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In a conference call on Monday morning, Feb. 29, 2016, members of CMAJ ’s Journal Oversight Committee (JOC) were informed that the editor-in-chief (EIC) had been relieved of duty and the JOC itself disbanded — all in direct contravention of processes the CMA had put in place to protect editorial

During acute pulmonary hypertension, both the pericardium and the right ventricle (RV) constrain left ventricular (LV) filling; therefore, pericardiotomy should improve LV function. LV, RV, and pericardial pressures and RV and LV dimensions and LV stroke volume (SV) were measured in six anesthetized dogs. The pericardium was closed, the chest was left open, and the lungs were held away from the heart. Data were collected at baseline, during pulmonary artery constriction (PAC), and after pericardiotomy with PAC maintained. PAC decreased SV by one-half. RV diameter increased, and septum-to-LV free wall diameter and LV area (our index of LV end-diastolic volume) decreased. Compared with during PAC, pericardiotomy increased LV area and SV increased 35%. LV and RV compliance (pressure-dimension relations) and LV contractility (stroke work-LV area relations) were unchanged. Although series interaction accounts for much of the decreased cardiac output during acute pulmonary hypertension, pericardial constraint and leftward septal shift are also important. Pericardiotomy can improve LV function in the absence of other sources of external constraint to LV filling.

Academic Health Sciences Centres have provided and continue to provide valuable service to society. However, the lack of a clear mandate, structure, governance and administration results in their full potential not being met. As the Canadian healthcare system undergoes the reform that must occur to make the publicly funded system sustainable into the future, it is essential that AHSCs have clarification of their roles, develop a distinct governance structure and be provided a distinct budget for a set of deliverables within an agreed-upon accountability framework.

The Frank-Starling Law accounts for many changes in cardiac performance previously attributed to changes in contractility in that changes in contractility might have been incorrectly inferred from changing ventricular function curves (i.e. systolic performance plotted against filling pressure) if diastolic compliance also changed. To apply the Frank-Starling Law in the presence of changing diastolic compliance, it is necessary to measure end-diastolic volume directly or to calculate end-diastolic transmural pressure, which requires that pericardial pressure be known. Under most normal circumstances, increased intrathoracic pressure (and other interventions, such as vasodilators or lower-body negative pressure, that decrease central blood volume) decreases the transmural end-diastolic pressures of both ventricles, their end-diastolic volumes and stroke work. However, when ventricular interaction is significant, the effects of these interventions might be quite different; this may be important in patients with heart-failure. Although these interventions decrease RV transmural pressure, they may increase LV transmural pressure, end-diastolic volume, and thus stroke work by the Frank-Starling mechanism.

Over the past several years, the editors of leading international cardiovascular journals have met to form the HEART Group and to discuss areas of growing, common interest. Recently, the HEART Group has developed a document that addresses general ethical principles in the conduct of the scientific process with which all of the editors concur. Published essentially simultaneously in all of the participating journals, including this journal, this document presents the ethical tenets accepted by all of the undersigned editors that will (continue to) guide their decisions in the editorial process. These are the general principles on which the HEART Group is based and by which we, as a group, abide; however, please note that individual journal members and their respective societies may have their own rules and regulations that supersede the guidelines of the HEART Group. Acta Cardiologica Hugo Ector, MD, PhD Editor-in-Chief Patrizio Lancellotti, MD Editor-in-Chief American Journal of Cardiology William C. Roberts, MD Editor-in-Chief American Journal of Geriatric Cardiology Nanette K. Wenger, MD Editor-in-Chief Annals of Noninvasive Electrocardiology Arthur J. Moss, MD Editor-in-Chief Canadian Journal of Cardiology Eldon R. Smith, MD Editor-in-Chief Cardiology Jeffrey S. Borer, MD Editor-in-Chief Cardiosource Review Journal Kim A. Eagle, MD Editor-in-Chief Cardiovascular Drug Reviews Jane Freedman, MD Incoming Editor-in-Chief Henry Krum, PhD Incoming Editor-in-Chief Chim Lang, MD Incoming Editor-in-Chief Cardiovascular Drugs and Therapy Willem J. Remme, MD, PhD Editor-in-Chief Cardiovascular Research Hans Michael Piper, MD, PhD Editor-in-Chief Catheterization and Cardiovascular Interventions Christopher J. White, MD Editor-in-Chief Circulation Joseph Loscalzo, MD, PhD Editor-in-Chief Circulation Research Eduardo Marban, MD, PhD Editor-in-Chief Coronary Artery Disease Burton E. Sobel, MD Editor Current Opinion in Cardiology Robert Roberts, MD Editor Current Problems in Cardiology Shahbudin H. Rahimtoola, MD Editor Europace A. John Camm, MD Editor-in-Chief European Heart Journal Frans Van de Werf, MD Editor-in-Chief European Journal of Heart Failure Karl Swedberg, MD, PhD Editor-in-Chief Heart Adam D. Timmis, MD Editor Heart & Lung: The Journal of Acute and Critical Care Kathleen S. Stone, PhD, RN Editor-in-Chief Heart Rhythm Douglas P. Zipes, MD Editor-in-Chief International Journal of Interventional Cardioangiology David G. Iosseliani, MD Editor-in-Chief Journal of Cardiovascular Computed Tomography Allen J. Taylor, MD Editor-in-Chief Journal of Cardiovascular Pharmacology Michael R. Rosen, MD Editor Journal of Interventional Cardiology Cindy L. Grines, MD Editor-in-Chief Journal of the American College of Cardiology Anthony N. DeMaria, MD Editor-in-Chief JACC: Cardiovascular Imaging Jagat Narula, MD, PhD Editor-in-Chief JACC: Cardiovascular Interventions Spencer B. King III, MD Editor-in-Chief Journal of Electrocardiology Galen S. Wagner, MD Editor-in-Chief Journal of Interventional Cardiac Electrophysiology Sanjeev Saksena, MD Editor-in-Chief Journal of the American Society of Echocardiography Alan S. Pearlman, MD Editor-in-Chief Journal of Heart Valve Disease Endre Bodnar, MD, PhD Editor-in-Chief Robert W. Emery, MD Incoming Editor-in-Chief Journal of Thoracic and Cardiovascular Surgery Lawrence H. Cohn, MD Editor-in-Chief Netherlands Heart Journal Ernst E. van der Wall, MD Editor-in-Chief Pediatric Cardiology Ra-id Abdulla, MD Editor-in-Chief Progress in Cardiovascular Diseases Michael Lesch, MD Editor Revista Espanola de Cadiologia Fernando Alfonso, MD, PhD Editor-in-Chief Scandinavian Cardiovascular Journal Rolf Ekroth, MD Chief Editor

