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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute coronary syndrome (ACS) is associated with a number of abnormalities in inflammation, endothelial function, and coagulation, all of which appear to be modulated by statins. We examined the time to benefit of different statin regimens in the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) trial and other ACS trials that compared statin therapies in patients with ACS. In PROVE IT-TIMI 22, apparent clinical benefit was observed as early as 30 days, with significant reduction in all-cause mortality, myocardial infarction, unstable angina requiring rehospitalization, revascularization performed 30 days postrandomization, or stroke observed as early as 4 months. In PROVE IT-TIMI 22, atorvastatin 80 mg lowered both low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP) at 30 days and 4 months to a greater extent than pravastatin 40 mg. Those who achieved the lowest LDL and the lowest CRP levels at 30 days after ACS had the lowest risk of acute cardiac events. The very early benefits of statin therapy appeared to be correlated with CRP reductions, which may relate to the intensity of the pleiotropic effects of statins.
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PMID:Early time to benefit with intensive statin treatment: could it be the pleiotropic effects? 1612 24

Cerebral and myocardial ischemia, two of the leading causes of morbidity and mortality worldwide, are associated with inflammation that can lead to multiple organ failure and death. High-mobility group box 1(HMGB1), a recently described mediator of lethal systemic inflammation, has been detected in individuals with severe sepsis and hemorrhagic shock, but its role during ischemic injury in humans is unknown. To determine whether systemic HMGB1 levels are elevated after ischemic injury, a prospective observational study was performed in subjects with a diagnosis of either Acute Coronary Syndrome (ACS) or cerebral vascular ischemia (transient ischemic attack or cerebral vascular accident). Subjects (n, 16; age [mean], 67+/-16.3 years) were enrolled in the North Shore-LIJ emergency department within 24 h of symptom onset. Blood samples were collected, and HMGB1 levels analyzed by Western blot analysis using previously described methods (Wang et al. Science. 1999). Control samples were obtained from healthy age- and sex-matched volunteers (n, 16; age [mean], 68+/-15.8 years). Here, we report that serum HMGB1 levels were significantly elevated in both myocardial ischemia subjects (myocardial control serum HMGB1, 1.94+/-2.05 ng/mL, vs. myocardial ischemia serum HMGB1, 159+/-54.3 ng/mL; P<0.001); and in cerebral ischemia subjects (cerebral control serum HMGB1, 16.8+/-10.9 ng/mL, vs. cerebral ischemia serum HMGB1, 218+/-18.8 ng/mL; P<0.001). These results suggest that systemic HMGB1 levels are elevated in human ischemic disease.
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PMID:Elevated high-mobility group box 1 levels in patients with cerebral and myocardial ischemia. 1672 Dec 63

A 70-year-old female was admitted for syncope preceded by chest pain. On admission ECG showed signs of myocardial ischaemia and cardiac troponin I (cTnI) was mildly elevated. Acute coronary syndrome without ST elevation was diagnosed. During hospitalization transthoracic echocardiography (TTE) revealed the presence of a round echogenic pedunculated mass adherent to the aortic valve. Cardiac catheterization revealed normal coronary arteries. According to the hypothesis that the lesion could be responsible for both acute coronary syndrome and syncope, surgical intervention was scheduled. The mass was removed and the histological examination revealed a cardiac papillary fibroelastoma (CPF). CPF is the most common tumour of the cardiac valves, it is often found incidentally but it can cause myocardial infarction, sudden death, syncope and stroke; its embolization is the most common complication. For symptomatic patients surgical excision is curative.
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PMID:Cardiac papillary fibroelastoma presenting with acute coronary syndrome and syncope. 1686 62

