Correlation Between Myocardial Deformation and Coronary Artery Tortuosity in Patients With Hypertrophic Cardiomyopathy
Correlation Between Myocardial Deformation and Coronary Artery Tortuosity in Patients With Hypertrophic Cardiomyopathy
Correlation between myocardial deformation and coronary artery tortuosity in patients with
 hypertrophic cardiomyopathy
Excessive tortuosity of the coronary arteries (TCA) is a somewhat common finding in patients
 referred for coronary angiography, reported in 14-40% of patients referred for angiography.
 The presence of TCA has been associated with chest pain and myocardial perfusion
 abnormalities during stress in the absence of obstructive coronary artery disease. Fluid
 dynamic modeling suggests that stress-induced ischemia may be attributable to a reduction in
 distal coronary artery perfusion pressure from viscous and turbulence energy losses. The
 physiologic reasons for TCA are unclear. Pre-clinical studies where elastases and
 collagenases were used to alter arterial morphology together with genetic and pathologic
 analysis of rare clinical disorders such as arterial tortuosity syndrome have indicated that
 arterial tortuosity arises from abnormalities in arterial elastin fibers and extracellular
 matrix. Apart from inherited disorders, some but not all studies have linked TCA with
 hypertension and female sex, and with increased left ventricular (LV) mass from pressure but
 not volume overload and smaller heart size.

 Hypertrophic cardiomyopathy (HCM) is associated with an increased left ventricular (LV) wall
 thickness. HCM is the most common genetic heart disease, characterized by marked clinical and
 morphologic heterogeneity. Diagnosis is usually based on the echocardiographic finding of
 unexplained left ventricular (LV) hypertrophy, defined by increased wall thickness in 1 or
 more LV segments. LV mass is generally assumed to be increased in patients with
 phenotypically expressed HCM, based largely on early pathological studies. TCA among HCM
 patients have not been studied.

 Disruption of the ordered arrangement of myofibers alters normal cardiac mechanical function,
 resulting in temporal and spatial heterogeneity in regional myocardial contractility.
 Although global LV function is generally unaltered, asynchrony and asynergy in regional
 function lead to delayed diastolic relaxation and impaired diastolic filling. Whilst LV
 ejection fraction is frequently normal in both, LV strain assessment could differentiate,
 compared to normal person. Cardiovascular magnetic resonance (CMR), by virtue of its
 high-resolution volumetric reconstruction of the LV chamber, currently affords a highly
 accurate and reproducible quantitative assessment of mass . We sought to establish if
 cardiovascular magnetic resonance myocardial feature tracking (CMR-FT), an emerging method
 allowing accurate assessment of myocardial deformation, differentiates between HCM with or
 without TCA. Additionally, CMR assessment of fibrosis and LV hypertrophy allowed association
 analyses and comparison of diagnostic capacities.

 This is a single-center, retrospective, case control study that will evaluate the difference
 of TCA between HCM and control in the first part. In the second part, we will use CMR-FT to
 compare the myocardial strain between HCM with or without TCA and analyze the relationship of
 strain and TCA.
Inclusion Criteria:

 -  Subjects must meet all the following inclusion criteria to be eligible for
 participation in this study

 1. 18<age≤85；

 2. Patients with hypertrophic cardiomyopathy and without hypertrophic cardiomyopathy
 undergoing coronary angiography and echocardiography;

 3. Willing to sign informed consent.

 Exclusion Criteria:

 -  Subjects who meet any of the following exclusion criteria are not to be enrolled in
 this study

 1. All coronary arteries can not be shown clearly in coronary angiography

 2. Prior coronary artery bypass surgery, valve prosthesis

 3. Connective tissue disease

 4. Cardiac dilatation(left ventricular end diastolic diameter, ≥55mm male，≥50mm
 female )

 5. Congenital heart failure, LVEF<35%

 6. Coronary total occlusion, changes in coronary morphology, such as long stents
 implantation