Surgery – Diagnostic testing – Detecting nuclear – electromagnetic – or ultrasonic radiation
Reexamination Certificate
2001-01-24
2004-11-09
Lateef, Marvin M. (Department: 3737)
Surgery
Diagnostic testing
Detecting nuclear, electromagnetic, or ultrasonic radiation
C600S476000, C600S478000, C600S479000, C382S128000, C382S130000
Reexamination Certificate
active
06816743
ABSTRACT:
FIELD OF THE INVENTION
The present invention relates to the field of atherosclerosis intervention. More specifically, the invention relates to near-infrared imaging for in vivo identification and characterization of tissue including vulnerable atherosclerotic plaques.
BACKGROUND OF THE INVENTION
Over the past two decades, valuable studies have been conducted using new intracoronary technologies to characterize coronary lesions in living patients. These new technologies include angioscopy, ultrasound, and atherectomy. Studies based upon these approaches have further added to the knowledge gained from post-mortem studies. While much has been learned during post-mortem studies, by definition, these investigations cannot provide prospective data. Furthermore, the procedures used in living patients, cannot usually provide detailed information on the chemical composition of the diseased tissue. A significant amount of relevant information, however, has been derived over the years through various studies on coronary lesions.
The characterization of lesions causing acute coronary syndromes has been advanced significantly by post-mortem observations. It was earlier observed that in human autopsy specimens of thrombosed coronary arterial segments, the thrombus was situated at the site of a plaque where an intimal fracture allowed the exposure of soft, abscess-like lipoid material into the lumen of the blood vessel (Constantinides P, Plaque fissures in human coronary thrombosis, J Atheroscler Res 1966; 6:1-17 (cited references are incorporated herein by reference)). Subsequently, it was shown that coronary thrombi responsible for fatal myocardial infarction were almost exclusively found at the site of disrupted plaques (Davies M J, Thomas A C, Thrombosis and acute coronary artery lesions in sudden cardiac ischemic death, N Engl J Med 1984; 310:1137-40; Davies M J, A macro and micro view of coronary vascular insult in ischemic heart disease, Cir 1990; 82(3):38-46; Falk E, Plaque rupture with severe pre existing stenosis precipitating coronary thrombosis: Characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi, Br Heart 1983; 50:127-34). The lipid content of human aortic plaques displaying ulceration and thrombosis was observed to be greater than that of non-disrupted plaques. Similarly, in patients dying of acute myocardial infarction, previous research revealed that while culprit lesion morphology in myocardial infarction is heterogeneous with respect to plaque architecture and cellular composition (van der Wal A C, Becker A E, van der Loos C M, Das P K, Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology, Circulation 1994; 89:36-44), the immediate site of plaque rupture is marked by an inflammatory process. An incidence of plaque disruption of about 83% has been also reported, similar to that of infarction, in patients with unstable angina. Additional reports noted the occurrence of coronary thrombosis at sites that do not show typical signs of plaque rupture (Burke A P, Farb A, Malcom G T, Liang Y-H, Smialek J, Virmani R, Coronary risk factors and plaque morphology in men with coronary disease who died suddenly, N Engl J Med 1997; 336:1276-82). These have been termed sites of erosion, and it is estimated that they are responsible for approximately 30% of coronary thrombi, with plaque rupture accounting for the remainder. There is a frequent occurrence in these studies of lipid-rich plaques with thin caps, both ruptured and non-ruptured, as incidental findings in patients dying of other coronary lesions, or non-cardiac causes (Falk E, Shah P K, Fuster V, Coronary plaque disruption, Circ. 1995; 92:657-71). It has also been observed that approximately 80% of patients dying suddenly had such lesions in addition to their culprit lesions (Farb A, Burke A P, Tang A L et al, Coronary plaque erosion without rupture into a lipid core: A frequent cause of coronary thrombosis in sudden coronary death, Circulation 1996; 93:1354-63). Although many post-mortem studies have yielded valuable information, there are several important limitations to their use. Because of possible selection bias, the findings derived from autopsy studies can be generalized with certainty only to those who die of acute coronary syndromes. It is quite possible that the prevalence, nature, and degree of plaque disruption and/or associated thrombosis of culprit lesions, is different in those surviving the disease. Results from autopsy studies suggest nonetheless that most acute lesions arise from a plaque that includes a lipid pool, a thin cap, and macrophage infiltration. While prospective studies have been limited, these histologic features may be considered to represent a “vulnerable plaque”, a term first defined by Muller et al (Muller J E et al, Triggers, Acute Risk Factors and Vulnerable Plaques: The Lexicon of a New Frontier, JACC 1994; 23(3) 809-13). This type of plaque refers to its functional property of having an increased likelihood of rupture, and may include more than one histologic type.
The coronary angiogram is considered a primary source of information for living patients with lesions that cause acute coronary syndromes. Recently, retrospective analysis of coronary angiograms in patients who subsequently developed unstable angina and myocardial infarction demonstrated that many culprit lesions originate from plaques previously causing less than 50% stenosis (Ambrose J A, Tannenbaum M A, Alexopoulos D et al, Angiographic progression of coronary artery disease and the development of myocardial infarction, J Am Coll Cardiol 1988; 12, 56-62; Ambrose J A, Winters S L, Arora R R et al, Angiographic evolution of coronary artery morphology in unstable angina, J Am Coll Cardiol 1986; 5,472-8; Nobuyoshi M, Tanaka M, Nosaka H et al, Progression of coronary atherosclerosis: is coronary spasm related to progression? J Am Coll Cardiol 1991; 18, 904-10; Little W C, Downes T R, Applegate R J, The underlying coronary lesion in myocardial infarction: implications for coronary angiography, Clin Cardiol 1991; 14, 868-74). The residual stenosis, after successful thrombolytic therapy, was found to be of only moderate severity in many cases, supporting the concept that occlusive thrombus frequently develops at coronary sites without prior severe stenosis (Kereiakes D J, Topol E J, Sea G, Myocardial infarction with minimal coronary atherosclerosis in the era of thrombolytic reperfusion, J Am Coll Cardiol 1991; 17, 304-12; Brown G G, Gallary C A, Badger R S et al, Incomplete lysis of thrombus in the moderate underlying atherosclerotic lesion during intracoronary infusion of streptokinase for acute myocardial infarction, Circulation 1986; 73, 653-61). Despite these advances, the use of coronary angiography to study coronary atherosclerotic lesions in living patients has severe limitations including its inability to provide information about the sub-surface features of the plaque. The relatively low sensitivity and specificity of a plaque's geometric surface features to predict subsequent occlusion indicate that other plaque-related characteristics (i.e., plaque composition), not detectable by angiography, may be more important in the determination of plaque vulnerability (Taeymans Y, Theroux P, Lesperance J, Waters D, Quantitative angiographic morphology of the coronary artery lesions at risk of thrombotic occlusion, Circulation 1992; 85, 78-85).
The development of angioscopic imaging devices for the coronary arteries also provided a valuable opportunity to define the surface features of lesions which cause unstable angina and acute coronary syndromes. Angioscopic imaging devices were used percutaneously to obtain a clear view, with magnification, of the inner surface of the coronary lumen in patients undergoing catheterization. Normal segments of coronary arteries in living patients were observed to be white and smooth, while disrupted atherosclerotic plaques causing disea
Lodder Robert A.
Moreno Pedro
Muller James E.
O'Connor William
Fish & Richardson P.C.
Lateef Marvin M.
Lin Jeoyuh
University of Kentucky Research Foundation
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