Acute coronary syndrome is an inflammatory disease, during which the complement cascade is activated. We assessed the complement C3 and C4 concentration ratio (C3/C4 ratio) in serum as a potential measurement to predict cardiovascular attacks. Patients with acute coronary syndrome (n=148) were followed after an initial attack for subsequent ischemic cardiovascular events (composite end point of death, myocardial infarction, recurrent unstable angina, or stroke). During the follow-up period (average 555 days), 44 patients met an end point. Blood samples were taken at hospitalization, 1 week, 3 months, and 1 year after hospital admission. Serum complement C3 and C4 concentrations and the C3/C4 ratio were analyzed. Patients with an end point had, throughout the follow-up period, a higher C3/C4 ratio than patients without these end points (repeated measures analysis of variance, p=0.007). When all traditional cardiovascular risk factors and other potential confounding factors were included in a Cox multivariate logistic regression survival analysis, the C3/C4 ratio emerged as the novel risk factor for any new cardiovascular event (odds ratio 1.33, 95% confidence interval 1.08 to 1.63, p=0.007). When the C3/C4 ratio was divided into 4 quartiles, 24% in quartiles 1 and 2 (lowest) and 48% in quartile 4 (highest) had end points during follow-up (odds ratio 3.04, 95% confidence interval 1.27 to 7.29, p=0.01). In conclusion, increased serum C3/C4 ratio is a readily available and novel marker for recurrent cardiovascular events in acute coronary syndrome. The relative increase in serum C3 protein and decrease in C4 protein could explain changes in the C3/C4 ratio.
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PMID:Serum complement C3/C4 ratio, a novel marker for recurrent cardiovascular events. 1739 78

Venous thromboembolism (VTE) remains the most common preventable cause of in-hospital death and D-dimer (DD) is one of the essential diagnostic tools for it. Each risk factor for VTE can raise DD and they are numerous: 24 listed in 2008 European Guidelines. Acute coronary syndrome and stroke increase DD concentration, too. Thus, all three most important causes of cardiovascular death are capable of raising DD. Recent evidence suggests DD as a sensitive marker also for acute aortic dissection. Many other processes may raise DD concentration: atrial fibrillation, congestive heart failure, disseminated intravascular coagulation, etc. The adequate DD interpretation is additionally important due to the frequent usage of the test (probably millions of times a year in the world). Simple and concise classification is much easier to remember and such one is suggested.
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PMID:Pragmatic classification of the causes of high D-dimer. 1985 27

The management of antithrombotic therapy in atrial fibrillation patients presenting with acute coronary syndrome and/or undergoing percutaneous coronary inter vention/stenting cannot be done according to a regimented common protocol, and stroke and bleeding risk stratification schema should be employed to individualize treatment options. A delicate balance is needed between the prevention of thromboembolism, against recurrent cardiac ischemia or stent thrombosis, and bleeding risk. New guidance from a consensus document of the European Society of Cardiology Working Group on Thrombosis, endorsed by the European Heart Rhythm Association and the European Association of Percutaneous Cardiovascular Interventions on the management of Antithrombotic Therapy in Atrial Fibrillation Patients Presenting with Acute Coronary Syndrome and/or Undergoing Percutaneous Coronary Intervention/Stenting has sought to clarify some of the major issues and problems surrounding this practice, and will allow clinicians to make much more informed decisions when faced with treating such patients.
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PMID:Antithrombotic therapy in anticoagulated patients with atrial fibrillation presenting with acute coronary syndromes and/or undergoing percutaneous coronary intervention/stenting. 2069 60

Acute coronary syndrome in elderly can manifest with a variety of atypical presentation and may be associated with other comorbid conditions. We present an atypical presentation of ACS in an elderly left handed female presenting with sudden onset of slurred speech preceded by dizziness and vomiting. After through clinical examination and investigation she was managed as a case of non ST elevation myocardial infarction and ischaemic stroke.
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PMID:An unusual presentation of acute coronary syndrome. 2187 78