In the intact animal, it is difficult to discriminate between the independent effects of series and direct ventricular interaction (DI) or the individual contributions of the pericardium and septum to DI. Left ventricular (LV) venous return (LVVR) and right ventricular (RV) end-diastolic pressure (RVEDP) were varied independently in a right-heart bypass model. LV minor-axis diameters were measured, and the product of the two diameters was used as an index of LV volume (LVVI). At each RVEDP (0, 5, 10, and 15 mmHg), increased LVVR caused an increased LVVI. When RVEDP was increased, increased pump output was required to maintain a given LVVI. RV-to-LV pressure gain (DeltaLVEDP/DeltaRVEDP) reflects coupling and DI. With the pericardium closed, the gain was dependent on RVEDP; when RVEDP was increased from 0 to 5 mmHg, the gain was not statistically different from zero, indicating little or no DI. When RVEDP was increased from 10 to 15 mmHg, the gain was not statistically different from 1.0, indicating approximately 1:1 coupling of the ventricles. Opening the pericardium reduced the gain, but significant interaction remained. When the septal contribution was accounted for, the remaining interaction was eliminated. In conclusion, DI substantially affects LVEDP-volume relations. Considerable increases in RV output may be required to counterbalance increased constraint to LV filling. With the pericardium closed, RV-to-LV coupling is minimal when RVEDP is low and increases to 1:1 coupling when RVEDP is high. Opening the pericardium reduces DI, but significant septum-mediated interaction remains.

Background Acute right ventricular (RV) hypertension may result in hemodynamic collapse. The associated reduction in left ventricular (LV) end-diastolic volume is thought to result from reduced RV output (secondary to RV ischemia) and adverse direct ventricular interaction. Aortic constriction improves cardiac function in these circumstances; this has been attributed to a reversal of the RV ischemia caused by an increased coronary perfusion pressure. We hypothesized that altered ventricular interaction, potentially via altered septal mechanics, may also contribute to the beneficial effects of aortic constriction. Methods and Results We instrumented nine dogs with ultrasonic dimension crystals to measure RV segment length, septum–to–RV free wall and septum–to–LV free wall diameters, and LV anteroposterior diameter. Catheter-tipped manometers were used to measure LV and RV pressures. Pericardial pressure was measured with flat, liquid-containing balloon transducers. Inflatable cuff constrictors were placed on the pulmonary artery (PA) and aorta, and a flow probe was placed on the PA. The right coronary artery (RCA) was perfused independently by a roller pump calibrated for flow. During moderate PA constriction, while RCA pressure was maintained at control level, RCA flow did not change significantly (15.8±6.2 to 16.9±11.5 mL/min) and was similar during severe PA constriction (18.6±9.8 mL/min). During severe PA constriction, RV stroke volume decreased from a control value of 10.3±4.9 to 2.3±1.4 mL/beat ( P P P Conclusions In this model of acute RV hypertension, aortic constriction improves cardiac function, at least in part, by altering ventricular interaction independent of changes in RCA flow. Changes in RCA flow do not appear to have a significant impact on cardiac function in this model in which coronary artery pressure was maintained at normal or increased levels.

To define relative changes in intestinal vascular capacitance, we developed a model that allowed us to construct intestinal vascular pressure-volume relationships (PVR). Thirteen alpha-chloralose-anesthetized and splenectomized dogs were studied using a pneumatic constrictor and a small catheter to change and measure portal venous pressure. A small lead sheet was placed beneath the abdominal wall. Relative changes in intestinal blood volume (IBV) were determined by in vivo blood pool scintigraphy with 99mTc-labeled erythrocytes and were expressed as percentages corrected for specific activity and abdominal wall radioactivity. PVRs were constructed using data recorded during graded inflations of the portal venous constrictor. The abdominal wall contributed 32.4 +/- 7.7% (SD) of the total counts. During a 4-h control period, PVRs varied by no more than 6% (of IBV). In the isolated intestinal circulation, the change in IBV was precisely proportional to the volume of blood added, indicating that this method can detect very small changes in volume (< or = 5 ml). Nitroglycerin (25 micrograms.kg-1.min-1) increased capacitance by 20%. Although it measures only relative changes, the model is stable and sensitive, provides reproducible measurement of intestinal PVRs, and, with adaptation, may prove useful in patient studies.

