Troponin Release In Patients Research Articles

Del Nido versus blood cardioplegia in adult cardiac surgery: a meta-analysis.

Initially developed for myocardial protection in immature cardiomyocytes, del Nido cardioplegia has been increasingly used over the past decade in adult patients. Our aim is to analyse the results from randomized controlled trials and observational studies comparing early mortality and postoperative troponin release in patients who underwent cardiac surgery using del Nido solution and blood cardioplegia. A literature search was performed through three online databases between January 2010 and August 2022. Clinical studies providing early mortality and/or postoperative troponin evaluation were included. A random-effects meta-analysis with a generalized linear mixed model, incorporating random study effects, was implemented to compare the two groups. Forty-two articles were included in the final analysis for a total of 11 832 patients, 5926 of whom received del Nido solution and 5906 received blood cardioplegia. del Nido and blood cardioplegia populations had comparable age, gender distribution, history of hypertension and diabetes mellitus. There was no difference in early mortality between the two groups. There was a trend towards lower 24 h [mean difference -0.20; 95% confidence interval (CI) -0.40 to 0.00; I2 = 89%; P = 0.056] and lower peak postoperative troponin levels (mean difference -0.10; 95% CI -0.21 to 0.01; I2 = 0.87; P = 0.087) in the del Nido group. del Nido cardioplegia can be safely used in adult cardiac surgery. The use of del Nido solution was associated with similar results in terms of early mortality and postoperative troponin release when compared with blood cardioplegia myocardial protection.

Effects of Remote Ischemic Preconditioning on Decreasing Troponin Release in Patients Not Taking Sulfonylureas After Cardiac Surgery - A Meta-Analysis.

Remote ischemic preconditioning (RIPC) is a new noninvasive myocardial protection strategy that uses blood pressure cuf inflation to simulate transient non-fatal ischemia to protect the myocardium and reduce ischemia-reperfusion injury. Sulfonylureas may mask the effects of RIPC due to their cardioprotec-tive effect. This meta-analysis aimed to evaluate whether RIPC, in the absence of sulfonylureas, reduces troponin release in patients undergoing cardiac surgery. We conducted a meta-analysis of randomized controlled clinical trials to determine whether RIPC can reduce postoperative troponin release in cardiac surgery patients undergoing cardiopulmonary bypass without treatment with sulfonylureas. The data were normalized to equivalent units prior to the analysis. A random-effects model was used to provide more conservative estimate of the effects in the presence of known or unknown heterogeneity. Six studies with a total of 570 participants were included. The analysis showed that troponin release was lower in the RIPC group than in the control group at six hours (test of standardized mean differences = 0, Z=3.64, P<0.001) and 48 hours (Z=2.72, P=0.007) postoperatively. When the mean of cross-clamping time was > 60 minutes, RIPC reduced troponin release at six hours (Z=2.84, P=0.005), 24 hours (Z=2.64, P=0.008), and 48 hours (Z=2.87, P=0.004) postoperatively. In cardiac surgery patients who are not taking sulfonylureas, RIPC can reduce troponin release at six and 48 hours postoperatively; hence, RIPC may serve significant benefits in certain cardiac surgery patients.

Cardiovascular Biomarkers

The value of circulating biomarkers to care for patients with cardiovascular disease has grown significantly over the last few decades. The majority of clinical data focus on the use of natriuretic peptides (NPs) for the diagnosis, prognosis, and management of patients with heart failure (HF) and troponin measurements in patients with suspected or proven acute coronary syndrome (ACS). Part of the reason for the slow adoption of biomarkers beyond these two classes has been limitation in the optimal modes of application of new assays. Future studies are needed to clarify the use of biomarkers, with the ultimate goal of simplifying the diagnosis, prognosis, and patient care of complex cardiovascular conditions. This chapter reviews the use of established biomarkers for HF, ACS, and atrial fibrillation (AF). Tables include a summary of emerging and established cardiovascular biomarkers, characteristics of B-type natriuretic peptide and amino-terminal pro-B-type natriuretic peptide, cutoff points for NP measurement, differential diagnosis of elevated NP concentrations, biomarkers in HF with preserved ejection fraction, summary of NP management trials, third universal definition of myocardial infarction, and guidelines for recommendations of biomarkers in HF. Figures depict the various causes of NP release, the complex mechanism of troponin release in patients with HF, the ischemic and nonischemic etiologies of troponin release, timing of biomarker release during myocardial infarction, and the biomarkers involved in the pathogenesis of AF. Algorithms demonstrate evaluating outpatients with dyspnea in the clinic using NPs in their workup and the use of troponin to assist with determining an appropriate management strategy for a patient with ACS. This review contains 7 highly rendered figures, 8 tables, and 202 references.

