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These data suggest that SFA SI-PTA can be successfully used for limb salvage with minimal morbidity and mortality in a group of patients with severe lower extremity occlusive vascular disease.
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Recently the phenomenon of aspirin resistance has been object of several studies, but no data are available on the possible role of the haemorheologic parameters in affecting platelet function and resistance to antiplatelet agents. Aim of our study was to evaluate platelet function and haemorheology in patients with acute coronary syndromes (ACS), receiving double antiplatelet therapy with aspirin and clopidogrel. The study population included 301 (231M/70F; age: 66 +/- 13 yrs) consecutive adult patients admitted to the Coronary Care Unit of the Azienda Ospedaliero-Universitaria Careggi, with diagnosis of acute myocardial infarction or unstable angina. We assessed: whole blood viscosity (WBV) at shear rates of 0.512 s(-1) and 94.5 s(-1), plasma viscosity (PLV) at 94.5 s(-1) shear rate, erythrocyte deformability index (DI) and PFA-100 closure times with ADP (PFA/ADP) and epinephrine (PFA/EPI). We considered any PFA-100-EPI result < 203 sec (95th percentile of control distribution) to be indicative of aspirin resistance. 104/301 patients (34.5%) had PFA/EPI CTs in the reference range (group 1) whereas the remaining had values higher than 203 sec (group 2). WBV at 94.5 sec (-1) s.r. was similar in group 1 and 2 (WBV: 4.43 +/- 0.25 vs 4.45 +/- 0.61 mPa.sec, respectively). PLV and WBV at 0.512 sec (-1) s.r. were slightly higher, but not significantly, in group 1 than in group 2 (PLV: 1.47+/-0.13 vs 1.44 +/- 0.15 mPa.sec; p = 0.08 and WBV: 23.37 +/- 4.6 vs 22.54 +/- 3.90 mPa.sec; p = 0.07). DI was significantly lower in group 1 with respect to group 2 (4.05 +/- 2.93 vs 5.71 +/- 3.30, p < 0.0001). White blood count (WBC) was significantly higher in group 1 than in group 2 (11464 +/- 3504 vs 7867 +/- 2162, p < 0.0001). In conclusion, these results demonstrate that in patients with acute coronary syndromes the antiaggregant effect of aspirin is modulated not only by the direct action on platelets, but also by erythrocyte deformability and white blood cell count.
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We report the case of a 55-year-old man who underwent coronary angiography in 2004 for early angina following anterior ST-elevation myocardial infarction. Angiography disclosed a critical stenosis in the proximal left anterior descending artery and significant stenoses in the right coronary artery and first obtuse marginal branch, treated with two paclitaxel-eluting stents and a sirolimus-eluting stent, respectively. After completion of a six-month thienopyridine course and while still being on lifelong aspirin, in 2007 he was readmitted for lateral ST-elevation myocardial infarction: angiography revealed stent thrombosis beginning at the proximal edge of the sirolimus-eluting stent implanted in the first obtuse marginal branch. Intravascular ultrasound was performed after thrombectomy but before balloon dilation showing suboptimal stent expansion and a thrombus partially adhering to the sirolimus-eluting stent. The procedure was then successfully completed with the implantation of another sirolimus-eluting stent. This clinical vignette suggests that suboptimal drug-eluting stent deployment may be associated with stent thrombosis well after the traditional time frame of subacute thrombosis.
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Altogether, 10 RCT's and 1 retrospective study with a total number of 26,658 STEMI patients were included. Random-effects model with Mantel-Heanszel weighting was used to pool outcomes into a meta-analysis. Therapy with clopidogrel was associated with 2.76% 30-day STEMI mortality which was similar to that of ticagrelor (2.6%; OR=0.9395 [CI=0.76 to 1.17; p=0.58]), and for bivalirudin (2.8%; OR=1.02 [CI=0.82 to 1.27; p=0.86]), but was slightly higher for heparin (3.0%; OR=1.08 [CI=0.86 to 1.35; p=0.52]). There was a trend towards lower mortality after tirofiban (2.1%; OR=0.77 [CI=0.52 to 1.13; p=0.20]), and cangrelor (1.7%; OR=0.59 [CI=0.29 to 1.20; p=0.19]), although the sample size for both agents was woefully small. The only agent which offers a significant 30-day mortality benefit in STEMI was prasugrel with significant lowest 1.75% death rate (OR=0.63 [CI=0.46 to 0.86; p=0.03]).
