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Alterations in cerebrovascular reactivity to CO2, an index of cerebrovascular function, have been associated with increased risk of stroke. We hypothesised that cerebrovascular reactivity is impaired with increasing age and in patients with symptomatic coronary artery disease (CAD). Cerebrovascular and cardiovascular reactivity to CO2 was assessed at rest and during hypercapnia (5% CO2) and hypocapnia (hyperventilation) in subjects with symptomatic CAD (n=13) and age-matched old (n=9) and young (n=20) controls without CAD. Independent of CAD, reductions in middle cerebral artery blood velocity (transcranial Doppler) and cerebral oxygenation (near-infrared spectroscopy) were correlated with increasing age (r = -0.68, r = -0.51, respectively, P < 0.01). In CAD patients, at rest and during hypercapnia, cerebral oxygenation was lower (P < 0.05 vs. young). Although middle cerebral artery blood velocity reactivity was unaltered in the hypercapnic range, middle cerebral artery blood velocity reactivity to hypocapnia was elevated in the CAD and age-matched controls (P < 0.01 vs. young), and was associated with age (r = 0.62, P < 0.01). Transient drops in arterial PCO2 occur in a range of physiological and pathophysiological situations, therefore, the elevated middle cerebral artery blood velocity reactivity to hypocapnia combined with reductions in middle cerebral artery blood velocity may be important mechanisms underlying neurological risk with aging. In CAD patients, additional reductions in cerebral oxygenation may place them at additional risk of cerebral ischaemia. [ABSTRACT FROM AUTHOR]

Background: Elevated expression and increased activity of vascular epithelial sodium channel (ENaC) can result in vascular dysfunction in small animal models. However, there is limited or no knowledge on expression and function of ENaC channels in human vasculature. Hence, this study explored the expression and function of ENaC in human arteries and their association with hypertension., Methods: Human internal mammary artery (IMA) and aorta were obtained from cardiovascular patients undergoing coronary artery bypass graft surgery. Expression of the ENaC subunit was analyzed by polymerase chain reaction, Western blot, and immunohistochemistry. ENaC function was observed by patch-clamp electrophysiology in endothelial cells isolated from IMA. Levels of ENaC subunit expression levels were compared between arteries from normotensive, uncontrolled hypertensive, and controlled hypertensive patients., Results: For the first time, expression of α, β, γ, and δ was detected at mRNA and protein levels in human IMA and aorta. Single-channel patch-clamp recordings identified both αβγ- and δβγ-like channel conductance in primary endothelial cells isolated and cultured from IMA. Reduced expression of the δ subunit was observed in controlled hypertensive IMA, whereas reduced expression of γ-ENaC was observed in controlled hypertensive aorta., Conclusions: These data suggest that functional ENaC channels are expressed in human arteries and their expression levels are associated with hypertension.

Background and Purpose: Engagement in physical activity following coronary artery bypass graft (CABG) surgery has many benefits and also many potential barriers, especially during the first few months. It is important to explore current clinical practice before investigating ways to optimally prepare and support people to progressively increase their physical activity post-hospital discharge and to navigate the challenges. The aim of the study was to explore current practice in New Zealand hospital services for preparing and supporting people who have had CABG surgery to engage in physical activity following hospital discharge., Methods: Locality authorisation to participate in the study was sought from all 11 hospitals providing cardiac surgery services in New Zealand. The most senior health professional responsible for preparing people to engage in physical activity following CABG surgery was invited to participate by completing a purpose designed questionnaire on behalf of their hospital service. Respondents were also requested to provide any patient information handouts regarding progressive physical activity engagement following CABG surgery., Results: Responses were received from all nine hospitals that granted locality authorisation. All nine hospitals prepared people to engage in aerobic exercise prior to discharge, predominantly through the provision of a walking schedule. In contrast, no hospitals provided information about engagement in resistance exercise. There was wide variability in both the advice provided regarding sternal precautions and time to return to activities of daily living. Additionally, the facilitation of some elements of self-management for physical activity, in particular problem solving and providing follow up support outside of the cardiac rehabilitation setting was provided infrequently., Discussion: The findings demonstrated variability in service delivery in a number of areas and highlighted potential areas for improvement in light of what is known from the literature. Provision of follow up support for those unable to access outpatient cardiac rehabilitation is a key need., (© 2022 John Wiley & Sons Ltd.)

