Elevated circulating cardiac troponin I in patients with cirrhosis

It has been shown that certain patients with cirrhosis have asymptomatic cardiac abnormalities that have not yet been explained. Thus, cardiac troponin I, a specific marker of myocardial injury, has been measured in patients with cirrhosis without previous cardiac disease. Thirty-two consecutive patients (age 49 +/- 11) with cirrhosis and normal ECG were selected, 22 of which were alcoholic. Hemodynamic investigations were performed. Left ventricular function and mass were evaluated by echocardiography. Serum creatine kinase MB mass, myoglobin, and cardiac troponin I concentrations were measured. Cardiac troponin I concentrations were elevated in 10 patients (32%) (range 0.06-0.25 microg/L) whereas creatine kinase MB mass and myoglobin were normal in all patients. Abnormal troponin I values were not related to the severity of cirrhosis, to the degree of portal hypertension, or to other hemodynamic values. In contrast, elevated serum cardiac troponin I concentrations were related to a decreased stroke-volume index (P <. 05) and a decreased left ventricular mass (P <.05). These results show a high prevalence of slightly elevated serum cardiac troponin I in patients with cirrhosis, especially in those with alcoholic cirrhosis. Elevated troponin I is associated with subclinical left ventricular myocardial damage. These findings may be linked to a lack of left ventricular adaptation in certain patients with cirrhosis and alcoholic cardiomyopathy.     

Cardiac troponin I level correlates with chronic-phase left ventricular function after successful direct percutaneous transluminal coronary angioplasty in patients with acute myocardial infarction

OBJECTIVES: The relationships between cardiac troponin I, various biochemical markers, and chronic-phase left ventricular ejection fraction (LVEF) after successful direct percutaneous transluminal coronary angioplasty (PTCA) were examined in 36 patients with acute myocardial infarction. METHODS: Biochemical markers were measured on admission, immediately after, and from 6 hours to 9 days after PTCA. RESULTS: The time to peak values were: creatine kinase-MB 9.7 hours, cardiac troponin I 9.8 hours, myoglobin 10.7 hours, creatine kinase 10.6 hours, cardiac troponin T 18.6 hours, and myosin light chain 68.9 hours. Cardiac troponin T, cardiac troponin I and myosin light chain levels were elevated over 9 days after successful direct PTCA. Chronic-phase LVEF inversely correlated with peak values of creatine kinase-MB (r = -0.519, p < 0.01), cardiac troponin T (r = -0.500, p < 0.01), cardiac troponin I (r = -0.441, p < 0.05) and creatine kinase (r = -0.411, p < 0.05). The values of cardiac troponin I, cardiac troponin T, creatine kinase and creatine kinase-MB at each sampling point were significantly inversely related to chronic-phase LVEF. The value of cardiac troponin I at each time point for 7 days correlated well with chronic-phase LVEF. CONCLUSIONS: Cardiac troponin I has high specificity for predicting long-term cardiac function after successful direct PTCA when early values are unavailable.     

Circulating concentrations of cardiac proteins in complicated and uncomplicated Plasmodium falciparum malaria

In an unmatched case-control study of 63 non-immune European patients with uncomplicated (n = 52) and complicated (n = 11) falciparum malaria, serum levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), heart-type fatty acid-binding protein (H-FABP), myoglobin, troponin T and creatin kinase-muscle brain were compared. Elevated levels of NT-proBNP and H-FABP indicated myocardial impairment in complicated but not in uncomplicated falciparum malaria. The clinical impact of these findings remains to be evaluated. The pathophysiology of cardiac impairment in complicated falciparum malaria warrants further investigation.     

血清肌钙蛋白I、肌酸激酶同工酶-Ⅱ测定在肾衰患者中的作用

目的：观察慢性肾功能衰竭患者心肌肌钙蛋白、肌酸激酶同工酶一Ⅱ的异常变化,并分析其与预后的关系。方法：应用ACCESS2化学发光法检测慢性肾功能衰竭患者心肌肌钙蛋白、肌酸激酶同工酶一Ⅱ,彩色多普勒测定左室射血分数（EF）,同时对心肌肌钙蛋白升高患者进行APACHEⅡ评分。结果：48例患者血清肌钙蛋白I升高率为44．4％;APACHEⅡ评分在心肌肌钙蛋白升高患者中明显升高;血清肌钙蛋白I、肌酸激酶同工酶-Ⅱ同时升高患者,心衰发生率高。结论：慢性肾功能衰竭患者心肌损伤较为普遍且部分为亚临床损伤,需谨慎对待。     

Early release of glycogen phosphorylase in patients with unstable angina and transient ST-T alterations.

