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AIMS We aimed to demonstrate whether coronary microvascular function is improved after ticagrelor administration compared to clopidogrel administration in STEMI subjects undergoing thrombolysis. METHODS AND RESULTS MIRTOS is a multicentre study of ticagrelor versus clopidogrel in STEMI subjects treated with fibrinolysis. We enrolled 335 patients

L-RECORD (Left Radial Compared to Femoral Approach for Coronary Angiography in Patients With Previous CABG) is a randomized, prospective, multicenter study comparing coronary angiography (CAG) procedural parameters between left transradial access (L-TRA) and transfemoral access (TFA) in coronary

Coronary symptoms associated with conditions related to mast cell activation and inflammatory cell interactions, such as those involving T-lymphocytes and macrophages, further inducing allergic, hypersensitivity, anaphylactic, or anaphylactic insults, are currently referred to as the Kounis syndrome. Kounis syndrome is caused by inflammatory mediators released during allergic insults, post-inflammatory cell activation, and interactions via multidirectional stimuli. A platelet subset of 20% with high- and low-affinity IgE surface receptors is also involved in this process. Kounis syndrome is not just a single-organ but also a complex multisystem and multi-organ arterial clinical condition; it affects the coronary, mesenteric, and cerebral arteries and is accompanied by allergy–hypersensitivity–anaphylaxis involving the skin, respiratory, and vascular systems in the context of anesthesia, surgery, radiology, oncology, or even dental and psychiatric medicine; further, it has significantly influences both morbidity and mortality. Kounis syndrome might be caused by numerous and continuously increasing causes, with broad clinical symptoms and signs, via multi-organ arterial system involvement, in patients of any age, thereby demonstrating predominant anaphylactic features in terms of a wide spectrum of mast cell-association disorders. Cardiac symptoms, such as chest pain, coronary vasospasm, angina pectoris, myocardial infarction, stent thrombosis, acute cardiac failure, and sudden cardiac death associated with subclinical, clinical, acute, or chronic allergic reactions, constitute the clinical manifestations of this syndrome. Since its first description, a common pathway between allergic and non-allergic coronary events has been demonstrated. The hypothesis is based on the existence of a much higher degree of mast cell degranulation at plaque erosion or rupture sites compared with at the adjacent areas or even more distant segments in post-acute myocardial infarction of non-allergic etiology. Although mast cell activation, differentiation, and mediator release takes days or weeks, the mast cell degranulation may occur just before any acute coronary event, further resulting in coronary artery vasoconstriction and atheromatous plaque rupture. It seems that medications and natural molecules stabilizing the mast cell membrane as well as monoclonal antibodies protecting the mast cell surface can emerge as novel therapeutic modalities for acute coronary and cerebrovascular event prevention.

Objectives The aim of this study was to test the hypothesis that more intensive over standard anticoagulation administered during coronary angiography would significantly reduce rates of radial artery occlusion (RAO). Background RAO, although silent, remains a frequent and therefore worrisome complication following transradial coronary angiography. Anticoagulation is effective in reducing RAO, but the optimal heparin dose remains ill defined. Methods In this multicenter, randomized superiority trial, a high dose (100 IU/kg body weight administered in divided doses) and a standard dose (50 IU/kg body weight) of heparin during 5- or 6-F coronary angiography were compared. A total of 3,102 patients were randomized, of whom 1,836 patients not proceeding to percutaneous coronary intervention and without need for arterial access crossover entered the trial. Post-catheterization hemostasis did not follow a rigid protocol. Results A total of 102 early RAOs were found on ultrasonography (incidence 5.6%). In the high-dose heparin group, the rate of RAO was significantly lower compared with the standard-dose heparin group (27 [3.0%] vs. 75 [8.1%]; odds ratio: 0.35; 95% confidence interval: 0.22 to 0.55; p Conclusions High compared with standard heparin dose significantly reduced the rate of RAO in patients undergoing coronary angiography. High-intensity anticoagulation should be considered in transradial diagnostic procedures. (High [100IU/Kg] Versus Standard [50IU/Kg] Heparin Dose for Prevention of Forearm Artery Occlusion; NCT02570243 )

