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1. |
Alpha–adrenergic Blockade for Variant AnginaA Long–term, Double–blind, Randomized Trial |
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Circulation,
Volume 63,
Issue 6,
1983,
Page 1185-1188
MICHAEL WINNIFORD,
NEIL FILIPCHUK,
L HILLIS,
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摘要:
Recent reports have shown that /3-adrenergic blockade may exacerbate variant angina. On theoretical grounds, ca-adrenergic blockade may be beneficial in these patients. To test this hypothesis, we assessed the efficacy of prazosin, an ca-adrenergic blocking agent, in six men, mean age 49 years, with variant angina. Prazosin, 14.0 ± 2.4 mg/day (mean SD) in three equal doses, was compared with placebo in a double-blind, randomized, double-crossover trial lasting 41/2 months: 2 weeks of open-label prazosin followed by four 1-month periods of blinded alternating therapy. No other vasoactive medications were administered during the study. Prazosin reduced sitting systolic arterial pressure from 145 18 to 127 16 mm Hg (p = 0.02), but exerted no effect on diastolic arterial pressure or heart rate. Prazosin did not change the weekly number of episodes of chest pain (2.5 2.3 with placebo vs 3.1 3.0 with prazosin, NS), nitroglycerin tablets used (3.9 3.7 with placebo vs 4.6 4.2 with prazosin, NS), or transient ST-segment deviations (by calibrated two-channel Holter monitoring for 24 hours/week throughout the study) (6.5 ± 10.1 with placebo vs 11.8 17.4 with prazosin, NS). During prazosin therapy, three patients had orthostatic dizziness and one patient had headache. Thus, in a long-term, randomized, double-blind trial, prazosin exerted no obvious beneficial effect in patients with variant angina.
ISSN:0009-7322
出版商:OVID
年代:1983
数据来源: OVID
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2. |
Coronary‐prone Behavior and Coronary Heart DiseaseA Critical Review |
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Circulation,
Volume 63,
Issue 6,
1983,
Page 1199-1215
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摘要:
A panel of biomedical and behavioral scientists were charged with the task of critically evaluating all available research and theory linking behavior to coronary heart disease. The task was divided into five topic areas: (1) association of coronary-prone behavior and coronary heart disease; (2) assessment of the “type A” behavior pattern; (3) physiologic mechanisms linking behavior to coronary heart disease; (4) cultural and developmental factors; and (5) intervention strategies. The review panels developed summary statements which delineated the perceived strengths and shortcomings of the theory and data for their respective sections and provided recommendations to the National Heart, Lung, and Blood Institute concerning future research.
ISSN:0009-7322
出版商:OVID
年代:1981
数据来源: OVID
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3. |
The Linearity of the End‐systolic Pressure‐Volume Relationship in Man and Its Sensitivity for Assessment of Left Ventricular Function |
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Circulation,
Volume 63,
Issue 6,
1983,
Page 1216-1222
HELMUTH,
MEHMEL BENJAMIN,
STOCKINS KAI,
RUFFMANN KLAUS,
OLSHAUSEN GERHARD,
SCHULER WOLFGANG,
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摘要:
The linearity and sensitivity of the end-systolic pressure-volume (P-Ves) relation to the inotropic state of the left ventricle were investigated in 11 patients with coronary heart disease and one patient with congestive cardiomyopathy. To minimize autonomic reflex responses, propranolol, 0.15 mg/kg, and atropine, 1 mg, were administered i.v. at the beginning of the study. Three ventriculograms were performed: at rest, after oral isosorbide dinitrate, 10 mg (systolic pressure decrease 15 ⩾ mm Hg), and during infusion of methoxamine, 2 mg/min (systolic pressure increase ⩾ 10 mm Hg).The three points of the P-Vesrelation showed linearity (r⩾ 0.96). The relation between the slope k of the PVesrelation and the left ventricular ejection fraction at rest was best described by an exponential function (r= 0.94). The use of peak systolic pressure instead of end-systolic pressure showed equally good results. The intercept of the PVesline on the abscissa, which represents the theoretical end-systolic volume at zero pressure, was not related to the ejection fraction under control conditions. The P-Vesrelation in postextrasystolic beats was displaced toward the left (smaller end-systolic volumes) and became steeper.
