[An unexpected cause of dyspnea and degradation of performance]. / Dyspnoe und Leistungsminderung mit unerwartetem Ausgang.

HISTORY AND ADMISSION FINDINGS: A 55-year old man suffers from progressive, distinctive dyspnoea and physical weakness since 5 days. Due to ST-segment changes in the ECG and a positive troponin-test, the primary care physician initiates an hospitalization. INVESTIGATIONS: After admission, the laboratory tests confirm the elevated troponin-values, and show additionally elevated pro-brain-natriuric-peptide-values. The coronary angiography presents a highly reduced left ventricular function, an aortic insufficiency III° and a coronary heart disease. DIAGNOSIS, TREATMENT AND COURSE: After clinical deterioration and fever up to 42°C with consecutive tachycardia, the patient is taken over to the intensive care unit. Blood cultures are taken and an empirical antibiotic treatment is started. The patient dies within a few hours in catecholamine refractory circulatory failure. In the autopsy we find signs of an acute recurrent bacterial aortic valve endocarditis with a paravalvular abscess in the myocardium and a septic abscess in the left kidney. The patient died on acute left ventricular failure. DISCUSSION: The manifestation of an endocarditis can be presented very variable and can thus be a challenge in clinical practice. For one thing, the disease presents as an acute, rapidly progressive infection, on the other hand it acts as subacute or chronic disease with just little fever and nonspecific symptoms. To initiate an adequate therapy without loss of time, endocarditis should be included in the differential diagnosis where the risk profile is evident. There are risk factors (poor dental status, intravenous drug use, artificial valve or cardiological devices) for endocarditis. These risk factors with additional symptoms should always be given to a further diagnostics to detect an endocarditis. In addition to a multiple cultivation and laboratory analysis additional diagnostics such as ECG, echocardiography (transthoracic, transthoracic) and chest X-ray should be performed. Further stratification of patients is then performed using the modified Duke criteria. The anti-infective therapy is carried out using the new ESC Guidelines (2015). If a surgical procedure is indicated, this should be done in close consultation with the colleagues of Thoracic and Cardiovascular Surgery.

Clinical outcome and paravalvular leakage of the new balloon-expandable Edwards Sapien 3 valve in comparison to its predecessor model (Edwards Sapien XT) in patients undergoing transfemoral aortic valve replacement.

OBJECTIVES: The aim of this study was to compare the 30-day procedural, clinical and echocardiographic outcome of the new balloon-expandable Edwards Sapien 3 (ES3) valve with the Edwards Sapien XT (ESXT). BACKGROUND: Post-implant paravalvular leaks (PVL) after transfemoral aortic valve replacement (TAVR) resulting in residual aortic regurgitation (AR) are a major limitation for long term outcome. New TAVR-devices have to eliminate this problem. METHODS: Transfemoral TAVR was performed in 209 consecutive intermediate-high-risk surgical patients (pts) with symptomatic aortic stenosis (ESXT n = 102, ES3 n = 107). Transthoracic echocardiography (TTE) and 3-dimensional computed tomography were used for valve size selection. Primary endpoint of the study was none/trace AR derived by TTE 30-days after TAVR. RESULTS: All pts underwent successfully TAVR with a combined device success of 100/102 (99%) in ESXT and 107/107 (100%) in ES3 pts. Fluoroscopy time (ESXT 11.8 ± 0.5 min vs. ES3 10.0 ± 0.5 min, P = 0.003) and contrast (ESXT 188.9 ± 5.6 mL vs. ES3 170.4 ± 4.7 mL, P = 0.04) were significantly lower in ES3 patients. 30-day clinical events did not differ. Transvalvular mean pressure gradients were significantly reduced to 7.4 ± 0.8 mmHg after ESXT and to 10.1± 0.4 mmHg after ES3 implantation. After 30 days none/trace AR was found in 34.3% (n = 35) of all ESXT pts in contrast to 89.7% (n = 96) of all ES3 patients. Moderate-to-severe AR was found rarely (ESXT 2.9% vs. ES3 0%, P = 0.073). CONCLUSIONS: Although there was no significant difference in 30 day mortality, the newer ES3 valve reduced significantly residual paravalvular leakage. © 2016 Wiley Periodicals, Inc.

Platelet activation is less enhanced in the new balloon expandable Edwards Sapien 3 valve compared to its predecessor model (Edwards Sapien XT).