AIMS The aim of this study was to compare the performance of the Tiger-II with Judkins 3.5L/4R catheters in coronary angiography (CAG) via the transradial approach (TRA). METHODS AND RESULTS Consecutive patients undergoing non-urgent CAG via the right TRA were randomised to either the Tiger-II (Terumo) or Judkins (3.5L/4R; Medtronic) 5 Fr catheters; 320 patients in each group were randomised. Catheter or access site change was required in 57 (17.8%) vs. 68 (21.3%) patients allocated to the Tiger-II and Judkins group, respectively (p=0.3). The study's primary endpoint of contrast volume (ml) used until completion of CAG was lower for Tiger-II vs. Judkins group: 66.8 (54.0-82.0) vs. 73.4 (60.0-94.1), p

Percutaneous transluminal coronary angioplasty with coronary stent implantation is a life-saving medical procedure that has become, nowadays, the most frequent performed therapeutic procedure in medicine. Plain balloon angioplasty, bare metal stents, first and second generation drug-eluting stents, bioresorbable and bioabsorbable scaffolds have offered diachronically a great advance against coronary artery disease and have enriched our medical armamentarium. Stented areas constitute vulnerable sites for endothelial damage, endothelial dysfunction, flow turbulence, hemorheologic changes, platelet dysfunction, coagulation changes and fibrinolytic disturbances. Implant surface attracts several proteins such as albumin, fibronectin, fibrinogen, and complement that lead to complement system activation. Macrophages recognize the implant as foreign substance due to protein adsorption and its continuous presence results in macrophage differentiation and fusion into foreign body giant cells. Polymer coating, stent metallic platforms and the released drugs can act as strong antigenic complex that apply continuous, repetitive, persistent and chronic hypersensitivity irritation to the coronary intima. The concomitant administration of oral antiplatelet drugs and environmental exposures can induce hypersensitivity inflammation. A class of platelets, activated via high-affinity and low-affinity IgE hypersensitivity receptors FCγRI, FCγRII, FCeRI and FCeRII, can induce Kounis hypersensitivity-associated thrombotic syndrome inside the stented coronaries. Type III variant of this syndrome is diagnosed when coronary artery stent thrombosis is associated with thrombus infiltrated by eosinophils or mast cells and/or when coronary intima, media and adventitia adjacent to stent, is infiltrated by eosinophils or mast cells. Careful history of hypersensitivity reactions to all implanted materials and concomitant drugs with monitoring of inflammatory mediators as well as lymphocyte transformation studies to detect hypersensitivity must be undertaken in order to avoid disastrous consequences. Food and Drug Administration recommendations for coronary stent implantation should be applied also to bioresorbable scaffolds. Further studies with inert and non-allergenic implants are necessary.

In the interesting report of Pradhan, Christ and Trapper (1) published in the Journal of Cardiovascular Diagnosis and Therapy , a 22-year-old man developed acute retrosternal pain and chest tightness with ischemic changes in inferolateral wall (ST elevation =0.2 mV) and positive troponin following a single dose of amoxicillin administered for acute tonsillitis treatment. Urgent coronary angiography demonstrated normal coronary arteries. The initial diagnosis of acute ST elevation myocardial infarction (STEMI) was attributed to coronary artery spasm, whereas acute myocarditis considered as a differential diagnosis.

Patients with inflammatory bowel disease (IBD) have a higher incidence of coronary artery disease (CAD) compared with the general population. Left main coronary artery (LMCA) thrombosis constitutes a very rare but catastrophic manifestation of acute coronary syndrome. Case reports describing young patients with IBD and LMCA thrombosis are scarce. Most importantly, patients with a positive family history of thrombotic events and those with significant genetic or acquired risk factors such as the antiphospholipid antibody syndrome, advanced age, immobilization, pregnancy, oral contraceptive use, obesity, diabetes, and cigarette smoking may have a higher risk of thrombosis among those with active IBD. We describe a 28-year-old man who was admitted for coronary angiography (CA) due to ST-segment elevation myocardial infarction. He had a recent exacerbation of ulcerative colitis. The patient was a smoker without a family history of CAD. Proximal total occlusion of the left anterior descending (LAD) artery and left circumflex (LCX) artery with massive thrombus was shown on CA, whereas a normal dominant right coronary artery delivered collaterals to the LAD artery.

