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Background The prognosis of cardiovascular disease is worse in women than men, and coronary microvascular dysfunction explains the excess cardiovascular risk in women. In addition, age-related increases in pulsatile arterial load are greater in women than men; and lower arterial compliance has been shown to independently predict cardiovascular events. However, whether arterial load differentially affects the coronary microvasculature in men and women remains unknown. We hypothesized that lower arterial compliance would be associated with coronary artery microvascular dysfunction in women. Methods and results 285 subjects (60% women, age: 61.2 ± 11.0 yrs) undergoing cardiac 82Rb positron-emission tomography between 2010 and 2013, with ejection fraction ≥50%, no heart failure, dyspnea, coronary artery disease or regional perfusion defects were included. Left ventricular microvascular function was assessed by myocardial flow reserve (MFR). Pulsatile arterial load was estimated by indexed arterial compliance [ACi: (stroke volume/pulse pressure)/BSA]. Multivariable linear regression evaluated associations of arterial compliance with myocardial flow reserve after adjustment for confounders. ACi was lower in women than men [0.39 ± 0.15 vs. 0.52 ± 0.28 (mL/mm Hg)/m2, P Conclusions Lower ACi was associated with altered coronary microvascular function in women, but not in men. Our findings highlight low arterial compliance as a potential link between hypertension, coronary microvascular dysfunction and adverse cardiovascular events in women.

Cardiovascular disease (CVD) is a leading cause of morbidity and mortality in women. Peripheral arterial disease (PAD), a manifestation of CVD and a marker for other adverse CVD outcomes such as ischemic heart disease and stroke, remains underrecognized and undertreated in women. Contrary to the previous belief that PAD is mainly a disease of white men, contemporary data suggest equal, if not higher, prevalence rates in nonwhite women. Women often present with asymptomatic or atypical disease and seek medical attention with more advanced disease. Cardiovascular morbidity and mortality rates, as well as procedural mortality rates, remain elevated in women compared with men. There are sex-specific markers and comorbidities with a higher female prevalence that are associated with PAD. Greater focus on PAD in cardiovascular trials, equivalent enrollment of women in large trials, and focused prevention strategies may help reduce the economic burden and adverse outcomes associated with PAD in women.

States of estrogen imbalance or deprivation are associated with higher risks of hypertension and cardiovascular disease in women; however, the effects of estrogen on hypertension are multifactorial, complex, and not completely understood. Although controversial, hormone therapy may improve cardiovascular outcomes when initiated by recently menopausal women. Improved screening for hypertension, especially in specific groups of younger women at higher risk, is recommended. Further study is needed to determine whether sex-specific differences exist in therapeutic response to pharmacologic management of hypertension.

KEY POINTS Cardiovascular disease (CVD), which is largely preventable, is a leading cause of morbidity and mortality among Canadian women. For this article, we use CVD to refer to ischemic heart disease and stroke. Data for peripheral arterial disease in women are limited and are addressed elsewhere

Objective To determine if visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) depth in early pregnancy differs by maternal ethnicity. Methods We prospectively evaluated 482 women without pre-pregnancy diabetes. All underwent sonographic measurement of VAT and SAT depth at 11 to 14 weeks' gestation. Results SAT did not differ between groups, but VAT did. Compared with Canadian-born women (3.9 cm, 95% CI 3.7–4.1), mean VAT depth was higher among Latin American (4.6 cm, 95% CI 4.1–5.2), Sub-Saharan African (5.0 cm, 95% CI 4.0–6.1), and Caribbean (6.0 cm, 95% CI 4.8–7.3) women. Adjusting for age, parity, and 1/height 2 , the relative risks of having a VAT depth >80th percentile were 1.69 (95% CI 1.05–2.73) for Latin American, 2.24 (95% CI 1.28–3.93) for Sub-Saharan African, and 3.34 (95% CI 1.91–5.84) for Caribbean women, relative to Canadian-born women. Women from these world regions also had a greater percentage of preterm births and emergency CSs. Conclusion VAT differs appreciably among certain ethnic groups, which may reflect their predisposition to adverse pregnancy outcomes.

