Giant cell myocarditis:a fatal cause of dyspnea in pregnancy

The clinical course of a pregnant patient, who presented with progressive dyspnea and heart failure is described. Despite intensive care and resuscitative efforts to mother and child, both expired. The autopsy revealed giant cell myocarditis in the mother. Giant cell myocarditis can affect pregnant patients and should therefore be considered in the differential diagnosis of progressive dyspnea. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved

Sustained high levels of serum HHV-8 DNA years before multicentric Castleman's disease despite full suppression of HIV with highly active antiretroviral therapy

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No long-lasting or intermittent mast cell activation in acute coronary syndromes

Background: Unstable coronary syndromes, such as acute myocardial infarction and unstable angina pectoris are mostly due to rupture of an atherosclerotic plaque. Recently mast cells were found to participate actively in the inflammatory process of atherosclerosis by excreting proteolytic and pro-inflammatory substances with the ability to cause plaque instability and rupture. Mast cell activity can be determined by measuring serum levels of tryptase, as has been demonstrated in patients with anaphylaxis and mastcytosis. Hypothesis: Acute coronary events (acute myocardial infarction and unstable angina pectoris) are associated with increased mast cell activity, reflected by elevated serum tryptase levels. Methods: Serum levels of tryptase were determined in the following three groups of patients: 13 patients with acute myocardial infarction, 10 patients with unstable angina pectoris, and 14 patients without ischaemic cardiovascular disease who were used as controls. Patients with known IgE mediated allergic diseases and/or anti-histaminical drugs were excluded. Results: The groups were comparable for sex, blood pressure, smoking and cholesterol levels. The controls tended to be younger (P=0.05). Levels of tryptase did not differ between patients with acute myocardial infarction (7.9+/-4.6 mug/l), unstable angina pectoris (6.0+/-2.1 mug/l) or controls (6.9+/-4.1 mug/l), nor could a relation with levels of C-reactive protein be demonstrated. Conclusion: Serum levels of tryptase are not elevated in patients with acute coronary syndromes. This implies that increased mast cell activity, if any, in unstable coronary syndromes is not reflected systemically. Other, more specific methods will be needed to determine the activity of the mast cell in vivo. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved

Long term angiotensin converting enzyme-inhibition in patients after coronary artery bypass grafting reduces levels of soluble intercellular cell adhesion molecule-1

Objective: to examine the effect of angiotensin converting enzyme inhibition (ACEI) on soluble intercellular adhesion molecule 1 (sICAM-1) and C-reactive protein (CRP) in patients requiring coronary artery bypass grafting (CABG). Method: subgroup analysis of 42 patients randomised to Quinapril (40 mg daily determined) and 45 to placebo. sICAM-1 and CRP were greater than or equal to4 weeks before and 1 year after surgery. Results: there was no difference in sICAM-1 at baseline (142.2 mug/L vs 136.6 mug/L). There was significant reduction in sICAM-1 in patients receiving quinapril (142.2 +/- 10.8 mug/L vs 125.6 +/- 9.4 mug/L, p < 0.05) but not placebo (136.6 +/- 10.2 mug/L vs 131.2 +/- 11.7 mug/L, p = NS). Levels of C-reactive protein remained unchanged in both groups (3.70 +/- 0.85 vs 2.73 +/- 0.32 mg/L, 2.85 +/- 0.48 vs 3.16 +/- 0.50 mg/L). Conclusions: ACEI reduces sICAM-1 in patients undergoing CABG. The benefits of ACEI may partly be due to a reduction of the vascular inflammatory response

Antineutrophil cytoplasmatic antibodies in patients with premature atherosclerosis:prevalence and association with risk factors

Objectives. Autoimmunity is suggested to play a role in premature atherosclerosis. Antineutrophil cytoplasmatic antibodies (ANCA) are a group of autoantibodies found in several inflammatory disorders in which they supposedly amplify the inflammatory process. In this study the hypothesis is tested that ANCA play a role in premature atherosclerosis. Design. Cross-sectional study followed by nested case-control study. In a total of 286 consecutive patients with premature atherosclerosis (age <5 years) ANCA were tested. Within the same cohort, a nested case control study in 16 ANCA-positive patients and 32 ANCA-negative controls matched for sex, and site of atherosclerosis, was executed. Setting. University hospital outpatient clinic for lipids and premature atherosclerosis. Subjects. A total of 286 consecutive patients with premature atherosclerosis (age <55 years). Results. Prevalence of ANCA was 5.6% (16 of 286). All cases had perinuclear ANCA (pANCA); no cytoplasmatic ANCA was found. Mean age was 42 +/- 7 in the ANCA-positive vs. 42 9 years in the ANCA-negative group (P = ns). More female parents were ANCA-positive (8M/8F vs. 200M/70F, P = 0.03). Patients with ANCA had more often peripheral vascular disease (37.5 vs. 15.2%, P = 0.03). In the case-control study levels of Lp(a) were higher (43.8 vs. 15.6% > 300 mg L-1, P = 0.05), whereas levels of HDL-c were lower in ANCA-positive patients (0.84 +/- 0.26 vs. 1.06 +/- 0.27 mmol L-1, P = 0.01). Markers of inflammation, C-reactive protein (CRP) and serum amyloid A (SAA), did not differ, nor did antibodies against oxidized-LDL and malondialdehyde (MDA)-LDL, markers for the extent of atherosclerosis. Conclusions. Our results suggest that ANCA do not appear to play a major role in premature atherosclerosis as there was no increased prevalence of the autoantibody. Moreover, no differences in the incidence of classical cardiovascular risk factors nor in serum levels of markers of inflammation were found between the ANCA-positive group as compared with the ANCA-negative group