Variability of Automated Intraoperative ST Segment Values Predicts Postoperative Troponin Elevation.

The effect of postoperative myocardial ischemia on long-term survival after vascular surgery

Purpose: Patients undergoing carotid endarterectomy (CEA) or carotid artery stenting (CAS) are at substantially increased risk of short-term and long-term cardiac complications. Still, the role of perioperative troponin in predicting cardiac events remains unclear. The objective was to systematically summarize the existing evidence on the topic and provide directions for further research. Materials and Methods: Studies that examined perioperative troponin values and its association with myocardial injury, and/or myocardial infarction (MI), and/or major adverse cardiac events (MACE) and postoperative mortality in exclusively CEA/CAS patients, published in English until March 15, 2022, were retrieved through a systematic search of MEDLINE and Web of Science. The study selection process was independently performed by 2 authors, while the third researcher resolved disagreements. Results: Four studies with 885 participants met the inclusion criteria. Age, chronic kidney disease, presentation of carotid disease, type of closure (primary closure/venous patch/Dacron/polytetrafluoroethylene patch), coronary artery disease, chronic heart failure, and the long-term use of calcium channel blockers represent risk factors for troponin elevation, which occurred in 11% to 15.3%. Myocardial infarction and MACE occurred in 23.5% to 40%, that is, 26.5% of patients with troponin elevation, respectively, during the first 30 postoperative days. Elevated postoperative troponin levels were significantly associated with adverse cardiac events during the long-term surveillance period. The rates of cardiac-related and all-cause mortality were higher in patients with postoperative troponin elevation. Conclusion: Troponin measurement could be helpful in the prediction of adverse cardiac events. The predictive role of preoperative troponin, the patient population in whom routine troponin sampling should be used, and a comparison of different treatment methods/anesthesia techniques in carotid patients should be further examined. Clinical Impact The present scoping review critically appraises the extent and nature of the existing literature data on the predictive value of troponin on the occurrence of cardiac complications in patients undergoing CEA and CAS. In particular, it provides clinicians with essential insights by systematically summarizing the core evidence and identifying knowledge gaps that may direct future research. This, in turn, may significantly alter the current clinical practice and perhaps even reduce the incidence of cardiac complications in patients undergoing CEA/CAS.

The effects of oral propranolol, digoxin and combination therapy on the resting and exercise electrocardiogram

N-Terminal Pro-Brain Natriuretic Peptide and Angiotensin-Converting Enzyme-2 Levels and Their Association With Postoperative Cardiac Complications After Emergency Orthopedic Surgery

