Wellens syndrome is an abnormal electrocardiographic pattern characterized by biphasic (type A) or deeply inverted (type B) T waves in leads V2–V3. It is typically caused by temporary obstruction of the left anterior descending (LAD) coronary artery due to the rupture of an atherosclerotic plaque leading to occlusion. Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome and even a rarer cause of Wellens Syndrome. It occurs when an intramural hematoma forms, leading to the separation of the tunica intima from the outer layers and creating a false lumen that protrudes into the real lumen, ultimately reducing blood flow and thus resulting in myocardial infarction. Here we report a case of SCAD presenting as an acute coronary syndrome with self-resolving chest pain, slightly elevated myocardial necrosis markers and electrocardiographic changes consistent with Wellens pattern type A first, and type B afterwards, that were not present upon arrival to the emergency department.

Orazio Christian Trovato, Giuseppe Vadalà, Vincenzo Sucato, Monica Lunetta, Danilo Puccio, Oreste Fabio Triolo, Salvatore Evola, Alfredo Ruggero Galassi and Giuseppina Novo, Division of Cardiology, Dipartimento Emergenze-Urgenze, University Hospital Paolo Giaccone and Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE), University of Palermo, Italy

Atrial Fibrillation is the most common cardiac arrhythmia affecting people of all ages, principally the elderly. Cognitive decline and dementia are also prevalent diseases in elderly. The scientific community always showed interest in the possible association between these two pathological entities, both implicating social and economic burden. This has been confirmed by several longitudinal population-based studies. Some studies also revealed that the association between atrial fibrillation and dementia may be not related to history of stroke. Therefore, other pathophysiological mechanisms are likely implicated, so far unclear or undefined. The aim of the present review is to analyse the possible mechanisms underlying the frequent association between atrial fibrillation and cognitive impairment.

The pathogenesis of tako-tsubo syndrome remains, nowadays, unclear: it is likely that the relevance of the different proposed mechanisms differs among specific clinical contexts. In this paper, we describe the case of a 61-year-old woman admitted to the intensive cardiac care unit for pre-syncope and persistent hypotension. Clinical and echocardiographic data were suggestive of tako-tsubo syndrome with severe dynamic left ventricular outflow tract (LVOT) obstruction and severe mitral regurgitation. Coronary angiography was normal. Inotropic agents were not administered, because absolutely contraindicated in the presence of LVOT obstruction: indeed, they may worsen the dynamic gradient with further hemodynamic compromise. The patient was, therefore, initially treated with intravenous fluid infusion and, later on, with beta-blockers; the patient had a regular clinical recovery, with progressive disappearance of ECG and echocardiographic abnormalities. This case confirms that an early echocardiographic diagnosis of LVOT obstruction is essential for therapeutic decision-making, especially in the setting of tako-tsubo syndrome presenting with compromised hemodynamic status.

Background: Epidemiologic studies indicate that elevated heart rate (HR) is an independent risk factor for mortality and morbidity in patients (pts) with chronic heart failure (CHF). Clinical trials with β-blockers suggest that HR reduction is an important mechanism of their benefit in pts with stable CHF. Pharmacologic inhibition of the If current now provides the opportunity of pure HR reduction. The purpose of this study was to evaluate the impact of ‘‘Off-Label’’ use of ivabradine on exercise capacity, gas exchange, functional class, quality of life, and neurohormonal modulation in pts with ischemic CHF. Methods: Between January 2008 and June 2008, a graded maximal exercise test with respiratory gas analysis and an endurance test with constant workload corresponding to 85% of the peak VO2 at the baseline and after 3 months were performed, and at the same times, N-terminal probrain natriuretic peptide (NT-proBNP) levels were also measured, in 60 pts (45 M, 15 F, mean age 52.7 ± 5.3 years), with stable ischemic CHF, New York Heart Association (NYHA) functional classes II (n = 35)—III (n = 25), with left ventricular ejection fraction (LVEF) ≤ 40%, randomized to a ‘‘off-label’’ ivabradine use (n = 30) and a control group (n = 30). Results: The exercise capacity increased from 14.8 ± 2.5 to 28.2 ± 3.5 min (P < .0001) and the peak oxygen consumption tended to improve from 13.5 ± 1.3 to 17.9 ± 2.4 mL/kg per minute (P < .0001) in ivabradine group. Oxygen consumption at the anaerobic threshold (AT) increased from 11.9 ± 1.4 to 15.3 ± 1.4 mL/kg per minute (P < .0001). NTproBNP levels decreased from 2356 ± 2113 pg/mL to 1434 ± 1273 pg/mL (P = .045). No significant differences were found in control group at 3 months. The positive ivabradine effects were also associated with an improvement in the NYHA functional class and quality of life. Conclusion: The ‘‘Off-Label’’ use of ivabradine significantly improves the exercise capacity, gas exchange, functional heart failure class, quality of life, and neurohormonal modulation in pts with ischemic CHF.

The coagulation cascade, and particularly thrombin, plays a very important role in arterial and venous thrombosis. Thereby, it is clear that thrombin inactivation is an optimal strategy for thrombotic disease prevention and treatment. The direct thrombin inhibitors are a new class of anticoagulant drugs directly binding thrombin and blocking its interaction with fibrinogen. The group of direct thrombin inhibitors includes recombinant hirudin (lepirudin and desirudin), bivalirudin, melagatran and its oral precursor, ximelagatran, argotraban and dabigatran. These drugs have several advantages compared to other anticoagulant drugs, and the particular pharmacokinetic properties of some of them could be very important for future management of thromboembolic prophylaxis. The efficacy and safety of these new drugs are evaluated in several clinical trials; however today only few clinical indications are available for the majority of them.

Depressed mood and other depressive symptoms frequently appear after acute myocardial infarction and it is known how these patients have an increased risk for morbidity and mortality compared to patients without depression. Many risk factors promote the development of clinical depression in patients with recent myocardial infarction. Although a large number of studies underline the negative prognostic impact of depression on the infarcted patient, only rarely depressed patients are appropriately diagnosed and treated. Furthermore it should be borne in mind that the use of psychotropics in medically ill patients requires attention. These compounds, in fact, may interact with the disease causing several complications. In addition since the cardiologic patient is often treated with other drugs, the risk of clinically significant pharmacological interactions is obviously improved. It seems appropriate to give some considerations about therapy and management of the infarcted patient with depression.