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Biomedical subjects

A Pozzati

Publications and source records attributed to A Pozzati.

At least 19 recordsLinked to original sources
PubMed1996

Transient sympathovagal imbalance triggers "ischemic" sudden death in patients undergoing electrocardiographic Holter monitoring.

OBJECTIVES: The aim of this study was to investigate the relation between "ischemic" sudden death (arrhythmic death preceded by ST segment shift) and autonomic nervous system activity. Background. Mechanisms precipitating sudden death are poorly known despite the importance of detecting functional factors that may contribute to such a fatal event. METHODS: We analyzed the tapes of eight patients (seven men and one woman with a mean age of 66 +/- 8 years) who had ischemic sudden death during ambulatory electrocardiographic (Holter) monitoring. Four patients had unstable and four had stable angina; none was taking antiarrhythmic drugs. Twenty patients with angina and transient myocardial ischemia during Holter monitoring served as control subjects. Arrhythmias, ST segment changes and heart rate variability were analyzed by a computerized interactive Holter system. RESULTS: Five patients had ventricular tachyarrhythmias (ventricular fibrillation in three, ventricular tachycardia in two), and three had bradyarrhythmias (atrioventricular block in two, sinus arrest in one) as the terminal event; all eight patients showed ST segment shift (maximal change 0.46 +/- 0.16 mV; with ST elevation in two) that occurred 41 +/- 34 min (mean +/- SD) before sudden death. The standard deviation of normal RR intervals (SDNN) was 89 +/- 33 ms during the 10 +/- 6 h of Holter monitoring; 5 min before the onset of the fatal ST shift, SDNN measurements were significantly lower than during the initial 5-min period (48 +/- 10 vs. 29 +/- 9 ms; p=0.002). In control patients, the SDNN was 102 +/- 39 ms during Holter monitoring, whereas it measured 56 +/- 30 ms 5 min before the most significant episode of ST shift (p<0.01 vs. 29 +/- 9 ms [corrected] in the group with sudden death). CONCLUSIONS: Autonomic dysfunction, as detected by a marked decrease in heart rate variability, is present in the period (5 min) immediately preceding the onset of the ST shift precipitating ischemic sudden death. These data suggest that sympathovagal imbalance may trigger fatal arrhythmias during acute myocardial ischemia, thus resulting in sudden death.

Aged↗
PubMed1995

Relation of severity of symptoms to transient myocardial ischemia and prognosis in unstable angina.

OBJECTIVES: This study was undertaken to compare the relative power of the severity of angina versus that of any other clinical, electrocardiographic (ECG) and angiographic findings in predicting the risk of subsequent in-hospital coronary events in patients admitted to the coronary care unit for treatment of unstable angina. BACKGROUND: The presence or absence of chest pain has traditionally been used to guide management and therapy of unstable angina. However, recent studies raised the possibility that the cumulative duration of ischemia may be an additional index of prognosis. METHODS: We studied 104 consecutive patients admitted to the coronary care unit because of unstable angina. Diaries of symptoms were accurately kept. All patients underwent Holter ambulatory ECG monitoring during the 1st 24 h and angiography within 1 week of admission. RESULTS: During the hospital stay, 41 patients (group 1) had subsequent coronary events; the remaining 63 patients (group 2) had a good clinical outcome. Recurrence of chest pain after admission was observed in 76% of patients: 36 of the 41 group 1 patients (sensitivity 88%) and 43 of the 63 group 2 patients (specificity 32%). Anginal scores (frequency and persistence of pain, duration of each single episode and pain-free interval) showed high specificity but low sensitivity for detecting evolution toward subsequent coronary events. On Holter monitoring, the duration/24 h of the total number of ischemic episodes was consistently greater in group 1 than in group 2. A cumulative duration of ischemia > or = 60 min/24 h was observed in 34 of the 41 group 1 patients (sensitivity 83%) but in only 16 of the 63 group 2 patients (specificity 75%). High risk coronary artery lesions (left main coronary artery disease or complex stenosis) were detected in 36 of the 41 group 1 patients and in 26 of the 63 group 2 patients. CONCLUSIONS: Transient myocardial ischemia detected by Holter monitoring, but not chest pain, is the best predictor of unfavorable short-term clinical outcome. The decision to perform early angiography and revascularization cannot be based on symptoms alone.

Aged↗
PubMed1995

[A transient decrease in heart rate variability in patients with sudden "ischemic" death during Holter monitoring].