Editor, In a recently published, retrospective observational study of vascular surgery patients, Valentijn et al.1 showed that preoperative haemoglobin levels, postoperative haemoglobin levels and haemoglobin decrease were all related to an increased risk of 30-day postoperative cardiovascular adverse events. Strengths of this study include the large sample of patients, and the use of multivariable and sensitivity analyses to adjust, and to reduce, the influence of confounding variables on study endpoints. However, other than the limitations described in the discussion of the article, we have noted further issues of this study making the interpretation of their results questionable. First, health status, type of surgery and comorbidities are important determinants of postoperative cardiovascular adverse events. This study showed that patients with postoperative cardiovascular adverse events had more risk factors of the Revised Cardiac Risk Index, more comorbidities, lower preoperative or postoperative haemoglobin levels and larger haemoglobin decreases. Furthermore, they were older, more likely to undergo open surgery and to receive transfusion. In our opinion, no matter how refined the adjustment is for differences in health status, surgery burden and comorbidities, it is never possible to ensure a complete adjustment for differences between patients with and without postoperative cardiovascular adverse events. Additionally, preoperative anaemia is actually associated with a number of other comorbidities and known risk factors that can significantly affect postoperative cardiovascular adverse events, such as advanced age, poor left ventricular ejection fraction, renal dysfunction, congestive heart failure, myocardial infarction, unstable angina, and so on. This can further make it difficult to identify the specific role of preoperative anaemia, and even sophisticated multivariable analyses are probably inadequate to clarify whether anaemia is a risk factor or simply a marker of a more severe and complex preoperative clinical pattern. Recently, a retrospective study including 574 860 non-cardiac surgical patients has shown that preoperative anaemia was only associated with baseline diseases that markedly increased 30-day mortality and morbidity after surgery, whereas anaemia per se was only a weak and independent predictor of postoperative mortality and morbidity.2 Second, this study included and adjusted preoperative usage of many cardiovascular medications including β-blockers, but the authors did not specify whether patients taking these drugs before surgery continued their therapies after surgery. A systematic review of the literature showed that β-blockers lowered the perioperative risk of myocardial ischaemia and cardiovascular death among patients with clinical risk factors undergoing major vascular surgery.3 Furthermore, withdrawal of chronic β-blockade following vascular surgery has been shown to be associated with increased perioperative mortality.4 Third, this study did not include intraoperative haemodynamic data. In patients undergoing non-cardiac surgery, intraoperative hypotension, tachycardia and hypertension have been shown to be independently associated with postoperative myocardial injury and cardiac adverse events.5 Even short periods of an intraoperative mean arterial pressure less than 55 mmHg can result in myocardial injury, and there is an independent graded relationship between the duration of intraoperative hypotension and postoperative myocardial injury and cardiac complications.6 Finally, postoperative haemoglobin levels were measured within 0 to 3 days after surgery, but the authors did not specify the times when postoperative cardiovascular adverse events occurred and the times of postoperative troponin-T measurement. In high-risk patients undergoing vascular surgery under electrocardiographic monitoring, the majority of ischaemic events (67%) including those culminating in myocardial infarction, were reported to start between 50 min before and 60 min after the end of surgery and during the emergence from anaesthesia.7 Thus, in some patients who experienced postoperative cardiovascular adverse events, their postoperative haemoglobin levels might have been measured after occurrence of the events. Under these circumstances, great caution must be taken when interpreting the relationship of the measured postoperative haemoglobin levels with postoperative cardiovascular adverse events. Acknowledgements related to this article Assistance with the letter: none. Financial support and sponsorship: none. Conflicts of interest: none.

The Silent Burden of Perioperative Myocardial Infarction After Noncardiac Surgery

Association between postoperative mean arterial blood pressure and myocardial injury after noncardiac surgery

Our aim was to examine the predictive value of preoperative stress echocardiography regarding early myocardial ischemia and late cardiac events after carotid endarterectomy (CEA). Patients with coronary artery disease undergoing CEA were prospectively included in this study. All patients (n = 162) were classified into low, medium, and high cardiac risk group, according to preoperative stress echocardiography. Classification was based on the criteria of the American Society of Echocardiography. For all patients, cTnI was measured before surgery and on postoperative days 1, 3, and 7. Postoperative cTnI values ranging from 0.05 to 0.5 ng/mL were classified as myocardial ischemia; values >0.5 ng/mL were classified as myocardial infarction. Cardiac damage was defined as either myocardial ischemia or infarction. No deaths, strokes, or symptomatic coronary events were observed during the early postoperative period. There were 112 low cardiac risk patients, 42 medium-risk patients, and 8 high-risk patients, according to stress echocardiography findings. Overall, there were 22 patients (14%) that increased their cTnI values postoperatively (12 of low cardiac risk and 10 of medium cardiac risk), and all of them were asymptomatic. None of the high-risk patients showed any troponin increase. Late cardiac events were associated with cTnI increase, although no high-risk patients showed any late event. Preoperative stress echocardiography does not seem to independently recognize patients in high risk for asymptomatic cardiac damage after CEA. Postoperative troponin elevation seems to be more predictive for late adverse cardiac events than preoperative stress echocardiography.

Evaluation of Non-Cardiac Surgical Patients With Postoperative Troponin Elevation at a Tertiary Referral Hospital

Recent analyses have demonstrated significant associations between troponin elevations in both the preoperative and postoperative settings. In this infographic, we explore the relationship between mortality and positive preoperative troponins, and the diagnostic and management pathways associated with postoperative troponin elevation.1,2

Reticulated Platelets as Predictor of Myocardial Injury and 30 Day Mortality After Non-cardiac Surgery.

Postoperative hypotension and troponin elevation: association or causation?