Background: The heart has an intrinsic ability to regenerate, orchestrated by progenitor or stem cells. However, the relative complexity of non-resident cardiac progenitor cell (CPC) therapy makes modulation of resident CPCs a more attractive treatment target. Thiamine analogues improve resident CPC function in pre-clinical models. In this double blinded randomised controlled trial (identifier: ACTRN12614000755639), we examined whether thiamine would improve CPC function in humans., Methods and Results: High dose oral thiamine (one gram twice daily) or matching placebo was administered 3-5 days prior to coronary artery bypass surgery (CABG). Right atrial appendages were collected at the time of CABG, and CPCs isolated. There was no difference in the primary outcome (proliferation ability of CPCs) between treatment groups. Older age was not associated with decreased proliferation ability. In exploratory analyses, isolated CPCs in the thiamine group showed an increase in the proportion of CD34 - /CD105 + (endoglin) cells, but no difference in CD34 - /CD90 + or CD34 + cells. Thiamine increased maximum force developed by isolated trabeculae, with no difference in relaxation time or beta-adrenergic responsiveness., Conclusion: Thiamine does not improve proliferation ability of CPC in patients undergoing CABG, but increases the proportion of CD34 - /CD105 + cells. Having not met its primary endpoint, this study provides the impetus to re-examine CPC biology prior to any clinical outcome-based trial examining potential beneficial cardiovascular effects of thiamine., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Long-chain acylcarnitines (LCACs) are known to directly alter cardiac contractility and electrophysiology. However, the acute effect of LCACs on human cardiac function is unknown. We aimed to determine the effect of LCAC 18:1, which has been associated with cardiovascular disease, on the contractility and arrhythmia susceptibility of human atrial myocardium. Additionally, we aimed to assess how LCAC 18:1 alters Ca 2+ influx and spontaneous Ca 2+ release in vitro. Human right atrial trabeculae ( n = 32) stimulated at 1 Hz were treated with LCAC 18:1 at a range of concentrations (1-25 µM) for a 45-min period. Exposure to the LCAC induced a dose-dependent positive inotropic effect on myocardial contractility (maximal 1.5-fold increase vs. control). At the 25 µM dose ( n = 8), this was paralleled by an enhanced propensity for spontaneous contractions (50% increase). Furthermore, all LCAC 18:1 effects on myocardial function were reversed following LCAC 18:1 washout. In fluo-4-AM-loaded HEK293 cells, LCAC 18:1 dose dependently increased cytosolic Ca 2+ influx relative to vehicle controls and the short-chain acylcarnitine C3. In HEK293 cells expressing ryanodine receptor (RyR2), this increased Ca 2+ influx was linked to an increased propensity for RyR2-mediated spontaneous Ca 2+ release events. Our study is the first to show that LCAC 18:1 directly and acutely alters human myocardial function and in vitro Ca 2+ handling. The metabolite promotes proarrhythmic muscle contractions and increases contractility. The exploratory findings in vitro suggest that LCAC 18:1 increases proarrhythmic RyR2-mediated spontaneous Ca 2+ release propensity. The direct effects of metabolites on human myocardial function are essential to understand cardiometabolic dysfunction. NEW & NOTEWORTHY For the first time, the fatty acid metabolite, long-chain acylcarnitine 18:1, is shown to acutely increase the arrhythmia susceptibility and contractility of human atrial myocardium. In vitro, this was linked to an influx of Ca 2+ and an enhanced propensity for spontaneous RyR2-mediated Ca 2+ release.

