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Biomedical subjects

D Tousoulis

Publications and source records attributed to D Tousoulis.

At least 19 recordsLinked to original sources
PubMed1999

Effects of L- and D-arginine on the basal tone of human diseased coronary arteries and their responses to substance P.

OBJECTIVE: To assess the effects of substance P administration alone and in combination with L- and D-arginine in patients with normal angiograms and in patients with coronary artery disease. DESIGN: Intracoronary infusions of (a) normal saline, (b) the receptor mediated nitric oxide stimulant substance P (5.6 and 27.8 pmol/min) before and after L- or D-arginine (50 and 150 micromol/min), and (c) glyceryl trinitrate (250 microg bolus) were given to 17 patients with coronary artery disease and stable angina, and to six patients with normal angiograms. The diameter of angiographically normal proximal and distal segments and coronary stenoses were measured by computerised quantitative angiography. RESULTS: L-arginine administration was associated with significant dilatation of stenoses (p < 0.01) of proximal segments of both "normal" (p < 0.05) and diseased (p < 0.01) arteries, and of distal segments of diseased arteries (p < 0.01). No significant changes were associated with D-arginine administration. Dose dependent dilatation of all segments including stenoses, was observed with substance P both before and after L-arginine infusion (p < 0.01). The magnitude of dilatation of stenoses and all segments of both "normal" and diseased coronaries was greater after L-arginine (p < 0.05) but not D-arginine and substance P infusion, than it was after saline and substance P infusion. Administration of D- or L-arginine did not change the magnitude of substance P induced dilatation. CONCLUSIONS: Diseased and "normal" coronary arteries dilated in response to substance P and L-arginine but were unaffected by D-arginine infusion. The magnitude of the response to substance P was not increased by L-arginine administration, indicating that it is not critically dependent on the availability of substrate for nitric oxide synthase.

Analysis of Variance↗
PubMed1998

Effects of changing the availability of the substrate for nitric oxide synthase by L-arginine administration on coronary vasomotor tone in angina patients with angiographically narrowed and in patients with normal coronary arteries.

We assessed the effects of intracoronary administration of substance P, LNMMA, L-arginine, and nitroglycerin in patients with normal coronary angiograms and in patients with coronary artery disease. LNMMA constricted (p <0.01) and both substance P and nitroglycerin dilated normal and diseased proximal and distal segments and stenoses (p <0.01). L-Arginine reversed the effect of LNMMA in all segments and caused greater dilation of the diseased arteries, including stenoses (p <0.05), indicating that there is a relative deficiency of L-arginine in diseased coronary arteries.

Aged↗
PubMed1998

Effects of ergotamine on myocardial blood flow in migraineurs without evidence of atherosclerotic coronary artery disease.

The effects of intravenous ergotamine (0.25 mg) on basal and hyperemic (dipyridamole) myocardial blood flow (MBF), measured with positron emission tomography and H2(15)O, were assessed in 15 migraineurs in a double-blind, randomized, placebo controlled, crossover study. Ergotamine produced a 27% reduction in hyperemic MBF (2.62 +/- 0.11 vs 3.72 +/- 1.05 ml x min(-1) x g(-1); p <0.05), a 31% reduction in the coronary vasodilator reserve (1.81 +/- 0.50 vs 2.71 +/- 1.15; p <0.01), and a 55% increase in minimal coronary resistance (42.2 +/- 15 vs 26.7 +/- 8 mm Hg x min x ml(-1) x g(-1); p <0.001), suggesting vasoconstriction of the coronary microcirculation.

Aged↗
PubMed1998

Relation of von Willebrand factor to occurrence of Q waves and thrombolytic treatment in acute myocardial infarction.

We measured the changes of plasma von Willebrand factor antigen and fibrinogen levels in patients with acute myocardial infarction treated with recombinant tissue plasminogen activator and patients not given fibrinolytic drugs. The von Willebrand factor levels are greater in patients with Q-wave than in patients with non-Q-wave myocardial infarction and are independent of thrombolytic treatment. Fibrinogen levels are depressed by thrombolytic treatment but are unrelated to the presence or absence of Q waves.

