Cardiac disease is the most common cause of cardiac arrest, and to facilitate the prediction of the likelihood of cardiac arrest cardiac arrest in such patients, they can be divided into two types: organic and nonorganic cardiac disease, of which the former is divided into two types: acute coronary syndromes and noncoronary cardiac disease (Figure 1). In this article, we will discuss the mechanisms and clinical prediction of non-coronary organic heart disease and non-organic heart disease leading to cardiac arrest according to the content of the block diagram. Figure 1 Classification in predicting cardiac arrest in patients with heart disease Myocardial disease is a group of diseases other than coronary heart disease, pulmonary heart disease, congenital heart disease, hypertensive heart disease and heart valve disease, which are mainly characterized by cardiomyopathy. The literature reports that sudden death due to myocardial lesions accounts for 7% to 23% of all sudden cardiac deaths, with congestive heart failure and malignant arrhythmias accounting for 50% each. Myocardial diseases include cardiomyopathy and myocarditis (Figure 2), the former mostly being familial autosomal dominant disorders with mutated genes mainly involving myocardial fibrous membranes and cytoskeletal proteins, and the latter mostly being inflammatory myocardial lesions caused by infectious and non-infectious factors. Both can occur with fatal arrhythmias leading to sudden death of the patient. The incidence of HCM is about 0.2%, the average age of onset is 38±15 years, and the sudden death rate in adults is about 2-4%. The incidence of HCM is about 0.2%, the average age of onset is 38±15 years, and the rate of sudden death in adults is about 2-4%, and in children is about 4-6%. The main pathological features are myocardial asymmetric hypertrophy, disorganized myocyte arrangement, fibrosis and small ventricular chambers, on the basis of which many abnormalities occur, mainly myocardial ischemia, diastolic hypoplasia and left ventricular outflow tract obstruction, leading to congestive heart failure and arrhythmias, and even sudden death. The patient’s electrocardiogram shows left ventricular hypertrophy with strain, deep and narrow abnormal Q waves, symmetrical giant inverted T waves in the chest leads, and significant prolongation of QT or QTc. Arrhythmias may include atrioventricular block, paroxysmal atrial fibrillation, and ventricular arrhythmias. Preexcitation syndrome can be complicated by rapid ventricular rate atrial fibrillation or atrial fold tachycardia, which can easily induce sudden cardiac death. A small percentage of patients (5% to 10%) have progressive deterioration of left ventricular function and die from progressive congestive heart failure. 2. Dilated cardiomyopathy (DCM) DCM is a chronic cardiomyopathy characterized by left ventricular enlargement and systolic dysfunction and can be broadly classified into two categories: familial/hereditary and viral/immune. Up to 40% of patients have a family history of the disease, mostly autosomal dominant, but with a few X-linked inheritance (2% to 5%). the main lethal factor in DCM is heart failure, and up to 50% of patients experience cardiac arrest due to slow arrhythmias, pulmonary or body circulation embolism, or electro-mechanical separation, but malignant ventricular arrhythmias remain one of the most common causes of sudden death in patients with DCM, especially in The number of sudden deaths due to sudden arrhythmias is high in patients with mild clinical symptoms, and syncope is an independent predictor of sudden death in this disease. The arrhythmias in this disease are mainly slow arrhythmias, atrial fibrillation, bundle branch block, intraventricular block and ventricular tachycardia, with progressive QRS waveform hypovoltage and significant prolongation of QT or QTc. Patients with abnormal widening of QRS waveform (160ms) and double bundle branch block have a poor prognosis and are prone to sudden death due to ventricular arrhythmia. 3, right ventricular cardiomyopathy (ARVC) ARVC is also known as arrhythmogenic right ventricular cardiomyopathy, a cardiomyopathy in which the right ventricular myocardial tissue and extracellular interstitium are progressively replaced by fibrous adipose tissue. 