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Ischemic Events (ischemic + event)
Selected AbstractsRegular or "Super-Aspirins"?JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 4 2001A Review of Thienopyridines or Aspirin to Prevent Stroke PURPOSE: To review the evidence for the effectiveness and safety of the thienopyridines (ticlopidine and clopidogrel) compared with aspirin for the prevention of vascular events among patients at high risk of vascular disease. BACKGROUND: Atherosclerosis and resultant cardiovascular disease are important causes of morbidity and mortality in older people. In particular, atherosclerosis of the cerebral arteries can lead to transient ischemic attacks (TIAs) and stroke. Stroke ranks as the third-leading cause of death in the United States and in 1997 was responsible for over 150,000 fatalities.1 In addition to the mortality associated with this disease, stroke is also a leading source of long-term disability in survivors. Nearly 4.5 million stroke survivors are alive today,1 highlighting the fact that primary, but also secondary, prevention are extremely important for minimizing the complications of this illness. DATA SOURCES: Specialized trial registers of the Cochrane Stroke Group and the Antithrombotic Trialist's Collaboration, MEDLINE, and Embase were searched. Additional unpublished information and data were sought from Sanofi, the pharmaceutical company that developed and manufactures ticlopidine and clopidogrel, as well as the principal investigators of the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial,7 the largest of the trials identified. STUDY SELECTION CRITERIA: All unconfounded randomized trials comparing either ticlopidine or clopidogrel with aspirin among patients at high risk of vascular disease (those with symptoms of ischemia of the cerebral, coronary, or peripheral circulations) who were followed for at least 1 month for the recurrence of vascular events were included. DATA EXTRACTION: Data were extracted from four completed randomized trials completed in the past 20 years, which included 22,656 patients.7,10 Two authors independently extracted the data from these trials for the following information: the types of patients enrolled; the entry and exclusion criteria; the randomization method; the number of patients originally allocated to the treatment and control groups; the method and duration of follow-up; the number of patients in each group lost to follow-up; information on compliance with the treatment allocated; the definitions of outcome events; the number of outcome events in each treatment group; and any method used for blinding patients, treating clinicians, and outcome assessors to treatment allocation. MAIN RESULTS: Four completed trials involving a total of 22,656 patients were identified. Aspirin was compared with ticlopidine in three trials (3,471 patients)8,10 and with clopidogrel in one trial (19,185 patients).7 A recent TIA or ischemic stroke was the qualifying event in 9,840 patients, a recent myocardial infarction in 6,302 patients, and symptomatic peripheral arterial disease in 6,514 patients. The average age of the patients was approximately 63, with approximately two-thirds of the patients being male and white. The duration of follow-up ranged from 12 to 40 months. CONCLUSIONS: This systematic review demonstrates that, compared with aspirin, thienopyridines are only modestly more effective in preventing serious vascular events in high-risk patients. For patients who are intolerant of, or allergic to aspirin, the available safety and efficacy data suggest that clopidogrel is an appropriate, but more-expensive, alternative antiplatelet drug. It appears safer than ticlopidine and as safe as aspirin but it should not replace aspirin as the first-choice antiplatelet agent for all patients. Further studies are necessary to determine which, if any, particular types of patients would benefit most and least from clopidogrel instead of aspirin. [source] Does the Morphology of Atrial Septal Aneurysm Influence Cerebral Arterial Embolus Occurrence?ECHOCARDIOGRAPHY, Issue 9 2007Jacek Kurzawski M.D., Ph.D. Background and Purpose: Atrial septal aneurysm (ASA) is a rare heart defect regarded as a source of arterial emboli. The main objective of the study was to assess the role of ASA morphology in the etiology of embolism.Methods: Eighty-eight subjects were included after transthoracic echocardiography positive for ASA. Medical history of embolic events was obtained in 13 patients (14.8%). Magnitude, location, size of aneurysm, oscillation, direction of bulging, the presence of interatrial shunt and source of any potential cardiac embolus material were assessed, and the size of the left atrium, the area of both atria, and the presence of any valve prolapse syndrome were recorded. The occurrence of atrial fibrillation or flutter and the presence of concomitant diseases and other clinical features were also estimated.Results: The occurrence of arterial emboli was not related to ASA morphology. Coexisting diseases, smoking and left atrial dimension were significantly correlated with the occurrence of arterial emboli.Conclusions: Ischemic events were not significantly correlated with the ASA presence. The present findings suggest other causes of vascular events in patients with ASA. [source] Microsphere embolism-induced cortical cholinergic deafferentation and impairments in attentional performanceEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2005Tara K. S. Craft Abstract Ischemic