Cardiovascular Biomarkers

The value of circulating biomarkers to care for patients with cardiovascular disease has grown significantly over the last few decades. The majority of clinical data focus on the use of natriuretic peptides (NPs) for the diagnosis, prognosis, and management of patients with heart failure (HF) and troponin measurements in patients with suspected or proven acute coronary syndrome (ACS). Part of the reason for the slow adoption of biomarkers beyond these two classes has been limitation in the optimal modes of application of new assays. Future studies are needed to clarify the use of biomarkers, with the ultimate goal of simplifying the diagnosis, prognosis, and patient care of complex cardiovascular conditions. This chapter reviews the use of established biomarkers for HF, ACS, and atrial fibrillation (AF). Tables include a summary of emerging and established cardiovascular biomarkers, characteristics of B-type natriuretic peptide and amino-terminal pro-B-type natriuretic peptide, cutoff points for NP measurement, differential diagnosis of elevated NP concentrations, biomarkers in HF with preserved ejection fraction, summary of NP management trials, third universal definition of myocardial infarction, and guidelines for recommendations of biomarkers in HF. Figures depict the various causes of NP release, the complex mechanism of troponin release in patients with HF, the ischemic and nonischemic etiologies of troponin release, timing of biomarker release during myocardial infarction, and the biomarkers involved in the pathogenesis of AF. Algorithms demonstrate evaluating outpatients with dyspnea in the clinic using NPs in their workup and the use of troponin to assist with determining an appropriate management strategy for a patient with ACS. This review contains 7 highly rendered figures, 8 tables, and 202 references.

Cardiovascular Biomarkers

The value of circulating biomarkers to care for patients with cardiovascular disease has grown significantly over the last few decades. The majority of clinical data focus on the use of natriuretic peptides (NPs) for the diagnosis, prognosis, and management of patients with heart failure (HF) and troponin measurements in patients with suspected or proven acute coronary syndrome (ACS). Part of the reason for the slow adoption of biomarkers beyond these two classes has been limitation in the optimal modes of application of new assays. Future studies are needed to clarify the use of biomarkers, with the ultimate goal of simplifying the diagnosis, prognosis, and patient care of complex cardiovascular conditions. This chapter reviews the use of established biomarkers for HF, ACS, and atrial fibrillation (AF). Tables include a summary of emerging and established cardiovascular biomarkers, characteristics of B-type natriuretic peptide and amino-terminal pro-B-type natriuretic peptide, cutoff points for NP measurement, differential diagnosis of elevated NP concentrations, biomarkers in HF with preserved ejection fraction, summary of NP management trials, third universal definition of myocardial infarction, and guidelines for recommendations of biomarkers in HF. Figures depict the various causes of NP release, the complex mechanism of troponin release in patients with HF, the ischemic and nonischemic etiologies of troponin release, timing of biomarker release during myocardial infarction, and the biomarkers involved in the pathogenesis of AF. Algorithms demonstrate evaluating outpatients with dyspnea in the clinic using NPs in their workup and the use of troponin to assist with determining an appropriate management strategy for a patient with ACS. This review contains 7 highly rendered figures, 8 tables, and 202 references.

Clinically Suspected Myocarditis in the Course of Severe Acute Respiratory Syndrome Novel Coronavirus-2 Infection: Fact or Fiction?

