Examining Safety and Feasibility of Intravascular Thermographic Assessment

While the approach to identifying and treating a high-grade, symptomatic and ischemia-producing coronary stenosis is readily apparent, the optimal treatment of lesions without these characteristics is less established. The uncertainty is because plaque rupture and coronary thrombus development occurs with non-stenotic lesions.¹ Additionally, while it only takes one plaque rupture or erosion to cause myocardial infarction and its attendant consequences, numerous plaques often exist in a single coronary artery, let alone a single patient. These facts have led to increasing interest in identification of the vulnerable plaque. What constitutes a vulnerable plaque? By definition, a vulnerable plaque is one that is at high risk of progression, rupture, erosion leading to future complications.² This property transcends into various plaque characteristics. Plaques with thin fibrous caps, substantial necrotic debris, lipid and high degrees of inflammation are considered particularly vulnerable. Indeed, the site of plaque rupture is commonly associated with an inflammatory process.^3,4 Numerous modalities exist that attempt to identify vulnerable plaque from both a morphologic and functional standpoint. Morphologically, there exist the noninvasive modalities of computed tomography and magnetic resonance imaging⁵ as well as the invasive modalities of intravascular ultrasound, optical coherence tomography and intracoronary magnetic resonance imaging.⁶ Each of these techniques brings with it potential advantages and limitations in morphologic evaluation of coronary plaque. Plaque vulnerability can also be assessed from a metabolic perspective. Inflammation is characterized by macrophage infiltration and activity, which should lead to heat production.⁷ Intravascular thermography refers to evaluation of temperature heterogeneity as a surrogate measure of inflammation. Previous research has shown that patients with stable angina, unstable angina and myocardial infarction demonstrate increasing heterogeneity within diseased coronary artery segments. Additionally, increasing changes in temperature between diseased and non-diseased segments predict adverse outcomes.^8,9 However, blood flow through the coronary arteries has limited the accuracy of intravascular thermography due to a cooling effect,¹⁰ and this finding has led to the development of flow-occluding thermography devices.¹¹ In this issue of the Journal, Belardi et al. report on the safety and feasibility of a flow-occluding catheter in assessing temperature heterogeneity as a surrogate marker of inflammation in coronary lesions for which percutaneous intervention was planned. Fifteen patients were evaluated; however, in one patient (7%), the catheter could not access the lesion. In the remaining 14 patients, 20 lesions were assessed and 15 are included in the final analysis. The other 5 were excluded due to incomplete occlusion of blood flow. This represents a 75% success rate of blood flow occlusion by the catheter. In the study population, there were no procedural complications. Patients appeared to tolerate occlusion times of 30–60 seconds without event. The catheters showed remarkable temperature correlation, reflecting both the accuracy of the thermistors and the circumferential nature of temperature heterogeneity. With this study, the authors present the safety and feasibility of this flow occluding thermography catheter by demonstrating an overall success rate of flow occlusion in less that 75% of the intended lesions. Intravascular thermography was well tolerated and safe in all, but only 14 patients were fully tested. This small number of patients represent barely a day’s work in many catheterization laboratories, and cannot be used to draw meaningful conclusions regarding safety and efficacy. Further improvements in catheter design (reduced diameter, increased flexibility) will be necessary to allow improved access to all lesions of interest and additional study will be needed to determine true safety and accuracy. Once these milestones are achieved, pilot data from these more thorough safety and efficacy studies shall help determine the incremental value of flow occlusion thermography versus conventional thermography. In conclusion, identification of vulnerable plaque remains an attractive and clinically challenging task. Intravascular thermography, along with other modalities, has potential in helping us along this task, and flow occlusion has the potential to improve the detection of temperature heterogeneity. Once vulnerable plaque can be accurately identified, the true effects of interventions (dietary, medical, mechanical) can be assessed.12 If further study and clinical trials show improved outcomes, we may one day see a paradigm shift in interventional cardiology from tertiary prevention of complications to secondary prevention of coronary disease.

1. Casscells W, Naghavi M, Willerson JT. Vulnerable Atherosclerotic Plaque: A Multifocal Disease. Circulation 2003;107:2072–2075. 2. Naghavi M, Libby P, Falk E, et al. From Vulnerable Plaque to Vulnerable Patient: A Call for New Definitions and Risk Assessment Strategies: Part I. Circulation 2003;108:1664–1672. 3. van der Wal AC, Becker AE, van der Loos CM, Das PK. 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. 4. Piek JJ, van der Wal AC, Meuwissen M, et al. Plaque inflammation in restenotic coronary lesions of patients with stable or unstable angina. J Am Coll Cardiol 2000;35:963–967. 5. Fuster V, Fayad ZA, Moreno PR, et al. Atherothrombosis and high-risk plaque: Part II: Approaches by noninvasive computed tomographic/magnetic resonance imaging. J Am Coll Cardiol 2005;46:1209–1218. 6. MacNeill BD, Lowe HC, Takano M, et al. Intravascular modalities for detection of vulnerable plaque: Current status. Arterioscler Thromb Vasc Biol 2003;23:1333–1342. 7. Casscells W, Hathorn B, David M, et al. Thermal detection of cellular infiltrates in living atherosclerotic plaques: Possible implications for plaque rupture and thrombosis. Lancet 1996;347:1447–1451. 8. Stefanadis C, Diamantopoulos L, Dernellis J, et al. Heat production of atherosclerotic plaques and inflammation assessed by the acute phase proteins in acute coronary syndromes. J Mol Cell Cardiol 2000;32:43–52. 9. Stefanadis C, Toutouzas K, Tsiamis E, et al. Increased local temperature in human coronary atherosclerotic plaques: An independent predictor of clinical outcome in patients undergoing a percutaneous coronary intervention. J Am Coll Cardiol 2001;37:1277–1283. 10. Diamantopoulos L, Liu X, De Scheerder I, et al. The effect of reduced blood-flow on the coronary wall temperature. Are significant lesions suitable for intravascular thermography? Eur Heart J 2003;24:1788–1795. 11. Stefanadis C, Toutouzas K, Vavuranakis M, et al. New balloon-thermography catheter for in vivo temperature measurements in human coronary atherosclerotic plaques: A novel approach for thermography? Catheter Cardiovasc Interv 2003;58:344–350. 12. Nakamura M, Lee DP, Yeung AC. Identification and treatment of vulnerable plaque. Rev Cardiovasc Med 2004;5(Suppl 2):S22–S33.