In the current study, most patients who underwent posterior decompressive surgery for degenerative lumbar disorders achieved satisfactory clinical outcomes. However, 8.9% of the patients experienced postoperative symptomatic myocardial ischemia, resulting in the decreased overall surgical outcome and patient satisfaction. Most of these events occurred within the first four days after surgery, with the risk declining sharply after the third postoperative day. Age > 52 years, heart rate > 81 Bpm, daily liquid intake < 2140 mL, and cardiac surgery history were independently associated with postoperative symptomatic myocardial ischemia after posterior decompressive surgery for degenerative lumbar disorders. These results were not confounded by other variables potentially associated with PSMI.
Due to the frequently degenerative nature of the lumbar spine, the afflicted population tends to be older, often with multiple medical comorbidities, such as hypertension, diabetes, cardio-cerebrovascular disease, pulmonary disease, etc. Even in the absence of comorbid conditions, older patients demonstrate diminished physiologic reservation compared to the younger counterparts, including cardiac, renal, pulmonary, and immunologic functions contributing to an increased vulnerability to external insults. General anesthesia is a routine method in posterior decompressive surgery for degenerative lumbar disorders. Intraoperative decreases in pressure occur almost universally during inhalation anesthesia because halothane, isoflurane, and enflurane all produce a dose-related depression of myocardial contractility. The compensatory ability for hemodynamic changes (hypotension, bradycardia, and decreased pulmonary capillary wedge pressure) is diminished in elderly patients. The hemodynamic changes induced by anesthesia induction and revival procedure, intraoperative mass blood loss, may cause myocardial infarction. In the current study, age older than 52 years is found to be a potential risk factor for myocardial infarction, partly consistent with Goldman's findings, in which age over 70 years was identified as a risk factor for postoperative myocardial infarction [17]. The ten-year difference in age between our study and Goldman may be due to the racial disparity and the difference in diagnosis included in the two studies. Nitroglycerin was proved to prevent intraoperative myocardial infarction by improving coronary arterial blood flow in 1980 [18]. However, intraoperative prophylactic use of nitroglycerin in high-risk patients may have negligible benefits or may even be harmful, leading to cardiovascular decompensation through decreased preload [19]. Several studies demonstrate that nitroglycerin administered as a prophylactic against myocardial infarction caused hemodynamic changes that may have led to an increased incidence of intraoperative myocardial infarction due to the altered hemodynamic responses [20, 21]. However, older patients should not be excluded from the benefit of surgery, given that their overall improvements of Oswestry Disability Index (ODI) and pain relief were equivalent to those of patients without postoperative myocardial infarction. Given the correlation of age and the risk of postoperative myocardial infarction, a thorough understanding of the interplay between postoperative myocardial infarction and surgical outcomes will be vital to optimizing clinical decision-making and appropriate patient counseling before surgery. For spinal surgeons and anesthesiologists, avoidance of significant hemodynamic changes during the perioperative period should be followed.
Previous studies have demonstrated that patients with prior myocardial infarction, particularly those who had an infarction within six months before surgery, are at increased risk for postoperative infarction. Those with angina alone were not [22–25]. For patients with pre-existing coronary artery disease undergoing non-cardiac surgery, the risk of cardiac complications is known to be higher [16, 26]. Most of the degenerative lumbar disorders do not need an emergency operation; comprehensive preoperative assessment of surgical and anesthesia risks, especially the cardiovascular and respiratory function, is necessary as time permits. Based on the understanding of the above point, patients with myocardial infarction or angina within six months before are not recommended to receive surgery unless in particular circumstances in our medical center. However, we did find that patients who received cardiac surgical intervention six months ago, including coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI), assume a greater risk of postoperative myocardial infarction. There are two possible explanations for it. First, while at rest, the heart receives 4% of the cardiac output, although 10% of the systemic oxygen consumption is cardiac [27]. It results in a high degree of oxygen extraction across the coronary vascular bed. The heart increases its myocardial oxygen supply by increasing its oxygen extraction and increasing the total coronary blood flow. Under normal conditions, this increase can be up to five times the resting flow. Both the CABG and PCI are the recommended treatment methods for severe coronary artery disease involving multiple vessels or the left main stem; the patients always present poor cardiac function and lower compensatory capacity [28]. Second, revascularization with CABG and PCI are options for patients presenting with angina pectoris on optimal medical therapy. However, the repeat revascularization rate is 25.9% after PCI and 13.7% after CABG, both of which are not much higher. Delay of revascularization could result in irreversible loss of cardiac function. The surgical intervention could mechanically expand the narrowed coronary vessels but not improve vascular biological performance. Kappetein et al. [29] revealed that major adverse cardiac and cerebrovascular events (MACCE) were 26.9% in the CABG group and 37.3% in the PCI group after five years of follow-up. In other words, surgical intervention may temporarily relieve myocardial ischemia symptoms but not prevent the recurrence of myocardial infarction permanently.
The intraoperative blood loss varied from 300 mL to 1000 mL in the surgical treatment for degenerative lumbar disorders, depending on the surgery time, surgeon's experience, blood coagulation status, etc. Humans have a multitude of survival compensatory neuroendocrine mechanisms, which allow them to tolerate up to 30% of circulating blood volume loss before changes in traditional vital signs are evident, such as heart rate, blood pressure, respiratory rate, and oxygen saturation [30, 31]. Postoperatively, fluid resuscitation or blood transfusion should be implemented to maintain hemodynamic stability. The liquid intake and output volume need to be balanced. Gold JP et al. demonstrated that patients with larger hourly urine output did have a higher rate of ischemic complications, although this did not reach significance [32]. In the current study, the overall liquid output-intake difference of more than 800 mL was a potential risk factor for postoperative symptomatic myocardial ischemia.
In contrast, the amount of intraoperative blood loss is not. Postoperatively, if the liquid intake was not enough or the fluid output was excessive (use of mannitol or diuretic, somatosensory evaporation), the insufficient blood volume may induce a series of compensatory adaptations in the body, especially the increase of venous return and rapid heartbeat. Heart rate is an essential determinant of myocardial oxygen consumption: the faster the heart rate, the greater the amount of oxygen consumed per given time period. It is because the number of contractions per minute increased. Slogoff and Keats' showed a twofold increase in the frequency of ischemia associated with a heart rate above 100 bpm. By analyzing the ST segment trends, it appears that heart rate increase precedes ST depression, which suggests a cause-and-effect relationship [30]. Moreover, the autonomic nervous system plays a significant role in the pathophysiology of perioperative ischemia. There is evidence that sympathetic activation has an essential role in the onset of adverse cardiac events [30]. Adrenergic activity and plasma catecholamine levels change considerably in the postoperative period, which may predispose myocardial ischemia by altering the relationship between myocardial oxygen demand and supply [33].
There were several potential limitations in this study. First, this is a single-center study with a limited sample size. Only 256 patients were enrolled. Therefore, the study may be prone to type two error and underpowered to detect the significance of some potential risk factors. Thus, a multi-center large sample study is required. Second, only Chinese Han individuals were included in this study, and ethnic variation was not covered.