Mg Of Aspirin Research Articles

Thrombosis Prevention After Total Hip Arthroplasty

Thromboembolic disease is a common complication of total hip arthroplasty. The purpose of this study was to compare a new mobile compression device with low-molecular-weight heparin with regard to their safety and effectiveness for the prevention of venous thromboembolic disease. Patients who had a total hip arthroplasty were randomized to receive prophylaxis with a mobile compression device or low-molecular-weight heparin for ten days. Use of the compression device began intraoperatively, and the patients in this group could receive 81 mg of aspirin daily after the surgery. The first injection of the low-molecular-weight heparin began between twelve and twenty-four hours after the surgery. After ten to twelve days, all patients underwent bilateral lower-extremity duplex ultrasonography to screen for deep venous thrombi in the calf and thigh. Any clinical symptoms of pulmonary embolism were evaluated with spiral computed tomography lung scans. Bleeding events and utilization of (i.e., compliance with) prophylactic treatment in both groups were documented. Clinical evaluation to look for evidence of deep venous thrombi and pulmonary emboli was performed at twelve weeks postoperatively. Four hundred and ten patients (414 hips) were randomized; 392 of these patients (395 of the hips) were evaluable with regard to the safety of the intervention and 386 patients (389 hips) were evaluable with regard to its efficacy. Demographics were similar clinically between the groups. The rate of major bleeding events was 0% in the compression group and 6% in the low-molecular-weight heparin group. The rates of distal and proximal deep venous thrombosis were 3% and 2%, respectively, in the compression group compared with 3% and 1% in the heparin group. The rates of pulmonary embolism were 1% in the compression group and 1% in the heparin group, and there were no fatal pulmonary emboli. Within the twelve-week follow-up period, two events (one deep venous thrombosis and one pulmonary embolus) occurred in one patient in the compression group following negative findings on duplex ultrasonography on the twelfth postoperative day. There was no difference between the groups with regard to the prevalence of venous thromboembolism. When compared with low-molecular-weight heparin, use of the mobile compression device for prophylaxis against venous thromboembolic events following total hip arthroplasty resulted in a significant decrease in major bleeding events.

Platelet aspirin resistance in ED patients with suspected acute coronary syndrome

Background Platelet aspirin resistance is reported to be as high as 45%. The prevalence of emergency department (ED) platelet aspirin resistance in suspected acute coronary syndrome (ACS) is not described. Our purpose was to determine the prevalence of platelet aspirin resistance. Methods We determined platelet aspirin resistance in a convenience sample of ED suspected ACS patients. Eligible patients had longer than 10 minutes of chest pain or an ischemic equivalent. Two hours after receiving 325 mg of aspirin, blood was assessed for platelet function (Accumetrics, San Diego, CA). Definitions are as follows: aspirin resistance, at least 550 aspirin reaction units; positive troponin T, greater than 0.1 ng/mL; significant coronary lesion, at least 70% stenosis. The composite end point was prospectively defined as a 30-day revisit, positive cardiac catheterization, or hospital length of stay (LOS) longer than 3 days. Results Of 200 patients, 50.5% were male, 50.0% were black, troponin T was positive in 7.5%, cardiac catheterization was done in 10.5%, and 33.3% had a significant stenosis. Final diagnoses were noncardiac in 83.4%, stable angina in 8.0%, and unstable angina in 8.5%. Overall, 6.5% were resistant to aspirin; and high-risk patients trended to more aspirin resistance than non–high-risk patients (23.1% [3] vs 9.1% [17]; P value 95% confidence interval [CI], −0.0929 to 0.373). One-month follow-up found ED revisits in 12.5% of aspirin-resistant vs 4.9% of non–aspirin-resistant patients (95% CI, −0.114 to 0.182) and rehospitalization in 12.5% of resistant patients vs 4.3% of nonresistant patients ( P value 95% CI, −0.108 to 0.187). Although LOS was similar at index admission, if rehospitalized, LOS was 6.5 for aspirin-resistant patients vs 3.2 days in nonresistant patients ( P < .0001). Conclusion This first report of platelet aspirin resistance in patients presenting to the ED with suggested ACS finds that it is present in 6.5% of patients.

