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Background: To explore the relationship between comorbidity burden and mortality, peri-procedural complications, and length of stay in patients treated with TAVR in the National Inpatient Sample (NIS). Patients undergoing transcatheter aortic valve replacement (TAVR) often have multiple comorbidities. Whilst the impact of individual comorbid conditions on clinical outcomes following TAVR has been previously assessed, the impact of more global measures of comorbidity remains unknown in this cohort. To explore the relationship between comorbidity burden and mortality, peri-procedural complications, and length of stay in patients treated with TAVR NIS. Methods: TAVR procedures were identified between 2011 and 2014 and comorbidities were defined by the Elixhauser classification system (ECS) consisting of 30 comorbidity measures. Endpoints included in-hospital mortality, periprocedural complications, and length of stay. Patients were classified based on their ECS in five categories (ECS I < 0, ECS II = 0, ECS III = 1–5, ECS IV = 6–13, ECS V ≥ 14). Results: A total of 40,604 TAVR patients were identified. Mean age was 81.2 ± 8.5 years. Patients with ECS category V accounted for more than 40% of the cohort and experienced almost a 2.5-fold increase in in-hospital mortality (OR 2.42, 95% CI: 1.28–4.56), acute kidney injury (OR: 6.23, 95% CI: 4.13–9.41), major bleeding (OR: 2.26, 95% CI: 1.71–2.99), post-procedural stroke or TIA (OR: 2.02, 95% CI: 1.08–3.78). It was also associated with a mean 4.14-day increased length of stay (95% CI: 3.67 to 4.65) compared to patients with lower ECS category after adjusting for confounding factors. Conclusions: Our study of over 40,000 TAVRs shows that Elixhauser comorbidity score was independently associated with higher mortality, periprocedural complications, and length of stay. Global comorbidity burden is an important consideration for risk stratification in patients undergoing TAVR.

Fetal heart rate variability (FHRV) is a key index of antenatal and intrapartum fetal well-being. FHRV is well established to be mediated by both arms of the autonomic nervous system, but it remains unknown whether higher centers in the forebrain contribute to FHRV. We tested the hypothesis that selective forebrain ischemia would impair the generation of FHRV. Sixteen chronically instrumented near-term fetal sheep were subjected to either forebrain ischemia induced by bilateral carotid occlusion or sham-ischemia for 30 min. Time, frequency, and nonlinear measures of FHRV were assessed during and for seven days after ischemia. Ischemia was associated with profound suppression of electroencephalographic (EEG) power, which remained suppressed throughout the recovery period ( P < 0.001). During the first 5 min of ischemia, multiple time and frequency domain measures were increased (all P < 0.05) before returning back to sham levels. A delayed increase in sample entropy was observed during ischemia ( P < 0.05). For the first 3 h after ischemia, there was moderate suppression of two measures of FHRV (very-low frequency power and the standard deviation of RR-intervals, both P < 0.05) and increased sample entropy ( P < 0.05). Thereafter, all measures of FHRV returned to control levels. In conclusion, profound forebrain ischemia sufficient to lead to severe neural injury had only transient effect on multiple measures of FHRV. These findings suggest that the forebrain makes a limited contribution to FHRV. FHRV therefore primarily originates in the hindbrain and is unlikely to provide meaningful information on forebrain neurodevelopment or metabolism.

BACKGROUND There has been a revival of balloon aortic valvuloplasty (BAV) for severe aortic stenosis, as a result of an increasing number of patients undergoing trans-catheter aortic valve implantation (TAVI). However, there has not been universal adoption of BAV as a standalone, nor bridging therapy. METHODS A retrospective analysis of the practice at our institution between June 2009 and May 2016 was performed. Demographic, clinical, procedural, and follow-up data on all patients were collected. RESULTS A total of 200 patients with a median age of 82 years and severe symptomatic aortic stenosis underwent BAV from June 2009 to May 2016. All patients had appreciable comorbidity with a mean logistic Euro SCORE of 48 ± 11 and mean standard Euro SCORE 15 ± 4. BAV was performed for palliation in 118 (59%), as a bridging therapy for TAVI in 55 (27.5%) and bridging to surgical AVR in 27 patients (13.5%), respectively. Major complications occurred in 14 patients (7%) including 2 in-patient deaths (1%). A statistically significant improvement in symptoms and a decrease in trans-valvular gradient were observed. CONCLUSION BAV is an effective treatment strategy, either as a bridge to definitive therapy or as a palliative procedure, with an acceptable mortality. BAV is associated with a significant improvement in symptoms and is valuable as a palliative treatment in high-risk patients, where no other invasive option is available.

