Double blind randomised controlled trial of effect of metoprolol on myocardial ischaemia during endoscopic cholangiopancreatography.

OBJECTIVE--To evaluate the effect of metoprolol, a beta adrenergic blocking drug, on the occurrence of myocardial ischaemia during endoscopic cholangiopancreatography. DESIGN--Double blind, randomised, controlled trial. SETTING--University Hospital. SUBJECTS--38 (two groups of 19) patients scheduled for endoscopic cholangiopancreatography. INTERVENTIONS--Metoprolol 100 mg or placebo as premedication two hours before endoscopy. MAIN OUTCOME MEASURES--Heart rate, arterial oxygen saturation by continuous pulse oximetry, ST segment changes during endoscopic cholangiopancreatography (an ST segment deviation > 1 mV was defined as myocardial ischaemia), electrocardiogram monitored continuously with a Holter tape recorder. RESULTS--All patients had increased heart rate during endoscopy compared with rate before endoscopy, but heart rate during endoscopy was significantly lower in the metoprolol group compared with the placebo group (P = 0.0002). Twenty one patients (16 placebo, 5 metoprolol; P = 0.0008) developed tachycardia (heart rate > 100/min) during the procedure, and 11 patients (10 placebo, 1 metoprolol; P = 0.003) developed myocardial ischaemia. One patient in the placebo group had an acute inferolateral myocardial infarction. In the 10 other patients with signs of myocardial ischaemia during endoscopy the ST deviation disappeared when the endoscope was retracted. In all patients myocardial ischaemia was related to increases in heart rate, and 10 of the 11 patients had tachycardia coherent with myocardial ischaemia. CONCLUSIONS--Metoprolol prevented myocardial ischaemia during endoscopic cholangiopancreatography, probably through lowering the heart rate. Thus, tachycardia seems to be a key pathogenic factor in the development of myocardial ischaemia during endoscopy.     

Implications of troponin testing in clinical medicine

During the past decade considerable research has been conducted into the use of cardiac troponins, their diagnostic capability and their potential to allow risk stratification in patients with acute chest pain. Determination of risk in patients with suspected myocardial ischaemia is known to be as important as retrospective confirmation of a diagnosis of myocardial infarction (MI). Therefore, creatine kinase (CK)-MB - the former 'gold standard' in detecting myocardial necrosis - has been supplanted by new, more accurate biomarkers.Measurement of cardiac troponin levels constitute a substantial determinant in assessment of ischaemic heart disease, the presentations of which range from silent ischaemia to acute MI. Under these conditions, troponin release is regarded as surrogate marker of thrombus formation and peripheral embolization, and therefore new therapeutic strategies are focusing on potent antithrombotic regimens to improve long-term outcomes. Although elevated troponin levels are highly sensitive and specific indicators of myocardial damage, they are not always reflective of acute ischaemic coronary artery disease; other processes have been identified that cause elevations in these biomarkers. However, because prognosis appears to be related to the presence of troponins regardless of the mechanism of myocardial damage, clinicians increasingly rely on troponin assays when formulating individual therapeutic plans.     

Characteristics of a nickel–albumin binding assay for assessment of myocardial ischaemia

Background: The aim of this study was to describe a method to measure ischaemia-induced alterations of the binding capacity of serum albumin to exogenous nickel.

Methods: We measured the levels of cardiac troponin I (cTnI), serum albumin, ischaemia-modified albumin (IMA) measured by a cobalt–albumin binding assay (CABA), and a nickel–albumin binding assay (NABA) in the following groups: myocardial infarction (n?=?32) and non-ischaemic chest pain (n?=?64).

Results: IMA, cTnI and NABA levels were higher in the myocardial infarction group. NABA presented a higher ability to discriminate myocardial ischaemia than CABA.

Conclusions: Patients with myocardial infarction have reduced nickel binding to human serum albumin, and NABA may have an important role as an early marker of myocardial ischaemia.     

