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Black patients have higher incident fatal coronary heart disease (CHD) rates than do their White counterparts. Racial differences in out-of-hospital fatal CHD could explain the excess risk in fatal CHD among Black patients. We examined racial disparities in in- and out-of-hospital fatal CHD among participants with no history of CHD, and whether socioeconomic status might play a role in this association. We used data from the ARIC (Atherosclerosis Risk in Communities) study, including 4,095 Black and 10,884 White participants, followed between 1987 and 1989 until 2017. Race was self-reported. We examined racial differences in in- and out-of-hospital fatal CHD with hierarchical proportional hazard models. We then examined the role of income in these associations, using Cox marginal structural models for a mediation analysis. The incidence of out-of-hospital and in-hospital fatal CHD was 1.3 and 2.2 in Black participants, and 1.0 and 1.1 in White participants, respectively, per 1,000 person-years. The gender- and age-adjusted hazard ratios comparing out-of-hospital and in-hospital incident fatal CHD in Black with that in White participants were 1.65 (1.32 to 2.07) and 2.37 (1.96 to 2.86), respectively. The income-controlled direct effects of race in Black versus White participants decreased to 1.33 (1.01 to 1.74) for fatal out-of-hospital and to 2.03 (1.61 to 2.55) for fatal in-hospital CHD in Cox marginal structural models. In conclusion, higher rates of fatal in-hospital CHD in Black participants than in their White counterparts likely drive the overall racial differences in fatal CHD. Income largely explained racial differences in both fatal out-of-hospital CHD and fatal in-hospital CHD., Competing Interests: Disclosures The authors have no conflicts of interest to declare., (Copyright © 2023 Elsevier Inc. All rights reserved.)

High sensitive cardiac troponin I (hs-cTnI) increases with inducible myocardial ischemia in patients with coronary artery disease (CAD). We aimed to assess if the change in hs-cTnI levels with exercise stress testing is associated with major adverse cardiac events (MACE). A cohort of 365 (age 62 ± 9 years, 77% men) patients with stable CAD underwent 99mTc sestamibi myocardial perfusion imaging with treadmill testing. Plasma hs-cTnI level was measured at rest and at 45 min after stress. Multivariable Fine & Gray's subdistribution hazards models were used to determine the association between the change in hs-cTnI and MACE, a composite end point of cardiovascular death, myocardial infarction, and unstable angina requiring revascularization. During a median follow-up of 3 years, 39 (11%) patients experienced MACE. After adjustment, for each two-fold increment in hs-cTnI with stress, there was a 2.2 (95% confidence interval 1.3-3.6)-fold increase in the hazard for MACE. Presence of both a high resting hs-cTnI level (>median) and ≥ 20% stress-induced hs-cTnI elevation was associated with the highest incidence of MACE (subdistribution hazards models 4.6, 95% confidence interval 1.6 to 13.0) compared with low levels of both. Risk discrimination statistics significantly improved after addition of resting and change in hs-cTnI levels to a model including traditional risk factors and inducible ischemia (0.67 to 0.71). Conversely, adding inducible ischemia by SPECT did not significantly improve the C-statistic from a model including traditional risk factors, baseline and change in hs-cTnI (0.70 to 0.71). In stable CAD patients, higher resting levels and elevation of hs-cTnI with exercise are predictors of adverse cardiovascular outcomes beyond traditional cardiovascular risk factors and presence of inducible ischemia., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relations that could have appeared to influence the work reported in this study., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Neighborhood socioeconomic status (nSES) is associated with cardiovascular morbidity and mortality in the general population; however, its effect on high-risk patients with prevalent coronary artery disease (CAD) is unclear. We hypothesized "double jeopardy," whereby the association between nSES and adverse outcomes would be greater in high-risk patients with heart failure (HF) and/or previous myocardial infarction (MI) compared with those without. We followed 3,635 patients (mean age 63.2 years, 42% with HF, 25% with previous MI) with known or suspected CAD over a median of 3.3 years for all-cause death and cardiovascular death or nonfatal MI. Patients were categorized by a composite nSES score, and proportional hazards models were used to determine the association between nSES and outcomes. Cross-product interaction terms for previous MI × nSES and HF × nSES were analyzed. Compared with high nSES patients, low nSES patients had increased risk of all-cause death (hazard ratio [HR] = 1.61; 95% confidence interval [CI] = 1.20, 2.15) and cardiovascular death or MI (subdistribution HR [sHR] = 1.82; 95% CI = 1.30, 2.54). Associations were more pronounced among patients without HF or previous MI. Low nSES patients without HF had a higher risk of all-cause death (HR = 2.27; 95% CI = 1.41, 3.65) compared with those with HF (HR = 1.21; 95% CI = 0.82, 1.77, P interaction = 0.04). Similarly, low nSES patients without previous MI had a higher risk of cardiovascular death or MI (sHR = 2.72; 95% CI = 1.73, 4.28) compared with those with previous MI (sHR = 1.02; 95% CI = 0.58, 1.81, P interaction = 0.02). In conclusion, low nSES was independently associated with all-cause death and cardiovascular death or MI in patients with CAD; however, associations were greater in patients without HF or previous MI compared with those with HF or MI., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Background: Mental stress-induced myocardial ischemia is a frequent phenomenon in patients with coronary artery disease. Women with coronary artery disease tend to have more mental stress-induced myocardial ischemia and more chest pain/anginal symptoms than men, but whether the association between mental stress-induced myocardial ischemia and angina burden differs in women and men is unknown., Methods: This was a cross-sectional study with experimental manipulation of 950 individuals with stable coronary artery disease. Chest pain/angina frequency in the previous 4 weeks was assessed with the Seattle Angina Questionnaire's angina-frequency subscale. Mental stress-induced myocardial ischemia was assessed with myocardial perfusion imaging during mental stress (standardized public speaking task). Presence of mental stress-induced myocardial ischemia was based on expert readers and established criteria. A conventional (exercise or pharmacologic) stress test was used as a control condition., Results: Overall, 338 individuals (37%) reported angina; 112 (12%) developed mental stress-induced myocardial ischemia, and 256 (29%) developed conventional stress ischemia. Women who reported angina had almost double the probability to develop mental stress-induced myocardial ischemia (19% vs 10%, adjusted prevalence rate ratio, 1.90; 95% confidence interval, 1.04-3.46), whereas there was no such difference in men (11% vs 11%, adjusted prevalence rate ratio, 1.09; 95% confidence interval, 0.66-1.82). No association was found between angina symptoms and conventional stress ischemia for women or men. Results for ischemia as a continuous variable were similar., Conclusions: In women, but not in men, anginal symptoms may be a marker of vulnerability toward ischemia induced by psychologic stress. These results highlight the psychosocial origins of angina in women and may have important implications for the management and prognosis of women with angina., (Copyright © 2018 Elsevier Inc. All rights reserved.)

