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Is there a Role for Oral Triple Therapy in Patients with Acute Coronary Syndromes Without Atrial Fibrillation?
Spinthakis, N, Farag, M, Akhtar, Z, Gorog, DA
Current vascular pharmacology. 2018;(5):427-436
Abstract
BACKGROUND Acute Coronary Syndrome (ACS) patients, despite treatment with Dual Anti- Platelet Therapy (DAPT), have up to 10% risk of recurrent Major Adverse Cardiac Events (MACE) in the short term. METHODS Here we review studies using more potent antithrombotic agent combinations to reduce this risk, namely Triple Therapy (TT) with the addition of an oral anticoagulant, PAR-1 antagonist, or cilostazol to DAPT (mainly aspirin and clopidogrel), and discuss the limitations of trials to date. RESULTS Generally speaking, TT leads to an increase in bleeding. Vorapaxar showed a signal for reducing ischaemic events, but increased intracranial haemorrhage 3-fold in the subacute phase of ACS, although remains an option for secondary prevention beyond the immediate subacute phase, particularly if prasugrel or ticagrelor are not available. Non-Vitamin K Oral Anticoagulants (NOACs) all increased bleeding, with only modest reduction in MACE noted with low dose rivaroxaban. Rivaroxaban can be considered combined with aspirin and clopidogrel in ACS patients at high ischaemic and low bleeding risk, without prior stroke/TIA. The combination of P2Y12 inhibitor and NOAC, without aspirin, looks promising. DAPT may be replaced, not by TT, but by dual therapy comprising a NOAC with a P2Y12 inhibitor. CONCLUSION More potent antithrombotic regimens increase bleeding and should only be considered on an individual basis, after careful risk stratification. Accurate risk stratification of ACS patients, for both ischaemic and bleeding risk, is essential to allow individualised treatment.
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[high on-treatment platelet reactivity in patients with chronic renal failure using acetylsalicylic acid].
Horyniecki, M, Łącka-Gaździk, B, Dworaczek, W, Śnit, M, Łabuz-Roszak, B
Wiadomosci lekarskie (Warsaw, Poland : 1960). 2017;(6 pt 1):1102-1107
Abstract
Cardiovascular diseases (CVD) are the most common cause of mortality in the world. Acetylsalicylic acid (ASA) is a widely used medicine in primary and secondary prevention of cardiovascular diseases. About 1-60% patients taking aspirin have high platelet reactivity (HOPR) despite aspirin treatment. HOPR is significantly more frequent in patients with chronic kidney disease (CKD) and it increases the risk of adverse cardiovascular events in these patients. The cause of HOPR in patients with CKD may be oxidative stress and inflammation. To the risk factors belong diabetes, female sex or decreased HDL cholesterol level.
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3.
Administration of Traditional Chinese Blood Circulation Activating Drugs for Microvascular Complications in Patients with Type 2 Diabetes Mellitus.
He, L, Wang, H, Gu, C, He, X, Zhao, L, Tong, X
Journal of diabetes research. 2016;:1081657
Abstract
Traditional Chinese medicine (TCM) is an important complementary strategy for treating diabetes mellitus (DM) in China. Traditional Chinese blood circulation activating drugs are intended to guide an overall approach to the prevention and treatment of microvascular complications of DM. The core mechanism is related to the protection of the vascular endothelium and the basement membrane. Here, we reviewed the scientific evidence underpinning the use of blood circulation activating drugs to prevent and treat DM-induced microvascular complications, including diabetic nephropathy (DN), diabetic peripheral neuropathy (DPN), and diabetic retinopathy (DR). Furthermore, we summarized the effects and mechanism of TCM on improving blood rheology, inhibiting aggregation of platelet, forming advanced glycation end products (AGEs), regulating oxidative stress, reducing blood fat, and improving lipid metabolism. The paper provides a new theoretical basis for the clinical practice of TCM in the prevention and treatment of DM and its microvascular complications.
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4.
Mechanism of the anti-platelet effect of natural bioactive compounds: role of peroxisome proliferator-activated receptors activation.
