Biomedical subjects
Publications and source records attributed to E Tsiamis.
Explore the source record for details and available documents.
BACKGROUND: Recent studies have shown that patients with single vessel coronary artery disease (CAD) suffering from acute coronary syndromes (ACS) have increased coronary sinus (CS) blood temperature compared with the right atrium (RA). The aim of this study was to investigate whether there is a correlation between systemic inflammatory indexes and CS temperature and whether there is a difference in CS temperature between patients with single vs. multivessel disease. MATERIALS AND METHODS We included consecutive patients scheduled for coronary angiography for recent-onset chest pain evaluation. We measured C-reactive protein (CRP) levels in the study population. Coronary sinus and RA blood temperature measurements were performed by a 7F thermography catheter. DeltaTau was calculated by subtracting the RA from the CS blood temperature. RESULTS: The study population comprised 53 patients with ACS, 25 patients with stable angina (SA) and 22 subjects without CAD (control group). DeltaTau was greater in patients with ACS and with SA compared with the control group (0.22 +/- 0.10 degrees C, 0.18 +/- 0.04 degrees C vs. 0.14 +/- 0.07 degrees C, P < 0.01 for both comparisons). The ACS group had greater DeltaTau compared with the SA group, although the difference did not reach statistical significance (P = 0.09). Eighteen (39.1%) out of 46 patients with multivessel disease had three-vessel disease and 28 (60.8%) had two-vessel disease. DeltaTau between patients with multivessel and single vessel disease was similar (0.22 +/- 0.01 degrees C, 0.19 +/- 0.01 degrees C, P = 0.17). The levels of CRP were well correlated with DeltaTau (R = 0.35b, P < 0.01). CONCLUSIONS: Systemic inflammation is well correlated with CS temperature; thus, an inflammatory process could be the underlying mechanism for increased heat production from the myocardium.
Explore the source record for details and available documents.
AIMS: Heat released from atherosclerotic plaques as a result of the local inflammatory process, may be measured in vivo by a thermography catheter. Statins seem to have an antiinflammatory effect which results in plaque stabilization. The aim of this study was to investigate the effect of statins on plaque temperature. METHODS AND RESULTS: The study population included 72 patients: 21 with effort angina, 32 with unstable angina and 19 with acute myocardial infarction. In the study group, 37 patients received statins for more than 4 weeks and 35 were not receiving statins. We measured the temperature difference (deltaT) between the atherosclerotic plaque and the proximal vessel wall (background temperature) using a thermography catheter. The statistical analysis showed that the mean value of deltaT was higher in the untreated group compared to the treated-with-statin, group (0.56+/-0.41 vs 0.29+/-0.33 degrees C, P<0.01). Moreover, a progressive increase in deltaT by type of clinical syndrome was observed in both groups (statin group; effort angina: 0.24+/-0.15, unstable angina: 0.26+/-0.26, acute myocardial infarction: 0.40+/-0.28, vs untreated group; effort angina: 0.41+/-0.26, unstable angina: 0.44+/-0.28, acute myocardial infarction: 0.84+/-0.52, P<0.05). Multivariate analysis showed that treatment with statins was an independent factor in temperature variation, after taking into account the effect of the clinical syndrome (P<0.05). CONCLUSIONS: Patients on statin treatment produce less heat from the culprit coronary lesion than those not treated. Thus, statins seem to have a favourable effect on heat release from atherosclerotic plaques, and whether this effect has an impact on plaque stabilization needs to be investigated in future studies.
In this case report, we present the first clinical application of three thermography catheters for temperature measurements in the coronary arteries, the aorta, and the femoral arteries. The entire procedure was performed successfully without complications. Larger clinical studies are required in order to examine the feasibility for the application of the aortic and the peripheral artery thermography catheters and the clinical significance of temperature measurements in these arteries. Cathet Cardiovasc Intervent 2001;54:51-58.