The pooled cohort Atherosclerotic Cardiovascular Disease (ASCVD) risk calculator is designed to improve cardiovascular risk estimation compared with the Framingham Risk Score, particularly in blacks. Although the ASCVD risk score better predicts mortality and incident cardiovascular disease in blacks, less is known about its performance for subclinical vascular disease measures, including arterial stiffness and carotid intima-media thickness. We sought to determine if the ASCVD risk score better identifies subclinical vascular disease in blacks compared with the Framingham risk score. We calculated both the Framingham and ASCVD cohort risk scores in 1,231 subjects (mean age 53 years, 59% female, 37% black) without known cardiovascular disease and measured the extent of arterial stiffness, as determined by pulse wave velocity (PWV), central pulse pressure (CPP), and central augmentation index (CAIx), and subclinical atherosclerosis, as determined by carotid-IMT (C-IMT). Compared with whites, blacks had higher CAIx (23.9 ± 10.2 vs 22.1 ± 9.6%, p = 0.004), CPP (36.4 ± 10.5 vs 34.9 ± 9.8 mmHg, p = 0.014), PWV (7.6 ± 1.5 vs 7.3 ± 1.3 m/s, p = 0.004), and C-IMT (0.67 ± 0.10 vs 0.65 ± 0.10 mm, p = 0.005). In a multivariable analysis including race and Framingham risk score, race remained an independent predictor of all measures of subclinical vascular disease; however, models with race and the ASCVD risk score showed that race was not an independent predictor of subclinical vascular disease. In conclusion, greater subclinical vascular disease in blacks was not estimated by the Framingham risk score. The new ASCVD risk score provided a better estimate of racial differences in vascular function and structure., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Android fat is a surrogate measure of visceral obesity in the truncal region. Both visceral adiposity and oxidative stress (OS) are linked to cardiometabolic risk factors and clinical cardiovascular disease. However, whether body fat distribution (android vs gynoid) is associated with OS remains unknown. We hypothesized that increased android fat will be associated with greater OS. Body fat distribution and markers of OS, including plasma levels of reduced (cysteine and glutathione) and oxidized (cystine and glutathione disulfide) aminothiols, were estimated in 711 volunteers (67% female, 23% black, mean age 48 ± 11) enrolled in the Emory Georgia Tech Predictive Health study. At 1 year, 498 subjects had repeat testing. At baseline, anthropometric and fat distribution indexes, including body mass index, waist circumference, weight/hip ratio, and android and gynoid fat mass correlated with lower plasma concentrations of glutathione and higher cystine levels indicative of higher OS. At 1 year, the change in android but not gynoid fat mass or body mass index negatively correlated with the change in the plasma glutathione level after adjustment for cardiovascular risk factors. Increased body fat, specifically android fat mass, is an independent determinant of systemic OS, and its change is associated with a simultaneous change in OS, measured as plasma glutathione. In conclusion, our findings suggest that excess android or visceral fat contributes to the development of cardiovascular disease through modulating OS., (Copyright © 2017. Published by Elsevier Inc.)