events have been hypothesized to play a critical role on the pathogenesis of dementia and the acceleration of cognitive impairments. This experiment was designed to determine the consequences of microvascular ischemia on the cortical cholinergic input system and associated attention capacities. Injections of microspheres (,50 µm diameter; ,5000 microspheres/100 µL) into the right common carotid artery of rats served as a model of microvascular ischemia and resulted in decreases in the density of cholinergic fibers in the ipsilateral medial prefrontal cortex and frontoparietal areas. Furthermore, dense astrogliosis, indicated by glial fibrillary acidic protein (GFAP) immunohistochemistry, was observed in the globus pallidus, including the areas of origin of cholinergic projections to the cortex. Fluoro-Jade B staining indicated that loss of neurons in the cortex was restricted to areas of microsphere-induced infarcts. Attentional performance was assessed using an operant sustained attention task; performance in this task was previously demonstrated to reflect the integrity and activity of the cortical cholinergic input system. Embolized animals' performance was characterized by a decrease in the animals' ability to detect signals. Their performance in non-signal trials remained unaffected. The residual density of cholinergic axons in prefrontal and frontoparietal areas correlated with the animals' performance. The present data support the hypothesis that microvascular ischemia results in loss of cortical cholinergic inputs and impairs associated attentional performance. Microsphere embolism represents a useful animal model for studying the role of interactions between microvascular disorder and impaired forebrain cholinergic neurotransmission in the manifestation of cognitive impairments. [source] Beneficial effect of hyperbaric oxygen on island flaps subjected to secondary venous ischemia,MICROSURGERY, Issue 2 2002Thomas J. Gampper M.D. The potential for hyperbaric oxygen therapy (HBO) to decrease the untoward effects of a secondary ischemic event was studied in the rat superficial epigastric flap model. The secondary venous ischemic flap was created by cross-clamping the vascular pedicles for 2 h. Twenty-four hours later, the flap was reelevated and the venous pedicle was occluded for 5 h. Thirty-two rats were divided into three groups. In experimental group 1, animals received HBO treatment immediately prior to the initial flap elevation and ischemia at 2 atmosphere pressures for 90 min. In experimental group 2, the rats underwent a similar course except for a second 90-min HBO course immediately prior to the secondary venous occlusion. The rats without HBO therapy were used as controls. The results showed that all control flaps were nonviable at 1 week by clinical inspection and fluorescein injection. Complete flap survival occurred in 20% of group 1 flaps and 30.8% of group 2 flaps. Partial flap survival occurred in the rest of the flaps in these two groups, with mean survival areas of 48% and 55%, respectively. In conclusion, HBO treatments significantly increase the survival of flaps subjected to a secondary ischemia, even if administered before the primary ischemia. Administering HBO prior to secondary venous ischemia was marginal, which may be due to the effect of O2 given by HBO not lasting longer than 5 h. © 2002 Wiley-Liss, Inc. MICROSURGERY 22:49,52 2002 [source] Biventricular Pacing for Severe Mitral Reguritation Following Atrioventrgicular Nodal AblationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2p1 2003PATRICK J.S. DISNEY DISNEY, P.J.S., et al.: Biventricular Pacing for Severe Mitral Regurgitation Following Atrioventricular Nodal Ablation. A 69-year-old woman developed acute pulmonary edema and severe mitral regurgitation (MR) 2 days following an uncomplicated AV nodal (AVN) ablation and insertion of VVI pacemaker for chronic atrial fibrillation. There was no history of significant mitral valve disease. Left ventricular function was normal and there was no evidence of an acute cardiac ischemic event. Transthoracic echo and right heart catheterization studies showed reduction in the severity of MR with biventricular pacing as opposed to RV pacing alone. A permanent pacemaker configured for biventricular pacing was implanted with complete resolution of symptoms and significant reduction in degree of MR. (PACE 2003; 26[Pt. I]:643,644) [source] Intracranial atherosclerotic disease: An update,ANNALS OF NEUROLOGY, Issue 6 2009Adnan I. Qureshi MD The consensus conference on intracranial atherosclerosis provides a comprehensive review of the existing literature relevant to the epidemiology, diagnosis, prevention, and treatment of intracranial atherosclerosis, and identifies principles of management and research priorities. Patients who have suffered a stroke or transient ischemic attack attributed to stenosis (50,99%) of a major intracranial artery face a 12 to 14% risk for subsequent stroke during the 2-year period after the initial ischemic event, despite treatment with antithrombotic medications. The annual risk for subsequent stroke may exceed 20% in high-risk groups. In patients with intracranial atherosclerotic disease, short-term and long-term anticoagulation is not superior to antiplatelet treatment. Overall, the subgroup analyses from randomized trials provide evidence about benefit of aggressive atherogenic risk factor management. Intracranial angioplasty with or without stent placement has evolved as a therapeutic option for patients with