Repeated Successful Thrombolysis of a Jarvik 2000 Left Ventricular Assist Device in a Patient With Noncompaction Cardiomyopathy

28-year-old white man with history of end-stage heart failure caused by isolated left ventricular (LV) noncompaction cardiomyopathy had been implanted with the Jarvik 2000 LV assist device 3 years previously as a bridge to survival and to decision via a left posterolateral thoracotomy, off-pump, with outflow graft anastomosis to the descending aorta and postauricular pedestal. The patient had an excellent postoperative course free of adverse events for 1.5 years. The pump was operated at a rotational speed of 9000 rounds per minute. Anticoagulation included acenocoumarol aiming for an international normalized ratio of 3 to 3.5 and 100 mg of aspirin daily. On the 20th month of support, the patient presented with symptoms and signs of cardiogenic shock associated with a sudden increase in power consumption by the …

Effects of tirofiban and percutaneous coronary intervention in an old patient with acute myocardial infarction and cardiogenic shock

A 75 year old man presented in our institutition with acute inferoposterior and right ventricular ST-segment elevation myocardial infarction and cardiogenic shock, 40 minutes after the pain onset. He was pretreated with 300 mg of aspirin, 600 mg of clopidogrel, and was taken to the catheterization laboratory. Door to needle time was 35 minutes. Primary percutaneous coronary intervention with bare-metal stent implantation first in infarct related right coronary artery, with subsequent high-bolus dose (25 microg/kg) tirofiban, and then in suboccluded RCx were done. The procedures were done during the cardio-pulmo-cerebral reanimation because of relapsing ventricular fibrillation, with final TIMI 3 coronary flow established. Subsequently, intraaortic balloon pump was inserted Echocardiography taken on the second day showed globaly hypokinetic left ventricle, with 10% ejection fraction and competent valves. During the next three weeks of hospital follow-up, there were no major adverse cardiac events, a transient azotemia and fall in hemoglobin concentration without major bleeding, and no episodes of severe thrombocytopenia were recorded. After six months, the patient was without chest pains, 2/3 class according to the New York Heart Association, without major adverse events, and echocardiographic left ventricular ejection fraction increment for 30%.

Very Late Bare Metal Stent Thrombosis Presenting with Acute Myocardial Infarction: 14 Years after Coronary Stenting

Fourteen years previously, a 67-year-old man underwent percutaneous coronary intervention (PCI) for proximal left anterior descending artery lesion with a bare metal stent (BMS) for acute myocardial infarction (AMI) and attained an excellent result. Ticlopidine (200 mg) was administered for one month and 100 mg of aspirin was daily has been continued. One year after PCI, coronary angiography showed no restenosis. However, 14 years after PCI, he suffered from AMI due to stent thrombosis. Intracoronary aspiration thrombectomy and implantation of a drug-eluting stent were successful. This report demonstrates evidence of a very late case of stent thrombosis with the use of BMS.

This Month in Gastroenterology

This Month in Gastroenterology

Time-Dependent Effects of Low-Dose Aspirin on Plasma Renin Activity, Aldosterone, Cortisol, and Catecholamines

Studies have shown that aspirin may decrease blood pressure when given at bedtime but not when administered on awakening. However, until now, a biologically plausible mechanism of this striking phenomenon was not revealed. We investigated the effect of 100 mg of aspirin administered at bedtime compared with administration on awakening on plasma renin activity and aldosterone levels over 24 hours and excretion of cortisol and catecholamines in 24-hour urine samples. A randomized, placebo-controlled, double-blind, crossover trial was performed in 16 grade 1 hypertensive subjects. During 2 periods of 2 weeks separated by a 4-week washout period, participants used aspirin both at morning and at night, which was blinded with placebo. After both periods, subjects were admitted for 24 hours to measure the aforementioned parameters. Aspirin intake at bedtime compared with on awakening reduced average (24-hour) plasma renin activity by 0.08 microg/L per hour (95% CI: 0.03 to 0.13 microg/L per hour; P=0.003) without affecting aldosterone levels (95% CI: -0.01 to 0.01 nmol/L; P=0.93). Cortisol excretion in 24-hour urine was 52 nmol/24 hours (95% CI: 5 to 99 nmol/24 hours; P=0.05) lower, and dopamine and norepinephrine excretions were 0.25 micromol/24 hours (95% CI: 0.01 to 0.48 micromol/24 hours; P=0.04) and 0.22 micromol/24 hours (95% CI: -0.03 to 0.46 micromol/24 hours; P=0.02) lower in patients treated with bedtime aspirin. In conclusion, aspirin taken at bedtime compared with on awakening significantly diminished 24-hour plasma renin activity and excretion of cortisol, dopamine, and norepinephrine in 24-hour urine. Decreased activity of these pressor systems forms a biologically plausible explanation for the finding that aspirin at night may reduce blood pressure, whereas aspirin at morning does not.

