Number of Pregnancies and Risk of Atrial Fibrillation.

Pregnancy is associated with major structural and hemodynamic changes in the cardiovascular system that predispose women to an increased risk of atrial fibrillation. While these changes generally resolve after parturition, the impact of subsequent pregnancies on the risk of atrial fibrillation is unknown. We searched through PubMed for studies that have investigated the impact of multiparity on the risk of atrial fibrillation. The following Medical Subject Headings terms were used: ([repeated pregnancies] OR parity) AND ([Atrial fibrillation] OR AF). Studies with complete data were included in the current study. Out of 135 studies identified through the prespecified criteria, we selected 2 studies with relevant data. Increasing number of pregnancies was associated with an increased risk of atrial fibrillation in a dose-response relationship. Our systematic review suggests that multiparity is associated with an increased risk of atrial fibrillation. More studies are warranted to elucidate the association between repeated pregnancies and atrial fibrillation.

Implantable Cardioverter Defibrillators and Chronic Kidney Disease.

Use of implantable cardioverter defibrillators (ICDs) is the treatment of choice for heart failure patients with ejection fraction <35% to prevent sudden cardiac death. Whether this benefit remains among patients with chronic kidney disease (CKD) or end stage renal disease (ESRD) is yet to be elucidated. We conducted a systematic review of studies in PubMed that have investigated the use of ICDs among patients with CKD or ESRD. From the 470 studies identified, we selected 42 for the current review. Patients with CKD/ESRD were more likely to get antitachycardia pacing or shocks and had higher cardiac and/or all-cause mortality compared to patients without CKD/ESRD. These associations had an inverse dose-response effect with worse outcomes with decreasing kidney function. In conclusion, use of ICDs in CKD/ESRD is associated with increased antitachycardia pacing/shocks and mortality suggesting that their routine use in this patient population may be associated with more adverse outcomes than benefits.

Plasma Fatty Acids in Zambian Adults with HIV/AIDS: Relation to Dietary Intake and Cardiovascular Risk Factors.

Objective. To determine whether 24 hr dietary recalls (DR) are a good measure of polyunsaturated fatty acid (PUFA) intake when compared to plasma levels, and whether plasma PUFA is associated with markers of HIV/AIDS progression and cardiovascular disease (CVD) risk. Methods. In a cross-sectional study among 210 antiretroviral therapy-naïve HIV-infected adults from Lusaka, Zambia, we collected data on medical history and dietary intake using 24 hr DR. We measured fatty acids and markers of AIDS progression and CVD risk in fasting plasma collected at baseline. Results. PUFA intakes showed modest correlations with corresponding plasma levels; Spearman correlations were 0.36 (p < 0.01) for eicosapentaenoic acid and 0.21 (p = 0.005) for docosahexaenoic acid. While there were no significant associations (p > 0.05) between total plasma PUFA and C-reactive protein (CRP) or lipid levels, plasma arachidonic acid was inversely associated with CRP and triglycerides and positively associated with HDL-C, CD4+ T-cell count, and plasma albumin (p < 0.05). Plasma saturated fatty acids (SFA) were positively associated with CRP (ß = 0.24; 95% CI: 0.08 to 0.40, p = 0.003) and triglycerides (ß = 0.08; 95% CI: 0.03 to 0.12, p < 0.01). Conclusions. Our data suggest that a single DR is inadequate for assessing PUFA intake and that plasma arachidonic acid levels may modulate HIV/AIDS progression and CVD risk.

Intake of trans fat and incidence of stroke in the REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort.

BACKGROUND: Whether elevated intakes of trans fatty acids (TFAs) increase the risk of stroke remains unclear. Except for the Women's Health Initiative-Observational Study, most studies that directly assessed the association between TFA intake and stroke yielded null results. OBJECTIVE: The aim of this study was to investigate the association between TFA intake and stroke incidence. DESIGN: We prospectively investigated the association between TFA intake and stroke incidence in black and white men and women (n = 17,107) from the REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort. Participants were recruited between 2003 and 2007 from the continental United States and followed for incident stroke. Diet was assessed by using the Block 1998 food-frequency questionnaire. Cox regression was used to test whether energy-adjusted TFA intake in 1-SD increments was associated with incident stroke. RESULTS: During a median follow-up of 7 y, 479 strokes were identified, including 401 ischemic strokes. Sex modified the association between TFA intake and stroke (P-interaction = 0.06), and thus the results were stratified by sex. In fully adjusted models, a 1-SD (2-g/d) increase in TFA intake was associated with an increased risk of any stroke in men (HR: 1.14; 95% CI: 1.02, 1.28) but not in women (HR: 0.93; 95% CI: 0.79, 1.11). Similarly, our results showed an increased risk of ischemic stroke in men (HR: 1.13; 95% CI: 1.00, 1.28) but not in women (HR: 0.93; 95% CI: 0.77, 1.12). CONCLUSIONS: We show that sex modifies the association between TFA intake and stroke; for every 2-g/d increase in TFA intake, there was a 14% increase in the risk of stroke in men but not in women. Our findings provide further evidence to support the concerted effort to minimize TFAs in the diet.

