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Biomedical subjects

J M Levett

Publications and source records attributed to J M Levett.

At least 19 recordsLinked to original sources
PubMed1999

Measuring for improvement: from Toyota to thoracic surgery.

BACKGROUND: Measuring quality has become a high priority in the era of managed care. Nevertheless, it can be counterproductive to use the same methods for measuring improvement in surgical procedures and processes as we use for measurement in basic research. Techniques of statistical process control have been used for many years to measure process improvement in industry and are now being applied to health care. METHODS: Examples of using statistical process control charts to monitor coronary artery bypass grafting mortality, intensive care unit admission time, and length of stay are reviewed. RESULTS: The major advantage of using control chart methodology is that it allows one to determine whether the process being evaluated is in fact stable and to detect when significant or special cause variation occurs. CONCLUSIONS: Summary statistics currently provided to purchasers of care and regulatory agencies do not ensure that the processes being evaluated are stable. We need to look at data over time with statistically validated methods such as control charts to better monitor our processes of care and thereby provide accurate statistics.

Coronary Artery Bypass↗
PubMed1998

Bradycardia induced by intravascular versus direct stimulation of the vagus nerve.

BACKGROUND: Electrical stimulation of the parasympathetic nervous system results in slowing of the heart. We sought to determine whether cardiac vagal efferent axons can be stimulated adequately to induce bradycardia without disturbing the integrity of the thorax. METHODS: Cardiodepressor effects elicited by direct stimulation of a vagus nerve in anesthetized dogs and pigs were compared with those generated when the same nerve was stimulated indirectly through bipolar electrodes placed in the adjacent superior vena cava. RESULTS: The heart rate of dogs decreased by about 80% when electrical stimuli were delivered to the right thoracic vagus at the level of the thoracic outlet through bipolar electrodes placed either in the adjacent superior vena cava (intravascular method) or directly on the nerve (direct method). Maximal responses were achieved with 10-V, 5-ms, and 20-Hz stimuli. In anesthetized pigs, similar bradycardia occurred when the right cervical vagus or the right cranial thoracic vagus was stimulated either directly or indirectly through the intravascular method. Atrial dysrhythmias occurred when the stimulating electrodes were placed by either method within 1 cm of the right atrium in both animal models. CONCLUSIONS: Controlled bradycardia can be induced during operation without the risk of generating cardiac dysrhythmias using electrical stimuli (10 V, 5 ms, and 10 to 20 Hz) delivered to the right cervical vagus nerve or the right cranial thoracic vagus nerve through adjacent intravascular electrodes.

Animals↗
PubMed1996

Cardiac augmentation can be maintained by continuous exposure of intrinsic cardiac neurons to a beta-adrenergic agonist or angiotensin II.

The purpose of this work was to determine whether constant increases in cardiac rate and force can be induced by continuous exposure (20 min) of intrinsic cardiac neurons to pharmacological agents which activate such neurons. Intrinsic cardiac neurons within the ventral right atrial ganglionated plexus were activated by constant infusions of dobutamine or angiotensin II (100 microM/min for 10 min followed by 200 microM/min for 10 min) via their local arterial blood supply in 12 artificially ventilated, open chest anesthetized dogs while monitoring heart rate and indices of regional cardiac contractility. The results were as follows: (1) Dobutamine (100 microM/min for 10 min) enhanced intrinsic cardiac neuronal activity by 195% at first, neuronal activity declining thereafter to +79% of control values in the continued presence of this agonist. When the dose of dobutamine was doubled (200 microM/min for 10 min) neuronal activity increased +179% above control values and remained elevated, as did heart rate as well as right and left ventricular contractility. (2) Angiotensin II (100 microM/min) increased neuronal activity at first, with neuronal activity decreasing gradually thereafter such that after 5 min of exposure activity reached control values. Neuronal activity did not increase further when neurons were subsequently exposed to a higher dose of angiotensin II (200 microM/min). Heart rate and ventricular contractility were increased initially more by angiotensin II than by dobutamine. However, cardiac indices fell thereafter concomitant with reductions in neuronal activity as the exposure to angiotensin II continued. Thus although cardiac rate and force initially were increased more by angiotensin II than by dobutamine, similar augmentation of cardiac indices was achieved by sustained exposure of a population of intrinsic cardiac neurons to either agent. In conclusion, heart rate and ventricular contractility can be enhanced for relatively prolonged periods of time by continuous exposure of a population of intrinsic cardiac neurons to a beta-adrenoceptor agonist or angiotensin II, with the beta-adrenoceptor agonist inducing more consistent cardiac augmentation than angiotensin II.

