Acute streptococcal myocarditis presenting as acute ST-elevation myocardial infarction.

Acute streptococcal myocarditis is an uncommon diagnosis in the developed world. Its presentation masquerading as acute myocardial infarction is still uncommon. We describe a case of a young male presenting with a recent diagnosis of streptococcal pharyngitis followed by a classical presentation of post streptococcal myocarditis. This is an unusual presentation of acute rheumatic fever (ARF) masquerading as acute myocardial infarction, with a discussion on its diagnosis and management.

Chronic total occlusion angioplasty through supplying collaterals.

Chronic total occlusions are typically difficult to recannalize especially when adverse angiographic morphologies are identified. We describe a case of chronic total occlusion crossing retrograde through the supplying collaterals followed by successful angioplasty and stenting.

A role for CXCL12 (SDF-1alpha) in the pathogenesis of multiple sclerosis: regulation of CXCL12 expression in astrocytes by soluble myelin basic protein.

The pathogenic mechanisms that contribute to multiple sclerosis (MS) include leukocyte chemotaxis into the central nervous system (CNS) and the production of inflammatory mediators, resulting in oligodendrocyte damage, demyelination, and neuronal injury. Thus, factors that regulate leukocyte entry may contribute to early events in MS, as well as to later stages of lesion pathogenesis. CXCL12 (SDF-1alpha), a chemokine essential in CNS development and a chemoattractant for resting and activated T cells, as well as monocytes, is constitutively expressed at low levels in the CNS and has been implicated in T cell and monocyte baseline trafficking. To determine whether CXCL12 is increased in MS, immunohistochemical analyses of lesions of chronic active and chronic silent MS were performed. CXCL12 protein was detected on endothelial cells (EC) in blood vessels within normal human brain sections and on a small number of astrocytes within the brain parenchyma. In active MS lesions, CXCL12 levels were high on astrocytes throughout lesion areas and on some monocytes/macrophages within vessels and perivascular cuffs, with lesser staining on EC. In silent MS lesions, CXCL12 staining was less than that observed in active MS lesions, and also was detected on EC and astrocytes, particularly hypertrophic astrocytes near the lesion edge. Experiments in vitro demonstrated that IL-1beta and myelin basic protein (MBP) induced CXCL12 in astrocytes by signaling pathways involving ERK and PI3-K. Human umbilical vein EC did not produce CXCL12 after treatment with MBP or IL-1beta. However, these EC cultures expressed CXCR4, the receptor for CXCL12, suggesting that this chemokine may activate EC to produce other mediators involved in MS. In agreement, EC treatment with CXCL12 was found to upregulate CCL2 (MCP-1) and CXCL8 (IL-8) by PI3-K and p38-dependent mechanisms. Our findings suggest that increased CXCL12 may initiate and augment the inflammatory response during MS.

The Mayo Clinic Risk Score predicts in-hospital mortality following primary angioplasty.

BACKGROUND: The Mayo Clinic Risk Score (MCRS) is a validated numeric score that predicts outcome following primary percutaneous coronary intervention (PCI). PURPOSE: We evaluated the ability of MCRS to risk stratify patients undergoing primary angioplasty. METHODS: Patients undergoing primary angioplasty within 6 hours of the onset of chest pain in the New York State percutaneous coronary intervention reporting system (n = 3,005) had their MCRS calculated using predictive variables: age, presence of cardiogenic shock, renal failure, class III-IV congestive heart failure, left main coronary disease and multivessel coronary disease. All patients were presumed to have intra-coronary thrombus and undergoing an urgent/emergent procedure. Based on the MCRS, patients were classified into five risk categories: very low-risk (MCRS < 5), low risk (6-8), moderate (9-11), high (12-14) and very high risk (15-25). RESULTS: The mean age of the study population was 62 years, 70% were male; stents were used in 89% and glycoprotein IIb/IIIa antagonists in 72%. The prevalence of cardiogenic shock, multivessel disease and left main disease was higher in patients with MCRS > 12. Overall in-hospital mortality following primary angioplasty was 4.7%; it was 0% in the very low-risk category, 0.9% in the low-risk category, 3.2% in the moderate-risk category, 10.7% in the high-risk category, and 25.1% in the very high-risk category (p < 0.0001). The higher-risk MCRS category predicted increased risk even when 317 (10.5%) patients with cardiogenic shock were excluded from the analysis. The overall c-statistic for the prediction of in-hospital mortality by MCRS was 0.85. CONCLUSION: Increasing MCRS predicts in-hospital mortality following primary angioplasty.