Stroke and thromboembolic events after transfemoral aortic valve replacement (TAVR) continue to be a problem. The aim of our study was to compare platelet aggregation (Agg) and platelet activation (PA) observed with two different catheter valves, the ESV-XT and the newer ESV-3 valve in patients (pts) undergoing TAVR on dual antiplatelet therapy (DAPT). A total of 174 patients with severe aortic stenosis and high surgical risk successfully underwent TAVR (60 ESV-XT; 114 ESV-3). Platelet Agg and PA (CD62P expression) were evaluated before and the following three days after TAVR under DAPT. Platelet Agg was inhibited to the same extent in both valve types and there was no significant difference in platelet drop between both valve types between day 0 and day 3 [ESV-XT vs ESV-3: median (25th-75th percentile): platelet count (x1000): 55 (42-74) vs 61(42-93), p=0.280]. However, there was an enhanced CD62P expression directly after TAVR with the ESV-XT compared to the ESV-3 [CD62P (MIF): 7.4 (6.8-8.6) vs 6.6 (6-7.9), p=0.014]. Surface expression of platelet CD62P was associated with the occurrence of residual aortic regurgitation (AR) and was significantly higher in patients with residual AR [CD62P (mild AR) vs CD 62P (no or trace AR): 7.9 (7.3-9.1) vs 7.1 (6.4-8.0), p < 0.001)]. PA was significantly enhanced in patients with the ESV-XT compared to the ESV-3 valve and was associated with the amount of residual AR which was significantly reduced by ESV-3. This may have implications for thromboembolic events following TAVR procedure.

Fish-Free Diet in Patients with Phenylketonuria Is Not Associated with Early Atherosclerotic Changes and Enhanced Platelet Activation.

BACKGROUND AND PURPOSE: Since patients with phenylketonuria (PKU) have to follow a lifelong restriction of natural protein to lower phenylalanine-intake, they never eat fish. This diet may lead to a chronic deficit of omega-3 and omega-6 fatty acids with the risk of early atherosclerotic changes. The aim of the study was to analyse the fatty acid profile of PKU patients and to correlate the results with surrogate markers of early atherosclerotic changes [enhanced carotid intima media thickness (CIMT) and ß-stiffness index] and platelet activation. METHODS: In 43 PKU patients and in 58 healthy controls we prospectively examined the fatty acid profile, CIMT, ß-stiffness index and platelet activation (flow cytometric determination of markers of platelet activation). CIMT was measured bilaterally by ultrasound. CIMTmean was defined as the mean value of the sum of CIMTleft and CIMTright. RESULTS: Despite of lower HDL-cholesterol and higher triglyceride concentrations in the PKU group, there was no significant difference in the omega-6 or omega-3 fatty acid profile, CIMT, ß-stiffness index between both groups. Platelet activation was not enhanced in the PKU group. CONCLUSIONS: Fish-free diet does not induce early atherosclerotic changes or enhanced platelet activation in PKU patients.

Haemodialysis impairs clopidogrel but not aspirin responsiveness in patients with end-stage renal disease. Results of a pilot study.

Dual antiplatelet therapy (DAPT) with aspirin (ASA) and clopidogrel (Clp) is the standard treatment to reduce ischaemic coronary events, but in patients with end-stage renal disease (ESRD) the efficacy of Clp remains unclear. Patients with ESRD are at higher risk for coronary artery disease (CAD) and also their post-interventional outcome is worse compared to patients with normal renal function. Little is known about the influence of haemodialysis (HD) on ASA and Clp responsiveness. To assess the effect of HD on ASA- and Clp-responsiveness in patients with documented CAD and ESRD, 31 patients with ESRD (mean age 66.5 ± 1.8 years, 23 male) on DAPT were evaluated for their ASA and Clp responsiveness with the Verify Now System (Accumetrics Inc.) We measured the antiplatelet effect in all ESRD patients at three time points: T1: just before HD; T2: directly after HD; T3: steady state on a HD free day one week after T1. In our study at baseline 10 (32.3%) patients were ASA-low responder (ASA-LR) and 14 (45.2%) patients Clp-low responder (Clp-LR). There was a significant difference in the PRU values before (T1) and immediately after HD (T2) [PRU T1=234 (169; 274) vs PRUT2= 247 (199; 278); pT1,2=0.036; ]. Results were shown as median ARU T1 (25th, 75th percentile) or median PRU T1 (25th, 75th percentile). Hence HD seems to impair responsiveness to Clp, resulting in an increase of 6.5 % Clp-LR. No significant differences in the ARU values at the different time-points were found.