Angiotensin II↗
PubMed1995

Leiomyosarcoma of the superior vena cava and azygos vein.

A 40-year-old woman presented with facial swelling and pressure sensation of the ears and sinuses. Chest roentgenography revealed a right paratracheal mass, which was confirmed by a venogram, and transjugular biopsy showed low-grade leiomyosarcoma. The superior vena cava was resected and reconstructed using a spiral vein graft. Pathologic evaluation revealed a low-grade leiomyosarcoma arising from both the superior vena cava and the azygos vein with clear margins.

Adult↗
PubMed1994

Effects of beta-blockade on neurohumoral responses and neurochemical markers in pacing-induced heart failure.

We investigated neurohumoral profiles and transmitter and neuroenzyme markers of cardiac autonomic innervation in control (unpaced) dogs and three groups of dogs with pacing-induced heart failure (paced, paced + beta-adrenergic blockade, and paced + cardiac denervation). Left ventricular ejection fraction decreased significantly and to a comparable extent in all paced groups. Pacing increased plasma norepinephrine (NE); increases in NE were not attenuated but instead tended to be exaggerated by treatment with propranolol or cardiac denervation. Atrial hypertrophy occurred in all paced groups compared with the control group. However, atrial and right ventricular hypertrophy were not as pronounced in the paced plus cardiac denervation group as in the paced and paced plus propranolol groups. Pacing also depleted neuropeptide Y and NE from all heart chambers; propranolol treatment did not modify these local tissue changes. Pacing caused selective depletion of neuroenzymes predominantly in the left ventricle; again, propranolol did little to modify these changes. In this study of paced animals with experimentally maintained cardiac dysfunction, failure to modify noradrenergic responses with intrapericardial cardiac denervation suggests that noncardiac sources contribute predominantly to high plasma NE. Failure to modify neurohumoral, neuropeptide, and neuroenzyme responses with beta-antagonist suggests this treatment has little practical direct influence on sympathetic vasomotor activity or neuronal function in heart failure.

Animals↗
PubMed1993

Cardiac geometry and mass changes associated with pacing-induced cardiomyopathy in the dog.

We evaluated the effects of chronic rapid pacing (240 beats/min) on ventricular geometry and function and on cardiac mass in a canine model. Forty dogs were studied by two-dimensional echocardiography before and after 45 days of pacing. Compared with sham-operated control animals, the paced animals had significant increases in end-diastolic and end-systolic volume and a decrease in ejection fraction. The increase in ventricular volume was primarily the result of dilation of the short axis of the ventricular lumen, without significant changes in the long-axis dimension. Paced animals had biatrial hypertrophy but no change in ventricular or total cardiac mass.

Animals↗
PubMed1991

Beta receptor derangement in postinfarction left ventricular perianeurysm tissue.

The purpose of this study was to evaluate alterations in adrenergic receptor density in patients with post-infarction left ventricular aneurysms. Resected specimens from 4 patients with left ventricular aneurysm were studied using standard techniques to evaluate beta receptors, alpha receptors, and muscarinic receptors in the border zone, perianeurysm tissue, and infarcted aneurysm tissue. Only the beta receptors demonstrated up-regulation around the aneurysm (p = 0.0003). This indicates that infarction with aneurysm formation can alter adrenergic receptor density, which may affect cellular response and predispose to arrhythmogenesis.

Aged↗
PubMed1991

Determination of infundibular innervation and amine receptor content in cyanotic and acyanotic myocardium: relation to clinical events in tetralogy of Fallot.

