Predisposing factors of coronary atherosclerosis
Coronary atherosclerotic heart disease (i.e., coronary heart disease) is a serious health hazard that occurs mostly after the age of 46, more in men than in women, and more in brain workers, with nutrition, work and social environment playing an important role in the development of coronary heart disease. The main factors that induce coronary atherosclerosis are genetics, high serum cholesterol, low high-density lipoprotein (HDL) level, high blood pressure, diabetes, smoking, obesity, type A behavior style, and less exercise.
Clinical manifestations of coronary heart disease
Patients with coronary artery disease may have symptoms, but if no complications occur, there are usually no obvious signs. The main manifestations are angina pectoris, myocardial infarction, arrhythmia, heart failure and sudden cardiac death.
1, angina pectoris: angina pectoris is a clinical syndrome caused by insufficient coronary artery blood supply, acute and temporary ischemia and hypoxia of the heart muscle. It is characterized by paroxysmal anterior chest crushing pain sensation, mainly located in the posterior part of the sternum, can radiate to the precordial area and the left upper limb, often occurs during labor or emotional excitement, lasting several minutes, can be relieved by rest or with nitrate drugs. Usually there are no abnormal signs, and most patients have an ECG showing ST-segment depression of 0.1mV or more during an angina attack.
Angina pectoris is divided into the following three types.
①exertional angina pectoris
②Spontaneous angina pectoris
③ mixed angina pectoris
2. Myocardial infarction: myocardial ischemia lasting for more than a few hours can cause serious damage to the myocardium and myocardial cell necrosis.
3, arrhythmia: myocardial ischemia can cause a variety of arrhythmias, especially serious arrhythmias can occur after myocardial infarction. Bradycardia and tachycardia can both reduce cardiac output and lead to heart failure. Ventricular tachycardia and ventricular fibrillation are important causes of sudden death in patients.
4.Heart failure: Myocardial ischemia and necrosis reduce the contractile capacity of the heart, and the magnitude of the decline is related to the area of myocardial infarction. Cardiogenic shock can occur when about 40% of the left ventricle is damaged. Complications after myocardial infarction such as septal perforation and mitral valve closure insufficiency due to papillary muscle rupture often lead to rapid deterioration and acute heart failure.
5, sudden cardiac death: more than 90% of sudden cardiac death in adults is caused by coronary heart disease. The causes are ventricular arrhythmia, acute pump failure, conduction obstruction, coronary artery spasm, etc. Half of the patients who die from ischemic heart disease die within one hour of acute onset, including 25% to 35% who die immediately or are already dead when discovered. Accurate determination of imminent sudden cardiac death is often not possible.
Diagnosis of coronary heart disease
1.Diagnosis methods of coronary heart disease
① Clinical diagnosis: Based on the typical medical history, symptoms, signs and ECG performance, it is generally easy to diagnose coronary heart disease. However, for variant angina pectoris, close monitoring of dynamic electrocardiogram should be performed in combination with clinical to be alert to the occurrence of acute myocardial infarction. Serum enzyme activity measurement is beneficial to the diagnosis of acute myocardial infarction.
②X-ray examination: Most patients can suggest fullness of the left heart margin and widening, elongation and distortion of the aortic arch. During an angina attack, the heart beat is weakened and pulmonary vessels show varying degrees of stasis. In myocardial infarction, these manifestations are more pronounced, and even the heart is significantly enlarged. In ventricular wall tumors, there is limited apical bulging or reverse pulsation.
③Echocardiography: It is useful for the detection of post-infarction complications such as septal perforation, mitral valve insufficiency, ventricular wall tumor formation, etc., and for the evaluation of cardiac function.
④Selective coronary angiography and left ventriculography: Selective coronary angiography is an important and reliable method to show the anatomical and pathological changes of coronary arteries. It is mainly used to confirm the diagnosis of coronary artery disease and its complications, the selection of surgical indications and the related differential diagnosis. It is not recommended for patients with severe hepatic or renal insufficiency, severe intractable heart failure, severe arrhythmias and systemic infectious diseases. Coronary artery stenosis is classified into four grades according to the imaging results.
Mild stenosis: diameter stenosis <50%, usually without hemodynamic significance.
Moderate stenosis: 50% to 75% stenosis with hemodynamic significance.
Severe stenosis: 75% to 99% diameter stenosis, with definite hemodynamic significance.
Complete obstruction: 100% stenosis of the canal lumen.
Left ventriculography is an integral part of selective coronary angiography. It is used to evaluate overall LV pump function and segmental abnormalities by observing LV morphology, size and motor function on X-ray film. The myocardium of the normal left ventricular wall, including the papillary muscles, moves in a coordinated diastolic motion called a coordinated state.