BACKGROUND To determine the transmural pressure-dimension relations of the right atrium (RA) and right ventricle (RV) before and after pericardiectomy, six open-chest dogs were instrumented with pericardial balloons placed over the RA and RV free walls. METHODS AND RESULTS PA appendage dimensions and RV free-wall segment lengths were measured using sonomicrometry. Intact-pericardium RA and RV transmural pressures were calculated by subtracting the pericardial pressures (measured using balloons) from the cavitary pressures. Pooled data from six animals with pericardium intact indicate that at RA and RV cavitary pressures of 5, 10, and 15 mm Hg, RV pericardial pressure was 4.3 +/- 0.3, 8.6 +/- 1.0, and 13.3 +/- 1.5 mm Hg, respectively, and RA pericardial pressure was 4.8 +/- 0.3, 9.6 +/- 0.6, and 14.6 +/- 0.6 mm Hg, respectively (mean +/- SD). With calculated unstressed dimensions, the cavity dimension data were normalized to strain (in percent). We determined that in the dog, RV strain would increase by 14% and RA by 68% to maintain cavitary pressure at 10 mm Hg on pericardiectomy. To compare these results with clinical data, RV (n = 7) and RA (n = 6) transmural pressures were measured using balloons in patients (age, 19 to 76 years) undergoing cardiac surgery. RA transmural pressure of six patients was 1.0 +/- 1.5 mm Hg when central venous pressures (CVPs) ranged from 3 to 16 mm Hg. RV transmural pressure equaled 1.2 +/- 1.9, 2.3 +/- 1.9, and 3.4 +/- 2.0 mm Hg when CVP was 5, 10, and 15 mm Hg, respectively. CONCLUSIONS Pericardial constraint (as evaluated by the ratio of pericardial to intracavitary pressures when CVP is 10 mm Hg) accounted for 96% of RA cavitary pressure in the dog and 89% in humans and at least 86% of RV cavitary pressure in the dog and 77% in humans.

Canada spans 9,976,140 square kilometers and has an approximate population of 32 million people (Statistics Canada, 2001). More than 90% of Canada’s geography is considered rural or remote (Government of Canada, 2001). Despite the highly dispersed population, and, indeed, because of it, Canada is committed to the idea that a networked telehealth system could provide better access and equity of care to Canadians. Growing evidence of the feasibility and affordability of telehealth applications substantiates Canada’s responsibility to promote and to develop telehealth. Telehealth is the use of advanced telecommunication technologies to exchange health information and provide healthcare services across geographic, time, social, and cultural barriers (Reid, 1996). According to a systematic review of telehealth projects in different countries (Jennett et al., 2003a, 2003b), specific telehealth applications have shown significant socioeconomic benefits to patients and families, healthcare providers, and the healthcare system. Implementing telehealth can impact the delivery of health services by increasing access, improving quality of care, and enhancing social support (Bashshur, Reardon, & Shannon, 2001; Jennett et al., 2003a). It also has the potential to impact skills training of the health workforce by increasing educational opportunities (Jennett et al., 2003a; Watanabe, Jennett, & Watson, 1999). Therefore, telehealth has a strong potential to influence improved health outcomes in the population (Jennett et al., 2003a, 2003b). Fourteen health jurisdictions—one federal, 10 provincial, and three territorial—are responsible for the policies and infrastructure associated with healthcare delivery in Canada. This article presents a telehealth case study in one of Canada’s health jurisdictions—the province of Alberta. The rollout of telehealth in Alberta serves as an example of best practice. Significant milestones and lessons learned are presented. Progress toward the integration of the telehealth network into a wider province-wide health information network also is highlighted.

Diastolic ventricular interaction is associated with septal shift and deformation, the consequences of which have not been fully assessed. A model was therefore developed to describe the mechanisms involved in interaction between the ventricles under different loading conditions. We assumed a circular cardiac minor-axis geometry surrounded by a pericardial membrane with the left ventricle (LV) and septum described by three layers. To define the equilibrium condition, we required the net force-balance at the right ventricular (RV)-LV intersection points to equal zero. The model was tested with and without consideration of bending forces associated with a change of curvature of a thick-walled structure. Model results were compared with data from animal experiments subjected to aortic and pulmonary constriction. LV and RV end-diastolic pressures as well as pericardial pressure were measured. In six dogs, septal segment length was measured using sonomicrometry, and in seven dogs, endocardial curvature was measured using echocardiography. Model and experimental results show that 1) with severe RV loading, septal inversion occurs at a negative transseptal gradient, and 2) the end-diastolic septal segment length continues to shorten after septal inversion during pulmonary constriction. Model simulation suggests that bending moments account for the septal curvature at zero transseptal pressure. In addition, the model predicts the shift in the pressure-area relationship of each ventricle by a change in loading of the opposite ventricle and predicts that large transmural gradients in stress and strain are associated with septal inversion. Thus the model and the experimental data agree and describe the important factors that modulate diastolic septal mechanics during acute differential ventricular loading.

BACKGROUND Body surface maps of net QRST deflection areas (isointegrals) reflect regional ventricular repolarization properties. Vulnerability to ventricular tachyarrhythmias is associated with maps that feature multiple islands (extrema) of positive and negative values; such maps reflect regional disparity of ventricular recovery properties. The value of body surface mapping in prediction of the efficacy of antiarrhythmic therapy for ventricular tachyarrhythmias has not been determined. METHODS AND RESULTS Isointegral ECG body surface mapping was performed in 51 patients with inducible ventricular tachycardia having programmed stimulation studies at baseline and after oral quinidine therapy. The degree of nondipolarity of QRST isointegral distribution was expressed by the number of extrema and by the percentage contribution of nondipolar eigenvectors after Karhunen-Loeve transformation. QRST isointegral nondipolarity was greater in ventricular tachycardia patients than in 51 age- and sex-matched normal subjects expressed as mean number of extrema (4.1 +/- 2.8 versus 2.0 +/- 0.2, respectively), mean eigenvector-determined nondipolar content percentages (12.4 +/- 10.1% versus 4.5 +/- 4.9%), prevalence of abnormal numbers of extrema (63% versus 4%), or prevalence of abnormal nondipolar content percentages (33% versus 4%) (each p less than 0.01). Quinidine prevented ventricular tachycardia induction in 14 patients. Patients for whom quinidine was or was not effective had similar nondipolarity indexes at baseline. However, maps on quinidine differed as a function of antiarrhythmic efficacy. Although effective therapy produced no significant mean changes in nondipolarity, ineffective therapy increased the number of extrema compared with baseline (5.4 +/- 3.4 versus 3.8 +/- 2.5, respectively) (p = 0.002). Individually, 43% of patients on effective therapy had drug-induced decreases in numbers of extrema compared with 14% of those on ineffective therapy (p = 0.02). Furthermore, 29% of patients on effective therapy showed drug-induced increases in numbers of extrema compared with 62% of those on ineffective therapy (p = 0.03). CONCLUSIONS QRST isointegral body surface mapping shows promise as a noninvasive measure of drug efficacy in patients with ventricular tachycardia.