Adult↗
PubMed1998

A comparative study of eccentric and concentric coronary stenosis vasomotion in patients with Prinzmental's variant angina and patients with stable angina pectoris.

BACKGROUND AND HYPOTHESIS: In patients with stable angina pectoris, eccentric stenoses have a greater potential for dynamic changes of caliber in response to vasoactive stimuli than concentric lesions. It is not known whether in patients with coronary artery spasm the degree of coronary vasoconstriction differs in eccentric versus concentric stenoses. Therefore, we examined the relationship between coronary stenosis morphology and the vasomotor response to vasoactive stimuli in patients with variant angina. METHODS: Computerized quantitative angiography was used to measure minimum luminal diameter of eccentric and concentric stenoses before and after the administration of ergonovine and isosorbide dinitrate in 22 patients with Prinzmetal's variant angina and in 20 patients with chronic stable angina. RESULTS: In patients with variant angina, mean stenosis diameter reduction with ergonovine was -0.85 +/- 0.38 and -1.12 +/- 0.69 mm in eccentric and concentric stenoses, respectively (p = NS). Isosorbide dinitrate promptly relieved spasm in all patients and increased the diameter of eccentric stenoses by 0.26 +/- 0.34 mm and that of concentric stenoses by 0.24 +/- 0.32 mm (p = NS). In patients with chronic stable angina, mean diameter reduction with ergonovine was -0.23 +/- 0.12 and -0.12 +/- 0.10 mm for eccentric and concentric stenoses, respectively (p < 0.05). Isosorbide dinitrate increased coronary diameter by 10% from baseline in 70% of eccentric and 38% of concentric stenoses (p < 0.01). CONCLUSION: In patients with variant angina pectoris, eccentric and concentric spastic stenoses react similarly in response to vasoactive stimuli. In patients with chronic stable angina, eccentric stenoses are more likely to show vasomotor responses than concentric stenoses.

Adult↗
PubMed1998

Complex stenosis morphology predicts late reocclusion during follow-up after myocardial infarction in patients with patent infarct-related coronary arteries.

BACKGROUND: Whether angiographic morphology of infarct-related residual stenoses continues to affect prognosis after discharge is not known. METHODS: We studied 175 patients after their myocardial infarction who required nonurgent coronary angioplasty for residual myocardial ischemia. The findings at diagnostic coronary angiography were compared with those before angioplasty (mean of 7 months later). Infarct-related stenoses were classified as complex or smooth. Stenosis progression was defined as >0.5 mm diameter reduction. RESULTS: One hundred twenty-one (69%) infarct-related stenoses were complex. At restudy, total occlusion was found in 41 (35%) of the infarct-related complex stenoses compared with 7 (13%) smooth stenoses (P = .001). Reocclusion occurred in 16 (55%) of 29 complex infarct-related stenoses with thrombus, compared with 25 (28%) of 88 without thrombus (P = .01). During follow-up, 46 patients (26%) had cardiac events. Of these, 70% had complex lesions at study entry compared with 30% smooth (P < .05). CONCLUSIONS: Residual angiographically complex stenoses after an uncomplicated myocardial infarction are associated with a greater risk of reocclusion and may predispose to coronary events at follow-up.

Adult↗
PubMed1998

Angiographic characteristics of infarct-related and non-infarct-related stenoses in patients in whom stable angina progressed to acute myocardial infarction.

BACKGROUND: In patients with coronary artery disease, angiographic and postmortem studies have shown that coronary stenoses in infarct-related arteries often have complex morphology. It is not known whether in patients with multivessel disease stenosis morphology in non-infarct-related arteries is different from those of the infarct-related arteries. METHODS AND RESULTS: In 24 consecutive patients we examined the angiographic characteristics of both the infarct-related stenoses and non-infarct-related stenoses before and after spontaneous acute myocardial infarction, by visual inspection and computerized edge detection of coronary angiograms. Before myocardial infarction, the severity of the infarct-related stenoses was <50% in 14 patients and > or =50% in 10 patients (p=not significant) and of non-infarct-related stenoses was <50% in 16 and > or=50% in 13. A significantly greater proportion of infarct-related stenoses with severity > or =50% progressed to non-Q-wave than to Q-wave myocardial infarction (71% vs 50%, p < 0.05). Before myocardial infarction, the percentage of concentric, eccentric, and irregular infarct-related stenoses was 8%, 13%, and 50%, respectively, whereas in the non-infarct-related stenoses it was 62%, 17%, and 21%, respectively (p < 0.01). A similar proportion of irregular morphology progressed to Q-wave or non-Q-wave myocardial infarction. CONCLUSIONS: In patients with stable angina who had acute myocardial infarction develop, the infarct-related and non-infarct-related stenoses on average are similar in severity but different in morphology. Nonsevere stenoses more frequently progress to Q-wave than to non-Q-wave myocardial infarction.

