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- Low ADAMTS-13 in plavix induced thrombotic thrombocytopenic purpura. [JOURNAL ARTICLE]
- World J Clin Cases 2013 Apr 16; 1(1):31-33.
Thrombotic thrombocytopenia purpura (TTP) was first described in 1924 as a "pathologic alteration of the microvasculature, with detachment or swelling of the endothelium, amorphous material in the sub-endothelial space, and luminal platelet aggregation leading to compromise of the microcirculation". Ticlopidine induced TTP has been highly associated with autoimmune induced reduction in ADAMTS-13 activity. These findings, to a lesser extent, have also been found in clopidogrel induced TTP. We report a case of clopidogrel associated TTP in a patient that presented with acute stroke, renal failure, and non-ST elevation myocardial infarction.
- Direct oral anticoagulants and antiplatelet agents. Clinical relevance and options for laboratory testing. [JOURNAL ARTICLE]
- Hamostaseologie 2013 Dec 4; 34(1)
Oral anticoagulants and platelet receptor blockers are widely used in clinical practice with the aim of reducing the risk of thrombotic complications in patients with cardiovascular diseases. Their regular intake and adequate antithrombotic action is vital and this is way numerous assays have been developed for laboratory testing and monitoring of these agents. Available assays can be stratified into pharmacokinetic and pharmacodynamic assays. Such assays are increasingly used in clinical routine and their daily use is triggered by the advent of the novel direct oral anticoagulants (DOACs) as an alternative for vitamin K antagonist (VKA) treatment, which are dabigatran, rivaroxaban and apixaban, and by the advent of prasugrel or ticagrelor as an alternative for clopidogrel with regard to platelet P2Y12 receptor inhibition. In this review the most important and most commonly used laboratory assays are summarized as well as their clinical implications with the focus on DOACs as an alternative for VKAs and the different P2Y12 receptor blockers for antiplatelet treatment.
- Review of the accumulated PLATO documentation supports reliable and consistent superiority of ticagrelor over clopidogrel in patients with acute coronary syndrome: Commentary on: DiNicolantonio JJ, Tomek A, Inactivations, deletions, non-adjudications, and downgrades of clinical endpoints on ticagrelor: Serious concerns over the reliability of the PLATO trial, International Journal of Cardiology, 2013. [JOURNAL ARTICLE]
- Int J Cardiol 2013 Nov 13.
- Combined Cardioprotectant and Antithrombotic Actions of Platelet P2Y12 Receptor Antagonists in Acute Coronary Syndrome: Just What the Doctor Ordered. [JOURNAL ARTICLE]
- J Cardiovasc Pharmacol Ther 2013 Dec 2.
Since the P2Y12 receptor antagonists were first introduced, they have been extensively tested in patients with acute coronary syndrome and are now standard of care. These antiplatelet drugs are very effective in reducing subsequent cardiovascular events, stent thromboses, and mortality in patients with acute myocardial infarction undergoing reperfusion therapy. Although the prevailing view is that their benefit derives from their antithrombotic properties, other unrelated pleiotropic effects appear to be equally beneficial. Accumulating clinical and animal evidence indicates that, if present at the time of reperfusion, these drugs have a direct anti-infarct effect similar to that of ischemic postconditioning. Four oral antagonists have been developed in rapid succession: ticlopidine, clopidogrel, prasugrel, and ticagrelor. Each agent had a more consistent and rapid onset of action than the previous one, and this has correlated with improved clinical outcomes when given early in treatment. Unfortunately, gut absorption causes an appreciable delay in the onset of effect, especially when morphine is used, and the constant push to minimize the door-to-balloon time has made it difficult to achieve adequate platelet inhibition at the time of percutaneous coronary intervention with an oral agent. An intravenous P2Y12 antagonist such as cangrelor may optimize treatment because it produces nearly maximal inhibition of platelet aggregation within minutes. If antiplatelet agents do protect through postconditioning's mechanism, then they would render any other intervention that protects through that mechanism redundant. Indeed, animals treated with cangrelor cannot be further protected by pre- or postconditioning. However, interventions that use a different mechanism such as mild hypothermia or cariporide, a Na(+)-H(+) exchange blocker, do add to cangrelor's protection. Future research should be directed toward identifying interventions that can augment the protection from antiplatelet therapy and finding a way to optimize P2Y12 inhibition at reperfusion in all patients.
