hypertensive heart disease
Introduction
Introduction to 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 contractile 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. basic knowledge The proportion of sickness: 0.01% Susceptible people: people with high blood pressure Mode of infection: non-infectious Complications: coronary atherosclerotic heart disease, chronic pulmonary heart disease, hypertrophic cardiomyopathy, asymptomatic myocardial ischemia
Cause
Cause of hypertensive heart disease
Increased long-term systemic arterial pressure, resulting in a heart afterload, resulting in left ventricular hypertrophy and enlargement, and may further lead to a heart disease with symptoms of cardiac insufficiency.
Genetic factors (20%)
Many clinical investigations have found that hypertension is multi-gene inherited, and patients with hypertension in the same family are more concentrated. On the one hand, they have a common way of eating and eating, but mainly have genetic factors, and the family has induced hypertensive heart disease. The factors are also called other high.
Weight factor (10%)
There is a high correlation between body weight and blood pressure. The results of population studies in China have proved that the body mass index is high, whether it is a single factor or multi-factor analysis. It is an independent risk factor for blood pressure elevation and induces hypertensive heart disease.
Nutritional factors (15%)
Excessive salt, heavy drinking, excessive saturated fatty acids in the diet, or low ratio of unsaturated fatty acids to fatty acids can increase blood pressure and induce hypertensive heart disease.
Other factors (8%)
The smoking and psychological factors that have been proven have been closely related to the prevalence and aggravation of hypertension, and finally induced hypertensive heart disease.
Prevention
Hypertensive heart disease prevention
1. Early, sustained, and systematic antihypertensive medication is the most fundamental way to prevent this disease.
2. The disease is caused by long-term increase in blood pressure leading to heart damage caused by excessive cardiac load. Long-term system of antihypertensive treatment can prevent the occurrence and development of this disease.
3. Long-term, regular antihypertensive treatment can improve the degree of damage to the hypertrophic heart, or even completely return to normal form. Treatments that simply emphasize the purpose of blood pressure reduction and neglect heart protection are not comprehensive and unscientific.
Complication
Hypertensive heart disease complications Complications coronary atherosclerotic heart disease chronic pulmonary heart disease hypertrophic cardiomyopathy asymptomatic myocardial ischemia
Coronary atherosclerotic heart disease, chronic pulmonary heart disease, hypertrophic cardiomyopathy, asymptomatic myocardial ischemia.
Symptom
Hypertensive heart disease symptoms Common symptoms After nausea, palpitations, shortness of breath, difficulty, pulse, acceleration, dizziness, cardiac aortic regurgitation, palpitations, hypertension
1. Early clinical manifestations: Early manifestations are generally atypical, patients may have no obvious symptoms or only mild discomfort such as headache, chest tightness, etc. These symptoms are mainly the general symptoms of hypertension, no particularity.
2. Clinical manifestations in the advanced stage: In high blood pressure, the arterial blood pressure is too high, which hinders the heart from pumping out the blood. The heart's long-term high-load work shows an increase in cardiac hypertrophy and stiffness, which eventually leads to obstruction of the pulmonary vein blood entering the heart, resulting in pulmonary congestion. . When the heart muscle is hypertrophied, the oxygen demand is increased, and the blood supply is relatively insufficient, which often leads to heart attack. The clinical manifestations of diastolic heart failure and systolic heart failure are similar, and it is difficult to identify clinically. The clinical features of heart failure caused by hypertension are as follows:
(1) due to left ventricular diastolic/systolic function abnormalities, can lead to pulmonary congestion, mainly manifested as 1 labor dyspnea; 2 air rush during supine, improved after sitting up; 3 activity is not large, but breathing difficulties, In severe cases, the patient can wake up in his sleep; 4 in severe cases, he has a sitting breathing, coughing, coughing pink foamy sputum.
(2) left heart failure often involves the decline of right ventricular function, the formation of whole heart failure, mainly manifested as 1 jugular vein filling; 2 right upper quadrant pain, and hepatomegaly; 3 lower extremity edema, severe systemic edema ; 4 oliguria.
Examine
Hypertensive heart disease check
1. Electrocardiogram: The ECG can be normal, and left ventricular hypertrophy and strain can also occur. RV5+SV1>4.0mV (male), RV5+SV1> 3.5mV (female), the ST segment of the R-wave dominant lead can be moved down, or the T wave is inverted, and the electric axis is left-biased.
2. Chest X-ray: Aortic extension, the aortic extension is distorted, the upper edge of the aortic arch can reach or exceed the level of the sterno-lock joint, the aortic node is obviously protruding to the left, and the heart is depressed. It becomes a typical aortic type. heart".