OBJECTIVE--To determine whether transient ST-T alterations in patients with unstable angina are associated with an increase in plasma glycogen phosphorylase BB concentrations on admission to hospital. DESIGN--Prospective screening of patients with unstable angina for markers of myocardial cell damage. SETTING--Accident and emergency department of university hospital. PATIENTS--48 consecutive patients admitted for angina pectoris (18 with transient ST-T alterations). None of the patients had acute myocardial infarction according to standard criteria. MAIN OUTCOME MEASURES--Creatine kinase and creatine kinase MB activities, creatine kinase MB mass concentration, and myoglobin, cardiac troponin T, and glycogen phosphorylase BB concentrations on admission. RESULTS--All variables except for creatine kinase and creatine kinase MB activities were significantly higher on admission in patients with unstable angina and transient ST-T alterations than in patients without. However, glycogen phosphorylase BB concentration was the only marker that was significantly (p = 0.0001) increased above its discriminator value in most patients (16). In the 18 patients with transient ST-T alterations creatine kinase MB mass concentration and troponin T and myoglobin concentrations were significantly (p = 0.0001) less commonly increased on admission (in five, three, and two patients, respectively). CONCLUSIONS--The early release of glycogen phosphorylase BB may help to identify high risk patients with unstable angina even on admission to an emergency department. Glycogen phosphorylase BB concentrations could help to guide decisions about patient management.     

Serum troponins T and I after elective cardioversion.

AIMS: To describe the pattern of release of five myocardial proteins after elective cardioversion. METHODS AND RESULTS: We measured serum levels of the myocardial proteins creatine kinase, creatine kinase MB mass, myoglobin, troponin T and troponin I serially from baseline to 24 h after 72 elective cardioversion attempts. The total energy used for attempted cardioversion was 408+/-318 J (range 50 to 1280 J). Maximal creatine kinase levels (median 232 IU x l(-1), interquartile range 91 to 1152 IU x l(-1)) occurred at 24 h and correlated with the total energy delivered (r=0.75, P<0.0001). The peak creatine kinase MB mass levels exceeded the discrimination level for myocardial injury (>/=5 microg x l(-1)) in seven patients (10%). The peak myoglobin levels were elevated (>85 microg x l(-1)) in 40 patients (56%) and correlated with the peak creatine kinase levels (r=0.83, P<0.0001). Troponin T reached the discrimination level (0.10 microg x l(-1)) in one patient with a serum creatinine level of 0.16 mmol x l(-1)and severe left ventricular impairment. Twelve patients had baseline troponin I levels above our prespecified discrimination level of 0.4 microg x l(-1)(range 0.4 to 3.1 microg x l(-1)), which did not increase after cardioversion. In two patients the levels rose from <0.4 microg x l(-1) to 0.5 microg x l(-1) and 0.6 microg x l(-1) respectively. CONCLUSIONS: Troponin T levels do not rise after elective cardioversion. The minor increases in troponin I may reflect our choice of discrimination level. Cardiac troponins are useful in determining whether arrhythmias requiring emergency cardioversion are primary or secondary to myocardial infarction.     

Detection of myocardial injury during transvenous implantation of automatic cardioverter-defibrillators.

