What Is Arterial Tension?

The shape of the heart is like an inverted, slightly flat front and back cone. If you think of it as a head, the coronary arteries on the top of the head that almost surrounds the heart look like a crown. The coronary arteries are arteries that supply blood to the heart. They originate in the aortic sinus at the root of the aorta, divide into two branches, and run on the surface of the heart. Using the classification principle of Schlesinger et al., The distribution of coronary arteries is divided into three types: 1. right dominant type; 2. balanced type; 3. left dominant type.

[gun zhuàng dòng mài]

The shape of the heart is like an inverted, slightly flat front and back cone. If you think of it as a head, it is located on the top of the head and almost surrounds it.

The branches of the left and right coronary arteries and their terminal branches have less variation in the thoracic costal surface of the heart and greater variation in the plantar surface. Using Schlesinger's classification principle, the distribution of coronary arteries is divided into three types:

The left and right coronary arteries are ascending

According to the direction and distribution of the coronary branches, it is not difficult to guess the part of the nutritional heart.

1. Right atrium and right ventricle: blood is supplied by the right coronary artery.

2. Left ventricle: 50% of its blood supply comes from the left

In order to maintain normal life activities of various tissues and organs of the human body, the heart needs to keep beating to ensure blood flow. As a muscular power organ that pumps blood, the heart itself also needs sufficient nutrition and energy to provide heart nutrition.

There are many collaterals or anastomotic branches between the coronary arteries and their branches. It is a potential pipeline. Usually, under the physiological condition of good coronary blood supply, these collaterals or anastomotic branches do not participate in the circulation of the coronary arteries , Only when the main coronary artery is narrowed or blocked, and the collateral vessels appear at both ends

In different states of the body, the stroke output of the heart and its own energy consumption are different, so the coronary blood flow is also different. In a quiet state, human coronary blood flow is 60ml to 80ml per 100 grams of myocardium per minute. For people of medium weight, the total coronary blood flow is 225ml / min, which accounts for 4% to 5% of cardiac output. When myocardial activity strengthens, coronary arteries reach their maximum

Coronary heart disease

Coronary heart disease is a heart disease caused by ischemic hypoxia (angina pectoris) or myocardial necrosis (myocardial infarction) caused by narrowing or obstruction of the coronary arteries (atherosclerosis or dynamic vasospasm), also known as ischemia Sexual heart disease. Most of the coronary heart disease that we talk about is caused by arterial organic stenosis or obstruction, also known as coronary atherosclerotic heart disease. The coronary artery stenosis is caused by the accumulation of fatty substances along the inner wall of blood vessels. This process is called arteriosclerosis. Arteriosclerosis develops to a certain degree, and coronary stenosis gradually increases, restricting blood flow to the heart muscle. Without adequate oxygen to the heart, chest discomfort, angina pectoris, occurs. The performance of angina pectoris varies from person to person. Most people describe it as "chest pressure," "swelling," "sulking," and some patients feel released to the shoulders, back, neck, and throat, resting, or taking nitroglycerin. Myocardial infarction is another manifestation of coronary heart disease. It has persistent and severe chest pain symptoms. It is not effective to rest or take nitroglycerin. During myocardial infarction, the coronary arteries were completely obstructed, and the part of the heart muscle died because there was no blood supply. Most are caused by the formation of blood clots in the narrow part, rupture of atheromatous plaques or vasospasm.

Acute coronary syndrome

Acute coronary syndrome (ACS) is a group of clinical syndromes caused by acute myocardial ischemia, including acute myocardial infarction (AMI) and unstable angina pectoris (UA). AMI is divided into ST-segment elevated myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI). Platelet activation plays an important role in the occurrence of ACS.

Antithrombotic Therapy for Acute Coronary Syndrome

Acute Coronary Syndrome (ACS) is a group of clinical syndromes based on the pathology of coronary atherosclerotic plaque rupture or erosion, followed by complete or incomplete occlusive thrombosis. It is a series of clinical signs including unstable angina pectoris, non-Q wave myocardial infarction and Q wave myocardial infarction. It has been found in long-term clinical practice that many patients have different clinical symptoms, but their coronary arteries have very similar pathophysiological changes, that is, coronary atherosclerotic plaques change from stable to unstable, and then rupture leading to thrombosis. Therefore, antithrombotic therapy for acute coronary syndrome is very important, especially in non-ST-segment elevation ACS. Antithrombotic therapy can be divided into antiplatelet therapy and antithrombin therapy.

