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Adam E Saltman

Publications and source records attributed to Adam E Saltman.

18 recordsLinked to original sources
PubMed2006

Inflammation effects on the electrical properties of atrial tissue and inducibility of postoperative atrial fibrillation.

BACKGROUND: Atrial fibrillation is the most common complication after cardiac surgery. Postoperative atrial fibrillation (PAF) has been shown to increase length of stay, morbidity, and mortality. Because the clinical behavior of PAF parallels that of inflammation following surgery, we investigated the effect of the inflammatory mediator arachidonic acid on the electrical behavior of normal atrial tissue in vitro and assessed the efficacy of the topical application of anti-inflammatory drugs at suppressing PAF in an animal model. METHODS: To study changes in electrical behavior from inflammation, the conduction properties of six normal canine right atrial appendages were quantified as a function of the direction of impulse propagation with and without 80 mum arachidonic acid. To study the effect of topical anti-inflammatory drugs, 24 adult mongrel dogs were prepared according to the model of sterile talc pericarditis. Nine dogs received talc alone (T), seven received talc combined with 600 mg ibuprofen (T + I), and eight received talc combined with 10 mg methylprednisolone (T + M). Three days following preparation, programmed electrical stimulation was performed to quantify conduction characteristics and to attempt the induction of atrial fibrillation (AF). RESULTS: In vitro, arachidonic acid produced an anisotropic and rapidly reversible 36.1 +/- 3.4% (P = 0.01) decrease in conduction velocity transverse to the long axis only. In vivo, both ibuprofen and methylprednisolone significantly reduced the incidence of sustained AF (from 56 to 0% T + I and 12% T + M, respectively, P = 0.02). No differences in conduction velocities or refractory periods were seen during sinus rhythm among the groups. CONCLUSIONS: Acute inflammation as mimicked by arachidonic acid slows conduction anisotropically, mainly transverse to the long axis of the atrial myocardial fibers. This may set the stage for reentry. Preventing inflammation in vivo by the topical application of anti-inflammatory drugs supports this hypothesis, suggesting a possible role for inflammation in the genesis of postoperative atrial fibrillation and shedding light on the mechanism underlying PAF.

Animals↗
PubMed2006

Invited commentary.

Explore the source record for details and available documents.

Atrial Fibrillation↗
PubMed2006

High resolution mechanical function in the intact porcine heart: mechanical effects of pacemaker location.

The necessity to quantify the mechanical function with high spatial resolution stemmed from the advancement of myocardial salvaging techniques. Since these therapies are localized interventions, a whole field technique with high spatial resolution was needed to differentiate the normal, diseased, and treated myocardium. We developed a phase correlation algorithm for measuring myocardial displacement at high spatial resolution and to determine the regional mechanical function in the intact heart. Porcine hearts were exposed and high contrast microparticles were placed on the myocardium. A pressure transducer, inserted into the left ventricle, synchronized the pressure (LVP) with image acquisition using a charge-coupled device camera. The deformation of the myocardium was measured with a resolution of 0.58+/-0.04 mm. Within the region of interest (ROI), regional stroke work (RSW), defined as the integral of LVP with respect to regional area, was determined on average at 21 locations with a resolution of 27.1+/-2.7 mm2. To alter regional mechanical function, the heart was paced at three different locations around the ROI. Independent of the pacemaker location, RSW decreased in the ROI. In addition, a gradient of increasing RSW in the outward direction radiating from the pacemaker was observed in all pacing protocols. These data demonstrated the ability to determine regional whole field mechanical function with high spatial resolution, and the significant alterations induced by electrical pacing.

Animals↗
PubMed2006

The use of extracellular matrix as an inductive scaffold for the partial replacement of functional myocardium.

