Causes and Predictors of Death in Patients With Coronary Heart Disease (from the Heart and Soul Study).

Although the prevalence of coronary heart disease (CHD) in the United States has increased during the past 25 years, cardiovascular mortality has decreased due to advances in CHD therapy and prevention. We sought to determine the proportion of patients with CHD who die from cardiovascular versus noncardiovascular causes and the causes and predictors of death, in a cohort of patients with CHD. The Heart and Soul Study enrolled 1,024 participants with stable CHD from 2000 to 2002 and followed them for 10 years. Causes of mortality were assigned based on detailed review of medical records, death certificates, and coroner reports by blinded adjudicators. During 7,680 person-years of follow-up, 401 participants died. Of these deaths, 42.4% were cardiovascular and 54.4% were noncardiovascular. Myocardial infarction, stroke, and sudden death accounted for 72% of cardiovascular deaths. Cancer, pneumonia, and sepsis accounted for 67% of noncardiovascular deaths. Independent predictors of cardiac mortality were older age, inducible ischemia on stress echocardiography, higher heart rate at rest, smoking, lower hemoglobin, and higher N-terminal pro-brain natriuretic peptide (all p values <0.05); independent predictors of noncardiac mortality included older age, inducible ischemia, higher heart rate, lower exercise capacity, and nonuse of statins (all p values <0.05). In conclusion, mortality in this cohort was more frequently due to noncardiovascular causes, and predictors of noncardiovascular mortality included factors traditionally associated with cardiovascular mortality.

Traditional Risk Factors Versus Biomarkers for Prediction of Secondary Events in Patients With Stable Coronary Heart Disease: From the Heart and Soul Study.

BACKGROUND: Patients with stable coronary heart disease (CHD) have widely varying prognoses and treatment options. Validated models for risk stratification of patients with CHD are needed. We sought to evaluate traditional and novel risk factors as predictors of secondary cardiovascular (CV) events, and to develop a prediction model that could be used to risk stratify patients with stable CHD. METHODS AND RESULTS: We used independent derivation (912 participants in the Heart and Soul Study) and validation (2876 participants in the PEACE trial) cohorts of patients with stable CHD to develop a risk prediction model using Cox proportional hazards models. The outcome was CV events, defined as myocardial infarction, stroke, or CV death. The annual rate of CV events was 3.4% in the derivation cohort and 2.2% in the validation cohort. With the exception of smoking, traditional risk factors (including age, sex, body mass index, hypertension, dyslipidemia, and diabetes) did not emerge as the top predictors of secondary CV events. The top 4 predictors of secondary events were the following: N-terminal pro-type brain natriuretic peptide, high-sensitivity cardiac troponin T, urinary albumin:creatinine ratio, and current smoking. The 5-year C-index for this 4-predictor model was 0.73 in the derivation cohort and 0.65 in the validation cohort. As compared with variables in the Framingham secondary events model, the Heart and Soul risk model resulted in net reclassification improvement of 0.47 (95% CI 0.25 to 0.73) in the derivation cohort and 0.18 (95% CI 0.01 to 0.40) in the validation cohort. CONCLUSIONS: Novel risk factors are superior to traditional risk factors for predicting 5-year risk of secondary events in patients with stable CHD.

Usefulness of an Echocardiographic Composite Cardiac Calcium Score to Predict Death in Patients With Stable Coronary Artery Disease (from the Heart and Soul Study).