OBJECTIVES: The present study was designed to assess the extent of myocardial injury in patients undergoing transvenous implantation of an automatic implantable cardioverter-defibrillator (ICD) using cardiac troponin I (cTNI), which is a highly specific marker of structural cardiac injury. BACKGROUND: During ICD implantation, repetitive induction and termination of ventricular fibrillation (VF) via endocardial direct current shocks is required to demonstrate the correct function of the device. Transthoracic electrical shocks can cause myocardial cell injury. METHODS: Measurements of total creatine kinase (CK), CK-MB, myoglobin, cardiac troponin T (cTNT) and cTNI were obtained before and after ICD implantation in 49 consecutive patients. Blood samples were drawn before and 2, 4, 8, and 24 h after implantation. RESULTS: Elevations of CK, CK-MB, myoglobin, cTNT and cTNI above cut-off level were found in 25%, 6%, 76%, 37% and 14% of patients, respectively, with peak cTNI concentrations ranging from 1.7 to 5.5 ng/ml. Cumulative defibrillation energy (DFE), mean DFE, cumulative VF time, number of shocks as well as prior myocardial infarction (MI) were found to be significantly related to a rise of cTNI. Mean DFE > or = 18 J and a recent MI were identified as strong risk factors for cTNI rise. CONCLUSIONS: During transvenous ICD implantation myocardial injury as assessed by cTNI rise occurs in about 14% of the patients. Peak cTNI concentrations are only minimally elevated reflecting subtle myocardial cell damage. Patients with a recent MI and a mean DFE > or = 18 J seem to be prone to cTNI rise.     

Serum myoglobin levels in patients with ischemic myocardial insult

Serum myoglobin levels were studied in 178 consecutive patients admitted for chest pain due to ischemic cardiac injury. Serum myoglobin level was compared with the clinical condition, electrocardiographic changes, and serum creatine kinase levels. Elevated serum myoglobin concentration was present in all patients with acute myocardial infarction, as defined by World Health Organization, Geneva, criteria, and, in addition, in about 50% of patients with so-called acute coronary insufficiency. On this basis we could define two different groups of patients with acute coronary insufficiency: cases exhibiting elevated serum myoglobin levels (group 1) and those with normal levels (group 2). In group 1 although creatine kinase levels were in the normal range, they were significantly higher than in group 2. Four patients from group 1 developed heart failure and another a typical acute myocardial infarction during hospitalization, whereas no patients of group 2 had such complications. In patients with acute myocardial infarction, the elevation of serum myoglobin preceded that of creatine kinase in most cases. Myoglobin release appears to be related to infarct size, the highest levels were found in extensive myocardial infarction and less marked elevations in cases of subendocardial infarction and in half of the cases with acute coronary insufficiency. It is proposed that serum myoglobin is a reliable measure of myocardial necrosis and serves to detect a hitherto undefined population of small-size acute myocardial infarction, with its attendant clinical and prognostic implications.     

New cut-off values of cardiac markers for risk stratification of angina pectoris

BACKGROUND: The aim of this present prospective study was to investigate the accuracy of cardiac markers for the prediction of subsequent cardiac events (cardiac death, acute myocardial infarction and recurrent ischemia requiring coronary revascularization). METHODS: Fibrinogen, cardiac troponin T, troponin I, creatine phosphokinase myocardial fraction, C-reactive protein and myoglobin at baseline and after 6 h were measured on 154 patients (109 male, 63+/-11 years) with chest pain. Receiver operator characteristic analyses were performed to determine cut-off points of cardiac markers in prediction of adverse events. RESULTS: The following cut-off values for prediction of cardiac events were calculated: troponin I at baseline 0.3 ng/ml (predictive accuracy=0.870), troponin I at 6 h 0.50 ng/ml (p.a.=0.909); troponin T at baseline 0.05 ng/ml (p.a.=0.643), troponin T at 6 h 0.05 ng/ml (p.a.=0.612), creatine phosphokinase myocardial fraction at baseline 2.0 ng/ml (p.a.=0.721), creatine phosphokinase myocardial fraction at 6 h 2.5 ng/ml (p.a.=0.734), myoglobin at baseline 23 ng/ml (p.a.=0.623), myoglobin at 6 h 26 ng/ml (p.a.=0.617), C-reactive protein at baseline 0.31 mg/dl (p.a.=0.662), C-reactive protein at 6 h 0.55 mg/dl (p.a.=0.682), and fibrinogen at baseline 360 mg/dl (p.a.=0.701). The combination of baseline troponin I with different parameters resulted in a higher sensitivity of up to 98%, with a similar predictive accuracy, but a lower specificity. Additive measurements of cardiac troponin I at 6 h to baseline cardiac troponin T and I proved to be the best combination for prediction of subsequent cardiac events. CONCLUSIONS: Changes in cut-off levels of cardiac markers and inflammatory parameters results in a high accuracy of risk stratification in patients with chest pains. Combination of these measurements might further help in the identification of patients who would benefit from early coronary revascularization.     