Antiplatelet Treatment in Ischemic Stroke Treatment

Antiplatelets represent a diverse group of agents that share the ability to reduce platelet activity through a variety of mechanisms. Antithrombotic agents are effective in the secondary prevention of ischemic strokes. Most strokes are caused by a sudden blockage of an artery in the brain (called an ischaemic stroke) that is usually due to a blood clot. Immediate treatment with antiplatelet drugs such as aspirin may prevent new clots from forming and hence improve recovery after stroke. Several studies have evaluated the role of one antiplatelet agent, aspirin, in reducing stroke severity. The International Stroke Trial (IST) of 20,000 patients with acute stroke from other countries. In this study there was a significant 14% proportional reduction in mortality during the scheduled treatment period (343 [3.3%] deaths among aspirin-allocated patients vs 398 [3.9%] deaths among placebo-allocated patients; 2p = 0.04). There were significantly fewer recurrent ischaemic strokes in the aspirin-allocated than in the placebo-allocated group (167 [1.6%] vs 215 [2.1%]; 2p = 0.01) but slightly more haemorrhagic strokes (115 [1.1%] vs 93 [0.9%]. Few studies examined the role of ticlopidin in acute stroke setting the results showed treatment with ticlopidine improved the neurologic outcome. In the Examining the Safety of Loading of Aspirin and Clopidogrel in Acute Ischemic Stroke and TIA (LOAD) study, 40 consecutive ischemic stroke patients were treated with 325 mg of aspirin and 375 mg of clopidogrel within 36 hours of symptom onset. Overall, 37.5% (n = 15) of the patients had an improvement of 2 or more points on the NIHSS 24 hours after antiplatelet administration. The antiplatelet efficacy of aspirin in preventing secondary stroke was established by three studies conducted in the late 1980s and early 1990s: the Swedish Aspirin Low-dose Trial (SALT) trials have demonstrated that aspirin-even in doses as low as 30 mg/day-reduces secondary stroke, MI, or vascular death in patients with. Clopidogrel and aspirin have been used in combination in patients with diverse arterial vascular diseases However, combinations of antithrombotic agents do not necessarily improve clinical efficacy and are typically associated with increased toxicity.

Hereditary thrombophilia and recurrence of ischemic placental disease

We sought to evaluate whether testing for hereditary thrombophilia alone or in combination with second-trimester uterine artery Doppler (UAD) is useful in predicting recurrent complications in patients with previous preeclampsia, placental abruption, or stillbirth. Between 2001 and 2005, 110 consecutive women were included in the study and received 100 mg of aspirin daily. Adjustment was made for several maternal confounding factors using a logistic regression model. After multivariable logistic regression analyses, only abnormal UAD assessment was significantly associated with recurrent complications (odds ratio, 11.2; 95% confidence interval, 3.8-32.6) Combining the results of UAD and the presence of laboratory markers of thrombophilia failed to improve the accuracy of UAD to predict recurrent complications. Hereditary thrombophilia testing is not useful in predicting recurrent complications in subsequent pregnancy.

The Effect of Combined Clopidogrel and Aspirin Therapy after Off-Pump Coronary Surgery

