L. Kritharides

Quantitative and temporal differences in coagulation, fibrinolysis and platelet activation after on-pump and off-pump coronary artery bypass surgery.

BACKGROUND With the increasing use of OPCAB, potentially devastating thromboembolic events, including graft thrombosis may become increasingly evident. We present a study of the quantitative and temporal differences of the coagulation system, fibrinolysis and platelet activation after coronary artery surgery with or without cardiopulmonary bypass. METHODS Patients undergoing on-pump CABG (n=10) or OPCAB (n=10) had six blood samples taken before surgery and up to 24h post-operatively. Activation of the coagulation cascade (tissue factor pathway-factor VIIa), endothelial injury (von Willebrand Factor antigen), thrombin generation (prothrombin fragments FI+II), fibrinolysis (decreased plasminogen levels), fibrin degradation (D-Dimer), platelet counts and platelet activation (soluble P-selectin) were quantified. RESULTS CABG caused earlier and more significant generation of thrombin, however OPCAB caused a late and sustained generation of thrombin. CABG caused intraoperative activation of fibrinolysis and fibrin degradation, however, at 24h these parameters were equally elevated in both groups. Platelet activation was significant in the CABG group, but did not occur in the OPCAB group. CONCLUSIONS Late thrombin generation and reduced fibrinolysis in the presence of intact, functioning platelets may contribute to adverse thromboembolic events after OPCAB surgery. Thromboembolic prophylaxis and anti-platelet therapy may need to be more aggressive after OPCAB surgery.

Incidence and determinants of myocardial infarction following percutaneous coronary interventions according to the revised Joint Task Force definition of troponin T elevation.

BACKGROUND Elevations in troponin T (TnT) occur frequently following percutaneous coronary intervention (PCI) and are associated with an adverse prognosis. The Joint ESC/ACC/AHA/WHF Task Force have released a proposal for a universal definition of myocardial infarction (MI), including diagnostic criteria for PCI associated MI. This is based on a TnT cut-point of more than three times the 99th percentile (0.03 ng/ml), which better reflects the precision of the assay. Our study investigated the incidence and predictive factors of a PCI associated MI, using the revised definition. METHODS 325 patients were studied following PCI with stenting. TnT was collected at both 8 and 18 h following PCI in patients with either stable or unstable angina and normal baseline TnT levels. Comparison was made of both clinical and procedural characteristics of patients with and without a rise in TnT following intervention, using cut points of 0.01 and 0.03 ng/ml. RESULTS TnT was elevated > or = 0.03 ng/ml in 27% and > or = 0.01 ng/ml in 39% of patients following PCI. Troponin elevation was significantly more likely in those patients who experienced peri-procedural ischemic symptoms or EKG changes, or in whom abciximab was used. The variables associated with a troponin rise showed a greater difference between TnT positive and negative patients when using 0.03 ng/ml compared to 0.01 ng/ml, suggesting that this may be a better definition of PCI-related MI. CONCLUSIONS Approximately one-quarter of low risk patients experience a procedural MI according to the revised definition. Rises in troponin were significantly associated with peri-procedural ischemic symptoms and EKG changes, and abciximab use, consistent with this level of TnT reflecting true myocardial necrosis.

Follow-Up of Pulmonary Hypertension With Echocardiography

Individual patient response to effective therapies for pulmonary hypertension (PAH) is variable and difficult to quantify. Consequently, management decisions regarding initiation and continuation of therapy are highly dependent on the results of investigations. Registry data show that changes in cardiac index, mean right atrial pressure, and mean pulmonary artery pressure have the greatest influence on survival. It is recognized that pulmonary artery pressure (PASP) responses to PAH-specific drugs are heterogeneous. However, follow-up testing is strongly focused on assessing changes in PASP and functional status (6-min walk). The goals of therapy, which should be highlighted in follow-up imaging, include not only reduction of PASP, decrease in pulmonary vascular resistance, and improvements in right ventricular function, cardiac output, and tricuspid regurgitation. This paper reviews the echocardiographic follow-up of pulmonary hypertension, and especially focuses on right ventricular function-a major determinant of outcome, for which reliable echocardiographic assessment has become more feasible.

Endothelial Activation After Coronary Artery Bypass Surgery: Comparison Between On-Pump and Off-Pump Techniques

BACKGROUND The effects of off-pump coronary artery bypass (OPCAB) surgery on endothelial cell activation are poorly understood. Endothelial cell adhesion molecules (CAMs) are expressed and released when the endothelium is activated. We compared plasma CAMs (E-selectin, ICAM-1 and VCAM-1) and HUVEC expression of the same CAMs when exposed to plasma taken before, during and after OPCAB or on-pump coronary surgery (CABG). METHODS Patients undergoing first time CABG (n=10) or OPCAB (n=10) had 6 blood samples taken before surgery and up to 24h post-operatively. Plasma samples were assayed for E-selectin, ICAM-1 and VCAM-1. The same plasma samples were exposed to HUVEC cultures and cell-surface expression of E-selectin, ICAM-1 and VCAM-1 measured. Data are expressed as mean+/-SEM of n subjects. RESULTS Plasma E-selectin was unchanged. Plasma ICAM-1 and VCAM-1 were elevated 24h post-operatively in both groups (P<0.01), with no differences between the groups. Twenty-four hours post-OPCAB plasma increased basal and IL-1beta induced expression of endothelial VCAM-1 by 133+/-16% and 140+/-27% (P<0.05), respectively. Plasma taken 3h post-CABG decreased endothelial VCAM-1 expression by 76+/-10% (P<0.05). Peri-operative plasma had no effect on endothelial expression of E-selectin or ICAM-1 in either group. CONCLUSIONS OPCAB and CABG with CPB appear to generate qualitatively different inflammatory responses with respect to endothelial activation, which may have clinical implications.

A Rapid Access Chest Pain Clinic (RACPC): Initial Australian Experience

BACKGROUND Chest pain is the second most common presenting symptom to emergency departments (ED) in Australia, although up to 85% of these patients do not have an acute coronary syndrome (ACS). Cardiologist-led rapid access chest pain clinics (RACPC) have been proposed overseas to assist in the management of such patients, with prompt outpatient assessment if patients are deemed low risk and discharged from the ED. The use of RACPCs in Australia has been only recently proposed; we therefore sought to examine one such RACPC in an Australian context. METHODS AND RESULTS 1133 consecutive patients were seen at a metropolitan RACPC, between August 2008 and February 2017. There was a high preponderance of cardiovascular risk factors. Exercise stress testing (EST) was the default investigation upon discharge from ED, with a total of 1038 ESTs performed in 1113 patients (93%), with low numbers of other functional tests, and a small, but increasing number of coronary computed tomography (CT) scans performed over this period. Eighteen patients subsequently underwent revascularisation (1.6% of the total cohort), and none of these patients were readmitted at any time with an ACS between the interval of their index ED presentation to these investigations or treatments. Five (0.4%) patients represented to ED within 48hours, none due to a cardiovascular cause. A total of 24 (2.1%) patients represented between 2 and 28 days, with none of these due to an ACS. CONCLUSIONS Following ED assessment of acute chest pain as low risk-with direct ED referral for exercising testing followed by RACPC review-results in very low readmission rates at 48hours and at 28 days. Moreover, these readmissions were almost always not of cardiovascular aetiology, and occurred despite relatively longer waiting periods for both EST (8 days) and between EST and RACPC review (11 days), than the prespecified 72 to 96hours as defined by the clinic protocol. Further investigation into this model of care in Australia is suggested.