There are few scenarios in the cardiac catheterization laboratory quite as dramatic as a coronary artery perforation. While some instances of this mishap are subtle, others are quite dramatic. Fortunately this occurrence is rare, but carries with it a significant risk of serious adverse events. The potential for harm may be reduced by the brisk identification of the problem within the catheter laboratory, together with early implementation of treatment. A clear understanding of the mechanism, implications, and management of this complication are essential tools for the capable interventional cardiologist.

Background Aortic stenosis (AS) is a common valvular abnormality and transcatheter aortic valve implantation (TAVI) is being increasingly used to treat patients considered too high risk for conventional surgery. We aimed to assess the prevalence of comorbid conditions in patients undergoing TAVI using the Charlson Comorbidity Index (CCI) and to assess their impact on clinical and procedural outcomes. Methods We analysed 158 patients who underwent a TAVI at our institution between June 2009 and September 2015 to define their co-morbid burden as measured with CCI, and study its impact on procedural characteristics and mortality at 30 days. Results One hundred fifty-eight (158) patients with a mean age of 82 ± 8 years and a mean CCI score of 2.67 underwent a TAVI. Only 12/158 patients had a CCI of 0. The commonest cardiovascular comorbidities were previous myocardial infarction (24%), congestive heart failure (15%) and diabetes mellitus (23%) whilst the commonest non-cardiovascular comorbidities were renal disease (46%) and chronic obstructive pulmonary disease (COPD) (29%). After multivariable adjustment, CCI was not independently associated with adverse clinical outcomes. The addition of CCI to scoring systems such as Logistic EuroScore (LES) and Society of Thoracic Surgeons (STS) risk models improved the area under the curve from 0.75 (95%CI: 0.44–1.00) and 0.83 (95%CI: 0.64–1.00) to 0.78 (95%CI: 0.53–1.00) and 0.89 (95%CI: 0.78–1.00) respectively. Conclusions The burden of comorbid conditions in patients undergoing TAVI is significant. The CCI score was not independently associated with a higher risk of death but can be useful in addition to LES and STS risk models in informing decision making on the selection of patients for TAVI.

The cost of inpatient percutaneous coronary interventions (PCI) procedure is related to length of stay (LOS). It is unknown, how LOS may be associated with readmission rates and costs of index PCI and readmissions in elective PCI. This study aims to evaluate rates, predictors, causes, and costs associated with 30-day unplanned readmissions according to lLOS in patients, who underwent elective PCI. We included patients in the Nationwide Readmission Database, who were admitted to hospital from 2010 to 2014, who underwent uncomplicated elective PCI. LOS was defined as 0, 1, 2, and ≥3 days. A total of 324,345 patients were included in the analysis and the 30-day unplanned readmission was 4.75%, 4.67%, 6.44%, and 9.42% in the LOS groups 0, 1, 2, and ≥3 days, respectively. Prolonged LOS was associated with increased average total 30-day cost (index and readmission cost, 0 days $15,063, 1 day $14,693, 2 days $18,136, and ≥3 days $24,336). Compared with 0 days, the odds of readmissions were greater for 2 days (odds ratio 1.41, 95% confidence interval 1.07 to 1.87, p = 0.016) and ≥3 days (odds ratio 1.70, 95% confidence interval 1.28 to 2.24, p

Transcatheter aortic valve replacement over the last few years has revolutionized the way severe aortic stenosis patients are being managed [ [1] , [2] , [3] , [4] ]. Randomized clinical trials commonly excluded bicuspid aortic valves and pure native severe aortic regurgitation [ 2 , 4 ]. We present a case with severe acute aortic regurgitation complicated by refractory pulmonary oedema successfully managed by transfemoral transcatheter aortic valve replacement using a Sapien 3 valve.

