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The mechanism of aortic pulse pressure decline induced by acute rapid ventricular pacing remains incompletely understood. It has been ascribed to changes in stroke volume or aortic compliance. This becomes more complicated by the dependence of aortic compliance on the level of the mean aortic pressure as well as the aortic wall properties. To test the role of such mechanical factors, aortic pressure-diameter hemodynamics, derived from simultaneous tip-micromanometer aortic pressure recordings and high-fidelity ultrasonic intravascular aortic diameter recordings, were measured in 15 normal subjects during and after abrupt cessation of rapid ventricular pacing (up to 160 bpm). Immediately after terminating the pacing, diastolic aortic pressure declined (-9%, from 87.4 +/- 1.2 to 79.5 +/- 1.7 mmHg, P0.0001) while systolic aortic pressure increased (+19%, from 109.5 +/- 1.6 to 130.1 +/- 2.8 mmHg, P0.0001). Thus, pulse pressure increased from 22.1 +/- 2.2 to 50.6 +/- 3.1 mmHg, P0.0001. To quantify systolic and diastolic aortic pressure differences we compared the first postpaced beat (a) and the last paced beat (b). To estimate what the aortic pressure would have been for the paced beats had the aortic diameter differences due to the different heart rate not occurred we calculated the theoretical pressure of the paced beat P(b) = E(b). D(a), where E(b) was the instantaneous aortic elastance of the paced beat and D(a) was the aortic diameter for the postpaced beat. The corrected pressure difference was then calculated by the following: DeltaP(cor) = (D(a). E(b)) - P(a). It was found that systolic DeltaP(cor) was 25% of systolic DeltaP(raw) and diastolic DeltaP(cor) was 89% of diastolic DeltaP(raw). DeltaP(raw) was the pressure difference between paced and spontaneous beat measured from the raw data. DeltaP(cor) indicates the portion of DeltaP(raw) that results from a change in aortic stiffness as a consequence of viscous behavior or aorto-ventricular coupling. These data indicate that the majority of diastolic pressure decline after pacing was terminated, may reflect a change in aortic stiffness while the majority of systolic pressure rise, and may be attributable to differences in hemodynamics alone.

The vulnerable atherosclerotic plaque is associated with an increased number of acute coronary syndromes. Current techniques such as coronary angiography are unable to detect and prospectively evaluate these lesions. Recently, other techniques, both invasive and noninvasive, are being developed trying to detect the plaque that is at increased risk for rupture eventually resulting in increased thrombosis. This review describes briefly evolving techniques for imaging of vulnerable plaques and describes in detail intravascular thermography.

Background: Nonfluoroscopic electromechanical mapping (NEM) has been proposed as a new technique for the evaluation of electrical and mechanical functioning of the myocardium. In this system, linear local shortening (LLS) is the parameter used for assessment of local mechanical properties. To validate this parameter, we compared LLS with regional wall motion (RWM) data derived from contrast left ventriculograms acquired in the same patients. Methods and results: Angiographic left ventricular RWM was analyzed using the area–length method. The right anterior oblique view was divided in five segments, the left anterior oblique view in two. Through a comparison of enddiastolic and endsystolic areas drawn from a computer-defined central point to the respective wall delineation, RWM was calculated as change in area. In the first approach, we compared area changes to comparable NEM segments. In the second part of the study, LLS values for normokinetic, hypokinetic, akinetic and dyskinetic segments were correlated to the change in angiographic RWM. In the first approach, the overall comparison of segments yielded a correlation coefficient of 0.67 (P

Background —The aim of this study was to assess the sigmoid line of elasticity in the human aorta. Methods and Results —The pressure-diameter relation was measured in the descending aorta in 120 subjects. In an additional group of 6 subjects, transient vena caval occlusion produced 5 sets of pressure-diameter data. We found that the best fit curve of the pooled pressure-diameter data was a third-order polynomial. A polynomial equation was used to calculate the sigmoid line of elasticity in the entire population and after the administration of diltiazem (15 patients) or enalaprilat (10 patients). The sigmoid line of elasticity was significantly different with respect to age ( P P P P Conclusions —This approach provides a quantitative evaluation of the aortic line of elasticity, which can differentiate the intrinsic from the extrinsic aortic elastic properties. Furthermore, it is a powerful and independent risk factor for cardiovascular events.

