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1.
Am J Physiol Heart Circ Physiol ; 296(3): H655-61, 2009 Mar.
Article in English | MEDLINE | ID: mdl-19122164

ABSTRACT

Acute coronary artery occlusion triggers the release of atrial natriuretic peptide (ANP) from the heart. ANP affects vasodilation, natriuresis, and inflammation, but the integrated biological effects of ANP on myocardial infarction are unknown. To elucidate these effects, the left anterior coronary artery was ligated in anesthetized, ANP-deficient (ANP(-/-)) and congenic wild-type (ANP(+/+)) mice. The survival of ANP(-/-) mice was markedly better (56%) at 30 days postinfarction than the survival of ANP(+/+) mice (20%, P < 0.01). Surviving mice were comparable initially, but ANP(-/-) mice developed more cardiac hypertrophy (P < 0.001) and had lower contractility indexes 30 days after infarction (P < 0.05). An analysis 24 h after coronary occlusion showed that ANP(-/-) mice had smaller infarcts than ANP(+/+) mice (62.6 +/- 12.1 vs. 100.8 +/- 3.8%, P < 0.001) adjusted for comparable areas at risk for ischemia. The administration of ANP to ANP(-/-) mice via osmotic minipumps significantly enlarged infarct size to levels comparable with those observed in ANP(+/+) mice (P < 0.05). There was no difference in neutrophil migration into the noninfarcted myocardium of ANP(-/-) mice undergoing actual versus sham-operated coronary occlusion. By comparison, after coronary occlusion, the neutrophil infiltration into the myocardium was enhanced in ANP(+/+) (P < 0.0005) and ANP(-/-) mice administered ANP (P < 0.0005). The expression of P-selectin, a molecule that mediates neutrophil adhesion, was significantly greater after coronary occlusion in the vasculature of ANP(+/+) or ANP(-/-) mice treated with ANP than in ANP(-/-) mice (P < 0.002). Taken together, these results indicate that ANP increases P-selectin, neutrophil infiltration, infarct size, and mortality following experimental coronary occlusion.


Subject(s)
Atrial Natriuretic Factor/metabolism , Coronary Occlusion/complications , Inflammation/etiology , Myocardial Infarction/etiology , Myocardium/metabolism , Animals , Atrial Natriuretic Factor/administration & dosage , Atrial Natriuretic Factor/deficiency , Atrial Natriuretic Factor/genetics , Cardiomegaly/etiology , Cardiomegaly/metabolism , Coronary Occlusion/metabolism , Coronary Occlusion/pathology , Coronary Occlusion/physiopathology , Disease Models, Animal , Hemodynamics , Inflammation/metabolism , Inflammation/pathology , Inflammation/physiopathology , Infusion Pumps, Implantable , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Myocardial Contraction , Myocardial Infarction/metabolism , Myocardial Infarction/pathology , Myocardial Infarction/physiopathology , Myocardium/pathology , Neutrophil Infiltration , P-Selectin/metabolism , Time Factors
2.
J Invasive Cardiol ; 18(9): E241-3, 2006 Sep.
Article in English | MEDLINE | ID: mdl-16954590

ABSTRACT

Single coronary ostium is a very rare congenital anomaly with an incidence of 0.024% in angiographic series. This is the third case of Shirani-Roberts subtype IB4: solitary ostium in the left coronary sinus associated with a retroaortic-coursing right coronary artery that arises from the left main coronary artery. The patient is a 45-year-old male with no past medical history, and who was seen in the clinic for evaluation of a murmur. Echocardiography showed rheumatic heart disease with mild mitral regurgitation and moderate aortic regurgitation; no shunts were present. Coronary and aortic root angiography did not show a vessel originating from the right coronary cusp. The right coronary artery originated from the left main coronary artery and had an aberrant course which was dorsal to the ascending aorta. No associated congenital heart disease was present.


Subject(s)
Coronary Vessel Anomalies/diagnosis , Coronary Vessel Anomalies/pathology , Coronary Angiography , Echocardiography , Echocardiography, Transesophageal , Humans , Incidence , Male , Middle Aged
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