Search

Introduction: Non-traumatic lower limb amputations (LLA) represent an important complication of diabetes (DM) and peripheral arterial disease (PAD). In Quebec, Canada, the latest data between 1996 to 2004 suggested a reduction in the incidence of LLA while other Canadian provinces observed a recent increase between 2010 and 2016. Our objective was to update the incidence trends of LLA in Quebec from fiscal years 2006 to 2019. Methods: Age-standardized incidence of LLA among individuals ≥40 years was assessed using the Quebec Integrated Chronic Disease Surveillance System (n=4,527,533 in 2019). The mean age of incident cases and the presence / duration of DM and/or PAD was collected. Estimations were presented for all, by sexes and by types of LLA (minor: below the knee; major: knee and above), with 99% confidence intervals (CI). Results: Between 2006 and 2019, incident cases of LLA increased from 818 to 1,099 but age-standardized incidence remained stable (Figure 1) for both sexes. Men had a higher age-standardized incidence of LLA then women (32.7 per 100,000 [99% CI: 29.7-35.9] vs 12.9 per 100,000 [11.2-14.9] in 2019). From 2006 to 2019, the age-standardized incidence of major LLA showed a relative decrease of 48% while minor LLA remained stable (Figure 1). Reduction in age-standardized incidence of major LLA was attributable to men (3.8 per 100,000 [2.7-5.3] to 1.7 per 100,000 [1.1-2.6]). The mean age of incident cases went from 68.2 to 69.5 years from 2006 to 2019 (72.4 for women and 68.3 for men in 2019). Ninety-eight percent of LLA had DM, while 95% had PAD and 95% had both in 2019. Between 2006 and 2019, the average time between the first LLA and DM diagnosis increased from 7.0 to 14.7 years and from 2.0 to 2.6 years for PAD. Conclusions: Although the age-standardized incidence of LLA is stable, men remain at higher risk then women. The portrait of incident cases is changing towards an older average age, longer DM duration and a reduction of major LLA. These results emphasize the importance to improve further preventive care of LLA in Quebec.

Introduction: The progression of type 2 diabetes (T2D) is unique to each patient and can be depicted through individual temporal trajectories. Latent group trajectory methods (latent growth mixture models [LGMM] or latent class growth analysis [LCGA]) can be used to classify similar individual trajectories in a priori non-observed groups (latent groups), sharing common characteristics. Although increasingly used in the field of T2D epidemiology, many questions remain regarding the utilization of these methods. Objective: To review the literature of longitudinal studies using latent group trajectory methods among individuals with T2D. Methods: MEDLINE (Ovid), EMBASE, CINAHL and Web of Science were searched through August 25 th , 2021. Data were collected on the type of method used (LGMM or LGCA), characteristics of studies and quality of reporting using the GRoLTS-Checklist. Results: From the 4,694 citations screened, a total of 38 studies were included. The studies were published between 2010 and 2021. Total follow-ups ranged from 8 weeks to 11 years, with 95% (36 out of 38) studies with a follow-up of 1 year of more. The characteristics of studies are presented in Table 1. Regarding the quality of reporting, trajectory groups were adequately presented, however many studies failed to report important decisions made for the trajectory group identification. Many studies considered trajectory groups as exposures to a subsequent outcome. Yet, issues in relation with selection bias, immortal bias and residual confounding were suspected and poorly addressed. Conclusions: Although LCGA were preferred, the context of utilization, data sources and research questions were diverse and unrelated to the type of method used. We recommend authors to clearly report the decisions made in trajectory groups identification.

Introduction: The SYNERGIE study has documented the effects on the cardiometabolic risk (CMR) profile of a 1-year lifestyle intervention targeting physical activity (PA) and diet followed by an additional 2-year maintenance period in a sample of 144 men with visceral obesity and an atherogenic dyslipidemia. Previously published results, following the 1-year intervention, had reported significant improvements in CMR markers and a decrease in intramuscular lipids assessed by computed tomography (CT) using the area of low attenuation muscle (LAM) as a marker. However, following the 2-year maintenance period, a slight deterioration of CMR markers including visceral adiposity (VAT) was observed, with the exception of circulating insulin levels. Hypothesis: In this secondary analysis, we tested the hypothesis that variations in cardiorespiratory fitness (CRF) and LAM could explain the long-term improvement in insulin sensitivity indices. Methods: Anthropometric measurements and an oral glucose tolerance test were performed at 0, 1 and 3 years, as well as a submaximal exercise test to assess CRF. Areas and volume of VAT and areas of LAM at mid-thigh and L4-L5 (psoas and core) were measured by CT. Participants were classified into two groups based on CRF changes observed during the 2-year maintenance period: CRF increased (CRF+) and CRF decreased (CRF-). Results: Complete data were available in a subsample of 72 men (52±8 years). Mean annual PA decreased from 143 min/week during the intervention to 103 min/week after the 2-year maintenance period (p Conclusion: Despite some gain in VAT observed during the 2-year maintenance period following the initial 1-year lifestyle intervention, participants who were able to maintain or even increase their CRF during the 2-year maintenance period were those whose insulin sensitivity continued to improve, regardless of the changes in LAM. In conclusion, these results are consistent with the importance of targeting CRF for the long-term management of CMR in men with visceral obesity.

Introduction: Weight loss is often considered a key target in lifestyle interventions aimed at reducing cardiometabolic risk in people with overweight/obesity. However, evidence suggests that regular endurance exercise can induce a mobilization of visceral fat in the absence of weight loss. Therefore, the objective of the present study was to test the effect of an extreme exercise prescription not aimed at weight loss on visceral adiposity and on indices of cardiometabolic health. Hypothesis: Despite our attempt to keep the cyclists weight stable during the 1-week exercise intervention, a loss of visceral fat would be observed. Methods: Eleven male recreational cyclists, aged 50 to 66 years and asymptomatic for cardiovascular disease, cycled 1144 km (715 miles) over a period of seven consecutive days. During the intervention, body weight and composition were assessed daily by bioelectrical impedance and cyclists’ caloric intake was increased to keep them in energy balance and weight stable. Their cardiometabolic health profile was documented before and after the intervention and included a fasting blood test, a resting hemodynamic profile, anthropometric, body composition and body fat distribution measurements including visceral adiposity assessed by magnetic resonance. A maximal cardiopulmonary exercise test was performed at baseline. During the intervention, energy expenditure was calculated from the caloric equivalents of oxygen consumption for each heart rate value acquired with a heart rate monitor. Prepared foods were provided to participants and their energy intake was closely monitored. Results: Small decreases in body weight (-0.8 kg, P 2 , P P =0.0005) as well as a trend towards an increase in lean mass (+0.8 kg, P =0.07) were observed. Visceral adiposity (-14.1 mL, P P P P P P P P P Conclusion: This study showed that recreational master cyclists were not able to remain in energy balance when exposed to a very large exercise prescription performed over one week. However, despite trivial changes in body weight and no change in subcutaneous adiposity, a significant reduction in visceral adiposity was observed. This study shows the differential response of subcutaneous vs visceral adiposity to a very large prescription of endurance exercise, and the inability of body weight changes to fully appreciate the effects of endurance exercise on features of cardiometabolic risk.

