Giant pulmonary artery aneurysm caused by sibutramine-associated pulmonary arterial hypertension: First case in the literature.
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ABSTRACT:
SUBMITTER: Kultursay B
PROVIDER: S-EPMC8274892 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:This case presents a woman in her early 20s who died after the sudden onset of chest pain. Five years earlier, she was investigated for a cardiac murmur during pregnancy and an echocardiogram revealed a 6.0×3.0?cm blood-filled sac compressing the left atrium and anterolateral aspect of the left ventricle with communication to the aortic root. She later had a CT scan of the chest with contrast, which showed aneurysmal dilatation of the left main coronary artery. She was placed on aspirin but defaulted from clinic 11 months post partum. At autopsy, a left coronary aneurysmal sac measuring 10.0×9.0?cm. was identified with a rupture measuring 7.0?cm in length and the pericardial sac contained 900?mL of blood with clots. The cause of death was cardiac tamponade secondary to rupture of the coronary artery aneurysm.
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Project description:Basilar artery perforator aneurysms (BAPA's) are a rare entity. Their natural history and treatment are unclear. We describe the largest BAPA reported thus far in literature in a 64-year-old Caucasian woman. This patient did not present with subarachnoid hemorrhage, but with left hemiparesis due to pontine ischemia. The aneurysm was initially misdiagnosed as a tumoral mass in a referring center. Angiography confirmed the presence of a BAPA and a flow diverter was successfully placed. This case shows us that a BAPA can mimic a tumoral mass and can cause ischemia due to mass effect without having ruptured. Both conservative and flow diverter placement seems viable treatment options. Individual patient characteristics and preferences should be considered in decision-making for treatment.
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Project description:Pulmonary arterial hypertension (PAH), a rapidly fatal vascular disease, strikes women more often than men. Paradoxically, female PAH patients have better prognosis and survival rates than males. The female sex hormone 17β-estradiol has been linked to the better outcome of PAH in females; however, the mechanisms by which 17β-estradiol alters PAH progression and outcomes remain unclear. Because proximal pulmonary arterial (PA) stiffness, one hallmark of PAH, is a powerful predictor of mortality and morbidity, we hypothesized that 17β-estradiol attenuates PAH-induced changes in mechanical properties in conduit proximal PAs, which imparts hemodynamic and energetic benefits to right ventricular function. To test this hypothesis, female mice were ovariectomized and treated with 17β-estradiol or placebo. PAH was induced in mice using SU5416 and chronic hypoxia. Extra-lobar left PAs were isolated and mechanically tested ex vivo to study both static and frequency-dependent mechanical behaviors in the presence or absence of smooth muscle cell activation. Our static mechanical test showed significant stiffening of large PAs with PAH (P<0.05). 17β-Estradiol restored PA compliance to control levels. The dynamic mechanical test demonstrated that 17β-estradiol protected the arterial wall from the PAH-induced frequency-dependent decline in dynamic stiffness and loss of viscosity with PAH (P<0.05). As demonstrated by the in vivo measurement of PA hemodynamics via right ventricular catheterization, modulation by 17β-estradiol of mechanical proximal PAs reduced pulsatile loading, which contributed to improved ventricular-vascular coupling. This study provides a mechanical mechanism for delayed disease progression and better outcome in female PAH patients and underscores the therapeutic potential of 17β-estradiol in PAH.
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Project description:Left main coronary artery (LMCA) disease due to external compression by a dilated main pulmonary artery (MPA) is an uncommon clinical entity. Here, we describe a 52-year-old woman with pulmonary arterial hypertension (PAH) and anteroseptal old myocardial infarction (OMI). The cause of the OMI was external compression of the LMCA by the dilated MPA and aneurysm of the left coronary sinus of Valsalva. The patient's sister (aged 56 years) had also been diagnosed with PAH and both women had a novel heterozygous splicing mutation, IVS2-2A?>?G (c.374-2A?>?G in NM_001456), in the filamin A ( FLNA) gene. To our knowledge, this is the first report of HPAH which is likely to be due to FLNA mutation and compression of the LMCA between a dilated MPA and aneurysm of the left coronary sinus of Valsalva.
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Project description:BACKGROUND:Movement disorders after the clipping for an unruptured giant aneurysm are rare. The information on the pathogenesis and treatment options for this condition is largely unknown. CASE DESCRIPTION:An 82-year-old female with no neurological deficits underwent a clipping for a giant middle cerebral artery (MCA) aneurysm. Immediately after surgery, she presented with hemichorea-hemiballismus (HC-HB) on the left side. Postoperative angiograms and single-photon emission computed tomography demonstrated the hyperperfusion in the right frontal cortex and the decreased perfusion in the basal ganglia, indicating that the abrupt hemodynamic changes due to the obliteration of the giant aneurysm caused the dysfunction of the frontal cortical and subcortical pathway and the basal ganglia. Administration of tiapride hydrochloride was dramatically effective in controlling the HC-HB until the hyperperfusion resolved. Single-photon emission computed tomography obtained 8 weeks after surgery revealed that the cerebral blood flow had been normalized in the right frontal cortex. The relative hypoperfusion of the right basal ganglia was also resolved. Then tiapride hydrochloride was discontinued without a relapse of HC-HB. CONCLUSION:This case appears consistent with the theory that the connecting fibers responsible for the development of HC-HB are also located in the frontal lobe. The treatment of giant aneurysms involving the M1 portion can cause abrupt hemodynamic changes in both frontal cortex and the basal ganglia, which can potentially induce postoperative movement disorders.
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