Arrhythmias associated with myocardial ischaemia and infarction

The intention of this review has been to summarise the current state of knowledge regarding the arrhythmias induced by myocardial ischaemia and infarction. Both clinical and experimental aspects were considered. There has been some progress toward understanding the electrophysiological mechanisms responsible for the genesis of such arrhythmias but understanding is far from complete. We are still unable to trace the sequence of events which begin with the electrophysiological changes induced in cells by ischaemia and progress through macromechanisms such as re-entry, automaticity, etc., to the final arrhythmia. Exactly how the changes in individual cells translate into the macromechanisms is not known. Similarly, which macromechanism actually operate, and to what extent, is not known.We have very little information regarding the biochemical events responsible for the changes in intracellular potential seen with ischaemia. Similarly, we do not know whether arrhythmogenic mediators are involved in such a process. We have a fairly complete catalogue of the changes in biochemistry induced by ischaemia, but at the moment it is difficult to find causal relationships between such changes and ischaemia-induced disturbances in electrophysiology.Finally, we are in possession of a catalogue of drugs which may reduce the arrhythmias induced by ischaemia and infarction (both clinically and experimentally), but have no clear direction as how to develop the ideal antiarrhythmic (antifibrillatory) drugs.     

Value of thallium-201 imaging in detecting adverse cardiac events after myocardial infarction and thrombolysis: a follow up of 100 consecutive patients.

OBJECTIVE: To determine the prognostic role of thallium-201 imaging compared with that of exercise electrocardiography in patients with acute myocardial infarction treated by thrombolysis. DESIGN: Patients who remained free of adverse cardiac events six weeks after myocardial infarction had stress and rest 201TI imaging and exercise electrocardiography and were followed up for 8-32 months. Adverse cardiac events (death, reinfarction, unstable angina, and congestive heart failure) were documented. SETTING: Large district general hospital, Middlesex. SUBJECTS: 100 consecutive male and female patients who were stable six weeks after thrombolysis for myocardial infarction. MAIN OUTCOME MEASURES: Prediction of occurrence of adverse cardiac events after myocardial infarction by exercise cardiography and 201TI myocardial perfusion imaging. RESULTS: Reversible ischaemia on 201TI imaging predicted adverse cardiac events in 33 out of 37 patients with such events during follow up (hazard ratio 8.1 (95% confidence interval 2.7 to 23.8), P < 0.001). Exercise electrocardiography showed reversible ischaemia in 33 patients, of whom 13 had subsequent events, and failed to predict events in 24 patients (hazard ratio 1.1 (0.56 to 2.2), P = 0.8). CONCLUSION: 201TI imaging is a sensitive predictor of subsequent adverse cardiac events in patients who have received thrombolysis after acute myocardial infarction, whereas exercise electrocardiography fails to predict outcome.     

Thyroid hormone and myocardial ischaemia

Thyroid hormone has various effects on the cardiovascular system and its effects on cardiac contractility, heart rhythm and vascular function has long been recognized. However, new evidence is emerged on the importance of thyroid hormone in the response of the myocardium to ischaemic stress and cardiac remodelling following myocardial infarction. Based on this new information, this review highlights the role of thyroid hormone in myocardial ischaemia and cardiac remodelling, the possible underlying mechanisms and the potential therapeutic implications. Thyroid hormone or analogs may prove new therapeutic agents for treating ischaemic heart disease.     

Expression of dual Nucleotides/Cysteinyl‐Leukotrienes Receptor GPR17 in early trafficking of cardiac stromal cells after myocardial infarction

GPR17 is a G_i-coupled dual receptor activated by uracil-nucleotides and cysteinyl-leukotrienes. These mediators are massively released into hypoxic tissues. In the normal heart, GPR17 expression has been reported. By contrast, its role in myocardial ischaemia has not yet been assessed. In the present report, the expression of GPR17 was investigated in mice before and at early stages after myocardial infarction by using immunofluorescence, flow cytometry and RT-PCR. Before induction of ischaemia, results indicated the presence of the receptor in a population of stromal cells expressing the stem-cell antigen-1 (Sca-1). At early stages after ligation of the coronary artery, the receptor was expressed in Sca-1⁺ cells, and cells stained with Isolectin-B4 and anti-CD45 antibody. GPR17⁺ cells also expressed mesenchymal marker CD44. GPR17 function was investigated in vitro in a Sca-1⁺/CD31⁻ cell line derived from normal hearts. These experiments showed a migratory function of the receptor by treatment with UDP-glucose and leukotriene LTD4, two GPR17 pharmacological agonists. The GPR17 function was finally assessed in vivo by treating infarcted mice with Cangrelor, a pharmacological receptor antagonist, which, at least in part, inhibited early recruitment of GPR17⁺ and CD45⁺ cells. These findings suggest a regulation of heart-resident mesenchymal cells and blood-borne cellular species recruitment following myocardial infarction, orchestrated by GPR17.     