Background: Ticagrelor may exert pleiotropic actions, beyond platelet inhibition, which are possibly adenosine-mediated. It has been suggested that in patients with coronary artery disease (CAD) ticagrelor may influence endothelial function. Objective: We aimed to assess the possibility of endothelial function deterioration following ticagrelor treatment cessation. Methods: This was a prospective, observational study, in stable CAD patients with prior percutaneous coronary intervention (PCI) for acute coronary syndrome manifested 1 year earlier, under ticagrelor maintenance dose (90 mg bid) and due to discontinue ticagrelor. Endothelial function was assessed by Peripheral Arterial Tonometry (EndoPat 2000 system, Itamar Medical, Caesarea, Israel) immediately after receiving the last tablet of ticagrelor (Day 0) and at Day 2 and Day 5 post-ticagrelor cessation. Reactive hyperaemia index (RHI) was calculated by automated software and endothelial dysfunction (ED) was defined as a RHI

Background Kounis syndrome is a systemic complication following an allergic reaction, presenting with coronary artery spasm or thrombosis and occasionally with stent thrombosis that can have fatal outcome. Objectives Heparins can induce allergic reactions via tissue antigenicity, heparin induced thrombocytopenia and contact system-activating effects of contaminants but allergy bivalirudin has not been reported so far. Methods Herein, we describe a patient with fatal acute coronary in-stent thrombosis following an allergic reaction soon after an intra-arterial heparin dose and intravenous administration of bivalirudin during angioplasty. Results The patient received intense myocardial infarction protocol treatment including angioplasty and defibillation together with antiallergic therapy but despite all of these efforts and measures, he succumbed 2 h later. Conclusions Significant suspicion should be raised that life saving drugs such as heparin and bivalirudin could join forces with concurrent medication acting as antigens and induce fulminant and fatal stent thrombosis as a manifestation of Kounis syndrome

Radial artery (RA) occlusion (RAO) remains the Achilles heel of transradial coronary procedures. Although of silent nature, RAO is relatively frequent, results in graft shortage for future coronary artery bypass surgery, and may occur even after short-lasting, 5F coronary angiography (CAG). The most frequent predictors of RAO are RA size, body size, female gender, and periprocedural anticoagulation intensity. Methods to detect RAO are variable, of which the Barbeau test and ultrasonography have similar diagnostic accuracy. Data indicate that late RAO recanalization may occur. Meticulous handling of RA and the use of appropriate hemostatic devices and techniques along with sufficient heparin dose appear important measures to reduce RAO rates. Recent contradictory studies indicate that the decreasing incidence of RAO overtime is not as uniform as previously thought. In 2 meta-analyses, the benefit of higher over lower anticoagulation intensity became evident. As “it may all be appropriate anticoagulation” for a simplified approach against RAO, the results of an ongoing trial comparing 100 with 50 IU/kg body weight in transradial CAG are eagerly awaited.

BACKGROUND Delay in the onset of antiplatelet action occurs in patients with ST-elevation myocardial infarction (STEMI) and is likely due to disturbed absorption. We hypothesized that patients presenting relatively late after the onset of symptoms would have faster antiplatelet action. METHODS AND RESULTS We analyzed patient-level data from 5 studies of 207 P2Y12 receptor antagonist-naive patients with STEMI undergoing primary percutaneous coronary intervention (PCI). All patients had available platelet reactivity (PR) assessment with the VerifyNow assay (in P2Y12 reaction units; PRU) prior to and 2 h after loading. High PR (HPR) was defined as ≥ 208 PRU. Pain-to-antiplatelet loading time independently predicted PR at 2 h after loading: every 1-h increase in pain-to-antiplatelet loading time produced a 7% decrease in PR (P=0.001). Pretreatment PR, body mass index, morphine and novel P2Y12 receptor antagonist also affected PR 2 h after loading. Novel P2Y12 receptor antagonist use and per hour increase in pain-to-antiplatelet loading time were independently associated with lower probability for HPR with an OR (95% CI) of 0.145 (0.095-0.220) and 0.776 (0.689-0.873), P

