94 research outputs found
Diagnosis and treatment of asymptomatic left ventricular systolic dysfunction after myocardial infarction.
The increased survival after acute myocardial infarction induced an increase in heart failure with left ventricular systolic dysfunction. Early detection and treatment of asymptomatic left ventricular systolic dysfunction give the chance to improve outcomes and to reduce costs due to the management of patients with overt heart failure
The QRS narrowing index for easy and early identification of responder to cardiac resynchronization therapy.
Coronary artery perforation: How to treat it?
AbstractCoronary artery perforation fortunately represents a rare complication of coronary catheterization but, if not properly and promptly treated, it is burdened by a high mortality rate. Rates of coronary perforation may be potentially higher when atherectomy devices are used or very complex calcified lesions are treated. Cardiac tamponade constitutes the most severe clinical consequence.We report the case of an intra-stent coronary perforation at the end of revascularization of a non-ST elevation myocardial infarction (NSTEMI), followed by an immediate impairment of hemodynamic compensation, due to significant pericardial effusion and subsequent cardiac tamponade.The use of covered stents has revolutionized the management of coronary perforation and this has meant that the use of emergency CABG has decreased over the years with satisfactory immediate and short-term outcomes, reducing the incidence of acute cardiac tamponade and mortality without surgery
A rare case of Prinzmetal angina 3 days after coronary artery stenting with a second-generation drug-eluting stent.
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Pacing ventricolare destro: una risorsa o una minaccia?
Early after the beginning of the pacemaker era, endocardial right ventricular apex has been the most extensively used site for cardiac pacing because it was easily accessible and reliable in a long-term perspective. However many data have demonstrated that this kind of pacing is suboptimal from a physiologic point of view because it causes several adverse effects such as altered ventricular contraction geometry, mitral regurgitation, perfusion alterations and interference with myocardial ion channels which determine a worsening of left ventricular function. Several strategies have been proposed to solve these problems (alternative pacing sites, specific algorithms able to reduce the percentage of ventricular pacing) which are still under evaluation. In this review we analyzed the effects of right apical ventricular pacing and its possible alternatives
Psicosomatica e ischemia cardiaca:correlazio ne tra eventi stressanti,meccanismi di dife sa,personalitĂ e stili di vita.
G-protein-coupled receptor kinase 5 polymorphism and Takotsubo cardiomyopathy.
BACKGROUND:
Takotsubo cardiomyopathy (TTC) is an increasingly reported clinical syndrome that mimics acute myocardial infarction without obstructive coronary artery disease and is characterized by transient systolic dysfunction of the apical and/or mid-segments of the left ventricle. The syndrome mainly occurs in postmenopausal women with high adrenergic state conditions. Nowadays, the pathophysiology of TTC is not yet known and the possibility of a genetic predisposition is controversial.
AIMS:
The purpose of this study was to assess the genetic susceptibility to TTC through analysis of the L41Q polymorphism of the G-protein-coupled receptor kinase 5 (GRK5).
METHODS AND RESULTS:
In a cohort of 20 patients enrolled in two tertiary Italian centers with diagnosis of TTC, accordingly to the commonly accepted Mayo Clinic criteria and in 22 healthy individuals (control) we have evaluated the polymorphism in GRK5 gene. The TTC patients had a mean age of 65 ± 9 years and 19 of 20 were women. The presence of one or two L41 alleles of GRK5 was significantly more frequent in TTC group than in the control group (40 vs. 8%, P = 0.0372).
CONCLUSION:
In our study, we have found a significant difference in the frequency of GRK5 polymorphism between TTC patients and controls, supporting a genetic predisposition to this cardiac syndrome
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