Comparison of the ability of paramedics with that of cardiologists in diagnosing ST-segment elevation acute myocardial infarction in patients with acute chest pain.
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Aged↗
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Results for “Creatine Kinase, MB Form”
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Long-term prognosis of patients with clinical unstable angina pectoris without elevation of creatine kinase but with elevation of cardiac troponin i levels.
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Aged↗
Prognostic value of isolated troponin elevation across the spectrum of chest pain syndromes.
The risk of death or recurrent myocardial infarction (MI) in patients with chest pain and baseline isolated troponin elevation is unclear. To determine the early and short-term risk of death or MI associated with isolated troponin elevation across a spectrum of chest pain syndromes, we used baseline creatine kinase (CK)-MB and troponin data from the Platelet IIb/IIIa Antagonism for the Reduction of Acute Coronary Syndrome Events in a Global Organization Network (PARAGON) B troponin substudy, the Global Utilization of Strategies To Open Occluded Coronary Arteries (GUSTO) IIa troponin substudy, and the Chest Pain Evaluation by Creatine Kinase-MB, Myoglobin, and Troponin I (CHECKMATE) study. Patients were grouped into 1 of 4 categories based on marker status (troponin-positive/CK-MB-positive, troponin-positive/CK-MB-negative, troponin-negative/CK-MB-positive, or troponin-negative/CK-MB-negative). The adjusted odds of death or MI occurring at 24 hours and 30 days was assessed by baseline marker status using multivariable logistic regression, with the group negative for both markers used as the reference. Patients who were positive for both markers had the highest odds of the 24-hour and 30-day end point. The adjusted odds of the 30-day end point for patients with isolated troponin elevation were 1.3 (95% confidence interval 0.7 to 2.3) and 4.8 (95% confidence interval 1.4 to 16.0) for high- and low-risk patients, respectively. The risk for 24-hour and 30-day death or MI with isolated positive CK-MB results was lower than with isolated positive troponin results, and it was not significantly greater than if the 2 markers were negative. For patients with high- and low-risk chest pain, baseline troponin elevation without CK-MB elevation was associated with increased risk for early and short-term adverse outcomes. This suggests that these patients should be admitted to the hospital and monitored in either an intensive care or step-down unit.
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Prognostic implication of troponin I elevation after percutaneous coronary intervention.
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Angioplasty, Balloon, Coronary↗
Comparison of intravenous myocardial contrast echocardiography and low-dose dobutamine echocardiography for predicting left ventricular functional recovery following acute myocardial infarction.
Akinesia after acute myocardial infarction (AMI) may be reversible or irreversible. Distinguishing these 2 entities early after AMI is difficult, but clinically important. Previous studies have shown that myocardial contrast echocardiography (MCE) and low-dose dobutamine echocardiography (DE) may both be useful in this setting. However, there are few data regarding the relative and combined value of these techniques. The aim of this study was to compare the utility of real-time intravenous MCE and low-dose DE in the early prediction of functional recovery of akinetic myocardium after AMI. Thirty-seven patients were studied 3 +/- 2 days after an AMI. Each subject underwent real-time MCE using an intravenous infusion of perflutren microbubbles. Immediately after this, low-dose DE was performed. Contrast opacification and wall motion were determined by experienced observers blinded to clinical data. Repeat echocardiograms were obtained 51 +/- 19 days later and wall motion at rest was scored by an observer blinded to clinical data. Normal contrast opacification predicted functional recovery with a positive predictive value of 63%, a negative predictive value of 73%, and an accuracy of 66%. Residual contractility during low-dose DE had a positive predictive value of 82%, a negative predictive value of 72%, and a predictive accuracy of 76%. When the 2 tests were concordant (64%), they had a positive predictive value of 81%, a negative predictive value of 85%, and a predictive accuracy of 83%. Low-dose DE was superior to intravenous MCE in the prediction of functional recovery of akinetic myocardium after AMI, but the combination of both maximizes predictive accuracy.