Diabetes is associated with cardiac metabolic disturbances and increased heart failure risk. Plasma fructose levels are elevated in diabetic patients. A direct role for fructose involvement in diabetic heart pathology has not been investigated. The goals of this study were to clinically evaluate links between myocardial fructose and sorbitol (a polyol pathway fructose precursor) levels with evidence of cardiac dysfunction, and to experimentally assess the cardiomyocyte mechanisms involved in mediating the metabolic effects of elevated fructose. Fructose and sorbitol levels were increased in right atrial appendage tissues of type 2 diabetic patients (2.8- and 1.5-fold increase respectively). Elevated cardiac fructose levels were confirmed in type 2 diabetic rats. Diastolic dysfunction (increased E/e', echocardiography) was significantly correlated with cardiac sorbitol levels. Elevated myocardial mRNA expression of the fructose-specific transporter, Glut5 (43% increase), and the key fructose-metabolizing enzyme, Fructokinase-A (50% increase) was observed in type 2 diabetic rats (Zucker diabetic fatty rat). In neonatal rat ventricular myocytes, fructose increased glycolytic capacity and cytosolic lipid inclusions (28% increase in lipid droplets/cell). This study provides the first evidence that elevated myocardial fructose and sorbitol are associated with diastolic dysfunction in diabetic patients. Experimental evidence suggests that fructose promotes the formation of cardiomyocyte cytosolic lipid inclusions, and may contribute to lipotoxicity in the diabetic heart.

The adipocytokine resistin is released from epicardial adipose tissue (EAT). Plasma resistin and EAT deposition are independently associated with atrial fibrillation. The EAT secretome enhances arrhythmia susceptibility and inotropy of human myocardium. Therefore, we aimed to determine the effect of resistin on the function of human myocardium and how resistin contributes to the proarrhythmic effect of EAT. EAT biopsies were obtained from 25 cardiac surgery patients. Resistin levels were measured by ELISA in 24-h EAT culture media ( n = 8). The secretome resistin concentrations increased over the culture period to a maximal level of 5.9 ± 1.2 ng/mL. Coculture with β-adrenergic agonists isoproterenol ( n = 4) and BRL37344 ( n = 13) had no effect on EAT resistin release. Addition of resistin (7, 12, 20 ng/mL) did not significantly increase the spontaneous contraction propensity of human atrial trabeculae ( n = 10) when given alone or in combination with isoproterenol. Resistin dose-dependently increased trabecula-developed force (maximal 2.9-fold increase, P < 0.0001), as well as the maximal rates of contraction (2.6-fold increase, P = 0.002) and relaxation (1.8-fold increase, P = 0.007). Additionally, the postrest potentiation capacity of human trabeculae was reduced at all resistin doses, suggesting that the inotropic effect induced by resistin might be due to altered sarcoplasmic reticulum Ca 2+ handling. EAT resistin release is not modulated by common arrhythmia triggers. Furthermore, exogenous resistin does not promote arrhythmic behavior in human atrial trabeculae. Resistin does, however, induce an acute dose-dependent positive inotropic and lusitropic effect.

Background: Cardiac surgery risk scoring systems predict operative mortality but not outcomes related to preoperative frailty. The aim of this study was to assess frailty in a cohort of older cardiac surgery patients as a predictor of postoperative outcomes., Methods: Prospective data was collected on patients 65 years of age and older undergoing cardiac surgery between September 2015 and October 2016 at Dunedin Hospital. Frailty was assessed with the Edmonton frail scale and five-metre gait speed. The primary endpoint was length of hospital stay. Secondary outcomes included postoperative complications, major adverse events, death and 12-month readmission rate., Results: Among the 96 patients, median age was 74 (interquartile range 10.5) and 65 (68%) were males. Of the sample 64 (67%) were scored as not frail, 22 (23%) as vulnerable, and 10 (10%) as frail. The median (interquartile range) postoperative days' stay were: not frail 6 (2), vulnerable 9.5 (8), and frail 15 (13). Survival analysis adjusting for EuroSCORE II, age, sex and surgery type showed that greater Edmonton Frail Scale scores were independently predictive of longer post-surgery hospital stay with a hazard ratio for discharge of 0.83 (95% confidence interval 0.76-0.91, p<0.001) per point. The Edmonton Frail Scale score was associated with the 12-month post discharge number of readmissions (adjusted incidence rate ratio 1.24 (95% confidence interval 1.13-1.37, p<0.001) per point., Conclusions: The Edmonton Frail Scale score predicts length of hospital stay post cardiac surgery and 12-month readmission rate in patients older than 65 years of age., (Copyright © 2019 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.)