BACKGROUND: Mechanisms precipitating sudden death are poorly known, in spite of the importance to detect functional factors which may contribute to such fatal event. Aim of the study was to investigate the relationship between "ischemic" sudden death (ISD: arrhythmic death preceded by acute myocardial ischemia) and autonomic nervous system activity. METHODS: We analysed the tapes of 6 patients (pts) (5 males; 67 +/- 12 yrs) suffering ISD during Holter monitoring (HM). One pt had recent onset angina, 2 had unstable and 3 stable angina; none was taking antiarrhythmic drugs. Arrhythmias, ST segment and heart rate variability (HRV) were analysed by a computerized interactive HM system, in order to obtain data on transient ischemia and sympatho-vagal balance. RESULTS: Five pts showed ventricular tachyarrhythmias (2 VF, 3 VT), and 1 had a bradyarrhythmia (advanced A-V block) as the terminal event; all pts showed ST shift (max: 0.37 +/- 0.28 mV; 1 with ST elevation; 4 with anginal pain) 53 +/- 35 min before ISD. SD of normal R-R intervals (SDNN) was 112 +/- 26 msec in the 11 +/- 8 hrs of HM, whereas it was 97 +/- 48 msec in the initial hour and 59 +/- 21 msec in the initial 5 min segment. Measurements of SDNN showed a marked decrease 5 min before the onset of fatal ischemic ST shift: 32 +/- 14 msec (p = 0.003). Also, pNN50 (percent of adjacent R-R differing > 50 msec: marker of vagal activity) was significantly reduced before ISD, when compared to the initial 5 min segment (from 10 +/- 5 to 7 +/- 4%; p < 0.03). Such changes were not observed before uncomplicated (that is not associated with malignant arrhythmias) ST shift episodes during HM. CONCLUSIONS: Autonomic dysfunction, as detected by a marked decrease of HRV, is present in the period (5 min) immediately preceding the onset of ST shift precipitating ISD; simultaneous measurements of vagal signals showed similar changes. These data suggest that sympatho-vagal unbalance may trigger fatal arrhythmias during acute myocardial ischemia, hence resulting in ISD.

Aged↗
PubMed1993

Vasotonic angina: a spectrum of ischemic syndromes involving functional abnormalities of the epicardial and microvascular coronary circulation.

OBJECTIVES: The present study was undertaken to investigate the response of large and small coronary arteries in a subgroup of patients with no or minimal coronary artery disease found to have objective signs of myocardial ischemia. BACKGROUND: Many patients apparently have normal coronary arteries despite abnormal electrocardiographic (ECG) changes during spontaneous anginal attacks or exercise stress testing. METHODS: Twenty-five patients with no or minimal (< 30% stenosis) coronary artery disease were chosen from a pool initially selected on the basis of spontaneous anginal attacks and ST segment shifts in the anterior leads. Of these, 10 were grouped as having variant angina (at least one episode of ST elevation) and the remaining 15 as having syndrome X (exercise-induced anginal pain, ST depression and reversible thallium abnormalities). Data were compared with those obtained in 10 patients with stable angina and documented coronary artery disease. Eighteen patients with supraventricular arrhythmias and normal coronary arteries served as control patients. Patients showing focal spasm during ergonovine testing were not included in the subsequent angiographic analysis. Great cardiac vein blood flow, aortic pressure and changes in coronary artery diameter were measured at rest and 2 to 4 min after hyperventilation in the remaining study group. The same procedure was repeated after sublingual administration of 0.3 mg of nitroglycerin in eight patients (four with syndrome X and four with variant angina). RESULTS: Hyperventilation induced diffuse epicardial coronary diameter reduction, which was marginal in control patients (9 +/- 4%) and those with coronary artery disease (5 +/- 3%) but severe (p < 0.001) in those with variant angina (28 +/- 14%) or syndrome X (25 +/- 13%). Concomitant determination of coronary blood flow showed significant (p < 0.001) decreases in those with variant angina (25 +/- 11%) and syndrome X (28 +/- 10%) but not in control patients (5 +/- 8%) or those with coronary artery disease (4 +/- 5%). Changes in great cardiac vein blood flow during hyperventilation were similar before and after nitroglycerin. CONCLUSIONS: These findings indicate that vasoconstrictor stimuli may trigger a diffuse abnormal response of both epicardial and resistance vessels in some patients with chest pain and angiographically normal coronary arteries. Patients showing such diffuse vasoconstrictor abnormalities are suggested to have a single pathogenetic entity with a spectrum of ECG manifestations ranging from ST depression to ST elevation.