Objectives: We sought to characterize UK-wide balloon aortic valvuloplasty (BAV) experience in the TAVI era. Background: BAV for acquired calcific aortic stenosis is in a phase of renaissance, largely due to the development of transcatheter aortic valve implantation (TAVI). Methods: Data from 423 patients at 14 centers across the UK were analyzed. Results: Patients were aged 80.9 6 9.5 years; 52.5% were male. Mean logistic EuroScore was 27.3% 6 16.8%. Mean peak transaortic gradient fell from 62.0 6 26.3 to 28.3 6 16.2 mm Hg. Aortic valve area increased from 0.58 6 0.19 to 0.80 6 0.25 cm 2 echocardiographically. Procedural complication rate was 6.3%, comprising death (2.4%), blood transfusion � 2 U (1.2%), cardiac tamponade (1.0%), stroke (1.0%), vascular surgical repair (1.0%), coronary embolism (0.5%), and permanent pacemaker (0.2%). Mortality was 13.8% at 30 days and 36.3% at 12 months. Subsequently, 18.3% of patients underwent TAVI and 7.0% sAVR, with improved survival compared to those who had no further intervention (logrank < 0.0001). Multivariate Cox proportional hazard analysis demonstrated that survival was adversely effected by the presence of coronary artery disease (HR 1.53, 95%CI 1.08‐2.17, P 5 0.018), poor LV function (HR 1.54, 95%CI 1.09‐2.16, P 5 0.014), and either urgent (HR 1.70, 95%CI 1.18‐2.45; P 5 0.004) or emergent presentation (HR 3.72, 95%CI 2.27‐6.08; P < 0.0001). Conclusion: Balloon aortic valvuloplasty offers good immediate hemodynamic efficacy at an acceptable risk of major complications. Medium-term prognosis is poor in the absence of definitive therapy. V C 2013 Wiley Periodicals, Inc.

Background Preimplantation balloon aortic valvuloplasty ( BAV ) is considered a routine procedure during transcatheter aortic valve implantation ( TAVI ) to facilitate prosthesis implantation and expansion; however, it has been speculated that fewer embolic events and/or less hemodynamic instability may occur if TAVI is performed without preimplantation BAV . The aim of this study was to systematically review the clinical outcomes associated with TAVI undertaken without preimplantation BAV . Methods and Results We conducted a search of Medline and Embase to identify studies that evaluated patients who underwent TAVI with or without preimplantation BAV for predilation. Pooled analysis and random‐effects meta‐analyses were used to estimate the rate and risk of adverse outcomes. Sixteen studies involving 1395 patients (674 with and 721 without preimplantation BAV ) fulfilled the inclusion criteria. Crude device success was achieved in 94% (1311 of 1395), and 30‐day all‐cause mortality occurred in 6% (72 of 1282) of patients. Meta‐analyses evaluating outcomes of strategies with and without preimplantation BAV showed no statistically significant differences in terms of mortality (relative risk [ RR ] 0.61, 95% CI 0.32–1.14, P =0.12), safety composite end point ( RR 0.85, 95% CI 0.62–1.18, P =0.34), moderate to severe paravalvular leaks ( RR 0.68, 95% CI 0.23–1.99, P =0.48), need for postdilation ( RR 0.86, 95% CI 0.66–1.13, P =0.58), stroke and/or transient ischemic attack ( RR 0.72, 95% CI 0.30–1.71, P =0.45), and permanent pacemaker implantation ( RR 0.80, 95% CI 0.49–1.30, P =0.37). Conclusions Our analysis suggests that TAVI procedures with or without preimplantation BAV were associated with similar outcomes for a number of clinically relevant end points. Further studies including a large number of patients are needed to ascertain the impact of TAVI without preimplantation BAV as a standard practice.

Background— There are limited data on outcomes of patients with previous coronary artery bypass grafting (CABG) presenting with ST-segment–elevation myocardial infarction (STEMI) and undergoing primary percutaneous coronary intervention (PPCI). We report outcomes in patients with STEMI undergoing PPCI with or without previous CABG surgery in a large real-world, all-comer population. Methods and Results— Clinical, demographic, procedural, and outcomes data were collected for all patients undergoing PPCI in England and Wales from January 2007 to December 2012. All-cause mortality at 30 days and 1 year were evaluated in the whole and a propensity-matched cohort. Of 79 295 patients with STEMI studied, 2658 (3.4%) patients had prior CABG, of whom 44% (n=1168) underwent PPCI to native vessels and 56% (n=1490) to bypass grafts. There were significant differences in the demographic, clinical, and procedural characteristics of these groups. Patients with prior CABG (with primary PCI to native artery or graft) had higher mortality at 30 days (6.2% with PPCI to native artery, 6.1% with PPCI to bypass graft) than patients with no prior CABG (4.5%; P Conclusions— A prior history of CABG in patients presenting with STEMI and undergoing PPCI does not independently confer additional risk of mortality, although it is a marker of other high-risk features.

