Publications by authors named "Homans D"

Beta-actin is a cytoskeletal protein that has been implicated as a potentially important mediator of the growth, signaling, migration, and remodeling of cells. Beta-actin is upregulated in remodeling myocardium in response to either pressure or volume overload. The cellular localization of this response has, however, not been determined and is a necessary first step to begin to clarify the role of beta-actin in myocardial remodeling.

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The AngelWings device is a newer transcatheter device used for closure of secundum atrial septal defects (ASD) and patent foramen ovale (PFO), which consists of a self-centering, 2-disk system. Transesophageal echocardiography (TEE) plays a pivotal role in the deployment of the 2 disks of this device, on the appropriate sides of the atrial septum. The objective of this study is to describe the echocardiographic findings associated with successful deployment of the AngelWings device for closure of ASD and PFO.

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Background: Left ventricular (LV) hypertrophy secondary to volume overload can result in alterations in myocardial bioenergetics and LV dysfunction. This study examined whether bioenergetic abnormalities contribute to the pump dysfunction.

Methods And Results: Severe mitral regurgitation (MR) was produced in 10 dogs by disruption of the chordal apparatus.

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Recent studies have demonstrated that pulmonary artery diastolic (PAD) pressure can be measured from a transducer positioned in the right ventricle (RV) based on the finding that PAD and RV pressures are equal at the time of pulmonary valve opening, which is associated with the time of maximum positive rate of pressure development (dP/dtmax) in the ventricle. The objective of this study was to assess the correlation between estimated PAD (ePAD) pressure, obtained through a RV transducer, and actual PAD (aPAD) pressure in patients with heart failure who have abnormal hemodynamics, reduced systolic function, and variable degrees of mitral regurgitation (MR) and tricuspid regurgitation (TR). Simultaneous measurements of pulmonary artery and RV pressures were obtained with a high-fidelity Millar catheter (Millar Instruments, Houston, TX) in 10 patients with New York Heart Association class III-IV heart failure who were being evaluated for cardiac transplantation.

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Beta-actin, a cytoskeletal protein important in the maintenance of cytoarchitecture, has long been thought to be expressed constitutively in myocardial tissue. As such, beta-actin mRNA has been used as a control gene in a wide range of experiments. However, we have uncovered consistent changes in beta-actin mRNA expression in canine myocardium remodeling as a result of insult to the left ventricle.

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To determine the effects of dobutamine stimulation on myocardium distal to a coronary stenosis, transmural spatially localized phosphorus 31 nuclear magnetic resonance measurements of myocardial high-energy phosphate compounds (adenosine triphosphate and phosphocreatine), inorganic phosphate, and blood flow and systolic wall thickening were made in 8 open-chested dogs. Data were collected under (1) control conditions, (2) after the application of a moderate coronary stenosis, (3) during infusion of dobutamine with continuing stenosis, and (4) after the release of the stenosis with continuing dobutamine. Stenosis was associated with concordant reductions of subendocardial blood flow, wall thickening, and high-energy phosphate, and mild elevation of inorganic phosphate; subepicardial measurements were essentially unchanged.

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Background: Structural sympathetic reinnervation of the transplanted human heart is believed to occur > 1 year after cardiac transplantation. The functional effects of reinnervating neurons, however, are undefined.

Methods And Results: To test directly for functional sympathetic reinnervation, we measured left ventricular or coronary hemodynamics in 11 patients < or = 4 months after transplantation, in 45 patients > or = 1 year after transplantation, and in 13 untransplanted, normally innervated patients.

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We examined the effects of the alpha-adrenergic blocking agent urapidil on coronary blood flow (CBF) and myocardial O2 consumption during exercise in 11 dogs trained to run on a motor-driven treadmill. Left circumflex coronary artery (LCX) BF was measured with an electromagnetic flowmeter, and aortic and coronary sinus electromagnetic flowmeter, and aortic and coronary sinus catheters allowed determination of myocardial arteriovenous O2 extraction. During control conditions, graded treadmill exercise caused progressive increases in myocardial O2 consumption, which resulted from regular increases in CBF as well as increased O2 extraction by myocardium.

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Objectives: This study tested the hypothesis that there is preferential recovery of subepicardial wall thickening after nontransmural myocardial infarction.

Background: Previous studies have demonstrated gradual recovery of mechanical function after reperfusion in acute myocardial infarction. Because myocardial necrosis is primarily subendocardial, it was hypothesized that recovery of mechanical function would occur primarily in the subepicardial layers.

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This study examines the hypothesis that high-energy phosphate (HEP) compound levels in unstimulated in vivo myocardium are defined by 1) the level of perfusion and 2) non-perfusion-dependent metabolic characteristics. This hypothesis was tested by determining 1) the effects of pharmacological hyperperfusion of functioning myocardium on transmural HEP compound distribution, contractile function, and myocardial oxygen consumption rate (MVO2) as well as 2) the effect of KCl cardioplegia on transmural myocardial HEP compound distribution. Creatine phosphate (CP) and ATP were measured across the anterior left ventricular wall using spatially localized 31P-nuclear magnetic resonance (NMR).