Adult↗
PubMed1992

Coronary hemodynamic effects of systemic thrombolysis in patients with unstable angina.

Intracoronary (i.c.) thrombus is a frequent finding in patients with unstable angina (UA). Accordingly, thrombolytic treatment could be beneficial, as resolution of thrombus might result in increased delivery of blood flow to the ischemic regions. To test this hypothesis, we studied 13 patients with active UA and ST-segment shift in the anterior leads. Coronary angiography was performed and great cardiac vein blood flow (GCVF; thermodilution) was measured in all patients 25 +/- 14 h after the last chest pain episode. Following angiography, patients received i.v. urokinase (UK: 1,000,000 IU/30 min); aortic pressure and GCVF were measured before and every 10 min following drug infusion, for a total time of 90 min. At baseline angiography, 5 of 13 patients (Group 1) had evidence of i.c. thrombus (intraluminal filling defect or thrombotic subocclusion) in the ischemia-related left coronary artery, whereas 8 patients (Group 2) did not. Group analysis showed that UK increased GCVF and decreased anterior coronary resistance in Group 1 (respectively, from 86 +/- 33 to 114 +/- 41 ml/min: p less than 0.005; and from 1.37 +/- 0.68 to 1.01 +/- 0.44 mmHg/ml/min: p less than 0.05) but not in Group 2 (both: p = NS). In conclusion, UK has been shown to increase regional coronary blood flow in selected patients presenting with active UA, as well as evidence of i.c. thrombus at early angiography. Heterogeneity of angiographic findings could explain controversies in trials dealing with thrombolysis in UA.

Aged↗
PubMed1992

Transient ischaemia refractory to conventional medical treatment in unstable angina: angiographic correlates and prognostic implications.

Complex stenosis morphology is frequently seen in patients with unstable angina. However, its relation to transient myocardial ischaemia and clinical outcome has not been adequately elucidated. We studied 86 patients admitted to the Coronary Care Unit for unstable angina; all patients underwent ECG Holter monitoring during the first 2-4 days, while receiving intensive triple drug treatment. Coronary angiography and subsequent analysis of the ischaemia-related artery were performed within 12 days of admission. Patients were grouped according to their angiographic features: 45 showed complex coronary morphology (CM: 29 eccentric stenosis with irregular borders or overhanging edges; 16 intracoronary thrombus), 11 had documented coronary spasm as well as moderate atherosclerosis (CS), seven had left main coronary artery disease, and the remaining 23 patients showed regular and smooth morphology of coronary stenosis (RM). At admission, transient myocardial ischaemia (TMI) was greater in patients with CM (85 +/- 60 min .24 h-1) than in those with RM or CS (33 +/- 26 min .24 h-1; P less than 0.005). After 3 days of full medical treatment TMI decreased in all groups, but 34/45 patients with CM and 9/34 with RM or CS still showed residual ischaemia (greater than 0 min .24 h-1): 76% vs 26%, P less than 0.02. Follow-up was obtained at hospital discharge and after 1 year in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[Regional coronary blood flow in patients with acute myocardial infarct treated by systemic fibrinolysis].

Thrombolysis has been reported to restore coronary blood flow in patients with acute myocardial infarction (AMI). However, the relationship between fibrinolytic treatment and evidence of myocardial reperfusion has not been adequately assessed. Accordingly, we measured great cardiac vein blood flow (GCVF:thermodilution) in 12 patients (Group 1) presenting with AMI (chest pain < 4 hours and ST elevation in the anterior leads) before and following i.v. urokinase (UK:2 million U/90 min). Ten patients receiving conventional treatment served as controls (Group 2). UK induced a significant increase of GCVF (from 101 +/- 24 to 164 +/- 42 ml/min, p < 0.001). Maximal increase occurred after 50 +/- 54 min from drug infusion. Conversely, changes in GCVF were not significant in Group 2 (from 103 +/- 35 to 106 +/- 31 ml/min, NS). Following 24 hours changes in GCVF were still consistent only in Group 1 patients. Individual analysis during 24 hours showed marked fluctuations of GCVF peak values in Group 1 patients (62 +/- 43%), but not in Group 2 (29 +/- 21%). Thus, UK induces a marked increase of GCVF in most patients with anterior AMI; such increase suggests that reperfusion occurs early (i.e. within 1 hour) from UK administration. Fluctuations of GCVF during monitoring are magnified by thrombolysis, suggesting intermittent coronary reocclusion in the early hours of AMI.