OBJECTIVES: We investigated the midterm clinical significance of human coronary atherosclerotic plaques temperature after a successful percutaneous coronary intervention. BACKGROUND: Previous studies have shown an increased temperature in human atherosclerotic plaques. However, the prognostic significance of atherosclerotic plaque temperature in patients undergoing a successful percutaneous intervention is unknown. METHODS: We prospectively investigated the relation between the temperature difference (deltaT) between the atherosclerotic plaque and the healthy vessel wall and event-free survival among 86 patients undergoing a successful percutaneous intervention. Temperature was measured by a thermography catheter, as previously validated. The study group consisted of patients with effort angina (EA) (34.5%), unstable angina (UA) (34.5%) and acute myocardial infarction (AMI) (30%). RESULTS: The deltaT increased progressively from EA to AMI (0.132 +/- 0.18 degrees C in EA, 0.637 +/- 0.26 degrees C in UA and 0.942 +/- 0.58 degrees C in AMI). The median clinical follow-up period was 17.88 +/- 7.16 months. The deltaT was greater in patients with adverse cardiac events than in patients without events (deltaT: 0.939 +/- 0.49 degrees C vs. 0.428 +/- 0.42 degrees C; p < 0.0001). The deltaT was a strong predictor of adverse cardiac events during the follow-up period (odds ratio 2.14, p = 0.043). The threshold of the deltaT value, above which the risk for an adverse cardiac event was significantly increased, was 0.5 degrees C. The incidence of adverse cardiac events in patients with deltaT > or = 0.5 degrees C was 41%, as compared with 7% in patients with deltaT < 0.5 degrees C (p < 0.001). CONCLUSIONS: Increased local temperature in atherosclerotic plaques is a strong predictor of an unfavorable clinical outcome in patients with coronary artery disease undergoing percutaneous interventions.
We sought to assess the haemodynamic effects of clonidine on left ventricular (LV) pressure-volume relation in patients with diastolic heart dysfunction due to essential hypertension. Towards this end, simultaneous recordings of LV volume (acoustic quantification) and LV pressure (micromanometer) were obtained in 10 such patients before and after drug administration and compared to baseline findings on 10 matched normal controls. The following measurements and calculations were obtained: maximal positive and negative first derivative of LV pressure (peak +dP/dt and peak -dP/dt, respectively), LV minimal and end-diastolic pressure, peak systolic blood pressure, time constant of relaxation (TAU), LV stroke work and LV stiffness constant. The two invasive indexes, LV stiffness constant and TAU classified 10/10 patients as having abnormal LV diastolic function compared with 7/10 patients so classified by Doppler studies. Central sympathetic suppression by a single oral dose of clonidine 0.125 mg in these patients resulted within 60 min in a decrease of heart rate and mean arterial pressure as well as a significant improvement of LV diastolic function indexes. Specifically, the LV stiffness constant (ml(-1)), in normal subjects was 0.0028 vs 0.0152 (P < 0.001) in hypertensive subjects at baseline, vs 0.0053 in hypertensive after clonidine (P < 0.001 vs baseline). Likewise, the E/A ratio, was 1.08 in normal subjects vs 0.88 (P < 0.0001) in hypertensives at baseline, vs 1.28 in hypertensives after clonidine (P < 0.0001 vs baseline). With clonidine the diastolic portion of the pressure-volume curve was displaced downward. In conclusion, clonidine can improve diastolic dysfunction without depressing systolic LV performance. The improvement may be attributable in part to withdrawal of direct sympathetic influence on the myocardium and in part to the indirect effect of systemic, pulmonary and coronary artery relaxation.
Explore the source record for details and available documents.
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<0.001), history of hypertension (P<0.004), and hypercholesterolemia (P<0.02). The difference between the transition point and the peak systolic pressure was increased in normal subjects compared with patients (P<0.0001). The sigmoid line shifted leftward and upward with diltiazem, but it remained unchanged with enalaprilat. During an average of 3 years of follow-up, 19 of 88 patients developed stroke (n=4), unstable angina (n=8), acute myocardial infarction (n=4), or acute pulmonary edema (n=3). 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.
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 degrees 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 degrees C) and acute myocardial infarction (2.150 degrees C) compared with stable angina (0.300 degrees C), P<0.001 for each comparison. Furthermore, stable angina has increased temperature differences compared with controls (0.200 degrees C, P<0.001). There were very good correlations between CRP and SAA with the temperature (r=0.796, P=0.01 and r=0.848, P=0.01, respectively). Local heat at the site of lesion is increased in patients with acute coronary syndromes and may arise from an aggressive inflammatory response occurring in these situations. The sensitive measurement of plaque temperature as a prognostic marker may be useful in the management of coronary heart disease.