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We examined the impeding effects of exercise on coronary blood flow by analyzing exercise-induced changes in the pressure-flow relationship during maximal coronary vasodilation with adenosine in chronically instrumented dogs and assessed the individual contributions produced by heart rate, contractility, and alpha 1-adrenergic vasoconstriction. Treadmill exercise that increased heart rate from 118 +/- 6 beats/min at rest to 213 +/- 8 beats/min (P < 0.01) decreased maximum coronary blood flows by decreasing the slope of the linear part of the pressure-flow relationship for coronary pressures > or = 30 mmHg (slopeP > or = 30) from 12.

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Persisting coronary vasoconstrictor tone that is responsive to exogenous adenosine administration has been demonstrated during myocardial ischemia. Therefore, the role and extent of endogenous adenosine-mediated coronary vasodilation in opposing coronary vasoconstriction within regions of ischemic myocardium was investigated in 10 chronically instrumented exercising dogs. Studies were performed on dogs with left circumflex coronary artery stenosis during treadmill exercise (6.

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This study was performed to examine the effect calcitonin gene-related peptide (CGRP) on blood flow through well-developed coronary collateral vessels. Studies were performed in 9 adult mongrel dogs 4-6 months after embolic occlusion of the left anterior descending coronary artery (LAD) with a hollow intravascular plug to stimulate collateral vessel growth. At the time of study, the LAD was cannulated to determine inter-arterial collateral flow from measurement of retrograde blood flow.

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This study examined responses of coronary collateral blood flow to endothelial-dependent vasodilators. Studies were performed in 13 dogs 4-6 mo after embolic occlusion of the left anterior descending coronary artery (LAD). Collateral flow was determined as the sum of retrograde flow from the cannulated LAD, and continuing tissue flow was measured with microspheres administered during the retrograde flow collection.

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This study was designed to test the hypothesis that the oxygen free radical scavengers superoxide dismutase (SOD) and catalase may reduce myocardial "stunning" after exercise-induced ischemia. To test this hypothesis, 8 mongrel dogs performed treadmill exercise for 10 min in the presence of a flow-limiting coronary artery stenosis. Regional left ventricular function was measured with ultrasonic microcrystals implanted to measure regional wall thickening.

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Mechanical complications after heart transplantation are uncommon. We describe a case of hemodynamically significant suture line obstruction that was recognized immediately after heart transplantation using transesophageal echocardiography. Transesophageal echocardiography has proved to be a powerful tool in recognizing mechanical complications in the early posttransplant period.

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This study was performed to determine whether thromboxane A2 (as the analogue U46619) and serotonin can cause vasoconstriction of moderately well developed coronary collateral vessels. Studies were carried out in seven adult mongrel dogs 2 to 4 months after embolic occlusion of the left anterior descending coronary artery had been performed to stimulate collateral vessel growth. At the time of study this artery was cannulated to determine interarterial collateral flow from measurements of retrograde blood flow.

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To determine the frequency of occult right heart thromboembolism during endomyocardial biopsy, 51 cardiac transplant recipients undergoing routine endomyocardial biopsy were studied echocardiographically. Patients were randomized to two groups. In Group 1, the venous sheath was flushed between each biopsy attempt; in Group 2, it was flushed only at the time of initial placement.

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Background: Previous work has reported that coronary vasodilator reserve may persist in myocardium rendered ischemic by hypoperfusion. This study investigated the presence and extent of residual coronary vasomotor tone in myocardial regions made acutely ischemic by a flow-limiting coronary stenosis during exercise.

Methods And Results: Studies were done in chronically instrumented dogs undergoing treadmill exercise in the presence of a coronary stenosis that decreased distal left circumflex coronary artery perfusion pressure to approximately 40 mm Hg.

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Background: Transient reversible myocardial dysfunction has been documented after episodes of exercise-induced ischemia. This study was undertaken to determine whether the duration or intensity of exercise affects the severity of postischemic dysfunction in this setting.

Methods And Results: Ten dogs were instrumented with ultrasonic microcrystals for measurement of wall thickening, with circumflex coronary artery flow probes, and with hydraulic occluders.

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This study was carried out to test the hypothesis that alpha-adrenergic vasoconstriction limits coronary blood flow (CBF) during exercise in the chronically pressure overloaded, hypertrophied left ventricle. Studies were performed in dogs in which left ventricular hypertrophy had been produced by banding the ascending aorta at 9 wk of age. Left circumflex coronary artery blood flow and myocardial O2 consumption (MVO2) were examined at rest and during treadmill exercise during control conditions, after selective alpha 1-adrenergic blockade with prazosin, and after nonselective alpha-adrenergic blockade with phentolamine.

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This study was carried out to test the hypothesis that adrenergic coronary vasoconstriction limits blood flow to hypoperfused regions of myocardium during exercise. The vasoconstrictor influence of alpha-adrenergic receptor subtypes was assessed by use of selective adrenergic blocking agents. Dogs chronically instrumented with a circumflex coronary artery hydraulic occluder and an intra-arterial catheter underwent treadmill exercise in the presence of a coronary stenosis that decreased distal perfusion pressure to 40 mm Hg.

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This study was carried out to examine the effects of atrial natriuretic peptide on coronary collateral blood flow. Studies were performed in nine adult mongrel dogs 3.4 months after embolic occlusion of the left anterior descending coronary artery had been performed to stimulate collateral vessel growth.

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Although triple-drug immunosuppression with cyclosporine, prednisone, and azathioprine has reduced the incidence of acute graft rejection after cardiac transplant, its effect on the development of coronary artery disease is unknown. We have followed up 74 cardiac transplant recipients with yearly coronary angiograms. The probability of acute rejection was 10.

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