1,721,186 research outputs found

    MRI in acute myocardial infarction.

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    Although acute myocardial infarction (AMI) is still one of the main causes of high morbidity in Western countries, the rate of mortality has decreased significantly. The main cause of this drop appears to be the decline of the incidence of ST-segment elevation myocardial infarction (STEMI) along with an absolute reduction in case fatality rate once STEMI has occurred. Myocardial ischaemia progresses with the duration of coronary occlusion and the delay in time to reperfusion determines the extent of irreversibile necrosis from subendocarial layers towards the epicardium in accordance with the so-called 'wave-front phenomenon'. Coronary artery recanalization, either by thrombolitic therapy or primary percutaneous intervention, may prevent myocardial cell necrosis increasing salvage of damaged, but still viable, myocardium within the area at risk. Magnetic resonance imaging (MRI) can provide a wide range of clinically useful information in AMI by detecting not only location of transmural necrosis, infarct size and myocardial oedema, but also showing in vivo important microvascular pathophysiological processes associated with AMI in the reperfusion era, such as intramyocardial haemorrhage and no-reflow. The focus of this review will be on the impact of cardiac MRI in the characterization of AMI pathophysiology in vivo in the current reperfusion era, concentrating also on clinical applications and future perspectives for specific therapeutic strategies

    Mitral Valve Prolapse, Ventricular Arrhythmias, and Sudden Death

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    Despite a 2% to 3% prevalence of echocardiographically defined mitral valve prolapse (MVP) in the general population, the actual burden, risk stratification, and treatment of the so-called arrhythmic MVP are unknown. The clinical profile is characterized by a patient, usually female, with mostly bileaflet myxomatous disease, mid-systolic click, repolarization abnormalities in the inferior leads, and complex ventricular arrhythmias with polymorphic/right bundle branch block morphology, without significant regurgitation. Among the various pathophysiologic mechanisms of electrical instability, left ventricular fibrosis in the papillary muscles and inferobasal wall, mitral annulus disjunction, and systolic curling have been recently described by pathological and cardiac magnetic resonance studies in sudden death victims and patients with arrhythmic MVP. In addition, premature ventricular beats arising from the Purkinje tissue as ventricular fibrillation triggers have been documented by electrophysiologic studies in MVP patients with aborted sudden death. The genesis of malignant ventricular arrhythmias in MVP probably recognizes the combination of the substrate (regional myocardial hypertrophy and fibrosis, Purkinje fibers) and the trigger (mechanical stretch) eliciting premature ventricular beats because of a primary morphofunctional abnormality of the mitral valve annulus. The main clinical challenge is how to identify patients with arrhythmic MVP (which imaging technique and in which patient) and how to treat them to prevent sudden death. Thus, there is a necessity for prospective multicenter studies focusing on the prognostic role of cardiac magnetic resonance and electrophysiologic studies and on the therapeutic efficacy of targeted catheter ablation and mitral valve surgery in reducing the risk of life-threatening arrhythmias, as well as the role of implantable cardioverter defibrillators for primary prevention

    Cocaine and the heart: more than just coronary disease.

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    Juxtaposition of the atrial appendages is a rare congenital cardiac malformation, with the appendages both located on the left or right side of the great arteries. It is usually associated with cyanotic congenital heart disease. The aim of this report is to illustrate the anatomical features of normal and juxtaposed atrial appendages, with a review of the associated anomalies. In the Anatomical Collection of Congenital Heart Disease of the University of Padua, consisting in 1,526 specimens, we found 17 (1.1%) cases of atrial appendages juxtaposition with left juxtaposition in 15 (88%) and right juxtaposition in 2 (12%). Complete form was present in 11 cases and partial form in 6. In left juxtaposition, the situs was solitus in all, and the most frequent anomalies were complete transposition of great arteries in 9 (60%) and tricuspid atresia in 5 (33%); anomalies of position of the heart in the thorax (dextro-mesocardia) were present in 46% of cases, hypoplastic right ventricle in 73%, abnormal relation of the great arteries and subaortic or bilateral infundibulum in all. In right atrial juxtaposition, the atrial situs was solitus with mitral and pulmonary atresia in one case and left isomerism with aortic atresia and double-inlet right ventricle in the other. In describing this malformation, we propose to maintain the use of a positional definition using the terms right and left juxtaposition to describe the presence of both the appendages on the right or on the left side of the great arteries, respectively. The use of a morphological definition should be added in cases of situs inversus or isomerism, with description of the morphology of the appendage located in the wrong position

    Electrocardiographic J waves as a hyperacute sign of Takotsubo syndrome.

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    Typical electrocardiographic (ECG) signs of acute Takotsubo syndrome (TTS) consist of ST-segment elevation and/or T wave inversion. We report an unusual case of a 62-year-old woman with TTS who acutely exhibited on 12-lead ECG transient J waves preceding ST-T abnormalities. In the experimental model of myocardial ischemia, the appearance of J waves represents an early ECG abnormality and is followed by ST-segment elevation. Because of the similar ECG time course observed in TTS and myocardial ischemia, we speculate that common electrophysiologic mechanisms may account for J waves appearance in these 2 clinical conditions. Our case report shows that recording of ECG J waves in postmenopausal women presenting for acute chest pain may be a sign of an ongoing TTS and suggests a similarity to myocardial ischemia as the pathologic basis
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