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A 12-year-old male patient suffering from congenital glaucoma developed bradycardia, left ventricular failure, and hypotension after induction of anesthesia. Electrocardiography and echocardiography revealed a complete normalization of ECG and a complete spontaneous recovery in the cardiac function 72 hours from the beginning of the clinical manifestations, while cardiac Magnetic Resonance Imaging was performed, and coronary Computed Tomography scan revealed a myocardial bridge of a tract of the left anterior descendent coronary artery. Diagnosis of Kounis syndrome (KS) was made, a relatively novel, under-recognized clinical condition, defined as the manifestation of an acute coronary syndrome accompanied by mast cell activation and platelet aggregation involving interrelated and interacting inflammatory cells in the setting of allergic, hypersensitivity, anaphylactic or anaphylactoid insults. We described one of the first pediatric cases of KS related to anesthetic medications. In children, this syndrome has been only described in isolated case reports or small case series. Thus, it appears critical to report new cases of KS in children to increase the awareness of this disease in pediatric healthcare workers so as to enhance its early recognition and optimal therapeutic strategy. Furthermore, it appears of paramount importance the implementation of universal guidelines accepted by allergology and cardiology societies, in order to standardize the management of pediatric and adult patients with KS. Finally, a close collaboration between pediatric allergists and cardiologists seems fundamental for an optimal multidisciplinary patient care.

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.

In the very important meta-analysis published this month in Acta Cardiologica [1] that was performed to comprehensively evaluate the risk of major bleeding events, the authors found that non-vitami...

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 )

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.

Kounis syndrome is the concurrence of coronary spasm, acute myocardial infarction or stent thrombosis, with allergic reactions in the setting of mast-cell and platelet activation. In this report Kounis syndrome manifesting as stent thrombosis with left ventricular thrombus formation was triggered by a food-induced allergic reaction. The allergic reaction to food was confirmed by oral rice pudding ingredients challenge test while skin tests were inconclusive. To our knowledge, this is first report of early stent thrombosis secondary to food allergic reaction in a 70-year-old man patient who was found to have left ventricular thrombus and undiagnosed hypertrophic cardiomyopathy.

Objective To conduct a systematic review evaluating the utility of brain natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) as biomarkers in adult patients with septic shock. Materials and methods Pubmed/Medline databases were searched from inception to November 2018 using the search terms: (septic[Title/Abstract] AND shock[Title/Abstract]) AND bnp[Title/Abstract]) and (septic[Title/Abstract]) AND shock[Title/Abstract]) AND natriuretic[Title/Abstract]). No restriction was applied regarding date of publication. Comparative observational studies evaluating BNP and NT-proBNP in patients with septic shock aged ≥18 years were eligible for inclusion. Bibliographies from the extracted articles were also reviewed to identify additional relevant publications. Results In total, 46 studies met all eligibility criteria and were included. A strong body of literature has demonstrated that in patients with septic shock, increased values of BNP and NT-proBNP are associated with increased mortality. An increase from baseline BNP values has also been associated with increased mortality, whereas decreases from baseline values are not related to worse outcome. Brain natriuretic peptides have also been associated with cardiac dysfunction in patients with sepsis. Moreover, BNP values have been found to be significantly elevated in septic shock, regardless of cardiac dysfunction, and have been used to distinguish between septic and cardiogenic shock. Furthermore, BNP and NT-proBNP are significantly increased in patients with septic shock, compared to patients with sepsis and severe sepsis. Conclusions BNP and NT-proBNP appear to be reliable predictors of outcome in septic shock.

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.

Extracorporeal circulation has led to a great development in cardiovascular surgery during the last five decades. Its time-proven efficacy and safety have made on-pump coronary artery bypass grafting (CABG) the gold standard method of surgical revascularization. However, coronary revascularization on cardiopulmonary bypass and the accompanying aortic manipulation are related to plenty of deleterious complications. Therefore, off-pump CABG surgery was established to avoid complications. Nevertheless, despite the initial enthusiasm on this technique, only 20% of myocardial revascularization procedures worldwide are performed off-pump. Not only are off-pump cardiac procedures more technically difficult but also they do not provide better results in terms of graft patency, completeness of revascularization, repeat revascularization requirement, cost, and quality of life. Completeness of revascularization and anastomotic quality should not be compromised to avoid cardiopulmonary bypass.