Duration of ischaemia determines matrix metalloproteinase-2 activation in the reperfused rabbit heart

It has been hypothesised that activation of matrix metalloproteinase-2 (MMP-2) contributes to reversible myocardial dysfunction (stunning) following short-term ischaemia and reperfusion. Gelatin zymography was used to measure release of both pro-MMP-2 (72 kDa) and MMP-2 (62 kDa), into the coronary effluent from isolated, perfused rabbit hearts during 90 min aerobic perfusion (control), or low-flow ischaemia (15 or 60 min at 1 mL/min), followed by 60 min reperfusion. In controls, pro-MMP-2 was detected in the coronary effluent throughout the first 30 min of aerobic perfusion, but MMP-2 was not detected. In contrast, MMP-2 was detected in the coronary effluent during reperfusion after both 15 and 60 min ischaemia. However, while left ventricular systolic function was impaired after both 15 min and 60 min ischaemia, a significant increase in the release of MMP-2 was only detected in hearts following 60 min ischaemia. The dissociation between mechanical function and MMP-2 levels suggest that MMP-2 does not contribute to myocardial stunning in this model, but may contribute to myocardial dysfunction following prolonged ischaemia.     

Control of blood pressure and risk of first acute myocardial infarction: Skaraborg hypertension project.

OBJECTIVE--To analyse the relation between treated blood pressure and concomitant risk factor and morbidity from acute myocardial infarction. DESIGN--Prospective longitudinal study. Treated blood pressures and other variables were used to predict acute myocardial infarction. SETTING--Primary health care in Skaraborg, Sweden. SUBJECTS--1121 men and 1453 women aged 40-69 years at registration at outpatient clinics, 1977-81, with no evidence of previous myocardial infarction were followed up for an average of 7.4 years. Subjects were undergoing treatment with drugs to lower blood pressure or had blood pressure that exceeded the systolic or diastolic limits, or both, for diagnosis (> 170/> 105 mm Hg (patients aged 40-60 years) and > 180/> 110 mm Hg (older than 60 years)) on three different occasions, or both. MAIN OUTCOME MEASURES--First validated event of fatal or non-fatal acute myocardial infarction. RESULTS--In men but not in women there was a negative relation between treated diastolic blood pressure and risk of acute myocardial infarction. Left ventricular hypertrophy and smoking were contributory risk factors in both sexes, as was serum cholesterol concentration in men. In men with normal electrocardiograms (n = 345) risk increased with increasing diastolic blood pressure (P = 0.047), whereas the opposite was found in men with electrocardiograms suggesting ischaemia or hypertrophy, or both (n = 499, P = 0.009). In those with a reading of 95-99 mm Hg the relative risk was 0.30 (P = 0.034); at > or = 100 mm Hg it was 0.37 (P = 0.027). No similar relations were seen in women or for systolic blood pressure. CONCLUSION--It may be hazardous to lower diastolic blood pressure below 95 mm Hg in hypertensive men with possible ischaemia or hypertrophy, or both. Electrocardiographic findings should be considered when treatment goals are decided for men with hypertension.     

Application of the fourth universal definition of myocardial infarction in clinical practice

Abstract

Purpose: The Fourth Universal Definition of Myocardial Infarction (MI) has highlighted the different pathophysiological mechanisms that may lead to ischaemic and non-ischaemic myocardial injury and has emphasised that the diagnosis of myocardial infarction requires the presence of acute myocardial ischaemia in the setting of acute myocardial injury. This case based review intends to illustrate basic principles on how to apply this new, revised definition in clinical practice.

Methods and Results: The distinction between different types of MIs (type 1 or type 2) and the delineation of MI from acute non-ischaemic myocardial injury may be challenging in individual patients, which is illustrated by presenting and discussing real-life routine cases.

Conclusions: Type 1?MI is a consequence of coronary plaque rupture or erosion with intracoronary thrombus formation that is usually apparent on coronary angiography. Plausible triggering mechanisms causing myocardial oxygen supply/demand mismatch must be identified for the diagnosis of type 2?MI and its treatment should focus initially on management of the underlying disease attributable to acute myocardial ischaemia.     

