Case report
Double diagnosis of coronary artery disease and left ventricular non-compaction – case study

Case report

A 71-year-old man with a history of ischaemic heart disease and inferior myocardial infarction treated medically in 1989 was admitted to the Institute of Cardiology due to pulmonary oedema preceded by a short history of worsening symptoms of heart failure. ECG showed sinus rhythm with QS in leads III and aVF, lack of R wave progression in anterior leads and reversal of T waves in leads I-II and V4-V5. Levels of markers of myocardial injury were within the reference range. Echocardiographic examination demonstrated impaired left ventricular systolic function with ejection fraction of 30%, regional wall motion abnormalities with akinesis of the inferior and septal apical segments and hypokinesis of the lateral wall. There was also notably increased trabeculation of the lateral and posterior wall suggesting left ventricular non-compaction. Coronary angiography disclosed occlusion of all three coronary arteries: left anterior descending (LAD) artery and circumflex (Cx) artery of the left coronary artery and right coronary artery. The further diagnostic course included cardiovascular magnetic resonance (CMR) targeted at myocardial viability assessment before qualification for revascularization. The examination confirmed the presence of left ventricular non-compaction with an end-diastolic ratio of non-compacted to compacted myocardium > 2.3 (Fig. 1). There were also subendocardial areas of delayed enhancement not exceeding 25% of the left ventricular wall thickness located in the anterior and antero-septal left ventricular segments (Fig. 2). Delayed enhancement was not present in the trabeculae, which would have been a sign of gadolinium-based contrast medium retention in that area. Because of the preserved viability of all myocardial segments with coexisting regional systolic dysfunction and globally impaired left ventricular ejection fraction the patient was qualified for coronary artery bypass grafting (CABG). The surgical revascularization was only partial and consisted of left internal mammary artery implantation to the left anterior descending artery. This was determined by an increased peri-operative risk related to the markedly impaired left ventricular systolic function. Cardiovascular magnetic resonance was repeated three months after the procedure. In the meantime the patient did not complain of angina, he had a good exercise tolerance (NYHA I) and did not have any cardiovascular adverse events. Volumetric and functional left ventricular parameters before and after the CABG are presented in Table I. There was a marked improvement of the left ventricular systolic function with a decrease of end-systolic volume and an increase of ejection fraction. Improvement of contractility after revascularization is demonstrated in Figure 3 presenting end-systolic and end-diastolic frames in short axis and 4-chamber view.

Discussion

We present an interesting case of a patient with dual diagnosis consisting of ischaemic heart disease and left ventricular non-compaction (LVNC). Ischaemic heart disease is a major cause of death in the developed countries and is commonly diagnosed by physicians of any specialty. In contrast, the problem of left ventricular non-compaction is relatively not widespread as the frequency of this disease is estimated at below 1 : 50 000. There are no large multicenter studies on patients with left ventricular non-compaction in the literature. The first case report of LVNC was published in 1975 [1]. The diagnostic criteria have been a matter of controversy since then and currently there is still no universally accepted definition of LVNC. Echocardiographic criteria are based on the presence of at least 2-fold thicker layer of non-compacted than compacted myocardium in the end-systolic phase. However, most authors of reports on non-compaction using magnetic resonance follow the diagnostic criterion of non-compacted to compacted myocardial thickness ratio > 2.3 measured in end-diastole. This cut-off value was related to satisfactory diagnostic accuracy in the detection of LVNC in terms of sensitivity (86%) and specificity (99%) [2]. The advantage of cardiovascular magnetic resonance in comparison to echocardiography is its possibility of imaging in any chosen plane and better visualization of anterior, antero-lateral and infero-lateral segments as well as better spatial resolution of the technique allowing better discrimination between compacted and non-compacted layers [3]. However, there are no documents on the prognostic value of the extent of hypertrabeculation or the value of non-compacted to compacted (NC/C) ratio. Importantly, cardiovascular magnetic resonance can depict the areas of delayed enhancement not only in the segments with compacted myocardium, but also in myocardium with increased NC/C ratio [4]. In the presented case the qualification for revascularization was based on the assessment of myocardial viability in the presence of occlusion of all three coronary arteries and impaired left ventricular ejection fraction. Despite akinesis of the inferior and septal apical segments on the echocardiographic examination there were no signs of postinfarction scar on CMR in that localization. The presence of delayed enhancement encompassing up to 25% of the myocardial thickness only in the antero-septal wall suggested that there is a high probability that systolic performance of dysfunctional segments will improve after successful revascularization [5].

In the presented case, incomplete revascularization of the advanced ischaemic heart disease led to expected improvement of the left ventricular myocardial contractility without significant influence on the degree of myocardial non-compaction.

References

 1. Chin TK, Perloff JK, Williams RG, et al. Isolated noncompaction of left ventricular myocardium. A study of eight cases’ Circulation 1990; 82: 507-513.

 2. Petersen SE, Selvanayagam JB, Wiesmann F, et al. Left ventricular non-compaction: insights from cardiovascular magnetic resonance imaging. J Am Coll Cardiol 2005; 46: 101-105.

 3. Thuny F, Jacquier A, Jop B, et al. Assessment of left ventricular non-compaction in adults: Side-by-side comparison of cardiac magnetic resonance imaging with echocardiography. Arch Cardiovasc Dis 2010; 103: 150-159.

 4. Dodd JD, Holmvang G, Hoffmann U, et al. Quantification of left ventricular noncompaction and trabecular delayed hyperenhancement with cardiac MRI: correlation with clinical severity AJR 2007; 189: 974-980.

 5. Kim RJ, Shah DJ. Fundamental concepts in myocardial viability assessment revisited: when knowing how much is “alive” is not enough. Heart 2004; 90: 137-140.