: The purpose of this randomized study was to evaluate the effect on graft patency by adding clopidogrel to aspirin in off-pump coronary artery bypass (OPCAB) grafting and the possible side effects of such therapy. : Twenty patients who underwent standard OPCAB through median sternotomy were randomized immediately after surgery in two groups. Patients in group A (n = 10) received 100 mg of aspirin starting preoperatively, continuing indefinitely. Patients in group B received 100 mg of aspirin and, in addition, 75 mg of clopidogrel starting immediately after the operation and for 3 months. Postoperative bleeding and other perioperative parameters were compared. Angiography was repeated 3 months after surgery to determine the patency and quality of grafts. : Preoperative risk factors were similar in the two groups. There was no significant difference in average number of distal anastomosis (P = 0.572), operation time (P = 0.686), postoperative bleeding (P = 0.256), ventilation time (P = 0.635), and intensive care unit stay (P = 0.065). Length of stay was shorter in group B (P = 0.024). There was no postoperative complication in either groups. Eight of 27 grafts in group A and 2 of 29 grafts in group B (P = 0.037) were occluded at the time of control angiography. : Early administration of a combined regimen of clopidogrel and aspirin after OPCAB grafting is not associated with increased postoperative bleeding or other major complications. Despite the small number of patients in this study and small number of examined grafts, the results suggest that the addition of clopidogrel may increase graft patency after OPCAB grafting.

Ocular blood flow levels and visual prognosis in a patient with nonischemic type central retinal vein occlusion

We look at the case of a 39-year-old female patient suffering from a sudden decrease in her left visual acuity (0.08). Her macular edema was examined using optical coherence tomography, and her optic disc blood flow was examined with laser speckle flowgraphy (LSFG). Additionally, the degree of seriousness of the central vein occlusion was evaluated through fluorescein angiography (FA). Ocular fundus findings revealed central vein occlusion associated with macular edema, and FA determined her disease type as a nonischemic-central vein occlusion. Daily doses of 100 mg of aspirin were administered orally to the patient. Upon administration, her ocular blood flow almost immediately increased. In this study, we demonstrate the potential of LSFG as a means to investigate ocular blood flow.

Successful Retrial of ECT Two Months After ECT-Induced Takotsubo Cardiomyopathy

heart failure; however, recovery of cardiac function is often complete within the first week following the insult. Cardiac enzymes may be mildly elevated, but on cardiac catheterization there is usually no evidence of coronary artery disease, or only "mild luminal irregularities" may be noted (7). Contraction band necrosis may be seen on biopsy in the more serious cases. The cause of takotsubo cardiomyopathy is unknown, but several mechanisms have been suggested, including ischemia from coronary artery spasm, microvascular spasm, and direct myocyte injury (5).

Two-Year Clinical, Angiographic, and Intravascular Ultrasound Follow-Up of the XIENCE V Everolimus-Eluting Stent in the Treatment of Patients With De Novo Native Coronary Artery Lesions: The SPIRIT II Trial

Two-Year Clinical, Angiographic, and Intravascular Ultrasound Follow-Up of the XIENCE V Everolimus-Eluting Stent in the Treatment of Patients With De Novo Native Coronary Artery Lesions: The SPIRIT II Trial

“Intracoronary Whirling Current Phenomenon” and Thrombus Formation After Sirolimus-Eluting Stent Implantation Visualized by Optical Coherence Tomography

We present a case of imaged “intracoronary whirling current phenomenon.” A 60-year-old Japanese man was treated with 2 sirolimus-eluting stents (SES; 3.0×18 and 3.5×33 mm) in the right coronary artery (RCA) for chronic total occlusion in October 2007. After percutaneous coronary intervention, he was taking 200 mg of aspirin and 200 mg of ticlopidine. However, he had recurrent transient ischemic chest pain beginning at 7 months. A second coronary angiography at 8 months after SES implantation showed reocclusion at a site just proximal to the SES. A repeat percutaneous coronary intervention was performed for RCA chronic total occlusion (Figure 1). After crossing the guide wire to the distal portion of the RCA, the target lesion was dilated using a 1.25×10 mm balloon catheter. After minimum balloon dilatation, optical coherence tomography (OCT) was performed to evaluate in-stent reocclusion from the distal portion to the proximal portion (Figure 2). Two different types of tissue coverage (may be consistent with thrombus formations of different ages) were observed in the stent reocclusion.1 Moreover, in the patent distal portion of the RCA, an intracoronary whirling current …

The preventive factors for aspirin-induced peptic ulcer: aspirin ulcer and corpus atrophy