Introduction: Considering the contribution of the autonomic nervous system (ANS) in regulating both energy expenditure and energy intake, assessment of heart rate variability (HRV) may elucidate the etiology and adaptive processes in the development of obesity. Variations in the cardiac ANS are associated with changes in energy balance and eating behaviours, highlighting the potential key function of the ANS in the etiology of obesity. While it is broadly accepted that obesity impacts HRV, potential impacts of HRV patterns on obesity remain unexplored. We hypothesize that certain HRV patterns increase risk of excess weight in children. Methods: Participants included 406 White youth from the QUALITY cohort (56% boys). Children were considered at risk of CVD due to confirmed parental obesity status. Time- and frequency-domain HRV indices derived from short-term ECG recordings (SDNN, RMSSD, pNN50, LF, HF, and LF/HF ratio) were analyzed at baseline (mean = 9.6 years, SD = 0.9). Adiposity at 2-year follow-up was evaluated through dual-energy X-ray absorptiometry. Total body fat (BF) and BF distribution were captured; central adiposity was estimated using the android-to-gynoid ratio. Prospective associations between HRV at baseline and adiposity at 2-year follow-up were estimated using regression models including weights for well-established confounders (difference in adiposity measures over time, sex, age, sexual maturity, and physical activity). Results: 8-10 year olds with a sympathovagal imbalance described by a sympathetic predominance (LF/HF) presented with higher BF (β = 3.32, p < 0.001) and higher android-to-gynoid ratio (β =0.03, p Conclusions: Impaired cardiac ANS modulation appears associated with the occurrence of childhood obesity two years later. A sympathetic predominance paired with reduced parasympathetic indices in otherwise healthy children may foreshadow pathophysiological processes that lead to obesity and may help to identify intervention targets.

The global obesity epidemic is well established, with increases in obesity prevalence for most countries since the 1980s. Obesity contributes directly to incident cardiovascular risk factors, including dyslipidemia, type 2 diabetes, hypertension, and sleep disorders. Obesity also leads to the development of cardiovascular disease and cardiovascular disease mortality independently of other cardiovascular risk factors. More recent data highlight abdominal obesity, as determined by waist circumference, as a cardiovascular disease risk marker that is independent of body mass index. There have also been significant advances in imaging modalities for characterizing body composition, including visceral adiposity. Studies that quantify fat depots, including ectopic fat, support excess visceral adiposity as an independent indicator of poor cardiovascular outcomes. Lifestyle modification and subsequent weight loss improve both metabolic syndrome and associated systemic inflammation and endothelial dysfunction. However, clinical trials of medical weight loss have not demonstrated a reduction in coronary artery disease rates. In contrast, prospective studies comparing patients undergoing bariatric surgery with nonsurgical patients with obesity have shown reduced coronary artery disease risk with surgery. In this statement, we summarize the impact of obesity on the diagnosis, clinical management, and outcomes of atherosclerotic cardiovascular disease, heart failure, and arrhythmias, especially sudden cardiac death and atrial fibrillation. In particular, we examine the influence of obesity on noninvasive and invasive diagnostic procedures for coronary artery disease. Moreover, we review the impact of obesity on cardiac function and outcomes related to heart failure with reduced and preserved ejection fraction. Finally, we describe the effects of lifestyle and surgical weight loss interventions on outcomes related to coronary artery disease, heart failure, and atrial fibrillation.

Introduction: In the last decade, an increase in the prevalence and a reduction in the incidence of diabetes have been observed in many countries including Canada. Yet, some Canadian provinces depicted an elevation in incidence rates among younger age groups. Our objective was to document these trends in the province of Quebec from fiscal years 2001 to 2017. Hypothesis: Prevalence is increasing because of raising incidence in individuals aged Methods: Prevalence, incidence and all-cause mortality among cases of diabetes ≥20 years were assessed using the Quebec Integrated Chronic Disease Surveillance System (n=6,551,045 in 2017). Estimations were age-standardized or stratified by 10-year age groups. Results: In 2017, the crude prevalence and incidence of diabetes were 9.9% [99% confidence interval: 9.9-10.0] (n=651,370) and 6.0 per 1,000 inhabitants [5.9-6.0] (n=35,355), respectively. Between 2001 and 2017, the age-standardized prevalence increased by 43% (6.3% [6.3-6.3] to 9.0% [9.0-9.1]), while age-standardized incidence decreased by 29% (8.3 per 1,000 [8.2-8.4] to 5.9 per 1,000 [5.9-6.0]). In every age group, the prevalence increased steadily with progressive stabilization from 2011 and onward, except for the 60-69 years old group who depicted a reduction from 2012 to 2017. Incidence remained stable among Conclusions: The rise and stabilization of diabetes prevalence could be due to a reduction in incidence in patients aged ≥50 years and mortality among all age groups. Prevention of diabetes should be a priority among individuals aged

Background: Even with many direct oral anticoagulant options, brand-name or generic warfarin is still widely used to prevent atherothrombotic events in cardiology. Federal standards regulate bioequivalence of generic vs. brand-name drugs through comparative bioavailability studies but does not regulate clinical equivalence nor tolerability in a “real-life” settings. Through public health surveillance, we have evaluated the impact of the generic warfarin commercialization on health care utilization: emergency room (ER) consultations or hospitalizations. Methods: We used an interrupted time series analysis using the Quebec Integrated Chronic Disease Surveillance System, a surveillance system from the second populous province in Canada (~8.3 million in 2017). Rates of health care utilization for warfarin users (n=280,158) aged ≥ 66 years were calculated for 6-month periods, 5 years before up to 15 years after warfarin commercialization (from January 1996 to January 2016). Periods before and after generic warfarin commercialization were compared by negative binomial segmented regression models for all users with a specific variable for generic or brand-name users. Sensitivity analyses were also conducted. Results: Generic warfarin analogs (n=5) were commercialized from January 2001. There was an approximated mean rate of 1134 ER or hospitalizations for 1000 brand-name and generic users per 6-month period, similar before and after generics commercialization. After generics commercialization, there was an immediate increase in rates of health care utilization for generic (9.9%) vs. brand-name users (0%), a statistically significant difference (9.9% [95% confidence interval: 4.4% to 15.5%], p = 0.0001). Rates of health care utilization remained stable and higher for generic vs. brand-name users throughout the period after generics commercialization. Conclusion: Among generic warfarin users, we observed an increased rates of health care utilization soon after generics commercialization. Risk and survival analysis studies controlling for potential confounders are required to deepen this pharmacovigilance signal as stricter licensing process may be required.

