Antiplatelet Management for Coronary Heart Disease: Advances and Challenges

Abstract

Coronary heart disease (CHD) remains the leading cause of death in the USA. CHD accounts for 48 % of all cardiovascular mortality or approximately one of every seven deaths. Disruption of atherosclerotic plaques--usually by rupture or erosion--and superimposed thrombosis can result in acute coronary syndromes and sudden cardiac death. Silent plaque disruption may also occur and result in coronary plaque progression and ultimately the symptomatic manifestations of stable CHD. Antiplatelet agents remain the cornerstone therapy for acute thrombotic coronary syndromes and are essential for thromboprophylaxis against these events in patients with stable CHD. Antiplatelet drugs are also important adjunct therapies during percutaneous coronary intervention (PCI) as they mitigate equipment-associated thrombotic complications that are partially induced by iatrogenic plaque rupture by interventionalists during balloon angioplasty in the cardiac catheterization laboratory. Since the introduction of clopidogrel, there has been considerable development in this field with at least three novel P2Y12 antagonists approved by the Food and Drug Administration (FDA) over the past decade. Rapidly accumulating evidence is helping to guide the optimal duration of treatment with dual antiplatelet therapy after stenting, especially with the newer drug-eluting stents. More data are also emerging on the hazards and long-term safety of these agents. It is therefore prudent for clinicians to remain current on treatment options and recent advances in this area. We herein review current and emerging antiplatelet therapies and summarize their characteristics and indications of use as well as challenges and areas of ongoing research.

Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures

“…The pathological changes always begin with endothelial injury, followed by arterial inflammation, excessive release of growth factors, inflammatory factors, and vasoactive factors, and vascular remodeling led by proliferation of fibrocytes and smooth muscle cells, which induce plaque formation and atherosclerosis [14]. Rupture of vulnerable plaques activates the coagulation cascade, leading to thrombosis and blood flow interruption in coronary arteries [15]. NSTEMI occurs secondary to the imbalance between the demand and supply of blood and is usually accompanied by microthrombosis without complete obstruction of the coronary artery.…”

“…Unstable angina, classified into NSTE-ACS, is pathophysiologically similar to NSTEMI, but without myocyte death. STEMI most often results from rupture of vulnerable plaques followed by thrombus formation and complete coronary lumen occlusion [15]. …”

“…As a traditional risk factor for ACS [15], elevated blood pressure is a potential mechanism leading to PM 2.5 -related increased risk for ACS [93]. A recent meta-analysis reported that short-term exposure to PM 2.5 , but not long-term exposure, was positively associated with an increased risk for hypertension [94].…”

Direct Medical Cost Analysis Among Coronary Heart Disease and Heart Failure Outpatients at One Hospital

“…Not all patients in this study received antiplatelet drug class. The provision of antiplatelet to coronary heart patients is an attempt to prevent thrombosis which could occur at any time due to a rupture of the plaque in blood vessels 18 . The medical history or comorbidities of gastrointestinal bleeding can be the reason to not give antiplatelet, especially aspirin, to patients 19 .…”

9-(4'-dimethylaminophenyl)-2,6,7-trihydroxy-xanthene-3-one is a Potentially Novel Antiplatelet Drug which Antagonizes the Effect of Thromboxane A2

“…In sum, compound 8 had a comparable or even better effect than clinically used acetylsalicylic acid and a different mechanism of action. Since antiplatelet treatment is aimed at inhibition of platelet aggregation in among others, patients with coronary artery disease [22] and thromboxane A 2 receptors are upregulated in acute myocardial infarction [5], a (novel) compound acting as an antagonist at these thromboxane receptors could be a potentially interesting drug.…”