Objective. Current methods for early identification of cerebral white matter injury in the premature infant at the bedside are inadequate. This study investigated the utility of advanced spectral analysis of the neonatal electroencephalogram (EEG) in the early diagnosis of white matter injury in the premature infant. The critical measurement used, suggested largely by previous studies in animal models, was the spectral edge frequency (SEF), calculated here as the frequency below which 90% of the power in the EEG exists. Methods. Fifty-nine very low birth weight infants (87% of eligible infants) had electrodes placed over the central and parietal regions (C3, P3, C4, and P4 sites according to the 10-20 international system) for the collection of EEG amplitude, intensity, and SEF. All averaged signals were analyzed off-line using software (Chart Analyzer; BrainZ Instruments, Auckland, NZ). All infants had a magnetic resonance imaging scan at term to identify the presence and severity of white matter injury. Results. There was no significant difference between conventional EEG amplitude and intensity for infants with or without evidence of white matter injury. However, premature infants with increasingly severe white matter injury had progressively lower SEFs compared with infants who did not exhibit white matter injury. Conclusions. These data suggest that SEF-based measures are useful for defining the presence and severity of white matter injury at the bedside.

We read with interest the letter from Dr. Dastidar and colleagues in which they express their views and compare our report of the randomized CvLPRIT (Complete Versus Lesion-Only Primary PCI Trial) [(1)][1] with their in-house clinical experience. They suggest that the trial was not run according to

The role of C-type natriuretic peptide (CNP) and its guanylyl cyclase-linked receptors in mediating salt secretion by the rectal gland of the spiny dogfish shark ( Squalus acanthias) was investigated using HS-142–1, a competitive inhibitor of the binding of natriuretic peptides to their guanylyl cyclase receptors. CNP binds to receptors and activates guanylyl cyclase in rectal gland membranes in a way that is inhibited by HS-142–1. Guanylyl cyclase activation in rectal gland membranes is far more sensitive to CNP than to atrial natriuretic peptide, whereas the reverse is true for membranes derived from mammalian (rabbit) renal collecting duct cells. HS-142–1 inhibited the stimulatory effect of CNP on ouabain-inhibitable oxygen consumption by rectal gland tubules. In explanted rectal glands continuously perfused with blood from intact donor sharks, HS-142–1 inhibited the increase in salt secretion normally provoked by infusing isotonic saline solutions into the donor animal. These results strongly support the view that CNP released into the systemic circulation in response to volume expansion mediates the secretion of chloride by the rectal gland via receptors linked to guanylyl cyclase.

Objective: We assessed the effects of coronary bypass grafting on left ventricular (LV) function, exercise capacity and symptom profile in patients with LV impairment and evaluated the role of identifying myocardial hibernation in a prospective non-randomised study. Methods: Of 120 patients screened, 47 patients with LV ejection fraction B 35% and three vessel coronary artery disease were studied. All underwent stress:redistribution and separate day rest:redistribution Tl-201 imaging together with cine MRI at enrolment, and cine MRI at follow-up. Group 1, 30 patients undergoing bypass surgery, underwent symptom limited treadmill exercise testing with peak VO2 measurement, and symptom profile evaluation less than 3 months before, and 3‐6 months after operation. Revascularisation was assessed by post-operative Tl-201 imaging and repeat coronary angiography. Group 2, 17 patients treated on medical therapy alone underwent symptom profile assessment at enrolment and follow-up for those who survived. Segmental hibernation was defined as the equivalent of greater than 50% of maximal Tl-201 uptake where wall motion was severely impaired on resting imaging. Patients were considered to be hibernating where two of nine LV segments fulfilled these criteria. Results: In group 1, five patients died (17%), peri-or post-operatively, two defaulted and 23 attended follow-up studies. In group 2, three patients died prior to follow-up (18%). In the surgical group there was an increase in mean LVEF from 24.098% to 29.7911% (PB0.05) while in the medical group there was a fall from 25.79 10% to 20.698% (PB0.05). In group 1, the mean NYHA dyspnoea grade improved from 2.7 to 1.4 while in the medical group it was unchanged, 2.6 to 2.5. In patients with myocardial hibernation identified pre-operatively, 18:19 (95%) improved LVEF after CABG compared with 2:4 (50%) of patients without hibernation. 17:19 (86%) patients with hibernation improved NYHA dyspnoea class compared with 2:4 (50%) of patients without. 60:93 (65%) of hibernating segments improved function after revascularisation while 47:53 (89%) hibernating segments showed no improvement on medical therapy alone. Conclusion: In patients with severe LV impairment with myocardial hibernation, coronary artery bypass grafting improves both global and regional systolic LV function, and symptom profile. Medical treatment of patients with LV impairment and myocardial hibernation does not improve LV contractile function or symptoms. Both surgical and medical therapy carry a high mortality rate. © 1997 Elsevier Science B.V.

