It is well known that hypertension is by far the most common cardiovascular disease and is the biggest culprit of stroke, heart failure, renal insufficiency, and may also cause fatal arrhythmia-ventricular fibrillation, leading to sudden death. Hypertension is a cardiovascular syndrome that is linked to the function of all organs of the body, so it is important to look at the prevention and treatment of hypertension as a whole and pay attention to the various complications and dysfunctions caused by hypertension, of which arrhythmia is one. Left ventricular hypertrophy and left ventricular remodeling caused by hypertension is one of the causes of fatal arrhythmias. The heart can be seen as a “pump” with a large reserve function, and elevated blood pressure is equivalent to a “pump” working long hours and overload, which accelerates the wear and tear of the pump, making it prematurely retired or often in need of repair. What arrhythmias are likely to occur in hypertension? Common arrhythmias include: premature ventricular contractions, premature atrial contractions, paroxysmal ventricular tachycardia, atrial tachycardia, atrial fibrillation, atrioventricular block, and intraventricular block. What time of day do arrhythmias tend to occur? According to epidemiological statistics and clinical observation studies, 80%-90% of arrhythmias occur between 6-12 a.m., with 4-8 a.m. being the time of day when serious arrhythmias are likely to occur and the time of day when sudden cardiac death is more likely to occur. What changes in the heart caused by hypertension are prone to arrhythmias? 1, left ventricular hypertrophy: hypertension is not controlled, 2-5 years can appear ventricular hypertrophy, the reason is: (1) blood pressure rises, peripheral resistance increases, the heart work increases, the heart resistance load increases, in order to overcome these resistance, the myocardium must increase myofibers, or increase the myocytes, compensatory hypertrophy to counteract the resistance of increased blood pressure; (2) as blood pressure rises, the pressure in the ventricular cavity also rises, the heart (3) Myocardial energy metabolism is impaired and negative metabolic products increase, which, through a biofeedback mechanism, promotes the expression of abnormal proteins and leads to myocardial hypertrophy and structural reconstruction; (4) Hypertension is also prone to activation of the neurohumoral system, such as increased activity of the renin-angiotensin-aldosterone system, increased excitability of the sympathetic nervous system, and increased catecholamine secretion. (5) Hypertension makes some hormones, secretory factors and growth factors overreact to the immune response to myocardial hypertrophy, and increase metabolism and secretion, which accelerate myocardial hypertrophy, such as insulin-like growth factor, epidermal growth factor, transforming growth factor-β (TGF-β), fibroblast growth factor, platelet-derived growth factor, etc. 2. Left atrial remodeling: The role of the left atrium is to regulate the filling volume and filling rate of the left ventricle and to maintain normal left ventricular cardiac output, while left ventricular hypertrophy and increased ventricular cavity pressure in turn affect the function of the left atrium. Epidemiological and clinical observation studies show that left ventricular diastolic insufficiency is most commonly associated with hypertension, left ventricular hypertrophy, increased pressure and decreased compliance, which increases the work done by the left atrium and increases the load on the left atrium. In order for the left atrium, a memory and booster pump, to function properly, it must increase the contraction of the atrial muscle, and over time, the atrial muscle becomes hypertrophic, the muscle fibers become longer, and the left atrium remodels and reconfigures. 3. Ischemic changes in hypertrophied myocardium: It was found that in the absence of significant stenosis in the coronary artery trunk and its branches, myocardial ischemia occurs in the left ventricular hypertrophy itself under the exercise state. Evidence of myocardial ischemia, such as ST-T changes or absence of dilute flow area, was demonstrated by 24-hour ambulatory electrocardiogram and radionuclide myocardial imaging, and corresponding monitoring revealed a high incidence of premature ventricular contractions, with the degree increasing with the increase of ischemia . What is the mechanism of ischemia? (1) Hypertension is a result of myocardial hypertrophy, structural changes in coronary arteries, restricted coronary vasodilatation, thickening and fibrosis of the coronary middle layer, narrowing of the vascular lumen, resulting in reduced coronary blood flow and weakened reserve function; (2) Increased absolute oxygen demand of hypertrophied myocardium and relatively reduced myocardial perfusion, progressive decrease in coronary blood flow reserve capacity, and ischemic injury under stress; (3) Hypertension occurs in micro Vascular pathological changes, such as abnormal bifurcation of capillaries, distortion and deformation of capillaries, uneven distribution, and large changes in sparseness. (4) hypertrophic myocardial fibrosis, hypertension itself can cause an increase in the collagen component of blood vessels and connective tissue, while various growth factors such as secreted aldosterone, renin and angiotensin can cause intercellular and perivascular fibrosis. Chronic ischemia can also lead to cardiomyocyte fibrosis, so cardiac remodeling is a process in which cardiomyocytes themselves, blood vessels, interstitial, and neurohumoral factors are involved. The degree of arrhythmia that occurs depends on various factors such as the degree of myocardial hypertrophy, the size of the ischemic area, the severity of ischemia, the degree of fibrosis, and the degree of abnormalities in ventricular and atrial remodeling. In summary, hypertension is one of the main factors causing the development of arrhythmias. The left ventricular hypertrophy, atrioventricular remodeling and neuroendocrine activation caused by hypertension are the material basis for the occurrence of arrhythmias. Only on the basis of a healthy lifestyle, reasonable selection of hypertensive drugs, long-term and effective control of blood pressure and reversal of ventricular and atrial remodeling can the occurrence of arrhythmias be reduced.