Background: Major, noncoronary complications are rarely encountered following transradial coronary procedures. Methods and Results: Among 1600 prospectively studied patients with complete follow-up, 7 patients experienced major complications following coronary forearm procedures corresponding to an incidence of 0.44%. We found inadvertent symptomatic intramyocardial contrast medium injection, 2 cases with compartment syndrome of which 1 was managed surgically, exertional hand ischemia due to radial artery occlusion, a large ulnar artery pseudoaneurysm, an ulnar arteriovenous fistula, and 1 critical hand ischemia due to late occlusion of the distal brachial artery. Conclusions: Although infrequent, surveillance for major complications should be encouraged after forearm coronary procedures.

Background Radial artery occlusion (RAO) remains the Achilles' heel of transradial coronary procedures. Standard over lower systemic anticoagulation levels are believed to reduce RAO rates but this is ill-supported by scientific evidence. We compared whether standard in comparison with less intensive anticoagulation was superior in preventing vessel closure. Methods and results The two arms of this analysis included 731 pooled patients with the same inclusion and exclusion criteria. We assessed forearm arterial access site occlusion rate by unfractionated heparin (UFH) dose in an individual participant data meta-analysis of this randomized study and of consecutive eligible patients from our previous trial. We randomized 308 consecutive patients undergoing transradial coronary angiography with 5 French (5Fr) catheters without need to crossover to receive 2500 or 5000UFH units. The primary end-point was the ultrasonographically determined vessel occlusion rate. Incident RAOs in the randomized arm were 15.9% vs. 14%, in the low and standard UFH dose, respectively (p=0.7). Corresponding figures for forearm arterial occlusion rates in the pooled population were 13.0% vs. 9.9% (relative risk: 1.3, 95% confidence interval — CI: 0.88–1.98; p=0.2). Procedural and fluoroscopy duration was less than 15 and 3min, respectively. The mean UFH dose difference was 3.52 (95% CI: −0.45 to 7.49) units per kilo body weight between occluded (n=84) and patent forearm arteries (n=647); (p=0.053). Conclusions Incident forearm arterial occlusions were high despite using 5Fr catheters for a short-lasting procedure. Systemic anticoagulation with standard over lower UFH dose did not reduce the frequency of RAOs after coronary angiography.

Background Obstructive Sleep Apnea (OSA) is an independent risk factor for cardiovascular disease and has been linked to the development of atherosclerosis. However, the underlying role of metabolic derangements in the development of atherosclerosis in OSA patients is not well-defined yet. Objective The aim of this study was to test whether patients with newly diagnosed OSA have an increased probability to develop carotid atherosclerosis as compared to healthy individuals. Methods A total of 40 subjects without a previous history of cardiovascular disease that underwent full night polysomnography were included in the study. Subjects with an apnea/hypopnea index (AHI) ≥15/h) were classified as moderate/severe OSA. Ultrasound was used to measure the carotid mean intima media thickness (cIMT) and the presence of atheromatic plaques on both carotid arteries of the subjects. Results All participants were well matched and had a similar cardiovascular risk profile (Framingham risk factors). Moderate to severe OSA was diagnosed in 21 subjects. The two groups had similar measurements of cIMT (0.66±0.17 vs 0.75±0.20 p= 0.33) and presence of atheromatic plaque (50% vs 45%, p=1.00). Conclusion Our study suggests that in patients with a similar cardiovascular risk profile and without history of cardiovascular disease, the severity of newly diagnosed OSA is not correlated to carotid atherosclerosis.

Patients with diabetes mellitus are at increased risk of developing coronary artery disease (CAD) and have an increased incidence of recurrent events following revascularization. Choosing the most appropriate strategy to revascularize these high-risk patients is crucial for improving the clinical outcomes. Several studies, randomized trials and meta-analyses have compared short- and long-term outcomes following coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI) in diabetic patients suffering from CAD. The aim of this article is to review the currently available evidence on the role of PCI and CABG in the management of diabetic patients with CAD.