Regenerative medicine approaches for the treatment of damaged or missing myocardial tissue include cell-based therapies, scaffold-based therapies, and/or the use of specific growth factors and cytokines. The present study evaluated the ability of extracellular matrix (ECM) derived from porcine urinary bladder to serve as an inductive scaffold for myocardial repair. ECM scaffolds have been shown to support constructive remodeling of other tissue types including the lower urinary tract, the dermis, the esophagus, and dura mater by mechanisms that include the recruitment of bone marrow-derived progenitor cells, angiogenesis, and the generation of bioactive molecules that result from degradation of the ECM. ECM derived from the urinary bladder matrix, identified as UBM, was configured as a single layer sheet and used as a biologic scaffold for a surgically created 2 cm2 full-thickness defect in the right ventricular free wall. Sixteen dogs were divided into two equal groups of eight each. The defect in one group was repaired with a UBM scaffold and the defect in the second group was repaired with a Dacron patch. Each group was divided into two equal subgroups (n = 4), one of which was sacrificed 15 min after surgical repair and the other of which was sacrificed after 8 weeks. Global right ventricular contractility was similar in all four subgroups groups at the time of sacrifice. However, 8 weeks after implantation the UBM-treated defect area showed significantly greater (p < 0.05) regional systolic contraction compared to the myocardial defects repaired with by Dacron (3.3 +/- 1.3% vs. -1.8 +/- 1.1%; respectively). Unlike the Dacron-repaired region, the UBM-repaired region showed an increase in systolic contraction over the 8-week implantation period (-4.2 +/- 1.7% at the time of implantation vs. 3.3 +/- 1.3% at 8 weeks). Histological analysis showed the expected fibrotic reaction surrounding the embedded Dacron material with no evidence for myocardial regeneration. Histologic examination of the UBM scaffold site showed cardiomyocytes accounting for approximately 30% of the remodeled tissue. The cardiomyocytes were arranged in an apparently randomly dispersed pattern throughout the entire tissue specimen and stained positive for alpha- sarcomeric actinin and Connexin 43. The thickness of the UBM graft site increased greatly from the time of implantation to the 8-week sacrifice time point when it was approximately the thickness of the normal right ventricular wall. Histologic examination suggested complete degradation of the originally implanted ECM scaffold and replacement by host tissues. We conclude that UBM facilitates a constructive remodeling of myocardial tissue when used as replacement scaffold for excisional defects.

Actinin↗
PubMed2005

Multichannel data acquisition system for mapping the electrical activity of the heart.

BACKGROUND: Details of the electrical conduction pattern of the heart are revealed to the electrophysiologist when multichannel data are used for activation mapping. Commercial electronic systems are available for simultaneous acquisition of many surface electrograms; however, the cost of these systems may be prohibitive and they can be mostly inflexible for adaptation to other research projects. Furthermore, the hardware and software design is often proprietary. In this article we describe the in-house design and implementation of a 320-multichannel acquisition system for animal electrophysiologic research. METHOD AND RESULTS: Several modules comprise this system. The multichannel data are first preprocessed by amplification, filtering, and analog multiplexing. An algorithm for automatic adjustment of signal gains is implemented to maximize the voltage resolution and minimize noise pickup. Signals are then digitized, and sequenced to order the multichannel data and to add markers required for analysis. The digital data are streamed to archival storage media. Additionally, the electrocardiogram (ECG), blood pressure, and stimulus channel signals are stored simultaneously. Selected signals are then displayed in real-time for measurement and analysis and as a check of the system integrity. Examples of multielectrode arrays and surface recordings are provided. Costs for building such a system are estimated. CONCLUSIONS: Multichannel data acquisition systems that are designed and constructed in-house have several advantages over turnkey commercial systems, including the potential for considerable cost savings, flexibility in acquiring data, and the ability to subsequently add additional components.

Analog-Digital Conversion↗
PubMed2004

Effects of ischemia on epicardial deformation in the passive rabbit heart.

BACKGROUND: Surgically induced ischemia in the arrested heart can result in changes in the mechanical properties of the myocardium. Regions of ischemia may be characterized based on the amount of epicardial deformation for a given load. Computer aided speckle interferometry (CASI), which tracks the movement of clusters of particles, is developed as a technique for measuring epicardial deformation, thereby determining the perfusion status of the passive heart. MATERIALS AND METHODS: Silicone carbide particles and retroreflective beads were dispersed randomly onto the epicardial surface of 11 isolated rabbit hearts to form speckle images. The hearts were arrested with hyperkalemic Krebs-Henseleit buffered solution. Each heart was then exposed to a series of intracavitary pressures, and at each pressure speckle images were acquired with a charge-coupled device (CCD) camera. Nine hearts were exposed to global ischemia, and two hearts were exposed to regional ischemia by occluding the second diagonal branch of the left anterior descending artery (LAD). The hearts were again loaded and the speckle images were acquired. CASI was used to determine the distribution of deformation field. RESULTS: CASI was able to determine displacements with a spatial resolution of about 50 microns. Global ischemia resulted in a significant increase in the maximum principle strain and the first invariant of the 2-D strain tensor. In the regionally ischemic heart, a large difference in deformation between the ischemic and perfused regions was clearly observed. CONCLUSION: Based on epicardial deformation, CASI is able to distinguish between perfused and ischemic myocardium, with a spatial resolution of 50 microns.