Epicardial adipose tissue (EAT) deposition has a strong clinical association with atrial arrhythmias; however, whether a direct functional interaction exists between EAT and the myocardium to induce atrial arrhythmias is unknown. Therefore, we aimed to determine whether human EAT can be an acute trigger for arrhythmias in human atrial myocardium. Human trabeculae were obtained from right atrial appendages of patients who have had cardiac surgery ( n = 89). The propensity of spontaneous contractions (SCs) in the trabeculae (proxy for arrhythmias) was determined under physiological conditions and during known triggers of SCs (high Ca 2+ , β-adrenergic stimulation). To determine whether EAT could trigger SCs, trabeculae were exposed to superfusate of fresh human EAT, and medium of 24 h-cultured human EAT treated with β 1/2 (isoproterenol) or β 3 (BRL37344) adrenergic agonists. Without exposure to EAT, high Ca 2+ and β 1/2 -adrenergic stimulation acutely triggered SCs in, respectively, 47% and 55% of the trabeculae that previously were not spontaneously active. Acute β 3 -adrenergic stimulation did not trigger SCs. Exposure of trabeculae to either superfusate of fresh human EAT or untreated medium of 24 h-cultured human EAT did not induce SCs; however, specific β 3 -adrenergic stimulation of EAT did trigger SCs in the trabeculae, either when applied to fresh (31%) or cultured (50%) EAT. Additionally, fresh EAT increased trabecular contraction and relaxation, whereas media of cultured EAT only increased function when treated with the β 3 -adrenergic agonist. An acute functional interaction between human EAT and human atrial myocardium exists that increases the propensity for atrial arrhythmias, which depends on β 3 -adrenergic rather than β 1/2 -adrenergic stimulation of EAT.

Macroscopic deposition of epicardial adipose tissue (EAT) has been strongly associated with numerous indices of obesity and cardiovascular disease risk. In contrast, the morphology of EAT adipocytes has rarely been investigated. We aimed to determine whether obesity-driven adipocyte hypertrophy, which is characteristic of other visceral fat depots, is found within EAT adipocytes. EAT samples were collected from cardiac surgery patients (n = 49), stained with haematoxylin & eosin, and analysed for mean adipocyte size and non-adipocyte area. EAT thickness was measured using echocardiography. A significant positive relationship was found between EAT thickness and body mass index (BMI). When stratified into standardized BMI categories, EAT thickness was 58.7% greater (p = 0.003) in patients from the obese (7.3 ± 1.8 mm) compared to normal (4.6 ± 0.9 mm) category. BMI as a continuous variable significantly correlated with EAT thickness (r = 0.56, p < 0.0001). Conversely, no correlation was observed between adipocyte size and either BMI or EAT thickness. No difference in the non-adipocyte area was found between BMI groups. Our results suggest that the increased macroscopic EAT deposition associated with obesity is not caused by adipocyte hypertrophy. Rather, alternative remodelling via adipocyte proliferation might be responsible for the observed EAT expansion.