Interleukin-1beta (IL-1beta) polymorphisms are associated with peptic ulcer and atrophic gastritis. This study aimed to examine effects of corpus atrophy and the genotypes of genes related to peptic ulcer, including IL-1beta, on risk of aspirin ulcer. 232 patients taking 100 mg of aspirin for cardiovascular diseases, of whom 40 had peptic ulcer, were enrolled. IL1beta, interleukin-1 receptor antagonist (IL-1RN), tumor necrosis factor (TNF)-alpha, cyclooxygenase (COX)-1, cytochrome p450 2C9 (CYP2C9), UDP-glucuronosyltransferase (UGT1A6) genotypes were determined, and serum pepsinogen levels were measured. The polymorphisms of IL-1beta-511/-31 were significantly associated with peptic ulcer, but other genotypes were not. Serum pepsinogen I and II levels and I/II ratio were significantly higher in the ulcer group than in the non-ulcer group. Taking PPI [adjusted odds ratio (OR), 0.09; 95% confidence interval (CI), 0.02-0.39], pepsinogen I of less than 50 ng/ml (OR, 0.24; 95% CI, 0.10-0.56) and IL-1beta-511 T carrier (OR, 0.42; 95% CI, 0.18-0.93) were significantly associated with peptic ulcer. Hypoacidity related to corpus atrophy as well as taking PPI seems to be preventively associated with development of peptic ulcer among low dose aspirin users.

Influence of platelet reactivity and response to clopidogrel on myocardial damage following percutaneous coronary intervention in patients with non-st-segment elevation acute coronary syndrome

Introduction A wide variability in the response to clopidogrel and magnitude of post-treatment platelet reactivity has been described. However, this has been demonstrated by light transmittance aggregometry, a method too laborious for daily practice. Point-of-care devices may overcome this limitation, but little is known on the predictive value of such measurements. Our objective was to determine the relationship between platelet reactivity and the incidence of myocardial damage following percutaneous coronary intervention (PCI) in patients with Non-ST-segment Elevation Acute Coronary Syndrome (NSTEACS). Materials and Methods This prospective study included 93 patients with NSTEACS and PCI. All patients received a loading dose of 300 mg of clopidogrel and 250 mg of aspirin. Myocardial damage was defined as any elevation above upper limit of normal or previous levels of troponin T, assessed every 6 h for at least 24 h following PCI. Platelet reactivity not related to clopidogrel (BASE reactivity), related to P2Y12 inhibition (P2Y12 reactivity) and inhibition of platelet aggregation (IPA) were assessed immediately pre-PCI with the VerifyNow® device. Results Myocardial damage was detected in 60 patients (64.5%). Higher BASE reactivity was associated with myocardial damage (287.8 ± 62.6 vs. 260 ± 55.9 units, p = 0.043) while a trend was found for P2Y12 reactivity (173.4 ± 70.3 vs. 149.2 ± 58.4 units, p = 0.109). No relationship was detected for IPA. Multivariate logistic regression analysis confirmed that BASE reactivity (p = 0.04) and P2Y12 reactivity (p = 0.03) were independent predictors of myocardial damage. Conclusions Platelet reactivity before PCI appears to be better predictor of myocardial damage than does response to clopidogrel.

T1069 Effect of Low-Dose Administration of Lansoprazole On the Gastric Mucosal Lesions Induced By Low-Dose Aspirin in Relation to Intragastric pH in Healthy Volunteers with Different CYP2C19 Genotypes