The magnitude of pericardial pressure and therefore the shape of the right ventricular end-diastolic transmural pressure-volume relationship remains controversial. To investigate ventricular compliance, eight dogs anesthetized with fentanyl were instrumented as follows. Right and left ventricular intracavitary pressures were measured with micromanometer-tipped catheters. Right and left ventricular free wall segment lengths were measured by sonomicrometry. Pericardial pressure was measured over the right and left ventricles by means of flat liquid-containing balloon transducers, and transmural pressures were calculated as the difference between intracavitary and pericardial pressures. After defining the pressure-segment length relationship by vena caval constriction followed by release and blood transfusion, the pericardium and chest were opened widely and the cardiac volume manipulation was repeated; this allowed direct measurement of transmural right ventricular end-diastolic pressure for each level of strain recorded with the chest and pericardium closed. When intracavitary right or left ventricular end-diastolic pressure was raised from zero to 20 mm Hg, the respective transmural pressures increased from 0.2 ± 0.6 (SD) mm Hg to 2.5 ± 1.6 mm Hg and from 0.3 ± 0.7 mm Hg to 6.0 ± 2.5 mm Hg. Ventricular segmental strain increased by 7.0 ± 0.8% and 6.0 ± 0.2%, respectively. No statistically significant differences were found between right ventricular calculated (intracavitary minus pericardial pressure) and measured (open pericardium, open chest) transmural pressures at a given strain, thereby confirming the accuracy of our pericardial pressure measurements. In addition, there was a linear relationship between the pressure measured over the right and left ventricles: right ventricular pericardial pressure = 1.00 (left ventricular pericardial pressure) − 0.53 (r = 0.98, p < 0.0005). In conclusion, the right ventricle has a small but measurable end-diastolic transmural pressure, which increases slightly over a wide range of intracavitary pressures and myocardial segmental strain. The compliance of the right ventricle is three to four times that of the left ventricle. Furthermore, the pericardial pressures measured over the right and left ventricles are similar.

This issue of the Journal marks a couple of milestones. First, this represents the 25th anniversary of the first issue of The Canadian Journal of Cardiology (CJC). Second, after 13 years, it represents my last issue as Editor-in-Chief. The first issue of the Journal was published in January 1985, with the late Dr Bob Beamish as Editor-in-Chief, a position he held for 12 years. It is appropriate to reflect on that first issue for a number of reasons. First, in 1985, Pulsus Group Inc established the Journal with no more than a hope that it would become the official journal of the Canadian Cardiovascular Society (CCS). Eldon R Smith Interestingly, I was one of a number of CCS members who were outspoken opponents to the Journal, believing that the Canadian cardiovascular science community was too small to support a high-quality journal. But through the persistence of Mr Robert Kalina of Pulsus Group Inc, and of Dr Beamish, the CJC was successful in becoming indexed (not an insignificant achievement) and was being recognized internationally as the de facto ‘Canadian’ journal of cardiology. In 1990, I was President of the CCS when it was decided that we should explore with Mr Kalina his invitation to have the CJC named as the official journal of the CCS. These negotiations were successful and since 1990, the CJC has been the official journal of the CCS. It was perhaps ironic that in 1997, when Dr Beamish retired, it was I who succeeded him as Editor-in-Chief. And now, 13 years have passed. It is also of interest to look at some of the articles published in that first issue. There were papers authored or co-authored by (now Senator) Wilbert Keon, Drs John McCans, George Klein, William Kostuk, Charles Pollick, Martin Gardner, Naranjan Dhalla, Grant Pierce and the late Dr Robert Burns, among others. It is clear that Dr Beamish was successful in influencing these prominent Canadian cardiovascular clinician-scientists to devote time to writing papers for a journal that would not be indexed for years to come. I take my hat off to Mr Kalina, Dr Beamish and all of these authors for this ‘Premiere Issue’. The past 13 years have been interesting and therefore, often challenging, while at the same time, very enjoyable. Because the CJC is the official journal of the CCS, the CCS Council has had the responsibility of recruiting and evaluating the Editor-in-Chief. The CCS Council only recently came to grips with the realization that it was not possible to view the Journal as a significant revenue centre and communication vehicle for members while simultaneously creating a journal with a high international recognition and a high impact factor. This has created many challenges for the editor, and perhaps mistakenly, we tried to achieve both goals simultaneously. To this end, the CJC has published statements, positions and guidelines from the CCS. In addition, we have looked favourably on articles considered to be of potential importance to policy development in Canada. Both groups of publications have not always supported the goal of improving the impact factor of the Journal. There have been other challenges associated with being the Editor-in-Chief. In some instances, we developed strategies to deal with these challenges, which have been both a success and, subsequently, a failure. During the early days of my editorship, it was clear that we needed to attract more submissions. We were successful in this goal but then, the global economic conditions conspired to make this a less desirable outcome. The more articles a journal attracts, the more resources must be devoted to evaluation of these articles and, of course, there is a significant impact of accepting more papers for publication – at least unless the total number of published articles increases. Although we were successful in increasing the number of submissions by a factor of close to 8, as advertising revenues decreased over the past few years, we had to look at ways to discourage some of these submissions. Thus, we instituted a fee to have a manuscript evaluated, an intervention that clearly had a negative impact on submission numbers from the international community. In addition, as advertising revenues decreased, we were forced to publish fewer articles in fewer issues per year – interventions that have resulted in much longer wait times for publication of accepted articles and therefore, less incentive for authors to submit to the CJC. This has made the past two years particularly difficult as we have struggled to decrease the delay time to publication while wishing to continue to attract and accept good articles submitted to the Journal. I believe we have made significant progress. Although our total number of submissions has decreased by approximately one-third in the past two years, our acceptance rate has remained relatively low and because of online publication, we have been successful in clearing most of the backlog of articles accepted earlier for publication. At the same time, we have taken some positive steps toward decreasing the number of published articles considered in the calculation of our impact factor. As a result, the impact factor for 2008 increased to our highest level ever at 1.8, and we have every reason to believe that it will increase further for the 2009 year. Thus, despite some very difficult economic times during which we have decreased the number of issues per year and the number of papers per issue, we have managed to continue to publish articles of importance to Canadian cardiovascular medicine and at the same time, increased our impact factor. However, it needs to be noted that many of our authors have had to suffer long waits to publication during this difficult time and for this, we offer both our apologies and our appreciation. Cover of the Premiere Issue of The Canadian Journal of Cardiology / Page couverture du premier numero du Journal canadien de cardiologie And now it is time to pass the torch. I am delighted that the CCS has been successful in recruiting Dr Stanley Nattel of the Montreal Heart Institute (Montreal, Quebec) for the position of Editor-in-Chief. Dr Nattel is a successful researcher who brings a long record of experience in editing to the CJC and I am confident that he is ideally situated to lead the Journal to the next level of accomplishment. I sincerely believe that with Dr Nattel’s leadership, the CJC can move into the upper echelons of international cardiovascular journals, while at the same time, continuing to serve the Canadian cardiovascular community needs. This will not occur without challenges, and Dr Nattel and the CJC will need the support of our authors, reviewers and readers as we move forward. But I believe that while challenges exist, the future is bright. I will be watching attentively from the sidelines and am prepared to do whatever I can to support the future success of the Journal. I wish to thank the CCS for the opportunity to be the Editor-in-Chief, as well as Pulsus Group Inc (Mr Kalina and staff) for all their support over the years. I have learned much and hope I have contributed in some small way to Canadian cardiovascular medicine and the development of the CJC. I owe much to the Associate Editors, members of the Editorial Board, Ms Peggy Randall in my office, and particularly to the many reviewers for all their support over the years. I will miss it.