Mitral annular calcium and aortic valve sclerosis on transthoracic echocardiography (TTE) are independently associated with cardiovascular (CV) events in patients with coronary artery disease (CAD). However, the prognostic value of calcific deposits at multiple sites is unknown. We performed TTEs in a prospective cohort of 595 outpatients with stable CAD and graded the severity of calcific deposition at 6 sites: mitral annulus, aortic valve, aortic ring, sinotubular junction, papillary muscle tip, and left main coronary artery. For each site with moderate calcific deposition or greater, 1 point was given to generate a composite cardiac calcium score (maximum of 6). The primary end point was the occurrence of CV events-a composite of death, myocardial infarction, stroke, transient ischemic attack, and heart failure. The association of the composite calcium score with CV events was evaluated using multivariate Cox proportional hazards models. Over a median follow-up of 4.2 years, 205 CV events occurred. Participants with a composite calcium score ≥2 had a higher risk of CV events (11.1 events/100 person-years) than those with a score of 0 (5.5 events/100 person-years, unadjusted hazard ratio [HR] 2.01, p <0.001), but this association was not significant after multivariate adjustment. The risk of death was higher in participants with a composite calcium score of ≥2 (8.9 events/100 person-years) versus those with a score of 0 (3.6 events/100 person-years, unadjusted HR 2.51, p <0.001). After adjustment for age, diabetes mellitus, previous coronary revascularization, diastolic blood pressure, estimated glomerular filtration rate, and serum phosphorus level, the risk of death remained higher in participants with a composite calcium score of ≥2 compared with those with a score of 0 (adjusted HR 1.76, 95% confidence interval 1.10 to 2.81, p = 0.02). In conclusion, a simple TTE-derived composite cardiac calcium score was independently predictive of death in patients with pre-existing CAD.

Association of CHADS2, CHA2DS2-VASc, and R2CHADS2 scores with left atrial dysfunction in patients with coronary heart disease (from the Heart and Soul study).

The predictive ability of the CHADS2 index to stratify stroke risk may be mechanistically linked to severity of left atrial (LA) dysfunction. This study investigated the association between the CHADS2 score and LA function. We performed resting transthoracic echocardiography in 970 patients with stable coronary heart disease and normal ejection fraction and calculated baseline LA functional index (LAFI) using a validated formula: (LA emptying fraction×left ventricular outflow tract velocity time integral)/LA end-systolic volume indexed to body surface area. We performed regression analyses to evaluate the association between risk scores and LAFI. Among 970 subjects, mean CHADS2 was 1.7±1.2. Mean LAFI decreased across tertiles of CHADS2 (42.8±18.1, 37.8±19.1, 36.7±19.4, p<0.001). After adjustment for age, sex, race, systolic blood pressure, hyperlipidemia, myocardial infarction, revascularization, body mass index, smoking, and alcohol use, high CHADS2 remained associated with the lowest quartile of LAFI (odds ratio 2.34, p=0.001). In multivariable analysis of component co-morbidities, heart failure, age, and creatinine clearance<60 ml/min were strongly associated with LA dysfunction. For every point increase in CHADS2, the LAFI decreased by 4.0%. Secondary analyses using CHA2DS2-VASc and R2CHADS2 scores replicated these results. Findings were consistent when excluding patients with baseline atrial fibrillation. In conclusion, CHADS2, CHA2DS2-VASc, and R2CHADS2 scores are associated with LA dysfunction, even in patients without baseline atrial fibrillation. These findings merit further study to determine the role of LA dysfunction in cardioembolic stroke and the value of LAFI for risk stratification.

Mitral annular calcium, inducible myocardial ischemia, and cardiovascular events in outpatients with coronary heart disease (from the Heart and Soul Study).