Student tutors for hands-on training in focused emergency echocardiography--a randomized controlled trial.

BACKGROUND: Focused emergency echocardiography performed by non-cardiologists has been shown to be feasible and effective in emergency situations. During resuscitation a short focused emergency echocardiography has been shown to narrow down potential differential diagnoses and to improve patient survival. Quite a large proportion of physicians are eligible to learn focused emergency echocardiography. Training in focused emergency echocardiography usually comprises a lecture, hands-on trainings in very small groups, and a practice phase. There is a shortage of experienced echocardiographers who can supervise the second step, the hands-on training. We thus investigated whether student tutors can perform the hands-on training for focused emergency echocardiography. METHODS: A total of 30 volunteer 4th and 5th year students were randomly assigned to a twelve-hour basic echocardiography course comprising a lecture followed by a hands-on training in small groups taught either by an expert cardiographer (EC) or by a student tutor (ST). Using a pre-post-design, the students were evaluated by an OSCE. The students had to generate two still frames with the apical five-chamber view and the parasternal long axis in five minutes and to correctly mark twelve anatomical cardiac structures. Two blinded expert cardiographers rated the students' performance using a standardized checklist. Students could achieve a maximum of 25 points. RESULTS: Both groups showed significant improvement after the training (p < .0001). In the group taught by EC the average increased from 2.3±3.4 to 17.1±3.0 points, and in the group taught by ST from 2.7±3.0 to 13.9±2.7 points. The difference in improvement between the groups was also significant (p = .03). CONCLUSIONS: Hands-on training by student tutors led to a significant gain in echocardiography skills, although inferior to teaching by an expert cardiographer.

Clinical cardiac safety profile of nilotinib.

BACKGROUND: Nilotinib is a second-generation tyrosine kinase inhibitor with significant efficacy as first- or second-line treatment in patients with chronic myeloid leukemia. Despite preclinical evidence indicating a risk of prolongation of the QT interval, which was confirmed in clinical trials, detailed information on nilotinib's cardiac safety profile is lacking. DESIGN AND METHODS: Here, we retrospectively assessed cardiovascular risk factors in 81 patients who were being or had previously been treated with nilotinib therapy and evaluated cardiovascular parameters by longitudinal monitoring of the QT interval and left ventricular ejection fraction. Detailed information on the occurrence and management of defined cardiac adverse events was extracted. RESULTS: The median duration of nilotinib therapy was 26 months (range, 1-72). The median QT interval at baseline was 413 msec (range, 368-499 msec). During follow-up, the median QT was not significantly different from the baseline value at any time-point. Sixteen of 81 patients (20%) had new electrocardiographic changes. Cardiac function, as assessed by measurement of left ventricular ejection fraction, did not change significantly from baseline at any time-point. During a median follow-up of 44 months (range, 2-73), seven patients (9%), all of whom had received prior imatinib therapy, developed 11 clinical cardiac adverse events requiring treatment. The median time from the start of nilotinib therapy to an event was 14.5 months (range, 2-68). Five of seven patients were able to continue nilotinib therapy with only one brief interruption. CONCLUSIONS: Whereas new electrocardiographic abnormalities were recorded in 20% of all patients and some of them developed severe or even life-threatening coronary artery disease, QT prolongation, changes in left ventricular ejection fraction, and clinical cardiac adverse events were uncommon in patients treated with nilotinib.

Low responsiveness to clopidogrel increases risk among CKD patients undergoing coronary intervention.

Patients with CKD are at higher risk for major events after percutaneous coronary intervention (PCI) compared with subjects with normal renal function. The aims of this study were to evaluate responsiveness to clopidogrel in patients with CKD and to examine the effect of antiplatelet drug response on post-PCI outcome. We retrospectively evaluated a consecutive cohort of 1567 patients with symptomatic coronary artery disease undergoing PCI, 648 (41%) of whom had stage 3 to 5 CKD. We assessed responsiveness to clopidogrel by ADP-induced platelet aggregation after oral administration of a 600-mg clopidogrel loading dose and 100 mg of aspirin. In a multivariate survival analysis that included 1335 (85%) of the cohort, stage 3 to 5 CKD and low response to clopidogrel were independent predictors of the primary end point (composite of myocardial infarction, ischemic stroke, and death within 1 year). In summary, a low response to clopidogrel might be an additional risk factor for the poorer outcomes in patients with stage 3 to 5 CKD compared with patients with better renal function.