Atrial premature complexes (APCs) serve as acute triggers for atrial fibrillation (AF), but it is currently unknown whether the association between APCs and AF varies by race or sex. We examined the association between APCs and AF in 13,840 (mean age = 63 ± 8.4 years; 56% women; 37% black) participants from the REasons for Geographic And Racial Differences in Stroke study. APCs were detected on baseline electrocardiograms (2003 to 2007). Incident AF was identified by study-scheduled electrocardiograms and self-reported history at a follow-up examination. Logistic regression was used to compute odds ratios (OR) and 95% confidence intervals for the association between APCs and incident AF. A total of 950 participants (6.9%) had APCs at the baseline visit. After a median follow-up of 9.4 years, 1015 incident AF cases (7.3%) were detected. APCs were associated with an increased risk of AF (odds ratios = 1.92, 95% confidence intervals = 1.57, 2.35). The relation between APCs and AF did not vary by race (interaction p value = 0.56) or sex (interaction p value = 0.66). In conclusion, APCs detected on a routine electrocardiogram are associated with an increased risk of AF development, and this association does not vary by race or sex. The findings of this analysis suggest that the risk of AF associated with atrial ectopy does not account for the differential risk of AF that is observed in whites compared with blacks, and in men compared with women., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Mental stress-induced myocardial ischemia (MSIMI) has been associated with adverse prognosis in patients with coronary artery disease (CAD), but whether this is a uniform finding across different studies has not been described. We conducted a systematic review and meta-analysis of prospective studies examining the association between MSIMI and adverse outcome events in patients with stable CAD. We searched PubMed, EMBASE, Web of Science, and PsycINFO databases for English language prospective studies of patients with CAD who underwent standardized mental stress testing to determine presence of MSIMI and were followed up for subsequent cardiac events or total mortality. Our outcomes of interest were CAD recurrence, CAD mortality, or total mortality. A summary effect estimate was derived using a fixed-effects meta-analysis model. Only 5 studies, each with a sample size of <200 patients and fewer than 50 outcome events, met the inclusion criteria. The pooled samples comprised 555 patients with CAD (85% male) and 117 events with a range of follow-up from 35 days to 8.8 years. Pooled analysis showed that MSIMI was associated with a twofold increased risk of a combined end point of cardiac events or total mortality (relative risk 2.24, 95% confidence interval 1.59 to 3.15). No heterogeneity was detected among the studies (Q=0.39, I2=0.0%, p=0.98). In conclusion, although few selected studies have examined the association between MSIMI and adverse events in patients with CAD, all existing investigations point to approximately a doubling of risk. Whether this increased risk is generalizable to the CAD population at large and varies in patient subgroups warrant further investigation., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Atrial fibrillation (AF) is an independent predictor of mortality after acute myocardial infarction (AMI). We analyzed the relation between biomarkers linked to myocardial stretch (NT-pro-brain natriuretic peptide [NT-proBNP]), myocardial damage (Troponin-T [TnT]), and inflammation (high-sensitivity C-reactive protein [hs-CRP]) and new-onset AF during AMI to identify patients at high risk for AF. In a prospective multicenter registry of AMI patients (from the Translational Research Investigating Underlying disparities in recovery from acute Myocardial infarction: Patients' Health status registry), we measured NT-proBNP, TnT, and hs-CRP in patients without a history of AF (n = 2,370). New-onset AF was defined as AF that occurred during the index hospitalization. Hierarchical multivariate logistic regression models were used to determine the association of biomarkers with new-onset AF, after adjusting for other covariates. New-onset AF was documented in 114 patients with AMI (4.8%; mean age 58 years; 32% women). For each twofold increase in NT-proBNP, there was an 18% increase in the rate of AF (odds ratio [OR] 1.18, 95% confidence interval [CI] 1.03 to 1.35; p <0.02). Similarly, for every twofold increase in hs-CRP, there was a 15% increase in the rate of AF (OR 1.15, 95% CI 1.02 to 1.30; p = 0.02). TnT was not independently associated with new-onset AF (OR 0.96, 95% CI 0.85 to 1.07; p = 0.3). NT-proBNP and hs-CRP were independently associated with new in-hospital AF after MI, in both men and women, irrespective of race. Our study suggests that markers of myocardial stretch and inflammation, but not the amount of myocardial necrosis, are important determinants of AF in the setting of AMI., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Reduced heart rate variability (HRV) and increased C-reactive protein (CRP) levels are both predictors of coronary artery disease and correlate with each other. We examined whether these 2 phenotypes share a common genetic substrate and investigated the relations of the CRP gene polymorphisms with both CRP levels and HRV indexes. We examined 236 male twins free of symptomatic coronary artery disease, with a mean age +/- SD of 54 +/- 2.9 years. The plasma CRP levels were measured and the frequency domain measures of HRV were assessed using a 24-hour electrocardiographic recording, including ultra-low-, very-low-, low-, and high-frequency power. Three single-nucleotide polymorphisms in the CRP gene were genotyped. Generalized estimating equations were used to examine the association between CRP and HRV, as well as the genotype-phenotype association. Bivariate structural equation modeling was performed to estimate the genetic and environmental correlations between CRP and HRV and the explanatory effect of CRP gene polymorphisms on the CRP-HRV association. Both CRP (h(2) = 0.76) and HRV indexes (h(2) = 0.56 to 0.64) showed high heritability. Greater CRP levels were significantly associated with lower HRV. A robust genetic correlation was found between CRP and ultra-low-frequency power (r(G) = -0.3, p = 0.001). One CRP single nucleotide polymorphism (rs1205) was significantly associated with both CRP (p = 0.003) and ultra-low-frequency power (p = 0.005) and explained 11% of the genetic covariance between them. In conclusion, reduced HRV correlates significantly with increased CRP plasma levels and this correlation is due, in large part, to common genetic influences. A polymorphism in the CRP gene contributes to both CRP levels and HRV.