Animals↗
PubMed2004

The completely endoscopic treatment of atrial fibrillation: report on the first 14 patients with early results.

UNLABELLED: We report the early results of a new completely endoscopic technique for the treatment of atrial fibrillation (AF). METHODS: Fourteen patients underwent surgery solely for the treatment of AF. The thoracoscopic technique delivered microwave energy to the epicardial surface of the beating heart. Access was obtained through 3 right-sided and 3 left-sided thoracic ports. The AFx/Guidant Flex-10 catheter was employed to produce a box lesion around the pulmonary veins along with additional right- and left-sided lesions. The left atrial appendage was amputated. RESULTS: Ten patients had paroxysmal fibrillation, 1 had persistent fibrillation, and 3 were in permanent AF. Mean age of the group was 60 years, and their mean duration of AF was 74 months. Half had undergone unsuccessful attempts at chemical and/or electrical cardioversion. There were no deaths. Two patients required conversion to open procedure to control bleeding from the left atrial appendage. Average procedure time was 221 minutes, with the last 2 procedures taking less than 2 hours. Median length of hospital stay was 6 days, with 7 patients staying less than 3 days. Seventy-one percent of patients were in sinus rhythm at discharge, 100% at 6 months follow-up, and 67% at 12 months. CONCLUSION: Totally endoscopic microwave ablation of atrial fibrillation appears to be safe and truly minimally invasive. It is associated with a short length of stay, short procedure time, and acceptable rhythm results. This procedure has the potential to greatly expand the indications for surgery in patients suffering from AF and deserves longer-term investigation.

Adult↗
PubMed2003

Both metabolic inhibition and mitochondrial K(ATP) channel opening are myoprotective and initiate a compensatory sarcolemmal outward membrane current.

BACKGROUND: Blockade of oxidative phosphorylation may activate ATP sensitive mitochondrial potassium (mitoK(ATP)) channels. We examined whether both metabolic inhibition and mitoK(ATP) channel openers protect both the whole organ and isolated cells from ischemia. METHODS AND RESULTS: Using a Langendorff preparation, one group of isolated rabbit hearts were exposed to ischemic preconditioning (IPC) via 2 episodes of flow interruption. The second group of hearts was preconditioned with 2 episodes of either the metabolic inhibitor, sodium cyanide (NaCN), or the mitoK(ATP) channel opener, diazoxide. The third group of hearts was exposed to the mitoK(ATP) channel inhibitor, 5-hydroxydecanoic acid (5-HD) prior to preconditioning with NaCN, diazoxide or IPC. Controls had no drug infused. Then, ischemia was induced in all hearts by left anterior descending coronary artery occlusion and infarct size was determined. Compared with controls (40+/-3%), infarct size was significantly reduced in hearts preconditioned with NaCN, diazoxide or IPC (18+/-3%, 26+/-3%, 21+/-2%, respectively; P<0.05 versus control). These reductions were reversed by 5-HD (36+/-3%, 33+/-2%, 37+/-2%; NaCN, diazoxide, IPC, respectively). Secondly, whole cell patch clamped isolated guinea pig ventricular myocytes were preconditioned with 2 episodes of either NaCN or diazoxide followed by Tyrodes perfusion with membrane potential set to -70 mV. Control cells were exposed to Tyrodes solution. All cells were then clamped to -20 mV and exposed to NaCN, which caused induction of an outward potassium current. Compared with controls, the average time to induction of the outward current was significantly reduced in cells preconditioned with either brief application of NaCN (11.6+/-1.8 versus 5.1+/-1.0 minutes, control versus NaCN, P<0.05) or diazoxide (5.5+/-1.4 versus 2.0+/-0.8 minutes, control versus diazoxide, P<0.05). CONCLUSIONS: Preconditioning protects the heart through mitoK(ATP). This protection also alters a surface membrane current, which may be important in myocardial protection.

