Ventricular thrombus formation in DCM reflects the presence of factors that represent Virchow's triad in the ventricle including local myocardial injury, reduced wall motion, and slow flow of the blood [13]. The clinical importance of LVT is that it carries the risk of embolic events. The incidence of LVT in the current study was 28.3%, which was higher than the incidence in other prospective studies (0.7–8%) [14, 15]. This can be explained by that, in the current study, we made a zoom on LVT in patients with ischemic DCM who were suspected to have thrombus.
In the current study, there was no significant difference in clinical variables between the two groups of studied patients regarding hypertension, dyslipidemia, smoking and diabetes mellitus and these results matched with Jiang and others in 2015 [14].
In the current study, all patients were on beta-blockers. In the literature, there is a controversy regarding the negative influence of beta-blockers in the occurrence of LVT in patients with DCM. Many studies reported a higher frequency of thrombus development in those patients when treated with beta-blockers and could be explained by the negative inotropic action of these drugs and thus increased blood stasis that contributes as one of the three components of Virchow's triad facilities the formation of LVT. Turpie et al. in 1989; reported an increased occurrence of thrombus in patients with anterior myocardial infarction after oral b-blocker therapy [16]. Un matching results were described in the GISSI-2 study that observed the same rate of LVT in patients with or without atenolol [17].
Secondary mitral regurgitation (MR) is an important issue in DCM patients. It is not due to a disease of the leaflets but to the symmetrical or asymmetrical dilation of the left ventricle [18]. It was reported that MR prevents thrombus formation in patients with DCM and this protective effect can be explained by increasing early diastolic flow velocities at the mitral annulus level and along the entire length of the LV, protecting the LV cavity from a slow blood flow pattern which is thrombogenic [19]. In the currently studied patients, no statistically significant difference was found between patients with or without LVT in presence of functional MR. MR was detected in 40% of group A and 44.7% of group B, which is consistent with the study of Garg et al. in 2019 [19], suggesting that this is not a major discriminatory variable in the formation of thrombus. However, Maze and others in 1989 noted a higher prevalence of MR in the no thrombus group [20]. Therefore, whether MR in patients with DCM is capable of decreasing blood stasis and LVT formation needs to be furtherly evaluated.
LVT are typically located in areas of reduced wall motion and adjacent to scars. The wall motion abnormality at the apex, which was the site of the thrombus in all cases in the current study, was not significantly different between groups A and B. All studied patients had akinetic or dyskinetic apex. The current study results were concordant with Maze et al., as they stated that no significant statistical difference between the thrombus and non-thrombus groups concerning the motion abnormality at the apex [20].
The presence of LVT is significantly related to the severity of LV functional impairment in patients with DCM [21]. Blood stagnation in the weak non-contractile segment of the ventricle plays a major role in the formation of thrombi [22]. In the current study, the two groups of patients showed evidence of advanced systolic dysfunction but more in group A with thrombi than in group B without. Several studies have shown that increased left ventricular internal diastolic diameters and low EF are independent predictors of LVT formation [6, 23]. Timely identification of LVT in patients with reduced EF is necessary to avoid delays in treatment with systemic anticoagulation. This identification is pretty important in patients with LV-EF ≤ 30% and sinus rhythm as prophylactic systemic anticoagulation is not supported in this group of patients relative to the increased risk of bleeding [24]. Therefore, advanced systolic dysfunction per se could not be used as an independent factor and a rationale for early treatment with prophylactic anticoagulant therapy to reduce the likelihood of embolization among the patients with ischemic DCM as the risk of bleeding also increased.
It has been noticed that the increase in the prevalence of LVT was paralleled by an increase in the scar burden. In the current study, the myocardial scarring as detected by DE-CMRI was seen significantly more extensive in patients with LVT than in patients without thrombus which matched with Kaolawanich and Boonyasirinant in 2019 as they stated that extensive apical scarring was found more significant in patients with thrombus than those without thrombus (63.3% vs 23.3%; P value < 0.0001) [25]. Therefore, apical scarring can be considered as additional evidence demonstrating the significant value of apical changes and the amount of myocardial scarring as independent markers for thrombus formation.