In patients with heart failure (HF), mortality is lower in women versus men. However, it is unknown whether the survival advantage in women compared with men is present in both whites and African Americans with HF. The inception cohort consisted of adults > or =65 years with incident HF after enrollment in the CHS, a prospective population-based study of cardiovascular disease. Of 5,888 CHS subjects, 1,264 developed new HF and were followed up for 3 years. Subjects were categorized into 4 race-gender groups, and Cox proportional hazard regression models were used to examine whether 3-year total and cardiovascular mortality differed among the 4 groups after adjusting for sociodemographic factors, co-morbidities, and treatment. A gender-race interaction was also tested for each outcome. In subjects with incident HF, African Americans had more hypertension and diabetes than whites, and white men had more coronary heart disease than other gender-race groups. Receipt of cardiovascular treatments among the 4 groups was similar. Mortality rates after HF were lower in women compared with men (for white women, African-American women, African-American men, and white men, total mortality was 35.5, 33.6, 44.4, and 40.5/100 person-years, and cardiovascular mortality was 18.4, 19.5, 20.2, and 22.7/100 person-years, respectively). After adjusting for covariates, women had a 15% to 20% lower risk of total and cardiovascular mortality compared with men, but there was no significant difference in outcome by race. The gender-race interaction for either outcome was not significant. In conclusion, in older adults with HF, women had significantly better survival than men irrespective of race, suggesting that gender-based survival differences may be more important than race-based differences.

