Search PubMed⌕ Search

Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 127 records · Page 7Linked to original sources
PubMed1997

Contractile reserve of dysfunctional myocardium after revascularization: a dobutamine stress echocardiography study.

OBJECTIVES: We sought to investigate the effects of revascularization on the contractile reserve of dysfunctional myocardium. BACKGROUND: The improvement in dysfunctional but viable myocardium after revascularization is frequently less than expected from the amount of contractile reserve detected on dobutamine stress echocardiography. The fate of the contractile reserve, when it does not result in an adequate contractile recovery, is unknown. METHODS: Basal contraction and contractile reserve of infarct zones were assessed by dobutamine stress echocardiography in 21 postinfarction male patients before and > 3 months after revascularization (30 infarct zones; mean +/- SD left ventricular ejection fraction 35 +/- 8%). An infarct zone wall motion score index (WMSI) was calculated. RESULTS: Before revascularization, contractile reserve was present in 14 infarct zones (12 patients) and absent in 16 (9 patients). After revascularization, ejection fraction increased by 5 +/- 4% (p < 0.01) in patients classified as positive for contractile reserve and remained unchanged in those classified as negative. New York Heart Association classification improved in 58.3% and 22.2% of patients, respectively. Basal contraction improved in eight zones with previous contractile reserve (57.1%) and in one zone without (6.3%) (p < 0.01). Contractile reserve was still evident in 13 zones with previous contractile reserve (93%; 8 with contractile recovery), and it developed in 6 zones without (38%; none with contractile recovery). WMSI values after revascularization were decreased from values before revascularization during low dose dobutamine in zones with and without previous contractile reserve (p < 0.01 and < 0.05, respectively). CONCLUSIONS: After revascularization, contractile reserve is maintained or even increases in viable infarct zones that do not recover as expected. It may also develop in some infarct zones judged not to be viable before revascularization. This increased contractile reserve may play a role in the functional improvement of patients after revascularization.

Aged↗
PubMed1997

Targeting new thrombolytic regimens at specific patient groups: implications for research and cost-containment.

Fibrinolytic drugs and aspirin, compared with placebo, have reduced the 35-day mortality of patients with acute myocardial infarction from approximately 12% to about 8%. The mortality reduction with active treatment is most evident in high risk groups of patients. Moreover, mortality with a fully patent infarct-related artery at 90 min from the start of thrombolytic treatment is half that found with an occluded artery. Yet more than 50% of acute infarct patients receiving thrombolysis fail to achieve complete early coronary patency or develop re-occlusion. Although thrombolytic strategies are continually evolving to try to further reduce early mortality and increase coronary reperfusion rates, new regimens, when tested in unselected patients against successful active treatments, such as streptokinase and aspirin, are likely to show no, or only small, average benefits, even when applied to tens of thousands of patients. In contrast, the effect of a new thrombolytic regimen is likely to be most evident is selected patients showing large areas of potentially salvageable ischaemic myocardium, as these patients have a higher absolute risk of premature death than patients with smaller infarcts and therefore should gain greater benefit from successful reperfusion. Since the effect of the new treatment, if present, would be greatest in this group, a smaller number of patients would be needed to show an effect; moreover, the risk of the new treatment would be justified against the larger potential benefit to be gained. We propose to target future thrombolytic regimens, in the first instance, at homogenous groups of high-risk patients; for example, those with large areas of potentially salvageable myocardium. This approach seems a rational and cost-effective way to invest limited amounts of medical resources and offers patients the greatest potential benefit of the new therapy, while restricting possible complications to a smaller number. Continued clinical research aimed at identifying possibly different causes of coronary occlusion and the reasons for worse outcomes is also essential to assign the most appropriate treatments to selected groups of patients.

Clinical Trials as Topic↗
PubMed1997

Mechanisms of adenosine-induced epicardial coronary artery dilatation.