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One hundred and eighty-eight of the 2697 questionnaires were returned (response rate: 7 %). The respiratory physicians declared that they performed an average of 8 pleural procedures per month. One hundred and seventy-five responders (95 %) practised pleural procedures in patients receiving platelet aggregation inhibitors; 68 of them (39 %) reported experiencing haemorrhagic complications. The bleeding risk associated with thoracentesis and chest tube insertion was considered minor by 97.8 and 65 % of responders respectively, whereas it was considered major for blind pleural biopsies by 73.4 %. Respiratory physicians were more reticent about performing pleural procedures in patients treated with clopidogrel than in those taking aspirin.
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Paradoxical embolism (EP) occurs when a venous thrombus passes into the arterial circulation, most commonly through an intracardiac shunt. A patent foramen ovale (FOP) is present in 25-35%of people at all ages. It is now possible to detect FOP by contrast echocardiography and it has been shown that there exists quite frequently a spontaneous transient right-to-left shunt during systole and, moreover, a right-to-left shunt during Valsalva maneuver and coughing. Acute or chronic pulmonary hypertension are also causes of shunt. This phenomenon has been associated with catastrophic outcomes such as stroke, visceral infarction and ischemic limb. We report the case of a 31-year old man with multiple paradoxical thromboemboli into his right kidney, spleen, small bowel and left brachial artery. Paradoxical embolism was suspected and confirmed by transoesophageal contrast echocardiography, disclosing FOP with right-to-left shunt. Successful percutaneous closure of patent foramen ovale with Amplatzer(R) PFO occluder 18 mm allowed subsequent oral antiaggregation with acetilsalicilic acid 150 mg/day and clopidogrel 75 mg/day. A new case gives the opportunity to review mechanisms, diagnosis and therapeutic issues. Treatment strategies for FOP in recurrent PE include antiplatelet agents, anticoagulants, surgical closure, or percutaneous closure devices. The completion of ongoing, randomized clinical trials comparing percutaneous closure devices with medical management is urgently needed to clarify if the risks of invasive endovascular device placement are outweighed by a long-term reduction in recurrent vascular events.
A literature search was conducted in MEDLINE from 1966 to July 2010 using the MESH terms and key words AZD6140, ticagrelor, P2Y12 receptor antagonist. The search was limited to studies in English language with human subjects.
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Although there was an association between the CYP2C19 genotype and clopidogrel responsiveness, overall there was no significant association of genotype with cardiovascular events.
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It has been hypothesized that persistent presence of polymer may compromise the safety of drug-eluting stents, and that therefore biodegradable polymer coatings might reduce late adverse events.
The cysts may potentially affect any organ; adrenals cysts are rare. This is a review of the literature regarding adrenal cysts, focusing on children and young adults.
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Hospital-acquired gastrointestinal bleeding is uncommon in non-critically ill patients. Anticoagulation appears to be the most important risk factor for nosocomial GIB. Routine use of acid suppressant medications for prophylaxis is unnecessary in most hospitalized patients.
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At 30 days, 115 (6.5%) individuals assigned prasugrel had met the primary endpoint compared with 166 (9.5%) allocated clopidogrel (hazard ratio 0.68 [95% CI 0.54-0.87]; p=0.0017). This effect continued to 15 months (174 [10.0%] vs 216 [12.4%]; 0.79 [0.65-0.97]; p=0.0221). The key secondary endpoint of cardiovascular death, myocardial infarction, or urgent target vessel revascularisation was also significantly reduced with prasugrel at 30 days (0.75 [0.59-0.96]; p=0.0205) and 15 months (0.79 [0.65-0.97]; p=0.0250), as was stent thrombosis. Treatments did not differ with respect to thrombolysis in myocardial infarction (TIMI) major bleeding unrelated to coronary-artery bypass graft (CABG) surgery at 30 days (p=0.3359) and 15 months (p=0.6451). TIMI life-threatening bleeding and TIMI major or minor bleeding were also similar with the two treatments, and only TIMI major bleeding after CABG surgery was significantly increased with prasugrel (p=0.0033).