Low levels of high-density lipoprotein (HDL) cholesterol are a marker of coronary artery disease progression and are associated with cardiovascular events. However, whether low HDL cholesterol is a useful prognostic indicator after percutaneous coronary intervention (PCI) is not known. In a sample of 4,088 patients who underwent PCI we evaluated 1-year mortality and repeat revascularization as a function of baseline HDL levels classified into approximate quartiles of very low (<35 mg/dl), low (35 to 40 mg/dl), medium (41 to 47 mg/dl) and high (48 to 120 mg/dl) HDL cholesterol. Decreasing levels of HDL cholesterol were associated with younger age, male gender, smoking, diabetes mellitus, and a history of bypass surgery (p <0.0001 for all). One-year mortality and coronary revascularization were significantly higher in the very low HDL cholesterol group compared with the other groups (very low HDL cholesterol 6.5% and 25.4%, respectively; low HDL cholesterol 3.1% and 20.8%; medium HDL cholesterol 4.3% and 22.7%; high HDL cholesterol 3.1% and 20.6%, p = 0.0001 and p = 0.007). One-year mortality was significantly higher in men with an HDL cholesterol level <33 mg/dL and in women with an HDL cholesterol level <38 mg/dL. In multivariable analysis, very low HDL was associated with nearly twofold the risk of death after adjusting for other independent predictors of outcome. In conclusion, in patients with coronary artery disease undergoing PCI, a baseline HDL cholesterol level <35 mg/dl is an important prognostic indicator. Baseline HDL cholesterol levels <33 mg/dl for men and <38 mg/dl were associated with higher one-year mortality after PCI.

Women with coronary heart disease (CHD) have higher mortality compared with men. Atherosclerotic imaging risk markers are associated with higher mortality and relative risk of CHD events in women compared with men. However, data on the predictive accuracy of coronary artery calcium (CAC) in women are scarce. We performed a systematic review of the published literature from 2003 to 2006 on the prognostic value of CAC in women and men. Two investigators reviewed Medline for prospective registries on annual rates of CHD death or myocardial infarction (MI) by CAC results. Three studies in 6,481 women and 13,697 men reported results by gender. We also analyzed 2 observational registries for annual all-cause death rates by CAC scores in women (n = 17,779) and men (n = 17,850). Summary relative risk ratios and 95% confidence intervals were calculated using a random effects model. For all-cause mortality, rates were 0.1% to 1.6% per year for women and 0.1% to 2.6% for men with CAC scores from 0 to 10 to > or =1,000, respectively (p <0.0001). For CHD death or MI, annual rates were 0.2% to 1.3% in women and 0.3% to 2.4% for men with low- to high-risk CAC scores. For women with a CAC score of 0, annual CHD death or MI rates were 0.16%, similar to that of men (p = 0.55). Summary relative risk ratios increased 4.9-fold (p = 0.006), 5.5-fold (p = 0.002), and 8.7-fold (p <0.0001) for mild-, moderate-, and high-risk CAC scores, respectively. A comparative analysis of gender differences showed no significant differences between women and men for mild- to high-risk CAC scores (p = 0.66), suggesting an equivalent ability to risk stratify by gender. In conclusion, this meta- and pooled analysis revealed that CAC screening is equally accurate in stratifying risk in women and men.

Elevated blood pressure (BP) variability has been linked to an increased risk for adverse cardiovascular events, but the biologic factors that promote elevated BP variability are not entirely understood. This cross-sectional study examined whether inflammatory factors might be associated with elevated BP variability during 24-hour ambulatory BP monitoring. Subjects were 140 healthy, normotensive adults. Inflammatory markers included C-reactive protein (CRP) and tumor necrosis factor-alpha. BP variability was calculated as the within-subject SD of BP values obtained during the daytime, nighttime, and 24-hour periods. In linear regression models that were adjusted for mean BP and other factors, CRP quartiles were positively associated with daytime systolic BP variability; for subjects in the lowest to highest CRP quartiles, the mean within-subject SDs of daytime systolic BP were 9.31, 9.62, 10.55, and 11.17, respectively (p for linear trend = 0.001). CRP showed similar positive associations with nighttime and 24-hour systolic BP variability. In contrast, tumor necrosis factor-alpha was not independently associated with systolic BP variability during any of the time periods. With respect to diastolic BP variability, significant positive associations were found between CRP and diastolic BP variability during all time periods and between tumor necrosis factor-alpha and daytime diastolic BP variability. In conclusion, there are positive associations between markers of inflammation and BP variability in healthy, normotensive adults, suggesting that inflammation may be 1 of the factors that promotes increased BP variability.