Blood Flow Velocity↗
PubMed1992

[The differentiated effects of fibrinolysis on the coronary flow in patients with unstable angina].

BACKGROUND: Intracoronary (i.c.) thrombus is a frequent finding in patients (pts) with unstable angina (UA). Accordingly, thrombolytic treatment could be beneficial, as resolution of thrombus might result in increased delivery of blood flow to the ischemic regions. METHODS: To test this hypothesis we studied 13 pts with UA refractory to maximal medical treatment and ST segment shift in the anterior leads. Coronary angiography was performed and great cardiac vein blood flow (GCVF; thermodilution) was measured in all pts within 48 hours (mean 29 +/- 13 hrs) from the last chest pain episode. Following angiography, pts received i.v. wrokinase (UK: 1 million IU/30 min); aortic pressure and GCVF were measured before and every 10 min during drug infusion, for a total time of 90 min. RESULTS: At baseline angiography 5/13 pts (Group 1) had evidence of i.c. thrombus (intraluminal filling defect or thrombotic subocclusion) in the ischemia-related left coronary artery, whereas 8 pts (Group 2) did not. Overall, coronary hemodynamics did not change significantly following drug administration: GCVF was 103 +/- 65 on baseline and 117 +/- 68 ml. min after UK; p > 0.05. Conversely, group analysis showed that UK increased GCVF and decreased anterior coronary resistances (mean aortic pressure/GCVF) in Group 1 (respectively from 86 +/- 33 to 114 +/- 41 ml. min: p < 0.005; and from 1.37 +/- 0.68 to 1.01 +/- 0.44 mmHg/ml. min: p < 0.05) but not in Group 2 (both: p > 0.05), despite similar effects on aortic pressure. CONCLUSIONS: Fibrinolytic treatment can be of therapeutic value in UA; UK has shown to increase regional coronary blood flow in selected pts presenting with refractory angina as well as evidence of i.c. thrombus at early angiography. Heterogeneity of angiographic findings could explain controversies in trials dealing with thrombolysis in UA.

Aged↗
PubMed1991

Prognostic significance of silent myocardial ischemia in variant angina pectoris.

The present study investigates the prognostic significance of silent myocardial ischemia in variant angina. Forty-eight-hour Holter monitoring and coronary angiography were performed in 54 patients with transient ST elevation and no history of myocardial infarction admitted to the coronary care unit for worsening of symptoms. Coronary artery spasm was documented in most of these patients. Over the subsequent month, 20 patients (group 1) had a major coronary event (2 died, 6 had nonfatal myocardial infarction and 12 had urgent coronary revascularization), and the remaining 34 patients (group 2) had a good clinical outcome. From 2,578 hours of recording, 547 ischemic episodes were identified of which only 9% were associated with angina. The mean daily number of ST elevation in group 1 was similar to that in group 2 (4.8 +/- 5.1 vs 4.1 +/- 4.6; p = not significant). Conversely, the mean daily duration of such ischemic episodes was consistently greater in group 1 than in 2 (79 +/- 36 vs 37 +/- 25 minutes; p less than 0.005). The occurrence of greater than or equal to 1 long-lasting (greater than or equal to 10 minutes) episode of ST elevation was observed in 18 of 20 patients in group 1 (sensitivity 90%), but only in 4 of 34 in group 2 (specificity 88%). Significant coronary atherosclerosis (greater than 50% stenoses) was found at angiography in 18 of 20 patients in group 1, and in 18 of 34 in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris, Variant↗
PubMed1991

Angiographic morphology in unstable angina and its relation to transient myocardial ischemia and hospital outcome.

Complex stenosis morphology frequently occurs in patients with unstable angina pectoris. However, its relation to transient myocardial ischemia and hospital outcome has not been ascertained. To address this issue, 88 patients with significant (greater than or equal to 50%) coronary artery disease presenting with angina--new onset (n = 38), worsening (n = 20) or at rest (n = 30)-were studied. Patients with left main artery disease, normal coronary arteries or occlusion of the ischemia-related arteries were not included in the study. Continuous electrocardiographic recordings were obtained during the first 24 hours. Angiography was performed within 1 week from admission. Complex morphology was defined as any stenosis with irregular borders, overhanging edges or intracoronary thrombus. Only data referring to the in-hospital outcome were considered in this study. Adverse end points were sudden death, myocardial infarction and emergency revascularization. Analysis of the angiograms revealed a complex morphology in 58 patients (group 1). The remaining 30 patients served as control subjects (group 2). Thirty-two of the 58 group 1 patients had an unfavorable clinical outcome (positive predictive value, 55%). A similar outcome occurred in only 2 of the 30 group 2 patients (negative predictive value, 93%). Of the 32 group 1 patients who had an unfavorable clinical outcome, 29 had a cumulative duration of transient myocardial ischemia of greater than or equal to 60 minutes per 24 hours. A similar duration of ischemia, however, was observed in another 6 group 1 and in 8 group 2 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina, Unstable↗
PubMed1990