Aims Aortic elasticity is an important determinant of left ventricular performance and coronary blood flow. Moreover, it has been shown that aortic elastic properties deteriorate in patients with coronary artery disease. However, the predictive role of aortic elasticity in the occurrence of coronary events, has not been addressed so far. Therefore, we set out to test prospectively the hypothesis that invasive as well as non-invasive measures of aortic elastic properties, assessed at rest from pressure–diameter relationships, could predict the development of recurrent coronary events. Methods and Results Clinical variables and measures of aortic function were assessed in 54 normotensive patients with coronary artery disease. The aortic pressure–diameter relationship was derived invasively with a high-fidelity Y shaped catheter (developed in our Institution) for aortic diameter measurements, simultaneously with a Millar catheter for aortic pressure measurements. Aortic root distensibility was assessed by non-invasive techniques. During an average of 3 years follow-up, 12 of 54 patients either developed unstable angina (n=8) or acute myocardial infarction (n=4). By multivariate Cox model analysis, aortic stiffness was the strongest predictor of progression to any end-point (relative risk: 3·24, CI: 1·79 to 5·83; P =0·000). When aortic stiffness was not considered, aortic distensibility was the only independent predictor for acute coronary syndromes (relative risk: 0·37 CI: 0·21 to 0·65; P =0·000). Conclusion In patients with coronary artery disease, aortic elastic properties are powerful and independent risk factors for recurrent acute coronary events.

C. Stefanadis, L. Diamantopoulos, J. Dernellis, E. Economou, E. Tsiamis, K. Toutouzas, C. Vlachopoulos and P. Toutouzas. Heat Production of Atherosclerotic Plaques and Inflammation Assessed by the Acute Phase Proteins in Acute Coronary Syndromes. Journal of Molecular and Cellular Cardiology (2000) 32, 43–52. Several studies have shown that inflammation plays an important role in the pathogenesis of coronary heart disease (CHD). Serum amyloid A (SAA) and C-reactive protein (CRP) reactants of the acute phase of inflammation, have been shown to be increased in patients with CHD. Recently ex vivo studies demonstrated that some types of atherosclerotic plaques show substantially warmer regions. A catheter-based technique has been developed to measure the temperature of human arteries in vivo. Therefore, the aim of the present study was to measure the luminal surface temperature in patients with CHD and to correlate it with the acute phase proteins in order to discriminate the role of inflammation in heat production in acute coronary syndromes. Sixty patients were studied with CHD (20 with stable angina, 20 with unstable angina and 20 with acute myocardial infarction) and 20 sex- and age-matched controls without coronary artery disease, by measuring plasma levels of SAA, CRP, plasma lipids and intracoronary arterial luminal wall temperature. Intracoronary temperature was measured with a thermography catheter developed in our Institution: a thermistor probe with a temperature accuracy of 0.05°C, was attached at the distal end of a long 3F polyurethane shaft. It was found that the median temperature differences at the site of the lesion from the core temperature was increased in patients with unstable angina (1.025°C) and acute myocardial infarction (2.150°C) compared with stable angina (0.300°C), P

The radial artery has been used as a free bypass graft with excellent results. An autologous vein graft-coated stent, a novel type of stent developed at our institution, has been applied successfully under both experimental and clinical conditions. To extend the spectrum of biological linings for coated stents, we used an arterial graft. We describe the first application of the radial artery as an autologous coating for a conventional stent to be used in treatment of coronary artery disease.

An atherosclerotic plaque is considered vulnerable when it is at higher risk of inducing acute cardiac events. The early detection and follow-up of the vulnerable plaque are crucial to prevent these events from happening. To date there are no proven techniques to detect such a plaque. Arterial wall thermography, tracing the heat signature of the activated macrophages, is a new and promising method in this direction. However, the difficulties of applying such a method in vivo should not be neglected. Current science proposes several potential thermographic methods. They can be generally categorized as noninvasive and invasive. Magnetic resonance thermometry (MRT) is the most important noninvasive method. It is novel, accurate, and reproducible, but is unfortunately hampered by resolution limitations due to the size and motion of the target vessels. The "infrared" and the "contact-sensor" are the most important invasive thermographic methods. Mainly due to the difficulties of infrared radiation in penetrating the flowing blood, the contact thermographic methods seem to be the most feasible at present. The superiority of thermal mapping of the arterial wall versus the localized temperature measurements is clear. The use of multiple thermal sensors arranged around the vessel's circumference and the application of motorized catheter pullback, not only ensure a large area of coverage, but also enable us to build thermal maps and vascular thermoanatomical reconstructions by using modern computer technology. It is expected that arterial thermography will undoubtedly initiate debate, mainly concerning the most appropriate therapy for the vulnerable plaque. Data collection and correct interpretation are expected to lead us into making wise decisions.

