Coronary vasodilation by nitrates is not mediated by the prostaglandin system: a quantitative cineangiographic study.

The possible role of prostaglandins in mediating large coronary artery vasodilation by nitrates was investigated by quantitative magnification coronary angiography. The effects of aspirin (1 g systemically and 100 mg intracoronary) in preventing large coronary artery vasodilation induced by intracoronary isosorbide dinitrate was investigated in 16 patients. Of these, 5 received 0.3 mg (Group 1A) and 11 received 3 mg (Group 1B) intracoronary isosorbide dinitrate, before and 15 minutes after aspirin. Relative to control, 0.3 mg isosorbide dinitrate induced a 19 +/- 9% (mean +/- SD) (p less than 0.01) and 19.5 +/- 11% (p less than 0.01) increase in coronary diameter before and after aspirin, respectively (p = NS). Changes after 3 mg isosorbide were 23 +/- 12% (p less than 0.01) and 26.5 +/- 14% (p less than 0.01), respectively, before and after aspirin (p = NS). In 10 additional patients (Group 2), the effect of the same dose of aspirin on rest coronary artery tone was assessed: changes relative to control were 0.9 +/- 5.5% (p = NS) minutes after aspirin. The intracoronary administration of 3 mg isosorbide dinitrate produced a 24.7 +/- 11% increase in coronary diameter (p = NS versus pre- and postaspirin isosorbide in Group 1B). Urinary 6-ketoprostaglandin-F1 alpha values in urine samples collected in the 8 hours before and the 8 hours after the study in five patients in Group 1B and five patients of Group 2, revealed a 36 +/- 14% (mean +/- SD) reduction in excretion of prostacyclin (p less than 0.01). These data rule out a role for prostaglandins both in mediating dilation of large coronary arteries by nitrates and in affecting their vascular tone at rest.

Transient myocardial dysfunction during pharmacologic vasodilation as an index of reduced coronary reserve: a coronary hemodynamic and echocardiographic study.

Regional coronary flow reserve and regional myocardial contractility were evaluated in 29 patients after maximal pharmacologic coronary vasodilation (intravenous dipyridamole, 0.56 mg/kg body weight, administered over 4 minutes). Nineteen patients had a severe (80 to 99%) proximal and isolated stenosis of the left anterior descending coronary artery and 10 patients had normal coronary arteries; all had normal ventricular function under rest conditions. Myocardial contractility was assessed by means of continuous two-dimensional echocardiographic monitoring; coronary reserve was evaluated by coronary sinus thermodilution. After dipyridamole infusion, 9 of the 19 patients with left anterior descending artery stenosis had transient myocardial asynergy involving the septum or apex, or both (Group IA), whereas 10 patients showed no asynergy (Group IB). No impairment of contractility was observed in the 10 patients with normal coronary arteries (Group II). Coronary blood flow was measured under basal conditions and up to 10 minutes after the end of dipyridamole infusion. In patients in Group II, dipyridamole induced an increase in great cardiac vein flow of 167 +/- 68% (mean +/- SD). The 10 patients in Group IB showed a response comparable with that of the control group (Group II) (136 +/- 45% increase in great cardiac vein flow; NS versus Group II), whereas the 9 patients in Group IA had an increase of 46 +/- 30% (p less than 0.01 versus both Group IB and Group II). No significant difference was found in the angiographic severity of the stenosis expressed in terms of minimal cross-sectional area (Group IA = 0.30 +/- 0.13 mm2, Group IB = 0.34 +/- 0.18 mm2; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Possibilities, limitations, and technique for the study of regional myocardial perfusion in man by Xenon-133.

The theoretical possibilities and the practical limitations of the Xenon-133 (133Xe) method for the study of regional myocardial perfusion in man are discussed. The techniques for data acqusition and processing developed over the past 5 years are described in detail. Illustrative examples of experimental findings are reported. The practical interpretation of the data, at the light of the influence of injection site, initial tracer distribution, constancy of counting geometry, spatial resolution, and Xenon retention in fat, is presented.

Impact of chronic patency of infarct-related coronary artery on prevalence of myocardial ischemia during the pharmacologic and exercise stress test.

BACKGROUND: Even late restoration of anterograde coronary flow may have beneficial effects on left ventricular function, electrophysiology, and survival in postinfarction patients. HYPOTHESIS: The patency or occlusion of an infarct-related coronary artery in the chronic phase may also be associated with myocardial ischemia provoked by pharmacologic and physiologic stress tests. METHODS: High-dose dipyridamole echocardiography test (DET) (up to 0.84 mg/kg over 10 min), exercise electrocardiography (EET), and coronary angiographic data in a group of 127 in-hospital patients who had survived an acute myocardial infarction were analyzed. Patients who had only angiographic evidence of infarct-related single artery disease (> or = 50% luminal diameter reduction) and no previous revascularization were enrolled in the study. DET and EET were performed (DET in all, EET in 118 patients) within 5 days before coronary angiography. Fifty-seven patients had total occluded infarct arteries (Group 1) with various degrees of collateral circulation (2.6 +/- 1.1 collateral score, by a 3 grading system), whereas the other 70 patients had patent infarct arteries (Group 2) with significant residual stenoses (82 +/- 13% diameter reduction). RESULTS: The prevalence of rest angina or effort angina and topography of the infarct-related coronary artery did not differ between the two groups (all p = NS). There were more patients with Q wave in Group 1 than in Group 2 (72 vs. 57%, p = 0.08) compared with non-Q wave infarction (Group 1 = 28 vs. Group 2 = 43%, p = 0.08). Ischemia in the infarct-related artery territory detected by DET (defined as new wall motion dyssynergy or marked worsening of resting hypokinesia) was 61% in Group 1 and 41% in Group 2 (p = 0.025). EET was positive in 26 of 54 (48%) Group 1 and in 21 of 64 (33%) Group 2 patients (p = 0.09). CONCLUSIONS: Patients with occluded infarct-related arteries have a higher prevalence of ischemia during DET and EET regardless of the presence of collateral flow. These results suggest that the presence of partial anterograde flow in the prolonged period could have a favorable influence on prevalence of residual ischemia in these patients.

