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Biomedical subjects

D Tousoulis

Publications and source records attributed to D Tousoulis.

At least 73 records · Page 4Linked to original sources
PubMed1996

t-Plasminogen activator and von Willebrand factor in patients with unstable angina.

We investigated whether the clinical evolution of symptoms in patients admitted with unstable angina is associated with changes in t-plasminogen activator antigen (t-PA) and von Willebrand (vW) factor levels. Concentrations of vW factor antigen and t-PA antigen were measured by an enzyme-linked immunoassay method in 10 patients who became clinically stable within 24 h of admission and remained so for 5 days. A significant rise in morning t-PA plasma level occurred 24 h after the admission (15.15 +/- 2.1 ng/ml, P < 0.05), whereas the vW factor remained unchanged. No significant changes were found in the night concentration in t-PA and vW factor during the 5 day period. Thus t-PA level is significantly raised 24 h after admission in patients with unstable angina who stabilize in response to medical treatment.

Aged↗
PubMed1996

Coronary stenosis progression differs in patients with stable angina pectoris with and without a previous history of unstable angina.

OBJECTIVES: To compare the evolution of stenoses responsible for acute coronary events with those not associated with acute coronary syndromes. METHODS AND RESULTS: We prospectively studied angiographic stenosis progression in 190 stable angina patients, with single vessel disease, who were awaiting non-urgent coronary angioplasty. Sixty four patients had a previous history of unstable angina (Group 1) and 126 patients had no history of unstable angina (Group 2). Culprit stenoses were classified as "complex' or "smooth'. At restudy, 8 +/- 4 months after the first angiogram, 12 of 63 culprit stenoses in Group 1 had progressed and seven of 125 in Group 2 (19% vs 6%, P = 0.0044). Thirteen of 68 complex culprit stenoses had progressed, compared with only 6 of 120 smooth culprit stenoses (19% vs 5%, P = 0.003). Coronary events occurred in 12 Group 1 patients and nine Group 2 patients (P = 0.02). CONCLUSIONS: In patients with stable angina, stenoses associated with previous episodes of unstable angina are more likely to progress than stenoses not associated with previous unstable angina. Unstable coronary atherosclerotic plaques, even those that have been clinically stable for more than 3 months, may retain the potential for rapid progression to total occlusion.

Adult↗
PubMed1996

Variable coronary vasomotor responses to acetylcholine in patients with normal coronary arteriograms: evidence for localised endothelial dysfunction.

OBJECTIVE: The vasomotor responses of the epicardial coronary arteries to acetylcholine were examined in patients with normal coronary arteries and chest pain. DESIGN: Quantitative angiography was used to measure minimum lumen diameter of proximal and distal coronary artery segments at baseline, during intracoronary infusion of acetylcholine (10(-7) - 10(-3) mol/l), and following an intracoronary bolus (2 mg) of isosorbide dinitrate. PATIENTS: Coronary arteriograms were obtained in 15 patients (mean (SEM) age 48 (10) years) with normal coronary arteries and chest pain. MAIN RESULTS: In response to the low concentrations of acetylcholine (10(-7) - 10(-6) mol/1) 20 (61%) distal and 11 (41%) proximal segments showed dilatation (group 1), whereas 13 (39%) distal segments and 14 (52%) proximal segments showed constriction (group 2) (P < 0.05 v group 1). In group 1, the maximum dilatation induced by acetylcholine in the proximal and distal segments was 7.83 (1.19)% and 11.6 (2.2)% respectively. In group 2, the maximum constriction at higher concentration was 16.55 (3.3)% and 33.11 (11.63)% in the proximal and distal segments respectively. The two different patterns of the vasomotor response coexisted in eight (53%) of the 15 patients. Intracoronary isosorbide dinitrate caused a greater increase in the coronary luminal diameter of distal segments than in proximal segments in group 1 (25.63 (5.16)% v 12.43 (3.48)%, P < 0.01) but not in group 2 (12.65 (2.53)% v 10.82 (3.33)%. CONCLUSIONS: Constriction and dilatation may occur in proximal and distal coronary artery segments, suggesting local areas of endothelial dysfunction, in response to acetylcholine in patients with chest pain and angiographically normal coronary arteries.