When ischemia in a segment of the ventricle produces abnormal contraction timing and contraction pattern, it is called segmental (regional) dyskinesia (segmental asynergy).
asynergy, hypokinesis, akinesis, and deskinesis.
Radionuclide myocardial imaging: the imaging methods include myocardial blood pool imaging, myocardial perfusion imaging, myocardial metabolic imaging, myocardial receptor imaging, myocardial radioimmune imaging, pro-necrosis myocardial imaging, and hypoxic myocardial imaging. Nuclear imaging can provide information on anatomical morphology, cardiac function, myocardial perfusion, myocardial metabolism, myocardial receptors, and histological signs.
(6) Ultra high speed CT (UFCT) examination: The scanning speed of UFCT is tens of times higher than that of ordinary CT, which eliminates movement artifacts and can clearly show the anatomy of the heart and coronary arteries and quantitatively evaluate cardiac function and myocardial coronary perfusion, which has important value in the diagnosis of coronary heart disease and can be used for follow-up after coronary artery bypass grafting.
2.Diagnosis of post-myocardial infarction complications
①Heart rupture: history of myocardial infarction; sudden loss of consciousness and respiratory arrest; rapid drop in blood pressure, inaudible heart sounds and signs of pericardial filling; ECG may show sinus rhythm or sinus bradycardia in a short period of time, with low voltage of QRS in each lead; echocardiography can make a clear diagnosis.
②Ventricular septal perforation: history of acute myocardial infarction, sudden decompensation of cardiac function, left and right ventricular failure and pulmonary edema; a full systolic blowing rough murmur is heard between the 3rd and 4th ribs at the left edge of the sternum; echocardiography and right heart catheterization can make a clear diagnosis.
(iii) Ventricular wall tumor: history of myocardial infarction and embolism in some cases; persistent heart failure after acute myocardial infarction, continuous myocardial enlargement, systolic sensation of heart tumor lifting or double pulsation in the apical region, third or fourth heart sound may be present; electrocardiogram shows post-myocardial infarction changes; two-dimensional echocardiography shows reduced or absent local motion of the left ventricle, thinning of the ventricular wall, contradictory motion, sometimes visible attached thrombus; left ventricle The left ventricular wall can be seen to have reduced or absent motion in the ventricular wall tumor area, thinning of the ventricular wall, outward expansion, loss of trabecular structures in the inner layer, and may have signs of wall thrombus.
Mitral valve insufficiency: after acute myocardial infarction, sudden cardiogenic shock with pulmonary edema and rapid deterioration of the condition; systolic murmur like blowing wind is heard in the apical region, which is louder in the early and middle stages, but there may be no murmur in the apical region when the papillary muscle is completely broken and severe mitral regurgitation makes the heart function extremely reduced, and there is often a third heart sound; there are signs of pulmonary edema on X-ray plain film; echocardiography can clarify the lesion Echocardiography can clarify the nature and extent of the lesion, and cardiac catheterization may be performed if necessary.
Differentiation of coronary artery disease from other diseases
1.Differentiate from other heart diseases that cause pain in the precordial region: heart valve disease, pericarditis, aortic coarctation aneurysm, aortic sinus aneurysm rupture, cardiovascular neurosis, etc.
2. Differentiate from non-cardiac diseases causing chest discomfort: such as chronic nephritis, esophagitis, esophageal hiatal hernia, peptic ulcer, cholelithiasis, cholecystitis, herpes zoster, cervical spondylosis, costochondritis, non-specific chest wall pain, etc.
Treatment of coronary heart disease
1.Treatment methods of coronary heart disease
①Medical treatment: including removal of angina triggering factors, application of anti-angina drugs, interventional therapy, hyperbaric oxygen therapy, extracorporeal counterpulsation therapy and exercise therapy, etc.
②Surgical treatment: including coronary angioplasty, coronary artery endothelial debridement, laser myocardial revascularization (TMLR), coronary artery bypass grafting (CABG) and treatment of post-myocardial infarction complications, etc.
2.Commonly used anti-anginal drugs and their pharmacological effects and principles of use
①Nitrates: commonly used are nitroglycerin, isosorbide nitrate (cardiac pain) and isosorbide mononitrate (Lunan Xinkang, long-acting cardiac pain treatment) and so on. Pharmacological effects include dilating veins, reducing cardiac preload; reducing ventricular filling pressure, increasing diastolic coronary perfusion; relaxing vascular smooth muscle, reducing vascular tone, relieving spasm of side branches and transmission vessels; promoting prostacyclin (PGI2) production in the vascular wall, inhibiting platelet release of thromboxane A2 (TXA2); lowering blood pressure, but can reflexively cause a mild increase in heart rate; intracoronary use of drugs Can directly dilate coronary arteries.