The first reported human anaphylactic death is considered to be the Pharaoh Menes death, caused by a wasp sting. Currently, anaphylactic cardiovascular events represent one of most frequent medical emergencies. Rapid diagnosis, prompt and appropriate treatment can be life saving. The main concept beyond anaphylaxis lies to myocardial damage and ventricular dysfunction, thus resulting in cardiovascular collapse. Cardiac output depression due to coronary hypoperfusion from systemic vasodilation, leakage of plasma and volume loss due to increased vascular permeability, as well as reduced venous return, are regarded as the main causes of cardiovascular collapse. Clinical reports and experiments indicate that the human heart, in general, and the coronary arteries, in particular, could be the primary target of the released anaphylactic mediators. Coronary vasoconstriction and thrombosis induced by the released mediators namely histamine, chymase, tryptase, cathepsin D, leukotrienes, thromboxane and platelet activating factor (PAF) can result to further myocardial damage and anaphylaxis associated acute coronary syndrome, the so-called Kounis syndrome. Kounis syndrome with increase of cardiac troponin and other cardiac biomarkers, can progress to heart failure and cardiovascular collapse. In experimental anaphylaxis, cardiac reactions caused by the intracardiac histamine and release of other anaphylactic mediators are followed by secondary cardiovascular reactions, such as cardiac arrhythmias, atrioventricular block, acute myocardial ischemia, decrease in coronary blood flow and cardiac output, cerebral blood flow, left ventricular developed pressure (LVdp/dtmax) as well as increase in portal venous and coronary vascular resistance denoting vascular spasm. Clinically, some patients with anaphylactic myocardial infarction respond satisfactorily to appropriate interventional and medical therapy, while anti-allergic treatment with antihistamines, corticosteroids and fluid replacement might be ineffective. Therefore, differentiating the decrease of cardiac output due to myocardial tissue hypoperfusion from systemic vasodilation and leakage of plasma, from myocardial tissue due to coronary vasoconstriction and thrombosis might be challenging during anaphylactic cardiac collapse. Combined antiallergic, anti-ischemic and antithrombotic treatment seems currently beneficial. Simultaneous measurements of peripheral arterial resistance and coronary blood flow with newer diagnostic techniques including cardiac magnetic resonance imaging (MRI) and myocardial scintigraphy may help elucidating the pathophysiology of anaphylactic cardiovascular collapse, thus rendering treatment more rapid and effective.

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: 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.

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

In patients with chronic atrial fibrillation, 90% of clots are located in the left atrial appendage (LAA). Therefore, LAA exclusion is a means of preventing thrombus formation and subsequent thromboembolic events in these patients. The LAA can be excluded from the systemic circulation via surgical, percutaneous, or thoracoscopic approaches. The surgical aim is complete obliteration of the appendage without a significant increase in either postoperative complications (bleeding, arrhythmias) or recurrence. We discuss the current surgical techniques available for LAA obliteration and review their results.

The combination of diabetes mellitus and coronary artery disease (CAD) constitutes an aggressive disease characterized biologically by chronic inflammatory, proliferative and pro-thrombotic situation. In the "diabetic patient" the increased frequency and gravity of simultaneous myocardial infarction and the deterioration of congestive heart failure contribute to the inevitable unfavourable final result. Diabetes accelerates the natural course of atherosclerosis and involves a great number of coronary vessels with more diffuse atherosclerotic lesions. Moreover, the risks of plaque ulceration and thrombosis have been shown to be considerably higher in diabetic patients. The treatment should be also aggressive and be based on the combined treatment of CAD and the effective regulation of glucose levels. The decision of revascularization in the diabetic patient should be posed relatively earlier. The surgical choice of revascularization seems to be advantageous over the interventional, with better early and late results.

Aims: This study aims to evaluate atherosclerosis, oxidative stress, and arterial stiffness attenuation by simvastatin and ivabradine in hyperlipidemic rabbits. Methods and Results: Forty rabbits were randomly divided into 4 groups: atherogenic diet (group C), atherogenic diet plus simvastatin (group S), atherogenic diet plus ivabradine (group I), and atherogenic diet plus simvastatin and ivabradine (group S + I). After 9 weeks, rabbits were euthanized and descending aortas excised for mechanical testing. Atherogenic diet induced the development of significant atherosclerotic lesions in group C animals but in none of groups S, I, and S + I. RAM-11 and HHF-35–positive cells were significantly reduced in groups S, I, and S + I compared with group C ( P < .001). A significant neointimal hyperplasia and intima–media ratio reduction was demonstrated in groups S ( P = .015 and P < .001), I ( P = .021 and P < .001), and S + I ( P = .019 and P < .001) compared with group C. Protein nitrotyrosine levels were significantly decreased in group S compared with group C ( P = .009), and reactive oxygen species levels were decreased in group I compared with group C ( P = .011). Aortic stiffness was significantly reduced in groups S, I, and S + I compared with group C ( P = .003, P = .011, and P = .029). Conclusion: Simvastatin and ivabradine significantly inhibited intimal hyperplasia and oxidative stress contributing to aortic stiffness reduction in hyperlipidemic rabbits.