Right ventricular myocardium was assessed for cholinergic and adrenergic innervation, as well as alpha-adrenergic, beta-adrenergic, and muscarinic receptors, in 18 cyanotic patients with tetralogy of Fallot (TOF) and four acyanotic control patients with ventricular septal defect, each of whom underwent a cardiac repair from June through December 1987. Neurons containing acetylcholine (ACH), neuron-specific enolase (NSE), S-100 protein, neuropeptide-Y (NPY), dopamine-beta-hydroxylase (DBH), and calcitonin gene-related polypeptide (CGRP) were detected surrounding arterioles and myocytes in all specimens. NSE and S-100 immunoreactivities were also identified in the cytoplasm of TOF cardiocytes, possibly indicating a neuroendocrine origin of these cells. Cardiocyte size was increased in TOF (p = 0.05). Acetylcholine (cholinergic) (p = 0.04) and CGRP (cholinergic) positive neurons (p = 0.07) were decreased in the TOF as compared to controls. Adrenergic fiber content (p = 0.15) and beta receptors (p = 0.21) were similar in both groups. There was an increase in muscarinic receptors in the controls (p = 0.002), and a marked increase in alpha receptors in TOF (p = 0.019). There were no intragroup differences in the TOF patients according to degree of cyanosis. In conclusion, there were important differences in neuronal and amine receptor content between TOF and control patients. Increased alpha receptors in TOF could account for differences in clinical and hemodynamic events.

Acetylcholine↗
PubMed1988

Preservation of myocardial high energy phosphates during cardioplegic arrest with nifedipine.

Nifedipine used both as an additive to cardioplegia solution (CPS) and as pretreatment prior to arrest was studied in a rat model to determine its effect upon ischemic ventricular electromechanical work during arrest and upon high energy phosphate levels. Fifty-one normothermic rats were studied in vivo with infusion of hypothermic (4 degrees C) CPS into the cross-clamped aortic root according to one of the following eight protocols: Group 1, baseline beating hearts; Group 2, CPS containing 15 mEq potassium chloride/liter (KCl/liter); Group 3, CPS containing 30 mEq KCl/liter; Group 4, CPS containing 15 mEq KCl/liter combined with stimulation of the vagus nerve; Groups 5 and 6, CPS with 15 mEq KCl/liter and containing 250 or 500 micrograms of nifedipine per liter; Groups 7 and 8, pretreatment with 100 or 200 micrograms nifedipine/kg given as an intravenous bolus 15 min prior to infusion of CPS with 15 mEq KCl/liter. Time to arrest, number of ischemic ventricular contractions after aortic cross clamping, and ATP and creatine phosphate (CP) levels were recorded. All nifedipine groups arrested more quickly and with fewer ventricular contractions and had ATP and CP levels higher than those of Group 2 (P less than 0.05). There were no differences between the nifedipine groups and Group 3 except that Group 8 (200 micrograms/kg pretreatment) resulted in higher levels of CP than Groups 3, 5, and 6 (P less than 0.05 for all groups). When all groups were combined, time to arrest correlated negatively with ATP (r = -0.863, P less than 0.01) and CP (r = -0.824, P less than 0.01) levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1988

Total denervation stabilizes the infarcted canine myocardium.

The effect of total cardiac denervation upon the electrophysiology of infarcted canine myocardium was studied at both organ and cellular levels. Fifteen dogs underwent coronary ligation to produce an infarct at the apex of the left ventricle (Group 1, n = 15). A second group of dogs (Group 2, n = 14) underwent total intrapericardial denervation with subsequent infarct 15.0 +/- 0.3 (mean +/- SEM) days later. All animals had bipolar epicardial pacing electrodes placed on the right ventricle and the infarct border zone of the left ventricle. Strength-interval curves were performed one or two times per week in conscious animals to assess cardiac excitability. Animals were sacrificed 18.1 +/- 0.5 days following infarct and histologic studies were performed to determine infarct size. Standard microelectrode techniques were also utilized to determine cellular parameters. Denervation was found to lengthen the absolute refractory period and prevent increases in the relative refractory period which were observed in innervated animals following infarct. Isolated tissue data including measurements of maximal rate of depolarization, mean diastolic potential, action potential amplitude, action potential duration at 50% repolarization, and effective refractory period indicated that denervation protects against cellular deterioration and improves electrophysiologic cellular characteristics. These studies suggest that under conditions of myocardial ischemia, denervation produces an electrically more stable myocardium which is less excitable and probably less vulnerable to lethal arrhythmias.