A 52-year-old man came to the emergency department at 3:00 am with constant retrosternal pain that had awakened him at 1:47 am and was accompanied by nausea. A standard 12-lead electrocardiogram showed 1 mm of ST-segment elevation in lead III with slightly less elevation in lead aVF and >0.5 mm elevation in lead II (Figure ​(Figure11). The reciprocal ST-segment depression noted in leads I and aVL confirmed that the minor ST-segment elevation in leads II, III, and aVF represented inferior acute myocardial injury (1). Figure 1 Standard 12-lead electrocardiogram recorded when the patient first presented to the emergency department. See text for explication. In the presence of inferior acute injury, the minor ST-segment depression in leads V2 to V6 suggested changes reciprocal to acute posterior myocardial injury. Lead V1 did not participate in the ST-segment depression because of a neutralizing anterior current of injury resulting from acute infarction of the right ventricle, which was located immediately behind lead V1. A 12-lead electrocardiogram recorded 20 minutes later with the precordial leads on the right side of the chest showed obvious ST-segment elevation in leads V2R (lead V1L) through V6R, confirming acute infarction of the right ventricle (Figure ​(Figure22). Lead V1R (V2L) showed slight ST-segment depression rather than elevation because it did not face the right ventricle, had an unimpeded look at the injured posterior wall of the left ventricle, and thus showed reciprocal depression. Figure 2 In this electrocardiogram, recorded 20 minutes after the electrocardiogram shown in Figure ​Figure1,1, the limb leads were recorded in the standard fashion and showed slightly more ST-segment elevation in leads II, III, and aVF and slightly more ... Some 75% to 80% of inferior myocardial infarcts are due to occlusion of the right coronary artery, with most of the others due to occlusion of the left circumflex artery (2). In addition, five features of these two electrocardiograms indicate that the right, rather than the left circumflex, is the culprit coronary artery: 1) ST-segment elevation in lead III greater than that in lead II; 2) ST-segment depression in lead I; 3) an isoelectric ST segment in lead aVR; 4) ST-segment depression in lead V2 with an elevated or isoelectric ST segment in lead V1; and 5) ST-segment elevation >1 mm in any of the right-sided precordial leads (2). Coronary arteriography, performed a week after the onset of infarction, revealed a 95% narrowing in the midportion of the right coronary artery without significant disease in any other vessel. After the stenosis was dilated, a 2.5 × 28-mm Cypher stent was placed in the midportion of the right coronary artery. The patient's risk factors for coronary disease were long-standing systemic arterial hypertension, an 80-pack-year history of cigarette smoking, a family history of coronary artery disease, a C-reactive protein level of 2.40 mg/dL (normal 55%). Because the number of standard electrocardiographic leads with ST-segment elevation predicts the extent of left ventricular damage, and consequently the death rate, in ST-segment elevation myocardial infarction, this patient's electrocardiogram predicted a good outcome (3).

The PRINCE trial of remote ischaemic preconditioning in noncardiac surgery to reduce myocardial injury: sign o' the times.

Abstract: Although frequently in humans, hypoxic and ischemic heart diseases are poorly documented in dogs, with only few reports of acute myocardial infarction (AMI) in this species. Some electrocardiographic findings might suggest myocardium hypoxia/ischemia, like ST segment elevation or depression, but there are no studies showing whether deviations in ST segment are associated to myocardial injury and serum increase of creatine phosphokinase (CPK-MB). In order to investigate possible myocardial cells injury in poor perfusion conditions, 38 dogs were studied, 20 with normal electrocardiogram and 18 with ST segment elevation or depression, recorded in lead II, at a paper speed of 50 mm/sec and N sensibility (1mV=1cm). Serum measurement of creatine phosphokinase isoenzyme MB (CPK-MB) in normal dogs (group 1) determined control values (in ng/mL), which were compared to those obtained from dogs with deviation (group 2), which allowed confirmation or not of myocardial injury. CPK-MB mean values obtained from dogs in groups 1 and 2 were 0.540ng/ml (SD±0.890)ng/mL and 0.440ng/mL (SD±1.106), respectively. At a significance level of 5%, the relation of CPK-MB with age, mass and total creatine phosphokinase (CPK-T) was not significant in groups 1 and 2. CPK-MB showed no difference, at 5% level, between groups 1 and 2. In conclusion, it is possible to use the human chemiluminescent immunometric assay kit in canine species and that hypoxia/ischemia revealed by ST segment deviation does not mean significant myocardium injury.