The DENSE systolic strain maps show heterogeneous myocardial function in HCM which requires a heterogeneous mechanism rather than a diffuse or global process. LGE predicts some but not all of the heterogeneity of intramural contractile abnormalities. Since LGE is a highly sensitive method 11, 25
, myocardial scar and excess collagen deposition cannot explain the spectrum of heterogeneous intramural function encountered in HCM. Myofiber disarray is one mechanism that could impair function without showing abnormalities on late enhancement images4
. The frequently observed pattern of an inner ring of normal intramural strain provides a mechanism that can explain preserved global left ventricular function despite severe strain abnormalities in the remainder of that segment. That observation could not be predicted by “uniform models” or assumptions about cardiac contraction. There are several factors that lead to heterogeneity of intramural function in patients with HCM and most of these mechanisms cannot be visualized with transmural or low resolution methods. Thus, the ability to spatially register high resolution strain maps with LGE images allows interrogation of the relationships between function and myocardial scar/collagen at an unprecedented level.
Histopathological studies have identified more than one kind of intramural heterogeneity in HCM that could relate to contractile abnormalities. Sarcomeric disarray is highly heterogeneous 26, 27
and not even confined within hypertrophic segments 26
. Sarcomeric hypertrophy occurs in the endocardium and the mid-wall 28, 29
. Diffuse interstitial fibrosis and myocardial scarring are common in HCM 28, 30, 31
. Moreover, a high fraction of young patients with HCM but no coronary artery disease have patchy signs of acute-subacute ischemia postmortem 31
At a clinical level, HCM is characterized by many types of heterogeneous abnormalities. Resting myocardial blood flow is heterogeneous despite metabolic demands similar to that of normal myocardium 32
and is related to LGE 10
. Multi-focal patterns of LGE have also been identified in asymptomatic and mildly symptomatic HCM patients 23
. These patterns, which may represent infarction, fibrosis, or excess collagen deposition 33, 34
, were later correlated with progressive dilation of the ventricle and risk of sudden death 21
Characterization of intramural left ventricular strain based on simple geometrical models does not apply in HCM since the assumption of a homogeneously contracting medium is not valid. Based on such models, there is a largely linear endocardial to epicardial gradient of circumferential strain and HCM 35
. Pioneering myocardial tagging studies may have masked the intramural strain heterogeneity due to the coarse spatial resolution (tag spacing of 7mm) 35
. Other MRI tagging studies in patients with HCM have previously reported abnormal contractile function in the left ventricle. Both radial displacement 36
and circumferential shortening are reduced in the septum 37
. Similar results were also obtained for total systolic strain recently with methods that allow full cardiac cycle interrogations 38
whereas diastolic strain was reduced in all segments.
Late gadolinium enhancement is not as closely linked to the full range of contractile abnormalities detected in HCM whereas in coronary artery disease regional function varies inversely with the transmural extent of gadolinium delayed enhancement 20
. In patients with HCM, the extent of delayed enhancement is inversely related to systolic segmental percent wall thickening 23
. While the current study also found an inverse relationship between percent wall thickening and the extent of LGE, this only applied to the less severely hypertrophic segments (). In the thickest regions of the heart, transmural systolic contraction was independent of the extent of LGE (). While not addressed by this dataset, myocardial edema or inflammation may also explain the discrepancy between regional contractile function and LGE 39, 40
The DENSE MRI acquisition has many advantages in producing cardiac strain measurements. DENSE has been used to measure post-infarct recovery of function 41
. Myocardial tagging 42
, harmonic phase image processing 43
and DENSE have yield comparable strain measurements 43–46
and have been recently shown to rely on the same physics for mapping motion 47
. As implemented in this study, DENSE provided approximately 250 measurements of intramural contractile function per short axis slice -- an order of magnitude more measurements than conventional tagged MRI. Therefore, fitting the strain measurements to a predetermined model of the heart 48
was not necessary -- a significant advantage for the irregularly shaped heart in patients with HCM. Since a volumetric preparation is used to sensitize the image to motion, the method intrinsically avoids through-plane motion artifacts.
Regional wall motion assessment by cine MRI and echocardiography can potentially be misleading depending on whether one chooses to report percent wall thickening (i.e. transmural strain) or absolute systolic change in wall thickness (in mm). Percent wall thickening is inversely proportional to end diastolic wall thickness yet the average amount of wall thickening in mm remains normal or hypercontractile in the same hearts. However, the greatest hazard of interpreting percent wall thickening data is the extrapolation to infer the mechanisms leading to abnormalities in regional contractile function in HCM. High-resolution images of intramural systolic function can properly address this issue. The fact that LGE and intramural strain show abnormalities with different spatial distributions suggests that the information may be complementary. Larger studies will need to be performed to determine the prognostic significance of these findings.