Clinical Needs: Ischemic Heart Disease
Alexander Gotschy1,2

1Institute for Biomedical Engineering, University and ETH Zurich, Zurich, Switzerland, 2Department of Cardiology, University Hospital Zurich, Zurich, Switzerland

Synopsis

Cardiovascular magnetic resonance (CMR) has become an established non-invasive imaging modality for the diagnosis of ischemic heart disease (IHD) and contributes important information for therapeutic decisions regarding revascularization. For the identification of ischemia, CMR provides two methods, which are routinely used in clinical practice. Ischemia can be visualized either as regional hypoperfusion when using CMR-perfusion imaging during vasodilator induced hyperaemia, or as impaired regional wall motion under dobutamine stress CMR. CMR has proven its robustness, diagnostic performance and prognostic value in patients with IHD in several multicenter trials.

Target Audience

Cardiologists, radiologists and medical physicists with an emerging interest in the clinical applications and indications of cardiovascular magnetic resonance (CMR) for the assessment of ischemic heart disease.

Syllabus

Despite tremendous advances in the treatment of ischemic heart disease (IHD) over the last decade, IHD continues to cause a large portion of mortality and morbidity in the Western world [1]. The therapeutic armamentarium for IHD is nowadays wider than ever before ranging from new conservative strategies and innovative interventional methods to the use of assist devices in end-stage congestive heart failure. However, the COURAGE trial has shown that an invasive treatment strategy does not necessarily improve outcome in patients with stable coronary artery disease compared to optimal medical therapy alone [2]. Therefore, the versatility of treatment options requires diagnostic modalities that account for the different stages and characteristics of myocardial ischemia to guide clinical decision making. In particular, as the inappropriate use of invasive treatment strategies like percutaneous coronary intervention (PCI) are not only expensive but can also be associated with potential complications [3]. The FAME trials have shown, that the relevance of a coronary stenosis is not determined by its anatomical appearance but by its ability to induce ischemia, which was quantified by an invasive fractional flow reserve measurement [4]. In patients with ischemia, PCI in addition to optimal medical therapy decreased the need for urgent revascularization while in patients without ischemia, the outcome appears to be favourable with the best available medical therapy alone [5]. Thus, the proof of ischemia is of paramount importance to guide the decision for revascularization. To avoid the costs and potential complications of an invasive coronary angiography, current guidelines recommend performing non-invasive ischemia testing in patents with intermediate pre-test probability for stable coronary artery disease [6]. Those non-invasive test might be exercise ECG, stress echocardiography, SPECT, PET or CMR. However, in a large study, the unselected use of non-invasive imaging tests demonstrated a low diagnostic yield [7]. In addition, nuclear stress tests like SPECT or PET expose the patient to ionizing radiation. In contrast, CMR allows the assessment myocardial ischemia and viability in one examination with higher diagnostic accuracy compared to SPECT [8, 9] and without the exposure to ionizing radiation. For the detection of ischemia, CMR provides two techniques that are relevant in clinical practice. First, CMR-perfusion imaging during vasodilator (adenosine or regadenoson) induced hyperaemia, and second dobutamine stress CMR (DSMR) to reveal stress induced wall motion abnormalities caused by ischemia. Both methods have proven excellent prognostic value in patients with known or suspected IHD [10 - 12]. CMR-perfusion imaging visualizes the passage of a gadolinium-based contrast agent (CA) through the myocardium under hyperaemic conditions. Since coronary arteries with relevant stenoses cannot adequately respond to the vasodilator, CA influx is delayed leading to a dark delineation of ischemic territories. After the vasodilator stress, a CMR-perfusion at rest may be obtained to rule out false positive results due to imaging artefacts. Usually, three axial slices are acquired, to assess perfusion deficits in the basal, mid-ventricular and apical segments of the myocardium. Alternatively to CMR-perfusion imaging, DSMR can be performed to investigate myocardial ischemia. Under the pharmacologic stress of increasing doses of dobutamine, ischemic regions are identified by monitoring regional left ventricular wall motion. In a direct comparison with vasodilator CMR-perfusion imaging, DSMR showed similar performance for the assessment of CAD [13]. Governmental regulations and restrictions from health insurances brought the economic aspects of diagnostic tools and therapeutic interventions increasingly into focus. Advanced and complex techniques with relatively high operating expenses, such as CMR, are usually not considered to be cost saving for the health care sector. However, recent studies have shown that a strategy to first perform CMR for the assessment of myocardial ischemia and scar tissue and referring only positive patients to coronary angiography is cost effective compared to coronary angiography alone and to other non-invasive stress tests [14, 15].

Conclusion

CMR fulfils the clinical need for the detection of myocardial ischemia and viability to guide clinical decision making regarding revascularization or medical therapy in patients with ischemic heart disease. Thereby, CMR not only avoids unnecessary interventions with potential complication but also demonstrates that technological progress and enhanced patient comfort can go along with economic feasibility.

Acknowledgements


References

1. Townsend et al. Eur Heart J, 2015; 36(40):2673-4.

2. Boden et al. N Engl J Med, 2007. 356(15): p. 1503-16.

3. Pfisterer et al. J Am Coll Cardiol, 2006. 48(12): p. 2584-91.

4. Tonino et al. N Engl J Med, 2009. 360(3): p. 213-24.

5. De Bruyne et al. N Engl J Med, 2012. 367(11): p. 991-1001.

6. Montalescot et al. Eur Heart J, 2013. 34(38): p. 2949-3003.

7. Patel et al. N Engl J Med, 2010. 362(10): p. 886-95.

8. Schwitter et al. Eur Heart J, 2008. 29(4): p. 480-489.

9. Greenwood et al. Lancet, 2012. 379(9814): p. 453-60.

10. Jahnke et al. Circulation, 2007. 115(13): p. 1769-76.

11. Lipinski et al. J Am Coll Cardiol, 2013. 62(9): p. 826-38.

12. Gargiulo et al.Circ Cardiovasc Imaging, 2013. 6(4): p. 574-82.

13. Manka et al. Int J Cardiovasc Imaging, 2011. 27(7): p. 995-1002.

14. Walker et al. Heart, 2013. 99(12): p. 873-81.

15. Moschetti et al. J Cardiovasc Magn Reson, 2012. 14(1): p. 35.


Proc. Intl. Soc. Mag. Reson. Med. 25 (2017)