ABSTRACT
INTRODUCTION: Since the outbreak of the 2019 coronavirus (COVID-19), vascular specialists have faced dramatic changes in clinical and surgical practice. Although COVID-19 pulmonary signs and symptoms were the most pertinent problems initially, in the long term, cardiovascular complications became the most fearsome, with poor outcomes in terms of morbidity and mortality. Algorithms and decision-making procedures have been modified, not only to treat new clinical findings in COVID-19 positive patients, but also to avoid complications related to pulmonary and systemic infections. Additionally, COVID-19-negative patients experienced challenging management, due to hospital crowding, the risk of nosocomial COVID-19 transmission, and pandemic emergencies. In this context, aortic interventions were subject to several difficulties. First, in COVID-19-positive patients, there was the onset of new pathological scenarios including thrombotic manifestations and the subsequent complications. Second, in both COVID-19-negative and positive patients, there was a need to deliver optimal treatment with acceptable perioperative risks, forcing a rethinking of decision-making especially in terms of indications for treatments. The aim of this systematic review is to present evidence published on COVID-19 and aortic-related issues, highlighting some challenging aspects regarding management, treatment and outcomes. EVIDENCE ACQUISITION: Data search was performed on PubMed, Scopus and Web of Science, using as time range "January 1st, 2000 - May 1st, 2021." Only articles in English language were included. Key words used for the query were "Aorta" AND "COVID-19" OR "SARS-CoV-2." Furthermore, the NCBI database of "SARS-CoV-2 Resources" was interrogated to find further relevant studies. EVIDENCE SYNTHESIS: The search retrieved 416 papers; among these, 46 studies were eligible and reviewed in depth. The published literature suggests the existence of a hypercoagulable state in patients with COVID-19 disease occurring via direct and indirect mechanisms. COVID-19 infection seems to promote a prothrombotic status that aggravates vascular disease. Regardless of clinical laboratory or status, active COVID-19 infection is considered a risk factor for poor vascular surgery outcomes. Specifically, it is associated with a fourfold increased risk of death and a threefold increased risk of major adverse events. Prognosis of patients hospitalized with COVID-19 disease is often determined by the extent of pulmonary disease, although vascular complications also greatly affect outcomes. Nevertheless, although COVID19 is highly morbid, in highrisk operations good outcomes can still be achieved even in elderly patients with COVID19. CONCLUSIONS: In the case of aortic disease during active COVID-19 infection, poor outcomes are associated with COVID-19 vascular and non-vascular complications, while for COVID-19-negative patients not much changed in terms of outcomes, despite the difficulties in management. Endovascular repair, when possible, minimized the impact of treatment, reducing the risk of COVID-related postoperative complications or acquired infection in negative patients.
Subject(s)
Anticoagulants/therapeutic use , Aortic Diseases/surgery , Blood Coagulation/drug effects , COVID-19/therapy , Endovascular Procedures , Thrombophilia/drug therapy , Vascular Surgical Procedures , Anticoagulants/adverse effects , Aortic Diseases/blood , Aortic Diseases/mortality , COVID-19/blood , COVID-19/mortality , Endovascular Procedures/adverse effects , Endovascular Procedures/mortality , Humans , Postoperative Complications/etiology , Risk Assessment , Risk Factors , Thrombophilia/blood , Thrombophilia/mortality , Treatment Outcome , Vascular Surgical Procedures/adverse effects , Vascular Surgical Procedures/mortalityABSTRACT
Cardiovascular complications in patients undergoing non-cardiac surgery are associated with longer hospital stays and higher in-hospital mortality. The aim of this study was to assess the incidence of in-hospital myocardial infarction and/or myocardial injury in patients undergoing hip fracture surgery and their association with mortality. Moreover, we evaluated the prognostic value of troponin increase stratified on the basis of peak troponin value. The electronic records of 1970 consecutive hip fracture patients were reviewed. Patients <70 years, those with myocardial infarction <30 days, and those with sepsis or active cancer were excluded from the study. Troponin and ECG were obtained at admission and then at 12, 24, and 48 h after surgery. Echocardiography was made before and within 48 h after surgery. Myocardial injury was defined by peak troponin I levels > 99th percentile. A total of 1854 patients were included. An elevated troponin concentration was observed in 754 (40.7%) patients in the study population. Evidence of myocardial ischemia, fulfilling diagnosis of myocardial infarction, was found in 433 (57%). ECG and echo abnormalities were more frequent in patients with higher troponin values; however, mortality did not differ between patients with and without evidence of ischemia. Peak troponin was between 0.1 and 1 µg/L in 593 (30.3%). A total of 191 (10%) had peak troponin I ≥ 1 µg/L, and 98 died in hospital (5%). Mortality was significantly higher in both groups with troponin increase (HR = 1.37, 95% CI 1.1-1.7, p < 0.001 for peak troponin I between 0.1 and 1 µg/L; HR = 2.28, 95% CI 1.72-3.02, p < 0.0001 for peak troponin ≥1 µg/L) in comparison to patients without myocardial injury. Male gender, history of coronary heart disease, heart failure, and chronic kidney disease were also associated with in-hospital mortality. Myocardial injury/infarction is associated with increased mortality after hip fracture surgery. Elevated troponin values, but not ischemic changes, are related to early worse outcome.