Background Some patients with hypertrophic obstructive cardiomyopathy may gain symptomatic relief from a reduction in the extent of obstruction to left ventricular outflow. We present the outcome of the first series of patients treated with an alternative method of gradient reduction using catheter techniques. Methods and Results Eighteen patients were treated with selective intracoronary alcohol injection to induce localized septal infarction. Patients underwent echocardiographic measurement of left ventricular dimensions and Doppler echocardiographic evaluation of left ventricular outflow tract gradients before the procedure, on the first postoperative day, and at a median follow-up of 3 months after the procedure. In addition, patients underwent exercise testing and symptom evaluation before and 3 months after nonsurgical septal reduction. There was a significant reduction in left ventricular outflow tract obstruction after the procedure (preprocedure, 67 mm Hg [95% CI, 48 to 87 mm Hg]; postprocedure, 25 mm Hg [95% CI, 16 to 34 mm Hg]; P =.0006), which persisted at 3-month follow-up (22 mm Hg [95% CI, 12 to 32 mm Hg]; P =.001). This was associated with a significant improvement in symptoms. There was a small but not significant increase in exercise capacity (n=10; preprocedure, 418 seconds [95% CI, 273 to 563 seconds]; postprocedure, 452 seconds [95% CI, 283 to 621 seconds). Left ventricular dimensions were not significantly altered by nonsurgical septal reduction. Conclusions Nonsurgical septal reduction significantly reduces left ventricular outflow tract obstruction and improves symptoms in some patients with hypertrophic obstructive cardiomyopathy. The technique may provide an alternative to surgical myomectomy in selected patients.

Aims: Primary percutaneous coronary intervention (PPCI) is the preferred strategy for acute ST-segment elevation myocardial infarction (STEMI), with evidence of improved clinical outcomes compared to fibrinolytic therapy. However, there is no consensus on how best to manage multivessel coronary disease detected at the time of PPCI, with little robust data on best management of angiographically significant stenoses detected in non-infarct-related (N-IRA) coronary arteries. CVLPRIT will determine the optimal management of N-IRA lesions detected during PPCI. Methods and results: CVLPRIT (Complete Versus culprit-Lesion only PRimary PCI Trial) is an open-label, prospective, randomised, multicentre trial. STEMI patients undergo verbal “assent” on presentation. Patients are included when angiographic MVD has been detected, and randomised to culprit (IRA)-only PCI (n=150) or in-patient complete multivessel PCI (n=150). Cumulative major adverse cardiac events (MACE) - all-cause mortality, recurrent MI, heart failure, need for revascularisation (PCI or CABG) will be recorded at 12 months. Secondary endpoints include safety endpoints of confirmed ischaemic stroke, intracranial haemorrhage, major non-intracranial bleeding, and repair of vascular complications. A cardiac magnetic resonance (CMR) substudy will provide mechanistic data on infarct size, myocardial salvage index and microvascular obstruction. A cost efficacy analysis will be undertaken. Conclusions: The management of multivessel coronary artery disease in the setting of PPCI for STEMI, including the timing of when to perform non-culprit-artery revascularisation if undertaken, remains unresolved. CVLPRIT will yield mechanistic insights into the myocardial consequence of N-IRA intervention undertaken during the peri-infarct period.

We describe a novel treatment for hypertrophic obstructive cardiomyoparhy, in which septal reduction is achived via transluminal induction of focal septal infarction. The results of the first three patients treated in this fashion have been recently reported; in this preliminary series, intraventricular pressure gradients could be dramatically reduced by the creation of a localized infarction of the ventricular septum. The procedure is well tolerated and effective in reducing the obstruction to left ventricular ourflow. Further studies are underway to fully evaluate the usefulness of the technique. (J Interven Cardiol 1996;9:393–397)

This study evaluates changes in ischaemic threshold over a 5-year period in patients with stable angina pectoris, who did not suffer any intervening cardiac event. Changes in ischaemic threshold are related to alterations in symptomatic status and ambulatory ischaemia. Over long-term follow-up, there is a significant fall in ischaemic threshold in such patients (mean heart rate at onset of ischaemia fell from 104 +/- 17.8 to 97 +/- 17.4 bpm: P0.001), but this is not matched by a worsening of either symptoms or ischaemia during daily life. In the 68% of patients that had a reduction in ischaemic threshold ofor = 5 bpm, 68% had either definite reduction or no change in symptoms and 84% had either reduction, abolition or no change in transient ischaemic activity. The dissociation between ischaemic threshold, ambulatory ischaemia and symptoms has implications for long-term monitoring and management of the patient with stable angina.