② β-adrenergic receptor blockers: commonly used are aminoglutethimide (atenolol), metoprolol (betaxolol, medoxin) and esmolol. Pharmacological effects include inhibition of myocardial excitation to sympathetic nerves and catecholamine response, resulting in reduced myocardial oxygen consumption at the same level of exercise; slowing down the heart rate, reducing blood pressure and myocardial contractility; causing resistance vasoconstriction in non-ischemic areas and redistribution of blood flow to improve blood supply to ischemic areas; increasing diastolic coronary perfusion; and inhibiting platelet release of TXA2.
Calcium channel blockers: commonly used are Perdipine (Nicardipine), Verapamil, Diltiazem V (Hepesin, Hepesin, Tenelheart) and Nifedipine (Cardiac pain, Bayerone). The pharmacological effects include lowering the resistance of body circulation, dilating the veins, thus reducing the load on the heart; directly inhibiting the contraction of coronary smooth muscle, causing coronary artery dilation; reducing the tension of the ventricular wall, increasing coronary perfusion; slowing down the heart rate, thus reducing myocardial oxygen consumption and prolonging diastolic coronary perfusion; preventing the inward flow of extracellular calcium ions before and after ischemia to protect cells from hypoxia and early reperfusion damage; inhibiting platelet aggregation, and reducing TXA2 and 5-hydroxytryptophan. Reduce the release of TXA2 and 5-hydroxytryptamine; reduce myocardial contractility, but some drugs can be offset by the enhancement of myocardial contractility by reflex sympathetic excitation induced by reduced vascular resistance.
④ Platelet inhibitors and anticoagulants
Aspirin: Inhibits the acetylation of platelet cyclooxygenase, which reduces the production of TXA2 and PGI2; also inhibits the release of platelet TXA2, thus preventing vasoconstriction and thrombosis.
Pansentin: Inhibits platelet adenylyl cyclase activity and increases cyclic adenylate levels, thus inhibiting platelet aggregation and dilating blood vessels.
Dextran: exerts an antithrombotic effect by inhibiting platelet adhesion.
Heparin: inhibits the formation of thrombin and prevents the change of prothrombin to thrombin; reduces thrombin activity; inhibits fibrin formation; inhibits the coagulation and release function of platelets.
Warfarin (Comidine): It can competitively block the binding of vitamin K to the relevant lipoproteins in the liver, thus inhibiting the liver from using vitamin K to synthesize thrombinogen and the production of active coagulation factors II, VII, IX and X.
⑤ Activate blood circulation and resolve stagnation of Chinese medicinal preparations: such as heart-preserving pills, broad chest pills, Suhexiang pills, Yi Xin Fuxue Pulse Granules and Heart Tong Oral Liquid.
The principles of the use of anti-angina drugs are as follows.
① exertional angina or other angina induced by increased myocardial oxygen consumption, drug therapy is based on beta-blockers. For stable angina pectoris, β-blockers are used in combination with vasodilators. For primary angina, it is often treated with a combination of nitrates, calcium channel blockers, β-blockers, platelet inhibitors and other drugs. For worsening angina, nitrates and calcium channel blockers are often used, and intravenous nitroglycerin is often continuously administered when angina attacks are frequent.
②For spontaneous angina pectoris, the treatment drugs are mainly calcium channel blockers.
③ For mixed angina pectoris, where exertional and spontaneous angina coexist and the coronary reserve is low and cannot tolerate the load of daily activities, clinical emphasis is placed on β-blockers. To prevent coronary artery constriction, calcium channel blockers or nitrates are often used in combination. For those who have good coronary artery reserve and can tolerate general activities, calcium channel blockers and nitrates are often used to prevent attacks caused by reduced coronary blood flow, and beta-blockers are added when necessary.
3.Interventional treatment of coronary heart disease
Percutaneous coronary balloon dilatation and angioplasty (PTCA).
Indications: Single, double or triple vessel lesions with relatively isolated, incomplete obstruction, non-calcified and not at the bifurcation, causing intractable angina, with objective evidence of ischemia and indications for CABG; secondary stenosis of coronary bridges after CABG, causing intractable angina, with objective evidence of ischemia; stenosis with a high degree of feasibility for PTCA after thrombolytic therapy for acute myocardial infarction;
Those with complete obstruction within 3 months with intractable angina and evidence of myocardial ischemia; those with left main stenosis with life-threatening ischemia that are not suitable for CABG; those with multiple vascular lesions with relatively suitable anatomical location with intractable angina that are not suitable for CABG.
Conditions in which PTCA is inappropriate: coronary artery spasm; multiple, diffuse coronary artery lesions; coronary artery stenosis less than 50; left main stenosis or stenosis of the “last blood supply vessel”; multiple vessel lesions in which occlusion by PTCA of any one coronary artery can lead to cardiogenic shock; chronic complete or sub-total obstruction of more than 3 months Chronic total or sub-total obstructive lesions of more than 3 months; coagulation disorders.