Acute coronary syndromes are classified into ST-segment elevation and non-ST-segment elevation based on ECG manifestations. Non-ST-segment elevation is further divided into unstable angina pectoris and non-ST-segment elevation myocardial infarction, and ST-segment elevation. Type mainly refers to acute myocardial infarction. The difference in the physiology of the two may be that the physiological basis of the non-ST-elevation disease is that the thrombus does not completely block the artery or microembolism, while the ST-elevation type is that the thrombus completely blocks the artery. Although the physiological processes of the two diseases are similar, the two have great differences in clinical manifestations and treatment strategies.

I. Non-ST-segment elevation acute coronary syndrome

Non-ST-segment elevation acute coronary syndromes include unstable angina pectoris and non-ST-segment elevation myocardial infarction. In 2002, ACC / AHA introduced a new UA / NSTEMI treatment guideline, which contains recommendations on antiplatelet and anticoagulant treatments as follows:

Class I

Coronary artery

1. Antiplatelet therapy should be started quickly. Aspirin is preferred (Level of Evidence: A).

2. Patients with aspirin allergy or gastrointestinal disorders cannot tolerate clopidogrel (Level of Evidence: A).

3. For inpatients who are not planning to undergo early interventional treatment, in addition to aspirin, clopidogrel should be used as much as possible. The duration of medication is 1 (Level of Evidence: A)-9 months (Level of Evidence: B ).

4. In-patients who are preparing for intervention should use clopidogrel for more than 1 month (Level of Evidence: A), or 9 months if there are no high risk factors for bleeding (Level of Evidence: B).

5. Patients who are preparing for elective CABG and are using clopidogrel should be discontinued for 5-7 days (Level of Evidence: B).

6. In addition to aspirin or clopidogrel for antiplatelet therapy, intravenous unfractionated heparin or subcutaneous LMWH should be used for anticoagulation (Level of Evidence: A).

7. For patients preparing for cardiac catheterization and PCI, in addition to aspirin and unfractionated heparin, GPIIb / IIIa receptor antagonists (Level of Evidence: A) class IIa should be used .

1. For patients with persistent ischemia and elevated troponin, or patients who are not prepared for invasive treatment but have other high-risk manifestations, in addition to using aspirin and low molecular weight heparin.

2. Compared with unfractionated heparin, enoxaparin is preferred as an anticoagulant in UA / NSTEMI patients, unless CABG surgery is planned within 24 hours (Level of Evidence: A).

3. For patients who have already used unfractionated heparin, aspirin and clopidogrel and are preparing for cardiac catheterization and PCI, GPIIb / IIIa receptor antagonists should be used, or just before PCI (Level of Evidence: B).

Class IIb

GP IIb / IIIa receptor antagonists (Level of Evidence: A) in addition to aspirin and low-molecular-weight heparin for patients without persistent ischemia and other high-risk manifestations or patients who are not prepared for invasive treatment

Class III

1. Patients without acute ST-segment elevation, posterior posterior wall MI, or new LBBB, undergo intravenous thrombolytic therapy (Level of Evidence: A)

2.Use abciximab in patients who are not going to do PCI (Level of Evidence: A)

This guideline has long guided our clinical work. However, the development of medical science is very rapid. In recent years, with the development of various large-scale clinical studies and the continuous emergence of new drugs, many new evidence-based medical evidences are in front of us, and the guidelines should be updated accordingly. In 2004, the American Association of Chest Physicians launched the guideline ACCP7 on thrombotic diseases. We will talk about the antithrombotic strategy of acute coronary syndrome based on ACCP7.

(A) Anti-platelet therapy for NSTE-ACS

Antiplatelet drugs commonly used in clinical practice include: aspirin, ticlopidine, dipyridamole, and platelet glycoprotein IIb / IIIa receptor antagonists. Combined antiplatelet therapy will improve clinical prognosis.

