Andreas Mazarakis

Weight loss after bariatric surgery improves aortic elastic properties and left ventricular function in individuals with morbid obesity: a 3-year follow-up study.

Objective To investigate whether weight loss after bariatric surgery (gastric bypass) is associated with changes in aortic function (an important determinant of left ventricular function) and in left ventricular function, in morbidly obese individuals 3 and 36 months after surgery. Methods We used echocardiography to evaluate 60 obese individuals [body mass index (BMI) > 40 kg/m2] who underwent surgery and 20 obese individuals who neither underwent surgery nor lost weight, at baseline and at 3 and 36 months of follow-up, and 40 lean individuals (BMI < 25 kg/m2) of similar age, sex and risk factors, at baseline. We measured aortic strain, distensibility, stiffness index, pressure–strain modulus and Doppler indices of left ventricular diastolic dysfunction (ratio of peak early to peak atrial flow velocities, isovolumic relaxation time and deceleration time). Results Baseline aortic function and Doppler diastolic indices were impaired in obese individuals compared with those who were lean (P < 0.05). During 3 and 36 months of follow-up, BMI and left ventricular diastolic diameter, volume, mass and wall thickness were reduced, and indices of aortic function and left ventricular diastolic function were normalized, in obese individuals after surgery [aortic distensibility (cm2 × dyn−1 × 10−6): 1.9 before surgery, 3.4 at 3 months after surgery and 4.3 at 3 years after surgery, compared with 3.36 in lean controls; P < 0.01], but not in those who did not lose weight. The reduction in BMI after surgery was related to the concomitant improvement in indices of aortic function (P < 0.01) and isovolumic relaxation time (P < 0.05) after adjustment for age, sex and concomitant reduction in blood pressure, lipids and glucose concentrations. Conclusion Weight reduction after bariatric surgery normalizes aortic function, reduces left ventricular hypertrophy and, thus, improves left ventricular diastolic function in morbidly obese individuals over a 3-year period of follow-up.

Cefuroxime-induced coronary artery spasm manifesting as Kounis syndrome.

Allergic angina and allergic myocardial infarction (Kounis syndrome) occurring during the course of a drug-induced allergic reaction in the absence of angiographically stenosed coronary arteries, is rare in clinical practice.This paper reports the case of a 70-year-old woman with no significant risk factors for coronary artery disease who developed coronary artery spasm after intravenous injection of cefuroxime.A subsequent coronary angiogram revealed normal coronary arteries (type I variant of the syndrome). The allergic reaction following cefuroxime administration seems to have triggered the development of coronary artery spasm. Susceptible individuals expressing an amplified mast cell degranulation effect may be more vulnerable to coronary artery spasm. The clinical implications of this syndrome are also discussed.

Kounis syndrome: a manifestation of drug-eluting stent thrombosis associated with allergic reaction to contrast material.

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.

Nickel allergy, Kounis syndrome and intracardiac metal devices

Metal-induced allergic reactions are not rare in every day practice but nickel, cobalt and chromium are the most common offenders. Other metal anions and metal alloys represent also emerging causes for hypersensitivity reaction in humans. The metal struts of endovascular and intracardiac devices are usually alloys containing nickel and constitute causes for allergic reactions with possible intracardiac and intracoronary mast cell activation resulting in the Kounis hypersensitivity coronary syndrome. Newer intracoronary stents avoid nickel thus making them less allergenic. It is advisable that, before any device implantation, careful history of any metal allergy should be taken and efforts should be made for the development of new devices with better biocompatibility.

Kounis syndrome: Two extraordinary cases

Acute myocardial infarction occurring during the course of an allergic reaction constitutes the Kounis syndrome. This syndrome is caused by inflammatory mediators released mainly from activated mast cells and the interrelated via bidirectional stimuli macrophages and T-lymphocytes. Since activated mast cells abound at the areas of plaque erosion or rupture in patients suffering from acute myocardial infarction a common pathway between allergic and non allergic coronary events seems to exist. Two cases of this syndrome are described, the first following nicorette transdermal application and subsequent finger pricking by fish bone and the second after ciprofloxacin administration.