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, P < 0.0001) while systolic aortic pressure increased (+19%, from 109.5 +/- 1.6 to 130.1 +/- 2.8 mmHg, P < 0.0001). Thus, pulse pressure increased from 22.1 +/- 2.2 to 50.6 +/- 3.1 mmHg, P < 0.0001. 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.
AIMS/HYPOTHESIS: Type II (non-insulin-dependent) diabetes mellitus is associated with macrovascular disease. Therefore, we investigated the aortic elastic properties by a new method in patients with diabetes and control patients matched with them. METHODS: Patients with Type II diabetes (n = 20) and control patients without diabetes (n = 21) were enrolled in the study. All patients had coronary artery disease. Instantaneous aortic diameter was measured by an intravascular catheter developed in our institution. Instantaneous aortic pressure was measured simultaneously at the same aortic level with a catheter-tip micromanometer. Thus, aortic pressure-diameter loops were obtained and slope and intercept were calculated. Aortic distensibility, stiffness constant and energy loss were also calculated. RESULTS: The mean age and the heart rate were similar in the two groups. The pulsatile changes in aortic diameter were greater in the control group (0.94 +/- 0.4 vs 1.28 +/- 0.4 mm, p < 0.01). The stiffness of the aortic wall was greater in diabetic patients as indicated from the following variables: the distensibility was less in patients with diabetes (1.16 +/- 0.6 vs 1.95 +/- 0.9 cm2 x dyne(-1) x 10(-6), p <0.01); the slope was greater (113.4 +/- 120.1 vs 51.61 +/- 3.3 mmHg/mm, p < 0.01) and the intercept was less in diabetic patients (-2301.9 +/- 2692.9 vs -1114.45 +/- 295.6 mmHg, p < 0.01); the stiffness constant was greater in patients with diabetes (1.66 +/- 1.8 vs 0.77 +/- 0.8 mm(-1), p < 0.03). Aortic energy loss was, however, similar between the groups. CONCLUSION/INTERPRETATION: In patients with non-insulin dependent diabetes aortic elastic properties, evaluated by pressure-diameter relation, are impaired. This could play an important part in the development of vascular complications related to diabetes.
BACKGROUND: Previous experimental studies with a new covered stent, the autologous venous graft-covered stent (AVGCS), have shown favorable results. The aim of this study was to evaluate the feasibility and safety of this new technique in human coronary arteries and to compare the long-term outcome with uncovered stents. METHODS AND RESULTS: A venous graft was removed from an upper limb. A conventional stent then was covered by the venous graft. Fifty-eight AVGCS were implanted in 56 patients, including 16 patients with acute coronary syndromes (ACS). Additionally, in 114 patients, 138 uncovered stents were implanted, serving as a control group, including 38 patients with ACS. The procedure was successful in all patients. Stent thrombosis was observed in 3 patients in the control group and in 1 patient with an AVGCS. There was a trend for the minimal luminal diameter to be greater in the AVGCS group at follow-up (P =.07), and statistical significance was observed in patients with ACS (P <.01). The target vessel revascularization and the restenosis rates were similar between the 2 groups. In patients with ACS, the restenosis rate was less (P <.04) and there was a trend for target vessel revascularization to be less in covered stents (P =.09). The event-free survival rate at 4 years was 85% in the AVGCS group versus 81% in the control group (P = not significant); in ACS it was 94% versus 78%, respectively (P = not significant). Stents covered by thicker venous grafts were associated with improved clinical outcome. CONCLUSIONS: Stents covered by autologous venous grafts may be safely prepared without complications. This technique may prove to be a useful means, especially in patients with ACS.