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Usefulness of prodromal unstable angina pectoris in predicting better survival and smaller infarct size in acute myocardial infarction (The InTIME-II Prodromal Symptoms Substudy).
Prodromal unstable angina on presentation is a significant predictor of smaller infarct size, reflected by smaller creatine kinase-MB and creatine kinase total measurements and lower 30-day, 6-month, and 5-year mortality. These findings suggest that prodromal unstable angina is an important physiologic marker that should be routinely collected for risk stratification.
Angina, Unstable↗
Relation of temporal creatine kinase-MB release and outcome after thrombolytic therapy for acute myocardial infarction. TAMI Study Group.
Measuring biochemical marker release after acute myocardial infarction helps in estimating infarct size and prognosis. We sought to relate in-hospital outcomes and curve-fitted creatine kinase (CK)-MB variables after thrombolysis. We measured CK-MB mass initially and at 30 and 90 minutes, and at 3, 8, and 20 hours after thrombolysis in 130 patients also undergoing cardiac catheterization at 90 minutes and at 5 to 7 days. Data were fitted, and maximums and curve areas calculated. CK-MB maximums related to infarct location (p = 0.014) and time to therapy (p = 0.002); curve area did not. Neither maximums nor curve area related to Thrombolysis in Myocardial Infarction trial flow grade at 90 minutes. Maximums related to ejection fraction at 90 minutes (p = 0.0004) and at 5 to 7 days (p = 0.0014), as did curve area (p = 0.0076 and 0.030, respectively). Maximums related to infarct zone function at 90 minutes (p = 0.024) and at 5 to 7 days (p = 0.042); curve area related only at 90 minutes (p = 0.027). Both maximums and curve area predicted congestive heart failure (p = 0.008 and p = 0.042, respectively) and a composite of congestive heart failure or death (p = 0.004 and p = 0.047, respectively); however, after adjusting for maximums, curve area no longer predicted congestive heart failure (p = 0.92). Maximums predicted the composite outcome after adjustment for curve area, and showed a trend toward predicting congestive heart failure (p = 0.089). We conclude that CK-MB maximums relate to infarct zone function, left ventricular function, and in-hospital outcomes after thrombolysis for acute myocardial infarction.
Biomarkers↗
Association between admission white blood cell count and one-year mortality in patients with acute coronary syndromes.
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Acute Disease↗
Myocardial preservation during coronary surgery with and without cardiopulmonary bypass.
BACKGROUND: There is increased interest in coronary artery bypass grafting (CABG) without cardiopulmonary bypass (CPB), although the preservation of the myocardium under such circumstances has not been properly investigated. The aim of this randomized study was to compare the changes in myocardial metabolism during CABG with and without CPB. METHODS: Myocardial energy metabolism and tissue injury during CABG was monitored in a series of 22 patients (11 with and 11 without CPB). RESULTS: The maximum myocardial lactate production was significantly higher (p = 0.02) in the group operated with CPB (0.56 mmol/L) than without it (0.17 mmol/L). A similar phenomenon was seen in the transcardiac pH differences (0.085 and 0.034 with and without CPB, p = 0.007). The postoperative peak values of creatine kinase-MB mass (15.1 vs 6.3 microg/L) and troponin I (13.8 vs 5.2 microg/L) were significantly higher (p < 0.001 and p = 0.008) with than without CPB. CONCLUSIONS: CABG on a beating heart is associated with better myocardial energy preservation and less myocardial damage compared with conventional CABG with CPB and intermittent antegrade mild hypothermic blood cardioplegia.
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Retrograde versus antegrade crystalloid cardioplegia in coronary surgery: value of troponin-I measurement.