- Acquired pure red cell aplasia due to treatment with clopidogrel: first case report. [JOURNAL ARTICLE]
- J Thromb Thrombolysis 2013 Dec 3.
A 62-year-old woman with hypertension, type 2 diabetes mellitus, hyperlipemia and coronary heart disease started taking clopidogrel, with no addition of any other new drugs. However, with the addition of the drug, the patient was diagnosed as having acquired pure red cell aplasia (PRCA), and no any other inducing factors were detected from the patient. Furthermore, with the withdrawal of clopidogrel from the treatment, the patient recovered from the PRCA and did not recur. Therefore, we report PRCA as a rare side effect of clopidogrel for the first time.
- Ad hoc percutaneous left atrial appendage closure. [Journal Article]
- J Invasive Cardiol 2013 Dec; 25(12):683-6.
To investigate the feasibility of ad hoc left atrial appendage (LAA) closure in patients in atrial fibrillation.Feasibility of ad hoc LAA closure depends, among other things, on transesophageal echocardiography (TEE) being omittable.Patients underwent ad hoc LAA closure at the same sitting as coronary angiography. TEE guidance or sedation was omitted. Left atrial access was via coexisting patent foramen ovale (PFO) or a transseptal puncture. Arriving in the left atrium, a contrast medium injection was performed, avoiding LAA intubation to exclude thrombus in the LAA. Thereafter, the 13 Fr TorqVue delivery sheath (the largest one available and compatible with all occluders) was advanced into the LAA and the diameter of the landing zone was estimated using the outer diameter of the sheath as a reference. An accordingly selected Amplatzer Cardiac Plug was deployed in the LAA.Median CHA2DS2-VASc score of the 13 included patients (8 males; age 76 years; interquartile range [IQR], 68-84 years) was 5 (IQR, 3-5) and HAS-BLED score was 3 (IQR, 2-4). Contrast medium injection to the left atrium did not reveal a thrombus in the LAA in any patient. The LAA closure procedures were uneventful and follow-up transthoracic echocardiography before discharge confirmed correct device position. Patients were discharged on acetylsalicylic acid and clopidogrel without vitamin-K antagonists.Ad hoc LAA closure using local anesthesia and fluoroscopy alone appears feasible.
- What lies beneath: Posterior ST elevation myocardial infarction with underlying right ventricular-paced rhythm. [JOURNAL ARTICLE]
- Exp Clin Cardiol 2013; 18(1):e55-e56.
A 66-year-old man with a history of coronary artery disease, stage V chronic kidney disease, peripheral arterial disease and a dual-chamber pacemaker experienced persistent chest and shoulder discomfort following his daily hemodialysis treatment. Treatment with clopidogrel had been discontinued three days previously due to impending vascular surgery. Electrocardiography revealed a right ventricular-paced rhythm with ST abnormalities indicative of posterior ST elevation myocardial infarction. The patient underwent urgent cardiac catheterization and required percutaneous coronary intervention for an acutely occluded coronary artery. The present case report emphasizes the importance of careful and timely review of the electrocardiogram of any patient with a ventricular-paced rhythm who experiences signs and symptoms consistent with acute coronary syndrome. Certain characteristic electrocardiographic abnormalities have been demonstrated to predict acute myocardial infarction in such patients.
- No Effect of Clopidogrel Activity or Cessation on Vascular Function or Markers of Inflammation. [JOURNAL ARTICLE]
- Int J Angiol 2012 Dec; 21(4):195-200.