BACKGROUND: In order to ascertain whether human adenosine-induced dilatation of epicardial arteries is direct or flow-mediated, we compared the effects of intracoronary adenosine infusion on epicardial coronary arteries with those produced by dipiridamole, a selective arteriolar vasodilator. METHODS AND RESULTS: In 24 patients with angiographically normal coronary arteries, coronary blood flow velocity was measured by a Doppler wire during intracoronary infusion of adenosine or dipyridamole, which is known to increase intramyocardial adenosine concentration. Coronary angiograms were obtained at baseline and immediately after the end of each infusion period; coronary diameters 5 mm distal to the wire tip were measured by computer-assisted quantitative coronary angiography. Peak coronary blood flow velocities during adenosine or dipyridamole infusions were similar (52.0 +/- 15.5 and 47.9 +/- 24.2 cm.s-1, P = ns). Coronary diameters immediately after adenosine and dipyridamole infusions were similar and both higher than that at baseline (2.80 +/- 0.63 and 2.86 +/- 0.64 vs 2.44 +/- 0.69 mm, P < 0.05). The absolute and percentage increases of coronary artery diameters in response to adenosine were highly correlated to coronary blood flow velocity (R = 0.622, intercept -0.10 +/- 0.14, P = 0.002 and R = 0.617, intercept -15.2 +/- 9.9, P = 0.001, respectively); similar correlations were found in response to dipyridamole (R = 0.708, intercept -0.44 +/- 0.19, P < 0.001 and R = 0.649, intercept -13.5 +/- 8.7, P < 0.001, respectively). Finally the absolute and percentage changes of coronary artery diameters caused by adenosine were highly correlated to those caused by dipyridamole (R = 0.840 P < 0.001 and R = 0.836, P < 0.001 respectively). CONCLUSIONS: A significant correlation exists between epicardial coronary vasodilation and coronary blood flow velocity during intracoronary adenosine infusion, thus suggesting that epicardial coronary vasodilation induced by adenosine is predominantly flow-mediated rather than direct. This conclusion is supported by the observation that similar findings were obtained using dipyridamole, which can only dilate epicardial coronary arteries indirectly, through the increase in coronary blood flow velocity caused by the inhibition of intramyocardial adenosine re-uptake.

Adenosine↗
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↗
PubMed1997

Detection of hibernated myocardium using intracoronary technetium-99m-sestamibi.

A possible limitation of intravenously administered perfusion tracers in detecting hibernating myocardium is their poor availability in low-flow areas. We have hypothesized that intracoronary administration might overcome such a limitation. In two patients with a previous anterior myocardial infarction and a severe residual stenosis of the left anterior descending coronary artery, technetium-99m-sestamibi (74 MBq) was selectively injected into the infarct-related coronary artery before successful PTCA. SPECT imaging was carried out 1 hour after the PTCA. In patient 1, evident tracer uptake was detected in the majority of the antero-apical dys-synergic area, previously characterized by a severe irreversible defect (less than 50% of peak activity) at rest-redistribution thallium SPECT ("mismatched pattern"); in patient 2, no uptake of sestamibi was detected in the dys-synergic area showing a severe irreversible defect (less than 50% of peak activity) at rest-redistribution thallium SPECT, ("matched pattern"). Forty days after PTCA, contractile recovery as well as normalization of thallium uptake occurred in patient 1, confirming that most of the dys-synergic area was viable (hibernating), while neither wall motion nor thallium uptake improvement occurred in patient 2, confirming that most of the dys-synergic area was not viable (scar). We conclude that sestamibi retention in the dys-synergic area after selective intracoronary administration correctly identified viable and scarred myocardium. The potential diagnostic value of intracoronary sestamibi at the time of coronary angiography deserves to be validated as a possible alternative to other current procedures for detecting hibernating myocardium.

Angioplasty, Balloon, Coronary↗
PubMed1997

Effects of bamiphylline on exercise testing in patients with syndrome X.