Adult↗
PubMed1997

Inhibition of nitric oxide synthesis during the cold pressor test in patients with coronary artery disease.

The effects of a cold pressor test during intracoronary infusions of L-NMMA and normal saline were studied in patients with chronic stable angina and in patients with normal coronary arteriograms. The cold pressor test during saline infusion caused significant dilation of proximal and distal segments in patients with normal coronary arteriograms, and this dilation was abolished by L-NMMA infusion; in patients with coronary disease the cold pressor test during saline caused constriction of the stenoses and distal segments and this constriction was augmented by L-NMMA infusion.

Aged↗
PubMed1997

Basal and flow-mediated nitric oxide production by atheromatous coronary arteries.

OBJECTIVES: This study assessed the effects of inhibition of nitric oxide synthesis on epicardial human coronary arteries and on coronary flow velocity during baseline conditions and during atrial pacing. BACKGROUND: Epicardial coronary artery dilation occurs in response to an increase in heart rate. It is not known whether the dilation of both angiographically normal and diseased epicardial coronary arteries during atrial pacing is nitric oxide dependent in humans. METHODS: The effects of an intracoronary infusion (4 mumol/min for 8 min) of NG-monomethyl-L-arginine (LNMMA), an inhibitor of nitric oxide synthesis, was studied in 16 patients with coronary artery disease and in 6 patients with normal coronary arteriograms. In all patients atrial pacing was performed during normal saline and during LNMMA infusion. the lumen diameter of epicardial coronary arteries was assessed by quantitative angiography, and changes in blood flow velocity were measured with a Doppler catheter. RESULTS: During saline infusion a significant increase in the lumen diameter of the proximal (p < 0.05) and distal (p < 0.01) segments of both normal and diseased arteries occurred during atrial pacing. No significant lumen diameter changes occurred in either group when atrial pacing was performed during LNMMA infusion. Stenosis diameter decreased during LNMMA infusion but did not change with atrial pacing either during saline infusion or during LNMMA infusion. The mean percent change in coronary blood flow with atrial pacing was less (p < 0.05) during LNMMA infusion than during saline infusion in both groups. CONCLUSIONS: These findings confirm that epicardial coronary artery dilation induced by pacing is nitric oxide dependent. Nitric oxide production contributes to the vasomotor tone of coronary resistance vessels. Nitric oxide is produced at the site of atheromatous stenosis but is unaffected by pacing.

Blood Flow Velocity↗
PubMed1997

Comparison of dobutamine and treadmill exercise echocardiography in inducing ischemia in patients with coronary artery disease.