The heart seems to be the primary site and the target of anaphylaxis resulting in the development of Kounis syndrome

In a very important paper published in this journal [1], twopatients suffering from severe anaphylaxis developedelectrocardiographic ST segment elevation associated withprominent cardiovascular symptoms. The first patient’surticaria was accompanied by chest pain, tachycardia andhypotension, and skin prick tests were positive for beef,pork and milk. The second patient’s urticaria was devel-oped intra-operatively, and was accompanied by hypoten-sion culminating in ventricular tachycardia and ventricularfibrillation necessitating cardiac defibrillation. This patienthad received propofol, sevoflurane, fentanyl, atracariumand epinephrine and had positive skin prick tests to atra-carium and latex.All the above symptoms are characteristic for type Ivariant of Kounis syndrome for the first patient, and type IIvariant of Kounis syndrome for the second patient. Kounissyndrome is defined [2] as the concurrence of acute coro-nary syndromes with conditions associated with mast celldegranulation and other interacting and interrelatedinflammatory cells such as T lymphocytes and macro-phages. It is caused by inflammatory mediators such ashistamine, neutral proteases, arachidonic acid products,platelet-activating factor, and a variety of cytokines andchemokines released during the activation process. It seemspossible that the first patient suffered a type I variant ofKounis syndrome, which is seen in patients with normal ornearly normal coronary arteries without predisposing fac-tors for coronary artery disease, in whom the acute releaseof inflammatory mediators can induce either coronaryartery spasm with normal cardiac enzymes and troponins,or coronary artery spasm progressing to acute myocardialinfarction with raised cardiac enzymes and troponins.On the other hand, type II variant of Kounis syndromeincludes patients with culprit but quiescent preexisting ath-eromatous disease, in whom acute release of inflammatorymediators can induce either coronary artery spasm alone, orplaque erosion or rupture manifesting as acute myocardialinfarction with its consequences. A type III variant of Kounissyndrome has been described recently in patients with coro-nary artery stent thrombosis in whom aspirated thrombusspecimens stained with hematoxylin–eosin and Giemsa arefound infiltrated by eosinophils and mast cells, respectively.The second patient had positive skin prick tests in latexand atracarium but the other drugs he received duringanesthesia such as propofol, fentanyl and sevoflurane couldalso contribute to the allergic cascade. Therefore, thispatient was under the risk of five agents which were able toact directly or via IgE mechanism to degranulate mastcells. It is known that mast cell surface bears 500,000 to 1million IgE molecules and degranulation occurs when2,000 of these molecules, which is a critical number, make1,000 bridges with antigens. These bridges can be madewith antigens of different specificities as it happens inpatients during anesthesia [2]. It looks likely that the moreantigens an anesthetized patient is exposed to, the easierand quicker the degranulation occurs.It is generally believed, that myocardial involvementduring severe anaphylactic reactions is the result of sys-temic vasodilatation, reduced venous return, leakage ofplasma and volume loss due to increased vascular perme-ability that ensue leading to depression of the cardiacoutput, and contribute to coronary hypoperfusion withsubsequent myocardial damage.However, experimental and clinical studies have shownthat human heart is the primary site and the target of

Hypersensitivity to proton pump inhibitors: Lansoprazole-induced Kounis syndrome

Proton pump inhibitors are commonly used in clinical practice for the treatment of peptic ulcer and gastroesophageal reflux and are well tolerated by the patients. Their use is rarely associated with hypersensitivity and anaphylactic reactions. According to the reports in the Uppsala Monitoring Center database the frequency of hypersensitivity reactions out of all reported adverse reactions for proton pump inhibitors and H2-histamine receptor antagonists was between 0.2% and 0.7%. A few cases of hypersensitivity to lansoprazole have been reported. We report a patient who developed Kounis syndrome after taking 30 mg of lansoprazole. This is the first report of Kounis syndrome associated with lansoprazole administration in the world literature.