We sought to determine whether mitral annular calcium (MAC) is associated with inducible myocardial ischemia and adverse cardiovascular outcomes in ambulatory patients with coronary artery disease (CAD). MAC is associated with cardiovascular disease (CVD) in the general population, but its association with CVD outcomes in patients with CAD has not been evaluated. We examined the association of MAC with inducible ischemia and subsequent cardiovascular events in 1,020 ambulatory patients with CAD who were enrolled in the Heart and Soul Study. We used logistic regression to determine the association of MAC with inducible ischemia and Cox proportional hazards models to determine the association with CVD events (myocardial infarction, heart failure, stroke, transient ischemic attack or death). Models were adjusted for age, gender, race, smoking, history of heart failure, blood pressure, high-density lipoprotein, and estimated glomerular filtration rate. Of the 1,020 participants 192 (19%) had MAC. Participants with MAC were more likely than those without MAC to have inducible ischemia (adjusted odds ratio 2.06, 95% confidence interval 1.41 to 3.01, p = 0.0002). During an average of 6.26 ± 2.11 years of follow-up, there were 310 deaths, 161 hospitalizations for heart failure, 118 myocardial infarctions, and 55 cerebrovascular events. MAC was associated with an increased rate of cardiovascular events (adjusted hazard ratio 1.39, 95% confidence interval 1.08 to 1.79, p = 0.01). In conclusion, we found that MAC was associated with inducible ischemia and subsequent CVD events in ambulatory patients with CAD. MAC may indicate a high atherosclerotic burden and identify patients at increased risk for adverse cardiovascular outcomes.

The CHADS2 score predicts ischemic stroke in the absence of atrial fibrillation among subjects with coronary heart disease: data from the Heart and Soul Study.

BACKGROUND: We sought to evaluate the prognostic performance of the CHADS(2) score for prediction of ischemic stroke/transient ischemic attack (TIA) in subjects with coronary heart disease (CHD) without atrial fibrillation (AF). METHODS: In 916 nonanticoagulated outpatients with stable CHD and no AF by baseline electrocardiogram, we calculated CHADS(2) scores (congestive heart failure, hypertension, age ≥75 years, diabetes [1 point each], and prior stroke or TIA [2 points]). The primary outcome was time to ischemic stroke or TIA over a mean follow-up of 6.4 ± 2.3 years. RESULTS: Over 5,821 person-years of follow-up, 40 subjects had an ischemic stroke/TIA (rate 0.69/100 person-years, 95% CI 0.50-0.94). Compared with subjects with low (0-1) CHADS(2) scores, those with intermediate (2-3) and high (4-6) CHADS(2) scores had an increased rate of stroke/TIA, even after adjustment for age, tobacco, antiplatelet therapy, statins, and angiotensin inhibitors (CHADS(2) score 2-3: HR 2.4, 95% CI 1.1-5.3, P = .03; CHADS(2) score 4-6: HR 4.0, 95% CI 1.5-10.6, P = .006). Model discrimination (c-statistic = 0.65) was comparable with CHADS(2) model fit in published AF-only cohorts. CONCLUSIONS: The CHADS(2) score predicts ischemic stroke/TIA in subjects with stable CHD and no baseline AF. The event rate in non-AF subjects with high CHADS(2) scores (5-6) was comparable with published rates in AF patients with moderate CHADS(2) scores (1-2), a population known to derive benefit from stroke prevention therapies. These findings should inform efforts to determine whether stroke prevention therapies or screening for silent AF may benefit subjects with stable CHD and high CHADS(2) scores.

Association of resistin with heart failure and mortality in patients with stable coronary heart disease: data from the heart and soul study.

BACKGROUND: Resistin is a pro-inflammatory signaling molecule that is thought to contribute to atherosclerosis. We sought to evaluate whether resistin is predictive of worse cardiovascular outcomes among ambulatory patients with stable coronary heart disease (CHD). METHODS AND RESULTS: We measured baseline serum resistin in 980 participants with documented CHD. After a mean follow-up of 6.1 (range, 0.1 to 9.0) years, 358 (36.5%) were hospitalized for myocardial infarction or heart failure or had died. As compared with participants who had resistin levels in the lowest quartile, those with resistin levels in the highest quartile were at an increased risk of heart failure (hazard ratio [HR], 2.06; 95% confidence interval [CI], 1.26-3.39) and death (HR, 1.56; 95% CI, 1.11-2.18), adjusted for age, sex, and race. Further adjustments for obesity, hypertension, insulin resistance, dyslipidemia, and renal dysfunction eliminated these associations. Resistin levels were not associated with an increased risk of non-fatal myocardial infarction (unadjusted HR, 1.18; 95% CI, 0.68-2.05). CONCLUSIONS: Elevated serum resistin is associated with higher rates of mortality and hospitalization for heart failure. However, this appears to be explained by the association of resistin with traditional measures of cardiovascular risk. Thus, serum resistin does not add prognostic information among high-risk persons with established CHD.

