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Creatine kinase isoenzyme MB relative index as predictor of mortality on extracorporeal membrane oxygenation support for postcardiotomy cardiogenic shock in adult patients.

OBJECTIVE: Extracorporeal membrane oxygenation (ECMO) has been used as initial, biventricular circulatory support for patients with severe postcardiotomy cardiogenic shock (PCS). Due to its aggressiveness and limited weaning quote, concerns have been raised about maintenance of ECMO support regarding duration. However, it is frequently hazardous for physicians to make an individualized decision, whether and when discontinuation of ECMO support should be considered. We tried to find measurable values during ECMO support that could predict the patient mortality on ECMO support. METHODS: During a 9-year period, 32 patients (mean age 55.4+/-11.9; ranging from 30 to 75 years) with ECMO support for postcardiotomy cardiogenic shock were included in this study. RESULTS: Eighteen patients died without weaning (group I, 56.25%), while 14 patients could be weaned off the ECMO support (group II, 43.75%). In the group II, six patients (18.75%) died later in the postoperative course and eight patients (25%) survived to be discharged from hospital. The overall survival of all 32 patients at 30 days was 31.25% (n=10). At a follow-up period of 3.88+/-1.58 years, the overall survival rate was 12.5% (n=4). Mean duration of ECMO support was 2.7+/-1.7 days. The following variables were significantly different between the two groups: blood lactate level and the level of MB isoenzyme of creatine kinase (CK-MB) 48 h after ECMO initiation (p<0.01, p=0.001) as well as the CK-MB relative index as the ratio of CK-MB to total CK (p<0.001). Logistic regression identified that only the CK-MB relative index 48 h after ECMO initiation was associated with mortality on ECMO support (p=0.011, odds ratio=1.219, 95% confidence interval: 1.046-1.421). CONCLUSION: For adult non-transplantation patients with postcardiotomy cardiogenic shock, the CK-MB relative index 48 h after ECMO initiation can be a predictor of mortality on ECMO support. This might be a useful tool for considering a patient either for discontinuation of ECMO support or further treatment.

Adult↗

The role of leukocyte depleting filters in heart transplantation: early outcomes in prospective, randomized clinical trial.

OBJECTIVE: Leukocyte-mediated reperfusion injury to cardiac allograft in the perioperative period is most likely associated with the early and late mortality after heart transplantation (Htx). Our aim is to determine the efficacy and safety of using leukocyte-depleting filters in a cardiopulmonary bypass (CPB) and secondary blood cardioplegia (SBC) circuit in Htx. METHODS: A prospective, randomized trial was performed in 40 patients undergoing orthotopic Htx. These patients were divided into two groups, to be treated with either leukocyte-depleted (LD) reperfusion (n=20) in the LD group, or whole blood reperfusion (n=20) in the Control group. The SBC was used in both groups. RESULTS: Intraoperatively, the LD group presented the reduced markers of reperfusion injury. The course of the creatine kinase MB (CK-MB) releases was significantly lower in the LD group (p<0.05). The LD hearts showed better spontaneous rhythm resumption (60% vs 10%; p<0.001), and lower need for isoprenaline (0.02+/-0.01 microg/(kg min) vs 0.03+/-0.02 microg/(kg min); p<0.05) and epicardial pacing (25% vs 60%; p<0.05) for weaning off CPB. Postoperatively, lower and shorter need for inotropic support (48+/-46, median=35 h vs 131+/-68, median=109 h; p<0.001), shorter temporary epicardial pacing (6+/-14, median=0 h vs 25+/-52, median=1 h; p<0.01), and lower 24-h chest drainage (551+/-274, median=500 ml vs 973+/-836, median=665 ml; p<0.05) in the LD group contributed to the shorter mechanical ventilation time (8+/-3, median=7.5 h vs 14+/-12, median=8.5 h; p<0.05) and the shorter stay at an intensive care unit (ICU) (70+/-24 h vs 116+/-73 h; p<0.05). The 30-day mortality was zero in both groups. CONCLUSIONS: The use of leukocyte depleting filters in heart transplantation is an effective, easy and safe method of myocardial protection, reducing significant myocardial reperfusion injury and improving posttransplant graft functional recovery.