BACKGROUND: The optimal route for delivery of cardioplegia is still in debate in patients with ischemic heart disease. Cardiac troponin-I is a new marker with the potential for detection of minor differences in myocardial ischemia. METHODS: In a prospective randomized trial 58 patients undergoing elective coronary artery bypass grafting for two- or three-vessel coronary artery disease were divided into groups with antegrade (group A, n = 29) and retrograde (group R, n = 29) application of crystalloid cardioplegia (St. Thomas II). Patients with major risk factors were excluded. In addition to routine electrocardiogram monitoring, cardiac troponin-I and creatine kinase-MB activity were measured in all patients preoperatively at 2, 5, 8, 24, and 48 hours after aortic cross-clamp release, and at hospital discharge. RESULTS: In both groups, there were no differences regarding operative parameters. A significantly higher cardiac troponin-I concentration was observed in the antegrade group at 24 hours after cross-clamp (8.2 +/- 8.5 microg/L vs 3.2 +/- 3.1 microg/L; p = 0.02). Patients with subtotal stenosis or occlusion of one or more main coronary arteries showed significantly lower cardiac troponin-I levels after retrograde application. CONCLUSIONS: Lower concentrations of the cardiac troponin-I marker after retrograde application of cardioplegia indicate advantages of myocardial protection in ischemic heart disease.
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Lactate release during reperfusion predicts low cardiac output syndrome after coronary bypass surgery.
BACKGROUND: Cardioplegic arrest induces anaerobic myocardial metabolism with a net production of lactate from glycolysis. However, persistent lactate release during reperfusion suggests a delayed recovery of normal aerobic metabolism and may lead to depressed myocardial function necessitating inotropic or intraaortic balloon pump support (low output syndrome [LOS]). We examined the relation between perioperative myocardial metabolism and postoperative clinical outcomes in patients undergoing isolated coronary artery bypass surgery (CABG). METHODS: We reviewed 623 patients who were enrolled in clinical studies evaluating perioperative myocardial metabolism between 1983 and 1996. Arterial and coronary sinus blood samples were obtained intraoperatively to assess myocardial metabolism. Clinical data regarding patient demographics and postoperative outcomes were prospectively collected and entered into our institutional database. RESULTS: Low output syndrome developed in 36 patients (5.8%). Myocardial lactate release was higher in these patients compared with those who did not develop postoperative LOS. Advanced age and poor preoperative left ventricular function were independent predictors of lactate release during reperfusion. Persistent lactate release after 5 minutes of reperfusion was the only independent predictor of postoperative LOS in this low-risk population. CONCLUSIONS: Persistent lactate release during reperfusion occurs in a significant proportion of low-risk patients undergoing isolated CABG and is an independent predictor of postoperative low cardiac output syndrome. Persistent lactate release during reperfusion suggests a delayed recovery of aerobic myocardial metabolism and may be related to intraoperative misadventure or inadequate myocardial protection. Myocardial lactate release may be useful as an alternative end-point in clinical trials evaluating perioperative myocardial protection.
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Peroxynitrite formation from human myocardium after ischemia-reperfusion during open heart operation.
BACKGROUND: Current experimental studies have demonstrated that peroxynitrite (ONOO-) has both cytotoxic and cytoprotective effects on myocardial ischemia-reperfusion injury. However, even myocardial ONOO- formation has not yet been investigated in humans undergoing open heart operation. We measured plasma nitrotyrosine as an indicator of ONOO- formation during open heart operation and examined its association with myocardial ischemia-reperfusion injury. METHODS: Twenty adult patients undergoing mitral valve replacement under cardiopulmonary bypass between 1997 and 1998 were enrolled in this study (6 men and 14 women). Arterial blood (Ao) and coronary sinus effluent (CS) were obtained: (1) before the initiation of cardiopulmonary bypass, (2) just after aortic unclamping, (3) at 5 minutes, (4) at 10 minutes, (5) at 15 minutes, and (6) at 20 minutes after aortic unclamping. RESULTS: At every sampling point after reperfusion, plasma nitrate and nitrite was significantly lower in CS than in Ao, and the percentage ratio of nitrotyrosine to tyrosine (%NO2-Tyr; an index of ONOO- formation) was significantly higher in CS than in Ao. The CS-Ao difference in %NO2-Tyr, myocardium-derived ONOO-, reached its peak at 5 minutes after reperfusion (2.17+/-0.74%), which was significantly correlated with the peak CS-Ao difference in plasma malondialdehyde, and with postoperative maximum creatine kinase-MB. CONCLUSIONS: These results first demonstrate that ONOO- is produced from human myocardium after ischemia-reperfusion during open heart operation, and myocardium-derived ONOO- can be determined by the CS-Ao difference in %NO2-Tyr.