Acetylcholine↗
PubMed1996

Low-dose cyclosporine treatment fails to prevent coronary luminal narrowing after heart transplantation.

BACKGROUND: Cyclosporine has been reported to induce endothelial dysfunction, arterial vasculitis, and accelerated atherosclerosis in experimental models. The purpose of the present study was to evaluate whether low-dose cyclosporine treatment started 1 year after heart transplantation reduces graft coronary artery narrowing compared with conventional cyclosporine doses. METHODS: One year after heart transplantation, 30 patients were randomly assigned to receive low-dose cyclosporine A (whole-blood polyclonal cyclosporine target trough levels 200 to 400 micrograms/L; group A; n = 15) or usual cyclosporine dosage (target levels 400 to 600 micrograms/L; group B; n = 15). Proximal and distal diameters of the left anterior descending, circumflex, and right coronary arteries were measured by quantitative coronary angiography at baseline (1 year after transplantation) and at 2 and 3 years after transplantation. RESULTS: One major cardiac event occurred in group A (retransplantation) and two in group B (sudden deaths). Moderate to severe allograft rejection (International Society for Heart and Lung Transplantation score 3A or higher) occurred in seven patients in group A and five in group B during the study period. Mean biopsy sample rejection score during the same period was increased in group A compared with that in group B (1.44 +/- 0.63 versus 1.05 +/- 0.59; p < 0.05). New angiographic evidence of vascular disease was observed in four patients of group A and in one patient of group B. Proximal coronary artery diameter was slightly, although not significantly, reduced in both groups at follow-up angiography. Distal segments showed a significant diameter reduction, which was greater in group A than in group B (-9.7% +/- 1.1% and -5.2% +/- 1.3%, respectively; p < 0.05). CONCLUSIONS: Cyclosporine dose reduction started 1 year after heart transplantation is ineffective in reducing coronary luminal narrowing and may be associated with an increased prevalence of cardiac allograft vasculopathy, especially in the distal coronary tree. Low-dose cyclosporine treatment may slightly enhance the risk of allograft rejection. Further investigations are needed to evaluate the effects of cyclosporine dose reduction started at an earlier time after heart transplantation.

Adult↗
PubMed1995

Differential progression of complex and smooth stenoses within the same coronary tree in men with stable coronary artery disease.

OBJECTIVES: We sought to compare the evolution of complex and smooth stenoses within the same coronary tree in patients with stable coronary artery disease. BACKGROUND: Progression of coronary stenosis has prognostic significance and may be influenced by local and systemic factors. Stenosis morphology is a determinant of disease progression, but no previous study has systematically assessed progression of complex and smooth stenoses within the same patient. METHODS: We studied 50 men with stable angina who 1) had one complex coronary stenosis and one smooth stenosis in different noninfarct-related coronary vessels at initial coronary angiography, and 2) had a second angiogram after a median interval of 9 months (range 3 to 24). Patients with lesions > or = 10 mm long, at a major branching point or with > 85% diameter reduction were not included. Coronary lesions were measured quantitatively from comparable end-diastolic frames. Stenosis morphology was determined qualitatively by two independent observers. RESULTS: All patients remained in stable condition during follow-up. Progression, defined as an increase in diameter stenosis by > or = 15% was seen in only eight complex stenosis (16%) but in no smooth lesions (p < 0.01). The severity of complex stenoses changed more than that of corresponding smooth stenoses (mean +/- 1 SD 5.8 +/- 13% vs. -0.06 +/- 6%, p < 0.01). On average, the annual rate of growth was 11.4 +/- 28% and 1.5 +/- 14% for complex and smooth lesions, respectively (p < 0.01). CONCLUSIONS: Few coronary stenoses progress rapidly in stable angina. Complex and smooth coronary stenoses progress at different rates within the same coronary tree. complex stenosis morphology itself is an important determinant of progression of stenosis in patients with apparently clinically stable coronary artery disease.

Aged↗
PubMed1995

Early spontaneous intermittent myocardial reperfusion during acute myocardial infarction is associated with augmented thrombogenic activity and less myocardial damage.