Adult↗

Effects of KR-32570, a new sodium hydrogen exchanger inhibitor, on myocardial infarction and arrhythmias induced by ischemia and reperfusion.

The present study was performed to evaluate the cardioprotective effects of [5-(2-methoxy-5-chloro-5-phenyl)furan-2-ylcarbonyl]guanidine (KR-32570) in rat and dog models of coronary artery occlusion and reperfusion. In addition, we sought to clarify the efficacy of KR-32570 on reperfusion-induced fatal ventricular arrhythmia. In anesthetized rats subjected to 45-min coronary occlusion and 90-min reperfusion, KR-32570 (i.v. bolus) dose-dependently reduced myocardial infarct size from 58.0% to 50.7%, 35.3%, 33.5% and 27.0% for 0.03, 0.1, 0.3 and 1.0 mg/kg, respectively (P<0.05). In anesthetized beagle dogs that underwent 1.2-h occlusion followed by 3.0-h reperfusion, KR-32570 (3 mg/kg, i.v. bolus) markedly decreased infarct size from 28.9% in vehicle-treated group to 8.0% (P<0.05), and reduced the reperfusion-induced release in creatine kinase isoenzyme MB, lactate dehydrogenase, Troponin-I and glutamic-oxaloacetic transaminase. KR-32570 dose-dependently decreased the incidence of premature ventricular contraction, ventricular tachycardia or ventricular fibrillation induced by ischemia and reperfusion in rats. Similar results were obtained in dogs with reperfusion-induced arrhythmia. In separate experiments to assess the effects of timing of treatment, KR-32570 given 10 min before or at reperfusion in rat models also significantly reduced the myocardial infarct size (40.9% and 46.1%, respectively) compared with vehicle-treated group. In all studies, KR-32570 caused no significant changes in any hemodynamic profiles. Taken together, these results indicate that KR-32570 significantly reduced the myocardial infarction and incidence of arrhythmias induced by ischemia and reperfusion in rats and dogs, without affecting hemodynamic profiles. Thus, it could be potentially useful in the prevention and treatment of myocardial injuries and lethal ventricular arrhythmias.

Animals↗

Long-term prognostic value of asymptomatic cardiac troponin T elevations in patients after major vascular surgery.

BACKGROUND: Cardiac troponin T (cTnT) is a sensitive and specific marker for myocardial injury, but elevations of cTnT without clinical evidence of ischemia and persistent or new electrocardiographic (ECG) abnormalities are common in patients undergoing major vascular surgery. We explored the long-term prognostic value of cTnT levels in these patients. METHODS: A follow-up study was conducted between 1996-2000 in 393 patients who underwent successful aortic or infrainguinal vascular surgery and routine sampling of cTnT. Patients were followed until May 2003 (median of 4 years [25th-75th percentile, 2.8-5.3 years]). Total creatine kinase (CK), CK-MB, and cTnT were routinely screened in all patients, and included sampling after surgery and the mornings of postoperative days 2, 3 and 7. Electrocardiograms were also routinely evaluated for sign of ischemia. An elevated cTnT was defined as serum concentrations >/=0.1 ng/ml in any of these samples. All-cause mortality was evaluated during long-term follow-up. RESULTS: Eighty patients (20%) had late death. The incidence of all-cause mortality (41% vs. 17%; p<0.001) was significantly higher in patients with an elevated cTnT level compared to patients with normal cTnT. After adjustment for baseline clinical characteristics, the association between an elevated cTnT level and increased incidence of all-cause mortality (adjusted hazard ratio, 1.9; 95% CI, 1.1-3.1) persisted. Elevated cTnT had significant prognostic value in patients with and without renal dysfunction, abnormal levels of CK-MB, and in patients with transient ECG abnormalities. CONCLUSIONS: Elevated cTnT levels are associated with an increased incidence of all-cause mortality in patients undergoing major vascular surgery.

Aged↗

Peri-operative myocardial injury in patients undergoing surgery for critical limb ischaemia.

