ABSTRACT
Tetralogy of Fallot is characterized by a ventricular septal defect, a large, overriding aorta, subpulmonic stenosis, and right ventricular hypertrophy. These lesions can be associated with abnormal development of the pulmonary vasculature. This can include peripheral pulmonic stenosis, discontinuous pulmonary arteries, anomalous pulmonary venous return, and the development of aortopulmonary collateral vessels. Aortopulmonary collateral vessels develop to supply underperfused areas of the pulmonary bed and pose a unique and challenging problem at the time of surgical repair, which involves closure of the ventricular septal defect, relief of right ventricular outflow tract obstruction, maintenance of pulmonary valve competency when possible, and establishment of laminar pulmonary blood flow to all segments of the pulmonary bed. We describe a 36-year-old man with unrepaired tetralogy of Fallot with distinctive aortopulmonary collaterals, who underwent complete surgical repair with good outcome. Two-dimensional echocardiogram, cardiac magnetic resonance imaging, and cardiac catheterization each provided vital details allowing a stepwise approach to defining his unique anatomy for surgical correction.
Subject(s)
Aorta/physiopathology , Cardiac Surgical Procedures/methods , Collateral Circulation , Lung/blood supply , Pulmonary Artery/physiopathology , Pulmonary Circulation/physiology , Tetralogy of Fallot/pathology , Tetralogy of Fallot/surgery , Abnormalities, Multiple/surgery , Adult , Cardiac Catheterization , Cardiac Surgical Procedures/adverse effects , Collateral Circulation/physiology , Humans , Male , Postoperative Complications/surgery , Pulmonary Artery/pathology , Pulmonary Artery/surgery , Pulmonary Infarction/surgery , Tetralogy of Fallot/diagnostic imaging , Tetralogy of Fallot/physiopathology , UltrasonographyABSTRACT
INTRODUCTION: Aspirin's effectiveness in reducing cardiovascular disease events is inadequate in some individuals, a phenomenon termed aspirin "resistance". The hypothesis that combining low dose aspirin with eicosapentaenoic acid and docosahexaenoic acid (EPA+DHA) reduces platelet function in the acute setting has not been investigated. PATIENTS AND METHODS: We conducted a clinical trial of EPA+DHA and aspirin ingestion in healthy adults. Fasting blood samples were drawn at baseline and 4 h after supplementation with EPA/DHA (3.4 g/d), aspirin (81 mg), and both. Platelet function was measured using the Platelet Function Analyzer-100 (PFA-100). Plasma lysophosphatidylcholine (LPC), lysophosphatidic acid (LPA), autotaxin, angiogenesis activators, and cytokines were measured. RESULTS: Platelet function decreased with the combination of aspirin+EPA/DHA (p=0.03) but not with either alone (p>0.05). EPA-LPC increased (p=0.002). DISCUSSION AND CONCLUSIONS: Our results demonstrate that a potentially beneficial effect on platelet function occurred within 4h after ingestion of low-dose aspirin and EPA+DHA in healthy adults.
Subject(s)
Aspirin/pharmacology , Blood Platelets/drug effects , Docosahexaenoic Acids/pharmacology , Eicosapentaenoic Acid/pharmacology , Aspirin/administration & dosage , Docosahexaenoic Acids/administration & dosage , Drug Combinations , Eicosapentaenoic Acid/administration & dosage , Humans , Platelet Function TestsABSTRACT
The term obesity cardiomyopathy has previously been used to describe a clinical syndrome in obese patients typically consisting of eccentric left ventricular hypertrophy with preserved ejection fraction and diastolic dysfunction and is often associated with right ventricular dysfunction independent of the presence of the obstructive sleep apnea syndrome. Although several publications have described the early stages of this syndrome, little is known about the end stages of the disease. The authors conducted a retrospective study of a subset of edematous obese patients with multiple common medical comorbidities who present with a clinical syndrome in the setting of physiologic stress or infection. Under severe physiologic stress these patients developed pulmonary hypertension, right-sided volume overload, decreased effective arterial blood volume, and renal failure. Often, these findings were in the setting of obstructive sleep apnea. This retrospective study focuses on an obesity-related cardiorenal syndrome but also serves to provide a foreground for acknowledging the broad spectrum of cardiovascular pathology, including pulmonary hypertension, diastolic dysfunction, and sleep apnea, seen in the obese.