Background: The diabetic heart undergoes remodelling contributing to an increased incidence of heart failure in individuals with diabetes at a later stage. The molecular regulators that drive this process in the diabetic heart are still unknown., Methods: Real-time (RT) PCR analysis was performed to determine the expression of cardiac specific microRNA-208a in right atrial appendage (RAA) and left ventricular (LV) biopsy tissues collected from diabetic and non-diabetic patients undergoing coronary artery bypass graft surgery. To determine the time-dependent changes, cardiac tissue were collected from type 2 diabetic mice at different age groups. A western blotting analysis was conducted to determine the expression of contractile proteins α- and β-myosin heavy chain (MHC) and thyroid hormone receptor-α (TR-α), the negative regulator of β-MHC. To determine the beneficial effects of therapeutic modulation of miR-208a, high glucose treated adult mouse HL-1 cardiomyocytes were transfected with anti-miR-208a., Results: RT-PCR analysis showed marked upregulation of miR-208a from early stages of diabetes in type 2 diabetic mouse heart, which was associated with a marked increase in the expression of pro-hypertrophic β-MHC and downregulation of TR-α. Interestingly, upregulation of miR-208a preceded the switch of α-/β-MHC isoforms and the development of diastolic and systolic dysfunction. We also observed significant upregulation of miR-208a and modulation of miR-208a associated proteins in the type 2 human diabetic heart. Therapeutic inhibition of miR-208a activity in high glucose treated HL-1 cardiomyocytes prevented the activation of β-MHC and hence the hypertrophic response., Conclusion: Our results provide the first evidence that early modulation of miR-208a in the diabetic heart induces alterations in the downstream signaling pathway leading to cardiac remodelling and that therapeutic inhibition of miR-208a may be beneficial in preventing diabetes-induced adverse remodelling of the heart.

Aortic valve stenosis (AS) is a major cause of morbidity and mortality, with no effective medical therapies. Investigation into the underlying biology of AS in humans is limited by difficulties in obtaining healthy valvular tissue for use as a control group. However, micro-ribonucleic acids (miRNAs) are stable in post-mortem tissue. We compared valve specimens from patients undergoing aortic valve replacement for AS to non-diseased cadaveric valves. We found 106 differentially expressed miRNAs (p < 0.05, adjusted for multiple comparisons) on microarray analysis, with highly correlated expression among up- and down-regulated miRNAs. Integrated miRNA/gene expression analysis validated the microarray results as a whole, while quantitative polymerase chain reaction confirmed downregulation of miR-122-5p, miR-625-5p, miR-30e-5p and upregulation of miR-21-5p and miR-221-3p. Pathway analysis of the integrated miRNA/mRNA network identified pathways predominantly involved in extracellular matrix function. A number of currently available therapies target products of upregulated genes in the integrated miRNA/mRNA network, with these genes being predominantly more peripheral members of the network. The identification of a group of tissue miRNA associated with AS may contribute to the development of new therapeutic approaches to AS. This study highlights the importance of systems biology-based approaches to complex diseases.

Background: Diabetes promotes progressive loss of cardiac cells, which are replaced by a fibrotic matrix, resulting in the loss of cardiac function. In the current study we sought to identify if excessive autophagy plays a major role in inducing this progressive loss., Methods and Results: Immunofluorescence and western blotting analysis of the right atrial appendages collected from diabetic and non-diabetic patients undergoing coronary artery bypass graft surgery showed a marked increase in the level of autophagy in the diabetic heart, as evidenced by increased expression of autophagy marker LC3B-II and its mediator Beclin-1 and decreased expression of p62, which incorporates into autophagosomes to be efficiently degraded. Moreover, a marked activation of pro-apoptotic caspase-3 was observed. Electron microscopy showed increased autophagosomes in the diabetic heart. In vivo measurement of autophagic flux by choloroquine injection resulted in further enhancement of LC3B-II in the diabetic myocardium, confirming increased autophagic activity in the type-2 diabetic heart. Importantly, in-vitro genetic depletion of beclin-1 in high glucose treated adult rat cardiomyocytes markedly inhibited the level of autophagy and subsequent apoptotic cell death., Conclusions: These findings demonstrate the pathological role of autophagy in the type-2 diabetic heart, opening up a potentially novel therapeutic avenue for the treatment of diabetic heart disease., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

This data article contains full list of autophagy related genes that are altered in diabetic heart. This article also shows data from in vitro cultured cardiomyocytes that are exposed the high glucose treatment to simulate hyperglycemic state in vitro. The interpretation of these data and further extensive insights into the regulation of SG biogenesis by AMPK can be found in "Type-2 diabetes increases autophagy in the human heart through promotion of Beclin-1 mediated pathway" (Munasinghe et al., in press) [1].