[Variant angina which interacts with two phenomena: local hypersensitivity and abnormal response in the coronary tree to vasoconstrictor stimuli].

The aim of the present study was to evaluate the vasomotion of the entire coronary tree in variant angina, particularly focusing the attention on the behaviour of the "non spastic" epicardial vessels, using a quantitative coronary technique. Two different groups of patients served as controls. The first group consisted of 10 patients with accessory nodal pathway but without any sign of myocardial ischemia (Group I). The second group included 8 patients with stable exertional angina pectoris and coronary artery disease (Group II). The third group (Group III) consisted of 16 patients presenting with variant angina and spontaneous or hyperventilation-induced (HV: 30 cycles/min for 5 min) ST segment elevation. All patients underwent coronary angiography before and 2 min after HV testing; the evaluation of the coronary diameters was performed on baseline and after HV. In Group III, the HV testing caused a 26 +/- 12% reduction of the "non spastic" coronary vessels, with the mean control diameter of 2.00 +/- 0.61 mm that decreased to 1.48 +/- 0.55 mm. The patients of Group I showed only a mild degree of vasoconstriction (9 +/- 6%) of the epicardial coronary vessels; the Group II patients, also, showed a moderate response to vasoactive stimulus (11 +/- 8%), with the mean control diameter of 2.36 +/- 0.69 mm that decreased to 2.09 +/- 0.65 mm. The greater amount of vasoconstriction showed by patients with variant angina was statistically significant compared to both control groups (p less than 0.001). A further analysis of the coronary vasomotion, in Group III patients, showed that the 6 patients with normal or near normal coronary angiograms exhibited a 34% reduction in the vessel diameter. The remaining 10 patients who presented with a diffuse atherosclerotic involvement of the epicardial vessels (organic stenosis greater than or equal to 50% at the site of spasm) showed a lesser (20%) but yet significant extent of vasoconstriction compared to both control groups (p less than 0.001). In conclusion, our data indicate that: patients with variant angina exhibit a marked and diffuse coronary narrowing of the coronary vessels during vasoconstrictor stimuli; focal spasm occurs more frequently at the level of atherosclerotic coronary segments, whether they are critical or not. An interaction between these 2 phenomena, ie atherosclerosis and abnormal vasoconstriction, is supposed to be a cause of the occurrence of focal coronary spasm in variant angina.

Adult↗
PubMed1989

ST/HR slope during prostacyclin treatment: an improved method to identify patients with advanced coronary artery disease.

Constriction of atherosclerotic coronary segments during exercise may further reduce coronary flow reserve in patients with coronary artery disease. This could influence the linear regression analysis of the heart rate-related changes in ST-segment depression (ST/HR slope) thereby limiting the accuracy of this method in identifying the severity of the disease. To test this hypothesis, the exercise related ST/HR slopes on placebo were compared with those obtained during coronary vasodilation induced by a prostacyclin analogue (iloprost 6 ng kg-1 min-1) in 42 anginal patients with documented coronary artery disease. In seven of these, the same protocol was repeated during right heart catheterization. The overall diagnostic accuracy of the ST/HR slope on iloprost was better than on placebo in patients with advanced coronary artery disease. This was due mainly to a consistent rightward shift of the ST/HR slope in patients with one- and two-vessel, but not three-vessel disease or left main stem disease. The reason for the greater effects of iloprost on ST/HR slopes in patients with a lesser degree of atherosclerosis remains unclear. However, coronary blood flow was higher during drug infusion, which suggests that iloprost may prevent the occurrence of dynamic coronary events able to reduce the maximum coronary flow reserve during exertion. This mechanism may be predominant in patients with minor coronary artery disease.

Adult↗
PubMed1989

[Abnormal coronary response to vasomotor stimuli: analogies between variant angina and X syndrome].

