Rapid Fire Abstracts
Kristian Dimovski, MD
MD
Lund University and Skåne University Hospital, Lund, Sweden, Sweden
Kristian Dimovski, MD
MD
Lund University and Skåne University Hospital, Lund, Sweden, Sweden
Anders Nelsson, MD
MD, PhD Student
Lund University and Skåne University Hospital, Lund, Sweden, Sweden
Ellen Ostenfeld, MD, PhD
MD, PhD, Associate professor
Lund University and Skåne University Hospital, Lund, Sweden, Sweden
Robert Jablonowski, MD, PhD
MD, PhD
Lund University, Sweden
Peter Kellman, PhD
Director of the Medical Signal and Image Processing Program
National Heart, Lung, and Blood Institute, National Institutes of Health
J. Gustav Smith, MD, PhD
Professor, medical doctor
The Wallenberg Laboratory/Department of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University and the Department of Cardiology, Sahlgrenska University Hospital, SE-413 45 Gothenburg, Sweden, Sweden
Martin Magnusson, MD, PhD
Professor
Lund University, Skåne University Hospital, Sweden
Henrik Engblom, MD, PhD
Professor, MD
Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skåne University Hospital, Lund, Sweden, Sweden
Håkan Arheden, MD, PhD
MD, PhD, Professor
Lund University and Skåne University Hospital, Lund, Sweden, Sweden
Marcus Carlsson, MD, PhD
Professor
Lund University and Skåne University Hospital, Lund, Sweden, Sweden
Twenty-two HF patients (39%) had MVDMPR and twenty-six HF patients (44%) had MVDABS. Eighteen patients (32%) had combined MVDMPR and MVDABS. MPR was lower in HF patients compared to healthy controls (HFrEF 2.8±0.7 vs 3.8±1.2, p=0.001; HFmrEF 2.2±0.6 vs 3.8±1.2, p< 0.001 and HFpEF 2.7±1.0 vs 3.8±1.2, p=0.002; Figure 1). Myocardial perfusion at stress was lower in HF patients compared healthy controls (HFrEF 2.4 ±0.6 vs 3.4±0.8, p< 0.001; HFmrEF 2.0±0.6 vs 3.4±0.8, p< 0.001; HFpEF 2.6±0.7 vs 3.4±0.8, p< 0.001; Figure 1) but with no difference in perfusion between the HF cohorts. There was no significant correlation between EF and MPR (r=0.11, p=0.42), MP at stress (r=0.07, p=0.59) or MP at rest (r=0.23, p=0.08) in HF patients.
Female HF patients had higher myocardial perfusion at rest and stress compared to male HF patients (rest 1.0±0.2 vs 0.9± 0.2, p=0.021; stress 2.5±0.5 vs 2.1±0.7, p=0.008) (Figure 2). MPR did not differ between female and male HF patients (p=0.905). There was no difference in perfusion between hypertensive (n=35) and normotensive HF patients (rest p=0.214; stress p=0.968) or between HF patients with diabetes (n=12) and without diabetes (rest p=0.402; stress p=0.755). Multivariate regression analysis including age confirmed these results (Table 1).
Conclusion: Microvascular dysfunction is present in almost half of non-ischemic HF independent of EF. Female sex was associated with a higher myocardial perfusion than males across all groups of heart failure similar to results in healthy controls5, while there was no difference in MPR. Different cutoffs for males and females to detect MVD should be considered when using absolute perfusion. CMR with qFPP has potential in future HF trials of MVD to select patients with MVD.