Cardiac complications, including clinically suspected myocarditis, have been described in novel coronavirus disease 2019. Here, we review current data on suspected myocarditis in the course of severe acute respiratory syndrome novel coronavirus-2 (SARS-CoV-2) infection. Hypothetical mechanisms to explain the pathogenesis of troponin release in patients with novel coronavirus disease 2019 include direct virus-induced myocardial injury (ie, viral myocarditis), systemic hyperinflammatory response (ie, cytokine storm), hypoxemia, downregulation of angiotensin-converting enzyme 2, systemic virus-induced endothelialitis, and type 1 and type 2 myocardial infarction. To date, despite the fact that millions of SARS-CoV-2 infections have been diagnosed worldwide, there is no definitive proof that SARS-CoV-2 is a novel cardiotropic virus causing direct cardiomyocyte damage. Diagnosis of viral myocarditis should be based on the molecular assessment of endomyocardial biopsy or autopsy by polymerase chain reaction or in-situ hybridization. Blood, sputum, or nasal and throat swab virology testing are insufficient and do not correlate with the myocardial involvement of a given pathogen. Data from endomyocardial biopsies and autopsies in clinically suspected SARS-CoV-2 myocarditis are scarce. Overall, current clinical epidemiologic data do not support the hypothesis that viral myocarditis is caused by SARS-CoV-2, or that it is common. More endomyocardial biopsy and autopsy data are also needed for a better understanding of pathogenesis of clinically suspected myocarditis in the course of SARS-CoV-2 infection, which may include virus-negative immune-mediated or already established subclinical autoimmune forms, triggered or accelerated by the hyperinflammatory state of severe novel coronavirus disease 2019.

Myocardial Injury in Critically Ill Patients with Community-acquired Pneumonia. A Cohort Study

Rationale: Myocardial injury, as reflected by elevated cardiac troponin levels in plasma, is common in patients with community-acquired pneumonia (CAP), but its temporal dynamics and etiology remain unknown. Objectives: Our aim was to determine the incidence of troponin release in patients with CAP and identify risk factors that may point to underlying etiologic mechanisms. Methods: We included consecutive patients admitted with severe CAP to two intensive care units in the Netherlands between 2011 and 2015. High-sensitivity cardiac troponin I was measured daily during the first week. We used multivariable linear regression to identify variables associated with troponin release on admission, and we used mixed-effects regression to model the daily rise and fall of troponin levels over time. Results: Of 200 eligible patients, 179 were included, yielding 792 observation days. A total of 152 (85%) patients developed raised troponin levels greater than 26 ng/L. Baseline factors independently associated with troponin release included coronary artery disease (176% increase; 95% confidence interval [CI], 11-589), smoking (248% increase; 95% CI, 33-809), and higher Acute Physiology and Chronic Health Evaluation IV score (2% increase; 95% CI, 0.8-3.3), whereas Staphylococcus aureus as a causative pathogen was protective (70% reduction; 95% CI, 18-89). Time-dependent risk factors independently associated with daily increase in troponin concentrations included reduced platelet count (2.3% increase; 95% CI, 0.6-4), tachycardia (1.5% increase; 95% CI, 0.1-2.9), hypotension (6.2% increase; 95% CI, 2.1-10.6), dobutamine use (44% increase; 95% CI, 12-85), prothrombin time (8.2% increase; 95% CI, 0.2-16.9), white cell count (1.7% increase; 95% CI, 0-3.5), and fever (22.7% increase; 95% CI, 0.1-49.6). Conclusions: Cardiac injury develops in a majority of patients with severe CAP. Myocardial oxygen supply-demand mismatch and activated inflammation/coagulation are associated with this injury. Clinical trial registered with www.clinicaltrials.gov (NCT01905033).

Improvement of mitochondrial function in human atrial tissue by remote ischemic conditioning

IntroductionRemote ischemic preconditioning (RIPC), repeated cycles of brief limb ischemia/reperfusion, attenuates postoperative troponin release in patients undergoing surgical coronary revascularization and improves clinical outcome in some, but not all studies. Mitochondria are the end‐effectors of cardioprotection by local ischemic conditioning maneuvers in experimental studies. Here, we now analyzed mitochondrial function in response to RIPC in human atrial tissue.MethodsPatients undergoing elective surgical coronary revascularization under isoflurane anesthesia were randomized to RIPC by 3× 5 min/5 min upper arm blood pressure cuff inflation/deflation or placebo (n=30/30), and their right atrial appendages were harvested prior to ischemic cardioplegic arrest. Cardioprotection was reflected by a 14% decrease with RIPC vs. placebo in the area under the curve of serum troponin I/T concentrations over 72 h after surgery. Mitochondria were isolated from the atrial tissue (n=10/10). Mitochondrial function, i.e. mitochondrial respiration, adenosine triphosphate (ATP) production, reactive oxygen species (ROS) production and calcium retention capacity (CRC) to estimate mitochondrial permeability transition pore (mPTP) opening, was measured at physiological temperature of 37°C. Data are given as mean±SEM.ResultsAssociated with the observed cardioprotection in patients, mitochondrial function was improved by RIPC. Basal respiration was not different between RIPC and placebo. ADP‐stimulated complex I respiration was significantly greater with RIPC than with placebo. Mitochondrial complex IV respiration and maximal oxygen uptake of uncoupled mitochondria were not different between RIPC and placebo, reflecting an equal loading of viable mitochondria (Figure 1A). The mitochondrial ATP production (Figure 1B) was greater whereas mitochondrial ROS production (Figure 1C) was less with RIPC than with placebo. CRC of mitochondria (Figure 1D) was improved with RIPC in comparison to placebo, with and without cyclosporine A.ConclusionIn human myocardium, mitochondria are an intracellular target of protection by RIPC.Support or Funding InformationSupported by: German Research Foundation (SFB 1116 B8)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