INTRODUCTION: Although up to a half of patients undergoing abdominal aortic aneurysm (AAA) repair suffer myocardial injury, as indicated by a rise in cardiac troponin I (cTnI), this is infrequently accompanied by a rise in creatine kinase (CK)-MB fraction or electrocardiogram (ECG) changes. This study compares for the first time peri-operative cTnI, CK-MB and ECG changes in patients undergoing surgery for critical lower limb ischaemia (CLI). METHODS: Twenty-nine patients (20 men, median age 75 [range, 57-95] years) were studied prospectively. cTnI, CK/CK-MB ratio and ECG were performed pre-operatively and on post-operative days 1, 2 and 3. RESULTS: Eleven (38%) patients had an elevated cTnI >0.5 ng/ml. Five (17%) patients had an elevated CK-MB fraction >4% and all of these patients had an elevated cTnI. Eleven (38%) patients had ischaemic changes on ECG including seven of 11 (64%) patients with elevated cTnI and all five patients with elevated CK-MB fraction. There was no relationship between pre-operative cardiac status, antiplatelet use or type of anaesthesia and post-operative cTnI rise. Patients with a cTnI rise were younger (p=0.01), and were more likely to have presented with gangrene (p=0.04) and have a longer operation time (p=0.01) than patients who did not demonstrate a cTnI rise. Four patients developed clinically apparent cardiac complications: cardio-pulmonary arrest (n=1), cardiogenic shock (n=1), acute CCF (n=1) and rapid atrial fibrillation (n=1). Survival at 6 months was 26 of 29 (90%) patients. CONCLUSION: These data demonstrate that over a third of patients operated for CLI sustain peri-operative myocardial injury, many of which are not clinically apparent. Pre-operative medical optimisation may improve prognosis in this group of patients.

Aged↗

Experience and result of extracorporeal membrane oxygenation in treating fulminant myocarditis with shock: what mechanical support should be considered first?

BACKGROUND: Extracorporeal membrane oxygenation (ECMO), instead of ventricular assist device (VAD), could work as the first-line treatment of choice for fulminant myocarditis (FM) with profound shock if intraaortic balloon pumping was inadequate. We reviewed our experience in treating FM with ECMO and compared it with the literature that described the use of VAD. METHODS: Fifteen consecutive patients (age 27.1 +/- 19.3 years) who had FM with profound shock were rescued with ECMO emergently. Hypotension, depressed left ventricular ejection fraction (19.1% +/- 6.1%), and oliguria occurred in all patients with high-dose catecholamine (inotropic equivalents: 69.0 +/- 37.7 microg/kg/min) and ventilator support. Before ECMO support, 6 patients received intraaortic balloon pumping support, 5 received external cardiac massage, 5 needed a temporary pacemaker, and 4 needed continuous hemofiltration. The pre-ECMO cardiac enzyme and liver enzyme levels were abnormally high. RESULTS: Fourteen patients (93.3%) could be weaned off mechanical support. Three of 14 successfully weaned patients died later as a result of complications. Survival to discharge was 73.3%, and none of survivors needed heart transplantation. The ECMO duration was 137.7 +/- 74.5 hours. The ECMO-related neurological complication (6.7%) and the reexploration rate for hemostasis (8.9%) were lower than the myocarditis group supported by VAD from the literature review. The 11 survivors exhibited no cardiac dysfunction during the follow-up period. CONCLUSIONS: Owning to advantages of fewer complications, easier application, and biventricular support, ECMO can be considered as the first-line treatment of mechanical support for FM with profound shock when intraaortic balloon pumping is inadequate or infeasible.

Adult↗

A comparative study of cardiac preservation with Celsior or University of Wisconsin solution with or without prior administration of cardioplegia.

