Impact of complications on outcomes following aortic and mitral valve replacements in the United States.

AIM: Heart valve replacement surgeries account for 20% of all cardiac procedures. In-hospital mortality rates are approximately 6% for aortic valve replacements and 10% for mitral valve replacements. The objectives of the study are to provide nationally representative estimates of complications following aortic and mitral valve replacements and to quantify the impact of different types of complications on in-hospital outcomes. METHODS: The Nationwide Inpatient Sample was analyzed for years 2000-2003. The effect of complications on in-hospital mortality, length of stay (LOS), and hospital charges were examined using bivariate and multivariable logistic and linear regression analyses. The confounding effects of age, sex, primary diagnosis, type of valve replacement, type of admission, comorbid conditions, and hospital characteristics were adjusted. RESULTS: A total of 43,909 patients underwent aortic valve replacement as the primary procedure during the study period and 16,516 patients underwent mitral valve replacement. Complications occurred in 35.2% of those undergoing aortic valve replacements and in 36.4% of those undergoing mitral valve replacements. Almost half of these are cardiac complications and a quarter involve hemorrhage/hematoma/seroma. Complications were significantly associated with in-hospital mortality, LOS, and hospital charges even after adjusting for patient and hospital characteristics. CONCLUSION: Complications are prevalent and exert a considerable influence on outcomes following aortic and mitral valve replacements. Quality initiatives should focus on minimizing complications and improving processes of care that would enable complications to be better resolved if they occur.

Effect of sleep position on apnea and bradycardia in high-risk infants.

OBJECTIVE: The purpose of this investigation was to investigate, in high-risk infants, the occurrence of abnormalities in documented monitor downloads during the side versus prone position. STUDY DESIGN: Forty infants admitted to the A. I. duPont Hospital for Children with diagnoses associated with sudden infant death syndrome were included in this investigation. During an overnight hospitalization, infants were placed on home apnea monitors, with computer memory to capture alarms for apnea > 20 seconds, age-defined bradycardia, and tachycardia. Infants were studied for 12 hours. Each infant was assigned to 6 hours of prone and side during the 12-hour period, with order of position randomly assigned by random number generation. Differences between the two positions in alarm frequency and significant events, as determined by a blinded interpreting physician were analyzed by Fisher exact test, with p < 0.05. Power analysis necessitated 20 patients in each group, with beta error of 0.2. RESULTS: Eleven episodes of apnea occurred in the prone position, and 16 in the side position (p = NS). The mean numbers of apnea events per tracing in the prone position was 0.27 +/- 0.84 and 0.39 +/- 1.1 in the side position (p = 0.58). The mean number of bradycardia events per tracing in the prone position was 0.44 +/- 1.45 and 0.49 +/- 1.94 in the side position (p = 0.9). CONCLUSION: Clinicians need to be cautious when recommending the side or prone position in this group of high-risk infants. The results in this investigation provide support for the Back to Sleep Campaign recommendations to be applied, not only to healthy term infants, but higher risk infants as well. Studies of the high-risk infant in the supine position are warranted.

Infant sleep position. Nursing practice and knowledge.

PURPOSE: (1) to examine the extent to which maternal/child health nurses caring for children accept the American Academy of Pediatrics recommendations on infant sleep position, (2) to determine if nurses are practicing according to the AAP recommendations, and (3) to determine the type of bedding utilized in the two institutions for infants. METHODS: Descriptive survey using 103 nurses in 2 institutions, and an observational assessment of nurses' practice. RESULTS: Findings revealed that 97% of the nursing staff were aware of the AAP recommendations, although only 67% agreed with the recommendations. The observational component of the investigation evaluated the sleep position during hospitalization of 206 infants < 6 months old on both the pediatric and maternity units of the two institutions. Fifty-five percent of the infants were observed to be in the side-lying position, 29% in the recommended supine (back) position, and 16% in the prone (abdomen) sleeping position. The recommended firm bedding was observed with 63% of the infants, whereas the remainder of the infants were observed to be on foam mattresses, extra blankets, or gel packs. CLINICAL IMPLICATIONS: Because side sleeping position was observed in the majority of infants, and one-third of the nurses queried disagreed with the AAP recommendations, education of nurses about Sudden Infant Death Syndrome prevention through "Back to Sleep" is still necessary.

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.

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.

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.

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.

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.

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.

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.

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.

Depletion of myocardial high energy phosphates by induction of ventricular fibrillation prior to cardioplegic arrest.

The effects of a short period of ventricular fibrillation on myocardial high energy phosphates were assessed in two groups of rats. Group 1 underwent hypothermic crystalloid cardioplegia infusion and aortic cross-clamping. In Group 2, cardioplegia and cross-clamping were preceded by ten seconds of induced ventricular fibrillation. In rat hearts that had undergone ventricular fibrillation, adenosine triphosphate levels averaged only 70% (p less than .0001) and creatine phosphate levels averaged only 60% (p less than .0005) of levels measured following standard cardioplegic arrest without ventricular fibrillation. These findings are of potential importance in both routine cardiac surgical procedures and in organ procurement.

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).

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.

Technique for repair of left ventricular free wall rupture.

A case of postinfarction left ventricular free wall rupture is reported. The technique used to repair the rupture is described, along with a modification of the technique.

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).

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.

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)