Skeletal muscle involvement in falciparum malaria: biochemical and ultrastructural study.

Biochemical evidence of skeletal muscle damage is common in malaria, but rhabdomyolysis appears to be rare. To investigate the relationship between serum creatine kinase and myoglobin levels, muscle histology, and renal function in Plasmodium falciparum infections, we studied 13 patients with uncomplicated malaria, 13 with severe noncerebral malaria, and 10 with cerebral malaria. A muscle biopsy specimen was obtained from each patient for light microscopy and electron microscopy. Mean serum creatine kinase concentrations +/- SD were raised but similar for the three groups (258 +/- 277, 149 +/- 158, and 203 +/- 197 U/L, respectively; P = .5). The mean serum myoglobin level +/- SD was highest in cerebral malaria (457 +/- 246 vs. 170 +/- 150 and 209 +/- 125 ng/mL in uncomplicated and severe malaria, respectively; P < .01) and correlated with the mean serum creatinine level (r = .39 for 36 patients; P = .02). The number of intravascular parasites, proportion of mature forms, and glycogen depletion were highest in biopsy specimens from patients with cerebral malaria. Myonecrosis was not observed. Muscle appears to be an important site for P. falciparum sequestration, which could contribute to metabolic and renal complications.     

Coronary angiographic findings and troponin T in patients with unstable angina pectoris

This study sought to identify differences in coronary anatomic pathology in patients with unstable angina and elevated versus nonelevated serum troponin T values. Previous studies have shown a worse prognosis in unstable angina patients with elevated serum troponin T values. Consecutive patients (n = 117) with Braunwald class IIIB angina were included in the study. Serum samples for troponin T were obtained at admission and every 6 to 8 hours for 18 to 24 hours. Acute myocardial infarction was excluded by routine creatine kinase measurements. All patients underwent coronary angiography before discharge. Cardiac events including cardiac death and myocardial infarction were recorded. Two thirds of the patients with unstable angina had no increase in serum troponin T (<0.1 microg/L) (n = 80). They had a lower incidence of 3-vessel disease (26% vs 46%, p <0.001), left main disease (5% vs 16%, p = 0.04), visible thrombus (4% vs 22%, p = 0.006), and less severe stenosis of the culprit artery (65% vs 84%, p <0.004) than patients with elevated serum troponin T values (> or =0.1 microg/L) (n = 37). The 1-year cardiac event rate was 0% versus 19% in patients with troponin T values <0.1 microg/L compared with patients with serum troponin T values > or =0.1 microg/L (p <0.0001). It was concluded that patients with unstable angina and no release of troponin T have less severe coronary artery disease, and have an excellent prognosis. It is suggested that these patients may be managed more conservatively and without invasive evaluation before discharge.     

Comparison of different cardiac markers in monitoring percutaneous coronary interventions with frequent use of stents and gpIIbIIIa-antagonists

Studies from the early 1990s found elevations of creatine kinase (CK) and its isoform CK-MB in 5-30% of patients after PCI, indicating minor myocardial damage. Less is known about the influence of modern improved PCI-techniques on the frequency of elevated cardiac markers and the correlation between different commonly used markers, especially cardiac troponins. From 1997 to 2001, 1486 patients undergoing PCI during the regular working hours were included in the prospective "Ludwigshafen Infarctlet Registry". Myocardial infarction in the past 48 hours was an exclusion criterion. Clinical and procedural data were documented. Follow-up data were obtained from discharge up to one year. PCI-related elevations of troponin T were found in 18%, of total-CK in 11%, of CK-MB in 33% and of myoglobin in 23% of cases. The correlation between the different markers was poor. Compared with troponin T, other markers showed low sensitivity (total-CK 58%, CK-MB 27%, myoglobin 22%) and, especially total-CK, low specificity. Stenting, side branch occlusion or major dissection, complex lesion morphology, gpIIbIIIa-antagonist application, proximal stenosis and unstable angina were independent predictors of an elevated troponin T in multivariate analysis. Due to this weak correlation between more specific and sensitive troponins and the other markers, troponins are preferred in monitoring after PCI. In addition to lesion characteristics, particularly stenting is associated with an increased rate of elevated troponin.     