We sought in this study to examine the effects of diurnal blood pressure variations upon common carotid artery (CCA) elasticity in selected subjects with uncomplicated moderate essential hypertension. Towards this end, 174 non-smoker subjects with stage I-II essential hypertension and without diabetes mellitus, left ventricular hypertrophy and carotid atherosclerosis, were classified as dippers and non-dippers according to the diurnal variation of >10% between mean daytime and night-time systolic and diastolic blood pressure (BP) in 24-h non-invasive ambulatory BP monitoring. CCA distensibility was derived by a combination of surface ultrasonographic data and simultaneous BP measurements at the brachial artery. The dippers and non-dippers were similar with respect to demographic characteristics. Non-dippers had significantly greater office systolic BP, 24-h systolic BP and ambulatory pulse pressure (PP) and significantly less (daytime-night-time) systolic and diastolic BP fall (by 16 mm Hg and 11 mm Hg respectively, P< 0.0001) compared to dippers. CCA distensibility was significantly reduced in non-dippers compared to dippers (by 0.89 dyne(-1)/cm(2/)10(-6), P < 0.05). Multiple linear regression analysis identified patient age and ambulatory PP as significant predictors of the CCA elasticity index. When patient age, 24-h systolic and diastolic BP were used as covariates in an analysis of covariance, the difference of CCA elasticity between dippers and non-dippers ceased to reach statistical significance. In contrast, when patient age, ambulatory PP, systolic (daytime-night-time) BP fall and diastolic (daytime-night-time) BP fall were used as covariates, the difference of CCA distensibility between dippers and non-dippers continued to be statistically significant. In conclusion, the excessive impairment of CCA elastic properties in non-dippers compared to dippers hypertensive seems to be ascribed to the increased of total 24-h haemodynamic load and not to the circadian pattern of BP. Journal of Human Hypertension (2000) 14, 813-818
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.
UNLABELLED: A renewed interest in radial artery conduits for bypass surgery has emerged during the last few years. In order to combine a surgical with a percutaneous technique, stents were covered by radial arterial grafts. The purpose of this study was to evaluate the feasibility of, and the immediate and long-term results after, intracoronary implantation of stents covered by autologous arterial grafts. METHODS: A graft was removed from the radial artery. A conventional stent was then covered by the arterial graft. The autologous arterial graft was stabilized on the stent by sutures. Fifteen covered stents were implanted in 15 patients (56.1 +/- 17.3 years old) in all coronary vessels. RESULTS: The procedure of stent covering was feasible and short in duration. Procedural success was 100% with no in-hospital stent thrombosis, Q-wave myocardial infarction or death. In 14 patients (93.3%), including the patients with clinical restenosis, a repeat angiography was performed (minimum lumen diameter immediately after procedure: 3.01 +/- 0.22 mm, at follow-up: 2.56 +/- 0.90 mm). Target lesion revascularization was required in 2 patients. The event-free survival rate at 2 years was 87%. CONCLUSION: Intracoronary implantation of stents covered by an autologous arterial graft may be performed safely with excellent long-term results. A multicenter study is required to assess the efficacy.
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 degrees 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 degrees C in SA, 0.683+/-0.347 degrees C in UA, and 1. 472+/-0.691 degrees 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.
OBJECTIVE: The use of stents has improved results after balloon coronary angioplasty. Several materials have been proposed for covering the metallic surface of the stent to reduce the rate of subacute thrombosis and restenosis. In our institution, an autologous arterial graft was used for covering the external surface of a conventional stent. The angiographic and histological response in a porcine coronary artery model was investigated. METHODS: An autologous arterial graft was removed from the femoral artery and carefully prepared. Subsequently, a conventional stent was covered externally by the arterial graft. Twenty-two covered stents and 22 uncovered regular stents were implanted alternatively in the coronary arteries of 22 pigs. One animal died immediately after the procedure, due to thrombus formation in the uncovered stent. Six animals were sacrificed at seven days and the remaining animals were sacrificed at two months. Before the sacrifice, coronary angiography was performed in all animals. RESULTS: Thrombosis was detected in two control segments and in one covered stented segment. After seven days, the luminal surface of the covered stents was covered by a new endothelial layer in contrast to partial endothelial cell appearance in the control group. The angiographic parameters were similar between the two groups. Histologically, the covered stents were associated with less vascular injury compared to uncovered stents. In covered stents a trend towards reduction of maximal intimal hyperplasia was detected (covered: 116.6 +/- 47.75 vs uncovered: 150.25 +/- 46.81 microns, p = 0.08); also the thickness of the arterial media was reduced (covered: 21.34 +/- 10.28 vs uncovered: 102.63 +/- 18.71 microns, p = 0.02). The luminal and vessel areas were similar in the two groups. CONCLUSIONS: The preparation and implantation of the autologous arterial graft-covered stent is technically safe and feasible. This type of covered stent results in accelerated endothelialization, less vascular injury, thinning of the arterial media and a trend to reduce the intimal hyperplasia in normal coronary arteries.