Background: Diastolic dysfunction is a key factor in the development and pathology of cardiac dysfunction in diabetes, however the exact underlying mechanism remains unknown, especially in humans. We aimed to measure contraction, relaxation, expression of calcium-handling proteins and fibrosis in myocardium of diabetic patients with preserved systolic function., Methods: Right atrial appendages from patients with type 2 diabetes mellitus (DM, n = 20) and non-diabetic patients (non-DM, n = 36), all with preserved ejection fraction and undergoing coronary artery bypass grafting (CABG), were collected. From appendages, small cardiac muscles, trabeculae, were isolated to measure basal and β-adrenergic stimulated myocardial function. Expression levels of calcium-handling proteins, sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) and phospholamban (PLB), and of β1-adrenoreceptors were determined in tissue samples by Western blot. Collagen deposition was determined by picro-sirius red staining., Results: In trabeculae from diabetic samples, contractile function was preserved, but relaxation was prolonged (Tau: 74 ± 13 ms vs. 93 ± 16 ms, non-DM vs. DM, p = 0.03). The expression of SERCA2a was increased in diabetic myocardial tissue (0.75 ± 0.09 vs. 1.23 ± 0.15, non-DM vs. DM, p = 0.007), whereas its endogenous inhibitor PLB was reduced (2.21 ± 0.45 vs. 0.42 ± 0.11, non-DM vs. DM, p = 0.01). Collagen deposition was increased in diabetic samples. Moreover, trabeculae from diabetic patients were unresponsive to β-adrenergic stimulation, despite no change in β1-adrenoreceptor expression levels., Conclusions: Human type 2 diabetic atrial myocardium showed increased fibrosis without systolic dysfunction but with impaired relaxation, especially during β-adrenergic challenge. Interestingly, changes in calcium-handling protein expression suggests accelerated active calcium re-uptake, thus improved relaxation, indicating a compensatory calcium-handling mechanism in diabetes in an attempt to maintain diastolic function at rest despite impaired relaxation in the diabetic fibrotic atrial myocardium. Our study addresses important aspects of the underlying mechanisms of diabetes-associated diastolic dysfunction, which is crucial to developing new therapeutic treatments.

Background: Diabetic women are five times more likely to develop congestive heart failure compared with two fold for men. The underlying mechanism for this gender difference is not known. Here we investigate the molecular mechanisms responsible for this female disadvantage and attempt safeguarding cardiomyocytes viability and function through restoration of pro-survival Pim-1., Methods and Results: Diabetes was induced by injection of streptozotocin in CD1 mice of both genders. Functional and dimensional parameters measurement using echocardiography revealed diastolic dysfunction in female diabetic mice within 8 weeks after STZ-induced diabetes. This was associated with significant downregulation of pro-survival Pim-1 and upregulation of pro-apoptotic Caspase-3, microRNA-1 and microRNA-208a. Male diabetic mice did not show any significant changes at this time point (P < 0.05 vs. female diabetic). Further, the onset of ventricular remodelling was quicker in female diabetic mice showing marked left ventricular dilation, reduced ejection fraction and poor contractility (P < 0.05 vs. male diabetic at 12 and 16 weeks of STZ-induced diabetes). Molecular analysis of samples from human diabetic hearts confirmed the results of pre-clinical studies, showing marked downregulation of Pim-1 in the female diabetic heart (P < 0.05 vs. male diabetic). Finally, in vitro restoration of Pim-1 reversed the female disadvantage in diabetic cardiomyocytes., Conclusions: We provide novel insights into the molecular mechanisms behind the rapid onset of cardiomyopathy in female diabetics. These results suggest the requirement for the development of gender-specific treatments for diabetic cardiomyopathy.

A combination of cardiac surgery and thyroidectomy as a single stage operation has rarely been reported in the literature. We report on the management of a 64-year-old female undergoing a combined aortic valve replacement and excision of a primary (ectopic) intrathoracic goiter. The literature on combined cardiac surgery and thyroidectomy is also reviewed., (© 2012 Wiley Periodicals, Inc.)