BACKGROUND: We have previously reported the cardiac functional and metabolic benefits of administration of extracellular-type cardioplegia before preservation with University of Wisconsin solution. Celsior solution was designed to be used both as an arresting solution and a storage solution for heart transplantation. The objective of the present study is to compare cardiac function of hearts arrested and preserved with Celsior solution to hearts arrested with cardioplegia followed by preservation with UW solution. METHODS: Rabbit hearts were divided into 4 groups: in the Celsior group, hearts were arrested and preserved with Celsior solution; in the C-Celsior group, hearts were arrested by an extracellular-type cardioplegia and preserved with Celsior solution; in the UW group, hearts were arrested and stored in University of Wisconsin solution; and, in the C-UW group, hearts were arrested with extracellular-type cardioplegia and stored in University of Wisconsin solution. After 6 hours of preservation, cardiac function was measured using modified Frank-Starling curves in the isolated blood-perfused working heart. RESULTS: Cardiac function in the Celsior group was inferior to that in both the C-UW group and UW group. The C-Celsior group demonstrated inferior cardiac function compared with the Celsior group (p < 0.01), whereas no significant difference was observed between the C-UW and UW groups. CONCLUSIONS: Celsior solution did not surpass UW solution regardless of the use of cardioplegia. Further studies are required to develop optimal solution for use as both an arresting solution and a storage solution.

Adenosine↗

Age-associated increase in creatine kinase-MB-specific activity in human serum confounds its use as an injury marker.

This study retrospectively examined a consecutive series of patient CKMB samples for a relationship between age (242 subjects, aged from 20 to 96 years old), serum CKMB activity and corresponding mass results analyzed for CKMB-specific activity (activity per molecule, unit/mg). Patients were categorized into six age groups. The means for specific activity of CKMB, standard error and 95% confidence intervals of each group were calculated. CKMB-specific activity in human serum increases with age regardless of gender or MI severity. As this greater propensity for increased CKMB activity may be due to alteration in part due to protein modification of post-MI release in the blood circulation, these findings add further weight for the current move to the use of troponins and other markers of myocardial injury.

Adult↗

Prevalence of myocardial ischemia during mechanical ventilation and weaning and its effects on weaning success.

BACKGROUND: Myocardial ischemia may be considered both a consequence of weaning from ventilation and a potential cause of weaning failure. A limited number of investigations have evaluated myocardial ischemia during mechanical ventilation and weaning and its effect on weaning success. The purpose of this pilot investigation was to determine the prevalence of myocardial ischemia in a diverse group of medical intensive care unit (MICU) patients during baseline mechanical ventilation, during weaning using continuous positive airway pressure, and up to 24 hours after extubation and to evaluate the relationship between ischemia and weaning failure. METHODS: This study was a prospective, repeated-measure, descriptive investigation that studied 43 ventilated MICU patients. Slightly more than half of participants were male (53%), and participants had a mean age of 51.1 +/- 14.6 years and were ventilated an average of 11.7 +/- 11.3 days. Myocardial ischemia was evaluated by examination of plasma cardiac troponin I, creatine phosphokinase-myocardial band (CK-MB), and ST-segment changes on electrocardiogram. Continuous electrocardiographic data were obtained by a calibrated, frequency-modulated, continuous 3-channel electrocardiographic recorder using leads I, II, and V2. RESULTS: Seventy percent of these participants (n = 30) exhibited ST-segment deviation at some point during data collection (baseline mechanical ventilation, during weaning, after extubation). Twenty-four participants exhibited ST-segment deviation at baseline, 7 during weaning, and 8 after extubation. Nine participants exhibited ST-segment deviation at >1 data collection time point. None had ST-segment deviation at all 3 time points. Cardiac enzyme concentrations were highly variable; five participants demonstrated clinically important increases in either CK-MB and/or troponin I. Thirty-five percent of participants required >1 weaning trial. Participants who exhibited ST-segment deviation during baseline ventilation were 60% more likely to fail their initial weaning trial. There were no significant differences in CK-MB or troponin I levels between those participants who were successfully weaned with 1 trial and those who failed to wean during that first trial. CONCLUSIONS: Silent myocardial ischemia was a common occurrence in this diverse group of MICU patients, although only 21% had previously diagnosed coronary disease. Clinicians must be aware of the potential for silent ischemia, monitor and evaluate their patients for such, and intervene to promote optimal cardiovascular function, particularly during the stress of ventilator weaning.

Adult↗

Preinfarction angina does not alter infarct size and in hospital outcome after acute myocardial infarction with ST elevation.

