A comprehensive view of sex-specific issues related to cardiovascular disease Cardiovascular disease (CVD) is the leading cause of mortality in women. In fact, CVD is responsible for a third of all deaths of women worldwide and half of all deaths of women over 50 years of age in developing countries. The prevalence of CVD risk factor precursors is increasing in children. Retrospective analyses suggest that there are some clinically relevant differences between women and men in terms of prevalence, presentation, management and outcomes of the disease, but little is known about why CVD affects women and men differently. For instance, women with diabetes have a significantly higher CVD mortality rate than men with diabetes. Similarly, women with atrial fibrillation are at greater risk of stroke than men with atrial fibrillation. Historically, women have been underrepresented in clinical trials. The lack of good trial evidence concerning sex-specific outcomes has led to assumptions about CVD treatment in women, which in turn may have resulted in inadequate diagnoses and suboptimal management, greatly affecting outcomes. This knowledge gap may also explain why cardiovascular health in women is not improving as fast as that of men. Over the last decades, mortality rates in men have steadily declined, while those in women remained stable. It is also becoming increasingly evident that gender differences in cultural, behavioural, psychosocial and socioeconomic status are responsible, to various degrees, for the observed differences between women and men. However, the interaction between sex-and gender-related factors and CVD outcomes in women remains largely unknown. CMAJ 2007;176(6):S1-44 Although cardiovascular disease (CVD) is common, significant sex-related differences in its epidemiology have only recently been appreciated. The objective of this section is to demonstrate that there are sex-specific differences in the prevalence, complications and burden of CVD in terms of mortality, hospital admissions and quality of life. Abstract Search strategyA MEDLINE search was conducted using the MeSH terms "cardiovascular disease" OR "atrial fibrillation" OR "congestive heart failure." A second search used the terms "prevalence" OR "incidence" OR "mortality" and the final search combined the results of the first 2 searches and added the terms "gender" OR "sex." Articles identified in this manner were retrieved and their reference lists searched for additional relevant articles. The search was limited to English-language publications, but no other restrictions were applied. Other data sources included Web sites of the World Health Organization, the Canadian Institute for Health Information and the National Centre for Health Statistics. Thirty-three original studies were reviewed. Studies were included if they were cohort studies, case-control studies or nested cohort studies that examined the incidence, prevalence or mortality of CVD, congestive heart failure or atrial fibrillation. The studies had to include data on both ...

Background-Coronary artery disease is a significant risk factor for atrial fibrillation (AF), but the basis for this association is incompletely understood. The present study evaluated the hypothesis that atrial ischemia can create a substrate for AF maintenance. Methods and Results-Atrial ischemia was induced by occlusion of an atrial arterial branch that did not provide blood flow to the ventricles. Atrial-arterial occlusion increased the duration of AF induced by burst pacing from 57Ϯ32 seconds (control) to 803Ϯ214 seconds (PϽ0.001) after 0.5 hour of occlusion and to 887Ϯ209 seconds (PϽ0.001) after 3 hours of occlusion. Prolonged AF (Ͼ20 minutes) was induced in 0 of 16 dogs (0%) under control conditions, 7 of 16 (44%, PϽ0.01) at 0.5 to 3 hours, and 5 of 13 (38%, PϽ0.01) 3 to 5 hours after occlusion. Atrial conduction was slowed substantially within the ischemic zone: eg, conduction delay was 8Ϯ1 ms at a cycle length of 200 ms, control, versus 22Ϯ5 ms (PϽ0.01) after 0.5 hours and 27Ϯ5 ms (PϽ0.001) after 3 hours of ischemia. Refractoriness was initially unaffected but was prolonged 5 hours after occlusion. Phase-delay analysis and high-density mapping confirmed severe conduction slowing in the ischemic zone. Histological examination confirmed the location of ischemic regions and revealed extensive ischemia-induced necrosis at sites of conduction delay. Conclusions-Experimental atrial ischemia creates a substrate for AF maintenance, apparently by causing local conduction slowing that promotes reentry. These results suggest that atrial ischemia may significantly promote AF, and may be relevant to AF mechanisms in association with coronary artery disease.

Background— Antiplatelet therapy is often discontinued in patients with drug-eluting stents who are undergoing surgical procedures. However, discontinuation of antiplatelet therapy is an important risk factor for late stent thrombosis. Our objective was to examine the safety of short-term discontinuation of antiplatelet therapy. Methods and Results— We systematically searched Medline for reported cases of late stent thrombosis and very late stent thrombosis published between January 2001 and July 2008. We restricted our search to Academic Research Consortium–defined definite cases. We identified 161 cases of late stent thrombosis or very late stent thrombosis from 84 articles (79 from case reports, 61 from registries, and 21 from randomized clinical trials). Patients had a mean age of 58.4±13.4 years, and 88% were male. A total of 19 cases occurred in patients who were receiving dual antiplatelet therapy at the time of the event. If patients stopped both antiplatelet agents simultaneously, the median time to event was 7 days. If patients had previously stopped a thienopyridine with no ill effect and subsequently stopped acetylsalicylic acid, the median time to event was also 7 days from the time of acetylsalicylic acid cessation. If the thienopyridine was stopped but acetylsalicylic acid was maintained, the median time to event was 122 days. Among the 48 patients who stopped both agents, 36 cases (75%) occurred within 10 days. Among the 94 patients who discontinued a thienopyridine but continued acetylsalicylic acid, only 6 cases (6%) occurred within 10 days. Conclusion— If acetylsalicylic acid therapy is maintained, short-term discontinuation of a thienopyridine may be relatively safe in patients with drug-eluting stents.