Red blood cell and platelet microparticles (RBCm and PLTm, respectively) have drawn research attention as to their potential prothrombotic and vasoconstrictive effects in experimental settings. However, the relevance of circulating microparticles in clinical settings is largely undetermined.Circulating microparticles were quantified with a flow cytometric method in blood samples from consecutive STEMI patients after primary PCI. A matched cohort of healthy volunteers was used to derive reference values for comparison. STEMI patients were followed for 6 months for a composite clinical endpoint.Fifty-one STEMI patients (age 59.8 ± 8.8 years) and 50 controls (age 56.2 ± 9.2 years; p=0.155) were enrolled. RBCm concentration was 18,198 ± 6062/μl in the reference cohort versus 33,740 ± 21,169/μl in STEMI patients (p0.001). RBCm count was not correlated to total RBCs (standardized beta 0.018; p=0.861). PLTm did not differ between groups (17,529 ± 16,292/μl in STEMI patients versus 14,372 ± 6211/μl in controls; p=0.203). RBCm c-statistic was 0.832 (95% confidence interval 0.720 to 0.944), while PLTm prognostic value was not statistically significant (c-statistic 0.614, 95% confidence interval 0.444 to 0.784). In the multivariate analysis, RBCm concentration was independently associated with the occurrence of the clinical endpoint, after adjustment for age, ejection fraction, serum creatinine and presence of diabetes (adjusted p=0.034).The present study demonstrates for the first time that erythrocyte microparticles are elevated in patients with STEMI treated with primary PCI, with levels approximately double those measured in a reference population of healthy volunteers, and their concentrations appear to be positively associated with adverse clinical events.

It has been postulated that obstructive sleep apnea (OSA) induces atherosclerosis through direct and indirect atherogenic mechanisms. However, OSA patients carry a higher burden of conventional cardiovascular (CV) risk factors. Therefore, whether OSA is uniquely associated with atherosclerosis or it

Objectives The aim of the present study was to assess the efficacy of remote ischemic post-conditioning (RIPC) by repeated intermittent balloon inflations in preventing acute kidney injury (AKI) in patients with a non–ST-segment elevation myocardial infarction undergoing percutaneous coronary intervention (PCI). Background AKI complicating PCI is associated with increased morbidity and mortality. Remote ischemic preconditioning, using cycles of upper limb ischemia-reperfusion as a conditioning stimulus, has been recently shown to prevent AKI in patients undergoing elective coronary angiography. Methods Eligible patients were randomized to receive RIPC by cycles of inflation and deflation of the stent balloon during PCI or a sham procedure (control patients). The primary endpoint was AKI, defined as an increase of ≥0.5 mg/dl or ≥25% in serum creatinine within 96 h from PCI. The 30-day rate of death or re-hospitalization for any cause was one of the secondary endpoints. Results A total of 225 patients were included (median age, 68 years; 36% female). The AKI rate in the RIPC group was 12.4% versus 29.5% in the control group (p = 0.002; odds ratio: 0.34; 95% confidence interval: 0.16 to 0.71). The number needed to treat to avoid 1 case of AKI was 6 (95% confidence interval: 3.6 to 15.2). The 30-day rate of death or re-hospitalization for any cause was 22.3% in the control group versus 12.4% in RIPC patients (p = 0.05). Conclusions RIPC by serial balloon inflations and deflations during PCI was found to confer protection against AKI in patients with a non–ST-segment elevation myocardial infarction undergoing PCI. The reduction in the rate of AKI translated into a clear trend (of borderline significance) toward better 30-day clinical outcome.