symptomatic intracranial atherosclerotic disease, particularly those with high-grade stenosis with recurrent ischemic symptoms, medication failure, or both. A multicenter randomized trial is currently under way to compare stent placement with intense medical management for patients with high-grade symptomatic intracranial atherosclerotic disease. Ann Neurol 2009;66:730,738 [source] 2121: Sustained neuroprotection after a single intravitreal injection of PGJ2 in a rodent model of NAIONACTA OPHTHALMOLOGICA, Issue 2010V TOUITOU Purpose Prostaglandin-J2 (PGJ2) has been proposed as a potential neuroprotective agent. We wanted to evaluate the toxicity/efficacy of a single intravitreal (IVT) injection of PGJ2 in a rodent model of nonarteritic anterior ischemic optic neuropathy (NAION). Methods We used the laser-activated rose Bengal induction method to produce AION in Long-Evans rats. We evaluated IVT-PGJ2 retinal and ON toxicity. Following induction, PGJ2 was IVT-injected in the treatment-group. IVT phosphate-buffered-saline (PBS) was used as control. Functional studies (VEP) were performed at baseline and at 7days post-treatment. Structural studies included immunohistochemical (IHC), electron microscopic (EM) analysis of the optic nerve (ON), and stereologic analysis of retinal ganglion cell (RGC) numbers at30 day 30. Results Toxicity: IVT PGJ2 (5 eyes) did not induce any significant functional/structural changes in the retina or ON of treated animals compared with animals injected with PBS (5 eyes) 30 days post-injection. Efficacy: After a single IVT-injection, day7 VEPs in the PGJ2-treatment group (n=7) had amplitudes 103.6% of baseline, whereas the PBS-treated group (n=6) had VEPs that were 42.4% of the baseline. 30days post-stroke, EM of ON from the treatment-group demonstrated significant preservation of axons and decreased demyelination. Stereological RGCcounts confirmed significant (p<0.04) RGC preservation in PGJ2-treated animals (1462.6 cells/µm2) compared w the stroke+PBS group (1156.5 cells/µm2). Conclusion A single IVT of PGJ2 preserves RGCs and their axons, and provides sustained neuroprotection for at least 1 month following initial ischemic event. [source] Continuous 12-lead electrocardiographic ST monitoring adds prognostic information to the thrombolysis in myocardial infarction risk score in patients with non-ST-elevation acute coronary syndromesCLINICAL CARDIOLOGY, Issue 4 2005Michael N. Zairis M.D. Abstract Background: Continuous 12-lead electrocardiographic (ECG) ST monitoring and the Thrombolysis In Myocardial Infarction Risk Score (TIMI-RS), both have been shown to be useful for early risk stratification in patients with non-ST elevation acute coronary syndromes (NSTACS). Hypothesis: Transient ST ischemic events, detected by continuous 12-lead ECG ST monitoring, early in the course of NSTACS, may add prognostic information to the TIMI-RS. Methods: In all, 567 consecutive patients with a NSTACS underwent 24-h continuous 12-lead ECG ST monitoring. An ST ischemic event was defined as a transient ST shift in any lead of , 0.10 mV compared with the reference ECG, lasting for ,l min. Results: The incidence of the composite of death, nonfatal myocardial infarction (or reinfarction) and recurrent ischemia by Day 14 was 22.2%. By Day 30, the incidence of the composite of death and nonfatal myocardial infarction (or reinfarction) was 14.7%. There was a significantly increased risk of 14-day (p value for trend < 0.001) or 30-day (p value for trend <0.001) composite endpoint with increasing of TIMI-RS. Moreover, the occurrence of , 1 ST shifts during ST monitoring was associated with a significantly increased risk of 14-(p value < 0.001) or 30-day (p value < 0.001) composite end-point, and this was true throughout the groups of TIMI-RS. Conclusions: The present study suggests that continuous 12-lead ECG ST monitoring, early in the course of NSTACS, may serve as an affordable tool to add prognostic information to the TIMI-RS. [source] Diagnostic and Prognostic Use of Stress Echocardiography in Stable PatientsECHOCARDIOGRAPHY, Issue 5 2000Steven C. Smart M.D. Stress echocardiography is an effective diagnostic and prognostic technique in stable patients with known or suspected coronary artery disease (CAD), myocardial infarction, or chronic left ventricular dysfunction and those undergoing noncardiac surgery. Stress echocardiography is sensitive and specific for the detection and extent of CAD. Negative tests confer a high negative predictive value for cardiac events regardless of the clinical risk. Positive studies confer a high positive predictive value for ischemic events in patients with intermediate to high clinical risk. Stress echocardiography provides incremental prognostic information relative to clinical, resting echocardiographic, and angiographic data. Meta-analysis studies have shown that the diagnostic and prognostic information provided by stress echocardiography is comparable to that from radionuclide scintigraphic stress tests. Stress echocardiography may be more specific for the detection and extent of CAD, whereas radionuclide scintigraphy may be more sensitive for one-vessel disease. Sensitivities are similar for the detection and extent of disease in patients with multivessel CAD. [source] ADP-induced platelet aggregation in acute ischemic stroke patients on aspirin therapyEUROPEAN JOURNAL OF NEUROLOGY, Issue 12 2008J.