Backgrounds and Aims: Given the major role gastric acid plays in the development of aspirininduced gastric mucosal lesions, proton pump inhibitors (PPIs) are now employed as firstline therapy in treating aspirin-related gastrointestinal disorders. Low-dose PPIs are also expected to have a similar preventive effect on aspirin-induced gastric injury. PPIs are metabolized by CYP2C19 in the liver, and their therapeutic effects are influenced by CYP2C19 genotype status. However, the effect of low-dose PPI on aspirin-induced gastric mucosal injury in relation to gastric acidity in humans has not been examined. Here, we investigated the relationship between intragastric pH and aspirin-induced gastric mucosal lesions with regard to CYP2C19 genotype status in healthy subjects receiving aspirin with and without a low-dose administration of lansoprazole. Methods: Fifteen Helicobacter pylori-negative subjects with different CYP2C19 genotype statuses (5 RMs, 5 intermediate metabolizers [IMs], and 5 poor metabolizers [PMs]) were each administered a series of three 7-day regimens of 15 mg of lansoprazole alone, 100 mg of aspirin alone, and both 15 mg of lansoprazole and 100 mg aspirin, with the order randomized among individuals. A washout period of 2 weeks or more was provided between regimens. Gastric mucosal injury was endoscopically evaluated on day 7 of each dosing period based on the modified Lanza score (MLS). 24-hour intragastric pH monitoring was started after endoscopy. Results: Median values (range) of MLS were 0 (0-1) in controls, 0 (0-1) in subjects receiving 15 mg of lansoprazole alone, 3 (0-5) in subjects receiving aspirin alone, and 0 (0-1) in subjects receiving both aspirin and 15 mg of lansoprazole. Lansoprazole increased the intragastric pH and significantly prevented aspirin-induced gastric mucosal injury (p = 0.0009 for aspirin and lansoprazole 15 mg). MLSs were negatively correlated with 24-hour intragastric pH (r = -0.740, P < 0.0001), whereas aspirin had no effect on intragastric pH. With regard to treatment with aspirin and lansoprazole 15 mg, although median values of MLS did not differ among the three genotype groups, median values of intragastric pH during treatment with this regimen were higher in PMs than in RMs and IMs (P = 0.009 for RMs, P = 0.028 for IMs). Conclusion: We observed a significant relationship between 24-hour intragastric pH and grade of aspirin-induced gastric mucosal lesions. Further, the acid inhibition attained on administration of 15 mg of lansoprazole appeared sufficient to prevent aspirin-induced gastric mucosal damage, irrespective of CYP2C19 genotype status.

The Prevention of Progression of Arterial Disease and Diabetes (POPADAD) Trial: Factorial Randomised Placebo Controlled Trial of Aspirin and Antioxidants in Patients with Diabetes and Asymptomatic Peripheral Arterial Disease

Conclusion: Neither aspirin, antioxidant therapy, nor the combination of aspirin and antioxidant therapy is useful in the primary prevention of cardiovascular events and mortality in patients with diabetes and asymptomatic peripheral arterial disease (PAD). Summary: Patients with asymptomatic PAD are six times more likely to die from cardiovascular disease ≤10 years than patients without PAD (N Engl J Med 1992;326:381-6). Aspirin as a secondary preventative measure in patients with diabetes and cardiovascular disease is well established. This has led to recommendations for use of aspirin as primary preventative therapy as well; however, a meta-analysis has demonstrated no efficacy for aspirin as a primary preventative therapy in patients with diabetes (BMJ 2002;324:71-86). Some evidence also indicates that there is increase in oxidative stress in patients with diabetes, with free radicals increasing platelet aggregation and antioxidants decreasing platelet aggregation. Based on the strength of the data for secondary prevention of cardiovascular events with aspirin therapy, the lack of data investigating aspirin as primary preventative therapy, and potential effects of antioxidants in patients with diabetes, the authors sought to study these agents in a group of patients with diabetes and asymptomatic PAD. The objective was to determine whether aspirin and antioxidant therapy, combined or alone, was more effective than placebo in reducing cardiovascular events in patients with diabetes and asymptomatic peripheral arterial disease. This was a multicenter, randomized, double-blind, two by two, factorial, placebo-controlled trial, It was conducted in 16 hospitals in Scotland and involved 188 primary care groups. Entered into the trial were 1276 adults (aged ≥40 years) with type 1 or type 2 diabetes and an ankle-brachial index <0.99, and no symptoms of cardiovascular disease. The daily regimen was 100 mg of aspirin plus antioxidant capsule in 320 patients, or aspirin plus placebo in 318, or antioxidant plus placebo in 320, or two placebo capsules in 318). The main outcome measures consisted of two composite primary end points: (1) death from coronary heart disease or stroke, nonfatal myocardial infarction or stroke, or amputation above the ankle, and (2) and death from coronary heart disease or stroke. There was no evidence of any benefit of aspirin or antioxidant therapy. There were 638 primary events, of which 116 occurred in the aspirin groups compared with 117 in the no-aspirin group (18.2% vs 18.3%; hazard ratio [HR] 0.98, 95% confidence interval [CI], 0.76-1.26). There were 43 deaths from coronary heart disease or stroke in the aspirin groups compared with 35 deaths in the no-aspirin groups (6.7% vs 5.5%; HR, 1.23, 95% CI, 0.79-1.93). In the antioxidant groups, 117 primary events (18.3%) occurred; whereas in the no-antioxidant therapy groups, 116 (18.2%) occurred (HR, 1.03; 95% CI, 0.79-1.33). There were 42 deaths from coronary heart disease or stroke in the antioxidant groups compared with 36 deaths from coronary heart disease or stroke in the no-antioxidant groups (6.6% vs 5.7%, respectively; HR, 1.21; 95% CI, 0.78-1.89). Comment: Once again, aspirin fails as primary preventative therapy in patients with diabetes. This study extended that conclusion to patients with asymptomatic PAD. The study, however, should not be construed as justification for failure to use aspirin as secondary preventative therapy in patients with cardiovascular disease and diabetes. Aspirin may be a so-called wonder drug, but it does not seem to be good for everything.