30% of patients have familial onset, mostly autosomal dominant, and 80% of patients are between 7 and 40 years of age, so this disease is one of the causes of sudden death in young people. The disease is characterized by episodic syncope, right ventricular-derived ventricular tachycardia, right ventricular dilatation, and hypofunction or failure, with a higher mortality rate in those with left ventricular involvement. The electrocardiogram shows a right bundle branch conduction block pattern with inversion of V1 to V3 and especially V2T waves in the right thoracic leads and small spikes (Epsilon waves) at the end of the QRS wave group and at the beginning of the ST segment, which are caused by late onset of local excitation in the right ventricular wall and are clear in leads I, V1 and V2. The arrhythmia is mostly left bundle branch block type of ventricular precontraction and monomorphic ventricular tachycardia, often accompanied by rightward deviation of the electrical axis, the incidence of which is as high as 70% to 92%, and 50% to 90% of patients have positive ventricular late potentials. arVC can present with heart failure, but more often ventricular arrhythmia leads to sudden cardiac death. 4.Specific cardiomyopathies include ischemic cardiomyopathy (myocardial fibrosis due to long-term coronary perfusion disorders), diabetic cardiomyopathy (cardiomyopathy in diabetic patients that cannot be explained by other causes, characterized by microangiopathy within the myocardial wall and perivascular interstitial fibrosis), and alcoholic cardiomyopathy (seen in drinkers without heart disease who have consumed more than 150g of liquor or 4 bottles of beer per day for more than 6 consecutive years, characterized by The main features are heart enlargement and heart failure), perinatal cardiomyopathy (a condition similar to dilated cardiomyopathy occurring at the end of pregnancy or within 5 months after delivery, mainly manifesting as heart failure, the etiology of which is unknown and may be related to viral infection), amyloid cardiomyopathy (a cardiomyopathy related to genetics, immunity and inflammation, characterized by the phenomenon of amyloid deposition and infiltration in the heart, requiring endocardial biopsy and histochemical staining are required to confirm the diagnosis), pharmacological cardiomyopathy (cardiomyopathy caused by cardiotoxic drugs with clinical manifestations similar to dilated cardiomyopathy, often caused by the antineoplastic drugs adriamycin, erythromycin, the antipsychotic drugs chlorpromazine, endorphin and the tricyclic antidepressants chlorpromazine and amitriptyline) and Keshan disease. The main clinical manifestation of patients with the above conditions is gradually increasing heart failure, and some patients may die suddenly due to malignant arrhythmias. Myocarditis is an inflammatory cardiomyopathy involving myocardial cells, interstitial tissue, blood vessels and/or pericardium. The disease can be divided into two categories: infectious and non-infectious, resulting in myocardial damage no less than myocardial infarction. The main factors include direct myocardial damage by infectious agents, damage by myocardial toxins, and immune-mediated myocardial damage, as well as apoptosis by inducing abnormal expression of proto-oncogenes. These damaged or apoptotic myocardial cells often cause electrical activity disorders in the myocardium, resulting in a disorder in the coordination of myocardial electrical activity that can lead to fatal arrhythmias. Patients with myocarditis may show ST-segment and T-wave abnormalities on the ECG, as well as supraventricular and ventricular arrhythmias, atrioventricular and intraventricular conduction disturbances, and occasionally abnormal Q waves. Since the clinical manifestations of the disease are non-specific, its clinical diagnosis is not easy to establish, and subendocardial myocardial biopsy is a more accurate diagnostic method. Due to myocardial stromal changes such as inflammatory exudation, interstitial edema, myocardial necrosis and fibrosis, the patient is prone to sudden death due to ventricular arrhythmias. Some clinical data suggest that 10% to 44% of sudden cardiac deaths in young people are due to myocarditis, and it is thought that the incidence of sudden cardiac death due to myocarditis may be underestimated (Figure 2). Figure 2 WHO/ISFC classification of cardiomyopathy