Action Potentials↗
PubMed1988

A canine model to assess the electrical stability of the transplanted heart.

The electrophysiological stability of the transplanted heart under conditions of myocardial ischemia is largely unknown. This problem was studied using a canine model of total cardiac denervation as a substitute for transplantation. Group 1 (N = 3) served as control with placement of ventricular pacing wires only. Group 2 (N = 3) underwent total cardiac denervation with placement of ventricular wires. Group 3 (N = 8) underwent total cardiac denervation with subsequent ligation of the left anterior descending coronary artery and collaterals to the apex. Group 4 (N = 9) underwent coronary artery ligation only. Chronic electrophysiological studies were conducted in all groups in the conscious state. Electrophysiological variables were determined from continuous Holter monitoring of the ECG, determination of strength-interval curves, and assessment of the inducibility of ventricular tachycardia by premature programmed pacing. In general, the denervated, infarcted group (Group 3) consistently demonstrated a greater level of electrical stability than the infarcted animals with normal innervation (Group 4).

Animals↗
PubMed1988

Pacemaker system failure and other events in children with surgically induced heart block.

Of 1,193 consecutive pediatric (less than 18 years) patients undergoing intracardiac repair from 1975 to 1984, 38 (3.2%) developed surgically induced complete heart block and were treated by permanent pacemaker implantation. Anomalies included complete atrioventricular septal defect = 9 (24%), simple ventricular septal defect = 9 (24%), atrioventricular discordant connection = 8 (212), tetralogy of Fallot = 7 (182), and other complex anomalies = 5 (13%). There were no hospital deaths. follow-up was 100% complete. There were six late deaths = 16%. Actuarial survival was 79 + 9% at 10 years. None of the late deaths were related to disturbance of cardiac rhythm or pacemaker system failure. Twelve patients (32%), required 27 reoperations for various types of pacemaker system failure. Indications for reoperation included: lead failure (44%). Pulse generator failure (44%), and wound sepsis (12%). Actuarial freedom from any pacemaker related reoperation was 50 + 16% at 48 months and 25 + 15% at 96 months. Only first reoperation was found to be an incremental risk factor for subsequent reoperation (p = 0.03). Surgical heart block has been neutralized as a risk factor for hospital death after repair of congenital cardiac defects. The risk of the development of surgical heart block now approaches zero, as indicated by a decreased incidence (1 of 401 = 0.25%) in our institution from 1985 to 1987, as compared to the era 1975 to 1984 (p = 0.001).

Actuarial Analysis↗
PubMed1988

Safety of the right atrial approach for combined mitral and tricuspid valve procedures.

Patients undergoing operation for combined mitral and tricuspid valvular disease may have the repair performed through the right atrium and the interatrial septum. Although the transseptal method is an established procedure, recent reports have stressed the disadvantages of this operation and underscored the risk of the development of complete atrioventricular dissociation with this technique. A review of our results with this approach confirms the efficacy and safety of this method. The surgical protocols used are described.

Female↗
PubMed1987

Comparative studies of prosthetic materials in the left atrium of the dog.

To assess the healing process of various intracardiac prosthetic graft materials, we inserted autologous left atrium (control), autologous pericardium (AP), bovine pericardium (BP), polytetrafluoroethylene (PTEE) and woven Dacron (WD) patches into excised defects in the left atrial wall of 15 dogs. Two patches were implanted into each heart utilizing six patches for each material. Three months after graft placement, histological examination revealed chronic inflammation and fibrosis for all materials. Dense connective tissue surrounded the grafts in which fibrosis was most prominent. Cartilage formation occurred in 11 grafts: 5 BP, 4 PTFE, 1 control and 1 AP site. This change was not evident with WD. The extent of cartilage formation was greatest in BP. Bone formation occurred in 3 BP sites. 2 PTFE and 1 control site. Quantitative calcium concentrations were similar for all of the grafts without bone formation. Calcium concentrations at sites with bone formation averaged 15.13 mg/g +/- 6.39 mg/g compared to 0.939 +/- 0.419 for sites without bone formation (p less than 0.0001). We conclude that while inflammation, fibrosis and connective tissue thickening occur with healing of all graft materials, cartilage and bone formation differ with respect to the material employed.