Objectives This study sought to test the hypothesis that colchicine treatment after percutaneous coronary intervention (PCI) can lead to a decrease in in-stent restenosis (ISR). Background ISR rates are particularly high in certain patient subsets, including diabetic patients, especially when a bare-metal stent (BMS) is used. Pharmacological interventions to decrease ISR could be of clinical relevance. Methods Diabetic patients with contraindication to a drug-eluting stent, undergoing PCI with a BMS, were randomized to receive colchicine 0.5 mg twice daily or placebo for 6 months. Restenosis and neointima formation were studied with angiography and intravascular ultrasound 6 months after the index PCI. Results A total of 196 patients (63.6 ± 7.0 years of age, 128 male) were available for analysis. The angiographic ISR rate was 16% in the colchicine group and 33% in the control group (p = 0.007; odds ratio: 0.38, 95% confidence interval: 0.18 to 0.79). The number needed to treat to avoid 1 case of angiographic ISR was 6 (95% confidence interval: 3.4 to 18.7). The results were similar for IVUS-defined ISR (odds ratio: 0.42; 95% confidence interval: 0.22 to 0.81; number needed to treat = 5). Lumen area loss was 1.6 mm2 (interquartile range: 1.0 to 2.9 mm2) in colchicine-treated patients and 2.9 mm2 (interquartile range: 1.4 to 4.8 mm2) in the control group (p = 0.002). Treatment-related adverse events were largely limited to gastrointestinal symptoms. Conclusions Colchicine is associated with less neointimal hyperplasia and a decreased ISR rate when administered to diabetic patients after PCI with a BMS. This observation may prove useful in patients undergoing PCI in whom implantation of a drug-eluting stent is contraindicated or undesirable.

The metal platforms used in interventional cardiology can prevent the late luminal enlargement and induce advantageous vascular remodeling, but have failed to prevent restenosis which remains a problem due to neointimal hyperplasia. Therefore, the first and the second generation drug-eluting stents have been developed in an effort to prevent vessel restenosis. Indeed, drug-eluting stents have significantly reduced in-stent restenosis and target lesion revascularization rates compared with the bare metal stents, but a very dangerous and lethal side effect has emerged with these stents that is acute, late and especially very late stent thrombosis. The thrombus formation inside the stent lumen is the result of platelet adhesion, platelet activation by activating factors that is followed by platelet aggregation (1). This occurs because stented regions constitute an ideal substrate for foreign body reaction due to endothelial damage and dysfunction, hemorheologic changes and turbulence as well as platelet dysfunction, coagulation and fibrinolytic disturbances, at least until re-endothelialization will have been completed (2). Several important papers have been published concerning hypersensitivity toward metallic stent failure such as restenosis-thrombosis, with their authors urging for further studies to be carried out in an effort to prevent, diagnose and treat such dangerous complications. Indeed, in a recent report (3) concerning atopic patient sensitized to nickel, in-scaffold thrombosis had occurred at the mid segment of the absorb bioresorbable vascular scaffold (Abbott Vascular, Santa Clara, California, USA) implanted in-ZES (Resolute Integrity zotarolimus-eluting stent, Medtronic, Santa Rosa, California, USA) for in-stent restenosis. Furthermore, reports that have been published recently have raised important questions about the pathophysiology of allergy-associated in-stent restenosis and thrombosis, as well as their prediction, prevention and treatment (4). The general plea, therefore, for efforts to prevent hypersensitivity-associated complications and especially stent restenosis-thrombosis should take into account the followings

Background: Obstructive Sleep Apnea (OSA) has been associated with both subclinical and accelerated atherosclerosis; however, it remains unknown whether this association is unique or is mediated by the higher burden of co-existing cardio-metabolic disorders frequently seen in patients with OSA. Objective: To prospectively examine whether patients with newly diagnosed moderate/severe OSA carry a higher burden of carotid atherosclerosis as compared to healthy, well matched for all standard Framingham risk factors patients. Methods: A total of 40 subjects without clinically diagnosed cardiovascular disease referred for polysomnography test were included in the study. Subjects with apnea/hypopnea index (AHI) ≥15/h) were classified as moderate/severe OSA. Subclinical changes in carotid atherosclerosis were assessed using mean intima media thickness (cIMT) and presence of atheromatic plaques on both carotid arteries. Measurement was performed using B-mode ultrasonogram. Results: Moderate to severe OSA was diagnosed in 21 subjects. While patients with OSA had a higher BMI compared to healthy subjects, both groups were well matched and of similar cardiovascular risk profile. No significant differences were detected in terms of C-reactive protein levels. The two groups had similar cIMT (0.66±0.17 vs. 0.75±0.20 p=0.33) and presence of atheromatic plaque (50% vs. 45%, p=1.00). Conclusion: Our study suggests that among patients with similar cardiovascular risk profile and free of overt CVD, the severity of newly diagnosed OSA was not correlated with increased inflammation or subclinical carotid atherosclerosis.

