PubMed · 7902765
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E J Harris, M R Nehler, J M Porter. 1993. Arteritis.. https://pubmed.ncbi.nlm.nih.gov/7902765/
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PURPOSE: To investigate through the use of cerebral Doppler technology whether emboli are a more common cause of nonarteritic anterior ischemic optic neuropathy (NAION) than previously recognized. METHODS: Eleven patients with a recent (<121 days) history of nonarteritic anterior ischemic optic neuropathy and 10 age-matched controls (event > 121 days) were examined using a Nicolet Pioneer 2020 transcranial Doppler (TCD) unit with a 2-MHz bilateral continuous monitoring capability. The right and left middle cerebral arteries were evaluated simultaneously for 30 minutes at a depth of 50 to 55 mm, and the number of emboli, blood flow velocities, and pulsatility indices were recorded. Data were stored by computer, and hard-copy color recordings were made. RESULTS: None of 11 patients with a recent history of NAION demonstrated microemboli by TCD examination. One patient in the control group who had a remote history of NAION had a microembolic event rate of 12 per hour (six over 30 minutes). This patient had a history of prosthetic cardiac valve replacement and was taking anticoagulation medication at the time of the examination. CONCLUSIONS: Our study did not reveal an increased incidence of embolic events in patients with NAION when they were examined in a transcranial Doppler study of the middle cerebral arteries. This study does not support embolism as a frequent cause of NAION.
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Numerous pathological, clinical, angiographic and angioscopic studies have demonstrated that acute coronary syndromes (unstable angina, acute myocardial infarction and ischemic sudden death) are most frequently the consequence of plaque disruption (plaque rupture or superficial plaque erosion) and consequent coronary thrombosis. Several serial angiographic studies have demonstrated that nearly 60-70% of acute coronary syndromes evolve from mildly to moderately obstructive atherosclerotic plaques. Coronary plaque disruption appears to be a function of both the composition of the plaque (plaque vulnerability ) as well as extrinsic triggers that may precipitate plaque disruption in a vulnerable plaque. Vulnerability for plaque disruption appears to be largely determined by the size of the lipid-rich atheromatous core, the thickness of the fibrous cap covering the core, and the presence of ongoing inflammation within and underneath the cap. Inflammatory cells may play a critical role in plaque disruption through the elaboration of matrix degrading metalloproteinases or MMPs (collagenases, gelatinases, stromelysins and matrilysin) and by inhibition of function and survival of matrix-synthesizing smooth muscle cells. Inflammatory cells may also play a critical role in triggering thrombosis following plaque disruption through the tissue factor pathway. In addition, stresses resulting from hemodynamic and mechanical forces may precipitate plaque disruption, particularly at points where the fibrous cap is weakest, such as at its shoulders. The degree of thrombosis following plaque disruption is determined by the thrombogenicity of the disrupted plaque, disturbed local rheology and systemic thrombotic-thrombolytic milieu. Surges in sympathetic activity provoked by sudden vigorous exercise, emotional stress -- including anger, or cold weather, may also trigger plaque disruption. These observations have led to the concept of plaque stabilization as a new clinical strategy for the prevention of acute coronary syndromes. Plaque stabilization can be achieved through pharmacologic and lifestyle-modifying interventions that reduce vulnerability to plaque disruption by altering plaque composition and/or inflammatory activity within the plaque.