Nina van der Hoeven

Coronary angiography after cardiac arrest: Rationale and design of the COACT trial

BACKGROUND Ischemic heart disease is a major cause of out-of-hospital cardiac arrest. The role of immediate coronary angiography (CAG) and percutaneous coronary intervention (PCI) after restoration of spontaneous circulation following cardiac arrest in the absence of ST-segment elevation myocardial infarction (STEMI) remains debated. HYPOTHESIS We hypothesize that immediate CAG and PCI, if indicated, will improve 90-day survival in post-cardiac arrest patients without signs of STEMI. DESIGN In a prospective, multicenter, randomized controlled clinical trial, 552 post-cardiac arrest patients with restoration of spontaneous circulation and without signs of STEMI will be randomized in a 1:1 fashion to immediate CAG and PCI (within 2 hours) versus initial deferral with CAG and PCI after neurological recovery. The primary end point of the study is 90-day survival. The secondary end points will include 90-day survival with good cerebral performance or minor/moderate disability, myocardial injury, duration of inotropic support, occurrence of acute kidney injury, need for renal replacement therapy, time to targeted temperature control, neurological status at intensive care unit discharge, markers of shock, recurrence of ventricular tachycardia, duration of mechanical ventilation, and reasons for discontinuation of treatment. SUMMARY The COACT trial is a multicenter, randomized, controlled clinical study that will evaluate the effect of an immediate invasive coronary strategy in post-cardiac arrest patients without STEMI on 90-day survival.

Targeting the dominant mechanism of coronary microvascular dysfunction with intracoronary physiology tests

The coronary microcirculation plays a key role in modulating blood supply to the myocardium. Several factors like myocardial oxygen demands, endothelial and neurogenic conditions determine its function. Although there is available evidence supporting microvascular dysfunction as an important cause of myocardial ischaemia, with both prognostic and symptomatic implications, its diagnosis and management in clinical practice is still relegated to a second plane. Both diagnostic and therapeutic approaches are hampered by the broadness of the concept of microvascular dysfunction, which fails addressing the plurality of mechanisms leading to dysfunction. Normal microcirculatory function requires both structural integrity of the microcirculatory vascular network and preserved signalling pathways ensuring adequate and brisk arteriolar resistance shifts in response to myocardial oxygen demands. Pathological mechanisms affecting these requirements include structural remodelling of microvessels, intraluminal plugging, extravascular compression or vasomotor dysregulation. Importantly, not every diagnostic technique provides evidence on which of these pathophysiological mechanisms is present or predominates in the microcirculation. In this paper we discuss the mechanisms of coronary microvascular dysfunction and the intracoronary tools currently available to detect it, as well as the potential role of each one to unmask the main underlying mechanism.

Timing of revascularization in patients with transient ST-segment elevation myocardial infarction: a randomized clinical trial

Aims Patients with acute coronary syndrome who present initially with ST-elevation on the electrocardiogram but, subsequently, show complete normalization of the ST-segment and relief of symptoms before reperfusion therapy are referred to as transient ST-segment elevation myocardial infarction (STEMI) and pose a therapeutic challenge. It is unclear what the optimal timing of revascularization is for these patients and whether they should be treated with a STEMI-like or a non-ST-segment elevation myocardial infarction (NSTEMI)-like invasive approach. The aim of the study is to determine the effect of an immediate vs. a delayed invasive strategy on infarct size measured by cardiac magnetic resonance imaging (CMR). Methods and results In a randomized clinical trial, 142 patients with transient STEMI with symptoms of any duration were randomized to an immediate (STEMI-like) [0.3 h; interquartile range (IQR) 0.2-0.7 h] or a delayed (NSTEMI-like) invasive strategy (22.7 h; IQR 18.2-27.3 h). Infarct size as percentage of the left ventricular myocardial mass measured by CMR at day four was generally small and not different between the immediate and the delayed invasive group (1.3%; IQR 0.0-3.5% vs. 1.5% IQR 0.0-4.1%, P = 0.48). By intention to treat, there was no difference in major adverse cardiac events (MACE), defined as death, reinfarction, or target vessel revascularization at 30 days (2.9% vs. 2.8%, P = 1.00). However, four additional patients (5.6%) in the delayed invasive strategy required urgent intervention due to signs and symptoms of reinfarction while awaiting angiography. Conclusion Overall, infarct size in transient STEMI is small and is not influenced by an immediate or delayed invasive strategy. In addition, short-term MACE was low and not different between the treatment groups.

TCT-524 Invasive minimal Microvascular Resistance (mMR); a new index to assess microcirculatory dysfunction that is not modulated by the presence of angiographic coronary artery disease

TCT-523 Instantaneous Hyperemic Diastolic Velocity Pressure Slope for comprehensive physiological evaluation of epicardial and microvascular status Nina van der Hoeven, Alicia Quirós, Guus de Waard, Christopher Broyd, Sukhjinder Nijjer, Tim van de Hoef, Ricardo Petraco, Roel Driessen, Hernán Mejía-Rentería, Martijn van Lavieren, Martijn Meuwissen, Ibrahim Danad, Paul Knaapen, Jan Piek, Justin Davies, Niels van Royen, Javier Escaned Columbia University Medical Center, Amsterdam, Netherlands; The Heart Hospital Baylor Plano; VUMC, Amsterdam, Netherlands; Imperial College, London, United Kingdom; Imperial College London, London, United Kingdom; Academic Medical Center University of Amsterdam, Amsterdam, Netherlands; Imperial College, London, United Kingdom; Baylor Heart and Vascular Hospital, Dallas, Texas; Loyola Stritch School of Medicine; Academic Medical CenterUniversity of Amster, Amsterdam, Netherlands; Breda Amphia Ziekenhuis, Breda, Netherlands; Meenakshi Mission Hospital and Research Centre; VU University Medical Center, Amsterdam, Netherlands; University of Amsterdam, Amsterdam, Netherlands; Imperial College London NHS Trust, London, United Kingdom; VUmc Amsterdam, Amsterdam, Netherlands; Hospital Clínico San Carlos, Madrid, Spain BACKGROUND Instantaneous hyperemic diastolic velocity pressure slope (IHDVPS) is a measure of coronary conductance. IHDVPS is defined as the slope of the relationship between intracoronary hyperaemic pressure and Doppler flow velocity flow in mid to end diastole. In the presence of coronary artery disease, IHDVPS can be either calculated using the aortic pressure (IHDVPSPa) or distal coronary pressure (IHDVPSPd).

TCT-820 First Approach to Stimulate Arteriogenesis using Monoclonal Antibodies: Blocking the Interferon-alpha/beta Receptor Subunit 1 Stimulates Restoration of Perfusion in a Murine Hindlimb-ischemia Model Without Affecting Atherosclerosis

Purpose: Increased expression of interferon (IFN)-beta was shown in patients with insufficient coronary collaterals. Furthermore, mice treated with IFN-β demonstrate inhibition of collateral artery...