Background The aim of this study was to demonstrate a percutaneous transauricular method of balloon angioplasty in high-cholesterol fed rabbits, as an innovative atherosclerosis model. Methods Twenty male New Zealand rabbits were randomly divided into two groups of ten animals, as follows: atherogenic diet plus balloon angioplasty (group A) and atherogenic diet alone (group B). Balloon angioplasty was performed in the descending thoracic aorta through percutaneous catheterization of the auricular artery. Eight additional animals fed regular diet were served as long term control. At the end of 9 week period, rabbits were euthanized and thoracic aortas were isolated for histological, immunohistochemical and biochemical analysis. Results Atherogenic diet induced severe hypercholesterolemia in both group A and B (2802 ± 188.59 and 4423 ± 493.39 mg/dl respectively) compared to the control animals (55.5 ± 11.82 mg/dl; P

Cardiac events occur in 1% to 5% of patients undergoing non-cardiac surgery. Myocardial ischemia and nonfatal myocardial infarction constitute the most significant risk factors for mortality and cardiovascular morbidity, in patients with coronary artery disease. Perioperative b- blockade has been reported to reduce the risk of perioperative cardiac complications. Seven multicentre randomized trials have evaluated the impact of perioperative b-blocker administration on incidence of cardiovascular events.The Study of Perioperative Ischemia Research Group, the DECREASE and the BBSA trials focused on high risk patients for perioperative complications. The POBBLE, MaVS, and DIPOM trials did not target at patients with specific clinical risk factors, except DIPOM that included patients with diabetes. Finally, the POISE trial randomized patients with a wide variety of risk factors for perioperative cardiac complications. Interestingly, five meta-analyses reported a significant reduction in patients receiving b-blockers, with respect to perioperative myocardial ischemia and myocardial infarction. In conclusion, consistent evidence demonstrated a reduction in cardiac mortality and myocardial infarction by perioperative b-blockade in patients with clinical risk factors, undergoing high-risk non-cardiac surgery. However, patients with extensive preoperative ischemia were at high risk of perioperative cardiac complications, despite b-blocker therapy. Conversely, perioperative b-blocker therapy did not reduce the incidence of cardiac complications in patients without clinical risk factors. While, the safety and effectiveness of perioperative b-blockers in intermediate-risk patients, still remain a debatable issue.

It is common knowledge that cocaine has been linked to the development of various acute and chronic cardiovascular complications including acute coronary syndromes. We present a young, male patient, drug abuser who underwent CABG due to anterolateral myocardial infarction. Our presentation is one of the very rare cases reported in literature regarding acute thrombosis of left main coronary artery related to cocaine use, in a patient with normal coronary arteries, successfully operated. Drug-abusers seem to have increased mortality and morbidity after surgery and high possibility for stent thrombosis after percoutaneous coronary interventions, because of their usually terrible medical compliance and coexistent several problems of general health. There are no specific guidelines about treatment of thrombus formation in coronary arteries, as a consequence of cocaine use. So, any decision making concerning the final treatment of these patient is a unique and individualized approach. We strongly recommend that all these patients should be treated surgically, especially patients with thrombus into the left main artery.

Retroperitoneal fibrosis is best described as a chronic inflammatory process which may be idiopathic, but can rarely be brought about by medications, such as pergolide, used for treating Parkinson's disease. Pergolide can produce a fibrotic process in heart valves, resulting in valve insufficiency in up to 25% of cases. Herein we describe the case of a 68-year-old man who received pergolide for 2 years for Parkinson's disease. The patient developed retroperitoneal fibrosis resulting in renal failure from ureteral obstruction necessitating ureteral stenting, as well as significant aortic and mitral valve insufficiency. He successfully underwent surgery for combined aortic valve, mitral valve and ascending aorta replacement because of severe valve insufficiency and dilated (d = 5.8 cm) ascending aorta. Retroperitoneal fibrosis improved with pergolide cessation and corticosteroid treatment. This is the second case reported in the literature, of a patient who had double valve and ascending aorta replacement surgery because he suffered from this rare but serious adverse effect of dopamine agonists used for managing Parkinson's disease.