Background: Clopidogrel is widely used to prevent atherothrombotic events. Federal standards regulate bioequivalence of generic and brand-name drugs through comparative bioavailability studies but does not regulate clinical equivalence nor tolerability in “real-life” settings. We evaluated the impact of the generic clopidogrel commercialization on some adverse events: emergency room consultations (ER) or hospitalizations. Methods: This is an interrupted time series analysis using the Quebec Integrated Chronic Disease Surveillance System. Rates of adverse events for clopidogrel users (n=75,130) aged ≥ 66 years were calculated monthly, 12 months before and 12 months after generics commercialization. Periods before and after generics commercialization were compared by negative binomial segmented regression models for all users with a specific variable for generic and brand-name users after generics commercialization. Results: Generic clopidogrel analogs (n=6) were commercialized in 2012. There was an approximated monthly mean rate of 157 adverse events per 1000 brand-name and generic users-month. After generics commercialization, there was an immediate increase in rates of adverse events for generic vs. brand-name users (22 vs. 2%, p < 0.0001, Figure 1). This was explained by increased rates of ER (+22%) and hospitalizations (+20%) the month of generic clopidogrel commercialization. Hospitalization trend up to 1 year after generics commercialization was stable for generic users but reduced for brand-name users (-0.9 vs. -2.9%, p = 0.01), while ER trends were comparable (-1.1 vs. -1.8%, p = 0.2443). Conclusion: Among generic clopidogrel users, increased rates of ER and hospitalizations were observed soon after generics commercialization. The trend of hospitalizations was also affected following generic clopidogrel commercialization. Risk and survival analysis studies controlling for potential confounding are required to better characterize generic substitution.

Background: Substitution from brand-name to generic drugs is one way to reduce costs of pharmacological treatments. Generic drugs licensing is obtained through comparative bioavailability studies for which a variation of up to 20% is generally accepted. However, “real-life” efficacy and tolerance of generic drugs are not studied prior to commercialization. We aimed to evaluate the impact of brand-name to generic losartan, valsartan or candesartan substitution on serious adverse events (hospitalizations, emergency room consultations [ER] or mortality). Method: Three cohorts of persistent angiotensin II receptor blockers (ARB) users (losartan [brand-name and 8 generics], valsartan [brand-name and 5 generics] and candesartan [brand-name and 3 generics])aged ≥ 66 years were constituted using data from the Quebec Integrated Chronic Disease Surveillance System. Generic exposition was determined by substitution time-distribution matching. Time free of adverse events up to 365 days after the onset of generic exposition was compared between groups by survival analysis using Cox regression models adjusted for age, sex, comorbidities, concomitant treatments, socioeconomic status, previous brand-name drug, healthcare resources utilization and prescriber’s speciality, to provide hazard ratio (HR). Sensitivity analysis including non-persistent users was also conducted. Results: Within cohorts (losartan, n = 15,469; valsartan, n = 17,205; and candesartan, n = 25,008), proportions of exposed to generic substitution vs. unexposed who had at least one adverse event were respectively: 35% vs. 25%, 34% vs. 28% and 31% vs. 27% (all, p p < 0.0001]; 1.22 [ p < 0.0001] and 1.08 [ p = 0.0317]) and ER (HR: 1.55; 1.20 and 1.16, all = p < 0.0001). Regarding mortality, HR were respectively: 0.63 [ p = 0.1456]; 0.95 [ p = 0.8487] and 0.43 [ p < 0.0001]). Survival was not significantly different for exposed to generic losartan and valsartan substitution. However, even if the time free of hospitalizations and ER was 8% and 16% shorter for patients exposed to generic candesartan substitution, their survival was 2.3 times better when compared to patients who remained on brand-name candesartan (unexposed). Sensitivity analysis yield similar results. Conclusion: Substitution to generic antihypertensive drugs is associated with a significantly reduced delay before hospitalizations and ER for the three ARBs but a better survival for patients exposed to generic candesartan substitution only. Better bioavailability of generics versions of candesartan or differences in health cares between users could explain these differences.

Humans are increasingly approaching an era where cardiovascular health seems to be one of the major upper limits on achievable life span. An increasing body of scientific research and observational evidence indicates that resting heart rate (HR) is inversely related to the life span among homeothermic mammals and within individual species. HR not only reflects the status of the cardiovascular system but also serves as an indicator of cardiac autonomic nervous (sympathetic and parasympathetic) system activity and metabolic rate. There is a remarkable amount of variation in HR among species; it can be as low as 30 to 35 beats per minute (bpm) in large animals like whales and elephants or as high as 600 to 700 bpm in mice (Figure 1). Mammals that have a slower average HR tend to live much longer than those that have a faster HR.1,2 Although some variability inevitably exists and is observed in humans, estimations yield a mean value of ≈1 × 109 (1 billion) heartbeats in a lifetime across almost all homeothermic mammals (Figure 2). Figure 1. Semilogarithmic relation between resting heart rate and life expectancy in 15 mammal species. Excluding humans, heart rate (HR) is inversely correlated with life span. Adapted from Levine1 with permission of the publisher. Figure 2. Relation between life expectancy and total heartbeats over a lifetime of 15 mammal species. Data fall in a relatively narrow range, ≈1 billion beats. Adapted from Levine1 with permission of the publisher. Article see p 2100 Regularly engaging in moderate-to-vigorous physical activity has been shown to reduce the risk of all-cause mortality, cardiovascular mortality, cancer mortality, stroke, heart disease, breast cancer, and colon cancer, as well as numerous other undesirable health outcomes.3 Endurance physical exercise can reduce HR and promote the overall health profile. It is well …