Through survival analysis, there was no statistical difference in the effect of the 4 interventions on the variation of carotid stenosis rates or ischemic cerebrovascular events (P > 0.05). The occurrence of ischemic cerebrovascular events could be postponed by about 4 months in those treated with platelet antagonists + CDABCRBS and platelet antagonists + atorvastatin +CDABCRBS. By multivariate Logistic analysis, age, hypertension, and clopidogrel were associated with stenosis of extracranial carotid arteries (P <0.05). Age, diabetes, aspirin, clopidogrel, CDABCRBS were correlated with cerebrovascular accidents (P < 0.05).
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We included patients admitted for ACS or elective percutaneous coronary intervention (PCI) and discharged with ASA (acetylsalicylic acid; 100-160 mg) and clopidogrel (75 mg) or ticagrelor (90 mg twice a day). Chemistry was assessed at admission (baseline) and after a 30-90-day period of DAPT (together with platelet reactivity). The absolute and percentage variations of SUA after DAPT introduction were considered. Multiple-electrode aggregometry was used to assess platelet function. A total of 378 patients were enrolled, with 145 treated with aspirin and clopidogrel (AC) and 233 with aspirin and ticagrelor (AT). The AC patients were older (p = 0.003) and more often showed elective PCI as an indication to DAPT (<0.001); they received chronic therapy with ARB (angiotensin II receptor blocker; p = 0.001), nitrates (p = 0.044), CCB (calcium channel blocker; p = 0.005) and diuretics (p = 0.044). The AT patients displayed a higher percentage of ACS diagnosis (p < 0.001) and received chronic therapy with ACE (angiotensin-converting enzyme) inhibitors (p = 0.001), beta blockers (p = 0.001) and statins (p = 0.013). The AC patients displayed higher platelet reactivity at COL (collagen) test, ASPI test and ADP (adenosine diphosphate) test (p = 0.03, 0.001 and <0.001, respectively) and a higher percentage of HRPR (high residual platelet reactivity) in the ADP test (p = 0.001). No difference was found in the baseline uric acid and creatinine levels between AC and AT patients. At 30-90 days, a significant absolute and percentage increase in the SUA levels was found in AT as compared to AC patients (0.204 mg/dl vs. -0.165 mg/dl, p = 0.034; 6.26% vs. -0.005%, p = 0.018, respectively). Results were not influenced by variations in renal function. At multivariate analysis, in fact, ticagrelor therapy emerged as an independent predictor of increase in the uric acid levels (odds ratio (OR; 95% confidence interval (CI)) = 2.79 (1.66-4.67), p < 0.001). However, the variation in the SUA levels did not affect platelet reactivity or HRPR in both AC and AT patients.
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The aim of this study was to investigate the incidence of bleeding after dental extraction without stopping antiplatelet therapy. Postoperative bleeding was assessed in a total of 1271 patients who were divided into two groups: a study group comprising 183 patients on antiplatelet therapy (aspirin 125 patients/185 occasions; clopidogrel 42 patients/65 occasions; dual therapy 16 patients/24 occasions) who underwent 548 dental extractions on 274 occasions, and a control group comprising 1088 patients who were not receiving any antiplatelet or anticoagulant therapy and underwent 2487 dental extractions on 1472 occasions. The incidence of postoperative bleeding was higher in the study group (5/274, 1.8%) than in the control group (10/1472, 0.7%), and also in the dual antiplatelet subgroup (1/24, 4.2%) than in the single antiplatelet subgroups (clopidogrel: 2/65, 3.1%; aspirin: 2/185, 1.1%); however, these differences were not significant. Postoperative bleeding was managed successfully by repacking with Gelfoam impregnated with tranexamic acid powder in 12 patients and by resuturing in three of the control patients undergoing extraction of impacted teeth with flap elevation. These findings indicate that there is no need to interrupt antiplatelet drugs before dental extraction.
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At baseline, the incidence of aspirin resistance, defined as aspirin reaction unit (ARU) ≥ 550, was 9.2%, that of clopidogrel resistance, defined as P2Y12 reaction unit (PRU) ≥ 230, was 46.5%, and that of percent inhibition of PRU < 20% was 32.4%. At follow-up, the incidence of resistance by ARU value was 7.0%, 50.0% by PRU value, and 35.9% by percentage inhibition of PRU, respectively. The mean values of ARU (431.5 ± 63.6 vs. 439.8 ± 55.2; p = 0.216) and PRU (227.5 ± 71.4 vs. 223.3 ± 76.0; p = 0.350) were not significantly different before versus after antiplatelet-combination single-pill therapy. Five adverse events (3.5%) were observed during the study period.
