Background Coronavirus disease-2019 (COVID-19) is thought to predispose patients to thrombotic disease. To date there are few reports of ST-segment elevation myocardial infarction (STEMI) caused by type 1 myocardial infarction in patients with COVID-19. Objectives The aim of this study was to describe the demographic, angiographic, and procedural characteristics alongside clinical outcomes of consecutive cases of COVID-19–positive patients with STEMI compared with COVID-19–negative patients. Methods This was a single-center, observational study of 115 consecutive patients admitted with confirmed STEMI treated with primary percutaneous coronary intervention at Barts Heart Centre between March 1, 2020, and May 20, 2020. Results Patients with STEMI presenting with concurrent COVID-19 infection had higher levels of troponin T and lower lymphocyte count, but elevated D-dimer and C-reactive protein. There were significantly higher rates of multivessel thrombosis, stent thrombosis, higher modified thrombus grade post first device with consequently higher use of glycoprotein IIb/IIIa inhibitors and thrombus aspiration. Myocardial blush grade and left ventricular function were significantly lower in patients with COVID-19 with STEMI. Higher doses of heparin to achieve therapeutic activated clotting times were also noted. Importantly, patients with STEMI presenting with COVID-19 infection had a longer in-patient admission and higher rates of intensive care admission. Conclusions In patients presenting with STEMI and concurrent COVID-19 infection, there is a strong signal toward higher thrombus burden and poorer outcomes. This supports the need for establishing COVID-19 status in all STEMI cases. Further work is required to understand the mechanism of increased thrombosis and the benefit of aggressive antithrombotic therapy in selected cases.

A combination of prolonged SAPD, advanced age, and male sex identifies patients at high risk for development of AF after CABG.

Among adults undergoing noncardiac surgery, MINS is common and associated with substantial mortality.

BACKGROUND:The association between intraoperative cardiovascular changes and perioperative myocardial injury has chiefly focused on hypotension during noncardiac surgery. However, the relative influence of blood pressure and heart rate (HR) remains unclear. We investigated both individual and codependent relationships among intraoperative HR, systolic blood pressure (SBP), and myocardial injury after noncardiac surgery (MINS).METHODS:Secondary analysis of the Vascular Events in Noncardiac Surgery Cohort Evaluation (VISION) study, a prospective international cohort study of noncardiac surgical patients. Multivariable logistic regression analysis tested for associations between intraoperative HR and/or SBP and MINS, defined by an elevated serum troponin T adjudicated as due to an ischemic etiology, within 30 days after surgery. Predefined thresholds for intraoperative HR and SBP were: maximum HR >100 beats or minimum HR <55 beats per minute (bpm); maximum SBP >160 mm Hg or minimum SBP <100 mm Hg. Secondary outcomes were myocardial infarction and mortality within 30 days after surgery.RESULTS:After excluding missing data, 1197 of 15,109 patients (7.9%) sustained MINS, 454 of 16,031 (2.8%) sustained myocardial infarction, and 315 of 16,061 patients (2.0%) died within 30 days after surgery. Maximum intraoperative HR >100 bpm was associated with MINS (odds ratio [OR], 1.27 [1.07–1.50]; P < .01), myocardial infarction (OR, 1.34 [1.05–1.70]; P = .02), and mortality (OR, 2.65 [2.06–3.41]; P < .01). Minimum SBP <100 mm Hg was associated with MINS (OR, 1.21 [1.05–1.39]; P = .01) and mortality (OR, 1.81 [1.39–2.37]; P < .01), but not myocardial infarction (OR, 1.21 [0.98–1.49]; P = .07). Maximum SBP >160 mm Hg was associated with MINS (OR, 1.16 [1.01–1.34]; P = .04) and myocardial infarction (OR, 1.34 [1.09–1.64]; P = .01) but, paradoxically, reduced mortality (OR, 0.76 [0.58–0.99]; P = .04). Minimum HR <55 bpm was associated with reduced MINS (OR, 0.70 [0.59–0.82]; P < .01), myocardial infarction (OR, 0.75 [0.58–0.97]; P = .03), and mortality (OR, 0.58 [0.41–0.81]; P < .01). Minimum SBP <100 mm Hg with maximum HR >100 bpm was more strongly associated with MINS (OR, 1.42 [1.15–1.76]; P < .01) compared with minimum SBP <100 mm Hg alone (OR, 1.20 [1.03–1.40]; P = .02).CONCLUSIONS:Intraoperative tachycardia and hypotension are associated with MINS. Further interventional research targeting HR/blood pressure is needed to define the optimum strategy to reduce MINS.