Introduction: Physical activity is an integral part of type 2 diabetes (NIDDM) rehabilitation. Historically, NIDDM rehabilitation has employed low intensity, sustained exercise. Recent studies have demonstrated cardiometabolic benefits of high intensity burst exercise in healthy volunteers. The impacts of burst exercise in NIDDM have yet to be assessed. This study compared the impacts of burst and sustained exercises on cardiometabolic factors including: BMI, exercise adherence, cardiopulmonary fitness, HbA1C and lipid profiles in newly diagnosed NIDDM. Hypothesis: High-intensity burst physical activity may yield greater cardiometabolic benefits than low intensity, sustained exercise. Methods: This was a single center, single blind randomized trial. 76 patients, within three months of diagnosis of NIDDM, were recruited. Patients were randomized to a control group prescribed 30 minutes of exercise five days a week at 65% of target heart rate or an intervention group prescribed ten minutes of exercise three times a day, five days a week at 85% of target heart rate. All patients underwent routine blood tests, stress tests and logged exercise duration and frequency in logbooks. Patients were excluded from the study if they had evidence for diabetic end organ damage or cardiovascular disease, or took medications which would impact the cardiometabolic parameters assessed in this study. Results: Of 225 patients screened, 76 patients were recruited for the study with an average age of 67; 70% were male. No significant differences in demographics were noted between groups. Patients prescribed the burst regimen exercised 27% more than the control (p Conclusions: The burst exercise regimen significantly improved the cardiometabolic and fitness status of newly diagnosed NIDDM. This regimen may represent a simple and effective way to improve diabetes rehabilitation.

Background and objective: The impact of bariatric surgery on sub-clinical alteration of cardiac function assessed using speckle-tracking strain and its relationship with metabolic changes is unknown. We assessed in obese patients with normal left ventricle (LV) systolic function who underwent the biliopancreatic diversion with duodenal switch (BPD-DS); 1) prevalence of subclinical cardiac dysfunction and dyssynchrony in comparison with gender-matched subjects and, 2) the impact of bariatric surgery on myocardial function and its association with changes in NT-proBNP levels and insulin sensitivity. Methods: Prospective, observational study of the effect of BPD-DS after six months on strain, strain rate (SR) and displacement curves using a repeated measures mixed linear regression model analysis. Changes in systolic (LV end-systolic dimension, longitudinal strain) and diastolic (E/A, ESr) parameters were correlated with changes in body mass index (BMI), HOMA and NT-proBNP. Results: Thirty-eight severely obese patients (BMI 48.4±7.4 Kg/m 2 ) had decreased longitudinal strain (-17.0±2.5%) in comparison with 20 patients without obesity (-19.7±1.5%) (p2 . Eighteen patients (47%) had a global longitudinal strain considered clinically abnormal. Following surgery, 94% of these patients improved their LV mechanics, with normalization of their global longitudinal strain (p Conclusions: There is significant subclinical cardiac dysfunction in patients with severe obesity with normal systolic function. Improvement in longitudinal strain after surgery was not explained by improved insulin sensitivity or changes in NT-proBNP.

Background— Systematic use of coronary stents and optimized platelet aggregation inhibition has greatly improved the short-term results of percutaneous coronary interventions. Transradial percutaneous coronary interventions have been associated with a low risk of bleeding complications. It is unknown whether moderate- and high-risk patients can be discharged safely the same day after uncomplicated transradial percutaneous coronary interventions. Methods and Results— We randomized 1005 patients after a bolus of abciximab and uncomplicated transradial percutaneous coronary stent implantation either to same-day home discharge and no infusion of abciximab (group 1, n=504) or to overnight hospitalization and a standard 12-hour infusion of abciximab (group 2, n=501). The primary composite end point of the study was the 30-day incidence of any of the following events: death, myocardial infarction, urgent revascularization, major bleeding, repeat hospitalization, access site complications, and severe thrombocytopenia. The noninferiority of same-day home discharge and bolus of abciximab only compared with overnight hospitalization and abciximab bolus and infusion was evaluated. Two thirds of patients presented with unstable angina and ≈20% presented with high-risk acute coronary syndrome prior to the procedure. The incidence of the primary end point was 20.4% in group 1 and 18.2% in group 2 ( P =0.017 for noninferiority) with a troponin T–based definition of myocardial infarction; the incidence of the primary end point was 11.1% in group 1 and 9.6% in group 2 ( P =0.0004 for noninferiority) with a creatinine kinase myocardial band–based definition of myocardial infarction. No death occurred. Rate of major bleeding in both groups was extremely low at 0.8% and 0.2%, respectively. From 504 patients randomized in group 1, 88% were discharged home the same day. Conclusion— Our data suggest that same-day home discharge after uncomplicated transradial coronary stenting and bolus only of abciximab is not clinically inferior, in a wide spectrum of patients, to the standard overnight hospitalization and a bolus followed by a 12-hour infusion. This novel approach offers a safe strategy for same-day home discharge after uncomplicated coronary intervention.

Background— The early response of C-reactive protein to initiation of a hydroxymethylglutaryl coenzyme A reductase inhibitor (statin) is not known. The purpose of this study was to determine the rate at which highly sensitive C-reactive protein (hsCRP) levels change after initiation of simvastatin and whether this occurs independently of the change in LDL cholesterol. Methods and Results— The study was a crossover, double-blind design including 40 subjects with elevated LDL cholesterol. Subjects were randomly assigned to 1 of 2 groups: simvastatin 40 mg for 14 days, then placebo for 14 days, or placebo first, then simvastatin. Simvastatin decreased LDL cholesterol by 56±4 mg/dL ( P P =0.02) at day 14. Baseline log(hsCRP) levels were similar in the 2 groups. By day 14, log(hsCRP) was significantly lower in patients on simvastatin when compared with placebo ( P =0.011). Although there was no significant difference in fibrinogen levels, simvastatin produced a modest increase in log[lipoprotein(a)] ( P =0.03) at days 7 and 14. There were no relationships between the decrease in LDL cholesterol and the decrease in hsCRP. Conclusions— Simvastatin lowers hsCRP by 14 days, independent of its effect on LDL cholesterol. This rapid impact of a statin on hsCRP has potential implications in the management of acute coronary syndromes.

