A microvascular myocardial infarction in a 16-year-old girl with antiphospholipid syndrome: a case report.

Objective and importance: The antiphospholipid syndrome can manifest itself by silent (or not) myocardial infarction. Clinical presentation: We report the case of a 16-year-old girl who presented a myocardial infarction for whom a coronary-computer tomography did not reveal any coronary abnormalities or obstruction. She had a livedo reticularis on her physical exam. Intervention: The echocardiography showed a normal left ventricular function and a mild eccentric mitral regurgitation. A myocardial magnetic resonance imaging demonstrated transmural necrosis with microvascular obstruction at the inferobasal segment of the left ventricle, suggestive of a microvascular myocardial infarction. The blood test showed elevation of the three antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, and anti-ß2-glycoprotein). The lupus anticoagulant remained positive 12 weeks later, fulfilling the laboratory criteria for antiphospolipid carrier. The associated presence of this microvascular coronary obstruction was strongly suggestive of antiphospholipd syndrome, according to the revised Sapporo criteria. To our knowledge, this is the first reported case of antiphospholipid syndrome manifesting as an acute microvascular myocardial infarction, confirmed by myocardial magnetic resonance imaging. Conclusion: The antiphospholipid syndrome can manifest itself early by a microvascular myocardial infarction. The clinician has to be alerted by a livedo reticularis in these patients, which will be frequently associated with manifestations of antiphospholipid syndrome such as arterial thrombosis and valvulopathies.

At high cardiac output, diesel exhaust exposure increases pulmonary vascular resistance and decreases distensibility of pulmonary resistive vessels.

Air pollution has recently been associated with the development of acute decompensated heart failure, but the underlying biological mechanisms remain unclear. A pulmonary vasoconstrictor effect of air pollution, combined with its systemic effects, may precipitate decompensated heart failure. The aim of the present study was to investigate the effects of acute exposure to diesel exhaust (DE) on pulmonary vascular resistance (PVR) under resting and stress conditions but also to determine whether air pollution may potentiate acquired pulmonary hypertension. Eighteen healthy male volunteers were exposed to ambient air (AA) or dilute DE with a particulate matter of <2.5 µm concentration of 300 µg/m(3) for 2 h in a randomized, crossover study design. The effects of DE on PVR, on the coefficient of distensibilty of pulmonary vessels (α), and on right and left ventricular function were evaluated at rest (n = 18), during dobutamine stress echocardiography (n = 10), and during exercise stress echocardiography performed in hypoxia (n = 8). Serum endothelin-1 and fractional exhaled nitric oxide were also measured. At rest, exposure to DE did not affect PVR. During dobutamine stress, the slope of the mean pulmonary artery pressure-cardiac output relationship increased from 2.8 ± 0.5 mmHg · min · l (-1) in AA to 3.9 ± 0.5 mmHg · min · l (-1) in DE (P < 0.05) and the α coefficient decreased from 0.96 ± 0.15 to 0.64 ± 0.12%/mmHg (P < 0.01). DE did not further enhance the hypoxia-related upper shift of the mean pulmonary artery pressure-cardiac output relationship. Exposure to DE did not affect serum endothelin-1 concentration or fractional exhaled nitric oxide. In conclusion, acute exposure to DE increased pulmonary vasomotor tone by decreasing the distensibility of pulmonary resistive vessels at high cardiac output.