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Biomedical subjects

C Stefanadis

Publications and source records attributed to C Stefanadis.

At least 55 records · Page 3Linked to original sources
PubMed2001

Increased local temperature in human coronary atherosclerotic plaques: an independent predictor of clinical outcome in patients undergoing a percutaneous coronary intervention.

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.

Aged↗
PubMed2001

Acute effect of clonidine on left ventricular pressure-volume relation in hypertensive patients with diastolic heart dysfunction.

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.

Aged↗
PubMed2001

Echocardiographic and signal averaged ECG indices associated with non-sustained ventricular tachycardia after repair of tetralogy of fallot.

OBJECTIVE: To identify any possible association between different readily available non-invasive indices and potential malignant ventricular arrhythmias in patients with repaired tetralogy of Fallot. DESIGN: 27 consecutive patients, mean (SD) age 27.3 (11.7) years, were studied 15.7 (6.7) years after corrective surgery for tetralogy of Fallot, using 12 lead ECG, 24 hour Holter recordings, signal averaged ECG, and echocardiography. The following variables were measured: standard QRS duration, filtered QRS duration (fltQRS), low amplitude signal duration, and root mean square voltage of the last 40 ms of the fltQRS (RMS-40), as well as right ventricular systolic pressure, right ventricular ejection fraction, and the ratio of the maximum short axis diameters of the right and left ventricles (RD:LD). RESULTS: All patients had right bundle branch block, with a mean QRS duration of 137.1 (14.9) ms. There were no patients with sustained arrhythmia. Five patients had runs of non-sustained ventricular tachycardia (group A) and the other 22 patients did not (group B). Univariate analysis showed that fltQRS and RD:LD ratio were significantly associated with non-sustained ventricular tachycardia. In addition, a fltQRS >/= 148 ms, low amplitude signal >/= 32.5 ms, RMS-40 </= 23 microV, and RD:LD ratio >/= 1.05 were cut off points with a high sensitivity for detecting patients with non-sustained ventricular tachycardia. CONCLUSIONS: Abnormal signal averaged ECG and echocardiographic variables are associated with potentially malignant ventricular arrhythmias on the Holter recordings in asymptomatic patients with repaired tetralogy of Fallot.

Adult↗
PubMed2001

Vasomotor effects of L- and D-arginine in stenotic atheromatous coronary plaque.

OBJECTIVE: To examine the effects of exogenous L- and D-arginine on coronary stenosis vasomotion in relation to stenosis morphology. DESIGN: Intracoronary infusions of normal saline, L- and D-arginine (50 and 150 micromol/min), and glyceryl trinitrate (250 microg bolus) were given in 24 patients with coronary artery disease and stable angina. Coronary stenoses were classified as smooth or complex (irregular borders). The diameter of the coronary stenoses and their adjacent reference segments was measured by computed quantitative angiography. RESULTS: During L-arginine infusion a larger proportion of complex stenoses than smooth stenoses dilated by >/= 10% (p < 0.01), and the magnitude of dilatation was greater at the site of complex stenoses (p < 0.05). Irrespective of the type of morphology there was a positive correlation (p < 0.01) between the severity of stenoses and the magnitude of vasodilatation to L-arginine. The response to glyceryl trinitrate was similar in the two groups. No significant change was found in either group in response to D-arginine. CONCLUSIONS: In patients with coronary artery disease, coronary stenoses-particularly those of complex morphology-dilate in response to the administration of L-arginine but not D-arginine. This finding is consistent with partial deficiency of the substrate for nitric oxide synthesis, L-arginine, at the site of complex stenoses.

Analysis of Variance↗
PubMed2001

Risk stratification of coronary heart disease through established and emerging lifestyle factors in a Mediterranean population: CARDIO2000 epidemiological study.