-K. Cha Background and purpose:, Aspirin is an important therapeutic regimen to prevent the recurrent ischemic events or death after acute ischemic stroke. In this study, we evaluated the relationship between the extent of adenosine diphosphate (ADP) -induced platelet aggregation and outcome in acute ischemic stroke patients on aspirin therapy. Methods:, We selected 107 acute ischemic stroke patients who had been prescribed aspirin and evaluated platelet function test by using optic platelet aggregometer test after 5 days of taking it and investigated the prognosis 90 days after ischemic events. Kaplan,Meyer curve was used for survival analysis. Results:, After stratification of the subjected patients by tertiles of ADP-induced platelet aggregation, the events rates were 7.4%, 9.3% and 30.8% (P = 0.023). In multiple logistic regression analysis, old age over 70 years (OR, 13.7; 95% CI, 2.14,88.07; P = 0.001) and the increased ADP-induced platelet aggregation had independent significance to the risk of primary end-points after acute ischemic stroke (OR, 1.1; 95% CI 1.01 to 1.20; P = 0.026). Conclusions:, This study showed that the increased ADP-induced platelet aggregation under using aspirin is associated with poor outcome after acute ischemic stroke. [source] The Rationale for and Comparisons of Different Antiplatelet Treatments in Acute Coronary SyndromeJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 2008PAUL A. GURBEL M.D. Fundamentally, acute coronary syndromes are platelet-centric diseases, resulting from platelet-rich thrombi that develop at the site of vessel wall injury. In addition to aggregation, platelets modulate a plethora of other important pathophysiologic processes, including inflammation and coagulation. Therefore, a primary goal of therapy in the acute setting should be treatment with agents that provide predictable and superior platelet inhibition to prevent further ischemic events that develop from unchecked high platelet reactivity. Translational research studies of patients undergoing percutaneous revascularization have clearly demonstrated that adverse thrombotic outcomes are associated with high platelet reactivity and the latter is now emerging as a potent measurable cardiovascular risk factor. The intensity of antithrombotic therapy is influenced by patient risk. In the highest risk patients with elevated cardiac biomarkers indicative of myonecrosis, current guidelines support the use of early therapy with glycoprotein IIb/IIIa inhibition, aspirin, and clopidogrel. [source] Current Update on Glycoprotein IIb-IIIa and Direct Thrombin Inhibition in Percutaneous Coronary Intervention for Non-ST Elevation Acute Coronary Syndromes: Balancing Bleeding Risk and Antiplatelet EfficacyJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 2 2008ANDREW T. KWA M.D. Appropriate pharmacologic treatment for patients with acute coronary syndromes (ACS) remains a matter of controversy. Additionally, a substantial gap exists between recommended guidelines and current clinical practice. Questions remain regarding which antiplatelet/antithrombotic treatment strategies are appropriate for individual patients, based on their risk. We explore the role of glycoprotein IIb-IIIa inhibitors and the direct thrombin inhibitor bivalirudin in ACS patients, and consider the difficulties involved in reducing ischemic events while limiting bleeding risks. In patients with ACS who are undergoing percutaneous coronary intervention, high levels of microembolization and myocardial necrosis are potential risk factors for adverse long-term outcomes. Intensive antiplatelet/antithrombotic regimens may substantially affect these factors. Determination of risk levels, with the goal of targeting aggressive antithrombotic and interventional therapies to patients at higher risk, will help physicians choose appropriate pharmacologic therapy for patients with ACS. [source] Characteristics and Predictors of Aortic Plaques in Patients with Transient Ischemic Attacks and StrokesJOURNAL OF NEUROIMAGING, Issue 1 2004Abutaher M. Yahia MD ABSTRACT Objective. To identify the prevalence and characteristics of aortic atherosclerotic plaque disease and its association with cerebrovascular risk factors in patients with cerebral ischemic events. Background. Aortic atheroma is associated with ischemic stroke. Its characteristics, including morphology and distribution among different stroke subtypes, are not well described. Method. From July 2000 to August 2001, all patients evaluated by transesophageal echocardiography (TEE) with diagnoses of transient ischemic attacks (TIAs) and strokes were prospectively studied. Demographics, including age, gender, ethnicity, cerebrovascular risk factors, and stroke subtypes, were collected. Results. Thoracic aortic atheromas (TAAs) were present in 141 of 237 patients (59%) (mean age = 59 ± 14, 119 [50%] male). Mild plaque (<2mm) was present in 13 of 237 (5%), moderate plaque (2,4 mm) in 49 (21%), severe plaque (,4 mm) in 79 (33%), and complex plaque in 64 (27%). Patients' ages (odds ratio [OR] = 1.05, confidence interval [CI] 1.03,1.08, P < .001), coronary artery disease (OR = 2.2, CI 1.02,4.8, P < .042), and patent foramen ovale (PFO) (OR = 0.39, CI 0.22,0.70, P < .002) were associated with the severity and complexity of aortic plaque. In multivariate analysis, age (OR = 1.06, CI 1.03,1.08, P < .001) and the presence of PFO (OR = 0.35, CI 0.18,0.65, P < .001) continued to be significant to the severity and complexity of aortic atheroma. Gender, history of stroke, hypertension, diabetes mellitus, hyperlipidemia, and history of smoking were not associated with TAA. Conclusion. One