Advances in the mechanism and treatment of mitochondrial quality control involved in myocardial infarction

Mitochondria are important organelles in eukaryotic cells. Normal mitochondrial homeostasis is subject to a strict mitochondrial quality control system, including the strict regulation of mitochondrial production, fission/fusion and mitophagy. The strict and accurate modulation of the mitochondrial quality control system, comprising the mitochondrial fission/fusion, mitophagy and other processes, can ameliorate the myocardial injury of myocardial ischaemia and ischaemia-reperfusion after myocardial infarction, which plays an important role in myocardial protection after myocardial infarction. Further research into the mechanism will help identify new therapeutic targets and drugs for the treatment of myocardial infarction. This article aims to summarize the recent research regarding the mitochondrial quality control system and its molecular mechanism involved in myocardial infarction, as well as the potential therapeutic targets in the future.     

Early exercise testing after treatment with thrombolytic drugs for acute myocardial infarction: importance of reciprocal ST segment depression.

OBJECTIVE--To investigate the clinical importance of reciprocal ST depression induced by exercise testing early after acute myocardial infarction in patients treated with thrombolysis. DESIGN--Prospective observational study. SETTING--District general hospital in London. SUBJECTS--202 patients (170 men) aged 33-69 with acute myocardial infarction treated with thrombolysis. MAIN OUTCOME MEASURES--All patients underwent exercise testing and coronary arteriography. ST depression induced by exercise was classified as either reciprocal (associated with ST elevation) or isolated (occurring on its own). The relation between reciprocal ST depression and the following end points was studied: characteristics of the infarct, left ventricular ejection fraction, extent of coronary artery disease on arteriography, and presence of angina induced by exercise. RESULTS--Reciprocal ST depression occurred almost exclusively in Q wave infarctions and was associated with a lower overall ejection fraction than isolated ST depression. It tended to be associated with persistent occlusion of the coronary artery related to the infarct and did not indicate remote ischaemia due to multivessel coronary disease. Unlike isolated ST depression, reciprocal ST depression was not associated with angina induced by exercise. CONCLUSIONS--Reciprocal ST depression induced by exercise is usually associated with extensive Q wave infarctions and persistent occlusion of the artery related to the infarct. It does not seem to indicate reversible ischaemia and should not be used as a non-invasive marker of multivessel disease in the assessment of requirements for further investigation soon after acute myocardial infarction.     

Diagnostic re-classification and prognostic risk stratification of patients with acute chest pain

Unstable angina and myocardial infarction are prevalent manifestations of acute coronary artery disease, combined in the term ‘acute coronary syndromes’. The introduction of sensitive markers for myocardial necrosis has led to confusion regarding the distinction between small myocardial infarctions and ‘true’ unstable angina, and the application of ever more sensitive markers has accelerated the pace at which patients with unstable angina are being re-classified to non-ST-segment elevation myocardial infarction. But in how many patients with acute chest pain is myocardial ischaemia really the cause of their symptoms? Numerous studies have shown that most have <5 ng/l high-sensitivity cardiac troponin, and that their prognosis is excellent (event rate <0.5% per year), incompatible with ‘impending infarction’. This marginalisation of patients with unstable angina pectoris should lead to the demise of this diagnosis. Without unstable angina, the usefulness of the term acute coronary syndromes may be questioned next. It is better to abandon the term altogether and revert to the original diagnosis of thrombus-related acute coronary artery disease, myocardial infarction. A national register should be the next logical step to monitor and guide the application of effective therapeutic measures and clinical outcomes in patients with myocardial infarction.

     

Role of exercise testing early after myocardial infarction in identifying candidates for coronary surgery.

It has been suggested that ST depression in lead V5 or equivalent on early exercise testing after acute myocardial infarction predicts a high risk of death. To evaluate exercise testing and radionuclide ventriculography in this context 103 consecutive patients with myocardial infarction who were able to undertake a limited exercise test before discharge from hospital were exercised and underwent gated blood pool scanning. No serious complications resulted from exercise testing. Twenty nine patients developed ST depression in lead V5, 19 had exertional hypotension, 31 developed a heart rate of greater than or equal to 130 beats/min, and 15 had complex ventricular arrhythmias. Death during the first year after discharge from hospital was associated with exertional hypotension (p less than 0.001) and a heart rate on exercise testing of greater than or equal to 130 beats/min (p less than 0.05); these two variables identified all nine deaths. Inability to complete the exercise protocol for any reason was also predictive of death (p less than 0.01). Ventricular arrhythmias and ST depression in lead V5 induced by exercise were not significantly associated with an increased risk of death. The mean (SD) radionuclide ejection fraction in the patients who died was 29 (16%) compared with 43 (11)% in the patients who survived (p less than 0.001). ST changes on exercise testing after myocardial infarction appear to be less predictive of later complications than haemodynamic signs, which may indicate left ventricular damage rather than ischaemia.     

