile proteins on their early release from damaged myocardium.     

Antipsychotic drugs: is more worse? A meta-analysis of the published randomized control trials

OBJECTIVES: The purpose of this study was to evaluate the usefulness of transesophageal echocardiography before electrical cardioversion in patients with atrial fibrillation and to determine the mechanism of thromboembolism after cardioversion. BACKGROUND: Thromboembolic complications after electrical cardioversion of atrial fibrillation have been attributed to the dislodgment of preexistent left atrial thrombus during the resumption of atrial contraction. Transesophageal echocardiography has been proposed as a method of screening patients for left atrial thrombus before cardioversion. METHODS: Seventy transesophageal echocardiographic studies were performed in 66 patients, predominantly with nonvalvular atrial fibrillation, before direct current cardioversion. In addition, transesophageal echocardiography was performed during the cardioversion procedure in 15 patients and immediately after in 1 patient. RESULTS: Left atrial thrombus was detected in one patient (1.4%), and cardioversion was cancelled. Thromboembolic complications occurred in 4 patients, none of whom had evidence of left atrial thrombus before cardioversion. Within 10 s of successful cardioversion, left atrial spontaneous echo contrast appeared in five patients, increased in one patient and was unchanged in nine patients. Patients with new or increased spontaneous echo contrast had more impaired atrial contraction and slower initial heart rates after cardioversion than those without. Left ventricular contraction was also impaired transiently by cardioversion. CONCLUSIONS: Transesophageal echocardiographic detection of left atrial thrombus before direct current cardioversion is important but infrequent in patients with predominantly nonvalvular atrial fibrillation. The occurrence of thromboembolic complications in the absence of demonstrable left atrial thrombus and the new development of spontaneous echo contrast in association with the transient atrial dysfunction ("stunning") caused by cardioversion suggest that cardioversion may promote new thrombus formation, in which case all patients should receive full anticoagulant therapy at the time of cardioversion.     

Gallbladder volume and contractility in term and preterm neonates: normal values and clinical applications in ultrasonography

BACKGROUND: Normovolemic hemodilution is a well-accepted method for intraoperative blood salvage. However, some controversy exists concerning the possible risk of myocardial fiber injury as consequence of the reduced oxygen content. Laboratory diagnosis of perioperative myocardial fiber injury is difficult, since biochemical markers are elevated postoperatively due to the surgical trauma. Cardiac troponin I (cTnI) is a new, highly sensitive and specific marker for the detection of myocardial injury. The aim of our study was to investigate whether normovolemic hemodilution in patients with major orthopedic surgery (13 hemodiluted patients, 15 control) induces a release of cTnI. METHODS: cTnI as a highly specific and sensitive cardiac parameter, as well as total creatine kinase (CK), creatine kinase isoenzyme MB mass (CKMB mass) and myoglobin were measured after induction of anesthesia, after normovolemic hemodilution, prior to retransfusion of blood components, 3 h after surgery, and on the first and third postoperative days. RESULTS: Prior to retransfusion of blood components the hematocrit was decreased to 25.4 +/- 1.2% (mean +/- SEM; range: 18%-34%) in the control group and to 20.2 +/- 0.8% (mean +/- SEM; range: 17%-24%) in the hemodilution group. Total CK, CKMB mass as well as myoglobin concentration increased significantly in both groups, reaching their maxima within the first day of surgery. In contrast, cTnI was below the detection limit of assay (< 0.5 micrograms/L) at any time. CONCLUSIONS: We suggest that pre- and intraoperative hemodilution to a hematocrit of approximately 20% by maintaining normovolemia does not induce myocardial fiber injury in patients without preexisting cardiac diseases.     

An experimental model for infiltration of malignant lymphoma to the eye and brain

