Remco B. Grobben

One-Year Mortality, Causes of Death, and Cardiac Interventions in Patients with Postoperative Myocardial Injury

BACKGROUND:To evaluate the role of routine troponin surveillance in patients undergoing major noncardiac surgery, unblinded screening with cardiac consultation per protocol was implemented at a tertiary care center. In this study, we evaluated 1-year mortality, causes of death, and consequences of cardiac consultation of this protocol. METHODS:This observational cohort included 3224 patients ≥60 years old undergoing major noncardiac surgery. Troponin I was measured routinely on the first 3 postoperative days. Myocardial injury was defined as troponin I >0.06 &mgr;g/L. Regression analysis was used to determine the association between myocardial injury and 1-year mortality. The causes of death, the diagnoses of the cardiologists, and interventions were determined for different levels of troponin elevation. RESULTS:Postoperative myocardial injury was detected in 715 patients (22%) and was associated with 1-year all-cause mortality (relative risk [RR] 1.4, P = 0.004; RR 1.6, P < 0.001; and RR 2.2, P < 0.001 for minor, moderate, and major troponin elevation, respectively). Cardiac death within 1 year occurred in 3%, 5%, and 11% of patients, respectively, in comparison with 3% of the patients without myocardial injury (P = 0.059). A cardiac consultation was obtained in 290 of the 715 patients (41%). In 119 (41%) of these patients, the myocardial injury was considered to be attributable to a predisposing cardiac condition, and in 111 patients (38%), an intervention was initiated. CONCLUSIONS:Postoperative myocardial injury was associated with an increased risk of 1-year all-cause but not cardiac mortality. A cardiac consultation with intervention was performed in less than half of these patients. The small number of interventions may be explained by a low suspicion of a cardiac etiology in most patients and lack of consensus for standardized treatment in these patients.

Flexible mechanoprosthesis made from woven ultra-high-molecular-weight polyethylene fibres: proof of concept in a chronic sheep model

OBJECTIVES Ultra-high-molecular-weight polyethylene (UHMWPE) fibres are flexible, have high tensile strength, and platelet and bacterial adhesion is low. Therefore, UHMWPE may overcome limitations of current mechanical valves and bioprostheses. In this study, the biocompatibility and functionality of prototype handmade stented valves from woven UHMWPE (U-valve) was assessed in a chronic sheep model with acetylsalicylic acid monotherapy. METHODS Native pulmonary valves of 23 sheep were replaced by U-valves (n = 18) or Perimount bovine bioprostheses (reference group, n = 5). Sheep received 80 mg of acetylsalicylic acid daily. Follow-up was conducted at 1 week (n = 4), 1 month (n = 5), 3 months (n = 5) and 6 months (n = 4) in the U-valve group and at 3 months (n = 2) and 6 months (n = 3) in the reference group. Epicardial echocardiography and histology were used to assess valve function and tissue deposition, respectively. RESULTS Seventeen U-valve sheep (94%) and 3 reference sheep (60%) survived the perioperative period. One reference valve sheep was sacrificed after 4 months because of congestive heart failure. At explantation, all U-valves were intact without leaflet tearing. Up to 3 months, U-valves were flexible and free of stenosis. Regurgitation was mostly mild though gradually increasing; histology showed minimal connective tissue near the leaflet base and sparse calcification. At 6 months, connective tissue was diffusely observed on the leaflets with retraction and consecutive regurgitation and leaflet thickening. CONCLUSIONS Valves made from UHMWPE fibres demonstrated early feasibility in the pulmonary valve position with reasonably good haemodynamics and intact valve materials up to 6 months. Gradual leaflet thickening and retraction were observed after 3 months due to connective tissue overgrowth.

Detection and management of asymptomatic myocardial injury after noncardiac surgery

