amyloid/infarction

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Liraglutide Ameliorates β-Amyloid Deposits and Secondary Damage in the Ipsilateral Thalamus and Sensory Deficits After Focal Cerebral Infarction in Rats.

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Focal cerebral infarction causes β-amyloid (Aβ) deposition and secondary neuronal degeneration in the ipsilateral thalamus. Thalamus is the subcortical center of sensory, the damage of thalamus could cause sensory deficits. The present study aimed to investigate the protective effects of

[Myocardial rupture in primary chronic polyarthritis. Sequela of a rare combination of acute myocardial infarct, secondary amyloidosis and perimyocarditis].

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Severe chronic rheumatoid arthritis is sometimes associated with several internal organic lesions. This is the report of a patient with malignant chronic rheumatoid arthritis complicated by an acute myocardial infarction, left ventricular wall rupture and pseudoaneurysm besides reactive amyloidosis

Multiple infarcts and hemorrhages in the central nervous system of a dog with cerebral amyloid angiopathy: a case report.

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BACKGROUND β-amyloid (Aβ) can accumulate in the brain of aged dogs, and within vessels walls, the disease is called cerebral amyloid angiopathy (CAA). In humans, Alzheimer's disease and CAA are strongly correlated with cerebrovascular disease. However, in dogs, this association has not been

[Cerebral amyloid angiopathy complicated by multiple cerebral infarcts and intracerebral hemorrhages: case report].

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Recently, cerebral amyloid angiopathy is stressed as an unusual and infrequent cause of cerebral infarct or intracerebral hemorrhage. This report described a case of cerebral amyloid angiopathy complicated by multiple cerebral infarcts and multiple intracerebral hemorrhages. This 70-year-old man was

Fatal hemorrhage during anticoagulation of cardioembolic infarction: role of cerebral amyloid angiopathy.

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We report a patient with recurrent cardioembolism and hemorrhagic infarcts, who developed a fatal intracerebral hemorrhage 3 days after intravenous anticoagulation. At autopsy, cerebral amyloid angiopathy (CAA) was found. Because CAA and anticoagulation may add up to trigger cerebral hemorrhage, the

Serum amyloid A protein in acute myocardial infarction.

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Tissue injury including myocardial infarction leads to a variety of changes in plasma proteins commonly referred to as "the acute phase response". In this report the concentrations of serum amyloid A protein (SAA) were measured serially in 6 patients with myocardial infarction and 4 with angina. SAA

Amyloid, thrombosis, and acute myocardial infarction in association with a bicuspid aortic valve.

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A 34 year old man presented with an inferior non-Q-wave myocardial infarction. Echocardiography showed a bicuspid aortic valve with aortic outflow obstruction. Left coronary cusp morphology was normal but the right coronary cusp was grossly distorted and replaced by a mobile echodense mass

The spatial cerebral damage caused by larger infarct and β-amyloid toxicity is driven by the anatomical/functional connectivity.

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Large cerebral infarctions are major predictors of death and severe disability from stroke. Conversely, data concerning these types of infarctions and the affected adjacent brain circuits are scarce. It remains to be determined if the co-morbid concurrence of large infarct and β-amyloid (Aβ)

Time course of serum amyloid A response in myocardial infarction.

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Plasma concentrations of serum amyloid A (SAA), high density lipoprotein (HDL) cholesterol, non-HDL cholesterol, and apolipoproteins (Apo) A-I and B were measured daily for 6 days in 10 patients following myocardial infarction (MI) and in 10 secular controls admitted to a coronary care unit. SAA

Serum amyloid A protein in patients with acute myocardial infarction.

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The concentrations of four acute phase proteins were measured in sera of 40 patients with acute myocardial infarction (AMI) to evaluate their behaviour from day-to-day and to find out if they can serve for early prediction of postinfarction complications and mortality rate. Peak levels of serum

Left ventricular free wall rupture following acute myocardial infarction and cardiac amyloid.

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A 74-year-old man died of left ventricular free wall rupture 6 days following an acute inferoposterior wall myocardial infarction. His hospital course was complicated by pump failure which proved resistant to inotropic support, diuresis, and percutaneous transluminal coronary angioplasty. At

Amyloidosis of epicardial and intramural coronary arteries as an unusual cause of myocardial infarction and refractory angina pectoris.

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The present case report refers to a 65-year-old male patient with subocclusion of the right coronary artery who had an inferior myocardial infarction that was treated with coronary angioplasty. The patient subsequently developed intractable angina pectoris in the absence of critical coronary

Primary amyloidosis presenting as renal infarction.

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We report a case of primary amyloidosis affecting the kidney and presenting as a renal infarction on computed tomography and ultrasound examination. To our knowledge, it is the first case in the radio-logical literature with these imaging characteristics.

Scan findings in a case of splenic infarction due to amyloidosis: case report.

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Spleen images in a patient with monoclonal gammopathy showed numerous areas of decreased radiocolloid accumulation. Microscopic examination revealed areas of coagulation necrosis with diffuse amyloid infiltration in the spleen. In this patient, amyloidosis is considered to have caused the infarct.

Reversible myocardial oedema due to acute myocardial infarction as differential diagnosis of cardiac transthyretin amyloidosis

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Using bone-avid radiotracers, cardiac transthyretin (TTR) amyloidosis can be diagnosed by scintigraphy, thus obviating endomyocardial biopsy. Radiotracer accumulation, however, may also be due to other causes. A 68-year-old male with acute myocardial infarction underwent recanalization of the left

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