ISSN:0009-7322
出版商:OVID
年代:1981
数据来源: OVID
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4. |
EditorialThe End‐systolic Pressure‐Volume Relation of the VentricleDefinition, Modifications and Clinical Use |
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Circulation,
Volume 63,
Issue 6,
1983,
Page 1223-1227
KIICHI,
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ISSN:0009-7322
出版商:OVID
年代:1981
数据来源: OVID
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5. |
Left Ventricular Diastolic Performance At Rest and During Exercise in Patients With Coronary Artery DiseaseAssessment with First‐pass Radionuclide Angiography |
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Circulation,
Volume 63,
Issue 6,
1983,
Page 1228-1237
LAWRENCE,
REDUTO WILLIAM,
WICKEMEYER JAMES,
YOUNG LESLIE,
DEL VENTURA JOHN,
REID DONALD,
GLAESER MIGUEL,
QUINONES RICHARD,
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摘要:
We used first-pass radionuclide angiocardiography to assess filling fraction during the first third of diastole, peak filling rate and peak filling rate during the first third of diastole as indexes of left ventricular diastolic performance at rest and after upright bicycle exercise in 32 normal patients and 68 patients with coronary artery disease. The mean filling fraction was unchanged from rest to exercise in normal patients (47 ± 15% vs 46 ± 13%; NS). Even in 49 coronary patients with normal (⩾ 50%) ejection fraction at rest, filling fraction was less than that in normal patients at rest (35 ± 11% vs 47 ± 15%,p< 0.001). Despite similar resting heart rates, patients with coronary disease had lower (p< 0.001) peak filling rate and peak filling rate during the first third of diastole than normal patients. With exercise, filling fraction decreased (p< 0.001) from the resting value in coronary patients. These data suggest that (1) indexes of diastolic performance can be noninvasively assessed at rest and during exercise using first-pass radionuclide angiocardiography, (2) abnormalities in early diastolic performance are often present at rest in patients with coronary artery disease despite normal systolic performance, and (3) exercise-induced ischemia results in increased early diastolic dysfunction in patients with coronary disease.
ISSN:0009-7322
出版商:OVID
年代:1981
数据来源: OVID
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6. |
Transient Reduction of Regional Myocardial Perfusion During Angina at Rest with ST‐segment Depression or Normalization of Negative T Waves |
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Circulation,
Volume 63,
Issue 6,
1983,
Page 1238-1247
OBERDAN,
PARODI NILDA,
UTHURRALT Sit,
SEVERI WALTER,
BENCIVEFi1Ii CLAUDIO,
MICHELASSI ANTONIo,
ABBATE ATTILIO,
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摘要:
Previous studies have shown localized thallium-201 (201TI) defects during resting anginal episodes with ST-segment elevation. In this report, findings of201TI during spontaneous angina in 14 patients with ST-segment depression and seven with normalization of negative T waves are reported. One millicurie of201TI was injected i.v. during the ischemic episode and scintigrams were taken within 5–10 minutes and after 4 hours. One week later a new injection of201T1 in a basal state provided control scintigrams.Early scintigrams showed a regional reduction of201TI uptake in all patients With normalization of negative T waves and a close correspondence between the location of the defect and the site of the electrocardiographic changes. Conversely, scintigrams in patients with ST-segment depression showed a lesser relatively milder reduction of201TI activity in 12 and no defect in two. In these patients the defect, when present, was localized in eight and diffuse in four patients. The site of the201TI defect did not always correspond to the location of STsegment depression. Overall, 4-hour scintigrams were similar to those taken in the absence of symptoms.Heart rate and systolic blood pressure measured at the onset of the electrocardiographic changes were not significantly different from asymptomatic periods but were significantly lower than during effort-induced angina, so the defects should be related to a reduction of myocardial perfusion, as documented in variant angina, rather than to an inadequate increase of coronary blood flow.From this study, angina at rest with normalization of negative T waves appears related to localized uniform reduction of myocardial perfusion, while angina with ST-segment depression is associated with a less uniform reduction of perfusion, probably located in the subendocardial layers, in the presence of severe coronary lesions.
