Rapid Fire Abstracts
Theodor Lav, MD
PhD Student
Clinical Physiology, Department of Clinical Sciences Lund, Sweden
Theodor Lav, MD
PhD Student
Clinical Physiology, Department of Clinical Sciences Lund, Sweden
Kasper Kyhl, MD, PhD
MD
Zealand University Hospital, Denmark
David Nordlund, MD, PhD
Postdoctoral researcher
Skåne University Hospital, Lund University, Lund, Sweden
Henning Kelbæk, MD, PhD
Consultant Doctor
Zealand University Hospital, Denmark
Lars Køber, MD, PhD
Clinical Professor
University of Copenhagen, Denmark
Dan Höfsten, MD, PhD
Clinical Associate Professor
Copenhagen University Hospital,, Denmark
Jacob Lønborg, MD, PhD
Clinical Associate Professor
Copenhagen University Hospital, Denmark
Henrik Engblom, MD, PhD
Professor, MD
Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skåne University Hospital, Lund, Sweden, Sweden
David Erlinge, MD, PhD
Professor
Lund University, Department of Cardiology, Clinical Sciences, Lund, Sweden, Sweden
Håkan Arheden, MD, PhD
MD, PhD, Professor
Lund University and Skåne University Hospital, Lund, Sweden, Sweden
Thomas Engstrøm, MD, PhD
Professor
Copenhagen University Hospital, Denmark
There is a need for better prediction of outcomes after myocardial infarction to guide clinical treatment. We aimed to investigate if non-invasive pressure volume (PV)-loop variables by cardiovascular magnetic resonance imaging (CMR) have an incremental prognostic value for all-cause mortality or heart failure compared to conventional clinical measurements such as left ventricular ejection fraction (LVEF), infarct size (IS), mean arterial pressure (MAP) and stroke volume (SV) in patients with ST-elevation myocardial infarction (STEMI).
Methods:
A total of 653 STEMI-patients from the DANAMI-3 trial underwent CMR and brachial blood pressure registration after revascularization (1). Volumetric CMR-data and blood pressures were used for generation of PV-loops, as previously described and validated (2). The following PV-loop variables, shown in Figure 1, were calculated: arterial elastance (Ea), contractility (Emax), energy per ejected volume (EpV), external power, potential energy (PE), stroke work (SW), ventriculoarterial coupling (VAC), and ventricular efficiency (VE). The primary endpoint was a composite of all-cause mortality and hospitalization for heart failure. Secondary outcomes consisted of all-cause mortality, and hospitalization for heart failure respectively. Multivariate Cox proportional hazard models were applied with adjustments for age, sex, culprit vessel, and symptom duration in each model.
Results: A total of 39 (6%) patients suffered the primary endpoint during a median follow-up time of 3.2 years. Contractility (C-index 0.77), Ea (C-index 0.78), EpV (C-index 0.79), LVEF (C-index 0.78), IS (C-index 0.80), PE (C-index 0.79), VAC (C-index 0.79) and VE (C-index 0.79) were associated with the primary endpoint after adjustment for confounders (Figure 2). Infarct size and LVEF were associated with the primary endpoint (hazard ratio (HR) 1.64, 95% CI 1.16-2.31; and HR 0.57, 95% CI 0.40-0.81), whereas MAP and SV were not (HR 1.01, 95% CI 0.99-1.03; and HR 0.77, 95% CI 0.52-1.14). Associations with secondary outcomes are demonstrated in Figure 3. Emax was independently associated with all-cause mortality with a hazard ratio (HR) of 0.55 (95% CI 0.31-0.99), and Ea, PE, EpV and VAC were associated with hospitalization for heart failure with HR 1.94 (95% CI 1.43-2.63), HR 1.66 (95% CI 1.11-2.48), HR 1.99 (95% CI 1.47-2.69), and HR 2.00 (95% CI 1.50-2.68) respectively. No association was found between all-cause mortality and LVEF (or IS).
Conclusion:
CMR generated PV-loop variables provide incremental prognostic information to MAP, and SV but not to LVEF or IS with regard to all-cause mortality and development of heart failure in patients with STEMI treated with primary PCI.
