Table 1.
Drugs | Impact on the cardiovascular risk | Suggestion | References | |
---|---|---|---|---|
NSAIDs | Non- selectively NSAIDs | Its cardiovascular risk depends on the inhibition degree of COX-1 and COX-2. The smaller the inhibition degree of COX-1, the greater the inhibition degree of COX-2, and the greater its cardiovascular risk may be | People at high cardiovascular risk should use NSAIDs with caution. If necessary, use drugs that have a small inhibitory effect on COX-2, such as naproxen and ibuprofen | (8, 9, 12–15) |
Selective COX-2 inhibitors | Selective inhibition of COX-2 inhibits the synthesis of prostacyclin in endothelial cells, which destroys the balance between TXA2 and PGI2, leading to atherosclerosis, thrombosis, and other cardiovascular complications | |||
GC | The minimum effective dose of GC may reduce the increase of CV risk caused by inflammation by controlling the inflammatory process Increasing exposure time and cumulative dose may increase the risk of cardiovascular disease through changes in blood lipid levels, insulin resistance or diabetes, hypertension, obesity, etc. |
Use the smallest effective dose as much as possible and consider the course of treatment. At the same time, closely monitor the patient's blood pressure, blood lipids, blood sugar, etc., and add drugs when necessary to antagonize its side effects. | (18–24) | |
csDMARDs | MTX | It can inhibit atherosclerosis by anti-inflammatory, improving endothelial function, preventing intima-media thickening, and improving lipid status. However, with the prolongation of the course of disease, the CVD protective effect of MTX may be weakened because MTX increases homocysteine level |
Folic acid should be supplemented appropriately during medication | (26–34) |
SASP | By improving blood lipid level, controlling endothelial dysfunction and carotid artery remodeling induced by inflammation may help to ameliorate coronary heart disease and inhibit platelet aggregation mediated by arachidonic acid. | – | (37–39) | |
HCQ | HCQ can reduce the risk of cardiovascular disease by preventing thrombosis, lowering blood sugar, and improving lipid status However, some studies have shown that long-term use of HCQ can cause sodium and calcium channel block, which leads to membrane stabilization, atrioventricular block, QRS interval widening and QT interval lengthening, which leads to serious heart diseases such as conduction disorder, but it is rare |
Monitor electrocardiogram | (43–48) | |
LEF | It can relieve cardiac hypertrophy induced by pressure overload or angiotensin II in vivo and prevent the induction of cardiac fibrosis However, leflunomide has the risk of raising blood pressure |
Monitor blood pressure | (52, 53) | |
CsA | The decrease of intima-media thickness and plaque prevalence can prevent myocardial hypertrophy, but it can cause blood pressure increase and microvascular injury. | Monitor blood pressure | (32, 57–61) | |
AZA | By downregulating TLR4 signaling pathway, it can inhibit the excessive oxidative stress and inflammatory reaction caused by myocardial ischemia and reperfusion, promote the balance of oxidation and antioxidation, and alleviate the process of myocardial injury caused by ischemia and reperfusion to a certain extent | – | (63) | |
bDMARDs: | TNF antagonists | Improve insulin sensitivity and endothelial function to reduce the risk of cardiovascular disease But it is not recommended for patients with heart failure |
Use with caution in patients with heart failure | (67–79) |
Rituximab | By exhausting B cells, the infarct area is reduced and cardiac remodeling is improved, and a few patients may have peripheral edema, hypertension, hypotension or arrhythmia, and myocardial infarction. | Monitor blood pressure and electrocardiogram | (80, 81) | |
Abatacept | Improve endothelial function and insulin resistance to reduce the risk of cardiovascular disease | – | (83–87) | |
Tocilizumab | Inhibit the migration of human aortic smooth muscle cells and play an anti-atherosclerosis role | – | (91) | |
Anakinra | It can reduce heart remodeling after myocardial infarction without increasing the risk of heart failure, and can restore left ventricular diastolic function for patients with existing heart failure, especially patients with diastolic heart failure | Anakinra is suitable for patients with myocardial infarction | (92–96) | |
tsDMARDs | JAK inhibitors | Increased risk of venous thromboembolic events | Use with caution if there are high-risk factors for venous thromboembolism | (97–99) |
Botanic drug | Tripterygium wilfordii | It has protective effect on kidney damage and myocardial ischemia-reperfusion injury caused by salt-sensitive hypertension in rats It can cause cardiac toxicity, and its clinical manifestations are chest tightness, palpitation, arrhythmia, etc. In severe cases, it may cause insufficient blood supply to the heart, sudden drop in blood pressure, shock or heart failure, which is life-threatening |
Recommended for RA patients with angina pectoris and myocardial infarction. Monitor blood pressure and electrocardiogram |
(102–105) |
TGP | It can ameliorate hypertension and hyperlipidemia, inhibit the progression of atherosclerosis, and protect myocardial ischemia-reperfusion injury. | especially suitable for patients with myocardial infarction or insulin resistance. | (110–114) |