The role of cardiac troponin t and other new biochemical markers in evaluation and risk stratification of patients with acute chest pain syndromes

Background and hypothesis: Increased serum creatinine kinase (CK) and CK-MB enzyme levels have been used for years to detect myocardial infarction (MI). However, serum myoglobin and CK-MB mass or protein levels may indicate MI earlier; cardiac troponin T is the most specific marker of myocardial injury and it can detect even minor myocardial necrosis. The diagnostic and prognostic utility of the traditional and new markers of cardiac injury in the emergency evaluation of patients with acute chest pain syndromes were therefore compared. Methods: One hundred and fifteen consecutive patients with an acute coronary syndrome, and 64 controls recruited during the same period, were examined. The time elapsed from onset of symptoms to blood collection was recorded. Cardiac markers were measured in specimens collected upon arrival (0 h), and 2 and 5–9 h, and later in cases of longer observation. The major cardiac events occurring up to 40 months after the index examination were recorded. Results: cTnT levels provided unique information: they were the most specific indicators of myocardial damage and identified unstable angina patients at high risk of future major events. Up to 6 h after the onset of chest pain, the new markers were elevated more frequently than the traditional ones and permitted earlier MI recognition. The worst prognosis (nonfatal myocardial infarction or death) was noted in subjects with chest pain at rest within 48 h before the index examination and elevated cTnT levels. Conclusions: The new markers, particularly cardiac troponin T, offer considerable advantages and they should be more widely used in the diagnosis and risk stratification of acute coronary syndromes.     

Cardiac troponin I levels in patients with left heart failure and cor pulmonale

Cardiac troponin levels are regarded as the most specific of currently available biochemical markers of myocardial damage. Elevated levels of troponin have been previously reported in patients with left heart failure, reflecting small areas of undetected myocardial cell death. The aim of this study was to compare the levels of the cardiac troponin I (cTnI) in patients with left- and right-sided heart failure. Cardiac troponin I levels were studied with immunochemical methods in patients with right heart failure (n = 17) resulting from chronic obstructive pulmonary disease, ischemic left heart failure (n = 23), and nonischemic left heart failure (n = 18) who were admitted to departments of cardiology and chest diseases. Also, cTnI levels were measured in 32 healthy subjects as control group. Protein markers of myocardial injury (cTnI and myoglobin) in patients with left and right heart failure were collected approximately 12 to 36 hours after onset of obvious symptoms. Serum creatine kinase MB band was determined on admission and thereafter twice a day during the first 3 days. Elevated levels of serum cTnI were found in patients with nonischemic (0.83 +/- 0.6 ng/mL, p<0.01) and ischemic left heart failure (0.9 +/- 0.5 ng/mL, p<0.01) when compared to healthy subjects, whereas serum cTnI levels in patients with right heart failure due to chronic obstructive pulmonary disease were not significantly different from those of control subjects (0.22 +/- 0.1 vs 0.16 +/- 0.1 ng/mL, p>0.05). In addition, creatine kinase MB band and myoglobin levels were not significantly different between patient and healthy groups. The mean of cTnI levels in ischemic and even nonischemic left heart failure were increased compared to the mean of values in healthy individuals but without significant creatine kinase MB band and myoglobin elevations. But cTnI levels were not increased in patients with right heart failure due to chronic obstructive pulmonary disease. These data indicate that the cTnI levels are abnormal in left heart failure but not in cor pulmonale.     

