What is hypertensive heart disease? What are the pathophysiological changes in hypertensive heart disease?

Poor long-term control of hypertension can cause changes in cardiac structure and function, including hypertensive heart disease, including: early left ventricular diastolic dysfunction, left ventricular hypertrophy (LVH), progressive development of myocardial systolic dysfunction, and ultimately heart failure, Studies have shown that 70% of heart failure is caused by high blood pressure; there may be associated coronary heart disease, atrial fibrillation and other cardiac complications.

What is hypertensive heart disease? What are the pathophysiological changes in hypertensive heart disease?

Pathophysiological changes

1. Left ventricular hypertrophy (LVH)
LVH is a compensatory change of myocardial pressure on blood pressure, and the myocardial contractility is enhanced to maintain sufficient cardiac output, but long time can cause myocardial cell hypertrophy, muscle fiber thickening, degeneration, decreased capillary relative density, etc. change. Early myocardial remodeling phenomenon, that is, centripetal remodeling, myocardial cell hypertrophy, but the number does not increase, the arrangement changes, collagen fibers increase, and gradually collagen accumulation exceeds 20% to fibrosis, in order to replace the loss of function of cells, resulting in The heart is hypertrophic, and finally the increase in volume load causes centrifugal hypertrophy. Hypertension LVH is first reflected in the ventricular septal thickening, which is a common part of the heart size circulation, and plays an important role in the left and right ventricular systolic function.



2. Diastolic function is reduced
Diastolic heart failure is characterized by a decrease in left ventricular volume and an increase in end diastolic pressure, with normal or mild reduction in LVEF. This is mainly due to the normal ventricular systolic function, and the reduction of ventricular muscle relaxation and compliance reduces ventricular filling; to increase ventricular filling, the left ventricle must increase the filling pressure to obtain normal ventricular filling and stroke volume. In addition, LVH makes cardiomyocyte hypertrophy, especially myocardial fibrosis changes the myocardial diastolic pressure-capacity relationship, and also increases the diastolic blood pressure in the heart chamber, so LVH can cause diastolic dysfunction. Early cardiac structure changes in hypertension, diastolic dysfunction accounted for about 11%.

3. The contraction function is reduced
It is known that LVH is 10 times higher than heart failure in patients without LVH. This is because the increase in long-term pressure causes excessive post-loading, causing vascular wall thickness and cardiac centripetal hypertrophy and diastolic relaxation, and finally myocardial contractility. Decreased, enlarged heart chamber, increased ventricular end-diastolic volume, increased ventricular filling pressure and atrial pressure, blocked pulmonary venous return, acute or chronic left heart failure with hypertensive heart disease.