The purpose of this study was to investigate in vivo the arterial wall temperature after coronary stent implantation in pigs.We performed cardiac catheterization in 20 pigs with normal coronary arteries. Arterial wall temperature was studied with a thermography system that uses a 4-thermistor sensor tip. A segment was selected in the proximal right coronary artery. Temperature was mapped in this segment by means of a continuous catheter pullback. A stent was then implanted in the middle of this area, and the temperature scan was repeated. Pigs were randomized in two groups (10 + 10 pigs) for arterial temperature scanning: group A to be re-scanned after 5 days and then sacrificed, and group B to be re-scanned after 8 days and then sacrificed.The temperature of the arterial wall before stent implantation was equal to the adjacent areas. Immediately after stent implantation, the stented area had lower temperature than the adjacent areas (p0.001). Five days after implantation, the stented area was significantly warmer than the adjacent areas (p0.001); histopathology showed the highest macrophage population at the place of the stent. Eight days after implantation, the temperature differences were reduced to non-significant levels (p = NS) and the macrophage population was significantly lower.Stent implantation results in an immediate temperature decrease at the stented arterial segment, followed by a significant temperature increase around day 5 after stent implantation. These findings can be correlated with the peri-strut inflammation that follows the stent implantation.

The vulnerable atherosclerotic plaque is associated with an increased number of acute coronary syndromes. Current techniques such as coronary angiography are unable to detect and prospectively evaluate these lesions. Recently, other techniques, both invasive and noninvasive, are being developed trying to detect the plaque that is at increased risk for rupture eventually resulting in increased thrombosis. This review describes briefly evolving techniques for imaging of vulnerable plaques and describes in detail intravascular thermography.

Background —Activated macrophages play an important role in the pathogenesis of acute ischemic syndromes. It has been postulated that detection of heat released by activated inflammatory cells of atherosclerotic plaques may predict plaque rupture and thrombosis. Previous ex vivo studies have shown that there is thermal heterogeneity in human carotid atherosclerotic plaques. Methods and Results —To measure the temperature of human arteries in vivo, we developed a catheter-based technique. Ninety patients (45 with normal coronary arteries, 15 with stable angina [SA], 15 with unstable angina [UA], and 15 with acute myocardial infarction [AMI]) were studied. The thermistor of the thermography catheter has a temperature accuracy of 0.05°C, a time constant of 300 ms, and a spatial resolution of 0.5 mm. Temperature was constant within the arteries of the control subjects, whereas most atherosclerotic plaques showed higher temperature compared with healthy vessel wall. Temperature differences between atherosclerotic plaque and healthy vessel wall increased progressively from SA to AMI patients (difference of plaque temperature from background temperature, 0.106±0.110°C in SA, 0.683±0.347°C in UA, and 1.472±0.691°C in AMI). Heterogeneity within the plaque was shown in 20%, 40%, and 67% of the patients with SA, UA, and AMI, respectively, whereas no heterogeneity was shown in the control subjects. Conclusions —Thermal heterogeneity within human atherosclerotic coronary arteries was shown in vivo by use of a special thermography catheter. This heterogeneity is larger in UA and AMI, suggesting that it may be related to the pathogenesis.

The aorta acts as both a conduit and an elastic buffering chamber that modulates left ventricular function and coronary blood flow. Previous studies have shown that active smoking has unfavorable effects on aortic elasticity.To study the association between passive smoking and the elastic properties of the human aorta.Comparison of nonsmokers during passive smoking studies and smokers during active smoking or sham smoking studies.Academic medical center.16 male nonsmokers were assigned to passive smoking studies, and 32 current, long-term, male smokers were randomly assigned to either active smoking (16 patients) or sham smoking (16 patients) studies.All participants underwent diagnostic catheterization. In the passive smoking group, environmental tobacco smoke was vented into an exposure chamber for 5 minutes (mean carbon monoxide level, 30 parts per million). Each participant in the active smoking group smoked one filtered cigarette (1.0 mg of nicotine) under standardized conditions within 5 minutes; each participant in the sham smoking group performed a similar pattern of inhalation with one unlit cigarette.Aortic elastic properties were studied by measuring the aortic pressure-diameter relation before and for 20 minutes after passive, active, or sham smoking. Instantaneous diameter of the thoracic aorta was measured with a high-fidelity ultrasonic dimension catheter. Instantaneous aortic pressure and diameter were measured at the same site.Both passive and active smoking were associated with changes in the aortic pressure-diameter relation (change in mean distensibility in the passive smoking group, from 2.02 to 1.59 x 10(-6) cm2 x dyne(-1) [for comparisons of time course between passive and sham smoking groups, P0.001]; change in mean distensibility in the active smoking group, from 2.08 to 1.51 x 10(-6) cm2 x dyne(-1) [for comparisons of time course between active and sham smoking groups, P0.001]). These changes represent decreases of 21% and 27%, respectively. No changes in aortic elasticity were seen in the sham smoking group.Both passive and active smoking are associated with an acute deterioration in the elastic properties of the aorta. This association between exposure to tobacco smoke and aortic elasticity indicates that aortic function deteriorates during passive or active smoking.

A67-year-old man with a history of hypertension and hypercholesterolemia was scheduled for elective direct stent implantation for a severe proximal left descending artery stenosis. Using the femoral approach, a 7-French Judkins left guiding catheter was placed in the left coronary ostium. To keep the activated clotting time …