Cardiac surgical outcome prediction by blood pressure variability indices Poincaré plot and coefficient of variation: a retrospective study.

BACKGROUND: Recent literature suggests a significant association between blood pressure variability (BPV) and postoperative outcomes after cardiac surgery. However, its outcome prediction ability remains unclear. Current prediction models use static preoperative patient factors. We explored the ability of Poincaré plots and coefficient of variation (CV) by measuring intraoperative BPV in predicting adverse outcomes. METHODS: In this retrospective, observational, cohort study, 3687 adult patients (> 18 years) undergoing cardiac surgery requiring cardio-pulmonary bypass from 2008 to 2014 were included. Blood pressure variability was computed by Poincare plots and CV. Standard descriptors (SD) SD1, SD2 were measured with Poincare plots by ellipse fitting technique. The outcomes analyzed were the 30-day mortality and postoperative renal failure. Logistic regression models adjusted for preoperative and surgical factors were constructed to evaluate the association between BPV parameters and outcomes. C-statistics were used to analyse the predictive ability. RESULTS: Analysis found that, 99 (2.7%) patients died within 30 days and 105 (2.8%) patients suffered from in-hospital renal failure. Logistic regression models including BPV parameters (standard descriptors from Poincare plots and CV) performed poorly in predicting postoperative 30-day mortality and renal failure [Concordance(C)-Statistic around 0.5]. They did not add any significant value to the standard STS risk score [C-statistic: STS alone 0.7, STS + BPV parmeters 0.7]. CONCLUSIONS: In conclusion, BP variability computed from Poincare plots and CV were not predictive of mortality and renal failure in cardiac surgical patients. Patient comorbid conditions and other preoperative factors are still the gold standard for outcome prediction. Future directions include analysis of dynamic parameters such as complexity of physiological signals in identifying high risk patients and tailoring management accordingly.

Characterizing the Severity of Autonomic Cardiovascular Dysfunction after Spinal Cord Injury Using a Novel 24 Hour Ambulatory Blood Pressure Analysis Software.

Cardiovascular disease is one of the leading causes of morbidity and mortality in the spinal cord injury (SCI) population. SCI may disrupt autonomic cardiovascular homeostasis, which can lead to persistent hypotension, irregular diurnal rhythmicity, and the development of autonomic dysreflexia (AD). There is currently no software available to perform automated detection and evaluation of cardiovascular autonomic dysfunction(s) such as those generated from 24 h ambulatory blood pressure monitoring (ABPM) recordings in the clinical setting. The objective of this study is to compare the efficacy of a novel 24 h ABPM Autonomic Dysfunction Detection Software against manual detection and to use the software to demonstrate the relationships between level of injury and the degree of autonomic cardiovascular impairment in a large cohort of individuals with SCI. A total of 46 individuals with cervical (group 1, n = 37) or high thoracic (group 2, n = 9) SCI participated in the study. Outcome measures included the frequency and severity of AD, frequency of hypotensive events, and diurnal variations in blood pressure and heart rate. There was good agreement between the software and manual detection of AD events (Bland-Altman limits of agreement = ±1.458 events). Cervical SCI presented with more frequent (p = 0.0043) and severe AD (p = 0.0343) than did high thoracic SCI. Cervical SCI exhibited higher systolic and diastolic blood pressure during the night and lower heart rate during the day than high thoracic SCI. In conclusion, our ABPM AD Detection Software was equally as effective in detecting the frequency and severity of AD and hypotensive events as manual detection, suggesting that this software can be used in the clinical setting to expedite ABPM analyses.

High Thoracic Contusion Model for the Investigation of Cardiovascular Function after Spinal Cord Injury.

Cardiovascular disease is the leading cause of death for individuals with spinal cord injury (SCI). Because of a lack of a standardized and accessible animal model for cardiovascular disease after SCI, few laboratories have conducted pre-clinical trials aimed at reinstating descending cardiovascular control. Here, we utilized common contusion methodology applied to the midline of the upper-thoracic cord of adult Wistar rats accompanied with telemetric blood pressure monitoring and FluoroGold retrograde neuronal tracing, as well as lesion site and lumbrosacral afferent immunohistochemistry. We demonstrate widespread cardiovascular (i.e., impaired resting hemodynamics, autonomic dysreflexia) and hindlimb dysfunction at 1 month post-injury. Further, we provide a description of the neuroanatomical changes that accompany cardiovascular abnormalities. Specifically, we describe 1) the injury site including white matter sparing as well as lesion volume, and their correlations to cardiovascular as well as motor outcomes; 2) the severity of injury-dependent changes in sympathoexcitatory medullary neuron spinal connectivity, as measured using FluoroGold tracing; and 3) the extent of aberrant afferent plasticity within the lumbosacral region of the spinal cord, which has been linked to the development of autonomic dysreflexia. We believe that this model, which utilizes equipment common to numerous SCI laboratories, can serve as a research standard for studies specifically aimed at investigating autonomic neuroprotective and regenerative strategies following SCI.

Effects of early and delayed initiation of exercise training on cardiac and haemodynamic function after spinal cord injury.

