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Prognostic value of dobutamine stress technetium-99m-sestamibi single-photon emission computed tomography myocardial perfusion imaging: stratification of a high-risk population.
Calnon DA, McGrath PD, Doss AL, Harrell FE, Watson DD, Beller GA
(2001) J Am Coll Cardiol 38: 1511-7
MeSH Terms: Aged, Animals, Bias, Cardiotonic Agents, Coronary Disease, Disease Models, Animal, Dobutamine, Dogs, Drug Interactions, Female, Follow-Up Studies, Humans, Male, Middle Aged, Prognosis, Proportional Hazards Models, Radiopharmaceuticals, Referral and Consultation, Risk Assessment, Risk Factors, Survival Analysis, Technetium Tc 99m Sestamibi, Tomography, Emission-Computed, Single-Photon
Show Abstract · Added February 28, 2014
OBJECTIVES - This work was undertaken to define the intrinsic cardiac risk of the patient population referred for dobutamine stress perfusion imaging and to determine whether dobutamine technetium-99m ((99m)Tc)-sestamibi single-photon emission computed tomography (SPECT) imaging is capable of risk stratification in this population.
BACKGROUND - In animal models, dobutamine attenuates the myocardial uptake of (99m)Tc-sestamibi resulting in underestimation of coronary stenoses. Therefore, we hypothesized that the prognostic value of dobutamine stress (99m)Tc-sestamibi SPECT myocardial perfusion imaging might be impaired, owing to reduced detection of coronary stenoses.
METHODS - We reviewed the clinical outcome of 308 patients (166 women, 142 men) who underwent dobutamine stress SPECT (99m)Tc-sestamibi imaging at our institution from September 1992 through December 1996.
RESULTS - During an average follow-up of 1.9 +/- 1.1 years, there were 33 hard cardiac events (18 myocardial infarctions [MI] and 15 cardiac deaths) corresponding to an annual cardiac event rate of 5.8%/year, which is significantly higher than the event rate for patients referred for exercise SPECT imaging at our institution (2.2%/year). Event rates were higher after an abnormal dobutamine (99m)Tc-sestamibi SPECT study (10.0%/year) than after a normal study (2.3%/year) (p < 0.01), even after adjusting for clinical variables. In the subgroup (n = 29) with dobutamine-induced ST-segment depression and abnormal SPECT imaging, the prognosis was poor, with annual cardiac death and nonfatal MI rates of 7.9% and 13.2%, respectively.
CONCLUSIONS - Patients referred for dobutamine perfusion imaging are a high-risk population, and dobutamine stress (99m)Tc-sestamibi SPECT imaging is capable of risk stratification in these patients.
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23 MeSH Terms
Do NHE inhibition and ischemic preconditioning convey cardioprotection through a common mechanism?
Gumina RJ, Terzic A, Gross GJ
(2001) Basic Res Cardiol 96: 318-24
MeSH Terms: Animals, Cardiotonic Agents, Ischemic Preconditioning, Myocardial, Sodium-Hydrogen Exchangers
Added February 21, 2015
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4 MeSH Terms
Opposing effects of beta(1)- and beta(2)-adrenergic receptors on cardiac myocyte apoptosis : role of a pertussis toxin-sensitive G protein.
Communal C, Singh K, Sawyer DB, Colucci WS
(1999) Circulation 100: 2210-2
MeSH Terms: Adenylate Cyclase Toxin, Adrenergic beta-Agonists, Adrenergic beta-Antagonists, Animals, Apoptosis, Carbachol, Cardiotonic Agents, Cyclic AMP, GTP-Binding Protein alpha Subunits, Gi-Go, Heart, Imidazoles, Isoproterenol, Male, Muscarinic Agonists, Myocardium, Pertussis Toxin, Prazosin, Propanolamines, Rats, Rats, Sprague-Dawley, Receptors, Adrenergic, beta-1, Receptors, Adrenergic, beta-2, Second Messenger Systems, Virulence Factors, Bordetella
Show Abstract · Added March 5, 2014
BACKGROUND - beta-Adrenergic receptor (beta-AR) stimulation increases apoptosis in adult rat cardiac (ventricular) myocytes (ARVMs) via activation of adenylyl cyclase. beta(2)-ARs may couple to a G(i)-mediated signaling pathway that can oppose the actions of adenylyl cyclase.
METHODS AND RESULTS - In ARVMs, beta-AR stimulation for 24 hours increased the number of apoptotic cells as measured by flow cytometry. beta-AR-stimulated apoptosis was abolished by the beta(1)-AR-selective antagonist CGP 20712A (P<0.05 versus beta-AR stimulation alone) but was potentiated by the beta(2)-AR-selective antagonist ICI 118,551 (P<0.05 versus beta-AR stimulation alone). The muscarinic agonist carbachol also prevented beta-AR-stimulated apoptosis (P<0.05 versus beta-AR stimulation alone), whereas pertussis toxin potentiated the apoptotic action of beta-AR stimulation (P<0.05 versus beta-AR stimulation alone) and prevented the antiapoptotic action of carbachol.