Although previous studies have shown increased risk of morbidity and mortality in patients with diabetes mellitus (DM) who undergo coronary artery bypass grafting (CABG), data are conflicting on whether the gains in physical function and mental health after CABG achieved by patients with DM are similar to, or less than, those achieved by patients without DM. We compared the gains in physical function and mental health at 6 months after CABG surgery between 696 consecutive patients with DM and 376 without DM who underwent their first CABG from February 1999 to February 2001. Physical function and mental health were measured using the Short Form 36-item Health Survey. From the baseline and follow-up Short Form 36-item Health Survey data, the physical and mental component scales were derived. At 6 months, the patients with and without DM had significant improvement in physical function and mental health, but those without DM had improved significantly more than those with DM with respect to physical functioning. After adjusting for baseline characteristics, a lower proportion of patients with DM had experienced improvement (an increase of > or = 5 points) in the physical component scale score compared with those without DM (45.0% vs 58.0.%, RR = 0.78, p = 0.002). Moreover, a higher proportion of patients with DM experienced a decrease in the physical component scale score compared with those without DM (14.9% vs 7.8%, RR = 1.91, p = 0.006). In contrast, no significant differences were found in the mental component scale score changes by DM status. In conclusion, CABG is associated with lower gains in physical function in those with DM than in those without DM. Special attention should be paid to the physical function of patients with DM after CABG, and any barriers to functional recovery in this group should be promptly identified and addressed.

Recent studies have been inconsistent in demonstrating a decrease in the gender gap in short-term post-percutaneous coronary intervention (PCI) outcomes. We sought to determine gender differences in outcomes in younger and older patients who underwent PCI during the current stent era. We studied 4,768 elective PCI procedures performed at Emory University Hospital from 2001 to 2004. The baseline characteristics, periprocedural complications, angiographic success, procedural success, and major in-hospital complications (death, myocardial infarction, and emergency coronary artery bypass graft surgery) after PCI were compared between men and women. Women were more likely to be nonwhite and older, with a greater prevalence of hypertension and diabetes mellitus (all p <0.001) compared with men. After adjusting for baseline characteristics and coronary artery size, the incidence of coronary vascular injury complications was higher in women than in men, particularly in patients 55 years (OR 1.32, 95% CI 0.87 to 1.99, p = 0.047 for gender-age interaction). The adjusted odds of bleeding complications were also higher in women than in men (55 years OR 2.55, 95% CI 1.68 to 3.87, p = 0.121 for gender-age interaction). No significant gender differences were present in a combined end point of death, myocardial infarction, and emergency coronary artery bypass graft surgery. In conclusion, among patients who have undergone PCI, women, particularly younger women, are more likely than men to experience coronary vascular injury and bleeding complications unaccounted for by coronary artery size and other patient characteristics. No differences were found in major in-hospital complications by gender.

We examined gender and age differences for chief symptom complaints in a population-based sample of 881 women (43%) and 1,192 men (57%) hospitalized for acute myocardial infarction (AMI). Women, in particular older women, were less likely than men to have a chief complaint of chest pain associated with AMI. Overall, a large proportion of women and men whose AMI was ultimately diagnosed did not present with chest pain as their chief complaint.

Studies of the effects of menopausal hormone therapy on coronary artery disease (CAD) in postmenopausal women have provided contradictory results. Although recent experimental studies have revealed no beneficial effect of combination therapy with estrogen (E) and progesterone (P), the effect of monotherapy with E remains unknown. We retrospectively examined the medical records of 843 consecutive women aged > or =55 years who underwent their first cardiac catheterization between January 1996 and December 1998. We compared the presence and severity of CAD, defined as > or =1 diseased coronary vessel (with stenosis > or =50%), in women who only took E, E+P, or no menopausal hormone therapy. In all, 210 women (33%) took hormones, of whom 47 (22%) used E+P and 163 (78%) used E only. Women who used any hormones tended to be healthier than nonusers, but E+P users had a lower prevalence of risk factors and co-morbidities than E users. In unadjusted analyses, both the E and E+P groups were significantly less likely to have CAD than nonusers (relative risk [RR] 0.71, 95% confidence interval [CI] 0.58 to 0.84 for the E group; RR 0.76, 95% CI 0.54 to 0.99 for the E+P group). Demographic factors, CAD risk factors, co-morbidities, and primary prevention medication use explained the association between E+P and the presence of CAD (RR 1.14, 95% CI 0.74 to 1.39). In contrast, adjustment for these factors had a minimal effect on the association between E and CAD compared with nonusers (RR 0.79, 95% CI 0.59 to 0.98). Thus, the apparent protective effect of combination menopausal hormone therapy with E+P on CAD is due to differences in other patient characteristics. In contrast, unopposed E therapy may have a protective effect on CAD.