BACKGROUND: Preinfarction angina has been reported to limit infarct size, in a manner analogous to experimental preconditioning. However, other studies have reported inconsistent results. We aimed to investigate prospectively the role of preinfarction angina on infarct size and in hospital outcome. METHODS: Ninety-nine patients were divided into three groups according to the timing of angina: the group "< 48 h" reported angina within the last 48 h, the group "> 48 h" earlier than 48 h and the group "acute" no angina before infarction. Myocardial injury was estimated by creatine kinase, creatine kinase-MB, troponin I and C-reactive protein. In hospital events included death, recurrent ischemia, congestive heart failure and atrioventricular block. RESULTS: Clinical characteristics, thrombolysis administration and the magnitude of enzymes released were not statistically different among the three groups: peak creatine kinase was 2139+/-1714 U/l for the >48 h group, vs. 2344+/-1634 U/l for the acute group, vs. 2209+/-1384 U/l for the <48 h group (p=0.88). Peak creatine kinase-MB was 124+/-104 U/l for the >48 h group, vs. 168+/-182 U/l for the acute group, vs. 154+/-108 U/l for the <48 h group (p=0.62). Peak troponin I, peak C-reactive protein and in hospital outcome also did not differ statistically in the three groups; p=0.5, p=0.45. CONCLUSIONS: Infarct size estimated by cardiac enzymes and by the marker of C-reactive protein, as well as in hospital clinical prognosis are not different in patients with and without preinfarction angina. It seems, therefore, that preinfarction angina confers ischemic conditions inadequate to mimic preconditioning.

Angina, Unstable↗

Elevated serum cardiac troponin I in rhabdomyolysis.

OBJECTIVE: To examine the etiology and clinical significance of elevated serum cardiac troponin I (cTnI) in patients with rhabdomyolysis. METHODS: Data on 91 (63 men) consecutive patients with rhabdomyolysis were examined. RESULTS: The mean age was 57.8+/-19.6 years (range 24-97 years). Patients were divided into two groups: cTnI-positive with serum cTnI >0.6 ng/ml (n=19) and cTnI-negative with serum cTnI <0.6 ng/ml (n=72). Prevalence of cardiovascular risk factors was equal in both groups. Illicit substance use was more common in the cTnI-positive group (31% vs. 14%, P=0.04). Peak creatine kinase (CK) was higher in cTnI-positive group (34,811+/-38,309 vs. 15,070+/-21,655 U/l, P=0.04) but there was no difference in the MB isoenzyme (CK-MB) (118+/-132 vs. 89+/-451 ng/ml, P=0.63). In cTnI-positive group, there was a strong correlation between peak CK and CK-MB (r(2)=0.606, P=0.00008) but not between peak cTnI and peak CK (r(2)=0.164 and P=0.08) or CK-MB (r(2)=0.134 and P=0.12) levels. Serum creatinine was higher in cTnI-positive group (3.58+/-2.73 vs. 1.83+/-2.01 mg/dl, P=0.02) but there was no correlation between serum creatinine and cTnI (r(2)=0.121, P=0.158). None of the cTnI-positive patient had segmental wall motion abnormalities. Seventeen (89%) patients in cTnI-positive and 19 (26%) in cTnI-negative group required admission to intensive care unit (P=0.0001). Hypotension (37% vs. 6%, P=0.0002) and sepsis (47% vs. 11%, P=0.0003) were more common in cTnI-positive group. Duration of hospitalization was longer in cTnI-positive group (17.7+/-11.7 vs. 8.9+/-13 days, P=0.007) but there was no significant difference in mortality. CONCLUSION: In rhabdomyolysis, serum cTnI may be elevated unrelated to the degree of muscle damage, renal failure and cardiovascular risk factors, and is likely related to the etiology of rhabdomyolysis, as is evidenced by significantly higher serum cTnI with illicit substance use, hypotension, and sepsis. Elevated serum cTnI is associated with a higher morbidity.

Adult↗

Predictors and prognostic value of myocardial injury following stent implantation.