In the current study, the thrombus prevalence was often higher among patients with extensive myocardial scarring. This might confirm the concept of “the independent value of myocardial scarring” that might in part explain the marked difference in thrombus prevalence regardless of the severity of systolic dysfunction. In 2008 Weinsaft and others identified a low LVEF and myocardial scarring as independent risk factors of LVT formation [26].
Echocardiography is a widely employed modality in the diagnosis of LVT because it is readily available, safe, relatively cheap, and convenient but it is operator-dependent. In a setting of adequate imaging of the heart, TTE provides excellent specificity (85–90%) and sensitivity (95%) in detecting LVT [24]. In the current study, standard TTE was the first-line imaging modality used to screen for LVT. However, it was a challenge because TTE detects thrombus based on anatomical characteristics thus having a high ability to detect large and protuberant thrombi but limited in small and mural thrombi.
CMRI for detection of LVT in DCM is potentially more advantageous, compared with standard TTE not only in providing better morphological definition (anatomical characteristics) by providing cine imaging but also can characterize and differentiate LVT from other structures after contrast administration [27]. DE-CMR differentiates thrombus from surrounding myocardium as thrombus is avascular and thus characterized by an absence of contrast uptake. On the other hand, cine-CMRI without a contrast agent may be relatively insensitive for thrombus detection because thrombus may be camouflaged with the surrounding myocardium [4].
From the studied patients, routine TTE failed to detect thrombus in 12 out of 20 cases (60%). These results are consistent with Mollet et al. in 2002 who reported that among 12 patients with thrombus detected by CMRI, 58% (7 out of 12) were not detected by echocardiography [28]. Also, the current results matched the other studies that compared DE-CMRI and TTE and stated that DE-CMRI is superior for the detection of LVT [29, 30]. The limitations of TTE in detecting LVT were probably due to intra and inter-observer variation for detection of LVT that are lower for CMRI in comparison to TTE. One of the other factors that decreased detection of LVT in TTE is a poor acoustic window and it may be difficult to fully interrogate a very dilated ventricle if acoustic windows are limited. Broncano et al. in 2020 stated that cardiac MRI is not limited by acoustic windows as is TTE [31].
All of LVT in the current study patients involved the apical segments and it is well known that LVT is most frequently seen in the left ventricular apex as a common location in patients with ischemic as well as non-ischemic DCM [32].
Taken together, DE-CMR is usually interpreted in conjunction with cine-CMR, therefore the current study cannot permit conclusions to be made regarding the utility of DE-CMR alone for LVT detection. We used DE-CMRI as a gold standard in the detection of LVT as it is better than standard echocardiography and cine-CMRI alone. In the current study, cine-CMRI detected LVT in 13 out of 20 cases detected by DE-CMRI, with a prevalence of 65% which was not statistically significant when compared with TTE in the detection of LVT in the same group. These results matched with Weinsaft and others in 2011 who stated that DE-CMRI was the most accurate modality for detection of LVT, followed by cine-CMRI, and finally standard TTE [33].
Finally, it is very important to avoid false-positive results occasioned by endocardial elastosis, trabeculae, false tendons near-field clutter, lipomatous metaplasia, and artefacts among others [7]. In the current study, DE-CMRI did not detect LVT in cases of Group B, however, LVT was detected by TTE in two cases of this group, which may be false-positive results.
The present study has some limitations. Firstly, it was a small single-centre study and further studies which include more patients or multicenter studies are necessary for the validation of our results. Secondly, being a retrospective study, the outcome of LVT in the studied patients could not be evaluated. Thirdly, assessment of other clinical risk factors associated with LVT in patients with DCM has not been done, making the assessment of causality rather inconclusive.