The platelet adenosine diphosphate (ADP)-receptor blocker clopidogrel is effective in reducing the rate of thrombosis in cardiovascular disease, but may also have nonplatelet activity. However, there is variability in the suppression of platelet function in individuals, leading to the concept of clopidogrel resistance, that is, reduced platelet-suppressing activity. We tested the hypothesis that some of the beneficial effect of clopidogrel may be due to the variable activity of this drug on the vascular system (assessed by plasma markers von Willebrand factor and soluble E-selectin, and functional arterial pulse wave velocity) and inflammation (C-reactive protein and interleukin-6) while 32 patients with coronary artery disease taking 75 mg clopidogrel daily, and again 2 weeks after cessation of clopidogrel therapy. Platelet responsiveness to clopidogrel was assessed by the phosphorylation of intracellular regulatory protein-vasodilator-stimulated phosphoprotein method and aggregometry to ADP. Response to aspirin was assessed using arachidonic acid (AA), and soluble P-selectin and PAC-1 were also measured. While on clopidogrel, there were no relationships between any vascular or inflammatory index and the response to clopidogrel. After stopping clopidogrel, there were no differences in platelet aggregation to AA, or the expression of P-selectin or PAC-1 at rest, or after stimulation by AA, but platelet responses to ADP all increased (p < 0.01). Although soluble P-selectin increased when clopidogrel was stopped (p = 0.006), there were no changes in plasma markers or vascular function. We conclude that 75 mg/day clopidogrel has no effect of markers of vascular function or inflammation.
- A Review of the Role of Anticoagulation in the Treatment of Peripheral Arterial Disease. [REVIEW]
- Int J Angiol 2012 Dec; 21(4):187-194.
Peripheral arterial disease (PAD) is a major medical/surgical problem associated with high risk for coronary heart disease (CHD). Anticoagulation plays a significant role in the management of the PAD patient. However, evidence-based medicine supports only select anticoagulants, mainly antiplatelet agents. The available anticoagulant classes, their individual medications, and the mechanisms of action are described. Dextran 40, platelet glycoprotein (GP) IIb/IIIa receptor antagonists, direct thrombin (factor IIa, FIIa) inhibitors, and factor Xa (FXa) inhibitors do not, at this juncture, appear to have a significant role to play in the PAD patient. Aspirin has been used in PAD patients for a few decades, as has warfarin, but the role of warfarin is very limited. An attempt has been made to place each medication and its function in context all the way to the present with oral direct thrombin (FIIa) and FXa inhibitors described. These inhibitors may ultimately play an, as yet, undefined role in PAD. Specific use of anticoagulants in PAD patients is described and aspirin still stands out as a fundamental therapy. The thienopyridines, especially clopidogrel, have their established place and there is some evidence for benefit from the use of clopidogrel in dual therapy with aspirin. Dipyridamole, especially with aspirin as dual therapy, and cilostazol also have their evidence-based niches. The main role played by warfarin is for the patient with a vein graft in the arterial circulation. Heparin retains significant procedural importance. For now, Class I, Level of Evidence A center around aspirin for the PAD patient with clopidogrel, an alternative agent.
- Antiplatelet and anticoagulation therapy in acute cerebral infarction. [Journal Article]
- Rinsho Shinkeigaku 2013; 53(11):1172-4.
Effective treatments have recently been developed for acute cerebral infarction based on the pathophysiology.In atherothrombosis, artery-to-artery thrombosis plays a pivotal role in artery territory infarction and even in watershed infarction. In the latter, hemodynamic insufficiency is thought to prompt microembolism from the plaque in the area of borderzone of pial arteries. To suppress development of platelet thrombus on the ruptured plaque, strong antiplatelet therapy is required until the plaque stabilizes. Clinically dual antiplatelet therapy (DAPT) was reported to be more effective than mono therapy in suppressing microembolic signal in the middle cerebral artery. In addition, recent CHANCE trial reported that DAPT with aspirin and clopidogrel for the first 21 days is more effective in suppressing stroke recurrence than aspirin alone. Risk of cerebral hemorrhage was not enhanced in the DAPT group. Short term DAPT in the acute phase may soon be a standard treatment for acute atherothrombosis.For prevention of cardioembolism in patients with atrial fibrillation, new oral anticoagulants (NOAC) have recently been introduced. In cases where risk of hemorrhagic transformation is minimal, immediate anticoagulation with NOAC may provide clinical benefit including prompt anticoagulant effect, no need for drug dosing, and low risk of intracerebral hemorrhage.