Cardiac tumors require resection for diagnostic purposes and to avoid complications associated with an intracardiac mass. We present the case of a 41-year-old woman with a known uterine leiomyoma who presented 3 months after elective cesarian section and hysterectomy with a right ventricular mass that was confirmed histologically to be a benign leiomyoma of the same pathologic type as the uterine primary. Benign metastasizing leiomyoma is a rare pathologic entity occurring in women with a history of a uterine leiomyoma. This is the second reported case of cardiac metastasis from a benign uterine leiomyoma., (2010 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Saphenous vein graft aneurysm is a potentially fatal complication of coronary artery bypass grafting and usually requires surgery. This report describes endovascular coiling of a saphenous vein graft aneurysm that developed after redo coronary artery bypass grafting. The aneurysm occurred in a proximally occluded saphenous vein graft after revascularization of the same target vessel. The procedure required a retrograde approach through a patent left internal mammary and left anterior descending artery to reach and successfully thrombose the aneurysm.

Two cases of primary pulmonary sarcoma which were initially diagnosed as pulmonary thromboembolism are presented. The clinical and radiologic features of pulmonary sarcoma are reviewed, with special emphasis on the features which distinguish it from thromboembolism.

From 1971 to 1988, 303 patients underwent left ventricular aneurysm resection. We analyzed preoperative and procedure-related variables to ascertain risk factors for surgery. A distinction was made between akinetic and dyskinetic aneurysms to assess potential relation with postoperative outcome. Indications for surgery were arrhythmia in 20 patients, congestive heart failure in 81, angina in 133, congestive heart failure and angina in 42, and other combinations in the remaining 27 patients. The left ventricular aneurysm was dyskinetic in 180 patients and akinetic in 121. Risk factors and surgical procedures were similar in both groups. Left ventricular ejection fraction was less than or equal to 30% in 98 patients. Coronary bypass grafting was performed in 269 patients, with an average of 2.3 grafts per patient. Mitral valve replacement, the most common concomitant procedure, was performed in 16 patients. Intra-aortic balloon assist was required postoperatively in 47 patients. Overall operative mortality was 13% (38 patients) and was due to low cardiac output in 23 patients and arrhythmia in 12 patients. Univariate and multivariate analyses related early mortality to New York Heart Association functional classification of heart failure, the predominant indications of arrhythmia or congestive heart failure, left ventricular ejection fraction less than or equal to 30%, the need for intra-aortic balloon support, and the excision of an akinetic (18%) rather than dyskinetic (8%) left ventricular aneurysm. Over a follow-up period averaging nearly 5 years, the actuarial survival at 5 years was 63% in the dyskinetic group and 51% in the akinetic group.(ABSTRACT TRUNCATED AT 250 WORDS)

An experimental study to assess the performance of currently available pericardial substitutes is described with particular reference to their use after coronary artery bypass grafting. Seventy-two ewes, (six groups of 12 animals) had a 7 x 5 cm portion of the pericardium excised. Each group had either the defect left open, primarily resutured, replaced with coarse Dexon No. 2 mesh (American Cyanamid Co., Danbury, Conn.), replaced with fine Dexon No. 8 mesh, replaced with glutaraldehyde-preserved bovine pericardium, or replaced with polytetrafluoroethylene 0.1 mm surgical membrane. Six animals from each group were assessed at 3 months and the remaining six animals were assessed at 6 months. The open-defect and resutured groups served as control animals. None of the substitutes proved superior to the open-defect group in the prevention of chest wall/lung-to-pericardium adhesions at either 3 or 6 months. The limitations of the animal model in assessing this aspect of substitute performance are discussed. Whereas the bovine pericardium, polytetrafluorethylene, and Dexon No. 8 mesh groups were superior to the resutured group in the prevention of pericardium-to-epithelium adhesions in the area of the patch, this advantage was lost at 6 months when resuturing proved as effective as polytetrafluoroethylene and bovine pericardium. In all groups there was little tendency to produce generalized pericardial adhesions. At 3 months Dexon No. 8 mesh and bovine pericardium produced the least amount of significant epicardial reaction. In two animals in the 3-month polytetrafluoroethylene group and in one animal in the 6-month polytetrafluoroethylene group, a "fibrous peel" was encountered on the inner surface of the patch, which had also become adherent to the epicardium and had obscured the underlying anatomy. At 6 months the open-defect, resutured, and bovine pericardium groups had produced no significant epicardial reaction. In one animal at 6 months the bovine pericardium had become markedly thickened and degenerative. We do not recommend routine closure of the pericardium after coronary artery operations with any of the substitutes investigated in our study.

