Judith A. R. van Waes

Association between intraoperative hypotension and myocardial injury after vascular surgery

Background:Postoperative myocardial injury occurs frequently after noncardiac surgery and is strongly associated with mortality. Intraoperative hypotension (IOH) is hypothesized to be a possible cause. The aim of this study was to determine the association between IOH and postoperative myocardial injury. Methods:This cohort study included 890 consecutive patients aged 60 yr or older undergoing vascular surgery from two university centers. The occurrence of myocardial injury was assessed by troponin measurements as part of a postoperative care protocol. IOH was defined by four different thresholds using either relative or absolute values of the mean arterial blood pressure based on previous studies. Either invasive or noninvasive blood pressure measurements were used. Poisson regression analysis was used to determine the association between IOH and postoperative myocardial injury, adjusted for potential clinical confounders and multiple comparisons. Results:Depending on the definition used, IOH occurred in 12 to 81% of the patients. Postoperative myocardial injury occurred in 131 (29%) patients with IOH as defined by a mean arterial pressure less than 60 mmHg, compared with 87 (20%) patients without IOH (P = 0.001). After adjustment for potential confounding factors including mean heart rates, a 40% decrease from the preinduction mean arterial blood pressure with a cumulative duration of more than 30 min was associated with postoperative myocardial injury (relative risk, 1.8; 99% CI, 1.2 to 2.6, P < 0.001). Shorter cumulative durations (less than 30 min) were not associated with myocardial injury. Postoperative myocardial infarction and death within 30 days occurred in 26 (6%) and 17 (4%) patients with IOH as defined by a mean arterial pressure less than 60 mmHg, compared with 12 (3%; P = 0.08) and 15 (3%; P = 0.77) patients without IOH, respectively. Conclusions:In elderly vascular surgery patients, IOH defined as a 40% decrease from the preinduction mean arterial blood pressure with a cumulative duration of more than 30 min was associated with postoperative myocardial injury.

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.

Relationship Between Preoperative Evaluation Blood Pressure and Preinduction Blood Pressure : A Cohort Study in Patients Undergoing General Anesthesia

BACKGROUND: For outcomes research where changes in intraoperative blood pressure are a possible causative factor, it is important to determine an appropriate source for a reference value. We studied to what extent preinduction blood pressure values in the operating room differ from those obtained during preoperative evaluation outside the operating room. METHODS: Cohort study including 4408 patients aged 60 years or older undergoing noncardiac surgery. The outcome was the difference between the preinduction mean blood pressure (MBP) and the MBP obtained during preoperative evaluation. A difference of ≥10 mm Hg was considered clinically relevant. A paired samples t test was used to estimate the difference. Linear regression was used to obtain estimates adjusted for patient characteristics, comorbidity, medications, type of surgery, and preoperative blood pressure. RESULTS: Complete data were available for 3660 (83%) patients. There were 2228 (61%) patients with a difference of ≥10 mm Hg between the preinduction and preoperative MBP. The overall mean difference between both MBPs was 11 mm Hg (95% confidence interval, 10–11) with important variability among individuals. Patients with higher preoperative MBP values had smaller differences. After adjusting for patient characteristics, comorbidity, medications, type of surgery, and preoperative blood pressure, the difference decreased an estimated 5.0 mm Hg (95% confidence interval, 4.7–5.4) for every increase of 10 mm Hg in preoperative MBP. Patient characteristics, comorbidity, type of surgery, or medication were not strongly associated with the difference. CONCLUSIONS: The average preinduction blood pressure was higher than the preoperative blood pressure. This difference between the measurements can be explained by stress-induced effects and regression to the mean. To define an optimal reference value for research purposes or to arrive at a clinical perioperative blood pressure target, one should consider that there is important variability both within and between patients.

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.

Cardiac events within one year after a subarachnoid haemorrhage: The predictive value of troponin elevation after aneurysm occlusion

Background Patients who survive after an aneurysmal subarachnoid haemorrhage (ASAH) have an increased incidence of cardiovascular events compared with the general population. We assessed whether troponin elevation after aneurysm occlusion, as marker of myocardial injury, can predict long-term cardiac events. Methods We analysed a prospectively collected cohort of 159 patients with ASAH and early aneurysm occlusion, in whom routine post-intervention troponin I (TnI) measurements were performed. With competing risk regression modelling we estimated the association between TnI elevation after aneurysm occlusion and major adverse cardiac events within one year. Secondary outcome measures were all-cause mortality and neurological condition within one year. The predictive value of post-intervention TnI was compared with the predictive value of pre-intervention characteristics using c-statistics and the integrated discrimination improvement index. Results Subdistribution hazard ratios for TnI elevation and major adverse cardiac events at one year were 1.05 (95% confidence interval (CI) 1.03–1.07) per 10 ng/l increase in TnI and 7.91 (95% CI 1.46–43.0) for any TnI elevation. After adjustment for pre-intervention variables, the subdistribution hazard ratios were 1.47 (95% CI 0.81–2.67) per 10 ng/l and 9.00 (95% CI 1.62–50.1) for any elevation. The c-statistic was 0.71 for TnI elevation as a continuous measure and 0.69 for any TnI elevation. The integrated discrimination improvement index showed a minimum improvement in prediction of 0.08 (interquartile range 0.06 to 0.09) for TnI as a continuous measure and 0.003 (interquartile range −0.004 to 0.01) for any TnI elevation, when compared with pre-intervention characteristics. Conclusion TnI elevation after occlusion of a ruptured intracranial aneurysm predicts the occurrence of a major adverse cardiac event within one year after ASAH.

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.

Response to letter regarding article, "myocardial injury after noncardiac surgery and its association with short-term mortality".

We thank Dr Xue and colleagues for their careful reading of our study1 on the association between postoperative myocardial injury and short-term mortality. In this study, we showed that postoperative myocardial injury, identified by routine troponin measurement monitoring, predicts short-term mortality after noncardiac surgery. By adjusting this association for preoperative variables known to predict mortality, we showed that myocardial injury was an independent predictor of mortality. In response to the important comments raised by Dr Xue et al, we point out the following. First, Dr Xue and colleagues state that the association reported may be confounded by other preoperative and intraoperative factors that were not adjusted for. We wish to underline that we aimed to determine the prognostic value of postoperative myocardial injury on the occurrence of short-term death to answer the question of whether patients at higher …