Animals↗
PubMed1987

Effects of dimethyl sulfoxide on systemic and cerebral hemodynamic variables in the ischemic canine myocardium.

The effects of dimethyl sulfoxide (DMSO) infusion on cerebral blood flow (CBF) and systemic hemodynamics were studied in a canine model of myocardial ischemia. Immediately after ligation, cardiac output dropped from 2.09 +/- 0.11 (SEM) in the control group and 1.79 +/- 0.13 in the DMSO group to 1.07 +/- 0.21 and 1.0 +/- 0.08 L/min, respectively; there were no significant differences for 2 h. By the third hour and thereafter, the DMSO group had a significantly (p less than .05) higher cardiac output (1.65 +/- 0.08 L/min) than the control group (1.15 +/- 0.10 L/min). The cardiac output increase at 3 h was accompanied by significantly (p less than .05) lower systemic vascular resistance (SVR) in the DMSO group (5315 +/- 248 dyne X sec/cm5) as compared to the control group (7892 +/- 442 dyne X sec/cm5). There were no significant differences in heart rate, mean arterial pressure, pulmonary artery wedge pressure, or cerebral or pulmonary resistances in the control as compared to the DMSO group. Higher CBF values were noted at one hour and thereafter in the DMSO as compared to the control group (p less than .05). Low-dose DMSO given as an iv bolus improved cardiac output and CBF and lowered SVR in this canine model of experimental myocardial ischemia.

Animals↗
PubMed1986

Comparison of prosthetic graft materials as intracardiac right atrial patches.

An experimental animal model was developed to study the fate of prosthetic graft materials within the heart. Autologous pericardium, bovine pericardium, polytetrafluoroethylene, woven Dacron, and autologous right atrium (control) patches were implanted into the wall at three sites on the right atrium in each of 10 dogs (six patches for each graft material). The atria were harvested 90-100 days later and histologic examination and quantitation of calcium were performed. Chronic inflammation and fibrosis were found in 29 of 30 grafts. Cartilage formed in 26 of 30 sites and was found both in the center and around the edges of the grafts. In addition to cartilage, bone including marrow elements formed in the two autologous materials at 4 of the 12 sites and in 1 of the Dacron graft sites. Calcium content was greater in the control and the bovine pericardial grafts than in the other graft materials (P = NS). The incidence and degree of inflammation, fibrosis, calcification and cartilage, and bone formation were similar in all materials. We conclude that the healing process of these intracardiac graft materials is a generalized phenomenon independent of the inherent properties of a specific graft material.

Animals↗
PubMed1986

Preservation of myocardial high-energy phosphates with vagal stimulation and hypothermic cardioplegia.

We examined three methods of inducing hypothermic cardioplegic arrest and related each to preservation of high-energy phosphates. Levels of adenosine triphosphate (ATP) and creatine phosphate (CP) in baseline rat hearts were compared with levels found after vagal stimulation combined with cardioplegia containing 15 mEq of potassium chloride (KCl) per liter, cardioplegia with 15 mEq of KCl per liter alone, and cardioplegia with 30 mEq of KCl per liter alone. Vagal stimulation produced complete electromechanical arrest in a shorter time than either 15 or 30 mEq of KCl alone (p less than 0.001 for both cardioplegic solutions compared with vagal stimulation), with fewer ventricular beats after ischemia than cardioplegic solution containing 15 or 30 mEq of KCl (p less than 0.001 and less than 0.01, respectively). Levels of ATP and CP, although less than baseline levels (p less than 0.01 and less than 0.001, respectively), were greater with vagal stimulation than with either 15 or 30 mEq of KCl (p less than 0.001 and less than 0.05, respectively, for ATP and p less than 0.001 for both CP levels). Furthermore, when all groups were combined, ATP and CP levels were found to correlate negatively with arrest time (r = -0.851 and -0.788, respectively; both r values significant at p less than 0.01) and with the number of ventricular beats after ischemia (r = -0.927 and -0.851, respectively; both r values significant at p less than 0.01). We conclude that electromechanical work quantified as time to arrest after aortic cross-clamping and as number of ventricular beats after ischemia correlates negatively with ATP and CP levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