In-hospital management of acute heart failure: Practical recommendations and future perspectives.

Acute heart failure (AHF) represents the first reason for hospitalization in the elderly and despite therapeutic advances, remains a syndrome with significant morbidity and dismal prognosis. Hospitalization for AHF, on the other hand, is the single most important contributor to the huge financial burden related to HF. As a result, there is a significant unmet need for more effective in-hospital management of patients with AHF in order to improve outcomes, reduce readmission rate and alleviate the socioeconomic burden of the syndrome. The in-hospital management of AHF patients may schematically be divided into three phases, an early phase of intensive management of congestion and/or hypoperfusion, an intermediate phase of transition to oral life-saving medications and a late phase of discharge and transition to outpatient management. In the present paper, we attempt to provide a concise and practical roadmap for each of the above phases, focusing mainly on defining clinical and laboratory criteria for the evaluation of patients and on describing therapeutic algorithms that summarize the available evidence and guidelines. In addition, we highlight some key open issues that need to be addressed by future research.

Timing of clopidogrel loading before percutaneous coronary intervention in clopidogrel-naive patients with stable or unstable angina: A comparison of two strategies

BACKGROUND Clopidogrel-naive patients subjected to coronary angiography may be candidates for percutaneous coronary intervention (PCI). Clopidogrel loading with 600 mg at least 2 hours before the procedure is advised for such patients. However, there is no direct evidence that delaying PCI for 2 hours after clopidogrel loading is superior to ad hoc PCI. METHODS After coronary angiography, clopidogrel-naive patients (N = 199) with stable or unstable angina, candidates for PCI, were loaded with 900 mg of clopidogrel and then randomized to ad hoc PCI (ad hoc group, n = 103) or delayed PCI 2 hours after loading (delayed group, n = 96). Combined primary end point was death/periprocedural myocardial infarction (MI)/stroke/reintervention within 30 days post-PCI. Secondary end points were periprocedural MI; periprocedural creatine kinase-MB elevation >3 x upper limit of normal; any periprocedural increase of creatine kinase-MB, troponin-I, or myoglobin above upper limit of normal; Thrombolysis in Myocardial Infarction flow <3 after PCI; thrombocytopenia with platelet count of <70,000/mL; major bleeding defined according to the Thrombolysis in Myocardial Infarction criteria; and elevation of high-sensitivity C-reactive protein and soluble P selectin. RESULTS Primary end point occurred in 12.6% ad hoc group versus 15.6% delayed group patients (P = .34). High-sensitivity C-reactive protein increased in both groups post-PCI (analysis of variance P < .0001) without difference between groups (P = .5). Major bleeding occurred in 2.9% ad hoc group versus 3.1% delayed group patients (P = .9). No significant difference was observed in any other secondary end point. CONCLUSIONS In clopidogrel-naive patients, a strategy of delaying PCI for 2 hours after high-dose clopidogrel loading does not seem to confer any benefit compared to ad hoc PCI.

The conundrum of hypersensitivity cardiac disease: Hypersensitivity myocarditis, acute hypersensitivity coronary syndrome (Kounis Syndrome) or both?

Abstract Hypersensitivity or allergic inflammatory processes can affect the cardiac structures during allergic insults. The myocardium, the conduction system and the coronary arteries can be the targets of these insults resulting in Kounis syndrome (hypersensitivity coronary syndrome) or hypersensitivity myocarditis. Kounis syndrome and hypersensitivity myocarditis can be clinically indistinguishable and masquerade each other. Simultaneous occurrence of both entities has not been reported. We report on a patient who presented with signs and symptoms of type I variant of Kounis syndrome but cardiac magnetic resonance imaging showed that he had hypersensitivity myocarditis.