Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
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Cardiovasc. Pathol. · Mar 2007
Intramyocardial injection of low-dose basic fibroblast growth factor or vascular endothelial growth factor induces angiogenesis in the infarcted rabbit myocardium.
Myocardial angiogenesis after the systemic administration of basic fibroblast growth factor or vascular endothelial growth factor at high therapeutic doses has been implicated in the occurrence of side effects that may undermine their safety. The aim of this study was to investigate the angiogenic effects of the intramyocardial administration of recombinant human basic fibroblast growth factor or vascular endothelial growth factor protein, at low doses, in the infarcted rabbit myocardium. ⋯ Low doses of recombinant human basic fibroblast growth factor or vascular endothelial growth factor protein, when administered intramyocardially, stimulate angiogenesis in the infarcted myocardium.
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Cardiovasc. Pathol. · Mar 2007
Plasma brain natriuretic peptide correlates with infarct size but not with subsequent remodeling in the rat heart.
Brain natriuretic peptide is a marker of the severity of congestive heart failure. However, the relation between its concentration and ventricular remodeling after myocardial infarction remains unknown. Thus, we studied plasma brain natriuretic peptide over 6 months after myocardial infarction in the rat and correlated it with parameters of left ventricular remodeling. ⋯ Thus, after a large myocardial infarction in the rat, despite progressive left ventricular dilation and increase in wall stress, plasma brain natriuretic peptide did not progress over time. This indicates that, although plasma brain natriuretic peptide is a good indicator of infarct size and left ventricular dilation, it cannot be used to trace progressive ventricular remodeling in the rat heart after myocardial infarction.
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Cardiovasc. Pathol. · Jan 2007
Case ReportsIrreversible intrapulmonary vascular changes after pulmonary vein stenosis complicating catheter ablation for atrial fibrillation.
Pulmonary vein stenosis is a recognized complication of catheter ablation of arrhythmias emanating from the pulmonary vein; however, there is little information on secondary effects of pulmonary vein stenosis on lung tissue. ⋯ Chronic pulmonary vein stenosis after radiofrequency ablation of atrial fibrillation results in irreversible venous and arterial morphologic changes throughout the lung, including areas both close to, and remote from, the site of catheter ablation. Because there are persistent pathological changes remote from the ablation site causing the pulmonary hypertension, stenting the site of ablation to reopen large pulmonary veins may not be effective in treating the pulmonary hypertension.
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The incidence of heart failure has been steadily increasing over the past several decades. High readmission rates in patients with acute decompensated heart failure led to the search for biomarkers that could predict future clinical course and would, in an ideal case, enable monitoring of patients with heart failure and guidance of their therapy. ⋯ Other known markers, such as atrial natriuretic peptide and endothelin-1, are currently used for research purposes. The development of additional biomarkers will be an important step from improving diagnosis and treatment of patients with chronic and acute decompensated heart failure.
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Cardiovasc. Pathol. · Jul 2005
ReviewTwenty years of progress and beckoning frontiers in cardiovascular pathology: cardiomyopathies.
In the last 20 years, with the advent of cardiac transplantation and the availability of molecular biology techniques, major advancements were achieved in the understanding of cardiomyopathies. Novel cardiomyopathies have been discovered (arrhythmogenic right ventricular, primary restrictive, and noncompacted myocardium) and added in the update of WHO classification. ⋯ The extraordinary progress accomplished in molecular genetics of inherited cardiomyopathies allowed to establish hypertrophic and restrictive cardiomyopathies as sarcomeric ("force generation") diseases, dilated cardiomyopathies as cytoskeleton ("force transmission") disease, and arrhythmogenic right ventricular cardiomyopathy (ARVC) as cell junction disease. If we consider also cardiomyopathy as ion channel disease (long and short QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia), because they are diseases of the myocardium associated with electrical dysfunction, then a genomic/postgenomic classification of inherited cardiomyopathies may be put forward: cytoskeletal cardiomyopathy, sarcomeric cardiomyopathy, cell junction cardiomyopathy and ion channel cardiomyopathy.