Information on the relative benefit of coronary artery bypass grafting (CABG) versus stent-assisted percutaneous coronary intervention (PCI) for improvement of cardiac-related health status in women and how it compares with men is limited. The Stent or Surgery trial compared randomly assigned CABG and stent-assisted PCI in 206 women and 782 men with multivessel disease. We examined longitudinal changes at 6 and 12 months from baseline by gender and treatment in 3 subscales of the Seattle Angina Questionnaire (SAQ): physical limitation, angina frequency, and quality of life. At the time of revascularization, women were older, more severely ill, and tended to have lower SAQ scores than men. At 6 months, SAQ scores after both procedures improved significantly in both genders, with greater improvement achieved with CABG. After adjustment for other factors, in men, CABG was associated with a 54.7% greater improvement in physical limitation compared with PCI, 31.3% greater improvement in angina frequency, and 18.3% greater improvement in quality of life. In women, these relative differences were 11.6%, 43.2%, and 39.3%, respectively. At 1 year, men continued to show greater improvement with CABG in all 3 dimensions (50.6%, 19.7%, and 15.3%, respectively), but in women the relative differences decreased substantially (1.6%, 11.1%, and 0.6%, respectively) due to a greater later improvement after PCI (p = 0.049 for the interaction among treatment, gender, and follow-up for the quality of life domain). Although CABG may be superior to PCI in men, in women, at 1 year after intervention, both procedures appear equally effective.

Pulse pressure has been related to higher risk of cardiovascular events in older persons. Isolated systolic hypertension is common among the elderly and is accompanied by elevated pulse pressure. Treatment of isolated systolic hypertension may further increase pulse pressure if diastolic pressure is lowered to a greater extent than systolic pressure. Little is known regarding pulse pressure as a predictor of cardiovascular outcomes in elderly persons with isolated systolic hypertension, and the influence of treatment on the pulse pressure effect. We assessed the relation between pulse pressure, measured throughout the follow-up period, and the incidence of coronary heart disease (CHD), heart failure (HF), and stroke in 4,632 participants in the Systolic Hypertension in the Elderly Program, a 5-year randomized, placebo-controlled clinical trial of treatment of isolated systolic hypertension in older adults. In the treatment group, a 10-mm Hg increase in pulse pressure was associated with a statistically significant 32% increase in risk of HF and a 24% increase in risk of stroke after controlling for systolic blood pressure and other known risk factors, as well as with a 23% increase in risk of HF and a 19% increase in risk of stroke after controlling for diastolic blood pressure and other risk factors. Pulse pressure was not significantly associated with HF or stroke in the placebo group, nor with incidence of CHD in either the placebo or treatment group. These results suggest that pulse pressure is a useful marker of risk for HF and stroke among older adults being treated for isolated systolic hypertension.

1.5 mg/dl. Based on the number of these factors, a patient's risk for developing worsening renal function ranged between 16% (< or =1 factor) and 53% (> or =5 factors). After adjusting for confounding effects, worsening renal function was associated with a significantly longer length of stay by 2.3 days, higher in-hospital cost by $1,758, and an increased risk of in-hospital mortality (odds ratio 2.72; 95% confidence interval 1.62 to 4.58). In conclusion, worsening renal function, an event that frequently occurs in elderly patients hospitalized with heart failure, confers a substantial burden to patients and the healthcare system and can be predicted by 6 admission characteristics.