Localized pleural fibromas are a definite clinical entity. Their origin is much debated. Though most arise from the mesothelial cell, occasionally some arise from the pleural fibroblast. The former retain the potential to become malignant. Distinguishing between the two origins can aid prognosis after treatment. The characteristic cell is a spindle-shaped fibroblast. Slits or clefts lined by flattened cells are often present in the tumor. Clinically, pleural fibromas are usually asymptomatic, space-occupying lesions. Chest symptoms are nonspecific. Extrathoracic symptoms, especially arthritis, are not uncommon and occur only in the benign variety. Excision is the treatment of choice, but long-term follow-up is essential, for recurrence is not unknown and is often heralded by the region of arthritic symptoms. Recurrences may be benign or malignant, the latter having a poor prognosis, with most patients dying within 2 years. Experience with benign pleural fibromas seen in 6 patients over a 25-year period is presented.

The relative risks associated with anti-inflammatory drug prescription for patients with an earlier history of drug-associated gastro-intestinal disturbance have been investigated in a retrospective study. Under these circumstances ibuprofen was well tolerated. The risks associated with modified salicylates (principally aspirin in enteric-coated form) and indomethacin suppositories also appeared to be relatively slight. Retreatment with phenylbutazone, oral indomethacin, naproxen and combination therapy was hazardous.

Twelve consecutive infants with interrupted aortic arch, ventricular septal defect, and persistent ductus arteriosus have had the anomaly repaired without the use of synthetic grafts. In two infants (5 and 9 months) the ductus arteriosus was used for the arch repair. In three patients (mean age 14 days) the left carotid artery was turned down to form the new arch. In the remaining seven (mean age 12 days) a direct anastomosis was achieved, but one of these patients died at operation. Two others in this group also had persistent truncus arteriosus. Five patients have required another operation (two for stenosis of the anastomosis with one death). The 10 survivors (mean follow-up 5 years) are well and support our belief that complete repair without the use of synthetic grafts is the treatment of choice in this rare and difficult group.

Survey of implantation of porcine heterograft valves in the Dunedin Cardiac Surgical Unit has been reviewed covering 140 patients and 166 valves with a follow-up ranging from 1-55 months. The low mortality, minimal complication rate and absence of long term anticoagulants in the post operative regime are emphasized. Discussion centres on the low rate of complications and the usefulness of this valve. As with all biological valves durability is still in question.

Two patients with lateral subluxation of the atlas resulting from rheumatoid disease involving the upper cervical spine have been described. The deformity can be suspected on clinical grounds and in one of our two patients spinal cord damage was a sequel. Erosion of the opposing surfaces of the odontoid and lateral masses of the atlas with detachment of the transverse ligament and deeper fibres of the posterior longitudinal ligament appear to underlie this deformity. Radiological confirmation may require AP views with the head tilted to one or other side.

Serial serum magnesium estimations, beginning before operation, were performed on 200 patients who underwent coronary artery bypass grafting. The results indicate that serum magnesium concentration is of no value in the diagnosis of myocardial infarction in the postoperative patient or in predicting which patients are susceptible to postoperative dysrhythmias. There was no statistically significant difference in serum magnesium values between those patients who had an uncomplicated course and patients who had sustained either myocardial infarction or postoperative dysrhythmia or both.