Introduction: Dyspnea is a cardinal symptom among patients with respiratory and cardiovascular diseases. Its underlying mechanisms are complex, including pathophysiological as well as psychological and environmental factors. There is no gold standard to its evaluation and it has been recognized that multidimensional tools could provide a more comprehensive evaluation of the symptom. Hypothesis: The purpose of this study was to examine the validation of the scores of the French-Canadian version of the Modified Dyspnea Index(MDI), a multidimensional measure of dyspnea, among chronic cardiovascular and pulmonary patients. Methods: This study includes 137 patients: 79 with pulmonary arterial hypertension and 58 with interstitial lung disease. The cross-cultural adaptation and reliability of the MDI were already reported. The hypothesis guiding the test of convergent validity were that the final score of MDI, which reflects the intensity of dyspnea and its functional impact, would have correlations with: pulmonary function (forced vital capacity-FVC and FVC%), physical capacity (6 Minutes Walk Test-6MWT and Veterans Specific Activity Questionnaire-VSAQ), the practice of physical activity (Godin-Shephard Leisure-Time Physical Activity Questionnaire - GSLTPAQ) and quality of life (SF-12). Partial correlations were performed controlling theses variables: diagnosis, age, sex, BMI, and schooling. Results: The following correlations were observed between the total score of MDI and the reference variables: FVC 0.36 ( p ); FVC% 0.29 ( p=0.008 ); 6MWT 0.58 ( p ); VSAQ 0.77 ( p ); GSLTPAQ 0.50 ( p ); SF12-Physical Component 0.73 ( p ); SF12-Mental Comp. 0.31 ( p ). Conclusions: The results confirmed the associations hypothesized. The total score of the MDI explained much more the variance of the quality of life and perceived physical capacity, than lung function explained the MDI score. It is aligned with the described impact of the symptom in the daily life of the patient and the complexity of the factors underlying its triggering and perception. The use of the MDI can be very helpful in the clinical follow-up, guiding the choice of the best therapeutic approach and evaluation the outcomes of the interventions implemented.

Background: The assessment of physical capacity (PC) is relevant to estimate prognosis and guide therapeutics for patients with chronic cardiopulmonary disease. The Veterans Specific Activity Questionnaire (VSAQ) is a self-reported tool designed to assess perceived physical capacity in METs according to a given patient’s level of physical activity limited by symptoms. The purpose of this study was to examine the validity of the score of the French-Canadian version of the VSAQ among patients suffering from cardiovascular symptoms and chronic pulmonary diseases. Methods: A total of 140 subjects referred for treadmill testing (TT group) and 134 patients with pulmonary hypertension or interstitial lung disease (PD group) were enrolled. Criterion validation was verified in the TT group by level of agreement (Bland-Altman coefficient) between the VSAQ and the workload estimated by the gold standard to assess PC, the maximal treadmill test (MTT). Convergent validation was tested using correlations between the VSAQ score and physical capacity (MTT and 6-min walking test - 6MWT); practice of physical activity (Godin-Shephard Leisure-Time Physical Activity Questionnaire-GSLTPAQ); pulmonary function (forced vital capacity- FVC) and quality of life (Minnesota living with Heart Failure Questionnaire-LHFQ and SF-12). Partial correlation coefficients were adjusted for sex, age, BMI and education. Results: The mean bias between VSAQ and estimated METs was -1.54 with limits of agreement (CI 95%) of 3.71 to -6.79 METs, being constant around all MET levels. Significant correlations (p Conclusion: The VSAQ French-Canadian version demonstrated acceptable criterion and convergent validation among two different groups of chronic disease patients. Its utilization by the nurse during routine clinical follow-up of these patients could be helpful to guide functional evaluations and interventions.

Background —At one end of the clinical spectrum of coronary artery disease (CAD) are subjects who have had repeated acute ischemic events, and at the other end are those with long-standing angina who have never been unstable. This study tests the hypothesis that a specific biological profile can distinguish these 2 extreme groups and predict acute coronary events. Methods and Results —Blood levels of lipoprotein(a), homocysteine, tissue plasminogen activator, plasminogen activator inhibitor-1, C-reactive protein (CRP), fibrinogen, and von Willebrand factor were compared in 3 groups of 50 subjects each: (1) those with previous multiple acute coronary events, (2) age-matched subjects with ≥3 years of stable angina and no prior acute coronary events, and (3) matched controls without evidence of atherosclerotic disease and a normal coronary angiogram. All subjects were followed for 4.0 years. Lipoprotein(a), homocysteine, tissue plasminogen activator, and plasminogen activator inhibitor-1 were similar in both CAD groups and significantly higher than in the control group. However, compared with subjects with long-standing stable angina, those with previous multiple coronary events had higher values of CRP (5.7±5.4 versus 3.0±5.2 mg/L, P =0.012), fibrinogen (3.38±0.75 versus 2.92±0.64 g/L, P =0.001), and von Willebrand factor (1.60±0.55 versus 1.25±0.36 U/mL, P =0.0003). On follow-up, myocardial infarction and unstable angina occurred in 42% of the group with multiple events, 4% of the stable angina group ( P P P =0.002). A baseline CRP >3.5 mg/L had a relative risk of 7.6 (2.6 to 21.7, P =0.0002) for subsequent acute events. Conclusions —An inflammatory biological profile distinguished patients with previous multiple acute coronary events from those with long-standing stable angina and predicted acute coronary instability.

Rationale: Maximal exercise testing is an absolute contraindication in patients with severe symptomatic aortic stenosis (SSAS). Instead of maximal testing, the 6 minutes-walk test (6MWT) may be recommended to evaluate functional capacity and to establish prognostic. The aim of this study was to compare the 6MWT with a maximal exercise test in patients with SSAS. Method: A ramp cardiopulmonary exercise test (CPET) on a cycle ergometer taken as control, and a 6MWT, both with a breath-by-breath gas analysis, were performed in a population with SSAS waiting for transcatheter aortic valve implantation (TAVI). During both tests, patients were monitored with continuous electrocardiogram. Blood pressure was taken every 2 minutes during CPET and at the beginning and the end of the 6MWT test. Patients underwent both tests. Results: A total of 12 patients aged 79.5 ± 5.9 years participated to these evaluations. During the 6MWT, patients walked a mean distance of 335±74 m, producing a mean maximal workload of 48.5±13.2 watts during CPET. Through CPET, patients achieved a maximal oxygen consumption (VO2peak) of 11.9±4.2 mL/kg/min, which was similar to the VO2peak reached during 6MWT (12.8±2.5 mL/kg/min, p=0.062). For both tests, the respiratory exchanged ratio exceeded 1.1 (CPET=1.16±0.06 and 6MWT=1.12±0.09, p=0.241), which is one criterion of a maximal exercise capacity test. In comparison to CPET, a higher proportion of the 6MWT was performed at high intensity level (>85% VO2peak); 74.2±29.0% of the 6MWT vs. 31.5±24.0% of CPET, p=0.004*. During CPET, 8 patients experimented abnormal blood pressure (BP) response (4 dropped their BP and 4 achieved maximal BP value during recovery). No complication occurred during both tests except for 3 patients who experienced angina pectoris. In this high-risk elderly cohort, lean body mass was the better anthropometric feature associated with better exercise capacity during CPET (r=-0.73, p=0.03*). Conclusion: Both exercise tests were very demanding for patients with SSAS waiting for TAVI. The 6MWT was a maximal effort and high intensity exertion was maintained for almost 75% of the test. The 6MWT was as intense as CPET suggesting the importance of an adequate monitoring while testing those patients. Considering that CPET allow blood pressure measure throughout the test and included a lower test portion in high intensity level, CPET may be more appropriate to evaluate functional capacity in patients with SSAS.