The aim of this study was to evaluate the effects of hyperventilation (HV) and of ic nitroglycerin (NTG) on coronary diameters and hemodynamics in 32 patients with angina pectoris. Of these, 10 patients had stable angina and critical coronary artery disease (CAD, Group I), 12 patients with variant angina (VA) and no or minor coronary atherosclerosis (Group II), and 10 patients with angina and normal coronary arteries (syndrome X (SX), Group III). All patients underwent coronary angiography as well as right heart catheterization; measurements of left anterior descending coronary diameters (mid segment), great cardiac vein blood flow, aortic pressure and coronary resistance were performed on baseline, after HV and following NTG. HV caused coronary spasm in 4 patients with VA and significantly (p less than 0.001) reduced coronary diameters and regional blood flow both in Groups II and III, but not in Group I. NTG resulted in increased coronary diameters in all patients, however variations were greater in VA and SX (44 and 39%, respectively) than in Group I (18%; p less than 0.025). NTG induced an increase of coronary blood flow only in patients with CAD. We conclude that patients with VA and SX present a similar coronary response to vasomotor stimuli, either after HV or following NTG. Response is abnormal if compared to that of patients of group I, and it involves both epicardial and intramural coronary vessels. Thus, we suggest that SX and VA belong to a single pathogenetic entity with a spectrum of clinical manifestations.

Adult↗
PubMed1987

Effect of oral levodopa and carbidopa on coronary spasm in variant angina pectoris.

The effect of oral administration of 500 mg of levodopa with 50 mg of carbidopa, a peripheral dopadecarboxylase inhibitor, on coronary vasomotion during vasoconstrictor stimuli was examined in 15 patients with variant angina presenting with hyperventilation-induced myocardial ischemia. Patients were studied during 3 noninvasive sessions and 1 angiographic session. In all sessions the basic protocol consisted of provocation of coronary spasm by hyperventilation before and 2 hours after levodopa and carbidopa administration. During angiography, great cardiac vein blood flow, right atrial and aortic pressures were measured, and coronary angiograms were recorded at baseline and 1 to 4 minutes after each hyperventilation. Samples for dopamine plasma levels were drawn before and throughout the studies. In 3 selected patients, levodopa and carbidopa were associated with 30 mg of domperidone, an antagonist of dopamine peripheral receptors. Levodopa and carbidopa consistently prevented the occurrence of ischemia after hyperventilation in 6 of the 15 patients. This was due to inhibition of local coronary spasm in 2 patients and reduced coronary constriction in 4. Ischemia due to hyperventilation was still prevented despite addition of domperidone with levodopa and carbidopa. Plasma dopamine levels were 23 +/- 15 before and 739 +/- 284 pg/ml 2 hours after administration of levodopa and carbidopa. These findings are consistent with either a decreased central dopaminergic activity and associated disregulation of vasomotor tone, or a peripheral vasodilatory effect of increasing dopamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1985

[The relation between myocardial oxygen consumption and ischemia during exertion in patients with angina pectoris: effect of propranolol].

Patients with coronary artery disease exhibit a reduced coronary vasodilator reserve in response to exercise testing. Drugs which block coronary beta adrenergic receptors could exacerbate this abnormality leaving the vasoconstrictor alpha tone unopposed and/or counteracting the beta 2-mediated vasodilation elicited by the increase in myocardial oxygen demand. To test this hypothesis we administered propranolol 40 mg qid and placebo, using a cross over randomized single blind protocol, to 14 patients each with effort angina and critical coronary stenosis (greater than or equal to 75%). We performed computer-assisted multistage bicycle ergometer testings (25 W increments at 2 min intervals) after 2 weeks open label placebo (control) and at 2 week intervals following daily administration of propranolol and placebo. Compared to placebo, propranolol reduced significantly (p less than 0.001) peak heart rate (x +/- SD: 114 +/- 6 vs 150 +/- 11 beats/min) and rate pressure product (20.1 +/- 2.1 vs 28.0 +/- 3.9 X 10(-3)) and increased exercise duration (462 +/- 91 vs 355 +/- 85 sec). Conversely 0.1 mV ST segment depression was observed at lower heart rate (106 +/- 9 vs 127 +/- 8 beats/min, p less than 0.001) and rate pressure product (16.9 +/- 3.6 vs 22.4 +/- 2.4 X 10(-3), p less than 0.001). No significant differences were found between placebo and control. Moreover, we assessed the regression lines of the relationship between ST segment depression (ST) and heart rate (HR) during exercise. These have been shown to be shifted to the right after surgical revascularization and are an indirect measure of coronary reserve.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