NEW FINDINGS: What is the central question of this study? How does early versus delayed initiation of passive hindlimb cycling, as well as detraining, affect cardiac function and blood pressure control in a rodent model of spinal cord injury? What is the main finding and its importance? Early or delayed initiation of hindlimb cycling improves cardiac and haemodynamic function in spinal cord injury, although the benefits of early administration are more pronounced. We also demonstrate the need for exercise to be maintained, because detraining rapidly reverses the cardiac and haemodynamic benefits. Spinal cord injury (SCI) reduces physical activity and alters descending supraspinal cardiovascular control, predisposing this population to early onset of cardiovascular disease. We used a T3 SCI rodent model to investigate the effect of early versus delayed passive hindlimb cycling (PHLC), as well as the effect of detraining on cardiac dysfunction and blood pressure control, including autonomic dysreflexia (AD). Twenty male Wistar rats were divided into an early PHLC initiation group followed by a period of detraining (PHLC starting day 6 post-SCI, for 4 weeks, followed by 4 weeks of detraining; 'early PHLC/detraining' group) and a delayed PHLC intervention group (no PHLC for first 5 weeks post-SCI, followed by PHLC for 4 weeks; 'no PHLC/delayed PHLC' group). At 5 weeks post-SCI, the no PHLC/delayed PHLC group exhibited a decline in almost all cardiac indices (all P < 0.029), which was maintained in the early PHLC/detraining group. Also, the severity of induced AD was reduced in the early PHLC/detraining versus no PHLC/delayed PHLC group (all P < 0.0279). At 9 weeks post-SCI, no PHLC/delayed PHLC animals exhibited a reversal of cardiac dysfunction such that all indices were not different from pre-SCI, whereas early PHLC/detraining rats exhibited a reduction in all cardiac indices relative to pre-SCI (all P < 0.049), except ejection fraction. Between weeks 7 and 9 post-SCI, the no PHLC/delayed PHLC rats exhibited fewer spontaneous AD events than the early PHLC/detraining rats (P < 0.01). We show, for the first time, that delayed exercise promotes similar improvements in cardiac and haemodynamic function to those observed with early initiation. Furthermore, exercise needs to be maintained, because detraining reduces these cardiohaemodynamic benefits.

Development of an Algorithm to Perform a Comprehensive Study of Autonomic Dysreflexia in Animals with High Spinal Cord Injury Using a Telemetry Device.

Spinal cord injury (SCI) is a debilitating neurological condition characterized by somatic and autonomic dysfunctions. In particular, SCI above the mid-thoracic level can lead to a potentially life-threatening hypertensive condition called autonomic dysreflexia (AD) that is often triggered by noxious or non-noxious somatic or visceral stimuli below the level of injury. One of the most common triggers of AD is the distension of pelvic viscera, such as during bladder and bowel distension or evacuation. This protocol presents a novel pattern recognition algorithm developed for a JAVA platform software to study the fluctuations of cardiovascular parameters as well as the number, severity and duration of spontaneously occurring AD events. The software is able to apply a pattern recognition algorithm on hemodynamic data such as systolic blood pressure (SBP) and heart rate (HR) extracted from telemetry recordings of conscious and unrestrained animals before and after thoracic (T3) complete transection. With this software, hemodynamic parameters and episodes of AD are able to be detected and analyzed with minimal experimenter bias.

Characterizing the temporal development of cardiovascular dysfunction in response to spinal cord injury.

Spinal cord injury (SCI) is associated with rapid and sustained impairments in cardiovascular function that ultimately cause an early onset of cardiovascular disease. We know remarkably little about the temporal progression of cardiovascular disturbances, but such an understanding is critical to inform clinical management and develop appropriate intervention strategies. To characterize the cardiovascular response to SCI, six male Wistar rats were instrumented with telemetry and assessed for continuous arterial blood pressure (BP), core body temperature, and heart rate (HR) 7 days before and up to 28 days after T3 SCI. Hemodynamic variables were averaged day by day and hour by hour. Spontaneously occurring autonomic dysreflexia (AD) was characterized by applying a novel algorithm to continuous BP and HR data, and induced AD was assessed weekly via the BP response to colorectal distension. Systolic BP was reduced at all time points after SCI compared with before SCI (p<0.003), except at 4 and 6 days post-injury. Core body temperature was reduced at 2 days post-SCI only (p=0.001). The nocturnal dip in BP and temperature observed pre-SCI was absent during the first 14 days post-SCI, but returned from 21 days post-SCI on (p<0.024). The frequency and severity of spontaneously occurring AD events were significantly less between days 6 and 10 post-SCI compared all other time points (p<0.037). The pressor response to colorectal distension was greater at 14, 21, and 28 days post-SCI compared with at 7 days post-SCI (all p<0.004). In conclusion, SCI induces rapid and profound alterations in basal hemodynamics and diurnal rhythms that partially recover by 14 days post-SCI. AD, on the other hand, is acutely present post-SCI, but the frequency and severity of AD events increase substantially from 14 days post-SCI on.