Intraventricular injection of insulin-like growth factor 1 (IGF-1) 2 h after hypoxic–ischemic injury reduces neuronal loss. To clarify the mode of action, we compared histological outcome between treatment groups in the following three studies: 0, 0.5, 5, and 50 μg IGF-1 given 2 h after injury; 0 and 20 μg IGF-1 given 1 h before; and 20 μg IGF-1 and insulin or vehicle alone given 2 h after. Unilateral hypoxic-ischemic injury was induced in adult rats by ligation of the right carotid and exposure to 6% O2 for 10 min. Histological outcome was evaluated in the cortex, striatum, and hippocampus 5 days later. Five to 50 μg IGF-1 reduced the incidence of infarction and neuronal loss in a dose-dependent manner in all regions (p < 0.05), and 50 μg reduced the infarction rate from 87 to 26% (p < 0.01). Pretreatment did not alter outcome. IGF-1 improved outcome compared with equimolar doses of insulin (p < 0.05) and did not affect systemic glucose concentrations or cortical temperature. The results indicate that the neuronal protective effects of IGF-1 are specific and are not mediated via insulin receptors, hypothermia, or hypoglycemic mechanisms. Centrally administered IGF-1 appears to provide worthwhile trophic support to cells within most cerebral structures after transient hypoxic-ischemic injury.

Aims To compare the performance of apolipoproteins (Apo) and oxidized LDL against routine clinical lipid profiles in the discrimination of atherosclerotic burden and cardiac function in stable coronary artery disease (CAD) patients. Methods and results Using a cross-sectional approach, we measured oxidized LDL, Apo AI and B in 199 patients (34–81 years) with stable symptomatic CAD. The discrimination of (i) atherosclerotic burden (coronary atheroma scores, the number of diseased coronary vessels), and (ii) cardiac function [NYHA classification, left-ventricular systolic dysfunction (LVSD)] were judged using receiver operating characteristic (ROC) curves. The ratio of Apo AI to B was correlated to oxidized LDL (Spearman, r = 0.37, P < 0.001); however, oxidized LDL was unrelated to measures of cardiac function or CAD severity. Concentrations of Apo AI decreased from 1.38 to 1.20 g/L with increasing atheroma scores (P = 0.02), while triglyceride levels increased from 1.50 to 2.23 mmol/L (P = 0.016). High-density lipoprotein (HDL) cholesterol and Apo AI levels were higher among those with heart failure (P = 0.002), and increased ordinally with NYHA class (P = 0.005). On ROC analysis, reduced levels of Apo AI and HDL cholesterol were discriminators for patients in the upper quartile for atheroma score (P < 0.004). Raised indices of HDL were associated with heart failure (P < 0.002). Conclusion Apo AI levels are a consistent discriminator of atherosclerotic burden among patients with stable CAD. However, heart failure presents an element of confounding in the diagnostic and prognostic utility of Apo monitoring among these patients.