Acute coronary syndrome (ACS) is a major health burden, resulting in increased hospital admissions and significant morbidity and mortality. Platelet activation, which leads to thrombin generation, is highly implicated in ACS, and antiplatelet agents represent the current standard of care. Established antiplatelet agents include acetylsalicylic acid (ASA), thienopyridines (clopidogrel, ticlopidine), and glycoprotein IIb/IIIa inhibitors. Recently, antiplatelet therapy for ACS has evolved to include more potent inhibitors (e.g., prasugrel, cangrelor, and ticagrelor). During the acute phase of an acute coronary event, both anticoagulation and dual antiplatelet therapy with aspirin and a thienopyridine are guideline recommended as first-line treatment. While anticoagulation is usually limited to the acute in-patient phase, dual antiplatelet therapy is recommended for 12 months. Despite the efficacy of antiplatelet agents in ACS, in many patients the residual risk of death from cardiac events, myocardial infarction, stroke, and refractory ischemia remains high. Dual therapy (i.e., ASA or clopidogrel plus a vitamin K antagonist [VKA]), and triple therapy (two antiplatelets plus a VKA) are associated with increases in bleeding complications. New oral anticoagulants that offer a novel mechanism of action may, when added to the current standard of care, provide a more comprehensive response to thrombin generation. In this review, we examine the pathology of ACS, investigate antiplatelet therapies and describe emerging anticoagulants that may be of benefit when used as combination therapy with antiplatelet agents for secondary prevention in ACS patients.
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PMID:Improving long-term ACS management: is there a role for the new antiplatelets? 2257 44

Despite therapeutic advances, patients with worsening heart failure (HF) requiring hospitalization have unacceptably high post-discharge mortality and re-admission rates soon after discharge. Evidence suggests a hypercoagulable state is present in patients with HF. Although thromboembolism as a direct consequence of HF is not frequently clinically recognized, it may contribute to mortality and morbidity. Additionally, many patients with HF have concomitant disorders conferring additional thrombotic risk, including atrial fibrillation (AF) and coronary artery disease (CAD). Acute coronary syndrome (ACS), a known consequence of coronary thrombosis, is a common precipitating factor for worsening HF. Coronary thrombosis may also cause sudden death in patients with HF and CAD. Because data are largely derived from observational studies or trials of modest size, guideline recommendations on anticoagulation for HF vary between organizations. The recently presented Warfarin versus Aspirin in Reduced Cardiac Ejection Fraction trial of HF patients in sinus rhythm suggested anticoagulation reduces the risk of stroke, although rates of the combined primary endpoint (death, ischemic stroke, or intracerebral hemorrhage) were similar for acetylsalicylic acid and warfarin. Newer oral anticoagulants dabigatran, apixaban, and rivaroxaban have successfully completed trials for the prevention of stroke in patients with AF and have shown benefits in the subpopulation of patients with concomitant HF. Positive results of the Anti-Xa Therapy to Lower Cardiovascular Events in Addition to Standard Therapy in Subjects with Acute Coronary Syndrome-Thrombolysis in Myocardial Infarction 51 (ATLAS ACS 2-TIMI 51) trial of rivaroxaban in ACS are also encouraging. These data suggest there is a need to assess the potential role for these newer agents in the management of patients hospitalized for HF who continue to have a high post-discharge event rate despite available therapies.
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PMID:Anticoagulation in heart failure: current status and future direction. 2298 20

Acute coronary syndrome (ACS) occurs as a result of atherosclerotic plaque rupture and subsequent platelet activation and coagulation leading to thrombus formation and coronary occlusion. Thrombin and activated factor X (FXa) are key elements in the coagulation cascade. The use of anticoagulants in ACS, both in the acute phase and in the long term, has improved prognosis by reducing thrombotic events, but is associated with an increased risk of bleeding. In recent years, new oral anticoagulants have been developed that do not require monitoring and produce a lower risk of bleeding. Rivaroxaban is the only drug with a favorable risk-benefit profile in patients with ACS. The ATLAS ACS TIMI 2-51 is the first phase III trial demonstrating that the addition of low-dose rivaroxaban to optimal antiplatelet therapy reduces mortality, cardiovascular mortality, infarct or stroke without significantly increasing fatal bleeding.
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PMID:[Contribution of the new oral anticoagulants to the treatment of acute coronary syndrome]. 2349 72


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