Symptoms of cardiac hypertrophy
summary
Myocardial hypertrophy is a powerful form of compensation, but it is not unlimited. If the cause of the disease can not be eliminated for a long time, the function of hypertrophic myocardium will not be normal for a long time, and eventually turn to heart failure. Chronic heart failure generally develops on the basis of myocardial compensatory hypertrophy. Symptoms of cardiac hypertrophy? Let's talk about it
Symptoms of cardiac hypertrophy
Why does hypertrophic myocardium turn to failure? This is a problem that has been discussed and studied for a long time. At present, compensatory cardiac hypertrophy is considered to be an unbalanced growth form. This kind of unbalanced growth has its own characteristics at different levels of organs, tissues, cells and molecules, which is the basis of hypertrophic myocardium turning to dysfunction.
From the view of the whole heart, the unbalanced growth shows that the growth of heart weight exceeds the growth of sympathetic nerve axons which dominate the heart, so the density of sympathetic nerve distribution in the heart is significantly lower than that in the normal. Moreover, the synthesis of catecholamine in hypertrophic myocardium is decreased and the consumption is increased, so the content of norepinephrine in the heart is significantly reduced. This change in the content of innervation and neurotransmitters will promote the disturbance of excitation contraction coupling of myocardium, resulting in the weakening of myocardial contractility.
The ratio of heavy segment (head) to light segment (tail) of myosin decreased, that is, the proportion of head in the whole molecule decreased. The head is just where the ATPase is located, and the decrease of the specific gravity of the head can make the ATPase activity decrease correspondingly. In addition, ATPase is activated by Ca2 +. In heart failure, the activity of ATPase is further decreased because Ca2 + is transported slowly to myosin transverse bridge. In vitro, the activity of ATPase decreased by 20-30%. The decrease of ATPase activity leads to the disturbance of energy utilization of myocardium, which leads to the decrease of myocardial contractility.
matters needing attention
Patients with cardiac hypertrophy should avoid overwork and excessive mental stress, β Propranolol, a receptor blocker, can reduce myocardial contractility, alleviate left ventricular outflow tract obstruction, improve left ventricular wall compliance and left ventricular filling, and also has antiarrhythmic effect. Dosage: 10mg orally, 3 times a day. It can be increased gradually, up to 480mg / day. Calcium channel blockers can also be used, verapamil 40 mg orally, 3 times a day, nifedipine 10 mg orally, 3 times a day. It can improve the ventricular diastolic function, so we should pay attention to the observation of blood pressure to prevent the blood from falling too low.