In recent years improvements in obstetric and paediatric management have resulted in increased survival of infants from 24 weeks of gestation. However, these infants have continued to have a significantly increased risk of cerebral palsy, neurological morbidity and mortality (Volpe, 1997). There is increasing evidence to show that the neurological sequelae in many of these infants are the consequence of asphyxia during fetal life (Nelson & Leviton, 1991). Further it has been strongly suggested that haemodynamic factors both during asphyxia and during the post-asphyxial reperfusion phase contribute considerably to the pathogenesis of neurological disorders in the preterm fetus (Volpe, 1997). Currently, however, our understanding of the cerebrovascular and cardiovascular response of the preterm fetus to asphyxia is very limited. The cardiovascular and cerebrovascular responses of the near-term fetus to episodes of reduced oxygen supply have been well described (Jensen & Berger, 1991; Hanson, 1997; Volpe, 1997). These responses, particularly the redistribution of combined ventricular output (CVO) away from the periphery, contribute significantly to protecting essential organs such as the heart and brain. It has been suggested that immaturity of cardiovascular development may leave the preterm fetus more vulnerable to asphyxia (Jensen & Berger, 1991; Volpe, 1997). However, the current evidence regarding this hypothesis is both limited and contradictory. Several studies in the 0.6 gestation sheep fetus, an age broadly equivalent in neuronal development to a human fetus of 27-28 weeks gestation (McIntosh et al. 1979), have shown that unlike the near-term fetus redistribution of blood flow and bradycardia does not occur during hypoxia and that there is no rise in blood pressure (Boddy et al. 1974; Iwamoto et al. 1989). Similar observations were made during partial umbilical cord occlusion, although in this study there was evidence of redistribution of CVO (Iwamoto et al. 1991). Further, the ability of the fetal cerebrovasculature to vasodilate during hypoxia appears to be blunted and cerebral oxygen consumption is sustained in part by an increase in fractional oxygen extraction (Gleason et al. 1990). It has been suggested that these preterm fetal responses reflect relative immaturity of chemoreceptor function and neurohormonal modulators as well as an incomplete development of the autonomic nervous system (Walker et al. 1979; Iwamoto et al. 1991; Jensen & Berger, 1991). In contrast to these studies others have demonstrated that the 0.6 gestation sheep fetus appears to have a qualitatively similar cardiovascular response to complete occlusion of the umbilical cord to that of the near-term fetus, with an initial significant rise in blood pressure and a pronounced bradycardia (Mallard et al. 1994; Keunen et al. 1997). However, neither study evaluated the redistribution of blood flow. The study by Keunen et al. demonstrated the capacity of the immature animal to survive at least 20 min of complete umbilical cord occlusion, compared with a terminal duration for survival in the near-term sheep fetus of 10-12 min (Mallard et al. 1992). This capacity of the preterm fetus to survive longer periods of reduced oxygen supply is well described by others and is due to such factors as greater glycogen stores, greater anaerobic capacity in many tissues and lower basal metabolic activity (Dawes et al. 1959; Duffy et al. 1975). Speculatively, these data suggest that the very premature fetus may preferentially utilize this metabolic reserve during moderate hypoxia, and would only mount a full cardiovascular response to profound, near-terminal episodes of asphyxia. In pilot experiments we have determined that the preterm fetus is capable of surviving 30-33 min of complete umbilical cord occlusion. The cardiovascular response of the preterm fetus to such a near-terminal duration of asphyxia and the degree of haemodynamic compromise, including hypotension and cerebral hypoperfusion, that may occur is unknown. Furthermore the effects of such a profound insult on the post-asphyxial cardiovascular and cerebrovascular recovery of the preterm fetus have not been evaluated. There is considerable data from the more mature brain to suggest that the early post-asphyxial period is an important time during which further cerebral injury may occur. Ischaemia-reperfusion is associated with vascular dysfunction leading to post-insult impairment of blood flow and its regulation in many organs (Conger & Weil, 1995). A delayed, secondary fall in cerebral blood flow has been reported in both adult and neonatal preparations following asphyxia or ischaemia and is suggested to contribute to further injury (Rosenberg, 1988; Rosenberg et al. 1989; Gunn et al. 1997; Pourcyrous et al. 1997; Dorrepaal et al. 1997). Therapeutic intervention during this phase can significantly improve recovery of cerebral function (Gunn et al. 1997). It was the purpose of this study, therefore, to examine the cardiovascular, cerebrovascular and electroencephalographic (EEG) response of the 0.6 gestation fetal sheep to 30 min of asphyxia induced by complete umbilical cord occlusion and to evaluate the haemodynamic changes during the first 3 days after asphyxia.

Coronary artery disease is the leading cause of heart failure in the Western world. Left ventricular function is an important determinant of prognosis and parameters which reflect function such as left ventricular ejection fraction (LVEF), end-diastolic volume, end diastolic pressure, and exercise capacity can all be used to help predict outcome 1,2. The advent of drugs such as ACE inhibitors3, angiotensin II inhibitors4, and more recently beta-blocking agents such as carvedilol5 have provided means of improving prognosis in heart failure, but nevertheless overall outcome on medical treatment remains poor. Data from the CASS registry showed that in patients with left ventricular dysfunction on medical therapy, mortality increased in a curvilinear fashion in relation to reduction in LVEF 6. Furthermore it was shown that a survival benefit was conferred by surgical revascularization even in patients where LVEF was less than 25%, with a 1 year mortality of 15% in the surgical group and 24% in the medical group. Surgical and anesthetic techniques have improved since this data was published and most recent reports suggest an advantage of revascularization over medical therapy in patients with ischemic left ventricular dysfunction.7,8