An abnormal stimulation of adenosine A1-receptors has been suggested to play a role in the pathogenesis of both chest pain and ischemia-like electrocardiographic changes in patients with syndrome X and a nonselective adenosine antagonist (theophylline) has been reported to be beneficial in these patients. In this study we investigated the acute effects of bamiphylline, a specific A1-receptor antagonist, in 16 patients with syndrome X (14 women, age 57 +/- 6 years), with both angina and ST-segment depression inducible during exercise testing. All patients underwent two treadmill exercise tests (Bruce modified protocol) on 2 separate days, 5 minutes after the end of randomized intravenous infusion of either placebo (saline solution) or bamiphylline (300 mg). Severity of chest pain was assessed by a 100 mm visual analogic scale. There were no significant differences in resting heart rate and blood pressure after bamiphylline or placebo. Rate-pressure product (20 600 +/- 5000 vs 20 200 +/- 5200 bpm.mmHg), time to 1 mm ST depression (549 +/- 196 vs 581 +/- 201 sec), time to angina (519 +/- 209 vs 571 +/- 196 sec), and exercise duration (717 +/- 134 vs 676 +/- 166 sec) were also not significantly different after bamiphylline or placebo, but there was a mild reduction of the severity of exercise-induced chest pain (30 +/- 22 vs 39 +/- 20 mm, p < 0.05) with the active drug. Thus, in patients with syndrome X, bamiphylline does not improve exercise-induced ST changes, suggesting that A1-receptors are not significantly involved in their appearance. In addition, bamiphylline had little effect on anginal pain, suggesting that this cannot be mediated exclusively by A1-receptor stimulation in these patients.

Angina Pectoris↗
PubMed1996

Plasma protein acute-phase response in unstable angina is not induced by ischemic injury.

BACKGROUND: Elevated levels of C-reactive protein (CRP) are associated with an unfavorable clinical outcome in patients with unstable angina. To determine whether ischemia-reperfusion injury causes this acute-phase response, we studied the temporal relation between plasma levels of CRP and ischemic episodes in 48 patients with unstable angina and 20 control patients with active variant angina, in which severe myocardial ischemia is caused by occlusive coronary artery spasm. METHODS AND RESULTS: Blood samples were taken on admission and subsequently at 24, 48, 72, and 96 hours. All patients underwent Holter monitoring for the first 24 hours and remained in the coronary care unit under ECG monitoring until completion of the study. On admission, CRP was significantly higher in unstable angina than in variant angina patients (P < .001). In unstable angina, 70 ischemic episodes (1.5 +/- 2 per patient) and in variant angina 192 ischemic episodes (9.6 +/- 10.7 per patient) were observed during Holter monitoring (P < .001), for a total ischemic burden of 14.8 +/- 30.2 and 44.4 +/- 57.2 minutes per patient, respectively (P < .001). The plasma concentration of CRP did not increase in either group during the 96 hours of study, even in patients who had episodes of ischemia lasting > 10 minutes. CONCLUSIONS: The normal levels of CRP in variant angina, despite a significantly larger number of ischemic episodes and greater total ischemic burden, and the failure of CRP values to increase in unstable angina indicate that transient myocardial ischemia, within the range of duration observed, does not itself stimulate an appreciable acute-phase response.

Acute-Phase Reaction↗
PubMed1996

Autonomic changes associated with spontaneous coronary spasm in patients with variant angina.

OBJECTIVES: This study sought to investigate whether changes in nervous autonomic tone may have a role in the mechanisms triggering spontaneous coronary spasm in variant angina. BACKGROUND: Previous studies have suggested that both sympathetic and vagal activation may act as a trigger of epicardial artery spasm in patients with variant angina, but the actual role of autonomic changes in spontaneous coronary spasm remains unknown. METHODS: We analyzed the changes in heart rate variability associated with episodes of ST segment elevation detected on Holter monitoring in 23 patients with variant angina (18 men, 5 women; mean [+/-SD] age 59 +/- 12 years). For study purposes, episodes of transmural ischemia lasting > or = 3 min and without any ST segment changes in the previous 40 min were selected for analysis. Heart rate variability indexes were calculated at 2-min intervals, at 30,15,5 and 1 min before ST elevation and at peak ST segment elevation. Ninety-three of 239 total ischemic episodes (39%) fulfilled the inclusion criteria. RESULTS: The results showed that 1) high frequency (HF) (0.04 to 0.15 Hz), a heart rate variability index specific for vagal activity, decreased in the 2 min preceding ST segment elevation (p < 0.001) and returned to basal levels at peak ST segment elevation; 2) heart rate and low frequency (0.04 to 0.15 Hz), which are partially correlated with sympathetic activity, showed a significant increase at peak ST segment elevation (p < 0.001 for both); 3) the pattern of the HF reduction before ST segment elevation was consistently confirmed in several subgroups of ischemic episodes, including those of patients with or without coronary stenoses, those of patients with anterior or inferior ST segment elevation, those occurring during daily or nightly hours and silent episodes. There were no significant variations in heart rate variability in control periods selected from Holter tapes of patients and before ST segment elevation induced by balloon inflation in 20 patients undergoing coronary angioplasty. CONCLUSIONS: Our data show that changes in autonomic tone are likely to contribute to trigger or predispose to epicardial spasm. In particular, although not excluding an active role for adrenergic mechanisms, our data suggest that a vagal withdrawal may often be a component of the mechanisms leading to spontaneous coronary vasospasm.