OBJECTIVES: We sought to compare the magnitude of ischemia precipitated by both treadmill exercise and dobutamine stress echocardiography. BACKGROUND: Although it is alleged that dobutamine stress produces ischemia similar in degree and extent to that produced during treadmill exercise, a direct comparison with treadmill exercise, the most common form of exercise, has not been performed. METHODS: Eighty-five consecutive patients with known coronary artery disease underwent both stress tests on the same day, in random order. RESULTS: Sixty-two patients (73%) had positive results on exercise echocardiography compared with 53 (62%) who had positive results on dobutamine stress (p = NS). Of the 53 patients with positive dobutamine test results, wall motion abnormalities appeared after the addition of atropine in 35 patients (66%). During dobutamine infusion, 22 patients (26%) had a hypotensive response that was reversed in 16 by prompt administration of atropine. At peak dobutamine-atropine stress, heart rate was higher than that at peak exercise (p < 0.001), whereas systolic blood pressure and rate-pressure product were higher at peak exercise than at peak dobutamine-atropine stress (p = 0.0001). In the 53 patients with positive results on both tests, peak wall motion score index was greater with treadmill exercise than with dobutamine-atropine infusion ([mean +/- SD] 1.73 +/- 0.45 vs. 1.57 +/- 0.44, p < 0.001). CONCLUSIONS: Echocardiography immediately after treadmill exercise induces a greater ischemic burden than dobutamine-atropine infusion. In the clinical setting, exercise echocardiography should therefore be chosen over dobutamine echocardiography for diagnosing ischemia, when possible. When dobutamine echocardiography is used as an alternative modality, maximal heart rate should always be achieved by the addition of atropine.

Atropine↗
PubMed1997

Effects of inhibition of nitric oxide synthesis in patients with coronary artery disease and stable angina.

AIMS: Inhibition of nitric oxide synthesis causes a decrease in the basal diameter of normal distal epicardial coronary arteries in normal subjects. The effects of inhibition of nitric oxide in atheromatous coronary arteries is unknown. This study assessed the effects of the inhibition of nitric oxide synthesis in epicardial coronary arteries in patients with coronary artery disease. METHODS AND RESULTS: The effects of an intracoronary infusion of NG-monomethyl-L-arginine (LNMMA, an inhibitor of nitric oxide synthesis), were studied in 13 patients with chronic stable angina and coronary artery disease. The diameter of angiographically normal proximal and distal segments and coronary stenoses was measured by quantitative angiography. In response to an LNMMA infusion of 16 mumol min-1 for 4 min there was a significant reduction (P < 0.01) in the luminal diameter of the distal segments of diseased arteries (from 1.32 +/- 0.07 to 1.17 +/- 0.06 mm) and at the site of stenosis (from 1.15 +/- 0.22 to 1.06 +/- 0.20 mm), but no change (P = NS) in the luminal diameter of the proximal segments (from 3.16 +/- 0.12 to 3.08 +/- 0.14 mm) of diseased arteries. CONCLUSIONS: The average effect of inhibition of basal nitric oxide synthesis in epicardial coronary arteries in patients with stable angina and coronary artery disease was only distal constriction. Coronary stenoses constricted at the highest LNMMA concentration.

Angina Pectoris↗
PubMed1997

Impairment of the myocardial vasomotor response to cold pressor stress in collateral dependent myocardium.

OBJECTIVE: To study the vasomotor response (cold pressor/basal flow) in myocardium perfused entirely by collaterals, using the reflex sympathetic stimulation of cold pressor stress. DESIGN: Regional myocardial blood flow was measured in collateral dependent and in remote myocardium using positron emission tomography with 15O water at basal and at cold pressor stress. Regional ischaemia was measured with 18F-fluorodeoxyglucose (FDG). PATIENTS: Nine patients (mean (SD) age 53 (6) years) with an occluded coronary artery supplied entirely by collaterals from other angiographically normal arteries. RESULTS: In remote myocardium, basal and cold pressor flow were 0.99 (0.26) and 1.46 (0.60) ml/min/g (P < 0.05), respectively, a myocardial vasomotor response of 1.46 (0.45). In collateral dependent myocardium, basal and cold pressor flow were 0.91 (0.20) and 0.87 (0.35) ml/min/g, respectively (the latter value, P < 0.05 v remote region), a myocardial vasomotor response of 0.97 (0.43) (P < 0.05 v remote region). The myocardial vascular resistance (mean arterial pressure/flow) during cold pressor was higher in the collateral dependent than in remote myocardium, at 147.0 (61.1) and 85.6 (32.3) mm Hg.min.g/ml (P < 0.05), respectively, but with no relative increase in FDG uptake. CONCLUSIONS: In contrast to the decrease in myocardial resistance in remote myocardium with cold pressor, an increase was observed in collateral dependent myocardium suggesting a vasoconstrictor response in resistive vessels, without demonstrable myocardial ischaemia.

Cold Temperature↗