This report highlights the rare presentation of atrial myxoma with intracranial metastases and reviews previously reported examples. This is only the second case report of a glandular variant of atrial myxoma with metastases to the brain. A pathologist, unaware of this unusual variant of primary atrial myxoma, may mistake the intracranial lesion for a metastatic adenocarcinoma.

A 65-yr-old woman presented in May 1998 with a left parotid mass of 2 yr duration. The cytology and histopathology of the parotid lesion showed features of a columnar cell carcinoma. In November, 1967, she was diagnosed to have a classic papillary thyroid carcinoma (PTC). Ultrasound examination revealed a persistent thyroid nodule, the aspiration cytology of which confirmed columnar cell variant of papillary thyroid carcinoma (CCV-PTC). CCV-PTC is a recently described rare tumor of the thyroid that has been associated with an aggressive clinical course. Our case was peculiar in that the patient presented with an isolated metastasis in the parotid gland. Second, after an indolent course following the initial diagnosis of usual PTC 31 yr ago, she had now developed a more aggressive variant of the tumor.

In rheumatic MS, SR is associated with myocyte hypertrophy whereas AF is associated with myocytolysis. Endocardial inflammation is more common in left atrial appendage irrespective of rhythm. Interstitial fibrosis is seen in >90% of patients distributed in both the atria and is independent of the rhythm. Amyloid and Aschoff bodies are uncommon and the rest of the changes are uniformly distributed across both the atria.

The molecular mechanisms behind the rupture of intracranial aneurysms remain obscure. MiRNAs are key regulators of a wide array of biological processes altering protein synthesis by binding to target mRNAs. However, variations in miRNA levels in ruptured aneurysmal wall have not been completely examined. We hypothesized that altered miRNA signature in aneurysmal tissues could potentially provide insight into aneurysm pathophysiology. Using a high-throughput miRNA microarray screening approach, we compared the miRNA expression pattern in aneurysm tissues obtained during surgery from patients with aneurysmal subarachnoid hemorrhage (aSAH) with control tissues (GEO accession number GSE161870). We found that the expression of 70 miRNAs was altered. Expressions of the top 10 miRNA were validated, by qRT-PCR and results were correlated with clinical characteristics of aSAH patients. The level of 10 miRNAs (miR-24-3p, miR-26b-5p, miR-27b-3p, miR-125b-5p, miR-143-3p, miR-145-5p, miR-193a-3p, miR-199a-5p, miR-365a-3p/365b-3p, and miR-497-5p) was signi cantly decreased in patients compared to controls. Expression of miR-125b-5p, miR-143-3p and miR-199a-5p was signi cantly decreased in patients with poor prognosis and vasospasm. The target genes of few miRNAs were enriched in Transforming growth factor-beta (TGF-β) and Mitogen-activated protein kinases (MAPK) pathways. We found signi cant negative correlation between the miRNA and mRNA expression (TGF-β1, TGF-β2, SMAD family member 2 (SMAD2), SMAD family member 4 (SMAD4), MAPK1 and MAPK3) in aneurysm tissues. We suggest that miR-26b, miR-199a, miR-497and miR-365, could target multiple genes in TGF-β and MAPK signaling cascades to in uence in ammatory processes, extracellular matrix and vascular smooth muscle cell degradation and apoptosis, and ultimately cause vessel wall degradation and rupture.

Presence of a mutant allele of VKORC1 (-1639A & 1173T) and CYP2C9 genes increased the odds of requiring a lower mean dosage of acenocoumarol. Studying the combination of genotypes in RHD patients could predict acenocoumarol dose requirement more accurately.