Aged↗
PubMed1996

Serum lipoprotein(a) level is related to thrombin generation and spontaneous intermittent coronary occlusion in patients with acute myocardial infarction.

BACKGROUND: Thrombotic occlusion of the infarct-related coronary artery is often intermittent in the early, evolving phase of acute myocardial infarction. To assess their relationship to this pattern of coronary occlusion, serum or plasma concentrations of cholesterol, triglyceride, lipoprotein(a), and coagulation and fibrinolytic factors were measured in venous blood before the initiation of thrombolytic therapy. METHODS AND RESULTS: Thirty-two patients (23 men, 9 women: age, 30 to 70 years) with acute myocardial infarction received intravenous recombinant tissue plasminogen activator (20 to 60 megaunits) within 6 hours of the onset of symptoms. Continuous ECG ST-segment recording demonstrated intermittent occlusion of the infarct-related coronary artery in 12 patients (group 1) before the start of thrombolytic treatment and persistent occlusion in 20 patients (group 2). Groups 1 and 2 were similar in age, sex, race, duration of symptoms, blood sample collection time, location of the infarct-related coronary artery, and extent of coronary artery disease. The serum level (median [interquartile range]) of lipoprotein(a) was 34 (13 to 47) mg/dL versus 11.5 (5 to 27) mg/dL (P = .02), and the plasma level (median [interquartile range]) of thrombin-antithrombin III complex was 10.85 (6.4 to 21.5) versus 6.8 (4.2 to 8.7) micrograms/L-1 (P < .04) in groups 1 and 2, respectively. The levels of the other factors were similar in both groups. CONCLUSIONS: The phenomenon of spontaneous intermittent closure and reopening of coronary arteries early during acute myocardial infarction in humans is associated with a higher level of lipoprotein(a) and of a marker of thrombin generation, suggesting that lipoprotein(a) and thrombin are closely related to coronary patency in these patients.

Acute Disease↗
PubMed1996

Preconditioning by transient myocardial ischemia confers protection against ischemia-induced ventricular arrhythmias in variant angina.

BACKGROUND: In experimental models, ischemic preconditioning of the heart protects against ischemic damage and ventricular arrhythmias during subsequent coronary occlusion. In this study, we investigated whether protection against ischemic suffering and ischemia-induced arrhythmias may occur after spontaneous transmural ischemia in humans. METHODS AND RESULTS: We performed 24-hour Holter monitoring in 10 patients with variant angina who developed complex ventricular arrhythmias (CVAs, more than five premature ventricular beats per minute or repetitive ventricular arrhythmias) during episodes of ST-segment elevation. A total of 150 episodes of ST-segment elevation were detected on Holter monitoring, 21 (14%) of which showed CVAs. Episodes separated from the previous one by a time interval of < or = 30 minutes or by a time interval of > 30 minutes did not differ in either magnitude or duration of ST-segment elevation, but CVAs occurred more frequently in the second group (3% versus 29%, P < .0001). The time interval from the preceding ischemic episode was longer for the episodes with compared with those without CVAs (197 +/- 275 versus 57 +/- 87 minutes, P < .001), but these two groups of episodes also had similar severities and durations of ST-segment elevation. Finally, when we analyzed 13 clusters of two to six ischemic episodes, CVAs were found much more frequently in the first (92%) than in the last (23%, P = .009) episode of the clusters, while ST-segment elevations were similar (2.1 +/- 1.6 versus 2.2 +/- 1.1 mm) and ischemia durations shorter in the first than in the last episode (3.9 +/- 3.6 versus 6.1 +/- 1.7 minutes, P = .03). CONCLUSIONS: Our data indicate that preconditioning by transient ischemia induces a significant protection against ischemia-induced CVAs in patients with variant angina. This beneficial effect was not related to a reduction in either severity or duration of ischemia, suggesting that arrhythmic protection was a direct consequence of preconditioning rather than an epiphenomenon of ischemic protection.