Adult↗
Metabolic changes and myocardial injury during cardioplegia: a pilot study.
BACKGROUND: The timing, nature, and severity of both increased cardiac troponin I (cTn-I) levels and myocardial injury during ischemic arrest with cardioplegia are unknown. To define them more accurately, we studied myocardial metabolic activity and the release of markers of myocardial cell injury into the coronary sinus before, during, and after cardioplegia. METHODS: We simultaneously measured creatine kinase, creatine kinase-MB, cTn-I, lactate, phosphate, and blood gases in coronary sinus and systemic arterial blood from 12 patients before cardiopulmonary bypass, after removal of the aortic cross-clamp, and after discontinuation of cardiopulmonary bypass. We also measured coronary sinus flow and transmyocardial fluxes of all analytes and calculated myocardial oxygen consumption, myocardial carbon dioxide production, and myocardial energy expenditure. RESULTS: Myocardial lactate release increased 10-fold after removal of the aortic cross-clamp (p = 0.012) and was accompanied by a surge in myocardial phosphate uptake (p = 0.056). These events were associated with only partial cardioplegia-induced suppression of myocardial oxygen consumption (p = 0.0047), myocardial carbon dioxide production (p = 0.0022), and myocardial energy expenditure (p = 0.0029). Simultaneously, coronary sinus cTn-I levels increased from a mean of 0.76 to 2.43 ng/mL after removal of the aortic cross-clamp, and 2.51 ng/mL after cardiopulmonary bypass (p = 0.014), leading to an increase in arterial cTn-I concentration from 0.18 to 0.98 and 3.01 ng/mL (p = 0.0002). Thus, cTn-I release across the myocardium was absent at baseline, became detectable (p = 0.012) after removal of the aortic cross-clamp, and correlated with cross-clamp and pump times. Similar changes occurred with creatine kinase-MB. CONCLUSIONS: Metabolic myocardial stress occurs during ischemic arrest with cardioplegia and is associated with inadequate suppression of metabolism and with a surge in cTn-I and creatine kinase-MB release, which is maximal after removal of the aortic cross-clamp. These changes are likely to represent structural myocardial cell injury.
Aged↗
Glucose-insulin-potassium infusion for myocardial protection during off-pump coronary artery surgery.
BACKGROUND: The purpose of this randomized, double-blind, placebo-controlled pilot study was to determine the effectiveness of an intravenous glucose-insulin-potassium (GIK) infusion in preventing myocardial damage and maintaining cardiac performance in patients undergoing "off-pump" myocardial revascularization. METHODS: Forty-six adult patients undergoing elective off-pump coronary artery bypass received either normal saline or a GIK infusion immediately after the induction of anesthesia through the first 12 hours of intensive care unit convalescence. Measurements of blood glucose, circulating creatine kinase MB and troponin I concentrations, as well as cardiac index (CI) and mixed venous oxygen saturation (SvO2), were obtained immediately before starting the infusion (baseline) and at 6, 12, and 24 hours post-initial coronary artery occlusion. RESULTS: Five patients (8%) requiring cardiopulmonary bypass were excluded from data analysis. Twenty patients received saline. Twenty-one received GIK. Blood glucose was significantly higher in the GIK group. The concentration of circulating creatine kinase MB and troponin I significantly increased over time after off-pump coronary artery bypass, with no significant intergroup differences. Cardiac index and SvO2 did not differ significantly between groups. CONCLUSIONS: A GIK infusion protocol commonly used as an adjunct to reperfusion therapy for acute myocardial infarction causes insulin-resistant hyperglycemia in elective off-pump coronary artery bypass patients with no demonstrable benefit. The finding of significant release of cardio-specific enzymes in individual patients implies an ongoing need to develop more effective strategies for myocardial protection during off-pump coronary artery bypass.