Background— There remains limited insight into the pathophysiology and therapeutic advances directed at improving prognosis for patients with heart failure with preserved ejection fraction (HFpEF). Recent studies have suggested a role for coronary microvascular dysfunction in HFpEF. Rb-82 cardiac positron emission tomography imaging is a noninvasive, quantitative approach to measuring myocardial flow reserve (MFR), a surrogate marker for coronary vascular health. The aim of this study was to determine whether abnormalities exist in MFR in patients with HFpEF without epicardial coronary artery disease. Methods and Results— A total of 376 patients with ejection fraction ≥50%, no known history of obstructive coronary artery disease, and a confirmed diagnosis of heart failure (n=78) were compared with patients with no evidence of heart failure (n=298), further stratified into those with (n=186) and without (n=112) hypertension. Global and regional left ventricular MFR was calculated as stress/rest myocardial blood flow using Rb-82 positron emission tomography. Patients with HFpEF were more likely to be older, female, and have comorbid hypertension, diabetes mellitus, dyslipidemia, atrial fibrillation, anemia, and renal dysfunction. HFpEF was associated with a significant reduction in global MFR (2.16±0.69 in HFpEF versus 2.54±0.80 in hypertensive controls; P P Conclusions— HFpEF, in the absence of known history for obstructive epicardial coronary artery disease, is associated with reduced MFR independent of other risk factors.

Angiotensin-converting enzyme 2 (ACE2) is expressed in the kidney and may be a renoprotective enzyme, since it converts angiotensin (Ang) II to Ang-(1-7). ACE2 has been detected in urine from patients with chronic kidney disease. We measured urinary ACE2 activity and protein levels in renal transplant patients (age 54 yrs, 65% male, 38% diabetes, n = 100) and healthy controls (age 45 yrs, 26% male, n = 50), and determined factors associated with elevated urinary ACE2 in the patients. Urine from transplant subjects was also assayed for ACE mRNA and protein. No subjects were taking inhibitors of the renin-angiotensin system. Urinary ACE2 levels were significantly higher in transplant patients compared to controls (p = 0.003 for ACE2 activity, and p≤0.001 for ACE2 protein by ELISA or western analysis). Transplant patients with diabetes mellitus had significantly increased urinary ACE2 activity and protein levels compared to non-diabetics (p

BACKGROUND: 51 years ago, the first Mustard operation was performed at our institution and was successful; the patient is still alive today. The procedure’s success was such that many thought they were “cured”. They were not; “failing Mustards” with severe RV failure, TR and often pulmonary hypertension present to us with increasing frequency. We reviewed our experience with an emphasis on this “Mustard dilemma”. METHODS: In 2010-2013, we undertook multiple iterations of cross-sectional follow-up of all 546. Mustard procedures as part of a “double-switch” operation were not included. All points of last known contact were pursued via as many avenues (primary cardiologists, surgeons, institutions, family physicians). RESULTS: Institutional data protection policies were extremely difficult obstacles, as were breaks in follow-up continuity caused by physician retirement or death. The 546 Mustards (1963 2007) were performed at mean age 2.1 years for diagnoses including predominantly variants of arterial transposition or DORV. Most had undergone prior palliation via atrial septectomy (249), systemic-pulmonary shunt (19), PA band (44) or cavopulmonary connection (3). DHCA was used in w60% (mean 55 minutes). In-hospital mortality was 9%. Following discharge, late survival was excellent, with very slow rising late hazard for death over the subsequent decades (instantaneous risk w1%/ year after 40 years). Estimated survival 50 years after surgery is w46% overall (but 58% for isolated TGA). There have been 184 known deaths (33%). Of the 372 presumed survivors, the median age today would be 36 years (IQ range 30 40). More than 20% of adult Mustards we follow have decompensated heart failure by age 36, and this proportion rises disproportionately thereafter (figure). At last follow-up, prevalence of moderate TR was 20% and RV dysfunction 34%. Nevertheless, follow-up with a cardiologist is known for only 50% (182/372) of presumed survivors since 2010, and 60% (224/372) since 2000. The remaining 148 (40% of survivors) only had last known points of cardiology contact in the 1980s or 1990s. CONCLUSION: The bulk of adult Mustard survivors are approaching high-risk periods for onset of heart failure. The insidious onset of RV dysfunction, TR and pulmonary hypertension emphasizes the need for national tracking registry for this and other complex CHD patients, similar to those for cancer patients, to prevent patients re-presenting with excessive risk for any intervention, including transplantation. Canadian Cardiovascular Society (CCS) Poster HEART FAILURE: IMAGING, TREATMENT AND OUTCOMES Sunday, October 26, 2014

s S279 Young Investigator Award Winner e Clinical Science 528 CORONARY ARTERY MICROVASCULAR DYSFUNCTION: ROLE OF SEX AND ARTERIAL LOAD T Coutinho, L Mielniczuk, K Srivaratharajah, R deKemp, RS Beanlands