Animals↗
PubMed2003

Myocardial recovery from ischemia is impaired in CD36-null mice and restored by myocyte CD36 expression or medium-chain fatty acids.

Long-chain fatty acid uptake, which provides a large part of myocardial energy, is impaired in human and murine hearts deficient in the membrane fatty acid translocase, FAT/CD36. We examined myocardial function in CD36-null mice using the working heart. Fatty acid oxidation and stores of glycogen, triglycerides, and ATP were reduced in CD36-deficient hearts and were restored to WT levels by rescue of myocyte CD36. Under normal perfusion conditions, CD36-null hearts had similar cardiac outputs and end-diastolic pressures as WT or transgenic hearts. After 6 min of ischemia, cardiac output decreased by 41% and end diastolic pressure tripled for CD36-null hearts, with no significant changes in WT or transgenic hearts. Null hearts also failed more frequently after ischemia as compared with WT or transgenics. To dissect out contribution of fatty acid uptake, a perfusate-lacking fatty acids was used. This decreased cardiac output after ischemia by 30% in WT hearts as compared with 50% for CD36-deficient hearts. End diastolic pressure, a negative index of myocardial performance, increased after ischemia in all heart types. Addition to the perfusate of a medium-chain fatty acid (caprylic acid) that does not require CD36 for uptake alleviated poor ischemic tolerance of CD36-null hearts. In summary, recovery from ischemia is compromised in CD36-deficient hearts and can be restored by CD36 rescue or by supplying medium-chain fatty acids. It would be important to determine whether the findings apply to the human situation where polymorphisms of the CD36 gene are relatively common.

Animals↗
PubMed2003

Modeling stroke risk after coronary artery bypass and combined coronary artery bypass and carotid endarterectomy.

BACKGROUND AND PURPOSE: The goals of this study were to compare the ability of statewide and institutional models of stroke risk after coronary artery bypass (CAB) to predict institution-specific results and to examine the potential additive stroke risk of combined CAB and carotid endarterectomy (CEA) with these predictive models. METHODS: An institution-specific model of stroke risk after CAB was developed from 1975 consecutive patients who underwent nonemergent CAB from 1994 to 1999 in whom severe carotid stenosis was excluded by preoperative duplex screening. Variables recorded in the New York State Cardiac Surgery Program database were analyzed. This model (model I) was compared with a published model (model II) derived from analysis of the same variables using New York statewide data from 1995. Predicted and observed stroke risks were compared. These formulas were applied to 154 consecutive combined CAB/CEA patients operated on between 1994 and 1999 to determine the predicted stroke risk from CAB alone and thereby deduce the maximal added risk imputed to CEA. RESULTS: Risk factors common to both models included age, peripheral vascular disease, cardiopulmonary bypass time, and calcified aorta. Additional risk factors in model I also included left ventricular hypertrophy and hypertension. Risk factors exclusive to model II included diabetes, renal failure, smoking, and prior cerebrovascular disease. Our observed stroke rate for isolated CAB was 1.7% compared with a rate predicted with model II (statewide data) of 1.56%. The observed stroke rate for combined CEA/CAB was 3.9%. When the Stony Brook model (model I) based on patients without carotid stenosis was used, the predicted stroke rate was 2.8%. When the statewide model (model II), which included some patients with extracranial vascular disease, was used, the predicted stroke rate was 3.4%. The differences between observed and predicted stroke rates were not statistically significant. CONCLUSIONS: Estimation of stroke risk after CAB was similar whether statewide data or institution-specific data were used. The statewide model was applicable to institution-specific data collected over several years. Common risk factors included age, aortic calcification, and peripheral vascular disease. The observed differences in the predicted stroke rates between models I and II may be due to the fact that carotid stenosis was specifically excluded by duplex ultrasound from the patient population used to develop model I. Modeling stroke risk after CAB is possible. When these models were applied to patients undergoing combined CAB/CEA, no additional stroke risk could be ascribed to the addition of CEA. Such models may be used to identify groups at increased risk for stroke after both CAB and combined CAB/CEA. The ultimate place for CEA in patients undergoing CAB will be defined by prospective randomized trials.