OBJECTIVES: This study investigated the influence of early spontaneous intermittent reperfusion on the extent of myocardial damage and its relation to endogenous hemostatic activity. BACKGROUND: In the early phase of acute myocardial infarction coronary occlusion is often intermittent, even before thrombolytic therapy is administered. The relation between this phenomenon, myocardial damage and hemostatic activity is unknown. METHODS: Holter ST segment recording and pretreatment plasma tissue-type plasminogen activator (t-PA) antigen, plasminogen activator inhibitor-1 (PAI-1) antigen, prothrombin fragment F1 + 2 and soluble fibrin levels were measured in 57 patients with acute evolving myocardial infarction. Spontaneous intermittent myocardial reperfusion, defined as two or more episodes of transient resolution of ST segment elevation to within 0.05 mV of baseline, lasting > or = 1 min, before the start of recombinant t-PA (rt-PA) treatment was present in 28 patients (group 1) and absent in 29 (group 2). Left ventriculography and coronary angiography were performed 90 min after intravenous rt-PA administration. Plasma creatine kinase-MB fraction (CK-MB) levels were measured every 6 h for 24 h, and C-reactive protein levels were measured daily for 3 days. RESULTS: Group 1 had lower peak plasma CK-MB (141.9 +/- 28.3 vs. 203.8 +/- 23.3 IU/liter [mean +/- SEM], p < 0.014) and C-reactive protein levels (16 +/- 4 vs. 28 +/- 4 mg/liter on day 1; 26.6 +/- 5.5 vs. 61.8 +/- 14.4 mg/liter on day 2; 19.6 +/- 4.2 vs. 40.6 +/- 6.5 mg/liter on day 3, p < 0.012) and a higher left ventricular ejection fraction (62.9 +/- 4% vs. 51.1 +/- 5%, p < 0.04) than group 2. Group 1 had lower plasma t-PA antigen levels (15.6 vs. 27 micrograms/liter, p < 0.006) but higher prothrombin fragment F1 + 2 (1.8 vs. 1.1 nmol/liter, p < 0.003) and soluble fibrin levels (66.8 vs. 31 nmol/liter, p < 0.01). Coronary patency at 90 min was similar. CONCLUSIONS: Early spontaneous intermittent reperfusion during acute myocardial infarction is associated with augmented thrombogenic activity and less subsequent myocardial damage. This finding is consistent with a protective effect of intermittency on the myocardium and a procoagulant effect of spontaneous lysis on blood. It may also reflect a different rate of evolution of coronary thrombosis and myocardial infarction in patients with and those without spontaneous intermittent myocardial reperfusion.

Analysis of Variance↗
PubMed1995

The reactivity of the contralateral artery at the time of balloon dilation during coronary angioplasty.

The response of the contralateral arteries was investigated during balloon angioplasty of the left anterior descending artery. Thirty patients were studied. Coronary arteriograms were obtained at baseline, during maximal balloon inflation and at the end of the procedure. Luminal diameter was measured by a quantitative coronary arteriography analysis system. During balloon inflation the luminal diameter of the proximal segment of the right coronary artery increased by 2.4 +/- 6% (P < 0.05), and that of the left circumflex artery increased by 0.6 +/- 6% (P = ns). Both returned to near baseline values after angioplasty. In patients with increased collaterals during balloon inflation the left circumflex proximal segment increased more significantly than in patients with unchanged collaterals. The luminal diameter of the distal segment of the right coronary artery increased by 9 +/- 8% (P < 0.001) and that of the left circumflex artery by 8 +/- 11% (P < 0.01) during balloon inflation, returning to near baseline values after angioplasty. Thus, vasodilation of the contralateral arteries during balloon inflation at the time of coronary angioplasty occurs mainly in the distal segments, and appears to be related to an increase in collateral filling.

Adult↗
PubMed1995

Early remodelling of coronary stenoses after thrombolytic treatment in patients with acute myocardial infarction.