Impact of inflammatory markers on platelet inhibition and cardiovascular outcome including stent thrombosis in patients with symptomatic coronary artery disease.

BACKGROUND: There is cumulative evidence that the degree of inflammation correlates with prognosis after percutaneous coronary interventions (PCI). Additionally, there is a cross-link between platelet activation and inflammatory pathways. The aim of the present analysis was to evaluate the association of inflammatory markers and effects of dual antiplatelet therapy on platelet function and outcome in patients undergoing PCI. METHODS AND RESULTS: In a pilot study, 157 patients with symptomatic coronary artery disease (CAD) undergoing PCI were consecutively evaluated. Platelet response to clopidogrel and acetylsalicylic acid was assessed using whole blood multiple electrode aggregometry (MEA). Baseline levels of IL-6, RANTES and MCP-1 were measured by Bio-Plex Cytokine assay. C-reactive protein (CRP) was determined by Immunoassay. Levels of IL-6, RANTES, and CRP correlated well with ADP and arachidonic acid (AA)-induced MEA. In a second step, a retrospective analysis of a cohort of 903 PCI-patients was performed to evaluate the association of on-treatment residual platelet aggregation (RPA) and baseline CRP levels on the incidence of myocardial infarction (MI), death and stent thrombosis (ST). Patients suffering a subsequent event had a significantly higher level of baseline CRP and higher RPA compared to patients without events. After multivariate adjustment high baseline CRP and high RPA were independent predictors for combined major events and ST after PCI. CONCLUSION: To our knowledge this is the first study linking inflammation, antiplatelet drug responsiveness and outcome in a large CAD-patient cohort. The results suggest a relevant interaction of these parameters and encourage multimodal therapeutic approaches to treat cardiovascular risk after PCI.

Interaction of platelets and inflammatory endothelium in the development and progression of coronary artery disease.

An expanding body of evidence emphasizes the role of platelets as initial actors in inflammatory diseases such as atherosclerosis. Platelets interact with leukocytes and endothelial cells and enforce monocyte transformation into macrophages. Platelets not only mediate the recruitment of leukocytes. They also bind oxidized phospholipids and may promote foam cell formation. Platelets furthermore recruit progenitor cells to the scene, which are able to differentiate into foam cells or endothelial cells, presumably depending on the local microenvironment. Furthermore, platelets are capable of promoting the recruitment of circulating dendritic cells and influencing their functions, thereby presumably modulating immune reactions in atherogenesis. Taken together, platelets may participate in the initiation, development, and total extent of atherosclerotic lesions.

Oxidized LDL-activated platelets induce vascular inflammation.

Platelets are involved in the initiation of atherosclerosis by adherence to inflamed endothelium. Monocytes bind to these platelets and transmigrate into the vessel wall, transforming into macrophages and foam cells. We have previously shown that lipid-laden platelets are phagocytosed by macrophages. In this study we investigated the functional consequences of oxidized low-density lipoprotein (oxLDL) uptake on platelet function and interaction with the endothelium. Human platelets were isolated from healthy donors and activated by adenosine diphosphate. Immunofluorescence microscopy and flow cytometry revealed that oxLDL is located intracellularly in vesicles. With mepacrine costaining and confocal microtomography, we were able to identify dense granules as the vesicles that contain oxLDL. OxLDL-laden platelets induced intercellular adhesion molecule 1 expression in endothelial cells more than exogenous native LDL, oxLDL, and oxLDL-negative platelets. Furthermore, oxLDL-laden platelets induced foam cell development from CD34(+) progenitor cells. On endothelial regeneration, oxLDL-laden platelets had the opposite effect: The number of CD34(+) progenitor cells (colony-forming units) able to transform into endothelial cells was significantly reduced in the presence of oxLDL-platelets, whereas native LDL had no effect. Our results demonstrate that activated platelets internalize oxLDL and that oxLDL-laden platelets activate endothelium, inhibit endothelial regeneration, and promote foam cell development. Platelet oxLDL contributes significantly to vascular inflammation and is able to promote atherosclerosis.

Diagnostic and therapeutic potentials of platelet glycoprotein VI.

Platelets respond immediately to vascular injury by adhesion, aggregation, and thrombus formation. Disruption of the endothelial cell layer exposes extracellular matrix to the bloodstream. Collagen binding to platelet glycoprotein VI (GPVI) mediates the initial adhesion of the rolling platelet to the vascular wound. Signaling by GPVI leads to the onset of the platelet activation cascade that is finally crowned by a firm and shear-resistant integrin-based adhesive clot. Blockade of collagen binding to GPVI would prevent initial adhesion and further activation of the platelet and would have an enormous impact in antithrombotic therapy. Besides the therapeutical implication, radiolabeled GPVI gives us a valuable diagnostic means that may be used clinically for plaque imaging in the near future.