The 2008 Canadian Journal of Cardiology Symposium was held at the Canadian Cardiovascular Congress in Toronto on October 26, 2008, in collaboration with the Libin Cardiovascular Institute of Alberta. This annual Symposium is supported by the Pulsus Group Inc – the publisher of the Journal – and by the Canadian Cardiovascular Society. The subject of the 2008 Symposium was on recent advances in risk prediction, a subject of great importance to cardiovascular health and disease. We are pleased to make these excellent presentations available to readers of the Journal. The ability to predict risk for and from cardiovascular disease is increasingly important for several reasons. Perhaps foremost among these is the need to determine individual risk to better plan investigation and management with the greatest accuracy and safety for patients and lowest costs for the health care system. This will be even more important as personalized medicine becomes more widespread. However, we also need the ability to predict risk for public health planning. In Canada, this will require improved information systems to provide the population profile so that risk can be predicted to better inform population health planning. And finally, we need new predictors of risk that are modifiable in response to therapy – such markers do not only serve to identify populations for inclusion in clinical trials of new therapies, but can also serve as surrogate outcomes to decrease the need for ever increasing clinical trial size and cost. Our ability to predict risk is actually quite limited. Although risk scores are available to assess individual cardiovascular risk, these are neither very sensitive nor specific. Therefore, there is an urgent need for new and improved predictors. Ideally, these markers will be simple to measure, reproducible, highly sensitive and specific with excellent positive and negative predictive value. We have a significant way to go to achieve this goal. But progress is being made with increasing numbers of genomic, proteomic and metabolomic markers being identified as potential markers of risk. Dr Bruce McManus (pages 9A–14A) provided an excellent summary of this subject at the Symposium and reviewed the rigorous process required to validate newly identified markers before they can be widely used. One of the promising markers of risk for atherosclerosis is endothelial dysfunction. Dr Todd Anderson (pages 15A–20A) provided an objective overview of the current evidence that this marker will be useful to identify those likely to develop disease, but also pointed out the additional research needed to prove validity. Perhaps one of the greatest challenges we face is predicting which patients with myocardial infarction are likely to go on to experience sudden death, a mechanism that causes the death of approximately 40,000 Canadians each year. Dr Derek Exner (pages 21A–27A) described recent work that utilizes various data extraction approaches from electrocardiographic recordings that, together, might prove useful in this regard. Dr Exner is heading a new clinical trial that will help determine whether such analyses can be useful in the selection of patients to receive an implanted defibrillator. The final speaker at the Symposium was Dr Merril Knudtson (pages 29A–36A) who utilized his vast experience with the APPROACH database to assess risk for acute coronary events. This review emphasizes the value of explicit risk assessment particularly to identify the patient group most likely to benefit from a specific therapeutic approach. Overall, this was an excellent Symposium, and was very well attended. It obviously addressed subjects of considerable interest to attendees. The papers in this Supplement will serve to bring the insights of the speakers and their colleagues to the readers of The Canadian Journal of Cardiology.