ISSN:0009-7322
出版商:OVID
年代:1981
数据来源: OVID
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7. |
In Vivo Quantitation of Regional Myocardial Blood Flow by Positron‐emission Computed Tomography |
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Circulation,
Volume 63,
Issue 6,
1983,
Page 1248-1258
GERALD,
WISENBERG HEINRICH,
SCHELBERT EDWARD,
HOFFMAN MICHAEL,
PHELPS GERALD,
ROBINSON CARL,
SELIN JOHN,
CHILD DAVID,
SKORTON DAVID,
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摘要:
The potential of positron-emission computed tomography (PCT) for external quantitation of myocardial indicator concentrations and regional myocardial blood flow (RMBF) and the effect of left ventricular wall thickness on tracer concentration recovery by PCT was examined in seven open-chest dogs. RMBF was determined by the arterial reference technique in vivo and in vitro. Together with gamma-emitting Ce-141 microspheres, positron-emitting Ga-68-labeled microspheres were injected into the left atrium and their myocardial concentrations determined in vivo from gated and ungated cross-sectional PCT images. The loss in count recovery related to object size was corrected using postmortem and in vivo echocardiographic left ventricular wall thickness measurements. In vivo measurements of RMBF by PCT correlated linearly with invitro-derived RMBF (r= 0.98; n = 84), but they underestimated in vitro RMBF by an average of 40%. After correcting for wall thickness effect, in vivo measured RMBF agreed with the in vitro measurements in a one-toone relationship (r= 0.99). The accuracy of the in vivo PCT measured RMBF was maintained when corrections for wall thickness were made from in vivo echocardiographic instead of from postmortem measurements. Gating of the PCT images improved the accuracy of the in vivo RMBF determinations. Moreover, the increase in regional count recovery during systole provided an estimate of systolic wall thickening. Changes in left ventricular wall thickness from end-diastole to end-systole measured by PCT closely correlated with the changes in wall thickness observed by echocardiography. We conclude that (1) myocardial indicator tissue concentrations, and thus, RMBF, can be accurately measured by PCT provided corrections are made for the effect of wall thickness on count recovery; (2) these corrections can be made using in vivo echocardiography; and (3) gated PCT imaging can be used to evaluate regional myocardial systolic wall thickening as an index of regional function and combined with measurements of RMBF or regional metabolism. The results represent a framework for the noninvasive measurement of RMBF and metabolism by PCT in the experimental animal and in man.
ISSN:0009-7322
出版商:OVID
年代:1981
数据来源: OVID
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8. |
N‐13 Ammonia as an Indicator of Myocardial Blood Flow |
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Circulation,
Volume 63,
Issue 6,
1983,
Page 1259-1272
HEINRICH,
SCHELBERT MICHAEL,
PHELPS SUNG-CHENG,
HUANG NORMAN,
MACDONALD HERBERT,
SELIN DAVID,
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摘要:
We have characterized N-13 ammonia as a myocardial blood flow imaging agent suitable for positron-emission computed tomography. However, the mechanisms of uptake and retention of this agent in myocardium are not known, and effects of altered metabolism were not considered. Therefore, we studied the uptake and retention of N-13 ammonia in myocardium under various hemodynamic and metabolic conditions in open-chest dogs. N-13 ammonia was extracted nearly 100% during its initial capillary transit, followed by metabolic trapping that competed with flow-dependent back diffusion. At control flows, the first capillary transit extraction fraction (E) of N-13 ammonia averaged 0.82 ± 0.06. It fell with higher flows by E = 1 − 0.607 exp − 125/F. Myocardial N-13 tissue clearance half-times were similarly inversely related to blood flow, and ranged from 110–642 minutes. Cardiac work and changes in the myocardial inotropic state induced by isoproterenol and propranolol did not affect E or the tissue clearance half-times. Low plasma pH reduced E by an average of 20%, while elevated plasma pH had no effect. Decreases in flow below control also were associated with a fall in E. Inhibition of glutamine synthetase with L-methionine sulfoximine impaired metabolic trapping of N-13 ammonia and implicates the glutamic acid-glutamine reaction as the primary mechanism for ammonia fixation. The product of E times flow predicts the myocardial N-13 tissue concentrations, which increased by 70% when flow was doubled. Thus, blood flow and metabolic trapping are the primary determinants of myocardial uptake and retention of N-13 ammonia. The relative constancy of metabolic trapping over a wide range of hemodynamic and metabolic conditions demonstrates the value of N-13 ammonia as a myocardial blood flow imaging agent.