Introduction: Patients with coronary artery diseases (CAD) are often characterized by impaired fasting glucose (IFG), impaired glucose tolerance (IGT) or type 2 diabetes (T2D), conditions which have also been related to high levels of visceral adipose tissue (VAT) and ectopic fat. Secondary prevention intervention involving physical activity should therefore also target VAT/ectopic fat to improve the cardiometabolic risk (CMR) profile. Objectives: The objective of the present pilot study was to compare the response of CMR variables in recent post coronary bypass graft patients with either normal glucose tolerance (NGT), IFG/IGT, and T2D to a 1-year intervention targeting the improvement of lifestyle habits. Methods: Anthropometric measurements, assessment of lipid profile, magnetic resonance imaging of the heart and the abdomen, an oral glucose tolerance test and a maximal exercise treadmill test were performed before and after the intervention (n=44). Results: No significant difference was found in baseline characteristics of the three subgroups, except that patients with IFG/IGT and T2D had significant higher levels of VAT than NGT patients. In response to the lifestyle intervention, patients with IFG/IGT and T2D improved their CMR profile with decreases in waist circumference (Δ=-5.1cm, p Conclusion: Results of this pilot study suggest that increasing CRF is a relevant target to mobilize VAT/ectopic fat in order to improve the CMR profile including plasma glucose homeostasis in CAD patients, irrespective of their glucose tolerance status.

Introduction: A coronary artery bypass graft (CABG) surgery induces an important physiological stress which could impact on cardiometabolic risk (CMR) variables. Furthermore, lifestyle modification programs are effective in secondary prevention. Objective: The present pilot study explored the response of CMR variables to a CABG surgery followed by a 1-year intervention targeting the improvement of lifestyle habits (nutrition/physical activity) in patients with established coronary artery disease (CAD). Methods: Anthropometric measurements, assessment of lipid profile and magnetic resonance imaging were performed before and after CABG surgery (n=32) and 1 year after the lifestyle modification program (n=26). An oral glucose tolerance test (OGTT) and a maximal treadmill test (modified Bruce) were also performed after surgery and at the end of the intervention program. Results: Six weeks after surgery, but before initiation of the lifestyle modification program, patients significantly reduced their body mass index (BMI) (Δ=−1.0 kg/m 2 , p3 , p=0.007) and total abdominal adipose tissue volumes (Δ=−27.4 cm 3 , p=0.008). They also significantly decreased their LDL-C (Δ=−0.7 mmol/L, p=0.0003) and total cholesterol (Δ=−0.7 mmol/L, p2 , p=0.02) and waist circumference (Δ=−4.3 cm, p=0.002) as well as visceral (Δ=−36.2 cm 3 , p=0.03), subcutaneous (Δ=−29.1 cm 3 , p=0.005) and total abdominal adipose tissue volumes (Δ=−61.1 cm 3 , p=0.01). They also significantly reduced glucose area under the curve (Δ=−128.6 ρmol/L, p=0.0005) measured during the OGTT, TG/HDL-C ratio (Δ=−0.47, p=0.0006), triglycerides (Δ=−0.12 mmol/L, p=0.03), total cholesterol/HDL-C ratio (Δ=−0.34, p=0.003) and increased HDL-C levels (Δ=+0.2 mmol/L, p=0.0002). Cardiorespiratory fitness (CRF) was also improved significantly as reflected by an increase in VO 2 max (Δ=+4.0 mlO 2 /kg/min, p2 =0.61, p=0.0003) the improvement in 2-hours plasma glucose (OGTT) in response to the lifestyle modification program. Conclusion: Results of this pilot study suggest that the CMR profile of high risk patients with CAD is improved by the CABG surgery itself. In addition, a 1-year lifestyle modification program generates further cardiometabolic benefits.

Introduction: Ventricular premature beats (VPB) predict cardiovascular mortality among several adult populations. Controlled dietary magnesium (Mg) depletion studies demonstrated that diminished Mg intake and status induced VPB and other arrhythmias. Thus, we hypothesized that the prevalence of VPB is closely associated with serum Mg concentrations in a general adult population at high cardiovascular risk. Methods: Anthropometric, demographic and lifestyle characteristics were assessed in 750 Cree adults, >18yrs, who participated in an age-stratified, cross-sectional health survey in Quebec, Canada. Holter electrocardiograms recorded heart rate variability and cardiac arrhythmias for two consecutive hours. Multivariate logistic regression was used to evaluate potential associations between serum Mg and VPB. Results: VPB prevalence in adults with hypomagnesaemia (serum Mg ≤ 0.70mmol/L) was over twice that of adults without hypomagnesaemia (50% vs. 21%, p =0.015); results were not materially altered when adults with cardiovascular disease history were excluded. All hypomagnesaemic adults with VPB had type 2 diabetes. Prevalence of VPB declined across the serum Mg concentration gradient in adults with type 2 diabetes only ( p 0.70 mmol/L was 0.24 (95%CI: 0.06-0.98; p =0.046). Conclusions: Prevalence of VPB significantly declined across the serum Mg concentration gradient in adults with type 2 diabetes, indicating that future interventions to increase levels of serum Mg among adults with type 2 diabetes may confer protection against cardiac arrhythmia.