1.Aspirin

Aspirin is the basis of antiplatelet therapy. It acts on platelet cyclooxygenase-1 (COX-1), inhibits its activity, thereby reducing arachidonic acid degradation, reducing TXA2 production, inhibiting GpIIb / IIIa receptor activation, and thereby inhibiting platelet activation. ACCP7 recommends aspirin as follows:

For all patients with NSTE ACS who are not allergic to aspirin, oral aspirin 75 to 325 mg is recommended, followed by 75 to 162 mg daily (Grade 1A).

Walletin et al.'S study confirmed that long-term aspirin use can significantly reduce the risk of death and myocardial infarction in patients with ACS, and this advantage gradually increases with time. Another meta-analysis suggests that ACS that still occurs with aspirin means a poor clinical prognosis.

2. Ticlopidines

Including cleavide and clopidogrel. They are both antagonists of platelet ADP receptors. Acting on the ADP receptor, inhibits the activation of platelet GpIIb / IIIa receptors, thereby achieving the effect of inhibiting platelet activation. ACCP7's recommendations for Ticlopidine are as follows:

For all patients with NSTE ACS who do not have a clear aspirin allergy, oral clopidogrel 300 mg is recommended immediately followed by 75 mg / day (Grade 1A)

For patients with NSTE-ACS who cannot perform CABG within 5 days after diagnostic catheterization or coronary angiography, oral clopidogrel 300 mg is recommended immediately, followed by 75 mg daily to 9 to 12 months with aspirin (Grade 1A)

For patients with NSTE-ACS who will undergo coronary angiography within 24 hours, it is recommended to start clopidogrel after clearing the coronary anatomy (Grade 2A)

For patients taking clopidogrel and preparing for CABG surgery, we recommend discontinuing clopidogrel for 5 days before surgery (Grade 2A)

The purpose of the CURE trial is to investigate whether platelet aggregation caused by blocking the ADP pathway can benefit from aspirin therapy. The trial enrolled 12,562 UA / NSTEMI patients and randomly divided them into placebo and clopidogrel (loading 300 mg, then 75 mg per day) within 24 hours, followed by 3 to 12 months. All patients were given aspirin. The incidence of combined endpoint events (cardiovascular death, myocardial infarction, or stroke) was 11.5% in the placebo group and 9.39% in the clopidogrel group (RR 0.80, P <0.001). PCI-CURE is a subgroup study of the CURE trial. 2658 patients were enrolled. They were randomly and double-blindly divided into placebo group (n = 1345) and clopidogrel group (n = 1313). All patients were given aspirin. Eligible patients received placebo or clopidogrel for an average of 10 days before coronary intervention (PCI). Most patients received open-label drugs (clopidogrel or clopidogrel) for 2 to 4 weeks after surgery, and then Use study medication for 8 months. The primary endpoint (combined with cardiovascular death, myocardial infarction, or urgent target vessel revascularization) was 86 in the placebo group (6.4%) and 59 in the clopidogrel group (4.5%, RR0.7, P = 0.03). The incidence of cardiovascular death and myocardial infarction in the clopidogrel group decreased by 31%. The CURE test establishes the status of clopidogrel in ACS antiplatelet therapy.

3.Dipyridamole

Dipyridamole, Pansentin, is a phosphodiesterase inhibitor that inhibits platelet activation by inhibiting cAMP production. Dipyridamole does not increase the risk of gastrointestinal bleeding compared to aspirin, even when combined with warfarin. But there is no evidence in the acute phase of NSTE-ACS patients that dipyridamole can replace or be used in combination with aspirin and clopidogrel

4. Platelet glycoprotein IIb / IIIa receptor antagonists Platelets play a very important role in the pathogenesis of atherosclerosis, thrombosis and acute coronary syndromes. Glycoprotein (GP) receptors on platelet membranes are closely related to platelet viability. The binding of GPIIb / IIIa receptors to fibrinogen is the last common pathway for platelet aggregation caused by various platelet agonists. The platelet glycoprotein GPIIb / IIIa receptor antagonist is a new generation of platelet inhibitors by inhibiting platelet aggregation by binding to the GPIIb / IIIa receptor. ACCP7 recommends the following for Glycoprotein IIb / IIIa inhibitors:

For patients with NSTE-ACS at intermediate and high risk, early application of eptifibatide or tirofiban is recommended, with aspirin and unfractionated heparin (Grade 1A); for patients with NSTE-ACS who are taking clopidogrel, early and simultaneous Treatment with etibeptide or tirofiban (Grade 2A)

For patients with NSTE-ACS, it is recommended not to use abciximab as an initial treatment, unless the coronary anatomy is clear, PCI will be performed within 24 hours (Grade 1A)

Clinical trials show that the combined use of GPIIb / IIIa receptor antagonists and aspirin can reduce the incidence of ischemic complications, including death, acute myocardial infarction, and emergency coronary artery bypass graft (CABG) compared with aspirin and placebo alone. ) Or re-interventional therapy; GPIIb / IIIa receptor antagonists can also benefit patients with unstable angina pectoris and ST-free AMI. Clinical studies have been performed including: PURSUIT, PRISMPLUS, PRISM, and PARAGON. In the PURSUIT trial, 30-day mortality and MI in patients with unstable angina pectoris decreased in the EPtifibatide group (14.2%) compared to the placebo group (15.7%) (P = 0.04). The 96-hour, 7-day, and June mortality and MI rates also decreased by 1.2% to 1.5%. The 7- and 30-day mortality, MI, and refractory angina pectoris in patients with unstable angina pectoris and ST-free AMI with aspirin, heparin, and Tirofiband in the PRISM-PLUS trial were lower than those with aspirin and heparin alone.7 The time of day is 12.9% and 17.9% (P = 0.04); the time of 30 days is 18.5% and 22.3% (P = 0.03); the absolute value in June still fell by 3.0% -3.2%. The PRISM trial compares the efficacy of Tirofiband ten aspirin and heparin ten aspirin in patients with unstable angina pectoris. The former 48-hour combined endpoint (death, MI, and refractory ischemia) occurred in 3.8%, which was a 32% decrease over the latter (5.6%) ( P = 0.01). GPIIb / IIIa receptor inhibitors, as highly effective and specific antiplatelet drugs, are currently the most prominent advances in acute coronary syndromes, but large-scale prospective clinical studies are still underway to further understand their doses, effects, and safety.

(Two) anticoagulant therapy for NSTE-ACS

The commonly used anticoagulants in clinical practice are: ordinary heparin, low molecular weight heparin, selective indirect anti-factor Xa inhibitor (synthetic pentose), selective direct anti-factor Xa inhibitor (DX-9065a), and direct thrombin inhibitor .

1.Unfractionated heparin

The combination of unfractionated heparin and antithrombin III increases AT-III activity, thereby inactivating coagulation factors such as IIa and Xa. ACCP7's recommendations for unfractionated heparin are as follows:

For patients with NSTE-ACS, short-term combination of unfractionated heparin and antiplatelet therapy is recommended instead of pure antiplatelet therapy (Grade 1A). It is recommended that the dose of unfractionated heparin should be adjusted according to kg of body weight and maintain aPTT at 50 to 75 seconds (Grade 1C).

A meta-analysis confirmed that antiplatelet combined with short-term unfractionated heparin reduced mortality and myocardial infarction in patients with NSTE-ACS within 2 weeks. Unfractionated heparin is an important foundation for ACS anticoagulation.

2. Low-molecular-weight heparin

Low-molecular-weight heparin (LMWH) is a product of enzymatic hydrolysis or chemical degradation of ordinary heparin. Its anticoagulant effect is about the same as that of ordinary heparin. Due to its small molecular weight (average molecular weight of 4,500 Daltons), its anti-Xa and anti-IIa activity ratio increases. Factor Xa combined with platelets also has an inhibitory effect, so the antithrombotic effect is more obvious. LMWH has low non-specific binding capacity with plasma proteins, so it has higher bioavailability, longer half-life, and obvious anticoagulant effect. It is good for subcutaneous injection, almost 100%. The following are ACCP7 recommendations for low molecular weight heparin:

For NSTE-ACS patients, low molecular weight heparin is recommended instead of unfractionated heparin (Grade 1B)

It is not recommended to routinely monitor the anticoagulant effect of low molecular weight heparin (Grade 1C)