The present supplement contains papers based on the presentations at the outstanding Canadian Journal of Cardiology (CJC) Symposium held at the Canadian Cardiovascular Congress in Quebec City in October 2007. The CJC Symposium is an annual plenary session at the Canadian Cardiovascular Congress, cosponsored by the Canadian Cardiovascular Society and Pulsus Group Inc, publisher of the Journal. The format that has evolved uniquely features Canadian science; each year, the symposium has a subject focus and is held in collaboration with a Canadian research institution with expertise in that specific area of research. One of the four speakers, however, usually comes from another Canadian institution. In 2007, the focus of the symposium was on abdominal obesity and the metabolic syndrome. An obvious Canadian centre of excellence with international recognition is the Quebec Heart Institute at the Universite Laval – the Institute also happened to be celebrating its 50th anniversary in 2007. The symposium was co-chaired by Dr Jean-Pierre Despres, whose paper entitled “Abdominal obesity: The cholesterol of the 21st century?” is the first manuscript in this supplement. The second paper, also from the Quebec Heart Institute, is authored by Dr Paul Poirier and is entitled “Targeting abdominal obesity in cardiology: Can we be effective?” The third paper, entitled “Abdominal obesity and the metabolic syndrome: A surgeon’s perspective”, is by Dr Patrick Mathieu, a clinician scientist who is a cardiac surgeon at the Institute in Quebec. Dr Robert Ross from Queen’s University in Kingston, Ontario, completed the excellent group of speakers at the symposium and his paper entitled “Is weight loss the optimal target for obesity-related cardiovascular disease risk reduction?” completes this supplement. The CJC Symposium was very well attended, with excellent content; the papers in this supplement to the Journal will serve as a valuable overview on this important subject area. We greatly appreciate the collaboration of exceptional faculty from the Quebec Heart Institute and of Dr Robert Ross, who have made this supplement possible.

The key to understanding ventricular interaction is to have an appreciation of how constraint to left ventricular (LV) filling can affect the true LV distending pressure (i.e., LV transmural pressure) and how the diastolic position and systolic function of the ventricular septum is affected by the relationship between LV and right ventricular (RV) end-diastolic pressures (i.e., the end-diastolic transseptal pressure gradient).

The purpose of this study was to investigate the dependence of tau, the time constant of left ventricular (LV) isovolumic relaxation, on pericardial pressure and to compare values of tau as determined by the methods of previous investigators and by a standard exponential curve fit. All of the more recent methods involve an additional parameter--the pressure to which the exponential relaxation finally declines (PB, the pressure intercept in the method of Craig and Murgo and the asymptote in the exponential fits). An additional purpose of the study was to determine the relation of these parameters to pericardial pressure. In eight closed-chest anesthetized dogs, tau was calculated from intracavitary (Plv) and transmural LV pressure (Plv = Plv-Pper) by each method as pericardial (Pper) and LV end-diastolic pressure were changed by pericardial infusion and intravenous volume loading. The time constant determined by the method of Weiss et al was dependent on pericardial pressure; the time constants determined by the other methods were not. PB and the asymptotes were found to be similar and to increase almost equally with pericardial pressure. When pericardial pressure was zero, these values were approximately -20 mm Hg. Thus, both these parameters seem to indicate the same baseline pressure, a pressure that increases pari passu with pericardial pressure. Reported changes in the value of tau calculated from intracavitary LV pressure by the method of Weiss et al may reflect factors other than changes in LV diastolic function.

La Societe canadienne de cardiologie (SCC) a 60 ans cette annee. Certains peuvent trouver que c’est tres vieux, mais pour d’autres, c’est encore jeune. Cette perception de jeunesse s’avere particulierement pour les organismes, qui sont nombreux a subsister pendant des siecles. Eldon R Smith Pour continuer a exister, les organismes doivent demeurer pertinents pour leurs membres. A la SCC, on s’y est toujours efforce. L’elaboration reguliere de plans strategiques, des mesures d’approche aupres de categories precises de membres, l’appel a la participation des jeunes et la creation de valeur ajoutee pour les membres en sont le secret. La Societe s’engage dans le perfectionnement professionnel continu, la tenue d’un excellent congres annuel de formation et de recherche en sante cardiovasculaire, la recherche de l’excellence pour la formation des professions et la prise de position pour l’elaboration de politiques visant a ameliorer les soins cardiovasculaires au Canada. Bien sur, le Journal canadien de cardiologie est la revue officielle de la SCC et cherche a l’aider a realiser ses objectifs dans certains de ces secteurs. Dans un effort pour contribuer aux celebrations du 60e anniversaire, le journal a pris plusieurs mesures. Peut-etre avez-vous remarque que la page couverture a ete modifiee pour inclure le theme du 60e anniversaire. De plus, a compter du present numero, nous publions une serie d’articles prepares par d’anciens presidents de la Societe. Ces « reflexions » visent a familiariser les lecteurs actuels du journal a des aspects du riche passe de la Societe, a demontrer qu’il existe des defis a toutes les generations et qu’en travaillant ensemble, les membres d’une Societe peuvent foisonner et etre utiles en periode de calme comme en temps de crise. Les messages des anciens presidents seront publies tous les mois, de juin a octobre. Ceux qui ont accepte de collaborer sont le docteur T Edward Cuddy (1974–1976), le docteur Robert N Anderson (1978–1980), le Senateur Wilbert J Keon (1988–1990), le docteur Gilles Dagenais (1992–1994) et le docteur Ruth L Collins-Nakai (1999–2002). Je les remercie d’avoir pris le temps de preparer ces articles pour le journal. Ils continuent de participer a la SCC. Je me joins a eux pour souhaiter a la SCC de nombreuses autres annees fecondes.