High-sensitivity troponin I concentrations are a marker of an advanced hypertrophic response and adverse outcomes in patients with aortic stenosis

AimsHigh-sensitivity cardiac troponin I (cTnI) assays hold promise in detecting the transition from hypertrophy to heart failure in aortic stenosis. We sought to investigate the mechanism for troponin release in patients with aortic stenosis and whether plasma cTnI concentrations are associated with long-term outcome.Methods and resultsPlasma cTnI concentrations were measured in two patient cohorts using a high-sensitivity assay. First, in the Mechanism Cohort, 122 patients with aortic stenosis (median age 71, 67% male, aortic valve area 1.0 ± 0.4 cm2) underwent cardiovascular magnetic resonance and echocardiography to assess left ventricular (LV) myocardial mass, function, and fibrosis. The indexed LV mass and measures of replacement fibrosis (late gadolinium enhancement) were associated with cTnI concentrations independent of age, sex, coronary artery disease, aortic stenosis severity, and diastolic function. In the separate Outcome Cohort, 131 patients originally recruited into the Scottish Aortic Stenosis and Lipid Lowering Trial, Impact of REgression (SALTIRE) study, had long-term follow-up for the occurrence of aortic valve replacement (AVR) and cardiovascular deaths. Over a median follow-up of 10.6 years (1178 patient-years), 24 patients died from a cardiovascular cause and 60 patients had an AVR. Plasma cTnI concentrations were associated with AVR or cardiovascular death HR 1.77 (95% CI, 1.22 to 2.55) independent of age, sex, systolic ejection fraction, and aortic stenosis severity.ConclusionsIn patients with aortic stenosis, plasma cTnI concentration is associated with advanced hypertrophy and replacement myocardial fibrosis as well as AVR or cardiovascular death.

Troponin rise in patients with atrial fibrillation: A marker of adverse prognosis and increased thromboembolic risk

We have read with interest the article by Parwani and colleagues addressing the role of atrial fibrillation (AF) in induction of troponin release in patients presenting to the Emergency Department with AF and clinical symptoms suggestive of myocardial ischemia [1]. In face of their findings in 100 patients undergoing coronary angiography, of whom 23 had an elevated cardiac troponin I (N0.09 μg/L), the authors have suggested that troponin rise may be “falsely elevated” in this setting, since the prevalence of significant stenosis was similar irrespective of troponin rise: 26% in patients with positive troponin vs. 33% in patients with normal troponin (p = ns). However, we feel that, contrary to the author's opinion, troponin rise in this setting must be addressed with care in face of the recent evidence that we will shortly present. Conti and colleagues have recently shown that elevated cardiac troponin I is a predictor of poor outcome (a composite of stroke, acute coronary syndrome, revascularization, and global death) in patients presenting to the Emergency Department with AF lasting for less than 12 h [2]. The association of minor troponin elevations with an adverse prognosis in patients with AF has also been previously addressed by Van den Bos et al. in a prospective cohort study of 407 consecutive patients with AF admitted to the cardiology ward or intensive coronary unit (patients with ST elevation myocardial infarction were excluded) [3]. These authors have found that minor rises (N0.015 ng/ mL) were present in 20% of patients and associated with death, fatal myocardial infarction and major cardiovascular events (all-cause mortality, myocardial infarction and revascularization). As far as risk stratification of AF is concerned, minor rises in troponin seem also to have a major role in the prediction of thromboembolic events and may improve the discriminative capability of current risk classification schemes (CHADS2 and CHA2DS2-VASc), according to data from the “Randomised Evaluation of Long Term Anticoagulant Therapy” (RE-LY) trial biomarkers substudy [4]. Based on data from patients with AF undergoing transesophageal echocardiogram, this may be explained by the increased prevalence of markers of left atrial stasis (i.e., left atrial and left atrial appendage thrombi, dense spontaneous echocardiographic contrast and low flow velocities in the left atrial appendage), which are known to very strongly associate with embolism, and to increase in prevalence as troponin levels rise [5]. Therefore, we feel that minor elevations of troponin in patients with AF should be handled with care and not promptly assumed as false positives. In a first instance, ongoing myocardial ischemia should be ruled out if the clinical context is suggestive and the pretest probability is moderate or elevated. Then, even if the results are negative or the context is not suggestive of myocardial ischemia, an adequate prevention of thromboembolism should be considered, preferentially with anticoagulants, according to data of the RE-LY Biomarkers sub-analysis, if the bleeding risk of each particular patient is not prohibitive. The authors of this manuscript have verified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology and complies with the Statement on Matching Language to the Type of Evidence Used in Describing Outcomes Data [6].