third of TAA plaques are severe and complex in nature and more frequently present in the descending aorta and the arch of the aorta than in the ascending aorta. TEE should be considered for the early detection and treatment of TAA in patients without identified causes of stroke. [source] Platelet activation, myocardial ischemic events and postoperative non-response to aspirin in patients undergoing major vascular surgeryJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 10 2007S. RAJAGOPALAN Summary.,Objectives:,Myocardial ischemia is the leading cause of postoperative mortality and morbidity in patients undergoing major vascular surgery. Platelets have been implicated in the pathogenesis of acute thrombotic events. We hypothesized that platelet activity is increased following major vascular surgery and that this may predispose patients to myocardial ischemia.Methods:,Platelet function in 136 patients undergoing elective surgery for subcritical limb ischemia or infrarenal abdominal aortic aneurysm repair was assessed by P-selectin expression and fibrinogen binding with and without adenosine diphosphate (ADP) stimulation, and aggregation mediated by thrombin receptor-activating peptide and arachidonic acid (AA). Cardiac troponin-I (cTnI) was performed.Results:,P-selectin expression increased from days 1 to 3 after surgery [median increase from baseline on day 3: 53% (range: ,28% to 212%, P < 0.01) for unstimulated and 12% (range: ,9% to 45%, P < 0.01) for stimulated]. Fibrinogen binding increased in the immediate postoperative period [median increase from baseline: 34% (range: ,46% to 155%, P < 0.05)] and decreased on postoperative day 3 (P < 0.05). ADP-stimulated fibrinogen binding increased on day1 (P < 0.05) and thereafter decreased. Platelet aggregation increased on days 1,5 (P < 0.05). Twenty-eight (21%) patients had a postoperative elevation (> 0.1 ng mL,1) of cTnI. They had significantly increased AA-stimulated platelet aggregation in the immediate postoperative period and on day 2 (P < 0.05), and non-response to aspirin (48% vs. 26%, P = 0.036).Conclusions:,This study has shown increased platelet activity and the existence of non-response to aspirin following major vascular surgery. Patients with elevated postoperative cTnI had significantly increased AA-mediated platelet aggregation and a higher incidence of non-response to aspirin compared with patients who did not. [source] Safety and Efficacy of Bivalirudin in High-risk Patients Admitted Through the Emergency DepartmentACADEMIC EMERGENCY MEDICINE, Issue 8 2009Chadwick D. Miller MD Abstract Objectives:, The objective was to assess the safety and efficacy of bivalirudin monotherapy in patients with high-risk acute coronary syndrome (ACS) presenting to the emergency department (ED). Methods:, Data from the Acute Catheterization and Urgent Intervention Triage StrategY (ACUITY) trial were used to conduct a post hoc subgroup analysis of high-risk ACS patients (cardiac biomarker elevation or ST-segment deviation) who initially presented to the ED. The ACUITY trial randomized patients to receive heparin (unfractionated [UFH] or enoxaparin) plus glycoprotein IIb/IIIa inhibition (GPI), bivalirudin plus GPI, or bivalirudin monotherapy. Endpoints included composite ischemia, major bleeding (not coronary artery bypass graft (CABG) related), and net clinical outcome (major bleeding plus composite ischemia). Results:, Of 13,819 participants in the ACUITY trial, 6,441 presented initially to the ED, met high-risk criteria, and were included in the primary analysis. Bivalirudin alone when compared to heparin plus GPI, after adjusting for covariates, was associated with an improvement in net clinical outcome (12.3% vs. 14.3%, adjusted odds ratio [OR] = 0.81, 95% confidence interval [CI] = 0.66 to 0.99), similar composite ischemia (9.3% vs. 9.1%, adjusted OR = 0.98, 95% CI = 0.77 to 1.24), and less major bleeding (4.0% vs. 6.8%, adjusted OR = 0.57, 95% CI = 0.42 to 0.75). Bivalirudin plus GPI when compared to heparin plus GPI had similar net clinical outcome (13.8% vs. 14.3%, adjusted OR = 0.91, 95% CI = 0.75 to 1.11), composite ischemia (8.8% vs. 9.1%, adjusted OR = 0.87, 95% CI = 0.69 to 1.11), and major bleeding (6.8% vs. 6.8%, adjusted OR = 1.01, 95% CI = 0.79 to 1.30). Conclusions: Bivalirudin monotherapy decreases major bleeding while providing similar protection from ischemic events compared to heparin plus GPI in patients with high-risk ACS admitted through the ED. [source] Sequence of Electrocardiographic and Acoustic Cardiographic Changes and Angina during Coronary Occlusion and Reperfusion in Patients Undergoing Percutaneous Coronary InterventionANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2009A.N.P., Eunyoung Lee R.N., Ph.D. Background: Previous studies have suggested that ventricular function may be impaired without or prior to electrocardiographic changes or angina during ischemia. Understanding of temporal sequence of electrical and functional ischemic events may improve the detection of myocardial ischemia. Methods: A prospective study was performed in 21 subjects undergoing percutaneous coronary intervention (PCI) who had both ST amplitude changes >2 standard deviations above baseline on 12-lead electrocardiography (ECG), and new or increased third or fourth heart sound (S3 or S4) intensity measured by computerized acoustic cardiography. The sequence of the onset and resolution of these signs of ischemia were examined following coronary balloon inflation and deflation. Results: Electrocardiographic