BACKGROUND: Troponin I concentrations are frequently elevated following percutaneous coronary intervention (PCI) even in procedures without complications and are considered, by some, as predictive of long-term morbidity and mortality. We assessed whether post-PCI troponin I concentrations bore any relationship to clinical, angiographic and in-laboratory minor adverse events indicative of myocardial injury and evaluated, in follow-up, whether these levels are useful as a predictive markers of adverse events. METHODS: Patients (n=147) who were scheduled for PCI for stent placement were prospectively studied. In-laboratory events recorded were protracted chest pain, electrocardiographic changes, slow flows, dissections and lateral branch affectation. Troponin I and creatinine kinase MB fraction (CK-MB) mass were measured at baseline and post-procedure. Mean clinical follow-up was for 10.4+/-3.6 months. RESULTS: During PCI, at least one adverse event occurred in 34% of patients and, in 38% of them, there was an elevation of troponin I as compared to 5.1% of those patients without any adverse event (relative risk=7.4; P<0.001). Elevation of troponin I concentrations occurred in 16.3% of all patients, 79.2% associated with an AE. CK-MB was elevated in 15.6% of patients. On multivariate analysis, protracted chest pain, lateral branch involvement and slow flow remained statistically significant in relation to post-procedure elevations of troponin I concentrations. Clinical follow-up showed a poorer prognosis in patients who had had elevated troponin I concentrations. CONCLUSIONS: In-laboratory adverse event predict elevated post-procedure troponin I concentrations which are associated with myocardial injury. These elevations, in turn, predict poorer medium-term clinical outcomes.

Aged↗

Long-term prognosis of clinical variables, coronary reserve and extent of coronary disease in patients with a first episode of unstable angina.

Clinical and ECG prognostic markers, ischemic threshold (IT) and extent of coronary disease were analyzed in 383 patients with unstable angina (UA) and correlated with long-term events. Patients >74 years or those with severe heart failure or previous revascularization procedures were excluded. There were 369 events in 245 patients: 87 deaths, 96 myocardial infarction (MI), 111 coronary artery bypass grafting (CABG), and 75 angioplasty procedures (PTCA). Follow-up was obtained in 367 hospital survivors (99%, 114 (44) months) and ST depression on admission ECG, a modest enzyme rise, refractory angina (>2 episodes), two to three vessel coronary disease and a reduced IT (<==130 beats/min) were each associated with cardiac events. A multivariate analysis, however, showed refractory angina (p<0.001) and multivessel disease (p<0.001) as most significant predictors. After their exclusion, IT was most relevant predictor (p<0.001). However, the predictive value of these markers was essentially centered on first-year events (249, 67%). Moreover, refractory angina, minor enzyme rise and admission ST depression were each highly correlated with a reduced IT (p<0.006) and with multivessel disease (p<0.0001). Therefore, these findings underscore that the prognostic value of conventional clinical markers in patients with UA is limited to first-year events and that their remarkable correlation with extensive coronary disease and reduced coronary reserve reveal the anatomical substrate of this prognostic significance.

Aged↗

Temporal pattern of cardiac troponin I after thoracotomy and lung surgery.

BACKGROUND: Several studies have shown that patients with perioperative myocardial infarction (MI) are at higher risk for subsequent cardiac events and the identification of these patients is important. However, the diagnosis of perioperative MI can be difficult in many cases. The cardiac troponins are biomarkers with high cardiospecificity, and the aim of this study was to assess cTnI and cTnT among other cardiac biomarkers after thoracotomy and lung surgery. METHODS: 24 consecutive patients were included in the final analysis. Venous blood samples were drawn prior to the procedure, 1-3, 4-6, 16-18 and 30-32 h after surgery. Thoracotomy was performed as a standard posterolateral incision on the left or right side under general anesthesia. RESULTS: Both cTnI and cTnT were completely unaffected by the thoracotomy and the lung surgery. Furthermore, no single value of the troponins was above the 99th percentile at any time. In contrast, CK-MB was elevated in nearly half the patients, although the mean values complied well with the reference limit. CK and myoglobin were both considerably elevated and did not discriminate between acute myocardial infarction and release of the markers due to extracardiac injury. CONCLUSIONS: Only the troponins were unaffected by extracardiac surgery and were, thus, reliable markers of myocardial injury in patients who underwent thoracotomy and lung surgery. If the troponins are unavailable, CK-MB mass combined with the CK-MB/CK percentage should be preferred.