Epidermal growth factor protects against myocardial ischaemia reperfusion injury through activating Nrf2 signalling pathway

Alleviating the oxidant stress associated with myocardial ischaemia reperfusion has been demonstrated as a potential therapeutic approach to limit ischaemia reperfusion (I/R)-induced cardiac damage. It is reported that EGFR/erbB2 signalling is an important cardiac survival pathway in cardiac function and activation of EGFR has a cardiovascular effect in global ischaemia. Epidermal growth factor (EGF), a typical EGFR ligand, was considered to have a significant role in activating EGFR. However, no evidence has been published whether exogenous EGF has protective effects on myocardial ischaemia reperfusion. This study aims to investigate the effects of EGF in I/R-induced heart injury and to demonstrate its mechanisms. H9c2 cells challenged with H₂O₂ were used for in vitro biological activity and mechanistic studies. The malondialdehyde (MDA) and Superoxide Dismutase (SOD) levels in H9c2 cells were determined, and the cell viability was assessed by MTT assay. Myocardial I/R mouse administrated with or without EGF were used for in vivo studies. Pretreatment of H9c2 cells with EGF activated Nrf2 signalling pathway, attenuated H₂O₂-increased MDA and H₂O₂-reduced SOD level, followed by the inhibition of H₂O₂-induced cell death. In in vivo animal models of myocardial I/R, administration of EGF reduced infarct size and myocardial apoptosis. These data support that EGF decreases oxidative stress and attenuates myocardial ischaemia reperfusion injury via activating Nrf2.     

Regulation and actions of activin A and follistatin in myocardial ischaemia–reperfusion injury

Activin A, a member of the transforming growth factor-β superfamily, is stimulated early in inflammation via the Toll-like receptor (TLR) 4 signalling pathway, which is also activated in myocardial ischaemia–reperfusion. Neutralising activin A by treatment with the activin-binding protein, follistatin, reduces inflammation and mortality in several disease models. This study assesses the regulation of activin A and follistatin in a murine myocardial ischaemia–reperfusion model and determines whether exogenous follistatin treatment is protective against injury. Myocardial activin A and follistatin protein levels were elevated following 30 min of ischaemia and 2 h of reperfusion in wild-type mice. Activin A, but not follistatin, gene expression was also up-regulated. Serum activin A did not change significantly, but serum follistatin decreased. These responses to ischaemia–reperfusion were absent in TLR4^−/− mice. Pre-treatment with follistatin significantly reduced ischaemia–reperfusion induced myocardial infarction. In mouse neonatal cardiomyocyte cultures, activin A exacerbated, while follistatin reduced, cellular injury after 3 h of hypoxia and 2 h of re-oxygenation. Neither activin A nor follistatin affected hypoxia-reoxygenation induced reactive oxygen species production by these cells. However, activin A reduced cardiomyocyte mitochondrial membrane potential, and follistatin treatment ameliorated the effect of hypoxia-reoxygenation on cardiomyocyte mitochondrial membrane potential. Taken together, these data indicate that myocardial ischaemia–reperfusion, through activation of TLR4 signalling, stimulates local production of activin A, which damages cardiomyocytes independently of increased reactive oxygen species. Blocking activin action by exogenous follistatin reduces this damage.     