Aged↗
PubMed1996

Elevated levels of interleukin-6 in unstable angina.

BACKGROUND: Elevated plasma levels of C-reactive protein have been found in the majority of patients with unstable angina. The evidence of elevated levels of acute-phase proteins in unstable angina is in line with a growing body of evidence that suggests that inflammation plays a role in this syndrome and is an indirect sign of increased production of interleukin-6, which is the major determinant of acute-phase-protein production by the liver. However, in unstable angina, there is no direct proof of the role played by interleukin-6. METHODS AND RESULTS: We measured levels of interleukin-6 in 38 patients with unstable angina at the time of their admission to the coronary care unit and in 29 patients with stable angina. In the same groups of patients, we also measured C-reactive protein. Interleukin-6 (undetectable, ie, < 3 pg/mL, in healthy volunteers) was detectable in 23 (61%) of 38 patients with unstable angina but in only 6 (21%) of 29 with stable angina (P < .01). Median interleukin-6 levels were 5.25 pg/mL (range, 0 to 90 pg/mL) in patients with unstable angina but were below the detection limit of the assay in patients with stable angina (range, 0 to 7 pg/mL). A significant correlation was observed between interleukin-6 and C-reactive protein levels (r = .4, P = .013). CONCLUSIONS: Our study demonstrates that raised levels of interleukin-6 are common in unstable angina, correlate with C-reactive protein, and are associated with prognosis, thus confirming the importance of the cytokine pathway for the production by the liver of acute-phase proteins and strengthening the importance of inflammation in this syndrome. Further studies are required to elucidate better the role of interleukins in unstable angina.

Aged↗
PubMed1996

Noninvasive quantification of regional myocardial metabolic rate for oxygen by use of 15O2 inhalation and positron emission tomography. Theory, error analysis, and application in humans.

BACKGROUND: A method has been developed to measure the regional myocardial metabolic rate of oxygen consumption (rMMRO2) and oxygen extraction fraction (rOEF) quantitatively and noninvasively in humans by use of 15O2 inhalation and positron emission tomography. This article describes the theory, an error analysis of the technique, and procedures of the method used in a human feasibility study. METHODS AND RESULTS: Inhaled 15O2 is transported to peripheral tissues, where it is converted to 15O-labeled water of metabolism, which exchanges with the relatively large extravascular tissue space. Quantification of this buildup of radioactivity allows the calculation of rMMRO2 and rOEF. However, a correction for the spillover of the pulmonary gas radioactivity signal into myocardial regions is required and has been made by use of a gas volume distribution estimated from the transmission scan. This was validated by comparative measurements using the inert gas [11C]CH4 in four greyhounds. Spillover of the cardiac chamber radioactivity has been corrected for with an inhaled [13O]CO (blood volume) scan. The underestimation of myocardial radioactivity due to wall motion and thickness has been corrected for by use of values of tissue fraction obtained from the flow measurement [15OKCO2 scan). Values of rOEF were similar (within 4%) whether obtained from gas volume measurements determined from the transmission or [11C]CH4 scan data. 15O2 scan information from six healthy volunteers showed a clear distribution of myocardial radioactivity after the vascular and pulmonary gas 15O background was subtracted. Subsequent compartmental analysis resulted in values for rOEF and rMMRO2 of 0.60 +/- 0.11 and 0.10 +/- 0.03 mL.min-1.g-1 in the human myocardium at rest. CONCLUSIONS: The results of this study are in good agreement with established values. This is the first known approach to allow the direct quantitative determination of rOEF and oxygen metabolism to be made noninvasively on a regional basis.

Adult↗
PubMed1996

Noninvasive quantification of regional myocardial metabolic rate of oxygen by 15O2 inhalation and positron emission tomography. Experimental validation.

