MAA-Adduction and its Implications.

<p>MAA-Adduction and its Implications.</p

Serum Concentrations of IgM, IgG and IgA Antibodies 24 Hours post-AMI.

<p>A subgroup of patients (n = 10) were evaluated 24 hours post-AMI for the presence of circulating IgM, IgG and IgA anti-MAA antibody levels (Figure 3A) and the total serum IgM, IgG, and IgA concentrations (Figure 3B). Results are expressed as relative mg/L or g/L of Human IgM, IgG, and IgA using a standard curve. *P<0.01 significantly different comparing AMI and 24 hours post-AMI.</p

Relative Serum Concentrations of anti-MDA LDL and anti-MAA LDL IgG Antibody are not Different in Individuals with Coronary Artery Disease (CAD) and in Individuals who Present with an Acute Myocardial Infarction (AMI).

<p>CAD patients were grouped in the following categories; control patients (n = 82), patients with chest pain and CAD (Non-Obstructive CAD, n = 40), patients presenting with AMI (n = 42), and patients with significant Multi-Vessel Obstructive CAD requiring coronary bypass grafting (n = 72). Serum anti-MDA LDL (Figure 2A) and anti-MAA LDL (Figure 2B). There is no significant difference in serum antibody levels when comparing all study groups (p>0.5).</p

Light and Confocal Microscopy of MAA in the Culprit AMI Aspirated Tissue.

<p>Panel A and B illustrates a Masson’s Trichrome staining at low (20X) and high magnification (80X) with panel B as the inset box of panel A. Panel C is the rabbit IgG isotype control stain. Panel D illustrates the rabbit anti-MAA staining with Cy3 reporter (80X). Note the absence of collagen or fibrosis and the presence of cholesterol clefts in Panel A which are typical of an atheroma. Also note the localization of MAA in Panel D (white arrows) to cellular vacuolization and necrosis as noted by the arrows on the Masson’s Trichrome in Panel B (black arrows).</p

Relative Serum Concentrations of anti-MAA IgM, IgG and IgA Antibodies are Increased in Individuals with Coronary Artery Disease (CAD) and in Individuals who Present with an Acute Myocardial Infarction (AMI).

<p>CAD patients were grouped in the following categories; control patients (n = 82), patients with chest pain and CAD (Non-Obstructive CAD, n = 40), patients presenting with AMI (n = 42), and patients with significant Multi-Vessel Obstructive CAD requiring coronary bypass grafting (n = 72). Serum anti-MAA antibodies were evaluated for the isotypes IgM (Figure 1A), IgG (Figure 1B), and IgA (Figure 1C). *P<0.001 significantly increased compared to controls. #P<0.03 significantly increased compared to Non-Obstructive CAD. $P<0.003 significantly increased compared to Multi-Vessel Obstructive CAD.</p

Patient demographics.

a<p>P<0.01 significantly increased compared to control.</p>b<p>P<0.05 significantly increase compared to Non-Obstructive and Acute AMI.</p>c<p>P<0.001 significantly increased compared to control.</p>d<p>P<0.01 significantly increased compared to control.</p>e<p>P<0.001 significantly increased compared to control, Non-Obstructive CAD, and Obstructive Multi-Vessel CAD.</p>f<p>P = 0.03 significantly decreased compared to control, Non-Obstructive CAD, and acute.</p>g<p>P<0.02 significantly decreased compared to control, acute.</p><p>*#Control subjects reported they were healthy with no medical problems or medications.</p><p>Patient demographics.</p