This study will include patients with different types of cardiomyopathy from multiple centers were prospectively enrolled in a retrospective study to establish a natural population cohort of cardiomyopathy patients. By collecting clinical data and biological samples from surgical patients, we will construct a prognostic system for cardiomyopathy, optimize risk stratification, explore new strategies for the early prevention and treatment of cardiomyopathy, and improve the efficiency of clinical cardiomyopathy patients' diagnosis and treatment.
Age >18 years old.
The diagnosis of cardiomyopathy was confirmed by cardiac ultrasound, electrocardiogram, magnetic resonance angiography, pathological examination and gene sequencing.
Patients or their families agreed to participate in the study and authorized informed consent.
Incomplete clinical data.
Do not agree to the inclusion or refuse to authorize the informed consent.
Patients diagnosed with cardiomyopathy at all centers including The First Affiliated Hospital of Xi'an Jiaotong University.
Cohort
Other
Diagnosis of HCM
Biological/VaccineHypertrophic cardiomyopathy (HCM) is defined as the presence of increased LV wall thickness (with or without RV hypertrophy) or mass that is not solely explained by abnormal loading conditions.
Diagnosis of DCM
Biological/VaccineDilated cardiomyopathy (DCM) is defined as the presence of LV dilatation and global or regional systolic dysfunction unexplained solely by abnormal loading conditions (e.g. hypertension, valve disease, CHD) or CAD.Very rarely, LV dilatation can occur with normal ejection fraction (EF) in the absence of athletic remodelling or other environmental factors; this is not in itself a cardiomyopathy, but may represent an early manifestation of DCM. The preferred term for this is isolated left ventricular dilatation. Right ventricular dilatation and dysfunction may be present but are not necessary for the diagnosis.
Diagnosis of ARVC
Biological/VaccineArrhythmogenic right ventricular cardiomyopathy (ARVC) is defined as the presence of predominantly RV dilatation and/or dysfunction in the presence of histological involvement and/or electrocardiographic abnormalities in accordance with published criteria.
Diagnosis of NDLVC
Biological/VaccineThe NDLVC phenotype is defined as the presence of non-ischaemic LV scarring or fatty replacement regardless of the presence of global or regional wall motion abnormalities (RWMAs), or isolated global LV hypokinesia without scarring.
Diagnosis of RCM
Biological/VaccineRestrictive cardiomyopathy (RCM) is defined as restrictive left and/or RV pathophysiology in the presence of normal or reduced diastolic volumes (of one or both ventricles), normal or reduced systolic volumes, and normal ventricular wall thickness.Restrictive cardiomyopathy commonly presents as biatrial enlargement. Left ventricular systolic function can be preserved, but it is rare for contractility to be completely normal. Restrictive pathophysiology may not be present throughout the natural history, but only at an initial stage (with an evolution towards a hypokinetic-dilated phase). Restrictive physiology can also occur in patients with end-stage hypertrophic and dilated cardiomyopathy; the preferred terms are 'hypertrophic' or 'dilated cardiomyopathy with restrictive physiology'. Restrictive ventricular physiology can also be caused by endocardial pathology (fibrosis, fibroelastosis, and thrombosis) that impairs diastolic function
Diagnosis of LVNC
Biological/VaccineThe term 'left ventricular non-compaction' (LVNC) has been used to describe a ventricular phenotype characterized by prominent LV trabeculae and deep intertrabecular recesses. The myocardial wall is often thickened with a thin,compacted epicardial layer and a thickerendocardial layer. Left ventricular non-compaction is frequently a familial trait and is associated with variants in a range of genes, including those encoding proteins of the sarcomere, Z-disc, cytoskeleton, and nuclear envelope. Left ventricular non-compaction has also been used to describe an acquired and sometimes transient phenomenon of excessive LV trabeculation (e.g. in athletes, during pregnancy, or following vigorous activity)that must reflect increased prominence of an otherwise normal myocardial architecture, given that cardiomyocytes are terminally differentiated and the formation of new cardiac structures is impossible.The Task Force does not consider LVNC to be a cardiomyopathy in the general sense.
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Treatment groupsSee each treatment group below.
Change in the incidence of mortality rate
The survival status will be obtained from the medical records and phone calls to patients or their family members
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