Myocardial damage during percutaneous transluminal coronary angioplasty as evidenced by troponin T measurements

Aim The present study was undertaken to assess the effect ofballoon inflation during percutaneous transluminal coronaryangioplasty on markers of myocardial damage. Methods and results Seventy-five patients undergoing electivepercutaneous transluminal coronary angioplasty were evaluatedwith serum creatine kinase MB and cardio-specific troponin Tbefore and 1 and 4 days after the procedure. On day 1, 28% ofthe patients had increased cardiospecific troponin T valuesand 18% had increased creatine kinase MB values. On day 4, 24%had increased cardiospecific troponin T values, whereas allcreatine kinase MB values were normal. A high degree of correlationbetween creatine kinase MB and cardiospecific troponin T onday 1, as well as between both markers on day 1 and cardiospecifictroponin T on day 4 were found. The increased levels of cardiospecifictroponin T on day 4 was significantly correlated with the totalballoon inflation time (P<0·001). Conclusion We conclude that irreversible myocardial damage,as evidenced by increased cardiospecific troponin T values onday 4, occurs in an appreciable number of patients during percutaneoustransluminal coronary angio-plasty, and that this damage isstrongly correlated with the total balloon inflation time.     

Evaluation of "new" cardiac markers for ruling out myocardial infarction after coronary artery bypass grafting

STUDY OBJECTIVES: This study was conducted to evaluate the value of serum troponin T, myoglobin, and creatine kinase (CK)-MB mass concentrations for ruling out perioperative myocardial infarction (poMI) early after cardiac surgery. DESIGN: Retrospective study. SETTING: Cardiothoracic surgery department in a university hospital. PATIENTS: One hundred eighty-one patients undergoing coronary artery bypass grafting (CABG) with cardiopulmonary bypass were included. METHODS: Serum concentrations of troponin T, myoglobin, and CK-MB mass were measured preoperatively (baseline), on arrival at the cardiosurgical ICU (CICU), and at 2, 4, 8, 12, 16, and 20 h after arrival at the CICU. The strength of markers studied for ruling out poMI was studied using receiver operating characteristics curves. Based on these curves, the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) for each marker at every time point were calculated. RESULTS: poMI developed in 14 patients. On arrival at the CICU, all markers were significantly increased from baseline concentrations in both patient groups. In patients with poMI, serum concentrations of troponin T, myoglobin, and CK-MB mass were significantly higher than in control patients from 8, 2, and 0 h after arrival on the CICU, respectively. CK-MB mass was the earliest marker, and its NPV reached 98.6% 12 h after arrival at the CICU. On arrival at the CICU, the NPV for CK-MB mass already reached 96.7%. The NPV for myoglobin reached 98.4% 12 h after arrival at the CICU. Troponin T was not an early marker for ruling out poMI, with an NPV reaching 98.6% 12 h after arrival on the CICU. During the first 8 h after arrival at the CICU, sensitivity, specificity, PPV, and NPV of CK-MB mass exceeded those of myoglobin and troponin T. In later measurements (until 20 h after arrival at the CICU), troponin T gave the most sensitive definition of poMI. CONCLUSIONS: For ruling out poMI on the CICU after CABG, CK-MB mass is a better marker than myoglobin and troponin T during the first 12 h after arrival on the CICU. Using these markers, postoperative treatment of cardiac surgical patients might be further improved.     

Prognostic value of troponin T, myoglobin, and CK-MB mass in patients presenting with chest pain without acute myocardial infarction.

OBJECTIVE: To assess the prognostic value of minor myocardial damage in patients presenting with chest pain without myocardial infarction. DESIGN: The relative risk of suffering a cardiac event in the next six months was assessed in patients with minor myocardial damage assessed by the cardiac markers CK-MB, myoglobin, and troponin T. SETTING: Emergency department of a large university hospital. PATIENTS: In 128 consecutive patients with chest pain, acute myocardial infarction (by WHO criteria) was ruled out; of these, 39 had a rise and fall of one or more markers, indicating minor myocardial damage. The presence of a documented history of coronary artery disease was assessed on admission. RESULTS: 24 patients had a subsequent event (cardiac death, acute myocardial infarction, percutaneous transluminal coronary angioplasty, coronary artery bypass grafting) in the next six months. An abnormal troponin T predicted a subsequent event while abnormal CK-MB or myoglobin did not. The relative risk for troponin T was 2.8 (95% confidence interval: 1.0 to 7.9), for myoglobin 1.0 (0.3 to 3.2), and for CK-MB 0.9 (0.2 to 3.4). A documented history of coronary artery disease predicted subsequent events with a relative risk of 3.9 (1.3 to 11.3). CONCLUSIONS: Troponin T was the only marker that predicted future events, but a documented history of coronary artery disease was the best predictor in patients in whom an acute myocardial infarction had been ruled out.     

