I. Drug treatment
The main objectives of pharmacological treatment of chronic stable angina are:to prevent myocardial infarction and sudden death and to improve survival; to reduce symptoms and ischemic attacks and to improve quality of life. When choosing therapeutic drugs, prevention of myocardial infarction and death should be considered first. In addition, risk factors should be actively addressed.
(A) Drugs to improve prognosis
1. Aspirin:
Anti-platelet aggregation is achieved by inhibiting the synthesis of cyclooxygenase and thromboxane (TXA2), and should be taken by all patients as long as there are no contraindications to the use of the drug. Randomized controlled studies have demonstrated a reduction in the risk of myocardial infarction, stroke, or cardiovascular death with aspirin in patients with chronic stable angina. The optimal dose range for aspirin is 75-15Omg/d. The main adverse effects are gastrointestinal bleeding or hypersensitivity to aspirin. Patients who cannot tolerate aspirin.
2.Clopidogrel:
Effectively reduces ADP-mediated platelet activation and aggregation by selectively and irreversibly inhibiting platelet ADP receptors while blocking ADP-dependent activation complexes. It is mainly used after stent implantation and in patients with contraindications to aspirin. The drug has a rapid onset of action, with an effective blood concentration achieved 2 hours after a 30Omg dose. Commonly used maintenance dose is 75mg/d, l oral dose.
3.β-blockers:
A recently published meta-analysis of the effect of multiple beta-blockers on mortality showed that long-term secondary prevention treatment with beta-blockers in post-myocardial infarction patients reduced relative mortality by 24%. Beta-blockers with intrinsic sympathomimetic activity are less cardioprotective. It is important to note that there is no clear evidence that the beta-blocker atenolol, which is currently widely used, affects patient mortality.
4.Lipid-regulating therapy:
To achieve better lipid-lowering effects, the cholesterol absorption inhibitor ezamibe can be added to statin therapy. Patients at high risk for hypertriglyceridemia or low HDLemia may be considered for a combination of LDL-C lowering drugs and a fibrate (fenofibrate) or niacin. When high-risk or moderately high-risk individuals receive drug-lowering therapy, the intensity of treatment should be sufficient to reduce LDL-C levels by at least 30-40%.
When statins are applied, biochemical indicators such as transaminases and creatine kinase should be closely monitored to detect possible drug-induced liver damage and myopathy in a timely manner. When using intensive lipid-lowering therapy, more attention should be paid to monitoring the safety of drugs.
5.Angiotensin converting enzyme inhibitor (ACEI):
The results of the HOPE study showed that ramipril reduced the relative risk of primary endpoint events (cardiovascular death, myocardial infarction, and stroke) by 22% in patients with high-risk vascular disease without heart failure, and the results of the EUROPA study showed that perindopril reduced the relative risk of primary endpoint events (cardiovascular death, nonfatal myocardial infarction, and cardiac arrest with successful resuscitation) in patients with stable angina without heart failure. combined incidence) by 20%.
In patients with stable angina, ACEIs should be used in high-risk patients with combined diabetes, heart failure, or left ventricular systolic insufficiency. all patients with coronary artery disease benefit from ACEI therapy, but low-risk patients may benefit to a lesser extent.
Recommendations for drug therapy to improve prognosis:
Class I:
(1) Oral aspirin for those without contraindications to use (e.g., active gastrointestinal bleeding, aspirin allergy, or a history of aspirin intolerance).
(2) All patients with stable angina pectoris with coronary artery disease receiving statin therapy with a target LDL-C value <2, 60 mmol/L (100 mg/dl).
(3) ACEI in all patients with combined diabetes mellitus, heart failure, left ventricular systolic insufficiency, hypertension, and left ventricular insufficiency after myocardial infarction.
(4) Beta-blockers in patients with stable angina pectoris or heart failure after myocardial infarction.
Class IIa:
(1) Use ACEI in all patients with definite coronary artery disease.
(2) Use clopidogrel as an alternative therapy for patients who cannot use aspirin, such as those with aspirin allergy.
(3) Very high-risk patients (annual cardiovascular mortality >2%) with definite coronary artery disease receive intensive statin therapy.
Class IIb:
Patients with diabetes mellitus or metabolic syndrome combined with low HDL-C and hypertriglyceridemia receive fibrates or niacin.
II. Non-pharmacological treatment
(i) Revascularization therapy
The revascularization treatment for chronic stable angina includes percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG). For patients with chronic stable angina pectoris, PCI and CAB.
(II) Drugs to reduce symptoms and improve ischemia
Symptom-reducing and ischemia-improving drugs should be used in combination with drugs to prevent myocardial infarction and death, some of which, such as beta-blockers, have both effects. At present, the main drugs to reduce symptoms and improve ischemia include three categories: beta-blockers, nitrates and calcium antagonists.