Adult↗
PubMed2003

A completely endoscopic approach to microwave ablation for atrial fibrillation.

BACKGROUND: Surgical therapy for atrial fibrillation is extremely effective but not widely applied. Minimally invasive methods may be more attractive. We report a case of complete pulmonary vein isolation performed entirely through a thoracoscopic approach. METHODS: A 74-year-old woman with paroxysmal atrial fibrillation underwent a microwave ablation procedure using 3 access ports in the right pleural space and 3 access ports through the left pleural space. RESULTS: After the 3-hour procedure the patient was extubated in the operating room and discharged home in sinus rhythm on the second postoperative day. CONCLUSIONS: Endoscopic pulmonary vein isolation is a safe and effective procedure that may be applied to a wide variety of patients.

Aged↗
PubMed2002

Gap junction uncoupling protects the heart against ischemia.

BACKGROUND: Many stimuli can successfully protect the heart against ischemia. We investigated whether gap junction uncoupling before ischemia was myoprotective. We also studied the function of the adenosine triphosphate-dependent potassium channel, which has been implicated in the mechanism of pharmacologic preconditioning, with respect to gap junction physiology. METHODS: Twenty-eight rabbit hearts were placed on a Langendorff perfusion apparatus. Five were given a 5-minute infusion of 1 mmol/L heptanol (a gap junction uncoupler), 5 were given 10 micromol/L 2,3-butanedione monoxime (an electromechanical uncoupler), and 6 were given no drug. The left anterior descending coronary artery was then occluded for 1 hour and reperfused for 2 hours. Six hearts received 10 micromol/L glybenclamide before heptanol to evaluate the role of the adenosine triphosphate-dependent potassium channel. Six hearts underwent ischemic preconditioning with 2 cycles of 5 minutes of global ischemia and reperfusion. Action-potential duration of the ischemic zone, left ventricular developed pressure, and coronary flow were measured continuously. Infarct size was determined at the end of reperfusion. RESULTS: Heptanol significantly reduced infarct size (from 46% +/- 2% to 22% +/- 5%, P <.01), an effect that was not prevented by glybenclamide. Butanedione monoxime decreased developed pressure but did not significantly reduce infarct size (46% +/- 5% vs 46% +/- 2%, P = not significant). There were no differences among groups with regard to developed pressure or action-potential duration. CONCLUSION: Directly blocking gap junctions preconditions the heart. This protection is not a direct result of a decrease in developed pressure before a prolonged ischemic period nor is it achieved through a mechanism involving the adenosine triphosphate-dependent potassium channel.

Action Potentials↗
PubMedDate not supplied

Thrombogenic performance of a st. Jude bileaflet mechanical heart valve in a sheep model.

The sheep model is preferred for chronic evaluation of prosthetic heart valves, surgical techniques, and endocardiographic studies. A bileaflet mechanical heart valve (MHV) was implanted into a sheep model to study its in vivo performance and to evaluate the thrombogenic potential of the valve. Transesophageal echocardiography and transcranial Doppler ultrasonography measurements were conducted before and after the valve implantation. Platelet activity state (PAS) assay measurements were also conducted before and after the implantation surgery. After sheep euthanasia, the MHV was explanted and scanning electron microscopy (SEM) was performed on the explanted valve to examine changes to the MHV surface. Tissue blocks were taken from the sheep brain, left ventricle, aorta, spleen, and lung lobes for histological examination. Our results indicated that after the MHV implantation, more embolic signals were detected in the sheep carotid artery, increasing monotonously as a function of implantation time. Echocardiographic parameters including blood aortic velocity, transvalvular pressure gradient, and velocity time integral increased. PAS increased significantly after valve implantation. SEM pictures demonstrated calcium and phosphate deposition on the valve surfaces. Histological examination demonstrated hemorrhage in the lung tissue, pulmonary thrombosis, and osteogenesis in heart tissue.

Animals↗