This study explores gender differences in symptom presentation associated with coronary heart disease (CHD). In this prospective study, nurse data collectors directly observed 550 patients as they presented to the Emergency Department (ED) of Yale-New Haven Hospital. The final sample included 217 patients (41% women) diagnosed with CHD (acute coronary ischemia or myocardial infarction). Chest pain was the most frequently reported symptom in women (70%) and men (71%). Unadjusted analyses revealed that women were more likely than men to present with midback pain (odds ratio [OR] 9.61, 95% confidence interval [CI] 2.10 to 44.11, p = 0.001), nausea and/or vomiting (OR 2.29, 95% CI 1.19 to 4.42, p = 0.012), dyspnea (OR 1.82, 95% CI 1.05 to 3.16, p = 0.032), palpitations (OR 3.42, 95% CI 1.02 to 11.47, p = 0.036), and indigestion (OR 2.13, 95% CI 1.03 to 4.44, p = 0.040). After adjustment for age and diabetes, women were more likely to present with nausea and/or vomiting (OR 2.43, 95% CI 1.23 to 4.79, p = 0.011) and indigestion (OR 2.13, 95% CI 1.10 to 4.53, p = 0.048). Women (30%) and men (29%) were equally likely to present without chest pain, and dyspnea was the most common non-chest pain symptom. In the subgroup of patients without chest pain, unadjusted analyses revealed that women were more likely to report nausea and/or vomiting compared with men (OR 4.40, 95% CI 1.30 to 14.84, p = 0.013). Although we found some significant gender differences in non-chest pain symptoms, we conclude that there were more similarities than differences in symptoms in women and men presenting to the ED with symptoms suggestive of CHD who were later diagnosed with CHD.

Purpose: The risk factors for the development of heart failure are not clearly defined, particularly for older adults. We undertook the current investigation to examine the associations of traditional cardiovascular risk factors, comorbidity, and psychosocial factors with the risk of heart failure during 10 years of follow-up in a community-based elderly population., Subjects and Methods: We evaluated 1,749 subjects, 65 years of age or older, free of heart failure, myocardial infarction, and angina at baseline, who were participating in the New Haven, Connecticut cohort of the Established Population for Epidemiologic Studies of the Elderly program. Cox proportional hazards regression models were used to determine risk ratios (RR) and 95% confidence intervals (CI)., Results: During 13,811 person-years of follow-up, 173 subjects developed incident heart failure, as confirmed by chart review. Five factors were independent predictors of heart failure: male sex (RR = 1.7; CI, 1.3 to 2.4), older age (RR = 1.9; CI, 1.3 to 2.7 for age 75 to 84 years, RR = 3.0; CI, 1.7 to 5.5 for age 85 years and older, compared with < or = 74 years), diabetes (RR = 2.9; CI, 2.0 to 4.3), pulse pressure > or = 70 mm Hg (RR = 2.3; CI, 1.3 to 4.3, compared with <50 mm Hg), and body mass index > or = 28 kg/m2 (RR = 1.6; CI, 1.0 to 2.4, compared with <24 kg/ m2). Myocardial infarction occurred during follow-up in 8% of the cohort and was also an important predictor of heart failure (RR = 21; CI, 15 to 31)., Conclusions: Age and traditional cardiovascular risk factors are associated with the development of heart failure in the elderly. Preventive strategies should focus on the management of diabetes, blood pressure, and weight, in addition to the prevention and management of myocardial infarction.

We sought to determine how often angiotensin-converting enzyme (ACE) inhibitors are prescribed as a discharge medication among eligible patients > or = 65 years old with an acute myocardial infarction; to identify patient characteristics associated with the decision to prescribe ACE inhibitors; and to determine the factors associated with the decision to obtain an evaluation of left ventricular function among patients who have no contraindications to ACE inhibitors. We addressed these aims with an observational study of consecutive elderly Medicare beneficiary survivors of an acute myocardial infarction hospitalized in Alabama, Connecticut, Iowa, and Wisconsin between June 1992 and February 1993. Among the 5,453 patients without a contraindication to ACE inhibitors at discharge, 3,528 (65%) had an evaluation of left ventricular function. Of the 1,228 patients without a contraindication to ACE inhibitors who had a left ventricular ejection fraction < or = 40%, 548 (45%) were prescribed the medication at discharge. In a multivariable analysis, an increased prescribed use of ACE inhibitors at discharge was correlated with several factors, including diabetes mellitus, congestive heart failure, ventricular tachycardia, and loop diuretics as a discharge medication. Patients admitted after the publication of the Survival and Ventricular Enlargement (SAVE) trial were significantly more likely to receive ACE inhibitors, although the absolute improvement in utilization was small in the 6 months after the trial results were published. In conclusion, improving the identification of appropriate patients for ACE inhibitors and increasing the prescription of ACE inhibitors for ideal patients may provide an excellent opportunity to improve care.