Gregory S. McGee

Elastin content, cross-links, and mRNA in normal and aneurysmal human aorta

Although elastin depletion is thought to be an etiologic factor in abdominal aortic aneurysm, little is known about its transcription and posttranslational modification in normal and diseased human aorta. Our objectives were to quantify total elastin and elastin cross-links (desmosine/isodesmosine [DID]) and to determine if elastin mRNA was detectable in the disease-prone infrarenal aorta from patients with abdominal aortic aneurysm and a comparative group with no aneurysmal diseases. After preliminary extraction and thermolysin digestion, content of DID and the elastin tetrapeptide, valine-alanine-proline-glycine (VAPG), were determined by high-performance liquid chromatography. Tissue mRNA was studied by Northern blot analysis. Mean values (+/- SE) were compared by Students t test. The proportion of insoluble elastin was markedly decreased in abdominal aortic aneurysm tissue (1.3% +/- 0.04% vs 12% +/- -2.8%; p less than 0.001). There was no difference in the small percentage of elastin solubilized during extraction in abdominal aortic aneurysm (5.3% +/- 1%) and no aneurysmal disease (6.0% +/- 1.2%; p = 0.71) tissues. The DID concentration of insoluble elastin was not different for abdominal aortic aneurysm and no aneurysmal disease tissue (0.18% +/- 0.07 vs 0.18 +/- 0.05 nm DID/nm VAPG; p = 0.97). On the basis of VAPG content, only 26% +/- 4% of the sodium hydroxide insoluble residue from abdominal aortic aneurysm was elastin; the predominate protein(s) was high in polar amino acids. Elastin mRNA was detectable in all tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

Distal embolization as a presenting symptom of aortic aneurysms

The records of 302 patients who underwent abdominal aortic aneurysm (AAA) repair between 1985 and 1990 were reviewed. Two hundred and forty-eight patients (82%) were asymptomatic, while 32 patients (11%) had ruptured aneurysms. During this period, 15 patients (5%) presented with distal embolization as the first manifestation of their AAA. The preoperative embolic event resulted in limb-threatening ischemia in 3 patients, digital ischemia in 11, and calf myonecrosis in 1. CT scan was performed in 14 of 15 patients demonstrating irregular, heterogeneous thrombus within the AAA. Only two of the AAAs were larger than 5 cm. Angiography demonstrated occlusive lesions but was not diagnostic for AAA in seven patients and resulted in three episodes of embolization. AAA was repaired with a tube graft in 4 patients while a bifurcated graft was required in 11 patients for aneurysmal (in 4 patients) and occlusive disease (in 7 patients) of the iliac arteries. All cases employed a transperitoneal approach, systemic heparin, and distal occlusion prior to aortic clamping. Complications included three major (below-knee) and five minor amputations, developing or worsening renal failure in five patients (33%), and death in two (13%). In comparison, mortality was 5% for elective repair and 66% for rupture during this same period. CT scan was safer and more informative than angiography. The morbidity of patients with AAA presenting with emboli is comparable with rupture. The risk of embolization does not correlate with size and indicates the potentially dangerous nature of small AAAs.