Direct current cardioversion does not cause cardiac damage: evidence from cardiac troponin T estimation

Aim—To determine whether elective direct current (dc) cardioversion of atrial fibrillation/flutter causes myocardial damage.
Methods and results—Cardiac troponin T and creatine kinase were estimated 20-28 hours after dc cardioversion in 51 patients who received dc shocks for elective cardioversion of chronic atrial fibrillation/flutter. Although creatine kinase was raised in 44 patients, cardiac troponin T was undetectable in all patients.
Conclusion—Cardiac damage does not occur as a result of cardioversion.

Keywords: cardioversion;  troponin T;  creatine kinase;  atrial fibrillation     

Non-invasive assessment of perioperative myocardial cell damage by circulating cardiac troponin T

Troponin T is a unique cardiac antigen which is continuously released from infarcting myocardium. Its cardiospecificity as a marker protein might be particularly useful in assessing myocardial cell damage in patients undergoing cardiac surgery. Therefore, circulating troponin T was measured in serial blood samples from 56 patients undergoing cardiac surgery and in two control groups--22 patients undergoing minor orthopaedic surgery and 12 patients undergoing lung surgery by median sternotomy. In both control groups no troponin T could be detected, whereas activities of creatine kinase were raised in all 12 lung surgery controls and activities of the MB isoenzyme were raised in five of the 12 patients in the lung surgery group and in four of the 22 patients in the orthopaedic surgery group, respectively. All the patients undergoing coronary artery bypass grafting (n = 47) and cardiac surgery for other reasons (n = 9) had detectable concentrations of troponin T. Five patients had perioperative myocardial infarction detected as new Q waves and R wave reductions. In these five patients troponin T release persisted and serum concentrations (5.5-23 micrograms/l) reached a peak on the fourth postoperative day. In the 51 patients without perioperative myocardial infarction serum concentrations and the release kinetics of troponin T depended on the duration of cardiac arrest. In patients in whom aortic cross clamping was short troponin T increased slightly on the first postoperative days; in patients with longer periods of aortic cross clamping troponin T concentrations were higher and remained so beyond the fifth postoperative day. In patients with non-specific changes on the electrocardiogram troponin T concentrations were significantly higher on days 1 and 4 after operation than in patients with normal postoperative electrocardiograms(11.2 (5) and 4.5 (2.6) v 8.2 (3.4) and 2.9 (1.6) 1microg/l). Serum concentrations of troponin T showed some myocardial cell damage in every patient undergoing cardiac surgery. The persistent increases that were more common in patients with longer periods of cardiac arrest must have been caused by damage to the contractile apparatus. These results suggest that perioperative myocardial cell necrosis may be more common than indicated by changes of the QRS complex on the electrocardiogram.     

Usefulness of cardiac troponin I in patients undergoing open heart surgery

BACKGROUND: Significant myocardial injury during cardiac surgery is associated with a 10-fold increase in 2-year complication rates, yet there remains no clinical gold standard for diagnosis. Troponin I has complete cardiospecificity and is clinically used for diagnosis of myocardial infarction in other settings. METHODS AND RESULTS: One hundred consecutive patients undergoing open heart surgery (71 coronary artery bypass grafts and 29 aortic valve replacements) were enrolled and blood samples were drawn preoperatively, at 5 AM and 5 PM on days 1 and 2 after surgery, and at 5 AM for 3 more days. Twelve-lead electrocardiograms were performed daily and echocardiographic studies were performed on patients with either; electrocardiographic changes signifying likely myocardial damage, intraoperative complications, or elevated creatine kinase subfraction MB or troponin values. Seventeen patients had either new wall motion abnormalities or new Q waves all with peak cardiac troponin I >40 ng/mL. Stratification of patients by peak troponin values <40 and >60 ng/mL was highly predictive (P <.001) of days in intensive care unit, days on ventilator, development of new arrhythmia, and especially cardiac events. These postoperative variables also showed a stronger correlation with peak cardiac troponin I than did peak creatine kinase subfraction MB. CONCLUSION: Peak troponin I values detect myocardial infarction the day after heart surgery and predicts patient outcome.