Il ne se passe pas une journee sans que la presse nationale ou locale n’aborde la question de la grave penurie de professionnels de la sante. Cependant, il s’est passe a peine plus d’une decennie depuis que les gouvernements provinciaux (encourages par le gouvernement federal) ont reduit le nombre d’inscriptions dans les facultes de medecine et de soins infirmiers. Je continue a me demander comment une erreur de jugement aussi grossiere a pu se produire. Eldon R Smith Bien sur, je connais la plus grande partie de la reponse. Il y a une douzaine d’annees, on s’inquietait (et on s’inquiete encore) de la viabilite du systeme de sante canadien. A l’epoque, on pensait que le nombre de medecins dans le systeme constituait le principal catalyseur des couts, et on prevoyait un potentiel desastreux d’escalade des effectifs. De toute evidence, ces evaluations etaient superieures aux besoins estimatifs pour l’avenir, mais ces besoins avaient ete calcules selon des modeles modifies (les equipes multidisciplinaires) de prestation des soins. Pour l’essentiel, ces modeles ne se sont pas materialises. Les gouvernements ont agi rapidement, sur plusieurs facettes. En plus de reduire le nombre de places dans les facultes de medecine, ils ont impose d’imposantes restrictions sur l’immigration des medecins et, qui plus est, sur les postes de formation clinique postdoctorale. Ces mesures ont etrangle simultanement les trois principales sources de nouvelles demandes de permis d’exercer au Canada. Les gouvernements les ont prises malgre des donnees probantes considerables qui predisaient une penurie marquee des effectifs avant 2010. Etant donne les importantes compressions d’effectifs et l’attrition prevue, les resultats etaient previsibles. Maintenant, chaque territoire de competence au pays s’inquiete de sa capacite de respecter les besoins de sante fondamentaux de sa population. Fait interessant, les principaux efforts pour ameliorer la situation semblent consister a attirer des professionnels de la sante d’autres provinces. Certains territoires de competence subissent plus de pression que d’autres. En Alberta, on manque deja d’environ 1 000 medecins, et ce nombre devrait augmenter considerablement au cours des prochaines annees. Plusieurs facteurs entrent en jeu. L’economie albertaine en rapide progression a favorise une rapide croissance de la population. Edmonton et Calgary sont touchees, mais les effets sont les plus aigus dans le nord de la province, avec la colossale mise en valeur des sables bitumineux. A Calgary, il existe d’autres facteurs, peut-etre pas aussi evidents. En raison de l’economie florissante dans le secteur de l’energie, les pressions marquees pour augmenter le cout de la main-d’œuvre se font sentir dans tous les secteurs de l’economie. Puisque pratiquement aucun bureau n’est vacant, les prix ont monte en fleche. Les medecins de famille sont particulierement touches. Comme ils n’ont pas eu droit a des augmentations recentes de leurs honoraires, que le cout de la main-d’œuvre et des baux augmente, certains medecins de famille ont decide qu’ils ne pouvaient pas se permettre de gerer un cabinet. Ils prennent leur retraite, demenagent ou acceptent d’autres postes au sein du systeme de sante, non greves de frais generaux. Et la situation s’aggrave. Alors, que faire ? Pas grand-chose a court terme, je pense. La plus grande partie du probleme actuel decoule des mauvais calculs d’il y a dix ans. Il faut donc eviter de repeter cette erreur. Le nombre d’inscriptions dans les facultes de medecine et de soins infirmiers a augmente, meme si on ne sait pas si elle suffira. Pour les medecins, le delai entre l’entree a la faculte de medecine et le debut de la pratique est tellement long que les changements implantes maintenant n’auront pas d’effets avant six a neuf ans. Par consequent, a court terme, la seule possibilite consiste a tenter d’attirer des medecins d’ailleurs. Comme on l’a souligne, on s’attache a « voler » les effectifs des autres provinces, meme si on s’efforce aussi d’attirer les medecins d’autres pays. Il est incontestable que c’est la une question ethique qu’il faut regler. Est-il moralement acceptable de recruter des medecins d’autres pays, souvent plus pauvres ? Par consequent, il me semble que, pour regler le probleme d’effectifs, il faudrait mieux utiliser les ressources. Les medecins consacrent beaucoup de temps a executer des tâches qui pourraient etre confiees a d’autres professionnels de la sante, mais pour l’instant, le mode de remboursement de ces activites est inexistant, ou du moins tres limite, a moins que le medecin voit reellement le patient et prodigue le service. Plusieurs autres modes de paiement et regimes relationnels sont en place au Canada pour financer la prestation des soins a une population. Dans le cadre d’un tel systeme, les equipes multidisciplinaires peuvent prodiguer les services requis, et, surtout, les dispensateurs peuvent etre remuneres pour leurs activites preventives. De telles dispositions pourraient contribuer nettement a inciter les dispensateurs de soins a agir dans l’interet de la population, c’est-a-dire a les aider a ajouter des annees de qualite de vie en portant attention a leur mode de vie, au depistage et a la prise en charge des facteurs de risque, ainsi qu’a l’usage rapide et pertinent des traitements probants. Il reste beaucoup de travail a faire.

