Comparison of outcomes of operative versus non-operative treatment of acetabular fractures in the elderly and severely comorbid patient.

BACKGROUND: Acetabular fractures in the elderly and severely comorbid patient can be associated with high morbidity and mortality; however, differences in outcomes of acute ORIF versus non-operative care of acetabular fractures in a subgroup of elderly (>75 years) and/or severely comorbid younger patients (>65) remain unclear. PATIENTS AND METHODS: A retrospective review of 243 patients who sustained an acetabular fracture between April 2005 and November 2014 was performed. Eighty-seven patients met inclusion criteria: age > 75 with or without comorbidities or age > 65 if complicated by two or more medical comorbidities. Outcomes measures evaluated were 1-year mortality, duration of hospital stay, return to pre-injury ambulation status and treatment failure marked by conversion to a total hip arthroplasty (THA) within 1 year of treatment. RESULTS: Thirty-seven patients with acetabular fractures were treated with surgical fixation, and 49 were treated non-operatively. Operative patients did not demonstrate a statistically significant difference in mortality within 1 year of treatment compared to non-operatively treated patients. Operative patients demonstrated a statistically significant increase in treatment failure marked by a conversion to a THA within 1 year when compared to conservatively treated patients. No differences in age, duration of follow-up, or ability to return to baseline at latest clinical follow-up were found between groups. However, non-operatively treated patients had a higher incidence of Alzheimer's disease/Dementia and Parkinson's compared to operatively treated patients. CONCLUSION: Analysis of our small cohort suggests that there may be a role for the non-operative treatment of acetabular fractures in this debilitated patient population despite a somewhat longer length of hospital stay at the time of injury. Conversion to THA was significantly higher at 1 year in our operated patients. No differences in mortality at 1 year were noted between patient groups. Return to baseline ambulation status was slightly higher in the non-operated group but not significantly so. However, a potential bias to more likely treat complex fractures operatively cannot be ruled out, as non-operative fractures were most often anterior column variants, usually more amenable to non-operative care. LEVEL OF EVIDENCE: Prognostic Level III.

Stress-dependent finite growth in soft elastic tissues.

Growth and remodeling in tissues may be modulated by mechanical factors such as stress. For example, in cardiac hypertrophy, alterations in wall stress arising from changes in mechanical loading lead to cardiac growth and remodeling. A general continuum formulation for finite volumetric growth in soft elastic tissues is therefore proposed. The shape change of an unloaded tissue during growth is described by a mapping analogous to the deformation gradient tensor. This mapping is decomposed into a transformation of the local zero-stress reference state and an accompanying elastic deformation that ensures the compatibility of the total growth deformation. Residual stress arises from this elastic deformation. Hence, a complete kinematic formulation for growth in general requires a knowledge of the constitutive law for stress in the tissue. Since growth may in turn be affected by stress in the tissue, a general form for the stress-dependent growth law is proposed as a relation between the symmetric growth-rate tensor and the stress tensor. With a thick-walled hollow cylinder of incompressible, isotropic hyperelastic material as an example, the mechanics of left ventricular hypertrophy are investigated. The results show that transmurally uniform pure circumferential growth, which may be similar to eccentric ventricular hypertrophy, changes the state of residual stress in the heart wall. A model of axially loaded bone is used to test a simple stress-dependent growth law in which growth rate depends on the difference between the stress due to loading and a predetermined growth equilibrium stress.

Coronary and total peripheral resistance changes during sleep in a porcine model.

Changes in autonomic tone in the vasculature during sleep may have important implications for silent ischemia and sudden cardiac death. Few models exist in which both cardiac output and coronary blood flow are continuously measured during natural sleep and autonomic mechanisms are assessed. Catheters were chronically implanted in the aorta to measure mean arterial pressure (MAP), and flow probes were placed on the ascending aorta and the circumflex coronary artery of 18 pigs. Electrodes determined sleep stage as either non-rapid eye movement (NREM) or rapid eye movement (REM) sleep. The MAP was 73 +/- 3 mmHg in the quiet awake state, did not change in NREM, and decreased to 64 +/- 2 mmHg in REM sleep (P < 0.05). In NREM sleep, heart rate did not change from awake state values of 136 +/- 8 beats/min but increased by 5 beats/min in REM sleep (P < 0.05). Coronary vascular resistance decreased from awake state values of 2.7 +/- 0.2 to 2.2 +/- 0.2 mmHg.ml-1.min in REM (P < 0.05); total peripheral resistance decreased from awake values of 0.061 +/- 0.004 mmHg.ml-1.min to 0.050 +/- 0.003 in REM sleep (P < 0.05). Those changes appear to have been mediated primarily by reduction of alpha-adrenergic activity. Spectral analysis of heart rate suggests that power in the high-frequency range (a presumed indicator of parasympathetic tone) was lower in REM sleep than NREM sleep.

Transmural changes in stress-free myocyte morphology during pressure overload hypertrophy in the rat.