Surgery and the subsequent recovery are serious circulatory stress tests that may result in symptomatic cardiac events in vulnerable patients. Despite efforts to prevent the occurrence of postoperative adverse events, myocardial infarction following noncardiac surgery remains common. Even more worrisome, the typical symptoms of myocardial ischaemia, such as chest pain, are easily masked by postoperative pain treatment including opioids. As a consequence, the clinical course of postoperative myocardial infarction is mainly silent. Yet, cardiac morbidity and mortality rates in patients with asymptomatic postoperative myocardial infarction reportedly are similar to those among patients with a clinical diagnosis of myocardial infarction. As postoperative myocardial infarction may go largely undetected, the available evidence further indicates significant elevations of risk in postoperative patients with increases in circulating biomarkers reflecting cardiac cell damage, such as troponin, but without a conventional clinical diagnosis of myocardial infarction. Silent myocardial injury, as documented by elevated cardiac biomarkers, may occur in 10–20% of the patients undergoing noncardiac surgery. A metaanalysis of studies in such patients showed isolated troponin elevations to be a strong independent predictor of mortality within the first year after surgery. Moreover, the VISION study, including over 15,000 noncardiac surgery patients, showed a strong association between any troponin elevation after surgery, which occurred in 11% of the patients, and 30-day mortality. After implementing routine postoperative troponin monitoring in elderly noncardiac surgery patients at our institution, we found similar results: 19% of the patients had a troponin elevation following surgery and such elevation was significantly associated with 30-day mortality. These patients go largely undetected, and if detected, clinical guidelines for the management of isolated increases in cardiac biomarkers do presently not exist. Coronary plaque rupture

Causes and prevention of postoperative myocardial injury

Over the past few years non-cardiac surgery has been recognised as a serious circulatory stress test which may trigger cardiovascular events such as myocardial infarction, in particular in patients at high risk. Detection of these postoperative cardiovascular events is difficult as clinical symptoms often go unnoticed. To improve detection, guidelines advise to perform routine postoperative assessment of cardiac troponin. Troponin elevation – or postoperative myocardial injury – can be caused by myocardial infarction. However, also non-coronary causes, such as cardiac arrhythmias, sepsis and pulmonary embolism, may play a role in a considerable number of patients with postoperative myocardial injury. It is crucial to acquire more knowledge about the underlying mechanisms of postoperative myocardial injury because effective prevention and treatment options are lacking. Preoperative administration of beta-blockers, aspirin, statins, clonidine, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, and preoperative revascularisation have all been investigated as preventive options. Of these, only statins should be considered as the initiation or reload of statins may reduce the risk of postoperative myocardial injury. There is also not enough evidence for intraoperative measures such blood pressure optimisation or intensified medical therapy once patients have developed postoperative myocardial injury. Given the impact, better preoperative identification of patients at risk of postoperative myocardial injury, for example using preoperatively measured biomarkers, would be helpful to improve cardiac optimisation.

Kinetics of troponin I in patients with myocardial injury after noncardiac surgery

Abstract Background: Myocardial injury after noncardiac surgery, as measured by troponin elevation, is strongly associated with mortality. However, it is unknown in which patients prognosis can be improved. The presence of kinetic changes of troponin may be associated with a worse prognosis and warrant more aggressive management. Therefore, we aimed to study the kinetics of troponin in patients with postoperative myocardial injury, and to determine the added predictive value of kinetic changes of troponin on mortality. Methods: This cohort study included patients with myocardial injury after noncardiac surgery. Troponin I (TnI) was measured on the first three postoperative days. The primary outcome was all-cause 1-year mortality. We studied both absolute and relative TnI changes, and determined the delta TnI that was associated with mortality to distinguish a rise-and-fall TnI pattern from a stable TnI pattern. Next, we determined the added predictive value of a rise-and-fall TnI pattern for mortality. Results: In total, 634 patients were included. The risk ratio (RR) for mortality increased significantly with an absolute delta TnI of ≥200 ng/L (RR 1.5, 99.4% CI 1.0–2.2, p=0.003). Using this delta TnI to define a rise-and-fall pattern, 459 patients (72%) had a stable TnI pattern and 175 patients (28%) had a rise-and-fall pattern. When added to a model including the highest TnI value and variables from the revised cardiac risk index (RCRI), the TnI pattern did not increase the predictive value for mortality. Conclusions: A postoperative TnI rise-and-fall pattern was associated with 1-year mortality, but had no added value in addition to the highest TnI level to predict 1-year mortality. Therefore, postoperative TnI kinetics are not useful for further mortality risk stratification in patients with myocardial injury after noncardiac surgery.

Cardiac markers following cardiac surgery and percutaneous coronary intervention

Differentiation between procedure-related necrosis and postprocedural myocardial infarction (MI) is challenging because of the inherent association of these procedures to varying levels of myocardial injury. To improve risk stratification of patients at risk of an acute MI, the universal definition of MI implemented cardiac biomarker thresholds. The cutoff points for these thresholds, however, are largely arbitrary and lack therapeutic implications. Measurement of cardiac marker concentrations after percutaneous coronary intervention and cardiac surgery should, therefore, be used as a marker of baseline risk, atherosclerosis burden, and procedural complexity rather than a conclusive marker to diagnose acute MI.