Cholecystectomy in the presence of a large patent foramen ovale: laparoscopic or open?

An obese patient with cholelithiasis and acute cholecystitis was scheduled for an emergency laparoscopic cholecystectomy. On preoperative workup, a 5-year-old echocardiogram showed a large patent foramen ovale (PFO) with a right-to-left shunt that was open at rest. Noting both the benefits of laparoscopic surgery and the substantial incidence of PFO in the general population (10% to 30%), the attending and consulting surgeons reasoned that the benefits of laparoscopy greatly exceeded an immeasurably small risk of paradoxical emboli.

Resistin, exercise capacity, and inducible ischemia in patients with stable coronary heart disease: data from the Heart and Soul study.

OBJECTIVE: Resistin is an adipocytokine involved in insulin resistance, inflammation, and atherosclerosis. Its role in the development and progression of coronary heart disease (CHD) is not yet well-characterized. We performed a cross-sectional study to evaluate the association between serum resistin levels, exercise capacity, and exercise-induced cardiac ischemia among patients with stable CHD. METHODS AND RESULTS: We measured serum resistin concentrations and determined treadmill exercise capacity and inducible ischemia by stress echocardiography in 899 outpatients with documented CHD. Of these, 215 (24%) had poor exercise capacity (<5 metabolic equivalent tasks), and 217 (24%) had inducible ischemia. As compared with participants who had resistin levels in the lowest quartile, those with resistin levels in the highest quartile were more likely to have poor exercise capacity (33% versus 16%, odds ratio [OR] 2.68, P<0.0001) and inducible ischemia (30% versus 17%, OR 2.08, P=0.001). Both associations remained robust after adjusting for numerous clinical risk factors, metabolic variables, and markers of insulin resistance (poor exercise capacity adjusted OR 1.73, P=0.04; inducible ischemia adjusted OR 1.82, P=0.01). However, further adjustments for C-reactive protein, interleukin-6, and tumor necrosis factor-α eliminated the association with poor exercise capacity (adjusted OR 1.50, P=0.14) and substantially weakened the association with inducible ischemia (adjusted OR 1.72, P=0.03). CONCLUSIONS: Elevated serum resistin is associated with poor exercise capacity and exercise-induced cardiac ischemia in patients with stable coronary disease. Adjustment for inflammatory markers attenuated these associations, suggesting a possible role for resistin in inflammation and CHD pathophysiology.

Association of serum phosphorus with left ventricular mass in men and women with stable cardiovascular disease: data from the Heart and Soul Study.

BACKGROUND: Higher serum phosphorus levels are associated with cardiovascular disease (CVD) events in the general population, an association that may be stronger in men. Estradiol has phosphaturic properties. Whether higher serum phosphorus levels are associated with left ventricular (LV) mass in persons without end-stage renal disease and whether the association is modified by sex is unknown. STUDY DESIGN: Cross-sectional observational study. SETTING & PARTICIPANTS: 978 outpatients with stable CVD. PREDICTOR: The primary predictor variable was serum phosphorus level. Sex was evaluated as an effect modifier. OUTCOME & MEASUREMENTS: LV mass using transthoracic echocardiography. RESULTS: The association of serum phosphorus level with LV mass differed by sex (interaction P=0.04). In models adjusted for age, race, kidney function, smoking, diabetes, blood pressure, cholesterol level, C-reactive protein level, and angiotensin-converting enzyme inhibitor/angiotensin receptor blocker use, each 1-mg/dL higher serum phosphorus level was associated with 4.52-g/m2 greater LV mass (95% CI, 1.04-8.01; P=0.01) in men. Conversely, in women, no statistically significant association was found between serum phosphorus level and LV mass. LIMITATIONS: Older adult population with stable CVD; 19% were women. CONCLUSIONS: In outpatients with stable CVD, higher serum phosphorus levels are associated with greater LV mass in men, but not women. Whether sex hormones may account for these differences requires future study.

