Hypertrophic cardiomyopathy is the most common heritable cardiovascular disorder, with myocardial fibrosis being one of its hallmarks .
MRI has recently become an important tool for the evaluation of suspected HCM. It can also be used as a guide for suitable therapy, risk stratification, and family screening tool [2, 5].
CMR can detect regional fibrosis by LGE but in diffuse fibrotic processes defining an area of normal myocardium to be a nulled reference may be impossible .
Consequently, several studies have proposed the measurement of T1 relaxation as a potentially valuable tool for the quantitative assessment of myocardial fibrosis .
Regarding the phenotype of HCM, the results agree with Bogaert and Olivotto , who stated that “In a recent analysis of the spatial 3D spread of hypertrophy, we found that the majority of patients with so-called asymmetrical septal HCM follow a spiral pattern of hypertrophy in longitudinal direction following a counter-clockwise spiral, when viewed from LV apex.”
However, Noureldin et al.  stated that the asymmetric phenotype with sigmoid septal contour is the commonest phenotype, and Hoey et al.  stated that the asymmetric septal type is the commonest phenotype. This difference is most likely attributed to the lack of overall 3D look on the LV, where in the counter-clockwise pattern, the most hypertrophied segment is usually the anteroseptal basal segment; however, the overall pattern of hypertrophy is spiral in an anteclockwise fashion when viewed from the cardiac apex.
Regarding the RV hypertrophy, the results are not far from Hoey et al.  who stated that 15–20% of HCM patients have associated RV hypertrophy. However, Noureldin et al. , said that RV hypertrophy is present in approximately 18% of HCM patients.
The results regarding the prevalence of obstruction among HCM patients agreed with Hoey et al.  who said that LVOT obstruction is present in up to 70% of HCM patients and Noureldin et al.  who stated that asymmetric septal hypertrophy with sigmoid septal contour is the commonest phenotype accounting for about two thirds of HCM patients and is associated with obstruction.
Regarding the ECV, the current study proved that it has a better predictive value for fibrosis than the LGE, through correlating the ECV with LGE.
This agrees with Kellman et al. , who stated that ECV mapping is a promising technique complementing LGE imaging in cases of diffuse myocardial disease states. Also, Taylor et al.  and Lu et al.  stated that the T1 mapping technique has enabled better, non-invasive evaluation of the extent and severity of myocardial fibrosis compared to the conventional LGE technique to a level that was previously achieved with invasive procedures such as cardiac biopsy.
The results for correlating the ECV to the native T1 values and the native T1 values to the LGE were in agreement with Dass et al. , who stated that T1 mapping is more efficient in detecting myocardial changes in patients with cardiomyopathies compared to the traditional ways of measuring the myocardial wall thickness and LGE. Also, Sibley et al.  stated that T1 time correlates with interstitial fibrosis in patients with cardiomyopathy including those without focal LGE.
However, Puntmann et al.  stated that native T1 has a better diagnostic accuracy than post-contrast T1 values and ECV. This could be due to the small sample size and the blind quantification of T1 without checking the LGE images. And that agrees with Nezafat  who conducted a study on ischemic patients and stated that visual detection of infarct on native T1 maps was only moderate (low 60%).
Regarding the relation of the EF% to the LV mass, we had a negative correlation indicating that as the mass of the left ventricle increases, the EF% decreases.
This agrees with Taylor et al.  who stated that diffuse fibrosis may play an important role in the pathophysiology of diastolic dysfunction where reduced LV ejection fraction is correlated to the increase of ECV in patients with non-ischemic cardiomyopathy. And as HCM patients have both interstitial and replacement fibrosis, therefore, the myocardial contractility is as well affected [1, 11].
Correlating the ECV to the presence and absence of obstruction, the results were of statistical significance in the basal anterior and antero-septal segments as well as the basal inferior segments, denoting that there is a positive relation between the expansion of the ECV at those segments and the presence of obstruction, knowing that in cases of left ventricular outflow obstruction, there is always hypertrophy of the basal anterior and antro-septal segments and those are the segments exposed to the maximum pressure. Similar findings were reported by Ooji et al.  who mentioned that there is a structure-function relationship between elevated LVOT pressure gradient and adverse myocardial remodeling.
The limitations of this study include the following: (1) The ECV expansion was considered at values ≥ 30% taking the published range of normal ECV value of 20–30% as a reference, while some papers consider the normal up to 25.3 ± 3.5% and others consider it as 25.4 ± 2.5%. (2) The ROIs were drawn blindly without checking the LGE images, to check the validity of T1 as a tool to replace LGE. (3) Some segments showed enhancement at one cut while the T1 mapping cut was planned at a different level from that showing enhancement. Those factors may attribute to the absence of ECV expansion in some segments that showed LGE where some segments showed focal insertion point enhancement and others showed subendocardial enhancement, while the T1 mapping ROI was drawn at the proper segment location.