Sevoflurane vs. propofol in patients with coronary disease undergoing mitral surgery: a randomised study

Myocardial ischemic damage is reduced by volatile anaesthetics in patients undergoing low-risk coronary artery bypass graft surgery; few and discordant results exist in other settings. We therefore performed a randomised controlled trial (sevoflurane vs. propofol) to compare cardiac troponin release in patients with coronary disease undergoing mitral surgery. Patients with coronary artery disease undergoing mitral surgery were randomly allocated to receive either sevoflurane (50 patients) or propofol (50 patients) as main hypnotic. The primary endpoint of the study was peak post-operative cardiac troponin release defined as the maximum value among the post-operative values measured at intensive care unit arrival, 4 h later, on the first and second post-operative day. There was no significant difference in post-operative peak troponin release, the median (25th-75th percentiles) values being 14.9 (10.1-22.1) ng/ml and 14.5 (8.8-17.6) ng/ml in the sevoflurane and propofol groups, respectively (P = 0.4). Fentanyl administration was different between the two groups: 1347 ± 447 μg in patients receiving sevoflurane and 1670 ± 469 μg in those receiving propofol, P = 0.002. The 1-year follow-up identified two patients who died in the propofol group (one myocardial infarction and one low cardiac output syndrome) and one in the sevoflurane group (myocardial infarction). In this study, patients with coronary artery disease undergoing mitral surgery did not benefit from the cardioprotective properties of halogenated anaesthetics. Sevoflurane anaesthesia was not associated to lower cardiac troponin release when compared with propofol anaesthesia.

Determinants of troponin release in patients with stable coronary artery disease: insights from CT angiography characteristics of atherosclerotic plaque

ObjectiveTo understand the determinants of troponin release in patients with stable coronary artery disease (CAD) by comparing high sensitive troponin T (hsTnT) levels with computed tomography angiography (CTA) characteristics of...

Influence of propofol–opioid vs isoflurane–opioid anaesthesia on postoperative troponin release in patients undergoing coronary artery bypass grafting

BackgroundIn experimental and clinical studies, volatile anaesthesia has proven to possess cardioprotective properties. However, no randomized controlled trials on the use of isoflurane during the entire cardiac surgical procedure are available. We therefore compared isoflurane–sufentanil vs propofol–sufentanil anaesthesia in patients undergoing coronary artery bypass grafting. MethodsOne hundred patients were randomly assigned to receive isoflurane–sufentanil (I) (n = 51) or propofol–sufentanil (P) (n = 49) anaesthesia, aimed at the same hypnotic depth. Postoperative concentrations of cardiac troponin I (cTnI) were followed for 72 h. Secondary outcome variables were length of stay (LOS) in the intensive care unit (ICU) and in hospital, and 30 day and 1 yr mortality and morbidity, defined as acute myocardial infarction, arrhythmias, and cardiac dysfunction. Groups were compared by an on-treatment analysis, using linear mixed models for repeated measures. ResultsEighty-four patients completed the protocol (I: 41 vs P: 43). Postoperative cTnI concentrations increased to a maximum of I: 2.72 ng ml−1 (1.78–5.85) and P: 2.64 ng ml−1 (1.67–4.83), but did not differ between groups (P=0.11). LOS in the ICU and in hospital was similar [ICU I: 18 (17.0–21.5) vs P: 19 (17.0–22.0) h; hospital I: 9 (6.5–8.0) vs P: 8 (6.0–9.0) days]. Cardiac morbidity and mortality in hospital and 30 days after surgery did not differ between groups. One year after surgery, two patients had died of non-cardiac causes. No between-group differences in cardiac morbidity were found. ConclusionsIn this study, the use of isoflurane–sufentanil in comparison with propofol–sufentanil anaesthesia does not afford additional reduction of postoperative cTnI levels.Clinical trial registration information: NCT00356746 (http://www.clinicaltrials.gov/ct2/show/NCT00356746?term=NCT00356746&rank=1).

