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Hypertension, Ahead of Print. BACKGROUND:Aberrant BMPR2 (bone morphogenetic protein receptor 2) signaling is associated with the pathogenesis of pulmonary hypertension. By contrast, mice with smooth muscle cell-specificSmad4deletion had no pulmonary hypertension but rather displayed evident aorticaneurysm and dissection.
Bronchial artery aneurysm (BAA) is a rare and fatal condition that requires immediate treatment. In the present case, a 76-year-old hypertensive woman was admitted with dizziness and diagnosed with an unruptured bronchial artery aneurysm, which was treated by transcatheter arterial embolization and aortic stent-graft.
BackgroundAbdominal aorticaneurysm (AAA) is a severe aortic disease for which no pharmacological interventions have yet been developed. Journal of the American Heart Association, Ahead of Print. Colocalization analysis pinpointed 13 proteins with strong evidence of colocalization with AAA.
Hypertension, Ahead of Print. BACKGROUND:The pathophysiology of familial thoracic aorticaneurysm and dissection (TAAD) is linked to genetic variants that affect aortic components. These findings establish a genetic link between systolic hypertension and TAAD.
Hypertension, Ahead of Print. BACKGROUND:Recent studies show that hyperactivation of mTOR (mammalian target of rapamycin) signaling plays a causal role in the development of thoracic aorticaneurysm and dissection. Echocardiography was performed to monitor the growth of the aortic root and ascending aorta.
Hypertension, Ahead of Print. BACKGROUND:Multiple pathways and factors are involved in the rupture of intracranial aneurysms. The EGFR (epidermal growth factor receptor) has been shown to mediate inflammatory vascular diseases, including atherosclerosis and aorticaneurysm.
Partial- or total loss of Sca-1 expression exacerbated aortic GFP+CD31-CD45-cell expansion, compared to Sca1GFP [Sca1KI-/-32±7-fold change of vehiclevs.Sca1KI+/-39±9vs.Sca1GFP 5±1; n=11-13/group; p<0.0001], suggesting disinhibited progenitor responses. Partial- or total loss of Sca-1 worsened aortic dilation [Sca1KI-/-1.25±0.06
Hypertension, Ahead of Print. Aortic diseases such as atherosclerosis, aorticaneurysms, and aortic stiffening are significant complications that can have significant impact on end-stage cardiovascular disease.
Clinical introduction The patient was a man in his 40s with a medical history of hypertension, Behcet’s disease (BD) and chronic renal dysfunction. The patient was receiving therapeutic doses of the following medications: sacubitril valsartan sodium tablets, prednisone acetate, cyclophosphamide and azathioprine.
The striking finding is the huge enlargement of the right pulmonary artery, almost aneurysmal dilatation of right pulmonary artery. This is the aortic knuckle. The possibillities here would be severe primary pulmonary hypertension versus atrial septal defect with severe pulmonary hypertension. It is not visible here.
This unique case highlights the diagnostic and therapeutic challenges of a patient with multiple vascular risk factors who suffered from strokes secondary to BHS.MethodsA 79‐year‐old man with a past medical history of peripheral artery disease, abdominal aorticaneurysm, myocardial infarction with drug eluding stents (on dual antiplatelet therapy (DAPT)), (..)
Hypertension, Ahead of Print. By these mechanisms, SMC-MR promotes disease progression in models of aging-associated vascular stiffness, vascular calcification, mitral and aortic valve disease, pulmonary hypertension, and heart failure.
Single-factor analysis indicated that age, hypertension, maximum aneurysm diameter, proportion of intraluminal thrombus, diameter of inferior mesenteric artery (IMA), and number of patent lumbar arteries (LA) were risk factors for T2EL-related reintervention. and aneurysm diameter of 53.55
A 69 year old woman with a history of hypertension presented to the emergency department by EMS for evaluation of chest pain and shortness of breath. There are no Q-waves to suggest old inferior MI, or inferior aneurysm as the etiology of the ST Elevation. What "initiates" the aortic stenosis cascade?
When there are QS-waves, one should always think about LV aneurysm, but ST to QRS ratio and T-wave to QRS ratio are far too large and not compatible with left ventricular aneurysm. Larger shunt volume means less blood exiting the left ventricle through the aortic valve and lower cardiac output. This ECG shows a lot of "acuity".
He carries the diagnoses hyperlipidemia, hypertension, and diabetes. No thoracic aortic hematoma, aneurysm or dissection. Here is the cardiology note, paraphrased to make it not identifiable: 50-something seen in cardiology consultation today at the request of Dr. XXXXXX for an NSTEMI. CT Angio Chest IMPRESSION 1.
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