ST amplitude and diastolic heart sound changes occurred contemporaneously, shortly after coronary occlusion (mean onset from balloon inflation; ST changes, 21 ± 17 seconds; S4, 25 ± 26 seconds; S3, 45 ± 43 seconds). In 40% of patients, a new or increased S3 or S4 developed earlier than ST changes. Anginal symptoms occurred in only 2 of the 21 subjects during ischemia with a mean onset time of 68 seconds. ST-segment changes resolved earliest (33 seconds after balloon deflation) while diastolic heart sounds (89 ± 146 seconds) and angina (586 ± 653 seconds) resolved later. Conclusion: A new or intensified S3 and/or S4 occurred contemporaneously with electrocardiographic changes during ischemia. These diastolic heart sounds persisted longer than ST changes following coronary reperfusion. Acoustic cardiographic assessment of diastolic heart sounds may aid in the early detection of myocardial ischemia, particularly in those patients with an uninterpretable ECG. [source] Cigarette smoking as a significant risk factor for digital vascular disease in patients with systemic sclerosisARTHRITIS & RHEUMATISM, Issue 12 2002Beverley J. Harrison Objective Patients with systemic sclerosis (SSc) are at high risk for digital vascular complications, including amputation and gangrene. Cigarette smoking is an important risk factor for vascular disease in the general population. We investigated the influence of cigarette smoking on digital ischemia in patients with SSc. Methods We studied 101 patients with SSc (87 women and 14 men, median age 53 years, median disease duration 13 years). Smoking history was defined in terms of current smoking status and total number of pack-years. Digital ischemic events were classified as debridement, hospital admission for intravenous (IV) administration of vasodilators, and digital amputation. The influence of smoking on digital ischemic events was examined using logistic regression, adjusting for age, sex, and disease duration. Results are expressed as the odds ratio (OR) and 95% confidence interval (95% CI). Results Of the 101 patients, 21 (21%) were current smokers, 37 (37%) were ex-smokers, and 43 (43%) had never smoked. After adjusting for age, sex, and disease duration, current smokers were significantly more likely than never-smokers to have had debridement (OR 4.5, 95% CI 1.1,18.3) or admission for IV vasodilators (OR 3.8, 95% CI 1.1,12.9). Patients smoking at higher intensity were more likely to require admission for IV vasodilators. Conclusion Among patients with SSc, current smokers are 3,4 times more likely than never-smokers to incur digital vascular complications. Resources should be directed to supporting smoking cessation in patients with SSc. [source] Is there a prognostic role for C-reactive protein in ischemic stroke?ACTA NEUROLOGICA SCANDINAVICA, Issue 3 2010G. Corso Corso G, Bottacchi E, Brusa A, Di Benedetto M, Giardini G, Lia C, Reggiani M, Veronese Morosini M. Is there a prognostic role for C-reactive protein in ischemic stroke? Acta Neurol Scand: 122: 209,216. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objectives,,, We investigated the relationship between C-reactive protein (CRP)-values in the acute phase of stroke and the risk of further fatal and non-fatal ischemic events. Materials and methods,,, We analysed 462 consecutive incident ischemic strokes. Patients were divided into two subgroups on the basis of a CRP cut-off level of 9 mg/l. Primary end points were any new vascular fatal and non-fatal event recorded during the follow-up period. Results,,, During a follow-up of 2.27 years, in 132 patients occurred a primary end point. Patients with CRP values ,9 mg/l had more frequently primary end point. The hazard ratio (HR) for cardiovascular events was 3.59; 1.93 for cerebrovascular events; 7.43 for vascular deaths and 5.78 for death from any cause. Cox proportional hazard multivariate analysis identified CRP values ,9 (HR = 4.19, 95% CI: 1.85,9.50, P = 0.001), the lack of secondary prevention therapy at discharge (HR = 4.35, 95% CI: 1.87,10.1, P = 0.001), age >70 years (HR = 3.09, 95% CI: 1.04,9.24, P = 0.04) as independent predictors of fatal events. Conclusions,,, CRP levels ,9 mg/l, evaluated in incident ischemic stroke within 24 h, predict a higher risk of further ischemic events and mortality. [source] Combination antiplatelet therapy in patients with peripheral arterial disease: Is the best therapy aspirin, clopidogrel, or both?,,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue S1 2009Emile R. Mohler III MD Abstract Patients with peripheral arterial disease (PAD) are at increased risk of atherothrombotic events. Antiplatelet therapy and risk-factor modification represent the basis of treatment to prevent the ischemic events associated with PAD. The efficacy of aspirin in the secondary prevention of myocardial infarction and stroke has been demonstrated in a large number of trials. More recently, however, the clinical benefit of clopidogrel compared with aspirin in patients with PAD was confirmed. Many clinical trials have evaluated the efficacy of combination antiplatelet therapy in the prevention of recurrent ischemic events in patients with atherosclerotic vascular diseases. Although the results of these studies appear promising, the benefits resulting from dual antiplatelet therapy are counterbalanced by a significant increase in bleeding. Further studies are needed to establish the optimal antiplatelet therapy in the management and prevention of PAD. © 2009 Wiley-Liss, Inc. [source] Antiplatelet