Troponin Release in Patients Admitted with Acute Decompensated Heart Failure and Renal Dysfunction: Results from the Pilot Phase of the PROTECT Trial

Troponin Release in Patients Admitted with Acute Decompensated Heart Failure and Renal Dysfunction: Results from the Pilot Phase of the PROTECT Trial

2007 in Review: A Dozen Steps Forward in Anesthesiology

Summary These 12 articles represent an inspiring collection ofadvances in our specialty. Yet another dozen could easilyhave been chosen, including: ● Long-term neuroprotection from isoflurane: Sakai et al .A NESTHESIOLOGY 2007; 106:92–9 ● The first human application of a novel local anesthetic:Rodriquez-Navarro et al .A NESTHESIOLOGY 2007; 106:339–45 ● Application of monitoring to measure in real time end-tidal concentrations of systemically administereddrugs: Takita et al .A NESTHESIOLOGY 2007; 106:659–64and Hornuss et al .A NESTHESIOLOGY 2007; 106:665–4 ● ASA practice guidelines for obstetric anesthesia: Con-nis et al .A NESTHESIOLOGY 2007; 106:843–63 ● The safety of low dose droperidol in the peri-operativeperiod: Nuttall et al .A NESTHESIOLOGY 2007; 106:531–6 ● Moving neuromuscular monitoring electrodes 2 cmmedially reduces the incidence of postoperative nau-sea and vomiting as much as pharmacologic therapy:Arnberger et al .A NESTHESIOLOGY 2007; 107:903–8 ● Laboratory studies suggesting a drug used orally totreat Alzheimer’s disease might also be used to treatchronic pain: Clayton

Desflurane Versus Propofol in Patients Undergoing Mitral Valve Surgery

Myocardial ischemic damage is reduced by volatile anesthetics in patients undergoing coronary artery bypass graft surgery, but it is unknown whether this benefit exists in patients undergoing valvular surgery with ischemia-reperfusion injury related to cardioplegic arrest and cardiopulmonary bypass. This study compared cardiac troponin release in patients receiving either volatile anesthetics or total intravenous anesthesia for mitral valve surgery. Randomized controlled study. University hospital. One hundred twenty patients undergoing mitral valve surgery. Fifty-nine patients received the volatile anesthetic desflurane for 30 minutes before cardiopulmonary bypass, whereas 61 patients received a total intravenous anesthetic with propofol. All patients had an opioid-based anesthetic for the mitral valve surgery. Peak postoperative troponin I release was measured as a marker of myocardial necrosis after mitral valve surgery. Patient mean age was 60 years, and 54% were men. There was no significant (p = 0.7) reduction in median (25th-75th percentiles) postoperative peak troponin, 11.0 (7.5-17.4) ng/dL in the desflurane group versus 11.5 (6.9-18.0) ng/dL in the propofol group. A subgroup of patients with concomitant coronary artery disease had the expected reduction (p = 0.02) of peak troponin I in those receiving desflurane, 14.0 (9.7-17.3) ng/dL, when compared with patients receiving total intravenous anesthesia, 31.6 (15.7-52.0) ng/dL. Myocardial damage measured by cardiac troponin release was not reduced by volatile anesthetics in patients undergoing mitral valve surgery, whereas it was reduced in patients with concomitant coronary artery disease.

