Overview of hypertensive cardiomyopathy
Hypertensive cardiomyopathy is a secondary cardiomyopathy caused by abnormal changes in the left ventricular wall or left ventricular cavity due to hypertension, which in severe cases leads to left ventricular hypertrophy, left ventricular cavity enlargement with diastolic and systolic cardiac insufficiency. Hypertensive patients may also have symmetrical or even asymmetrical left ventricular hypertrophy. However, hypertensive patients are usually not associated with left ventricular outflow tract obstruction.
Etiology
Hypertrophy of the left ventricular wall and abnormal changes in the left ventricular cavity as a result of chronic hypertensive disease, which was previously thought to be a beneficial compensatory mechanism, is now recognized as an independent risk factor for increased morbidity and mortality from cardiovascular accidents.
Symptoms
1. Stage of cardiac compensation
Hypertension and hypertensive cardiomyopathy are often found in this stage when there is a lack of obvious symptoms, physical examination or diagnosis and treatment of other diseases. If accompanied by arrhythmia, there may be palpitations. The heart boundary is normal or slightly enlarged to the lower left, and the apical beat is strong, and there may be a sense of lifting.
2. Restrictive cardiac dysfunction stage
Clinical manifestations and signs are similar to restrictive cardiomyopathy.
3. Systolic cardiac dysfunction stage
This stage shows symptoms of congestive heart failure. Gradually worsening dyspnea, organ perfusion insufficiency performance. The heart boundary is enlarged to the lower left, and there are signs of pulmonary stasis.
Examination
1. Electrocardiogram
The electrocardiogram may be normal, or there may be left ventricular hypertrophy and strain; RV5+SV1＞4.0mv (male), RV5+SV1＞3.5mv (female), ST segment may be shifted downward in the leads dominated by the R wave, or the T wave may be inverted, and the electrical axis may be deviated to the left.
2. Chest X-ray
The left ventricular rim is full and rounded, and may be enlarged to the lower left.
3. Echocardiography
(1) M-mode echocardiography (1) the septum and the posterior wall of the left ventricle increase in thickness, the septum and the posterior wall of the left ventricle are consistently and symmetrically thickened, when the absolute thickness of the septum and the posterior wall of the left ventricle is more than 12mm, the diagnosis of left ventricular hypertrophy can be confirmed. ② Increased myocardial weight of the left ventricle, the determination of myocardial weight is an important index for the evaluation of myocardial hypertrophy, in the past, only through the autopsy to understand the actual value of the myocardial weight, in recent years, a large number of clinical studies have shown that the application of echocardiography obtained myocardial weight value and the correlation with the results of the autopsy is very high, therefore, the American Society of Echocardiography recommends the application of the following formulae to calculate the weight of the myocardium and the index of the myocardial weight. .
LV weight (g) = 0.8 × 1.04 [(LVDd +IVST+ PWT)3-LVDd3) + 0.6
Left ventricular weight index (g/m2) = left ventricular weight/body surface area.
Normal values for LVWI are 135 g/m2 in men and 125 g/m2 in women.
(2) Two-dimensional echocardiography Left ventricular long-axis and short-axis views showed left ventricular wall hypertrophy, left ventricular hypertrophy with centripetal hypertrophy is common, and a few for irregular-type hypertrophy, centripetal hypertrophy septum and the posterior wall of the left ventricle was symmetric hypertrophy, and irregular-type septum and the posterior wall of the left ventricle was asymmetric hypertrophy, the left ventricular cavity was normal or slightly reduced, the amplitude of the ventricular wall movement was enhanced, the left atrium may be mildly enlarged, and the left atrial cavity may be mildly enlarged. The left atrium may be mildly enlarged, and the left ventricular myocardial thickness measured by two-dimensional echocardiography is more accurate than that by M-mode echocardiography, and enlargement of the left atrium and left ventricle can be seen in the stage of heart failure with systolic dysfunction.
(3) Doppler echocardiography Early cardiac contraction is hyperdynamic, the peak velocity of aortic blood flow increases, the cardiac output, ejection fraction is normal, and the mitral blood flow spectrum often has different abnormal changes. When diastolic compliance decreases in left ventricular hypertrophy, the left ventricular filling resistance increases, and in order to maintain the volume of cardiac output, the main compensatory mechanism is to increase the atrial filling pressures, which is reflected in the prolongation of the left ventricular isovolumic diastolic period, the E peak velocity decreases, acceleration time, deceleration time, prolongation of early diastolic duration, increase in peak A velocity, and decrease in E/A ratio, reflecting impaired left ventricular diastolic function.
Diagnosis
The diagnosis is not difficult to establish based on history, clinical manifestations, and laboratory tests.
Treatment
1. Angiotensin converting enzyme inhibitors
Animal experiments and clinical practice have confirmed that the most obvious effect of angiotensin-converting enzyme inhibitors is to inhibit the formation of myocardial hypertrophy. Observations show that 6 months of long-term treatment can reduce heart weight by 30% (the part of the reduction is myocardium or interstitial fibers is not certain), heart weight reduction and connective tissue reduction can improve the left ventricular diastolic function.
2. Calcium ion antagonists
Calcium antagonists are effective antihypertensive and anti-myocardial ischemic drugs. Although the pharmacological and chemical properties of these drugs vary considerably, the reversal of the effects on the ventricular muscle and arterial wall is consistent. Nifedipine (nifedipine) has a vasodilatory and reflex sympathetic stimulating effect similar to that of hydralazine, and may also reduce left ventricular hypertrophy. Diltiazem can also reduce left ventricular hypertrophy, the drug does not produce a reflex increase in heart rate, in addition, extended-release nicardipine in patients with hypertension also has a ventricular weight reduction effect.
3. β-blockers
β-blockers as antihypertensive drugs to reverse left ventricular hypertrophy effect is certain. For vasodilators that can lower blood pressure but cannot reverse left ventricular thickness, the addition of beta-blockers can reverse left ventricular thickness. Carvedilol is a new β-blocker, which can effectively control blood pressure and also dilate peripheral blood vessels through α1 receptor blockade. Therefore, it is used in antihypertension to both reverse left ventricular hypertrophy, correct diastolic filling abnormalities, and improve contractile function in damaged areas.
4. Angiotensin Ⅱ receptor antagonists
Angiotensin II is the effector molecule of renin-angiotensin system (RAS), so the most direct way to block the RAS system is to antagonize the action of Ang II at the receptor site.
5. Diuretics
Diuretics can reduce the incidence of stroke, so that hypertensive patients with cardiovascular disease mortality and disability rate reduced, is one of the most valuable antihypertensive drugs. Commonly used diuretics are hydrochlorothiazide, indapamide, furosemide, etc. Note that the use of too large a dose of abnormal glucose tolerance, lipid metabolism disorders, low potassium and other side effects.
6.α1 receptor blocking drugs
α1 receptor blocking drugs decrease blood pressure by lowering peripheral resistance. These drugs have obvious effects of dilating arteries and veins, improving cardiac function, improving tissue perfusion, having a protective effect on vital organs such as heart, brain and kidney, reversing left ventricular hypertrophy, and improving sugar and lipid metabolism. Commonly used α1 receptor blocking drugs include prazosin and terazosin.