There is a paucity of data regarding the early effectiveness of the proposed 600 mg clopidogrel loading dose (LD) on platelet reactivity (PR) in ST elevation myocardial infarction (STEMI) patients. If high on-treatment platelet reactivity (HTPR) is present, prasugrel reloading and subsequent maintenance dose (MD), might offer faster and stronger platelet inhibition than high clopidogrel MD. In 93 STEMI patients treated by primary percutaneous coronary intervention we assessed PR using the VerifyNow P2Y12 platelet function test, 2 h following 600 mg LD of clopidogrel. All the 60 (64.5 %) patients exhibiting HTPR (defined as PR ≥ 235 P2Y12 reaction units), were randomized to 1 of 2 therapeutic strategies: reloading with prasugrel 60 mg/10 mg MD or high (150 mg) clopidogrel MD. The primary endpoint of PR at 24 h post randomization was lower in the prasugrel compared to the clopidogrel group (51.3, 25.7–77.0 versus 242.4, 215.8–268.9 P2Y12 reaction units, least square estimates, 95 % confidence intervals, p

Objectives The study aimed to compare the antiplatelet action of ticagrelor with prasugrel in acute coronary syndrome (ACS) patients with high on-treatment platelet reactivity (HTPR) while on clopidogrel after percutaneous coronary intervention (PCI). Background Newer P2Y12 inhibitors like prasugrel and ticagrelor provide stronger platelet inhibition compared with clopidogrel. Both agents are efficacious in patients with HTPR while on clopidogrel, but direct comparison between them has not yet been reported. Methods In a prospective, single-center, single-blind study, 44 (of 139 screened, 31.7%) ACS patients with HTPR while on clopidogrel 24 h post-PCI were randomized to either ticagrelor 90 mg twice daily or prasugrel 10 mg once daily for 15 days with a crossover directly to the alternate treatment for another 15 days. HTPR was defined as platelet reactivity units (PRU) ≥235 as assessed by the VerifyNow P2Y12 function assay. Results The primary endpoint of platelet reactivity at the end of the 2 treatment periods was lower for ticagrelor (32.9 PRU, 95% confidence interval [CI]: 18.7 to 47.2) compared with prasugrel (101.3 PRU, 95% CI: 86.8 to 115.7) with a least squares mean difference of –68.3 PRU (95% CI: –88.6 to –48.1; p Conclusions In patients with ACS exhibiting HTPR while on clopidogrel 24 h post-PCI, ticagrelor produces a significantly higher platelet inhibition compared with prasugrel. (Ticagrelor Versus Prasugrel in Acute Coronary Syndromes After Percutaneous Coronary Intervention; NCT01360437 )

A 27-year-old primigravida presented with chest pain, ST-segment elevation in electrocardiogram leads I, aVL, and V1 to V6, positive troponin I, and apical hypokinesia with a left ventricular ejection fraction of 45%, 20 days following a cesarean section. The patient was a smoker, with no other

Percutaneous coronary interventions are increasingly applied in patients with complex coronary anatomy, including those with stem disease. Coronary artery bypass surgery confers a mortality reduction over optimal medical therapy in high-risk patients with both left main or multivessel coronary artery disease and left ventricular systolic dysfunction. Whether PCI might be preferred as an initial strategy in stable patients with multivessel disease and/or LM disease remains debatable. Emerging evidence suggests that patients with higher atheroma burden, as indicated by older age, presence of diabetes mellitus and extensive MVD in combination with LV dysfunction may derive the greatest benefit from CABG. PCI for unprotected LM with limited additional disease has been revised to a class II recommendation in the recent U.S. and European guidelines. An interdisciplinary team of both cardiac surgeons and cardiologists may optimize treatment in patients with intermediate-to-high disease severity characteristics. Ongoing trials will further strengthen evidence-base clinical decision making.