BACKGROUND: The purpose of this study was to validate a novel method for noninvasive quantification of regional myocardial oxygen consumption (MMRO2, mL.min-1 x 100 g-1) and oxygen extraction fraction (OEF) by use of positron emission tomography (PET) and inhalation of 15O-labeled molecular oxygen gas (15O2). METHODS AND RESULTS: Twenty-four measurements were performed in eight closed-chest anesthetized greyhounds at baseline and during infusions of adenosine (100 to 200 micrograms.kg-1.min-1), isoproterenol (1 to 10 microgram/min), and propranolol (5 mg botus +0.2 to 1 mg/min) with morphine (5 mg slow infusion +0.2 to 0.5 mg/ min) to obtain a wide range of oxidative metabolism. The PET imaging protocol consisted of 15O2 emission (OEF and MMRO2), transmission, [15O]CO emission (blood pool), and [15O]CO2 emission (myocardial blood flow: MBF(pets) mL.min-1.g-1) scans. OEF was calculated from the PET data (OEFpet) by three different analytical techniques: steady-state, 5-minute, and 8-minute autoradiographic analyses. Reference measurements of MBF (MBFref) and OEF (OEFref) were obtained during 15O2 inhalation with radiolabeled microspheres and paired arterial and coronary sinus blood sampling, respectively. MMRO2 was calculated from the PET (MMRO2pet) and the reference (MMRO2ref) data as follows: MMRO2 = OEF x MBF x (O2 content of arterial blood). OEF measured by the steady-state PET method was well correlated with the reference data over the range 0.16 to 0.73 (OEFpet = 1.03 OEFref -0.01, r = .97), as was MMRO2 over the range 2.4 to 27.5 mL.min-1 x 100 g-1 (MMRO2pet = 0.98 MMRO2ref +0.91, r = .94). OEFpet calculated by use of the 5-minute and 8-minute autoradiographic analyses were equally well correlated with the reference measurements (r = .95 and r = .97, respectively). There were no significant differences between values of MMRO2pet calculated by use of the steady-state, 5-minute, and 8-minute autoradiographic analyses (P = NS by ANOVA). Regional values of MBFpet, OEFpet, and MMRO2pet were homogeneously distributed and similar to the whole-heart values both at baseline and during the various pharmacological interventions. CONCLUSIONS: Accurate quantification of OEF and MMRO2 is feasible with 15O2 inhalation and PET imaging using both the steady-state and autoradiographic analytical approaches. These studies suggest the applicability of this method for quantitative assessments of regional cardiac oxidative metabolism in clinical studies.

Adenosine↗
PubMed1996

Low incidence of serotonin-induced occlusive coronary artery spasm in patients with recent myocardial infarction.

Intracoronary infusion of serotonin has been reported to induce varying degrees of coronary vasoconstriction in different coronary syndromes, but it has never been studied in patients after myocardial infarction. In patients with recent myocardial infarction, we found a low incidence (11%) of serotonin-induced occlusive spasm only in the infarct-related artery (IRA), and a significantly higher vasoconstriction in the distal segment of the IRA than in the same segment of the non-IRA.

Cardiac Catheterization↗
PubMed1996

Temporal relation between ischemic episodes and activation of the coagulation system in unstable angina.

BACKGROUND: Although a major role of coronary thrombosis in the pathogenesis of unstable angina has been demonstrated, the results of a series of studies have suggested that activation of the hemostatic system may not be confined to ischemic episodes. The purpose of this study was to investigate the temporal relation between ischemic episodes and activation of the coagulation system in unstable angina. METHODS AND RESULTS: Thrombin-antithrombin III (TAT) and prothrombin fragment 1 + 2 (F1 + 2) levels were measured in 13 patients during spontaneous ischemic episodes (time 0, 5, and 15 minutes and 1 hour) to evaluate the time course of the activation of the coagulation system associated with the development of ischemia (protocol A). TAT and F1 + 2 levels were also measured in 28 patients with unstable angina on admission to hospital (every 6 hours for 24 hours and daily for 3 days) to assess their temporal relation with ischemic episodes (protocol B). In protocol A, TAT and F1 + 2 levels were elevated in 10 of 13 patients (77%) in at least 1 sample. The median value of TAT showed a peak at 5 minutes and returned to baseline within 15 minutes (P < .05), consistent with its plasma half-life of 5 minutes, whereas the median value of F1 + 2 showed no significant changes, possibly because of its longer half-life, which tends to dampen sudden bursts of thrombin production. In protocol B, activation of the clotting system was found in 10 of 33 samples (30%) temporally related to ischemia and also in 23 of 150 (15%, P = .07) of those not temporally related to ischemia. CONCLUSIONS: Our study demonstrates that patients with active unstable angina develop frequent bursts of thrombin production not necessarily associated with ischemic episodes and that, conversely, some ischemic episodes are not associated with evidence of thrombin activation.