Fuentes, E, Fuentes, F, Palomo, I
Platelets. 2014;(7):471-9
Abstract
Platelets are crucial mediators of the acute complications of atherosclerosis causing life-threatening ischemic events throughout plaque development. The inhibition of the platelet function has been used for a long time in an effort to prevent and treat cardiovascular diseases. However, morbidity and mortality figures indicate that current anti-platelet strategies are far from a panacea. In this context, a large number of natural bioactive compounds (NBCs) (polyphenols, terpenoids, alkaloids and fatty acids, among others) have been reported with apparent inhibitory activity on human platelets and each constituent may possess multiple targets. In this sense, the article describes how the mechanism of anti-platelet action by NBCs peroxisome proliferator-activated receptors agonists is mediated by inhibition of protein kinase-α, cyclooxygenase-1, thromboxane A2, cytosolic calcium, and indirect stimulation of protein kinase A (increased in cyclic adenosine monophosphate levels) and protein kinase G (increased in cyclic guanosine monophosphate levels).
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5.
Influence of omega-3 polyunsaturated fatty acid-supplementation on platelet aggregation in humans: a meta-analysis of randomized controlled trials.
Gao, LG, Cao, J, Mao, QX, Lu, XC, Zhou, XL, Fan, L
Atherosclerosis. 2013;(2):328-34
Abstract
OBJECTIVE Increased platelet activity predicts adverse cardiovascular events. The objective was to assess the effects of long-chain omega-3 polyunsaturated fatty acid (n-3 PUFA)-supplementation on platelet aggregation. METHODS AND RESULTS We conducted a meta-analysis of randomized controlled trials identified using PubMed, Embase and the Cochrane Library. Fifteen studies were included. In comparison to placebo using the random-effect model, n-3 PUFA-supplementation significantly reduced adenosine diphosphate-induced platelet aggregation (standard mean difference [SMD] = -1.23 with 95% confidence interval [CI] -2.24 to -0.23, p = 0.02) and platelet aggregation units, determined using the VerifyNow(®) rapid platelet-function assay system (SMD = -6.78 with 95% CI -12.58 to -0.98, p = 0.02). There was a trend toward decreased collagen-induced (SMD = -0.70 with 95% CI -0.72 to 0.33, p = 0.18) and arachidonic acid-induced platelet aggregation (SMD = -0.43 with 95% CI -2.26 to 1.40, p = 0.64) compared with controls; however, statistical significance was not reached. CONCLUSIONS Our meta-analysis demonstrates that n-3 PUFA-supplementation is associated with a significant reduction in platelet aggregation when the participants were at poor health status, but not in healthy persons. High-risk patients with cardiovascular disease and even diabetics may potentially benefit from n-3 PUFAs therapy. However, n-3 PUFAs may not be effective in primary prevention. Larger trials need to be carried out to confirm the present findings.
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6.
Inflammation in atherosclerosis: from pathophysiology to practice.
Libby, P, Ridker, PM, Hansson, GK, ,
Journal of the American College of Cardiology. 2009;(23):2129-38
Abstract
Until recently, most envisaged atherosclerosis as a bland arterial collection of cholesterol, complicated by smooth muscle cell accumulation. According to that concept, endothelial denuding injury led to platelet aggregation and release of platelet factors which would trigger the proliferation of smooth muscle cells in the arterial intima. These cells would then elaborate an extracellular matrix that would entrap lipoproteins, forming the nidus of the atherosclerotic plaque. Beyond the vascular smooth muscle cells long recognized in atherosclerotic lesions, subsequent investigations identified immune cells and mediators at work in atheromata, implicating inflammation in this disease. Multiple independent pathways of evidence now pinpoint inflammation as a key regulatory process that links multiple risk factors for atherosclerosis and its complications with altered arterial biology. Knowledge has burgeoned regarding the operation of both innate and adaptive arms of immunity in atherogenesis, their interplay, and the balance of stimulatory and inhibitory pathways that regulate their participation in atheroma formation and complication. This revolution in our thinking about the pathophysiology of atherosclerosis has now begun to provide clinical insight and practical tools that may aid patient management. This review provides an update of the role of inflammation in atherogenesis and highlights how translation of these advances in basic science promises to change clinical practice.