ISSN:0009-7322
出版商:OVID
年代:1981
数据来源: OVID
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9. |
Myocardial Lactate MetabolismEvidence of Lactate Release During Net Chemical Extraction in Man |
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Circulation,
Volume 63,
Issue 6,
1983,
Page 1273-1279
EDWARD,
GERTZ JUDITH,
WISNESKI RICHARD,
NEESE J.,
BRISTOW GILBERT,
SEARLE J.,
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摘要:
Myocardial blood flow has been recognized to be heterogeneous in patients with coronary artery disease. Traditional arterial-coronary sinus sampling methods cannot demonstrate comparable heterogeneity of myocardial metabolism. In this study we used a tracer technique to investigate possible heterogeneity of myocardial lactate metabolism. Twenty-one patients with symptoms of ischemic heart disease were studied. We injected14C-I-lactate intravenously as a constant infusion after a priming dose. Coronary sinus and arterial samples were obtained for chemical and radioisotopic analyses. At rest, myocardial lactate extraction by chemical analysis was 24.6 ± 8.5% (mean ± SD). By radioisotopic analysis, the lactate extraction was 41.0 ± 10.2% (p< 0.001). Thus, certain areas of the myocardium were releasing lactate despite global net extraction of lactate. In the 12 patients with significant left main or both left anterior descending (LAD) and left circumflex (LCX) lesions, the calculated amount of lactate released at rest was 0.136 ± 0.045, umol/ml of blood (mean ± SD). In contrast, the amount released in the six patients with a significant lesion in only the LAD or LCX was 0.076 ± 0.019 μmol/ml, and in the three patients without left coronary arterial lesions it was 0.039 ± 0.004 μmol/ml.Using a tracer method, myocardial lactate metabolism was demonstrated to be heterogeneous at rest in patients with ischemic heart disease. A significant amount of lactate can be released by the myocardium at a time when chemical arterial-coronary sinus analysis indicates global myocardial extraction. The amount of lactate released appears to be related to the severity of the coronary artery disease.
ISSN:0009-7322
出版商:OVID
年代:1981
数据来源: OVID
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10. |
Myocardial Metabolic and Hemodynamic Effects of Dobutamine in Heart Failure Complicating Coronary Artery Disease |
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Circulation,
Volume 63,
Issue 6,
1983,
Page 1279-1285
RICHARD,
POZEN ROBERT,
DIBIANCO RICHARD,
KATZ REBECCA,
BORTZ ROBERT,
MYERBURG Ross,
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摘要:
Eighteen patients with congestive heart failure (CHF) complicating coronary artery disease (CAD) and seven patients with CHF due to primary cardiomyopathy (CM) were studied during infusions of dobutamine in doses of 2.5–15.0 μg/kg/min. There were statistically significant (p< 0.05) improvements in cardiac index, stroke volume index, left ventricular stroke work index and nuclear ejection fraction in both groups. Significant decreases (p< 0.05) in pulmonary capillary wedge pressure, right atrial pressure, and systemic and pulmonary vascular resistances were also observed in both groups. However, five patients increased an already elevated pulmonary capillary wedge pressure during dobutamine infusion, which was associated with either the development of angina pectoris or with a significant elevation of the mean arterial pressure. In the CAD patients, gated cardiac scans analyzed for segmental wall motion showed improvement in 27% of the abnormally contracting segments during dobutamine infusion. Finally, the effects of dobutamine on myocardial metabolism were assessed with arterial and coronary sinus lactate analysis. Fourteen of the 18 CAD patients (78%) showed no metabolic abnormality during dobutamine infusion; four CAD patients (22%), three of whom developed typical angina pectoris, displayed abnormal lactate metabolism. None of the CM patients developed angina pectoris or displayed abnormal lactate metabolism. Of the seven patients with an adverse hemodynamic or metabolic response, four had recently been withdrawn from propranolol therapy. In conclusion, dobutamine produced favorable effects on hemodynamics, left ventricular ejection fraction, and segmental wall motion abnormalities in most patients with CHF without a deleterious effect on myocardial metabolism.
ISSN:0009-7322
出版商:OVID
年代:1981
数据来源: OVID
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