drug response variability and the role of platelet function testing: A practical guide for interventional cardiologists,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 1 2009Dominick J. Angiolillo MD Abstract Antiplatelet therapy is the cornerstone of treatment for patients with acute coronary syndrome and is also of particular importance in those who undergo percutaneous coronary intervention with stent implantation. Dual antiplatelet therapy with aspirin and clopidogrel is associated with improvement in long-term clinical outcomes in such patients and is presently the antiplatelet therapy of choice for secondary prevention of thrombotic events. However, a significant number of patients experience recurrent events despite antiplatelet therapy. Although poor patient compliance can account for some of these events, particularly in those patients who receive a drug-eluting stent, increasing evidence indicates that there is variability in response to antiplatelet therapy and patients who have higher levels of platelet reactivity are at increased risk for recurrent ischemic events. However, the lack of a consistent definition of inadequate platelet response, as well as the lack of a standardized measurement technique, has made it difficult to define how to treat these patients. To translate findings associated with variability in platelet response into improved patient care, it is necessary to gain a better understanding of what variable platelet response is, how it is measured, who it should be measured in, and what its clinical relevance is. The objective of this review is to evaluate the data regarding interindividual response variability to antiplatelet therapy with the aim of providing practical considerations and where possible, recommendations, regarding this topic for interventional cardiologists. © 2008 Wiley-Liss, Inc. [source] Evolution of Anticoagulant and Antiplatelet Therapy: Benefits and Risks of Contemporary Pharmacologic Agents and Their Implications for Myonecrosis and Bleeding in Percutaneous Coronary InterventionCLINICAL CARDIOLOGY, Issue S2 2007Hector M. Medina M.D., M.P.H. Abstract Periprocedural myonecrosis, as evidenced by elevated creatine kinase,myocardial bound (CK-MB) levels, occurs in up to 25% of patients undergoing percutaneous coronary intervention (PCI) and has been linked with an increased risk of adverse short- and long-term clinical outcomes. Such myonecrosis arises from three main pathophysiological mechanisms: procedure-related complications, lesion-specific characteristics (e.g., large thrombus burden, plaque volume), and patient-specific characteristics (e.g., genetic predisposition, arterial inflammation). Periprocedural myonecrosis has not been definitively identified as the cause of postprocedural ischemic events, although agents that reduce or prevent thrombosis,including aspirin, thienopyridines, heparin, low-molecular-weight heparins, glycoprotein IIb/IIIa inhibitors, and direct thrombin inhibitors,have been shown to reduce the incidence of ischemic outcomes in this population, as have agents that reduce inflammation (aspirin, statins). At the same time, antithrombotic agents are known to increase the risk of bleeding and the use of transfusions, which have likewise been associated with worse outcomes in these patients. Thus, optimal management of patients undergoing PCI represents a balance between minimizing the risk of ischemic outcomes and simultaneously minimizing the risk of major bleeding. It may be that patients who have only minor, untreated postprocedural elevations in CK-MB level (with no clinical or angiographic signs of ischemia) might have a better prognosis than patients who have normal CK-MB levels but who suffer major bleeding complications. Copyright © 2007 Wiley Periodicals, Inc. [source] Bleeding Complications in Acute Coronary Syndromes and Percutaneous Coronary Intervention: Predictors, Prognostic Significance, and Paradigms for Reducing RiskCLINICAL CARDIOLOGY, Issue S2 2007Steven V. Manoukian M.D. Abstract In clinical trials up to 30% of patients with acute coronary syndromes (ACS) or undergoing percutaneous coronary intervention (PCI) experience bleeding complications, and even higher rates have been reported in contemporary practice. A growing body of data suggests a strong correlation between bleeding and both short- and long-term adverse outcomes, including mortality, which is independent of baseline characteristics and remains evident in most trials, despite variations in the definition of major bleeding. Although the value of antithrombin and antiplatelet therapy in reducing the risk of ischemic events is well established, the mechanisms of action that confer the benefits of these therapies have an inherent tendency to increase the risk of bleeding complications. As a result, characterization of baseline hemorrhagic risk is critical and must be accomplished before selecting an antithrombotic therapy. Risk factors for bleeding may be divided into two categories: nonmodifiable (including age, gender, race, weight, renal insufficiency, anemia, and acuity of presentation) and modifiable (including choice of antithrombotic therapy and PCI procedural characteristics). Of these predictive factors, the choice, dosage, and duration of the antithrombin and/or antiplatelet regimen are perhaps the most readily modifiable, especially in patients with an increased risk of bleeding. This review explores the nature of the association between bleeding and adverse outcomes, including mortality; evaluates