Pericardial effusion as primary manifestation of Takayasu arteritis.

Takayasu arteritis (TA) is a chronic vasculitis, affecting young women in 80-90% of cases with greatest prevalence in Asians. As exudative pericarditis is an extremely rare, but a possible manifestation of TA, we report on a young women who presented with recurrent febrile pericardial effusion as primary manifestation of TA.

Is routine ultrasound guidance really necessary for closure of patent foramen ovale using the Amplatzer PFO occluder?

OBJECTIVES: The aim of the study was to evaluate safety, efficacy, and long-term clinical outcome of percutaneous closure of patent foramen ovale (PFO closure) in a low volume center using the Amplatzer PFO occluder without echocardiographic guidance. BACKGROUND: Most centers perform PFO closure either by transesophageal echocardiography (TEE) or intracardiac echocardiography (ICE) guidance for optimal device selection. As TEE is poorly tolerated by patients in supine position and ICE is a costly alternative that increases vascular access complications, we wanted to assess the safety and efficacy of PFO closure by fluoroscopic guidance only. METHODS: Before PFO closure, all patients had a diagnostic contrast-TEE and morphological classification of PFO. All PFO closures were performed using the 25-mm Amplatzer PFO occluder with fluoroscopic guidance only. Intraprocedural echocardiography was replaced by right atrial opacification using contrast angiography. Contrast TEE was done after 6 weeks, contrast TTE after 3, 6, and 12 months postprocedural. RESULTS: In all 92 patients (52.4 +/- 1.5 years), a 25-mm Amplatzer PFO occluder was implanted in the correct position. Total fluoroscopic time was 8.4 +/- 0.6 minutes and the application of contrast medium was 122.5 +/- 5.8 mL. By contrast-TEE, 12 patients (13 %) showed a small residual shunt (grade 1). During follow-up (2.09 +/- 0.13 years) two patients (2.1%) suffered from a recurrent event (TIA in both cases). CONCLUSIONS: Percutaneous closure of PFO using the 25-mm Amplatzer PFO occluder guided by fluoroscopy only is a safe and efficacious intervention for nearly all patients.

Stress echocardiography for risk stratification of asymptomatic patients with type 2 diabetes mellitus.

BACKGROUND: The purpose of this study was to assess stressechocardiography (SE) for risk stratification of asymptomatic type 2 diabetic patients (DM2) without known coronary artery disease CAD. METHODS: A total of 211 consecutive, asymptomatic DM2 patients underwent exercise (n=177) or dobutamine (n=34) SE and were followed up for 11+/-2 months. Primary endpoint was a major cardiac or vascular event (MACCE; all-cause-death, non-fatal myocardial infarction, coronary revascularization procedures, cerebrovascular event, acute limb-ischemia). RESULTS: During follow-up 39 of these patients suffered a MACCE. SE correctly identified 33 of these 39 patients by demonstrating silent ischemia in advance. In a multivariate logistic regression analysis a positive SE turned out to be an independent predictor for the occurrence of a MACCE during 11+/-2 months. CONCLUSIONS: SE represents an effective tool for risk stratification of asymptomatic DM2 patients.

Electrical remodeling and cardiac dimensions in patients treated by cardiac resynchronization and heart failure controls.