Adult↗

Cardiovascular outcome in hospitalized patients with minimal troponin I elevation and normal creatine phosphokinase.

BACKGROUND: Among patients with acute coronary syndrome, elevated cardiac troponin and creatine phosphokinase MB fraction levels have both prognostic and diagnostic values. However, in hospitalized patients, cardiac biomarkers are measured in a variety of clinical situations including but not limited to acute coronary syndrome. Moreover, these patients may have elevated troponin levels with no increase in creatine phosphokinase MB fraction levels. OBJECTIVE: To evaluate the cardiovascular outcome of acutely ill, hospitalized patients with minimal troponin I increase with normal creatine phosphokinase MB fraction. METHODS: We identified 64 patients retrospectively from our database with minimal troponin I increase and normal creatine phosphokinase MB fraction hospitalized between November 1998 and April 2000. Discharged patients were questioned about re-hospitalization for myocardial infarction, unstable coronary syndrome, congestive heart failure and percutaneous coronary intervention by means of a structured questionnaire. For those patients who died during hospitalization, data were collected from hospital records. For patients who died at home or at a different institution, a surviving relative completed the questionnaire. Primary outcomes were death, myocardial infarction and the need for revascularization or re-hospitalization. RESULTS: Composite endpoint of death, myocardial infarction, percutaneous coronary intervention or coronary artery bypass grafting and re-hospitalization for cardiac cause occurred in 35.95% of patients within 1 year. CONCLUSIONS: There is a significant composite event rate of death, myocardial infarction or re-hospitalization for cardiac causes in acutely ill, hospitalized patients with normal creatine phosphokinase MB fraction and minimally elevated troponin I, regardless of the cause for hospitalization.

Aged↗

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.

Aged↗

Role of biochemical markers in diagnosis of myocardial infarction.

An ideal cardiac biochemical marker should have not only high sensitivity but also high specificity to myocardial infarction. The creatine kinase-MB, a relatively specific cardiac marker, could be elevated in situations other than acute myocardial infarction, such as renal failure, muscular injury, and myopathy. Although these are more specific than creatine kinase-MB, cardiac troponins have also been reported to be elevated in conditions other than acute myocardial infarction, such as chronic renal failure, acute myocarditis, cardiomyopathy, congestive heart failure, pulmonary embolism, rhabdomyolysis, sepsis, and left ventricular hypertrophy. With the ongoing research in this field, future holds hopes of finding an ideally specific marker of myocardial infarction, but until then biochemical markers should be used in conjunction with clinical assessment and electrocardiography in making the diagnosis of myocardial infarction, and the patients should not be treated merely on the basis of elevated serum levels of cardiac biochemical markers.

Biomarkers↗

Release of cardiac biochemical markers after percutaneous myocardial laser or sham procedures.

BACKGROUND: Percutaneous myocardial laser (PML) reduces symptoms in patients with intractable angina. PML leads to a certain loss of viable myocardium, we therefore assessed if troponin or cardiac markers release may explain the clinical effect, and furthermore assessed the markers release during percutaneous sham procedures. METHODS: Eighty-two patients with chronic refractory angina were randomized to either percutaneous myocardial laser or a true sham procedure. Cardiac markers were assessed before the procedure, and (1/2), 2, 4, 6, and 10-12 h postprocedure. RESULTS: Troponin I increased to median peak levels (range) of 4 (0.6-43) microg/L in the laser group vs. 1.5 (0.1-5.9) microg/L, p=0.001, and creatine kinase MB to 14 (6-357) microg/L vs. 11 (3-40) microg/L, p<0.05, within and between-group comparison, the rise of CK-MB occurred significantly earlier in the sham group, 3.8 vs. 2.5 h. A time-dependent between-group difference was only detected for troponin. 88% of sham and 100% of laser patients had marker levels above reference limits. There was no correlation between the number of laser/sham created channels, biomarker levels postprocedure, and changes in left ventricular ejection fraction or angina improvement during 12 months of follow-up. CONCLUSIONS: The release of cardiac markers is not related to relief of angina after myocardial laser. The use of intracardiac catheters induces a considerable marker release, which is not caused by acute ischemia.

Angina Pectoris↗