CONCLUSIONS - In ARVMs, stimulation of beta(1)-ARs increases apoptosis via a cAMP-dependent mechanism, whereas stimulation of beta(2)-ARs inhibits apoptosis via a G(i)-coupled pathway. These findings have implications for the pathophysiology and treatment of myocardial failure.
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24 MeSH Terms
Replacement by homologous recombination of the minK gene with lacZ reveals restriction of minK expression to the mouse cardiac conduction system.
Kupershmidt S, Yang T, Anderson ME, Wessels A, Niswender KD, Magnuson MA, Roden DM
(1999) Circ Res 84: 146-52
MeSH Terms: Animals, Animals, Newborn, Cardiotonic Agents, Electrocardiography, Gene Expression Regulation, Developmental, Gene Targeting, Heart Conduction System, Isoproterenol, Lac Operon, Long QT Syndrome, Mice, Mice, Knockout, Potassium Channels, Potassium Channels, Voltage-Gated, Recombination, Genetic, Staining and Labeling, beta-Galactosidase
Show Abstract · Added February 23, 2011
The minK gene encodes a 129-amino acid peptide the expression of which modulates function of cardiac delayed rectifier currents (IKr and IKs), and mutations in minK are now recognized as one cause of the congenital long-QT syndrome. We have generated minK-deficient mice in which the bacterial lacZ gene has been substituted for the minK coding region such that beta-galactosidase expression is controlled by endogenous minK regulatory elements. In cardiac myocytes isolated from wild-type neonatal mice, IKs is rarely recorded, while IKr is common. In minK (-/-) myocytes, IKs is absent and IKr is significantly reduced and its deactivation slowed; these results further support a role for minK in modulating both IKs and IKr. Despite these changes, ECGs in (+/+) and (-/-) animals are no different at adult and at neonatal stages. ECG responses to isoproterenol are also similar in the 2 groups. beta-Galactosidase staining in postnatal minK (-/-) hearts is highly restricted, to the sinus-node region, caudal atrial septum, and proximal conducting system. Moreover, as early as embryonal day 11, segmentally restricted beta-galactosidase expression is observed in the portions of the sinoatrial and atrioventricular junctions that are thought to give rise to the conducting system, thereby implicating minK expression as an early event in conduction system development. More generally, the restricted nature of minK expression in the mouse heart suggests species-specific roles of this gene product in mediating the electrophysiological properties of the heart.
2 Communities
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17 MeSH Terms
A randomized controlled trial of epoprostenol therapy for severe congestive heart failure: The Flolan International Randomized Survival Trial (FIRST).
Califf RM, Adams KF, McKenna WJ, Gheorghiade M, Uretsky BF, McNulty SE, Darius H, Schulman K, Zannad F, Handberg-Thurmond E, Harrell FE, Wheeler W, Soler-Soler J, Swedberg K
(1997) Am Heart J 134: 44-54
MeSH Terms: Aged, Angiography, Angiotensin-Converting Enzyme Inhibitors, Antihypertensive Agents, Cardiac Output, Cardiotonic Agents, Cause of Death, Digoxin, Diuretics, Epoprostenol, Exercise Tolerance, Female, Heart Failure, Humans, Infusions, Intravenous, Male, Middle Aged, Proportional Hazards Models, Pulmonary Wedge Pressure, Quality of Life, Risk Factors, Stroke Volume, Survival Rate, Vascular Resistance, Ventricular Dysfunction, Left, Walking
Show Abstract · Added February 28, 2014
This trial evaluated the effects of epoprostenol on patients with severe left ventricular failure. Patients with class IIIB/IV congestive heart failure and decreased left ventricular ejection fraction were eligible for enrollment if angiography documented severely compromised hemodynamics while the patient was receiving a regimen of digoxin, diuretics, and an angiotensin-converting enzyme inhibitor. We randomly assigned 471 patients to epoprostenol infusion or standard care. The primary end point was survival; secondary end points were clinical events, congestive heart failure symptoms, distance walked in 6 minutes, and quality-of-life measures. The median dose of epoprostenol was 4.0 ng/kg/min, resulting in a significant increase in cardiac index (1.81 to 2.61 L/min/m2), a decrease in pulmonary capillary wedge pressure (24.5 to 20.0 mm Hg), and a decrease in systemic vascular resistance (20.76 to 12.33 units). The trial was terminated early because of a strong trend toward decreased survival in the patients treated with epoprostenol. Chronic intravenous epoprostenol therapy is not associated with improvement in distance walked, quality of life, or morbid events and is associated with an increased risk of death.
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26 MeSH Terms