INTRODUCTION: The prevalence of severe obesity has tripled in Canada in the past few decades. Nevertheless, cognitions and eating behaviours in this population have not been extensively studied as for their relationships with anthropometric characteristics and comorbidities. Therefore, the aim of this study was to link 3 factors related to cognitions and eating behaviours: restraint, disinhibition and susceptibility to hunger, according to gender, body composition and hypertension (HTA) status. HYPOTHESIS: Cognitive and behavioural profiles of severely obese people differ in regard to gender and HTA status. METHODS: A total of 125 severely obese people [Body Mass Index (BMI) of ≥ 40 or ≥ 35 kg/m 2 with comorbidities] were recruited through the bariatric surgery clinic of our institution. They were invited to complete a validated French version of the Three-Factor Eating Questionnaire (51-items). Weight, fat-free mass, and body fat mass of participants were measured using a bioelectric impedance balance and HTA status was recorded. RESULTS: Participants were 41 ± 10 years, weighted 133.9 ± 27.4 kg with a BMI of 48.7 ± 7.6 kg/m 2 , a lean mass of 66.0 ± 14.1 kg, a fat mass of 32.6 ± 17.9 kg and a fat percentage of 50.3 ± 5.7%. Age and BMI were similar between men and women, but men’s weight, body fat, and fat-free mass were higher than in women. In the entire cohort, a negative correlation was observed between susceptibility to hunger and fat mass (r=-0.273; p=0.035). In men, positive correlations were observed between restraint vs. weight (r=0.394; p=0.016) and BMI (r=0.459; p=0.004). In women, negative correlations were observed between restraint vs. weight (r=-0.215; p=0.044) and lean mass (r=-0.278; p=0.009), while positive correlations were observed between disinhibition vs. weight (r=0.211; p=0.049) and fat mass (r=0.215; p=0.044). Overall, 56% (70/125) of all participants showed HTA. A greater proportion of participants with a higher restraint score suffered from HTA than in participants presenting a lower restraint score (67 vs. 48%; p=0.027). Restraint profile also differed between women suffering with HTA vs. without HTA (p=0.008). A greater proportion of participants showing a lower disinhibition score suffered from HTA than those with a higher disinhibition score (64 vs. 48%; p=0.051). CONCLUSION: Higher score of susceptibility to hunger observed in severely obese individuals is linked to a lower body fat mass. Despite similar eating behaviour profiles, different associations coexist according to gender between restraint vs. disinhibition factors and anthropometric characteristics. Among women, those suffering with HTA present a higher level of restraint, but lower disinhibition score. These findings in severely obese people differ from actual literature in overweight and obese people.

The prevalence of obesity in the United States and the world has risen to epidemic/pandemic proportions. This increase has occurred despite great efforts by healthcare providers and consumers alike to improve the health-related behaviors of the population and a tremendous push from the scientific community to better understand the pathophysiology of obesity. This epidemic is all the more concerning given the clear association between excess adiposity and adverse health consequences such as cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). The risks associated with overweight/obesity are primarily related to the deposition of adipose tissue, which leads to excess adiposity or body fatness. Furthermore, weight loss, specifically loss of body fat, is associated with improvement in obesity-related comorbidities. Before weight loss interventions can be recommended, however, patients must be assessed for their adiposity-related risk. Unfortunately, healthcare providers and systems have not done a good job of assessing for excess adiposity even in its simplest form, such as measuring body mass index (BMI). It is for these reasons that we must emphasize the importance of assessing adiposity in clinical practices. Although it can be argued that the entire population should be targeted as an important public health issue with a goal of prevention of weight gain and obesity, there are currently so many “at risk” individuals that simple strategies to identify and treat those individuals are necessary. We must identify those individuals at highest risk of comorbidities in order to identify those who might benefit the most from aggressive weight management. This scientific statement will first briefly review the epidemiology of obesity and its related comorbidities, supporting the need for improved assessment of adiposity in daily clinical practice. This will be followed by a discussion of some of the challenges and issues associated with assessing adiposity and then by a review …

The rate of obesity is rising logarithmically, especially in those with severe obesity (body mass index [BMI] >40 kg/m2). Cardiologists, endocrinologists, internists, family practitioners, and most healthcare professionals are increasingly confronted with the severely obese patient and with postoperative bariatric patients because obesity is associated with significant morbidity and increased mortality. In addition, more adolescents these days are severely obese. Substantial long-term successes of lifestyle modifications and drug therapy have been disappointing in this population. The National Institutes of Health has suggested that surgical therapy be proposed to those patients with BMI >40 kg/m2 or >35 kg/m2 with serious obesity-related comorbidities such as systemic hypertension, type 2 diabetes mellitus, and obstructive sleep apnea. When indicated, surgical intervention leads to significant improvements in decreasing excess weight and comorbidities that can be maintained over time. These include diabetes mellitus, dyslipidemia, liver disease, systemic hypertension, obstructive sleep apnea, and cardiovascular dysfunction. Recent prospective, nonrandomized, observational, or case-control population studies have also shown bariatric surgery to prolong survival in the severely obese. Different types of bariatric procedures are being performed. Historically, operative mortality was between 0.1% and 2.0% with more recent data not exceeding 1%. Early complications include pulmonary embolus (0.5%), anastomotic leaks (1.0% to 2.5%), and bleeding (1.0%). Late complications include anastomotic stricture, anastomotic ulcers, hernias, band slippage, and behavioral maladaptation. The number of bariatric operations being performed is increasing tremendously as a result of increasing medical need and the evolution of safer surgical techniques and guidelines. Currently, bariatric surgery should be reserved for patients who have severe obesity in whom efforts at medical therapy have failed and an acceptable operative risk is present. The terms overweight, obese, and severe obesity refer to a clinical continuum. Excess adiposity should be considered a chronic disease that has serious health consequences. An …

Obesity is associated with comorbidities that may lead to disability and death. During the past 20 years, the number of individuals with a body mass index >30, 40, and 50 kg/m 2 , respectively, has doubled, quadrupled, and quintupled in the United States. The risk of developing comorbid conditions rises with increasing body mass index. Possible cardiac symptoms such as exertional dyspnea and lower-extremity edema occur commonly and are nonspecific in obesity. The physical examination and electrocardiogram often underestimate cardiac dysfunction in obese patients. The risk of an adverse perioperative cardiac event in obese patients is related to the nature and severity of their underlying heart disease, associated comorbidities, and the type of surgery. Severe obesity has not been associated with increased mortality in patients undergoing cardiac surgery but has been associated with an increased length of hospital stay and with a greater likelihood of renal failure and prolonged assisted ventilation. Comorbidities that influence the preoperative cardiac risk assessment of severely obese patients include the presence of atherosclerotic cardiovascular disease, heart failure, systemic hypertension, pulmonary hypertension related to sleep apnea and hypoventilation, cardiac arrhythmias (primarily atrial fibrillation), and deep vein thrombosis. When preoperatively evaluating risk for surgery, the clinician should consider age, gender, cardiorespiratory fitness, electrolyte disorders, and heart failure as independent predictors for surgical morbidity and mortality. An obesity surgery mortality score for gastric bypass has also been proposed. Given the high prevalence of severely obese patients, this scientific advisory was developed to provide cardiologists, surgeons, anesthesiologists, and other healthcare professionals with recommendations for the preoperative cardiovascular evaluation, intraoperative and perioperative management, and postoperative cardiovascular care of this increasingly prevalent patient population.