Ischaemia alters the effects of cardiomyocyte‐derived extracellular vesicles on macrophage activation

Myocardial ischaemia is associated with an exacerbated inflammatory response, as well as with a deregulation of intercellular communication systems. Macrophages have been implicated in the maintenance of heart homeostasis and in the progression and resolution of the ischaemic injury. Nevertheless, the mechanisms underlying the crosstalk between cardiomyocytes and macrophages remain largely underexplored. Extracellular vesicles (EVs) have emerged as key players of cell‐cell communication in cardiac health and disease. Hence, the main objective of this study was to characterize the impact of cardiomyocyte‐derived EVs upon macrophage activation. Results obtained demonstrate that EVs released by H9c2 cells induced a pro‐inflammatory profile in macrophages, via p38MAPK activation and increased expression of iNOS, IL‐1β and IL‐6, being these effects less pronounced with ischaemic EVs. EVs derived from neonatal cardiomyocytes, maintained either in control or ischaemia, induced a similar pattern of p38MAPK activation, expression of iNOS, IL‐1β, IL‐6, IL‐10 and TNFα. Importantly, adhesion of macrophages to fibronectin was enhanced by EVs released by cardiomyocytes under ischaemia, whereas phagocytic capacity and adhesion to cardiomyocytes were higher in macrophages incubated with control EVs. Additionally, serum‐circulating EVs isolated from human controls or acute myocardial infarction patients induce macrophage activation. According to our model, in basal conditions, cardiomyocyte‐derived EVs maintain a macrophage profile that ensure heart homeostasis, whereas during ischaemia, this crosstalk is affected, likely impacting healing and post‐infarction remodelling.     

Anomalous origin of the left coronary artery connected to the pulmonary artery in a 31-year-old woman

Anomalous origin of the left coronary artery connected to the pulmonary artery (ALCAPA) is a rare congenital defect with a high mortality rate in infancy if left untreated. It may cause myocardial ischaemia and can lead to myocardial infarction, mitral dysfunction, cardiac arrhythmias, heart failure and sudden death. Without operation, survival into adulthood is rare. We report clinical findings, diagnostic characteristics and therapy in a 31-year-old woman with ALCAPA and preserved left ventricular function.     

Prognosis of patients with "chest pain ?cause".

All 662 patients admitted to the two coronary care units in Nottingham during 12 consecutive months were followed up prospectively for one year. At the time of discharge from hospital they were categorised according to set criteria into the following diagnostic groups: definite, probable, or possible myocardial infarction; ischaemia heart disease without infarction; chest pain ?cause; and other diagnoses. Eighty-nine patients (13% of admissions) were categorised as having chest pain ?cause. No deaths occurred among these patients during the observation period, although two were readmitted with myocardial infarction. Patients with chest pain ?cause had few problems during the year after admission, and at the end of that time 75% were in their original employment. Patients admitted with ischaemic heart disease had a similar death rate (between six weeks and one year after admission) to those with myocardial infarction, and only 36% were in their original employment one year after admission. Chest pain ?cause is a clinically useful diagnostic category to which patients may be allocated after only simple investigations.     

Clinical significance, angiographic characteristics, and short-term outcomes in 30 patients with early coronary artery graft failure

BackgroundDespite technical advances in coronary artery bypass grafting (CABG), early postoperative myocardial ischaemia still remains a challenging problem. The aim of this study was to determine the incidence, clinical features, angiographic characteristics, and management of early graft failure in the present CABG era. MethodsBetween January 1997 and December 2002, 1731 patients underwent CABG at our institution. Coronary angiography was performed in patients with clinical evidence of early postoperative ischaemia (≤3 months). Thirty of these patients with graft failure constituted the population of this study. ResultsOff-pump and on-pump CABG were almost evenly performed in these patients [n=16 (53%) and n=14 (47%) respectively]. Acute myocardial infarction and unstable angina were the leading indications for coronary angiography in the majority of patients [n=28 (93%)]. The most common cause of graft failure was occlusion / thrombosis [n=20 (67%)]. Percutaneous coronary intervention (PCI) was offered to the majority of patients [n=22 (73%)]. Of these patients, 14 underwent PCI to native coronary arteries, whereas eight underwent PCI to the culprit vessel. Three patients underwent reoperation, and five received medical management. Four patients (13%) died in hospital (two after redo CABG, one after unsuccessful PCI, and one patient managed medically). Two patients (7%) had nonfatal major complications (one non-ST-elevation myocardial infarction and one stroke). ConclusionEarly graft failure generally presents as acute coronary syndrome. Graft occlusion/ thrombosis is the leading cause of ischaemia. Patients with graft failure can undergo PCI with a relatively low risk, but the need for redo CABG in associated with a high mortality. (Neth Heart J 2009;17:13-7.)