Influence of different antiplatelet treatment regimens for primary percutaneous coronary intervention on all-cause mortality

The aim of this analysis was to examine the influence of different in-cath-lab antiplatelet regimens for the primary percutaneous coronary intervention (PCI) on all-cause mortality. The study group consisted of 7193 patients (pts) undergoing primary PCI in 38 centres in 2003 in Poland. All patients received pretreatment with 300 mg of aspirin, 992 pts (14%) received glycoprotein (GP) IIb/IIIa inhibitors, 2690 pts (37%) were treated with 300 mg loading dose of clopidogrel, and 1566 (22%) received combined antiplatelet treatment with both GP IIb/IIIa inhibitors and clopidogrel. Remaining 1945 patients (27%) did not receive GP IIb/IIIa inhibitors or clopidogrel. Primary endpoint of the study was all-cause mortality up to 1 year from ST-segment elevation myocardial infarction (STEMI). One year mortality rates in the four groups were: 10.4%, 9.0%, 9.7%, and 15.3%, respectively. Propensity-adjusted survival analysis showed significant reduction of mortality for combination therapy with GP IIb/IIIa inhibitors and clopidogrel, clopidogrel alone, and GP IIb/IIIa inhibitors alone over aspirin alone. No additive effect on survival was seen for a combination therapy with GP IIb/IIIa inhibitors and clopidogrel in comparison to treatment with clopidogrel alone. In this large cohort, multicentre STEMI registry in-cath-lab use of GP IIb/IIIa inhibitors and clopidogrel alone or in combination was associated with the reduction of 1 year all-cause mortality in the setting of primary PCI in comparison with aspirin only. However, the use of GP IIb/IIIa inhibitors on top of 300 mg loading dose of clopidogrel did not further reduce mortality.

Aspirin Use, Dose, and Clinical Outcomes in Postmenopausal Women With Stable Cardiovascular Disease

Background— Despite compelling evidence that aspirin reduces fatal and nonfatal vascular events among the overall population in various settings, women have frequently been underrepresented and their data underreported. We sought to evaluate the relationship between aspirin use, dose (81 or 325 mg), and clinical outcomes among postmenopausal women with stable cardiovascular disease (CVD). Methods and Results— Women with CVD (n=8928) enrolled in the Women’s Health Initiative Observational Study were used for this analysis. The primary outcome was the incidence of all-cause mortality and cardiovascular events (myocardial infarction, stroke, and cardiovascular death). Among 8928 women with stable CVD, 4101 (46%) reported taking aspirin, of whom 30% were on 81 mg and 70% were on 325 mg. At 6.5 years of follow-up, no significant association was noted for aspirin use and all-cause mortality or cardiovascular events. However, after multivariate adjustment, aspirin use was associated with a significantly lower all-cause (adjusted hazard ratio, 0.86 [0.75 to 0.99]; P =0.04) and cardiovascular-related mortality (adjusted hazard ratio, 0.75 [0.60 to 0.95]; P =0.01) compared with no aspirin. Aspirin use was associated with a lower risk of cardiovascular events (adjusted hazard ratio, 0.90 [0.78 to 1.04]; P =0.14), which did not meet statistical significance. Compared with 325 mg, use of 81 mg was not significantly different for all-cause mortality, cardiovascular events, or any individual end point. Conclusions— After multivariate adjustment, aspirin use was associated with significantly lower risk of all-cause mortality, specifically, cardiovascular mortality, among postmenopausal women with stable CVD. No significant difference was noted between 81 mg and 325 mg of aspirin. Overall, aspirin use was low in this cohort of women with stable CVD.