Adult↗
Minimal access aortic valve replacement: effects on morbidity and resource utilization.
BACKGROUND: The aim of this study was to compare outcomes in patients undergoing minimal access versus conventional aortic valve replacement (AVR). METHODS: We reviewed prospectively gathered data on all patients who were undergoing first-time AVR, with or without replacement of the ascending aorta, over a 1-year period at our institution. RESULTS: A total of 176 patients underwent minimal access and 258 underwent conventional AVR. The conventional group was older, had more incidence of diabetes, and more aortic stenosis (all p < 0.05). Eight minimal access AVR patients (2%) required conversion to a complete sternotomy. Minimal access AVR patients had longer aortic crossclamp times than conventional AVR patients (60 +/- 22 vs 55 +/- 23 minutes, p = 0.03) but similar CPB times (93 +/- 38 vs 88 +/- 42 minutes, p = 0.20). Postoperative creatine kinase-MB levels were similar for the two groups. Total postoperative blood loss was significantly lower in the minimal access group, and these patients received less red blood cell and fresh frozen plasma transfusions. Minimal access AVR patients were less likely to have postoperative respiratory failure (3% vs 10%); they had shorter intensive care unit stays (3.7 +/- 5.4 vs 4.5 +/- 5.6 days) and shorter hospital stays (10 +/- 6 vs 12 +/- 7 days, all p < 0.05). Mortality was lower in patients undergoing minimal access surgery (3% vs 9%, p = 0.008) by univariate analysis. Multivariate predictors of mortality were age, hypertension, and CPB time. CONCLUSIONS: Although patient selection may have influenced some of the observed differences between our patient groups, minimal access surgery appears to be associated with decreased morbidity and resource use when compared to conventional AVR.
Aortic Valve↗
Blood cardioplegic protection in profoundly damaged hearts: role of Na+-H+ exchange inhibition during pretreatment or during controlled reperfusion supplementation.
BACKGROUND: Inhibition of the Na+/H+ exchanger before ischemia protects against ischemia-reperfusion injury, but use as pretreatment before blood cardioplegic protection or as a supplement to controlled blood cardioplegic reperfusion was not previously tested in jeopardized hearts. METHODS: Control studies tested the safety of glutamate-aspartate-enriched blood cardioplegic solution in 4 Yorkshire-Duroc pigs undergoing 30 minutes of aortic clamping without prior unprotected ischemia. Twenty-four pigs underwent 30 minutes of unprotected normothermic global ischemia to create a jeopardized heart. Six of these hearts received normal blood reperfusion, and the other 18 jeopardized hearts underwent 30 more minutes of aortic clamping with cardioplegic protection. In 12 of these, the Na+/H+ exchanger inhibitor cariporide was used as intravenous pretreatment (n = 6) or added to the cardioplegic reperfusate (n = 6). RESULTS: Complete functional, biochemical, and endothelial recovery occurred after 30 minutes of blood cardioplegic arrest without preceding unprotected ischemia. Thirty minutes of normothermic ischemia and normal blood reperfusion produced 33% mortality and severe left ventricular dysfunction in survivors (preload recruitable stroke work, 23% +/- 6% of baseline levels), with raised creatine kinase MB, conjugated dienes, endothelin-1, myeloperoxidase activity, and extensive myocardial edema. Blood cardioplegia was functionally protective, despite adding 30 more minutes of ischemia; there was no mortality, and left ventricular function improved (preload recruitable stroke work, 58% +/- 21%, p < 0.05 versus normal blood reperfusion), but adverse biochemical and endothelial variables did not change. In contrast, Na+/H+ exchanger inhibition as either pretreatment or added during cardioplegic reperfusion improved myocardial recovery (preload recruitable stroke work, 88% +/- 9% and 80% +/- 7%, respectively, p < 0.05 versus without cariporide) and comparably restored injury variables. CONCLUSIONS: Na+/H+ exchanger blockage as either pretreatment or during blood cardioplegic reperfusion comparably delays functional, biochemical, and endothelial injury in jeopardized hearts.
