Lesion embolic

Fever is common as well as a heart murmur (sometimes new or changing). The patient may or may not have embolic phenomenon, splenomegaly, or skin manifestations (e.g, Osier s nodes, Janeway lesions). Laboratory tests... 

CHD = myocardial infarction (Ml), significant myocardial ischemia (angina), history of coronary artery bypass graft (CABG), history of coronary angioplasty, angiographic evidence of lesions, carotid endarterectomy, abdominal aortic aneurysm, peripharal vascular disease (claudication), thrombotic/embolic stroke, transient ischemic attack (TIA)... 

This is a critical step and requires careful attention since it is at this stage that embolic events are most likely to develop. The risk of embolization is minimized by conservative sizing of the balloon (5 mm) and by performing a single inflation. The balloon should be deflated slowly. Mild residual stenoses (<20%) or persistence of an ulcer at the lesion site should be accepted, since aggressive stent dilatation can produce cerbral embolization. 

Ohki T, Marin ML, Lyon RT et al. Ex vivo human carotid artery bifurcation stenting correlation of lesion characteristics with embolic potential. J Vase Surg 1998 27 463-471. 

Several studies have evaluated the effect of tPA treatment administered at variable timepoints after clot embolization (Brinker et al. 1999 Busch et al. 1998 Franke et al. 2000 Jiang et al. 2000). Early lesion expansion as visible on DWI could only be reversed or slowed down if thrombolysis-induced reperfusion was initiated early after the onset of ischemia (Fig. 4.14). For example, if tPA was given at 1.5 h post occlusion the DWI lesion did not further enlarge whereas thrombolysis at later timepoints did not attenuate lesion growth (Brinker et al. 1999). Correlation analysis with other MR parameters revealed that areas with increased lactate or T2 values did not improve when tPA was started > 3 h after the insult (Franke et al. 2000). By using histological means, other investigators however... 

Fig. 4.14. Maps of the apparent diffusion coefficient (ADC) measured before and after embolic occlusion of the right middle cerebral artery in an animal without therapy (upper row) and in two animals with thrombolytic treatment initiated 1.5 h (middle row) and 4.5 h (lower row) after onset of ischemia. In the untreated animal, a decline of ADC was observed immediately after MCA occlusion that increased in size over time. Thrombolysis with recombinant tissue-type plasminogen activator (tPA) lead to the partial reversal of the ADC lesion over the first 5 h of therapy if started early. Late-onset thrombolysis at 4.5 h post occlusion did not reverse lesion growth, but was followed by a further lesion enlargement of the ischemic lesion. [Reproduced with permission from Hoehn et al. (2001)]...

Busch et al. 2002 tPA rat embol MCAO slower lesion progression... 

Schuler OG, Eriskat J, Baethmann AJ, Back T (2001a) Thrombolysis induces a reperfusion-dependent inhibition of peri-infarct depolarizations in experimental thromboembolic stroke. J Cereb Blood Flow Metab 21 S396 Schuler OG, Plesnila N, Otto D, Baethmann AJ, Back T (2001b) Early thrombolysis inhibits periinfarct depolarizations in embolic MCA occlusion. NeuroReport 12 3943-3946 Schwindt W, Burke M, Pillekamp F, Luhmann HJ, Hoehn M (2004) Functional magnetic resonance imaging and somatosensory evoked potentials in rats with a neonatally induced freeze lesion of the somatosensory cortex. J Cereb Blood FlowMetab 24 1409-1418... 

With the use of DWI, small acute lesions lying in different vascular territories in addition to lacunar infarction provides evidence for the possibility of an embolic mechanism in a subset of classic lacunar syndromes (Gerraty et al. 2002 Ay et al. 

This was systematically studied with DWI in 62 consecutive patients who presented with a classic lacunar syndrome (Ay et al. 1999). DWI showed subsidiary acute lesion(s) in addition to the index lacunar lesion in ten patients (16%). The additional lesions were punctuate and lay within the leptomen-ingeal arterial territories in the majority. Patients with subsidiary infarction(s) more frequently harbored an embolic cause of stroke. This finding is critical because underlying embolic cause may give rise to recurrent strokes with more extensive brain injury. Identification of subsidiary infarctions on DWI should have an impact in prompting the physician to introduce the best effective treatment for secondary stroke prevention in a patient with lacunar infarction. 

Different topographical patterns of AMBI are associated with different vascular pathologies. Hemorheologic abnormalities or vascular anatomic variations may be contributing factors of AMBI in both hemispheres or in both the anterior and the posterior circulation (Roh et al. 2000). A scattered lesion pattern on DWI in patients with an initial negative CT is indicative of an arterial or embolic source and associated with favorable clinical outcome (Koennecke et al. 2001). Occlusion of the... 

DWI can demonstrate scattered lesions in acute stroke patients with initial negative CT (Koennecke et al. 2001) associated with an embolic etiology. In patients presenting with classical lacunar syndromes, DWI can demonstrate lesions not apparent in CT or conventional MR in addition to the lesion in the territory of a single perforator. The most common associated lesions are punctuate subsidiary lesions in the territory of the leptomeningeal arteries (Ay et al. 1990). 

Carotid loops may be associated with aneurysm formation and rarely with embolism, endothelial damage and thrombosis exceptionally there may be focal ischemia on head movement (Sarkari et al. 1970 Desai and Toole 1975). Rarely, these loops may cause hypoglossal nerve lesions or pulsatile tinnitus. 

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