Background: Systemic inflammation is pivotal in the pathogenesis of cardiovascular disease. As inflammation can directly cause cardiomyocyte injury, we hypothesised that established systemic inflammation, as reflected by elevated preoperative neutrophil-lymphocyte ratio (NLR) >4, predisposes patients to perioperative myocardial injury. Methods: We prospectively recruited 1652 patients aged !45 yr who underwent non-cardiac surgery in two UK centres. Serum high sensitivity troponin T (hsTnT) concentrations were measured on the first three postoperative days. Clinicians and investigators were blinded to the troponin results. The primary outcome was perioperative myocardial injury, defined as hsTnT!14 ng L À1 within 3 days after surgery. We assessed whether myocardial injury was associated with preoperative NLR>4, activated reactive oxygen species (ROS) generation in circulating monocytes, or both. Multivariable logistic regression analysis explored associations between age, sex, NLR, Revised Cardiac Risk Index, individual leukocyte subsets, and myocardial injury. Flow cytometric quantification of ROS was done in 21 patients. Data are presented as n (%) or odds ratio (OR) with 95% confidence intervals. Results: Preoperative NLR>4 was present in 239/1652 (14.5%) patients. Myocardial injury occurred in 405/1652 (24.5%) patients and was more common in patients with preoperative NLR>4 [OR: 2.56 (1.92e3.41); P<0.0001]. Myocardial injury was independently associated with lower absolute preoperative lymphocyte count [OR 1.80 (1.50e2.17); P<0.0001] and higher absolute preoperative monocyte count [OR 1.93 (1.12e3.30); P¼0.017]. Monocyte ROS generation correlated with NLR (r¼0.47; P¼0.03).

Clinical Trials.gov NCT00512109.

BackgroundIncreased baseline heart rate is associated with cardiovascular risk and all-cause mortality in the general population. We hypothesized that elevated preoperative heart rate increases the risk of myocardial injury after non-cardiac surgery (MINS).MethodsWe performed a secondary analysis of a prospective international cohort study of patients aged ≥45 yr undergoing non-cardiac surgery. Preoperative heart rate was defined as the last measurement before induction of anaesthesia. The sample was divided into deciles by heart rate. Multivariable logistic regression models were used to determine relationships between preoperative heart rate and MINS (determined by serum troponin concentration), myocardial infarction (MI), and death within 30 days of surgery. Separate models were used to test the relationship between these outcomes and predefined binary heart rate thresholds.ResultsPatients with missing outcomes or heart rate data were excluded from respective analyses. Of 15 087 patients, 1197 (7.9%) sustained MINS, 454 of 16 007 patients (2.8%) sustained MI, and 315 of 16 037 patients (2.0%) died. The highest heart rate decile (>96 beats min−1) was independently associated with MINS {odds ratio (OR) 1.48 [1.23–1.77]; P<0.01}, MI (OR 1.71 [1.34–2.18]; P<0.01), and mortality (OR 3.16 [2.45–4.07]; P<0.01). The lowest decile (<60 beats min−1) was independently associated with reduced mortality (OR 0.50 [0.29–0.88]; P=0.02), but not MINS or MI. The predefined binary thresholds were also associated with MINS, but more weakly than the highest heart rate decile.ConclusionsPreoperative heart rate >96 beats min−1 is associated with MINS, MI, and mortality after non-cardiac surgery. This association persists after accounting for potential confounding factors.Clinical trial registrationNCT00512109.

The development of percutaneous procedures to diagnose and treat coronary artery disease has transformed the lives of many patients. Patients with limiting symptoms can now often be returned to full activity by percutaneous coronary intervention (PCI), with a low risk of procedure related cardiac events. PCI has obvious advantages over coronary artery bypass grafting, and, because increasingly complex disease can be treated in patients with previously prohibitive comorbidity, the demand for both diagnostic and interventional procedures increases every year. 1In percutaneous coronary procedures a sheath with a haemostatic valve is introduced into a peripheral artery under local anaesthetic. Preshaped catheters are passed through the sheath to the ostium of the relevant coronary artery, thus allowing the delivery of radiography contrast medium, angioplasty wires, balloons, and stents. After completion of the procedure, the catheter and sheath are removed and haemostasis is achieved by manual compression, an arterial closure device, or direct repair.The femoral artery has traditionally been the preferred access site for coronary procedures, but this approach has several limitations. It is relatively contraindicated in the presence of severe peripheral vascular disease and in patients receiving anticoagulation treatment. A period of post-procedure recumbency is needed to avoid disruption of the arterial puncture site. This may be poorly tolerated by patients with left ventricular dysfunction, lung disease, or back and hip pain. Despite bed rest, the rate of complications at the femoral access site (haematoma, pseudoaneurysm, arteriovenous fistula, or need for blood transfusion or surgical arterial repair) is 2-8% after transfemoral PCI.2 3 These factors together affect patients' satisfaction, morbidity, length of hospital stay, and costs and have driven the development of alternative vascular access for coronary procedures. In this review we summarise the literature on transradial coronary procedures and discuss the potential clinical implications and technical considerations of this vascular approach.