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Underlying diseases were hypertension in 75%, hyperlipidemia in 78% and DM in 60% (15% on insulin), and 14% of the subjects received HD. Eighty-three percent of the patients had orally taken Statin, 85% ACE/ARB and 68% had beta blockers. Mean length and diameter of PES were 21.6 ± 7.2 mm and 2.9 ± 0.3 mm, respectively. Target lesion revascularization (TLR) rate 6 months after PES placement was 14.6% overall. In HD patients TLR was 43%, hypertension 15.0%, hyperlipemia 12.4%, DM with oral medication 12.5%, DM with insulin 12.0%, respectively. In multivariate analysis, HD was an independent risk factor for TLR (p=0.0001, OR: 6.61, 95% C.I.: 2.34-18.6).
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A 10-part questionnaire relating to pre- and postoperative clopidogrel use was mailed to all UK urology consultants listed in the British Association of Urological Surgeons' directory.
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In patients with ACS, the CYP2C19 LOF allele was associated with post-procedure HTPR and a subsequently increased risk of adverse clinical events at one-year follow-up following DES implantation and clopidogrel administration.
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A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was whether early administration of aspirin might optimize vein graft patency. More than 250 papers were found using the reported search, of which 4 new papers in addition to the previous 7 represented the best evidence to answer the clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and results of these papers are tabulated. Early postoperative aspirin administered within 6 h following coronary artery bypass grafting (CABG) has been shown to be optimal for prevention of vein graft occlusion. Early aspirin has significant benefit in reducing vein graft occlusion, mortality, myocardial infarction, stroke, renal failure and bowel infarction. The efficacy of early postoperative aspirin on vein graft patency diminishes the later it is administered. It has optimal benefit at 6 h, some benefit at 24 h and no benefit after 48 h post CABG. ACC/AHA, EACTS and ACCP have issued guidelines recommending administration of early aspirin or an alternative (clopidogrel, ticlopidine and indobufen) at 6 h or soon after bleeding has settled as the standard of care for optimization of vein graft patency. The ACCP guideline has also suggested that optimal prevention of cardiovascular complication should have higher value than prevention of postoperative bleeding. Several randomized, controlled studies, including a meta-analysis, have shown that early administration of aspirin following CABG is not associated with increased blood loss or transfusion requirement. Postoperative bleeding has been identified as a significant reason for non administration of early aspirin in a prospective study. It is essential to define/quantify the postoperative blood loss that precludes administration of early aspirin. This will enhance prompt administration in some cases and guide judgement, especially in patients with high-risk factors for vein graft thrombosis. Administration at 6 h is the optimal time to give aspirin as long as bleeding has settled.
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This modified method showed that when 12.5 microL CaCl2 (0.2 mmol/L) was added to the reaction system, MAT was appropriate (93 +/- 23 seconds). The CVs for the modified impedance assay and release assay were 9.31% and 6.13%, respectively. The mean VASP-PRI in the patient group treated with clopidogrel was significantly lower than that in the control group without antiplatelet therapy (54.88 +/- 16.81% vs. 79.86 +/- 10.24%, p < 0.001). MAT of the modified method in VASP PRI > 50% group were shorter than that in the PRI < 50% group [185 (154-241) vs. 214 (184-250), p < 0.051. Meanwhile, the RV of the modified method in VASP PRI > 50% group were higher than that in the PRI < 50% group [1.00 (0.72-1.47) vs. 0.82 (0.62-1.08), p < 0.051. However, the electrical resistance (omega) and RV of the original method showed no differences between the two groups [0 (0-2) vs. 0 (0-1.25), 0.05 (0-0.25) vs. 0.08 (0-0.24); p > 0.05, p > 0.05, respectively). Moreover, neither the original method nor the modified method showed differences in patients with CYP2C19 (*2 and *3) wild type and mutant type.
Our study provides evidence for a beneficial effect of a loading dose of 600mg of clopidogrel compared to the usual 300 mg in terms of platelet reactivity and platelet activation post treatment.