A comparison of echocardiography to invasive measurement in the evaluation of pulmonary arterial hypertension in a rat model.

Pulmonary arterial hypertension (PAH) is a life-threatening condition characterized by progressive elevation in pulmonary artery pressure (PAP) and total pulmonary vascular resistance (TPVR). Recent advances in imaging techniques have allowed the development of new echocardiographic parameters to evaluate disease progression. However, there are no reports comparing the diagnostic performance of these non-invasive parameters to each other and to invasive measurements. Therefore, we investigated the diagnostic yield of echocardiographically derived TPVR and Doppler parameters of PAP in screening and measuring the severity of PAH in a rat model. Serial echocardiographic and invasive measurements were performed at baseline, 21 and 35 days after monocrotaline-induction of PAH. The most challenging echocardiographic derived TPVR measurement had good correlation with the invasive measurement (r = 0.92, P < 0.001) but also more simple and novel parameters of TPVR were found to be useful although the non-invasive TPVR measurement was feasible in only 29% of the studies due to lack of sufficient tricuspid valve regurgitation. However, echocardiographic measures of PAP, pulmonary artery flow acceleration time (PAAT) and deceleration (PAD), were measurable in all animals, and correlated with invasive PAP (r = -0.74 and r = 0.75, P < 0.001 for both). Right ventricular thickness and area correlated with invasive PAP (r = 0.59 and r = 0.64, P < 0.001 for both). Observer variability of the invasive and non-invasive parameters was low except in tissue-Doppler derived isovolumetric relaxation time. These non-invasive parameters may be used to replace invasive measurements in detecting successful disease induction and to complement invasive data in the evaluation of PAH severity in a rat model.

Relation of beta-blocker use with frequency of hospitalization for heart failure in patients with left ventricular diastolic dysfunction (from the Heart and Soul Study).

Heart failure (HF) is a common public health problem, and many new cases are now recognized to occur in patients with preserved left ventricular ejection fraction. beta Blockers improve the outcomes of patients with known left ventricular systolic dysfunction, but whether beta blockers provide similar protection among patients with left ventricular diastolic dysfunction is unclear. We studied the association between use of beta blockers and subsequent hospitalization for HF in patients with diastolic dysfunction and stable coronary heart disease. We evaluated medication use and performed echocardiography at baseline in a prospective cohort of 911 outpatients with known coronary heart disease from the Heart and Soul Study. Hospitalizations for HF were assessed by blinded review of the medical records during an average follow-up of 5.2 years. Of the 911 participants, 118 (13%) had diastolic dysfunction, of whom 2 were lost to follow-up. Of the 116 remaining patients, 19 (25%) of the 77 using beta blockers were hospitalized for HF compared to 16 (41%) of the 39 not using beta blockers (age-adjusted hazard ratio 0.51, 95% confidence interval 0.26 to 1.00; p = 0.05). This association remained after additional adjustment for gender, smoking, history of myocardial infarction, diabetes, and creatinine (hazard ratio 0.46, 95% confidence interval 0.23 to 0.93; p = 0.03). The results were similar after excluding 31 participants with a history of self-reported HF (hazard ratio 0.33, 95% confidence interval 0.13 to 0.86; p = 0.02) and 24 participants with concurrent systolic dysfunction (hazard ratio 0.36, 95% confidence interval 0.14 to 0.89; p = 0.03). In conclusion, the use of beta blockers is associated with a decreased risk of hospitalization for HF in patients with diastolic dysfunction and stable coronary heart disease.