Animals↗
Ischemic preconditioning does not improve myocardial preservation during off-pump multivessel coronary operation.
BACKGROUND: The value of ischemic preconditioning during coronary operations has remained controversial. The aim of this study was to evaluate the effects of ischemic preconditioning on myocardial energy metabolism and tissue injury during off-pump multivessel coronary surgery. METHODS: Eleven patients with preceding preconditioning were compared with 11 patients without it. The preconditioning group underwent a 5-minute period of ischemia followed by a 5-minute reperfusion period before coronary occlusion for each of the first two anastomoses. RESULTS: The transmyocardial differences (coronary sinus - arterial) in inosine and the sum of adenine degradation products increased in both groups, but the differences in xanthine and hypoxanthine increased only in the preconditioning group. Myocardial lactate production increased to a maximum of 0.09 mmol/L with preconditioning and to a maximum of 0.17 mmol/L without it. Transmyocardial pH differences increased to 0.03 U in both groups. The maximum postoperative concentration of creatine kinase-MB mass was 14.8 microg/L with preconditioning and 6.3 microg/L without preconditioning, and that of troponin I 7.4 microg/L and 5.2 microg/L, respectively. There were no statistically significant differences between the groups, however. CONCLUSIONS: Ischemic preconditioning of 5 minutes followed by reperfusion of 5 minutes during off-pump multivessel coronary artery surgery did not prevent myocardial metabolic derangement and tissue injury and thus cannot be routinely recommended.
Adenosine↗
Modulation of calcium transport improves myocardial contractility and enzyme profiles after prolonged ischemia-reperfusion.
BACKGROUND: Ischemia-reperfusion (IR) injury causes myocardial dysfunction in part through intracellular calcium overload. A recently described pharmacologic compound, MCC-135 (5-methyl-2-[1-piperazinyl] benzenesulfonic acid monohydrate, Mitsubishi Pharma Corporation), alters intracellular calcium levels. This project tested the hypothesis that MCC-135 would influence regional myocardial contractility when administered at reperfusion and after a prolonged period of ischemia. METHODS: A circumflex snare and sonomicrometry crystals within remote and area-at-risk regions were placed in pigs (n = 18, 32 kg). Coronary occlusion was instituted for 120 minutes followed by 180 minutes of reperfusion. At 105 minutes of ischemia pigs were randomly assigned to IR only (n = 11) or MCC-135 (IR-MCC [300 microg. kg(-1). h(-1), n = 7]) administered intravenously. Regional myocardial contractility was determined by calculation of the regional end-systolic pressure-dimension relation (RESPDR [mm Hg/cm]). Myocardial injury was determined by measurement of plasma levels of myocyte-specific enzymes. RESULTS: At 90 minutes ischemia, mean troponin-I was 35 +/- 8 ng/mL with no significant difference between groups. At 180 minutes reperfusion, heart rate was increased by 18% +/- 5% in the IR only group (p < 0.05) and was reduced by 11% +/- 4% with IR-MCC (p < 0.05). At 90 minutes ischemia RESPDR was reduced from baseline by 51% +/- 6% (p < 0.05). By 30 minutes reperfusion, reductions in RESPDR were attenuated with IR-MCC compared with IR only values. The CK-MB levels were increased at 180 minutes reperfusion in the IR only group (52 +/- 9 ng/mL) compared with baseline (6 +/- 1 ng/mL, p < 0.05) but were attenuated with IR-MCC (24 +/- 4 ng/mL, p < 0.05) compared with IR only values. CONCLUSIONS: Despite similar degrees of injury at 90 minutes ischemia MCC-135 improved regional contractility and reduced the egress of CK-MB. Moreover MCC-135 was associated with decreased heart rate, a determinant of myocardial oxygen demand. Pharmacologic modulation of calcium transport ameliorates myocardial dysfunction in the acute IR period.
Animals↗