BACKGROUND: Cardiac resynchronization therapy (CRT) reduces the left ventricular diameter (LVEDD) in heart failure (HF) patients with left bundle branch block (LBBB). The study compares structural and electrical remodeling in HF patients on CRT and matched HF controls without LBBB. METHODS: In 42 patients (64 +/- 9 years left ventricular ejection fraction [LVEF] 25 +/- 8%, 16 coronary artery disease, 26 nonischemic cardiomyopathy, 21 with LBBB and CRT indication vs 21 controls [matched for gender, age, LVEF, and underlying disease]) an unpaced electrocardiogram (ECG) and echocardiogram were recorded at baseline (bl) and after 20.6 +/- 13.8 months (fup). LVEDD, left atrial (LA) width, mitral regurgitation (MR), P-wave, PR interval, QRS width, QRS vector, and QT interval were analyzed. RESULTS: LVEDD diminished with CRT (bl 68.7 +/- 10.3 vs fup 62.0 +/- 7.7 mm, P = 0.002). Controls showed no change (bl 64.1 +/- 9.4 vs fup 64.8 +/- 8.4 mm, P = n.s.). MR improved with CRT (bl 1.2 +/- 0.6 vs fup 0.8 +/- 0.7, P = 0.02), but not among controls. LA width tended to decrease on CRT (CRT bl 48.9 +/- 4.4 vs fup 46.9 +/- 7.2 mm, P = 0.17, controls bl 48.5 +/- 5.1 vs fup 47.5 +/- 6.5 mm, P = 0.49). PR interval lengthened in both groups (CRT bl 175 +/- 29 vs fup 188 +/- 30 ms, P = 0.03, controls bl 177+/-25 vs fup 187 +/- 19 ms, P = 0.27). QRS increased in both groups (CRT bl 165 +/- 22 vs fup 171 +/- 20 ms, P = 0.07, controls bl 111 +/- 17 vs fup 118 +/- 19 ms, P = 0.01). Analyses revealed no significant association of echocardiographic and ECG parameters. CONCLUSIONS: Despite LVEDD reduction with CRT, electrical activation does not recover. Electrical remodeling does not differ between LBBB patients under CRT and matched controls without CRT indication.

Baseline Doppler parameters are useful predictors of chronic left ventricular reduction in size by cardiac resynchronization therapy.

AIMS: The identification of responders to cardiac resynchronization therapy (CRT) in patients with left ventricular (LV) dysfunction and left bundle branch block (LBBB) remains difficult. We aimed to define the predictive value of conventional Doppler parameters. METHODS AND RESULTS: In 73 patients (65 +/- 9 years, 51 male, 36 ischaemic, 37 non-ischaemic cardiomyopathy, QRS 167 +/- 31 ms, LVEF 23 +/- 6%) with LBBB, a CRT device was implanted. LV pre-ejection interval (PEI), interventricular mechanical delay (IVMD), LV filling time (FT), and myocardial performance index (MPI) were assessed at baseline and on optimized CRT. Left ventricular end-diastolic diameter (EDD) was obtained at baseline and after 10.6 +/- 6.7 months. end-diastolic diameter diminished from 66.3 +/- 8.1 to 59.9 +/- 9.6 mm (P < 0.001). Initial LVPEI (r = 0.41, P < 0.001), baseline IVMD (r = 0.34, P = 0.003), acute LVPEI shortening (r = 0.33, P = 0.006), and baseline LVEDD (r = 0.32, P = 0.007) correlated with LVEDD reduction. An LVPEI > or =140 ms had a 82% accuracy to predict long-term LVEDD reduction (sensitivity 86%, specificity 67%, positive and negative predictive values 91 and 56%, respectively). Multivariate analysis solely revealed baseline LVPEI as predictor of LVEDD reduction. FT and MPI correlated only with their respective improvements. CONCLUSION: Left ventricular pre-ejection interval and IVMD predict favourable LV remodelling on CRT. The additional application of tissue Doppler parameters may further increase specificity and negative predictive value.

Hyperresponsiveness of platelets in ischemic stroke.

Platelet activation and aggregation are critical in the pathogenesis of acute ischemic cerebrovascular diseases. The aim of our study was to characterize platelet function in patients with acute ischemic stroke or transient ischemic attack (TIA), and to evaluate the effect of platelet activation on clinical outcome. One hundred thirty-eight consecutive patients with TIA (n = 74) or stroke (n = 64) were enrolled in this study. Platelet aggregation in response to ADP, epinephrine, arachidonic acid, or collagen, and expression of platelet activation receptors (CD62P, CD63, LIBS-1 and PAC-1) in the acute phase and at three months follow-up were evaluated. Platelets derived from stroke patients were more hyperaggregable in response to agonists in the acute phase compared to TIA patients (p[ADP] = 0.002, p[arachidonic acid] = 0.047, p[epinephrine] = 0.020). Platelet activation was enhanced in the acute phase irrespective of the severity of the disease (stroke or TIA) and returned to baseline levels three months later. Persistent elevated platelet activation at three months follow-up (PAC-1) was associated with increased incidence of recurrent stroke (median, [interquartile range] 3.4, [3.0-5.2] versus 2.9, [2.3-4.0], p = 0.048). In conclusion, platelets are hyperactive in acute stroke compared with TIA. A more intensified dual antiplatelet therapy may be of benefit for stroke patients.