The in vivo acoustic and structural characteristics of atherosclerosis in the descending thoracic aorta have not been well delineated. We prospectively evaluated the descending thoracic aorta of 147 patients (35 women and 112 men; age, 61 +/- 14 years) who underwent clinically indicated transesophageal echocardiography. Patients with suspected disease of the aorta were excluded. Thirty-eight patients (26%) had protruding plaques (men, 25%; women, 29%). Six patients had mobile intimal densities with the mobile area ranging up to 1 cm2. As expected, aortic lumen area was decreased (plaque-free, 3.53 cm2; plaque, 3.19 cm2; p less than 0.05) and wall area was increased (plaque-free, 1.51 cm2; plaque, 1.92 cm2; p less than 0.05) in the regions of the plaque. However, total arterial area was not increased (plaque-free, 5.04 cm2; plaque, 5.09 cm2; difference not significant) in a compensatory manner as observed in other arterial beds. Plaque gray scale was less than the gray scale of plaque-free wall (plaque-free, 141.2; plaque, 122.7; p less than 0.05) when compared at the same level of the descending thoracic aorta or with a second aortic plaque-free level (plaque-free, 150.4; plaque, 122.7; p less than 0.05). Standard deviation of gray scale level was similar between plaque and normal regions. Unsuspected protruding plaques in the descending thoracic aorta occurred in one quarter of the patients referred for routine transesophageal examination. Plaques tended to have lower echogenicity and were differentiated from plaque-free walls within patients. Plaque formation did not result in increased total arterial area. These data suggest that the degree or character of compensatory atherosclerotic remodeling in the highly elastic descending thoracic aorta may differ from other arterial beds.

Aorta, Thoracic↗

PubMedDate not supplied

Blood histamine is associated with coronary artery disease, cardiac events and severity of inflammation and atherosclerosis.

BACKGROUND: Mast cells are prevalent in the shoulder of unstable atheromas; cardiac mast cells secrete proteases capable of activating matrix metalloproteinases. Histamine is essential in the inflammatory cascade of the unstable plaque. Ascorbate depletion has been correlated with histaminemia which has been shown to impair endothelial-dependent vasodilation. This study evaluates whether oxidative stress as measured by isoprostanes (PGF(2alpha)) coupled with an inflammatory state characterized by histaminemia predisposes patients to acute coronary syndrome (ACS). METHODS: Whole blood histamine, serum vitamin C, and serum PGF(2alpha) levels were drawn on 50 patients with ACS as determined by standard diagnostic criteria, 50 patients with stable coronary artery disease (SCAD), and 50 age and sex matched normal controls (C). RESULTS: Data were analyzed by stepwise discriminant and Spearman's rank correlation coefficient. A significant relationship exists between histamine and PGF(2alpha). As PGF(2alpha) rises above 60 pg/mL, an increase in histamine occurs in both the ACS and SCAD groups. A significant inverse relationship exists between ascorbate and histamine in the ACS versus C groups (P < 0.01) and the SCAD versus C groups (P < 0.01). CONCLUSION: Histamine and isoprostane levels increase in SCAD and ACS patients. Mast cell activation and lipid oxidation generated during atherosclerosis manifest this inflammatory response. Accelerated isoprostane formation and depleted ascorbate paired with histaminemia is active in CAD and predispose patients to acute coronary syndrome. Blood histamine alone may be a better risk factor for coronary events, and a better prognostic indicator than CRP even when combined with lipid indexes.

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