3. Echocardiography
(1) M-mode echocardiography: 1 room interval and left ventricular posterior wall thickness increase ventricular septum and left ventricular posterior wall with uniform symmetry thickening, when the interventricular septum and left ventricular posterior wall absolute thickness is greater than 12mm, Diagnosis of left ventricular hypertrophy. 2 Left ventricular myocardial weight increase The measurement of myocardial weight is an important index to evaluate cardiac hypertrophy. In the past, the actual value of myocardial weight can only be understood through autopsy. In recent years, a large number of clinical studies have shown that the myocardial weight obtained by echocardiography is used. Values are highly correlated with autopsy results. Therefore, the American Society of Echocardiography recommends the use of the Devereux correction formula to calculate myocardial weight and myocardial weight index.
Left ventricular mass = 0.8 x 1.04 [(LVDd + IVST + PWT) - LVDd) + 0.6.
Left ventricular mass index (g/m) = left ventricular weight / body surface area.
The normal left ventricular mass index was 135 g/m for men and 125 g/m for women.
(2) Two-dimensional echocardiography: left ventricular long axis, short axis section showed left ventricular wall hypertrophy, left ventricular hypertrophy with centripetal hypertrophy, a few irregular irregular hypertrophy, centripetal hypertrophy ventricular septum and left ventricle The wall is symmetrical hypertrophy, the irregular type is asymmetrical hypertrophy between the ventricular septum and the posterior wall of the left ventricle, the left ventricular cavity is normal or slightly reduced, the amplitude of the wall motion is enhanced, and the left atrium can be slightly increased. Echocardiographic measurement of left ventricular myocardium thickness is more accurate than M-mode echocardiography, and heart failure during systolic dysfunction, as well as enlargement of the left atrium and left ventricle.
(3) Doppler echocardiography: early systole is hyperdynamic, the peak velocity of aortic blood flow is increased, the stroke volume is normal, the ejection fraction is normal, and the mitral blood flow spectrum often has different abnormal changes. When left ventricular hypertrophy and diastolic compliance decline, left ventricular filling resistance increases. In order to maintain cardiac output, the main compensatory mechanism is to increase atrial filling pressure, which is characterized by left ventricular isovolumic diastolic prolongation, E peak peak velocity. Decrease, acceleration time, deceleration time, prolonged duration of diastole, peak peak velocity of A peak, and decreased E/A ratio, reflecting impairment of left ventricular diastolic function.
(4) Tissue Doppler mitral annulus velocity: mainly manifested as decreased diastolic function. It is characterized by mitral annulus early diastolic velocity (E') and late diastolic velocity (A'), E'/A'<1. For patients with impaired myocardial relaxation, E' is reduced in the basal state and does not increase with the increase in preload as in normal subjects. Thus, E' reduction is one of the earliest manifestations of diastolic dysfunction. The European Society of Cardiology guidelines believe that E/E'15 can diagnose left ventricular diastolic dysfunction. When E/E' is 8-15, another diagnostic evidence of non-invasive left ventricular diastolic dysfunction, such as mitral or pulmonary venous flow spectrum, left ventricular mass index, etc., is required.
Diagnosis
Diagnosis and diagnosis of hypertensive heart disease
Diagnose based on
1. Have a history of long-term hypertension.
2, in the heart function compensation period only the general symptoms of hypertension; when the heart function is not fully compensated, there may be symptoms of left heart failure, lighter only after fatigue, breathing difficulties, severe cases of sitting breathing, heart Sexual asthma, and even acute pulmonary edema; patients with chronic disease can develop right heart failure and eventually lead to heart failure.
3, physical examination found that apical beat enhancement is lifted, the heart is enlarged to the left, the second heart sound in the aortic valve area can be metal tone, the pulmonary auscultation area can be second heart sound hyperactivity due to pulmonary hypertension, apical area or And) the aortic valve area can be heard in the II ~ III / IV systolic hairy murmur, left ventricular apex can be heard and diastolic gallop. In the case of whole heart failure, the skin and mucous membranes are severely purpura, jugular vein engorgement, hepatomegaly, edema, and chest and ascites.
4, ECG examination of unilateral or bilateral ventricular hypertrophy and / or strain, P wave widened or notched, V1 lead in the P wave terminal potential (PTF-V1) increased, a variety of arrhythmia and so on. Chest X-ray examination has aortic tortuosity, left ventricle or whole heart enlargement, lung septal line, pulmonary congestion and so on. Echocardiography showed unilateral ventricle or bilateral ventricular hypertrophy, mitral valve, aortic valve, tricuspid regurgitation, and decreased ejection fraction.
Differential diagnosis
Need to identify with aortic regurgitation.