BACKGROUND: In recent decades various lifestyle factors have been associated with the increasing risk of coronary heart disease. The aim of this study is to assess coronary risk, based on established and emerging lifestyle risk factors such as smoking habit, physical activity, alcohol consumption and depression in a Mediterranean population. METHODS: During 2000--2001, 535 male and 126 female patients with a first event of an acute coronary syndrome and 661 controls matched by sex, age and region were entered into the study. Conditional logistic regression analysis estimated the relative risks of developing coronary heart disease under several scenarios. RESULTS: The multivariate analysis showed that stopping smoking is exponentially related to the reduction of coronary risk. By contrast, passive smoking increases the risk from 48% to 112%. Familial smoking habits are related to current smoking status, increasing the coronary risk fourfold. The effect of depression on coronary risk differs according to gender (+15% in males vs. 32% in females), and interacts with retirement, current smoking, physical inactivity, alcohol consumption and social status, increasing the risk from 15% to 189%. A J-shape association was found between alcohol intake and coronary risk Physical inactivity doubles the coronary risk, while long-term physical activity plays a preventive role in the reduction of coronary risk, even in the elderly. CONCLUSION: Analysis of the data showed that the cluster of established and emerging lifestyle factors poses its particular role for further investigation in the aetiology of coronary heart disease.

Aged↗
PubMed2000

L-Arginine in coronary atherosclerosis.

Nitric oxide is formed from the N-guanido terminal of the amino acid L-arginine and from molecular oxygen by nitric oxide synthase enzymes. L-arginine administration improves the coronary blood flow response to acetylcholine in patients with normal coronary arteries and hypercholesterolemia, reverses the defective endothelium-dependent vasodilation associated with an elevated plasma low-density lipoprotein level or hypercholesterolemia, dilates coronary epicardial arteries and stenoses, enhances nitric oxide generation, and inhibits lesion formation after balloon angioplasty. Stimulation of endogenous nitric oxide production could inhibit atherogenesis, and therefore may be of benefit in patients with risk factors for atherosclerosis.

Arginine↗
PubMed2000

Assessment of aortic line of elasticity using polynomial regression analysis.

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.

Aorta↗
PubMed2000

Serum cholesterol level, cigarette smoking, and vasomotor responses to L-arginine in narrowed epicardial coronary arteries.

We examined the impact of serum cholesterol and cigarette smoking on the coronary vasomotor effects of L-arginine in patients with atherosclerotic coronary artery disease. The dilation of proximal and distal segments in response to low-dose L-arginine was greater in patients with a serum cholesterol level < or =200 mg/dl than in patients with a level >200 mg/dl, whereas the response was the same in smokers and nonsmokers.

Arginine↗
PubMed2000

Electromyographic evidence of subclinical myopathy in hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is due to a number of mutations of contractile protein genes such as beta-cardiac myosin, myosin binding protein-C, and troponin-T. Unlike troponin-T, beta-myosin is a constituent of slow skeletal muscle and its mutations generally have a better prognosis. In order to investigate the usefulness of electromyography in detecting skeletal muscle involvement in HCM, 46 patients were examined using both conventional electromyography (EMG) and quantitative electromyography (QEMG) methods. The QEMG involved motor unit potential (MUP) analysis, turns/amplitude (TAA) analysis, and power spectrum analysis of the interference pattern. Using conventional EMG, myopathic findings were demonstrated in 13 patients (28%). Receiver operating characteristic (ROC) analysis of the results of a discriminant function extracted using QEMG values, identified correctly 10 out of 11 normal controls and all 9 myopathic control patients, and displayed a 15% presence of myopathy (7 patients) among the cardiomyopathy group. The duration of MUPs was the most sensitive among the quantitative parameters in differentiating normal from myopathic subjects. Since skeletal muscle involvement may be due to distinct gene mutations, normal and myopathic EMG findings may reflect HCM subpopulations with a different genetic substrate.

Adolescent↗
PubMed2000

Heat production of atherosclerotic plaques and inflammation assessed by the acute phase proteins in acute coronary syndromes.

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.

Angina Pectoris↗
PubMed2000

Influence of Aortic Elastic Properties on Pulse Pressure Changes Induced by Rapid Ventricular Pacing.

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.

Journal Article↗
PubMed2000

Aortic pressure-diameter relation in patients with non-insulin dependent diabetes mellitus: new insights.

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.

Aorta, Thoracic↗
PubMed2000

Stents covered by autologous venous grafts: feasibility and immediate and long-term results.

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.

Coronary Angiography↗