The present supplement contains papers based on the content of the second annual Canadian Journal of Cardiology (CJC) Symposium held at the Canadian Cardiovascular Congress (CCC) in Montreal, Quebec, on October 23, 2005. The annual CJC Symposium is jointly sponsored by the Canadian Cardiovascular Society and Pulsus Group Inc, the publisher of the Journal, and in 2005 was presented in collaboration with the Montreal Heart Institute (MHI). The CJC Symposium has been established as an annual plenary session at the CCC to highlight important topics in cardiovascular medicine while featuring excellence in Canadian research. Beginning in 2005, the symposium is offered in collaboration with a Canadian centre – although not all of the speakers will necessarily come from that centre. For the 2005 CJC Symposium, it seemed natural to feature the MHI, Canada’s senior heart institute, which had just celebrated 50 years of excellence. The MHI has a rich tradition of exceptional patient care services, as well as outstanding research contributions. The Institute is respected internationally particularly for its many contributions to clinical research in the surgical and medical management of ischemic heart disease. These traditions continue as the Institute enters its second 50 years. For the 2005 CJC Symposium, we chose to focus on current and future challenges in cardiology. There are many such challenges despite the numerous advances of the past two decades, with none greater than the issue of developing better means to prevent progression, or cause regression, of coronary atherosclerosis. Dr Jean-Claude Tardif led off the symposium with a discussion of the demonstrated effects of statins in slowing atherosclerosis progression and perhaps promoting some regression, which, importantly, has translated into fewer cardiovascular events. Dr Tardif also reviewed some of the early results with approaches to increase levels of high density lipoprotein cholesterol and speculated on the potential for combinations of these approaches. Although Dr Tardif acknowledged the importance of these and other new pharmacological approaches, he reminded us of the increasing burden of atherosclerosis as a result of lifestyle choices and how we must continue (actually increase) our efforts to address these issues with our patients. Dr Pierre Theroux reviewed current challenges with acute coronary syndromes and pointed out the requirements for better algorithms for risk stratification, particularly the need to include markers of the activity status of the atherosclerotic process. From the viewpoint of pathophysiology, Dr Theroux focused on our deficient knowledge concerning the factors that determine why a plaque destabilizes, why some lesions are so thrombogenic and why the prognosis in some patients is impaired well beyond the acute phase. Dr Theroux also dealt with the need for new therapeutic approaches to this common clinical problem, particularly for improved antithrombotics and effective approaches to immune modulation. The most common arrhythmia, and the one that continues to challenge our therapeutic approaches, is atrial fibrillation. Dr George Wyse acknowledged that the major problem continues to be an incomplete understanding of the pathophysiology of this arrhythmia; therefore, therapeutic approaches continue to be empirical. An important modulating factor in the genesis of atrial fibrillation is inflammation, although therapeutic approaches to this issue have not yet been established. Dr Wyse also discussed the importance of structural and electrical remodelling, as well as genetic factors, to the genesis of atrial fibrillation and speculated on the potential of therapeutic options to address these factors. In a review of the therapeutic approaches currently used, Dr Wyse recognized the challenges and opportunities associated with each approach. The final presentation was by Dr Jean-Lucien Rouleau, who addressed the therapeutic challenges associated with chronic heart failure. Both the incidence and the prevalence of heart failure have been increasing, and, despite many advances in therapies, this remains a major challenge to health care systems. Dr Rouleau reviewed the surgical approaches to the management of heart failure, with a particular focus on coronary artery bypass grafting (CABG) and surgical ventricular restoration. There is a need for new studies to compare bypass surgery with current pharmacological management in heart failure patients, especially in patients in whom myocardial viability has been demonstrated. The Surgical Treatment for Ischemic Heart Failure (STICH) trial is an example of such a study in which CABG will be compared with pharmacological therapy; the study will also determine whether CABG and ventricular restoration surgery combined is better than CABG alone. The large attendance at the 2005 CJC Symposium and the spirited discussion period confirmed that the speakers addressed important questions, and were able to clarify the challenges and opportunities for these important cardiovascular problems. We thank each of the speakers for their participation, and certainly appreciate that they and their co-authors have provided these manuscripts so that their insights are available to a wider audience.

During mechanical ventilation, phasic changes in systemic venous return modulate right ventricular output but may also affect left ventricular function by direct ventricular interaction. In 13 anesthetized, closed-chest, normal dogs, we measured inferior vena cava flow and left and right ventricular dimensions and output during mechanical ventilation, during an inspiratory hold, and (during apnea) vena caval constriction and abdominal compression. During a single ventilation cycle preceded by apnea, positive pressure inspiration decreased caval flow and right ventricular dimension; the transseptal pressure gradient increased, the septum shifted rightward, reflecting an increased left ventricular volume (the anteroposterior diameter did not change); and stroke volume increased. The opposite occurred during expiration. Similarly, the maneuvers that decreased venous return shifted the septum rightward, and left ventricular volume and stroke volume increased. Increased venous return had opposite effects. Changes in left ventricular function caused by changes in venous return alone were similar to those during mechanical ventilation except for minor quantitative differences. We conclude that phasic changes in systemic venous return during mechanical ventilation modulate left ventricular function by direct ventricular interaction.

The cardiac effects of positive pressure ventilation and positive end-expiratory pressure are incompletely understood. External constraint due to increased intrathoracic pressure decreases left ventricular end-diastolic volume; the effects on venous return and ventricular interaction are less clear. Phasic changes in inferior vena caval flow, end-diastolic ventricular dimensions and output were measured in seven anesthetized, ventilated normal dogs. During inspiration, caval flow, right ventricular diameter and output decreased; end-diastolic transseptal pressure gradient, septum-to-left ventricular free wall diameter, left ventricular area (ie, left ventricular volume index) and output increased despite the decreased sum of the septum-to-free wall diameters. The reverse occurred during expiration. Increased positive end-expiratory pressure decreased the left ventricular area, but the end-expiratory right ventricular diameter was unchanged. At given airway pressures, right ventricular diameter was greater at higher positive end-expiratory pressures, suggesting that a leftward septal shift (direct ventricular interaction) added to the effect of external constraint on left ventricular end-diastolic volume. In conclusion, positive pressure ventilation reduced right ventricular end-diastolic volume during inspiration and increased the transseptal pressure gradient, which shifted the septum rightward, increasing left ventricular end-diastolic volume and output. The reverse occurred during expiration. Positive end-expiratory pressure constrained left ventricular filling and decreased left ventricular end-diastolic volume further by a leftward septal shift.

The degree to which the lungs and other mediastinal structures constrain the heart during cardiac surgery is uncertain.To assess the degree of constraint to left ventricular (LV) filling that is present during cardiac surgery.Central venous (CVP) and pulmonary capillary wedge pressures (PCWP), and an index of LV end-diastolic volume (LVEDV) - LV area, transesophageal echocardiography - were measured before and after sternotomy, after volume loading, after pericardiotomy, and before and after sternal closure following the clinically indicated procedure in 12 patients undergoing cardiac surgery. PCWP and estimated transmural LVEDP (PCWP-CVP) were plotted against the LV area.In all patients, the difference between PCWP and estimated transmural LVEDP-LV area relations over the full range of LV areas was substantial, indicating the presence of important constraint to filling. Even at small LV areas, when transmural LVEDP approached zero, PCWP was almost always greater than 10 mmHg. Because transmural LVEDP approached zero when areas were smallest, transmural LVEDP-LV area relations were judged to be more plausible than the corresponding PCWP-LV area relations.Considerable constraint to cardiac filling is effected by the lungs and other mediastinal structures. This constraint must be considered when assessing LV filling pressure - PCWP is not a reliable measure of LV preload in these circumstances.