For troponin T a characteristic biphasic change in the plasma time-concentration curve has been described, especially in patients with early reperfusion after thrombolytic therapy. As troponin T is bound to myofibrillar structures, treatment strategy or treatment outcome could influence the cumulative plasma release of this protein in a different way compared to the cumulative release of free cytoplasmic cardiac enzymes. The present study is the first study comparing the total quantity of troponin T released by the heart during the first 168 hours after acute myocardial infarction, both in patients treated with thrombolytic therapy (n = 16) and in patients not treated with thrombolytic therapy (n = 7). On the basis of clinical symptoms and coronary arteriogram within 24 hours, the patients treated with thrombolytic therapy were divided into two groups, reperfused (n = 9) and non-reperfused (n = 7). In the patients not treated with thrombolytic therapy, absence of spontaneous early reperfusion was judged only from clinical symptoms. Cumulative troponin T release into plasma was compared to the cumulative release of the cytoplasmic cardiac enzymes creatine kinase (EC 2.7.3.2) and hydroxybutyrate dehydrogenase (EC 1.1.1.27). Cumulative release, i. e., infarct size, was calculated using a two-compartment model for circulating proteins. Mean tissue contents, per gram wet weight, of 156 U/g for hydroxybutyrate dehydrogenase, 2.163 U/g for creatine kinase and 234 microg/g for troponin T, were used to express infarct size in gram-equivalents of healthy myocardium per litre plasma (g-eq/l). Release rates were represented by the ratio of cumulative quantities released in 10 hours and 72 hours for creatine kinase and hydroxybutyrate dehydrogenase and in 10 hours and 168 hours for troponin T. CONCLUSIONS: - Plasma time-concentration curves and release rates of troponin T in patients treated with thrombolytic therapy showing reperfusion differ significantly from those of patients not treated with thrombolytic therapy, showing no reperfusion. - Creatine kinase and hydroxybutyrate dehydrogenase release is completed within 72-100 hours in all patients, whereas troponin T release still continues after 168 hours. - Cumulative troponin T release at 168 hours is only a fraction (around 8%) of cumulative cytoplasmic enzyme release and the percentage released is not influenced by the treatment strategy or outcome, i. e., vessel patency. - Although troponin T release is only a fraction of the cumulative enzyme release (infarct size) there is a highly significant correlation between both, independent of the treatment strategy or treatment outcome.     

Mild hypothermia after cardiac arrest in dogs does not affect postarrest cerebral oxygen uptake/delivery mismatching

PURPOSE: To compare measurements of cerebral arteriovenous oxygen content differences (oxygen extraction ratios, oxygen utilization coefficients) in dogs after cardiac arrest, resuscitated under normothermia vs. mild hypothermia for 1-2 h or 12 h. METHODS: In 20 dogs, we used our model of ventricular fibrillation (no blood flow) of 12.5 min, reperfusion with brief cardiopulmonary bypass, and controlled ventilation, normotension, normoxemia, and mild hypocapnia to 24 h. We compared a normothermic control Group I (37.5 degrees C) (n = 8); with brief mild hypothermia in Group II (core and tympanic membrane temperature about 34 degrees C during the first hour after arrest) (n = 6); and with prolonged mild hypothermia in Group III (34 degrees C during the first 12 h after arrest) (n = 6). RESULTS: In Group I, the cerebral arteriovenous O2 content difference was 5.6 +/- 1.6 ml/dl before arrest; was low during reperfusion (transient hyperemia) and increased (worsened) significantly to 8.8 +/- 2.8 ml/dl at 1 h, remained increased until 18 h, and returned to baseline levels at 24 h after reperfusion. These values were not significantly different in hypothermic Groups II and III. The cerebral venous (saggital sinus) PO2 (PssO2) was about 40 mmHg (range 29-53) in all three groups before arrest and decreased significantly below baseline values, between 1 h and 18 h after arrest; the lowest mean values were 19 +/- 19 mmHg in Group I, 15 +/- 8 in Group II (NS), and 21 +/- 3 in Group III (NS). Postarrest PssO2 values of < or = 20 mmHg were found in 6/8 dogs in Group I, 5/6 in Group II and 4/6 in Group III. Among the 120 values of PssO2 measured between 1 h and 18 h after arrest, 32 were below the critical value of 20 mmHg. CONCLUSIONS: After prolonged cardiac arrest, critically low cerebral venous O2 values suggest inadequate cerebral O2 delivery. Brief or prolonged mild hypothermia after arrest does not mitigate the postarrest cerebral O2 uptake/delivery mismatching.     

Internal atrial defibrillation after failure of attempted pharmacological and electrical cardioversion. Mid- and long-term outcome

Cardioversion of atrial fibrillation by an endocavitary electrical shock was first proposed during the 1980s. The authors studied the efficacy of this technique at short and medium term in a population of 36 patients (28 men and 8 women) in whom atrial fibrillation persisted despite attempts to reduce it by antiarrhythmic drugs and external electrical cardioversion. The immediate success rate was high : 34 out of 36 patients (94%) and, at medium term, the number with sinus rhythm was comparable to that of studies evaluating the medium-term efficacy of external electrical cardioversion; 19 out of 33 patients (57%) were in sinus rhythm at 6 months and 9 out of 27 patients (33%) at 12 months. These results seem to justify attempts at internal atrial defibrillation in patients in whom the other two techniques of cardioversion have failed. Its use as the method of first intention could be proposed if the profile of "resistant" patients to classical techniques was known, which is unfortunately not presently the case.