A moderate weight loss of 5 to 10% has been shown to induce several improvements in the cardiometabolic profile of high risk obese patients and is therefore generally recommended as a clinically meaningful therapeutic target. The SYNERGIE study is a lifestyle modification program which aims at reshaping the nutritional and physical activity habits of sedentary men with visceral obesity. In the present analyses, 101 healthy men aged 30 to 65 years without diabetes but characterized by visceral obesity and by the high triglyceride-low HDL cholesterol atherogenic dyslipidemia were assigned to a personalized nutritional and physical activity management program which included a monthly visit. In response to the intervention program, men of the study decreased their body weight, waist circumference (Δ=−9 cm, p2 , p2 , n=65), men of the intervention group did not fully normalize their cardiometabolic profile after 1-year. In order to further explore this issue, men of the intervention group were classified into quartiles of VAT accumulation achieved after 1-year. In comparison with men in the top VAT quartile, men in the lowest VAT quartile had markedly improved cardiometabolic profile. Moreover, when compared to nonobese controls, men who reached low levels of VAT were characterized by a lower VAT accumulation (100 cm vs. 124 cm) despite higher body weight (80 kg vs. 73 kg) and body mass index (27 kg/m 2 vs. 24 kg/m 2 ) than healthy nonobese controls. These men were also characterized by “normalized” HDL cholesterol (1.17 mmol/l), triglycerides (1.58 mmol/l), glucose (5.8 mmol/l), apolipoprotein B (0.97 mg/dl) and apolipoprotein AI (1.35 g/l) compared to nonobese controls. These results suggest that VAT may represent a better therapeutic target than the normalisation of body weight in the management of cardiometabolic risk in high risk abdominally obese men.

Background: Diabetes is associated with accelerated vascular calcification and stiffening of the arteries. Reduced systemic arterial compliance (SAC) is regarded as a major factor in the development of hypertension, contributing to increased left ventricular afterload and myocardial oxygen demand and reduced coronary flow reserve. We thus hypothesized that reduced SAC is an independent predictor of mortality in patients with diabetes. Methods: We retrospectively analyzed data of 528 consecutive patients with type 2 diabetes who had a Doppler-echocardiographic exam in our institution. Blood pressure was measured in all patients at the time of echocardiography. SAC was calculated as the ratio of stroke volume index to arterial pulse pressure. Results: Follow up was completed in 97% of patients and mean follow-up time was 2.9±1.2 years. Mean age was 66±11 years with 68% males and 68% with coronary artery disease (CAD). Fifty percent of the patients had markedly reduced SAC on the basis of the cut-off value (SAC 2 /mmHg) previously reported to be associated with adverse outcome in patients with hypertension. Patients with reduced SAC were significantly older (68±11 vs. 65±10, p=0.002) and had a higher prevalence of hypertension (78 vs. 22%, p Conclusion : Reduced SAC is encountered frequently in patients with type 2 diabetes and is a major risk factor for total mortality in this population. The SAC, which is easily measurable in the context of routine echocardiographic exam, should be taken into consideration when evaluating these patients with regards to prognosis and treatment. Funded by: Québec Heart Institute Foundation

Obesity is a major contributor to the prevalence of cardiovascular disease in the developed world, and yet has only recently been afforded the same level of attention as other risk factors of coronary artery disease. Obesity is a chronic metabolic disorder associated with cardiovascular disease and increased morbidity and mortality. It is apparent that a variety of adaptations/alterations in cardiac structure and function occur as excessive adipose tissue accumulates, even in the absence of comorbidities. Shifts toward a less physically demanding lifestyle are observed today throughout different populations, and this scourge associated with obesity implicates a corresponding increase in the number of individuals afflicted with the metabolic syndrome, which defines the obese patient as being “at risk.” Adipose tissue is not simply a passive storehouse for fat, but an endocrine organ that is capable of synthesizing and releasing into the bloodstream a variety of molecules that may impact unfavorably the risk factor profile of a patient. Indeed, obesity may affect atherosclerosis through unrecognized variables and risk factors for coronary artery disease such as dyslipidemia, hypertension, glucose intolerance, inflammatory markers, and the prothrombotic state. By favorably modifying lipids, decreasing blood pressure, and decreasing levels of glycemia, proinflammatory cytokines, and adhesion molecules, weight loss may prevent the progression of atherosclerosis or the occurrence of acute coronary syndrome events in the obese high-risk population.

Obesity is becoming a global epidemic in both children and adults. It is associated with numerous comorbidities such as cardiovascular diseases (CVD), type 2 diabetes, hypertension, certain cancers, and sleep apnea/sleep-disordered breathing. In fact, obesity is an independent risk factor for CVD, and CVD risks have also been documented in obese children. Obesity is associated with an increased risk of morbidity and mortality as well as reduced life expectancy. Health service use and medical costs associated with obesity and related diseases have risen dramatically and are expected to continue to rise. Besides an altered metabolic profile, a variety of adaptations/alterations in cardiac structure and function occur in the individual as adipose tissue accumulates in excess amounts, even in the absence of comorbidities. Hence, obesity may affect the heart through its influence on known risk factors such as dyslipidemia, hypertension, glucose intolerance, inflammatory markers, obstructive sleep apnea/hypoventilation, and the prothrombotic state, in addition to as-yet-unrecognized mechanisms. On the whole, overweight and obesity predispose to or are associated with numerous cardiac complications such as coronary heart disease, heart failure, and sudden death because of their impact on the cardiovascular system. The pathophysiology of these entities that are linked to obesity will be discussed. However, the cardiovascular clinical evaluation of obese patients may be limited because of the morphology of the individual. In this statement, we review the available evidence of the impact of obesity on CVD with emphasis on the evaluation of cardiac structure and function in obese patients and the effect of weight loss on the cardiovascular system.

Background— The relation of the warm-up ischemia phenomenon to the presence and intensity of initial myocardial ischemia is unclear. We sought to determine whether the warm-up ischemia phenomenon requires initial myocardial ischemia or can be induced by exercise without ischemia and whether there is a relation between the intensity of initial ischemia and the attenuation of ischemia on reexercise. Methods and Results— Twelve subjects with exertional myocardial ischemia performed 2 exercise ECG tests (1 and 2) at a ±10-minute interval on 3 occasions (A, B, C) 1 month apart. A1 and A2 were symptom-limited. B1 was kept as long as A1, but its intensity was held under the ischemic threshold (heart rate×systolic pressure at 1-mm ST depression [STD]) noted at A1. B2 was symptom-limited. C1 was also kept as long as A1 but with an intensity adjusted to maintain one-half maximum STD of A1. C2 was symptom-limited. Exercise duration of A2, B2, and C2 increased similarly compared with A1 ( P =0.009). However, the ischemic threshold (×10 −3 ) increased at A2 (23.5±6.0) compared with A1 (20.3±4.8; P P Conclusions— Exercises under the ischemic threshold and of intermediate ischemic intensity increase short-term exercise capacity, but myocardial ischemia of more than moderate intensity is needed to induce the warm-up ischemia phenomenon.