Intake of trans fat and all-cause mortality in the Reasons for Geographical and Racial Differences in Stroke (REGARDS) cohort.

BACKGROUND: A high intake of trans fatty acids decreases HDL cholesterol and is associated with increased LDL cholesterol, inflammation, diabetes, cancer, and mortality from cardiovascular disease. The relation between trans fat intake and all-cause mortality has not been established. OBJECTIVE: The aim of this study was to determine the relation between trans fat intake and all-cause mortality. DESIGN: We used data from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study-a prospective cohort study of white and black men and women residing in the continental United States. Energy-adjusted trans fat intake was categorized into quintiles, and Cox-regression was used to evaluate the association between trans fat intake and all-cause mortality. RESULTS: During 7 y of follow-up, there were 1572 deaths in 18,513 participants included in REGARDS. From the first to the fifth quintile of trans fat intake, the mortality rates per 1000 person-years of follow-up (95% CIs) were 12.8 (11.3, 14.5), 14.3 (12.7, 16.2), 14.6 (13.0, 16.5), 19.0 (17.1, 21.1), and 23.6 (21.5, 25.9), respectively. After adjustment for demographic factors, education, and risk factors for mortality, the HRs (95% CIs) for all-cause mortality were 1.00, 1.03 (0.86, 1.23), 0.98 (0.82, 1.17), 1.25 (1.05, 1.48), and 1.24 (1.05, 1.48), respectively (P-trend = 0.004). The population attributable risk due to trans fat intake was 7% (95% CI: 5%, 8%). CONCLUSION: Higher trans fat intake is associated with an increased risk of all-cause mortality.

Cardiometabolic risk factors among HIV patients on antiretroviral therapy.

BACKGROUND: HIV and combination antiretroviral therapy (cART) may increase cardiovascular disease (CVD) risk. We assessed the early effects of cART on CVD risk markers in a population with presumed low CVD risk. METHODS: Adult patients (n=118) in Lusaka, Zambia were recruited at the time of initiation of cART for HIV/AIDS. Cardiometabolic risk factors were measured before and 90 days after starting cART. Participants were grouped according to cART regimens: Zidovudine + Lamivudine + Nevirapine (n=58); Stavudine + Lamivudine + Nevirapine (n=43); and 'other' (Zidovudine + Lamivudine + Efavirenz, Stavudine + Lamivudine + Efavirenz, Tenofovir + Emtricitabine + Efavirenz or Tenofovir + Emtricitabine + Nevirapine, n=17). ANOVA was used to test whether changes in cardiometabolic risk markers varied by cART regimen. RESULTS: From baseline to 90 days after initiation of cART, the prevalence of low levels of high-density lipoprotein cholesterol (<1.04 mmol/L for men and <1.30 mmol/L for women) significantly decreased (78.8% vs. 34.8%, P<0.001) while elevated total cholesterol (TC ≥5.18 mmol/L, 5.1% vs. 11.9%, P=0.03) and the homeostasis model assessment of insulin resistance ≥3.0 (1.7% vs. 17.0%, P<0.001) significantly increased. The prevalence of TC:HDL-c ratio ≥5.0 significantly decreased (44.9% vs. 6.8%, P<0.001). These changes in cardiometabolic risk markers were independent of the cART regimen. CONCLUSION: Our results suggest that short-term cART is associated with a cardioprotective lipid profile in Zambia and a tendency towards insulin resistance regardless of the cART regimen.

Short-term effect of fenofibrate on C-reactive protein: A meta-analysis of randomized controlled trials.

BACKGROUND: C-reactive protein (CRP) is positively associated with risk for cardiovascular disease and all-cause mortality. Some but not all randomized and non-randomized clinical trials found significant associations between fenofibrate therapy and CRP but the direction and magnitude of the association varied across studies. The duration of treatment, patient populations and sample sizes varied greatly, and most short-term studies (i.e., ≤ 12 weeks) had fewer than 50 patients. In this study we meta-analyzed randomized clinical trials to determine the short-term effect of fenofibrate on CRP. METHODS: Two reviewers independently searched PubMed and other online databases for short-term randomized clinical trials that reported CRP concentrations before and after fenofibrate treatment. Of the 81 studies examined, 14 studies with 540 patients were found eligible. Data for the change in CRP and corresponding measures of dispersion were extracted for use in the meta-analysis. RESULTS: The weighted mean CRP concentrations before and after fenofibrate therapy were 2.15 mg/L and 1.53 mg/L (-28.8% change), respectively. Inverse-variance weighted random effects meta-analysis revealed that short-term fenofibrate treatment significantly lowers CRP by 0.58 mg/L (95% CI: 0.36-0.80). There was significant heterogeneity between studies (Q statistic = 64.5, P< 0.0001, I2 = 79.8%). There was no evidence of publication bias and sensitivity analysis revealed that omitting any of the 14 studies did not lead to a different conclusion from the overall meta-analysis result. CONCLUSION: Short-term treatment with fenofibrate significantly lowers CRP concentration. Randomized trials that will recruit patients based with high baseline CRP concentrations and with change in CRP as a primary outcome are needed.