Cellular hypertrophy can alter the distribution of residual stress in the myocardium, hence can affect active and passive ventricular mechanics. It is hypothesized that an increase in stress-free cell cross-sectional area will tend to increase residual stresses. Therefore transmural distributions of myocyte cross-sectional areas and global ventricular dimensions in young rats 0-21 days following thoracic aortic handling with sham-operated and unoperated control groups were measured in tissue free of all external and residual stresses. Cell cross-sectional area increased in the stress-free state and was uniform across the wall except at 21 days when there was a transmural gradient with cells at the endocardium 46% larger in diameter than those in the outer wall. Cell area increased from a mean of 156 +/- 30 microM2 at 0 days to a mean of 627 +/- 164 microM2 at 21 days, although during this time there were no statistical changes in the opening angles of stress-free tissue sections. Because the time course of opening angle did not follow the changes in cell thickening, the cellular growth measured in this study is probably not the only factor responsible for the distribution of residual stress.

Effect of residual stress on transmural sarcomere length distributions in rat left ventricle.

It has been previously shown that the myocardium in the walls of the unloaded passive left ventricle (LV) is not stress free. To assess the functional significance of residual stress in the ventricular wall, we compared the transmural distributions of sarcomere length (SL) in specimens of rat LV myocardium fixed in the unloaded (residually stressed) and stress-free states. When a cross-sectional ring cut from the equatorial region of the freshly arrested rat hearts was cut radially to relieve residual stress, it sprang open into an arc with a mean opening angle of 45 +/- 15 degrees (SD) (n = 8). During immersion fixation in glutaraldehyde, the opening angle increased 9.3 +/- 7.1 degrees (SD) overall. SLs were measured at 16 equally spaced transmural locations from the free wall in the stress-free tissue sections and were compared with control measurements from adjacent cross-sectional rings in which residual stress had not been relieved. Average SL for the stress-free tissue (n = 11) was 1.84 +/- 0.05 (SD) microns and for the unloaded tissue was 1.83 +/- 0.06 (SD) microns. However, analysis of covariance on the pooled data showed that the transmural distributions were significantly different (P < 0.0001). Whereas SL was uniform across the wall in the stress-free state with a mean gradient of -0.014 +/- 0.044 (SD) microns/total wall thickness, there was a significant decrease (P = 0.001) in SL from epicardium to endocardium in the intact unloaded tissue [slope = -0.114 +/- 0.054 (SD) microns/total wall thickness].(ABSTRACT TRUNCATED AT 250 WORDS)

Unique strain history during ejection in canine left ventricle.

Understanding the relationship between structure and function in the heart requires a knowledge of the connection between the local behavior of the myocardium (e.g., shortening) and the pumping action of the left ventricle. We asked the question, how do changes in preload and afterload affect the relationship between local myocardial deformation and ventricular volume? To study this, a set of small radiopaque beads was implanted in approximately 1 cm3 of the isolated canine heart left ventricular free wall. Using biplane cineradiography, we tracked the motion of these markers through various cardiac cycles (controlling pre- and afterload) using the relative motion of six markers to quantify the local three dimensional Lagrangian strain. Two different reference states (used to define the strains) were considered. First, we used the configuration of the heart at end diastole for that particular cardiac cycle to define the individual strains (which gave the local "shortening fraction") and the ejection fraction. Second, we used a single reference state for all cardiac cycles i.e., the end-diastolic state at maximum volume, to define absolute strains (which gave local fractional length) and the volume fraction. The individual strain versus ejection fraction trajectories were dependent on preload and afterload. For any one heart, however, each component of absolute strain was more tightly correlated to volume fraction. Around each linear regression, the individual measurements of absolute strain scattered with standard errors that averaged less than 7% of their range. Thus the canine hearts examined had a preferred kinematic (shape) history during ejection, different from the kinematics of filling and independent or pre-or afterload and of stroke volume.

A method to reconstruct myocardial sarcomere lengths and orientations at transmural sites in beating canine hearts.

The ability to measure cyclic changes in myocardial sarcomere lengths and orientations during cardiac ejection and filling would improve our understanding of how the cellular processes of contraction relate to the pumping of the whole heart. Previously, only postmortem sarcomere measurements were possible after arresting the heart in one state and fixing it for histology. By combining such histological measurements with direct observations of the deformation experienced by the same myocardial region while the heart was beating, we have developed a method to reconstruct sarcomere lengths and orientations throughout the cardiac cycle and at several transmural layers. A set of small (1 mm) radiopaque beads was implanted in approximately 1 cm3 of the left ventricular free wall. Using biplane cineradiography, we tracked the motion of these markers through various cardiac cycles. To quantify local myocardial deformation (as revealed by the relative motion of the markers), we calculated the local deformation gradient tensors. As the heart deforms, these describe how any short vectorial line segment alters its length and orientation relative to a reference state. Specifically, by choosing the reference state to be the arrested and fixed heart and by measuring the sarcomere vector in that state, we could then use the deformation gradient tensors to reconstruct the sarcomere vector that would exist in the beating heart. As ventricular chamber volume varied over its normal range of operation, the range of reconstructed sarcomere lengths (approximately 1.7-2.4 microns) was comparable to other histological studies and to measurements of sarcomere length in excised papillary muscles or trabeculae. The pattern of sarcomere length changes was markedly different, however, during ejection vs. filling.