Cardiac protection by volatile anaesthetics

To evaluate the effects of total intravenous anaesthesia vs. volatile anaesthesia on cardiac troponin release in coronary artery bypass grafting with cardiopulmonary bypass, we performed a multicentre randomized controlled study to compare postoperative cardiac troponin release in patients receiving two different anaesthesia plans. We randomly assigned 75 patients to propofol (intravenous anaesthetic) and 75 patients to desflurane (volatile anaesthetic) in addition to an opiate-based anaesthesia for coronary artery bypass grafting. Peak postoperative troponin I release was measured as a marker of myocardial necrosis. There was a significant (P < 0.001) difference in the postoperative median (25th-75th percentiles) peak of troponin I in patients receiving propofol 5,5 (2,3-9,5) ng dL(-1) when compared to patients receiving desflurane 2,5 (1,1-5,3) ng dL(-1). The median (interquartile) troponin I area under the curve analysis confirmed the results: 68 (30.5-104.8) vs. 36.3 (17.9-86.6) h ng dL(-1) (P = 0.002). Patients receiving volatile anaesthetics had reduced need for postoperative inotropic support (24/75, 32.0% vs. 31/75, 41.3%, P = 0.04), and tends toward a reduction in number of Q-wave myocardial infarction, time on mechanical ventilation, intensive care unit and overall hospital stay. Myocardial damage measured by cardiac troponin release could be reduced by volatile anaesthetics in coronary artery bypass surgery.

Myocardial Damage Prevented by Volatile Anesthetics: A Multicenter Randomized Controlled Study

The purpose of this study was to evaluate the effects of volatile anesthesia versus total intravenous anesthesia on cardiac troponin release in off-pump coronary artery bypass grafting (OPCAB). The authors performed a multicenter randomized controlled study to compare cardiac troponin release in patients receiving either volatile anesthetics or total intravenous anesthesia for cardiac surgery on the beating heart, which is an excellent model of human myocardial ischemia. Three university hospitals. The authors randomly assigned 57 patients to desflurane (volatile anesthetic) and 55 patients to propofol (intravenous anesthetic) in addition to an opiate-based anesthesia for OPCAB. The 2 groups of patients received either desflurane (volatile anesthetic) or propofol in addition to an opiate-based anesthesia for OPCAB. Peak postoperative troponin I release was measured as a marker of myocardial necrosis. Prolonged hospitalization was considered as a secondary outcome. Patient mean age was 69 years, and 82% were men. There was a significant (p < 0.001) reduction in postoperative median (25th-75th percentiles) peak of troponin I in patients receiving volatile anesthetics, 1.2 (0.9-1.9) ng/dL, compared with patients receiving total intravenous anesthesia, 2.7 (2.1-4.0) ng/dL. This myocardial protection resulted in a reduced (p = 0.04) number (percentage) of patients requiring postoperative inotropes, 20 (35%) versus 31 (56%), and a reduced number (percentage) of patients submitted to prolonged hospitalization (> or =7 days), 7 (12%) versus 20 (36%) in the 2 groups (p = 0.005). One patient receiving total intravenous anesthesia died within 30 days of surgery. Myocardial damage measured by cardiac troponin release could be reduced by volatile anesthetics during OPCAB. Because patients underwent cardiac surgery on the beating heart, these results could have implications for cardiac patients undergoing noncardiac surgery.

Perioperative myocardial injury: individual and population implications

It is generally understood that patients who have cardiovascular disease are at risk of cardiac complications after surgery. In patients undergoing major or vascular surgery, the risk of such complications can be signi®cant. Eagle and colleagues studied patients enrolled on the CASS (Coronary Artery Surgery Study) registry who subsequently underwent non-cardiac surgery. They reported a perioperative myocardial infarction rate of 8.5% in patients with medically managed coronary artery disease who underwent vascular surgery. The authors de®ned high-risk surgery as surgery associated with a risk of perioperative death or myocardial infarction of greater than 4%. Abdominal surgery, thoracic surgery, and head and neck surgery fell into this category. For patients undergoing these types of surgery who had medically treated coronary artery disease, the overall perioperative myocardial infarction rate was 2.7% and the overall death rate 3.3%. This compared with rates of 0.8 and 1% respectively in patients undergoing similar surgery who did not have coronary artery disease. Data such as these are often considered with information on the prevalence of coronary artery disease to obtain some indication of the population burden of disease. For example, in 1990 Mangano stated that 25 million patients undergo major surgery in the USA each year and suggested that perhaps 6±7 million of these people are at risk of perioperative cardiac complications. Such estimates suggest that perioperative cardiac complications are both a major issue in the care of individual surgical patients and a major public health issue. This review will examine in more detail the population impact of perioperative cardiac morbidity and the implications of this for the individual patient.