risk factors for bleeding; and examines mechanisms for reducing bleeding complications through the selection of appropriate antithrombotic therapy. Copyright © 2007 Wiley Periodicals, Inc. [source] Continuous 12-lead electrocardiographic ST monitoring adds prognostic information to the thrombolysis in myocardial infarction risk score in patients with non-ST-elevation acute coronary syndromesCLINICAL CARDIOLOGY, Issue 4 2005Michael N. Zairis M.D. Abstract Background: Continuous 12-lead electrocardiographic (ECG) ST monitoring and the Thrombolysis In Myocardial Infarction Risk Score (TIMI-RS), both have been shown to be useful for early risk stratification in patients with non-ST elevation acute coronary syndromes (NSTACS). Hypothesis: Transient ST ischemic events, detected by continuous 12-lead ECG ST monitoring, early in the course of NSTACS, may add prognostic information to the TIMI-RS. Methods: In all, 567 consecutive patients with a NSTACS underwent 24-h continuous 12-lead ECG ST monitoring. An ST ischemic event was defined as a transient ST shift in any lead of , 0.10 mV compared with the reference ECG, lasting for ,l min. Results: The incidence of the composite of death, nonfatal myocardial infarction (or reinfarction) and recurrent ischemia by Day 14 was 22.2%. By Day 30, the incidence of the composite of death and nonfatal myocardial infarction (or reinfarction) was 14.7%. There was a significantly increased risk of 14-day (p value for trend < 0.001) or 30-day (p value for trend <0.001) composite endpoint with increasing of TIMI-RS. Moreover, the occurrence of , 1 ST shifts during ST monitoring was associated with a significantly increased risk of 14-(p value < 0.001) or 30-day (p value < 0.001) composite end-point, and this was true throughout the groups of TIMI-RS. Conclusions: The present study suggests that continuous 12-lead ECG ST monitoring, early in the course of NSTACS, may serve as an affordable tool to add prognostic information to the TIMI-RS. [source] Frequency of atrial septal aneurysm in patients with recent stroke: Preliminary results from a multicenter studyCLINICAL CARDIOLOGY, Issue 4 2001Michele Aquilina M.D. Abstract Background: The role of atrial septal aneurysm (ASA) as a risk factor for cerebral ischemia of unknown etiology is controversial. Recent studies have found an association between ASA and focal ischemic events, while results from other studies suggest a low incidence of embolism in patients with ASA. Hypothesis: The present study was designed to evaluate the frequency of ASA, a minor cardioembolic source, in patients with a recent stroke presenting with normal carotid arteries. Methods: In all, 394 patients with cerebral ischemic stroke were referred to our institutions. Patients underwent transthracic and transesophageal echocardiography and carotid artery ultrasound examination. The study population included 215 patients without significant arterial disease. Frequency and morphologic characteristics of ASA were evaluated. Results: Transthoracic examination showed ASA in 39 patients (18%), while transesophageal echocardiography showed ASA in 61 patients (28%). A patent foramen ovale was found in 47 patients (21.8%) and was associated with ASA in 40 patients (65.5%). We observed an increased thickness of the aneurysmatic wall (3.80 ± 1.7 mm) in all patients with ASA. Conclusions: The present study confirms the relationship between ASA and stroke in patients with normal carotid arteries. The most common abnormality associated with ASA was patent foramen ovale. We suggest that patients who have a stroke in the absence of significant carotid disease undergo transesophageal echocardiography to identify possible underlying septal abnormalities. [source] Overview of the relationship between ischemia and congestive heart failureCLINICAL CARDIOLOGY, Issue S4 2000PH.D., Willem J. Remme M.D. Abstract Ischemic heart disease is the principal etiology of heart failure in the Western world. Myocardial ischemia is important in cardiac remodeling, a process that leads to a progressive change in the shape and size of the heart and significantly worsens the prognosis of patients with heart failure. Preventing ischemic events, therefore, is an important goal in the management of patients with coronary artery disease. Statins have been shown to reduce the number of ischemic events in these patients, whereas the benefit of beta-blocker and aldosterone antagonist therapy on ischemic causes of heart failure remains unclear. Several large trials involving patients with asymptomatic left ventricular dysfunction after myocardial infarction or heart failure have shown that angiotensin-converting enzyme (ACE) inhibitors reduce the incidence of progressive heart failure, death, and ischemic events, thus establishing ACE inhibitors as first-line therapy for these patients. Other lines of evidence have suggested that ACE inhibitor therapy may also benefit patients with preserved left ventricular function, a hypothesis that is being evaluated in three large, controlled, randomized trials. One of these trials, the Heart Outcomes Prevention Evaluation (HOPE) study, was terminated prematurely because it demonstrated the significant positive effects of the ACE inhibitor ramipril on cardiovascular outcomes in patients with coronary artery disease and preserved left ventricular function. A growing body of data confirms the relationship between ischemia and heart failure and the benefits of ACE inhibitor treatment in a broad range of high-risk patients. [source] |