OBJECTIVE: To assess the frequency of early remodelling of coronary stenosis morphology after thrombolytic treatment in patients with acute myocardial infarction. DESIGN: Coronary angiograms were analysed by a computerised edge detection analysis system. Coronary stenosis severity was measured and morphology classified as smooth or complex. PATIENTS: Coronary arteriograms were obtained approximately 90 min and 24 h after thrombolytic treatment from 40 patients with acute myocardial infarction. MAIN RESULTS: Stenosis morphology was complex in 22 patients (65%) and smooth in 11 (32%) 90 min after thrombolysis. The morphology of 11 (50%) complex coronary stenoses and three (27%) smooth stenoses had changed at 24 h (P < 0.05). The transition from complex to smooth was associated with a reduction in stenosis severity from 65 (4)% to 51 (5)% (P < 0.05). The stenosis severity was 63 (4)% and 60 (5)% in those with persistently complex morphology, and 56 (7)% and 50 (5)% in those with persistently smooth morphology at 90 min and 24 h respectively (NS). CONCLUSIONS: Transition of morphology from complex to smooth within 24 h is common. This transition is associated with a reduction in stenosis severity of a degree greater than that found in persistently smooth stenoses over the same interval. 50% of stenoses are smooth at 24 h.

Adult↗
PubMed1994

Left ventricular function and coronary artery disease progression early after coronary bypass grafting.

To investigate the effects of coronary artery disease progression on left ventricular function in patients who suffer angina early after coronary artery bypass grafting, we studied the progression of coronary stenoses, the occurrence of graft occlusions, and measured left ventricular ejection fraction (regional and global) in 34 consecutive patients who underwent repeat angiography 25.2 +/- 3.5 (standard error of the mean) months postoperatively, from a total population of 550 patients who underwent bypass grafting. Resting left ventricular function and stenosis severity were assessed using a computerized, quantitative analysis system. Coronary stenosis progression was defined as an increase in the percentage of the stenotic occlusion by 30% or more, any increase in lesion severity that resulted in total coronary artery occlusion, or the occurrence of a new stenosis that occluded the artery by 50% or more. Group 1 comprised 21 patients with all grafts patent and group 2 comprised 13 patients with one or more grafts occluded (20 of 34 grafts). Coronary artery disease progressed in all patients in group 1, and this involved 22 of 54 (41%) grafted vessels and 3 of 15 (20%) nongrafted vessels (p < 0.05). Coronary artery disease progressed in 11 patients in group 2, involving 15 of 32 (47%) grafted vessels and 1 of 6 (17%) nongrafted vessels (p < 0.01). An increased collateral circulation was observed in both groups. The left ventricular ejection fraction remained unchanged in both groups (group 1, 0.60 +/- 0.03 versus 0.62 +/- 0.03; group 2, 0.62 +/- 0.05 versus 0.62 +/- 0.04 before and after bypass, respectively; p = not significant) and there was no difference between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Effects of ketanserin on epicardial coronary arteries after coronary angioplasty in patients with stable angina.

Previous studies have demonstrated the development of vasoconstriction immediately after percutaneous coronary angioplasty (PTCA), distal to the dilated stenosis, presumably resulting from endothelial injury. We have investigated the role of 5-HT2 receptors in mediating vasomotor changes in proximal and distal coronary segments and coronary stenoses, immediately after successful PTCA in patients with chronic stable angina. We compared the effects of the intracoronary infusion of 1 mg ketanserin (5-HT2 receptor antagonist) on proximal and distal coronary arterial segments immediately after PTCA in both vessels subjected to PTCA and control vessels. Coronary diameters, before and after angioplasty and after ketanserin administration, of proximal and distal segments and coronary stenoses were measured by computerized quantitative coronary angiography (CAAS system) in 12 patients (10 male, two female; mean age 54 +/- 6 years) with stable angina subjected to PTCA. After coronary angioplasty, vasoconstriction was observed in the segment distal to the dilated stenosis but not in the distal segments of control vessels (-0.12 +/- 0.04 and -0.02 +/- 0.02 mm respectively; P < 0.05). After ketanserin infusion significant dilatation was found in the distal segments of both PTCA vessels and control vessels, but the dilatation was greater in the PTCA vessels (P < 0.05). No significant changes were found in the proximal segments of either PTCA or control vessels, or at the PTCA site. In conclusion, the vasoconstriction distal to the site of PTCA is mediated, at least in part, via 5-HT2 receptors.

Angina Pectoris↗
PubMed1994

Coronary vasodilator reserve, pain perception, and sex in patients with syndrome X.