Objectives The primary aim of the study was to determine the antiplatelet effects of prasugrel versus high-dose clopidogrel in patients with high on-treatment platelet reactivity (HTPR) after percutaneous coronary intervention (PCI) and, secondarily, their relation to cytochrome (CYP) 2C19*2 carriage. Background High on-treatment platelet reactivity after clopidogrel administration after PCI is linked to the loss-of-function CYP2C19*2 allele and accompanied by an increased risk of adverse events. Methods We performed a prospective, randomized, single-blind, crossover study of platelet inhibition by prasugrel 10 mg/day versus high-dose 150 mg/day clopidogrel in 71 (of 210 screened; 33.8%) post-PCI patients with HTPR. Platelet function was assessed by the VerifyNow assay (Accumetrics, San Diego, California), and real-time polymerase chain reaction genotyping was performed for CYP2C19*2 carriage. Results The primary endpoint of platelet reactivity (measured in platelet reactivity units) at the end of the 2 treatment periods was lower after prasugrel compared with clopidogrel (least-squares estimates 129.4, 95% confidence interval [CI]: 111.1 to 147.7 versus 201.7, 95% CI: 183.2 to 220.2; p Conclusions In patients with HTPR after PCI, prasugrel is more effective compared with high clopidogrel in reducing platelet reactivity, particularly in CYP2C19*2 carriers. Genotyping guidance might be helpful only in case an increased clopidogrel maintenance dose is considered. (Prasugrel Versus High Dose Clopidogrel in Clopidogrel Resistant Patients Post Percutaneous Coronary Intervention (PCI); NCT01109784)

Objectives: β-Thalassemias are inherited hemolytic anemias with a broad phenotype and an increased rate of vascular complications despite a near absence of coronary artery disease. Methods: We investigated the presence of endothelial dysfunction and subclinical atherosclerosis in non-transfusion-dependent patients with β-thalassemia intermedia (β-TI) by means of flow-mediated (FMD) and flow-independent (FID) brachial artery dilatation and carotid artery intima-media thickness. Results: In 20 nondiabetic young adults with β-TI, FMD (6.6 ± 3.7 vs. 10.3 ± 3.1%; p = 0.002) and FID (14.0 ± 4.7 vs. 18.0 ± 5.6%; p = 0.02) were both lower relative to the values in 20 matched control subjects, whereas the intima-media thickness was increased (0.51 ± 0.09 vs. 0.46 ± 0.07 mm; p = 0.049). Fibrin generation, soluble endothelial activation markers, and proinflammatory proteins were higher in the patient group, while the plasma cholesterol level was lower. Conclusions: These findings indicate premature atherosclerosis among patients with β-TI; this is in accord with the high incidence of noncoronary vascular episodes in β-TI.

β-Thalassemia is an inherited hemoglobin disorder resulting in chronic hemolytic anemia that typically requires life-long transfusion therapy. Although traditionally prevalent in the Mediterranean basin, Middle East, North India, and Southeast Asia, immigration of those populations to North America and Western Europe has rendered β-thalassemia a global health problem. Cardiac complications represent the primary cause of mortality and one of the major causes of morbidity in those patients. Heart disease is mainly expressed by a particular cardiomyopathy that progressively leads to heart failure and death. The β-thalassemia cardiomyopathy is mainly characterized by 2 distinct phenotypes, a dilated phenotype, with left ventricular dilatation and impaired contractility and a restrictive phenotype, with restrictive left ventricular filling, pulmonary hypertension, and right heart failure. The pathophysiology of the disorder is multifactorial, with a central role of myocardial iron overload and the significant contribution of immunoinflammatory mechanisms. Patients’ management is demanding and requires a multidisciplinary approach, preferably in specialized centers.

Stent components acting as potential antigens and promoting intracoronary mast cell activation can lead to catastrophic intrastent thrombosis. Patients with drug-eluting stent (DES) implantation are prone to hypersensitivity reactions from five potential antigens namely, nickel strut, polymer coating, eluted drug, as well as, concomitant drugs clopidogrel and aspirin. These events may be more common than suspected because it is hard to document them, unless they become systemic, in which case they manifest themselves as the Kounis syndrome characterized by the concurrence of acute coronary events with hypersensitivity reactions. This report concerns of a patient with implanted DES who developed an acute myocardial infarction in the stent area following an allergic reaction to contrast material.