Background Treatment of patients with severe aortic stenosis with transcatheter aortic valve implantation (TAVI) has led to the revival of balloon aortic valvuloplasty (BAV). We assessed the indications, immediate outcome and durability following BAV. Methods A retrospective analysis of the practice at this institution between 2009 and 2012 was performed. Demographic, clinical, procedural and follow-up data were collected. Results 63 patients with severe symptomatic aortic stenosis underwent BAV. All had appreciable co-morbidity. The median age was 80 (75–86) years, 41 (65.1%) were male. Of the entire cohort 22% were diabetic, 11% had a history of bypass surgery, 27% had previous stroke, 27% stage IV renal failure, 33% has severe airways disease and 52.4% were in atrial fibrillation. With regard to echocardiographic variables; the mean peak gradient pre-procedure was 66.1±19.3 mm Hg, mean aortic valve area was 0.61±0.2 cm 2 . Most had impaired left ventricular systolic function, mean ejection fraction 42.6±18%. BAV was performed as a bridge to TAVI in 28 (44%), surgical aortic valve replacement in 23 (37%) and as a standalone therapy in 12 (19%) patients. Significant complications occurred in 4 (6.4%) of patients; of whom 1 had peri-procedural MI, 1 had renal failure, 1 cardiac tamponade and 1 had a retroperitoneal bleed. No patient suffered significant aortic regurgitation, stroke, nor required PPM implantation. Although there was no immediate peri-procedural mortality, 4 (6.4%) patients died of progressive deterioration later during the same admission. With respect to the procedural success, there was a significant reduction observed in the mean peak gradient to 50.2±18.1 mm of Hg (p 2 (p Conclusions BAV is a useful adjunct to allow definitive therapy for severe aortic stenosis in patients with significant co-morbidity. Even in those patients who are unsuitable for TAVI or surgical valve replacement, and who have the highest attendant risk for valve intervention, standalone BAV can provide an effective treatment.

A 67-year-old woman presented with a 2-year history of increasing exertional dyspnea without angina or syncope. There was a maternal family history of hypertrophic obstructive cardiomyopathy. On examination, she had a jerky pulse and an ejection systolic murmur, which increased in intensity on exercise. Echocardiography showed hypertrophic cardiomyopathy. Doppler ultrasound recorded an estimated outflow gradient of 20 mm Hg at rest, which rose to >100 mm Hg during dobutamine stress. Magnetic resonance cine imaging (field strength, 0.5 T; echo time, 6 ms) performed at rest and during dobutamine stress (Figure⇓) showed that during stress only, marked systolic signal loss …

A characteristic of perinatal encephalopathies are the distinct patterns of neuronal and glial cell loss. Cerebral hypoperfusion is thought to be a major cause of these lesions. Gestational age is likely to influence outcome. This study compares the cortical electrophysiologic and histopathologic responses to hypoperfusion injury between preterm and near term fetuses. Chronically instrumented 0.65 (93-99-d, n = 9) and 0.9 (119-133-d, n = 6) gestation fetal sheep underwent 30 min of cerebral hypoperfusion injury. The parasagittal cortical EEG and impedance (measure of cytotoxic edema) responses plus histologic outcome (3 d) were compared. The acute rise in impedance was similar in amplitude, but the onset was delayed (5.0 ± 0.7 versus 9.1 ± 1.1 min, p < 0.05) in the preterm fetuses relative to those near term. In contrast the extent of the secondary rise was reduced (p < 0.01) and peaked earlier in the preterm fetuses (19.8 ± 1.0 versus 40.5 ± 3.5 h,p < 0.01). Both groups had a similar fall in EEG spectral edge frequency. The preterm fetuses had a milder loss of EEG intensity at 72 h(-7.7 ± 1.5 versus -12.8 ± 0.9 dB, p < 0.05). At both ages there was a predominantly parasagittal cortical distribution of damage with a similar pattern of neuronal loss in the thalamus and striatum. There was extensive selective neuronal loss within the upper layers of the cortex in those near term. In contrast the preterm fetuses developed subcortical infarcts (p < 0.05). The cortical response to injury altered during the last trimester. The results suggest the severity of the delayed phase of cortical neuronal injury and selective neuronal loss increased near term. In contrast, the preterm fetuses had a more rapidly evolving injury leading to necrosis of the subcortical white matter.