For patients with NSTE-ACS who have received low-molecular-weight heparin anticoagulation, it is recommended to continue to use low-molecular-weight heparin anticoagulation during PCI (Grade 2C)

For patients with NSTE-ACS who have been treated with GP IIb / IIIa receptor antagonists, low molecular weight heparin is recommended instead of unfractionated heparin for anticoagulation (Grade 2B)

From the meta-analysis, we can see that the current standard antithrombotic therapy is unfractionated heparin (UFH) and aspirin. However, LMWH is more practical and clinically advantageous than UFH, and can be considered as an effective alternative to ACS medical treatment and surgical interventional preparations. Can significantly reduce the 30-day mortality and complex cardiac events in acute coronary syndromes.

3. Indirect anti-factor Xa inhibitor (synthetic pentose)

Large randomized trials evaluating the safety and effectiveness of fondaparinux in TE-ACS and NSTE-ACS are ongoing. In 2005, the results of OASIS-5, the first large-scale clinical study of fondaparinux for ACS, were published at ESC. The OASIS-5 study is a multicenter, randomized, double-blind, placebo-controlled clinical trial that enrolled 20,000 ACS patients from 576 centers in 41 countries. The objective was to evaluate the effectiveness and safety of fondaparinux in the treatment of ACS. The results showed that fondaparinux was as effective as enoxaparin in preventing cardiovascular events, death, and ischemic attacks within 9 days after ACS, and significantly reduced severe bleeding complications. Studies have shown that fondaparinux significantly reduced mortality within 1 month after an ACS event and was equally effective during a 6-month follow-up period. The findings suggest that fondaparinux is likely to be a new antithrombotic option for patients with ACS.

4, direct thrombin inhibitor

Hirudin and Bivalirutin can selectively bind to thrombin and inactivate it. It is mostly used for anticoagulation therapy of heparin-induced thrombocytopenic purpura in clinical practice. A meta-analysis of comprehensive clinical trials indicates that direct thrombin inhibitors compared with unfractionated heparin do not significantly reduce the risk of death and myocardial infarction in patients with ACS, and increase the risk of related bleeding. The following are ACCP7 recommendations for direct thrombin inhibitors: For NSTE-ACS patients, DTIs are not recommended as the first anticoagulant therapy (Grade 1B)

In order to make the guidelines more practical, ACC / AHA introduced the UA / NSTEMI GUIDELINE emergency diagnosis and treatment guidelines in 2005, emphasizing the treatment in the emergency room. According to the risk stratification of UA / NSTEMI, patients were divided into early conservative group and early intervention group. The treatment strategies of the two were different.

Early conservative strategies:

1. Aspirin (Class IA); choose clopidogrel (Class IA) when aspirin is contraindicated

2. Clopidogrel should be taken for at least 1 month (Class IA) to 9 months (Class IB); if early intervention is not possible, clopidogrel should be taken early in the emergency room.

3.Enoxaparin or common heparin (Class IA)

4. Etibabatin or tirofiban: persistent ischemia (Class IIaA), elevated TnI or TnT (Class IIaA), other high-risk factors (Class IIaA)

5. Unplanned PCI, abciximab should not be used early (Class IIIA)

Early intervention strategies:

1. Aspirin (Class IA); choose clopidogrel (Class IA) when aspirin is contraindicated

2. Low-molecular-weight heparin or unfractionated heparin (Class IA); Enoxaparin is preferred as an anticoagulant for UA / NSTEMI patients compared with unfractionated heparin, unless CABG surgery (Class IIaA) is planned within 24 hours

3.If preparing for early intervention, use GP IIb / IIIa receptor antagonist (Class IA) early.

4. If preparing for early intervention, GP IIb / IIIa receptor antagonists should be used in combination with aspirin, heparin, and clopidogrel (Class IIaB)

5. If preparing for PCI, take clopidogrel for at least 1 month (Class IA) to 9 months (Class IB)

This change will make the guide more operational and practical. Vascular endoscopy found to predict risk of acute coronary syndromes According to a recent article in the American Journal of Cardiology, Japanese scientists have found that endoscopy can effectively detect patients with unstable coronary syndromes. Patients with multiple yellow plaques in the blood vessels are predicted to be at higher risk.