Adult↗
PubMed1996

Significance of transient ST-T segment changes during dobutamine testing in Q wave myocardial infarction.

OBJECTIVES: We evaluated dobutamine stress electrocardiography for detecting potentially reversible contractile dysfunction or residual ischemia in the infarct-related area. BACKGROUND: ST-T segment changes in pathologic Q wave leads during stress testing may reflect contractile reserve, inducible ischemia or passive mechanical stretching. Dobutamine echocardiography allows detection of contractile reserve at low doses and inducible ischemia at high doses. METHODS: We used low (5 to 10 microg/kg body weight per min) and high doses (20 to 40 microg/kg per min) of dobutamine in 49 patients with a previous Q wave myocardial infarction and analyzed the relation between ST-T segment changes in pathologic Q wave leads and regional contraction. RESULTS: At low dose dobutamine, regional contraction improved in the infarct-related area in 23 patients. New or further ST segment elevation and pseudonormalization of negative T waves developed at low doses more frequently in patients with than without contractile reserve (both p < 0.001), giving a sensitivity of 43.5% and 60.9% and a specificity of 100% and 96.2%, respectively. At high dose dobutamine (43 patients), new or further ST segment elevation and pseudonormalization of negative T waves, occurring beyond those observed at low doses, had a low predictive accuracy for contractile reserve (sensitivity of 9.5% and 14.3% and specificity of 68.2% and 81.8%, respectively). Pseudonormalization of negative T waves at high dose dobutamine was 100% specific (but only 25% sensitive) for homozonal ischemia. CONCLUSIONS: ST segment elevation or pseudonormalization of negative T waves, or both, is indicative of contractile reserve in the infarct-related area when either develops at low dose dobutamine, but may be associated with worsening or no change in contractile function at high doses.

Aged↗
PubMed1996

Intracellular neutrophil myeloperoxidase is reduced in unstable angina and acute myocardial infarction, but its reduction is not related to ischemia.

OBJECTIVES: This study sought to assess neutrophil activation in acute coronary syndromes and its relation to ischemic episodes. BACKGROUND: Neutrophil activation has been reported in unstable angina and acute myocardial infarction; however, it is not clear whether it is related exclusively to ischemia-reperfusion injury. METHODS: We measured the index of intracellular myeloperoxidase in 1) patients with unstable angina, myocardial infarction, variant angina and chronic stable angina and in normal subjects (protocol A); and 2) in patients with unstable angina and acute myocardial infarction during the first 4 days of the hospital period (protocol B). To assess whether neutrophil activation was triggered by ischemia, the myeloperoxidase intracellular index was analyzed before and after spontaneous ischemic episodes and before and after ischemia induced by an exercise stress test in 10 patients with chronic stable angina. In 11 patients with unstable angina, we also compared values of the myeloperoxidase intracellular index at entry with those after waning of symptoms. RESULTS: In protocol A, the myeloperoxidase intracellular index was significantly reduced in patients with unstable angina and acute myocardial infarction compared with patients with stable and variant angina and normal subjects (p < 0.01). In protocol B, the myeloperoxidase intracellular index did not change over time in patients with unstable angina and myocardial infarction. However, in 11 patients with waning symptoms, the myeloperoxidase intracellular index was significantly higher afer symptoms had waned (p < 0.05). In patients with unstable angina, 23 ischemic episodes were studied; no changes in the myeloperoxidase intracellular index were observed. In 10 patients with chronic stable angina and positive exercise stress test results, no significant differences in the myeloperoxidase intracellular index were observed after stress-induced ischemia. CONCLUSIONS: Our study confirms that neutrophils are activated in acute coronary syndromes but suggests that their activation may not be only secondary to ischemia-reperfusion injury.

Adult↗