Regional myocardial perfusion in patients with atherosclerotic coronary artery disease, at rest and during angina pectoris induced by tachycardia.

We studied regional myocardial perfusion by scintigraphic computer-assisted analysis of initial distribution, washout rates, and residual activity of 133Xe injected into the left coronary artery of four patients with normal arteriograms and 14 patients with coronary stenosis. At rest, residual activity in poststenotic regions was always greater than in control regions, but initial washout rates were not slower. During angina, following xenon injections, the amount of indicator distributed to the poststenotic regions was markedly reduced; the increase of the initial washout rates was smaller than in control regions relative to rest, and residual activity was higher. Initial washout rates did not differ as much as from those of normal myocardium because in severe ischemia too little indicator is deposited initially in these regions to produce a change of any magnitude. Indeed, when angina was induced immediately after the xenon injection, poststenotic washout rates became much slower during angina than at rest, a finding that implicates functional factors in impairing poststenotic myocardial perfusion during angina.

Coronary vasodilation by nitrates is not mediated by the prostaglandin system: an angiographic and hemodynamic study.

The possible role of prostaglandins in mediating coronary vasodilation by nitrates was investigated in 13 patients. In nine patients (Group 1), the effects of ISDN on coronary-artery diameter and (in four of the nine) coronary sinus flow before and after administration of ASA were compared. In four additional patients (Group 2) the first ISDN administration was omitted in order to investigate the effect of ASA on resting coronary artery tone. Dosages used were 3 mg intracoronary ISDN and 1.0 g intravenous and 100 mg intracoronary ASA. Coronary artery diameter was analyzed by means of quantitative magnification coronary angiography. Coronary sinus flow was investigated by means of coronary sinus thermodilution. ASA was not able to induce significant changes in coronary artery diameter when injected before administration of ISDN or to prevent ISDN-induced vasodilation. At the coronary resistance level, ASA was not able to prevent the relative vasodilation induced by ISDN. It is concluded that coronary vasodilation by nitrates is not mediated by the prostaglandin system.

Coronary vasospasm as a source of false positive results during dobutamine echocardiography.

BACKGROUND: Several studies have demonstrated a consistently high sensitivity of dobutamine echocardiography whereas test specificity in these series has been variable. The aim of this study was to evaluate whether coronary vasospasm--elicited by alpha1 adrenoreceptor stimulation--may be a significant source of false positive responses during dobutamine stress. METHODS: From the data bank of four institutions we selected 113 patients (75 males, 38 females, mean age 55 +/- 12 years) with dobutamine echocardiography performed (up to 40 micrograms/kg/min and atropine 1 mg if needed) before a coronary angiography showing normal or near normal (visually assessed stenosis severity < 50%) coronary arteries. The following variables--which were previously reported influencing dobutamine echo specificity--entered the multivariate statistical analysis: age, sex, heart rate at baseline and at peak stress, baseline echo, hypertension, site of asynergy, and spasm at coronary angiography. RESULTS: Twenty-five patients had a positive dobutamine test. The positivity occurred in the left coronary territory in 15 and in the right coronary territory in 10 cases. All the 6 patients with spontaneous spasm during angiography had a false positive stress test result. By multivariate analysis only coronary artery spasm during angiography (p = 0.0015) and history of hypertension (p = 0.0031) were significant predictors of false positive results of dobutamine stress echocardiography. CONCLUSIONS: Coronary artery spasm may be an important source of false positive results during dobutamine stress echocardiography.

Effects of dilazep on coronary and systemic hemodynamics in humans.

The cardiovascular effects of dilazep, a new antianginal drug, were investigated in 18 patients, who underwent cardiac catheterization and coronary angiography for the evaluation of chest pain. Dilazep, 0.2 mg/kg, was injected intravenously over 1 to 2 minutes. The changes induced by dilazep in coronary tone were assessed by quantitative angiography in four patients, changes in systemic and coronary hemodynamics and blood gases in eight patients, and changes in systemic and pulmonary hemodynamics and blood gases in six. In 6 of the 18 patients the effects on hemoglobin-O2 oxygen binding were also investigated. Following dilazep administration, we observed a marked reduction of coronary resistance (six patients) (0.5 vs 1.0 mm Hg X min X ml-1, p less than 0.01) and of aortic-coronary sinus oxygen difference (seven patients) (4.6 vs 12.3 vol%, p less than 0.01), and a 23% increase in coronary diameter (four patients) (p less than 0.001). Total systemic resistance was also reduced by dilazep (six patients). Conversely, only minimal or insignificant changes were observed in heart rate (14 patients), aortic pressure (14 patients), total pulmonary resistance (six patients), myocardial oxygen consumption (six patients), double product (14 patients), blood gases (seven patients), and hemoglobin-oxygen affinity (six patients). We conclude that dilazep exerts a powerful dilating action on coronary vasculature without appreciable increase of myocardial oxygen consumption and cardiac work simultaneously with a reduction of peripheral resistance.