BACKGROUND: It remains unclear whether myocardial ischemia due to coronary microvascular dysfunction is the cause of chest pain in syndrome X (chest pain, ischemic-like stress ECG despite angiographically normal coronary arteries). To assess the function of the coronary microcirculation and its relation to pain perception, we measured myocardial blood flow (MBF) and coronary vasodilator reserve (CVR) in 29 patients with syndrome X and 20 matched normal control subjects. METHODS AND RESULTS: MBF at rest and after intravenous dipyridamole (0.56 mg.kg-1 over 4 minutes) was measured using positron emission tomography with H2(15)O. CVR was calculated as MBFdipyridamole/MBFrest. ECG changes and chest pain after dipyridamole in syndrome X were compared with those in 35 patients with coronary artery disease (CAD). Resting and postdipyridamole MBFs were homogeneous throughout the left ventricle in syndrome X patients and control subjects. MBF was 1.05 (0.25), mean (SD) versus 1.00 (0.22) mL.min-1.g-1 (P = NS) at rest and 2.73 (0.81) versus 3.00 (1.00) mL.min-1.g-1 (P = NS) after dipyridamole in patients and control subjects, respectively. CVRs were 2.66 (0.76) and 3.06 (1.08) (P = NS) and after correction of resting MBF for rate-pressure product were 2.35 (0.83) and 2.34 (0.90) (P = NS) in patients and control subjects, respectively. Female syndrome X patients had higher resting MBF than males, at 1.18 (0.20) versus 0.88 (0.19) mL.min-1.g-1 (P < .001). Chest pain after dipyridamole occurred in syndrome X as frequently as in CAD (21/29 versus 22/35, P = NS). CONCLUSIONS: When patients with syndrome X are compared with control subjects, no differences are found in MBF either at rest or after dipyridamole, despite syndrome X patients experiencing chest pain after dipyridamole to the same extent as patients with CAD. These findings, together with the absence of any relation among MBF, chest pain, and ECG changes under stress, cast further doubt on ischemia as the basis of the chest pain, at least in the majority of syndrome X patients.

Adult↗
PubMed1993

Left ventricular hypercontractility and ST segment depression in patients with syndrome X.

OBJECTIVES: This study was designed to assess the relation between rest left ventricular function and exercise capacity in patients with syndrome X. BACKGROUND: Clinical observation has suggested that some patients with syndrome X have a high rest left ventricular ejection fraction. In this study we determined the relation between left ventricular ejection fraction and exercise capacity and the electrocardiographic (ECG) changes that develop on exercise. METHODS: The pattern of left ventricular function, exercise capacity and 24-h ambulatory ECG monitoring were studied in 37 patients (9 men, 28 women; mean age 52 +/- 7 years) with syndrome X (angina with normal coronary arteries and a positive exercise test result). All patients had normal findings on echocardiogram and rest ECG. All treatment was discontinued for > or = 48 h. Left ventricular ejection fraction was determined by computerized analysis of the left ventricular angiogram. In patients with syndrome X, exercise duration and heart rate were measured at 1-mm ST segment depression and at peak exercise. RESULTS: Left ventricular hypercontractility (ejection fraction > or = 80%) was observed in 12 patients (32%) (group 1), whereas 25 patients (68%) had normal left ventricular contraction (group 2). The time to 1-mm ST depression on exercise testing was significantly earlier in group 1 than in group 2 (5.13 +/- 1.03 vs. 10.76 +/- 0.63 min, respectively, p < 0.001). The magnitude of the ST segment depression at peak exercise was significantly greater in group 1 than in group 2 (2.03 +/- 0.2 vs. 1.33 +/- 0.05 mm, respectively, p < 0.001). The mean time for ST segment depression to normalize was significantly greater in group 1 than in group 2 (4.76 +/- 0.78 vs. 3.16 +/- 0.39 min, respectively, p < 0.05). Linear regression analysis of all patients with syndrome X showed a significant correlation between exercise duration and ejection fraction (r = 0.55, p < 0.001). The mean circadian variation of heart rate and episodes of ST segment depression on 24-h ambulatory ECG monitoring were similar in the two groups of patients. CONCLUSIONS: These findings indicate that approximately one third of patients with chest pain, normal coronary angiograms and a positive exercise test have left ventricular hypercontractility, and this is associated with the development of ST segment depression at a lower heart rate and work load and a longer time to normalization of ST segment depression after exercise.

Adult↗