The association of uncarboxylated matrix Gla protein with mitral annular calcification differs by diabetes status: The Heart and Soul study.

OBJECTIVE: Mitral annular calcification (MAC) and aortic stenosis (AS) are associated with systemic calcification and cardiovascular disease (CVD) events. Matrix Gla protein (MGP) is an inhibitor of vascular calcification and lower levels of its precursor - uncarboxylated MGP (ucMGP) - are associated with vascular calcification in pilot studies. METHODS AND RESULTS: In this cross-sectional study of 839 outpatients with stable CVD, we measured serum ucMGP, and evaluated MAC and AS by echocardiography. The association of ucMGP with MAC differed by diabetes status (interaction P<0.001). Among participants without diabetes (n=615), higher ucMGP (per standard deviation [1178nM] increase) was associated with lower odds of MAC (odds ratio [OR] 0.73; 95% confidence interval [CI] 0.55-0.97) in models adjusted for traditional CVD risk factors, C-reactive protein, and kidney function. Among persons with diabetes (n=221), higher ucMGP was associated with higher odds of MAC (OR 1.89; 95% CI 1.29-2.78). Results were qualitatively similar for the association of ucMGP with AS although not statistically significant. CONCLUSIONS: Among outpatients with stable CVD, higher ucMGP is associated with lower odds of MAC in persons without diabetes, and higher odds of MAC in persons with diabetes. Future studies should determine whether ucMGP levels are associated with CVD events, and whether such associations differ by diabetes status.

Association of cystatin C with ischemia in patients with coronary heart disease.

BACKGROUND: Elevated concentrations of cystatin C are associated with greater cardiovascular morbidity and mortality. We sought to determine whether elevated concentrations of cystatin C were associated with inducible ischemia in patients with coronary heart disease (CHD). METHODS: We measured serum cystatin C and performed exercise treadmill testing with stress echocardiography in a cross-sectional study of 899 outpatients with CHD. RESULTS: Among the 241 participants in the highest quartile of cystatin C (>1.30 mg/L), 38% had inducible ischemia, compared with 13% of those in the lowest quartile of cystatin C < 0.92 mg/L; adjusted odds ratio [OR]: 2.1; 95% confidence interval [CI]: 1.2 to 3.8; p = 0.01). However, this association differed in participants with and without a history of coronary artery bypass graft (CABG), as well as in users and nonusers of beta-blockers and statins (p values for interaction < 0.1). Among participants without a history of CABG, 35% of those in the highest quartile and 9% of those in the lowest quartile of cystatin C had inducible ischemia (adjusted OR: 3.05; 95% CI: 1.3-6.9; p = 0.008). Among participants who were not using beta-blockers, 44% of those in the highest quartile and 7% in the lowest quartile of cystatin C had inducible ischemia (adjusted OR: 5.3; 95% CI: 1.8-15.5; p = 0.002). Among participants who were not using statins, 39% of participants in the highest quartile and 4% of those in the lowest quartile had inducible ischemia (adjusted OR: 10.3; 95% CI: 2.5-43.3; p = 0.001). CONCLUSIONS: Elevated levels of cystatin C are independently associated with inducible ischemia among outpatients with stable coronary disease.

Remote second-hand tobacco exposure in flight attendants is associated with systemic but not pulmonary hypertension.

BACKGROUND: Second-hand tobacco smoke has been associated with cardiopulmonary dysfunction. We sought to examine the residual effects of remote second-hand smoke exposure on resting and exercise cardiopulmonary hemodynamics. We hypothesized that remote secondhand smoke exposure results in persistent cardiopulmonary hemodynamic abnormalities. METHODS: Participants were non-smoking flight attendants who worked in airline cabins prior to the in-flight tobacco ban. Participants underwent clinical evaluations and completed smoke exposure questionnaires. We used Doppler echocardiography to measure pulmonary artery systolic pressure (PASP) and pulmonary vascular resistance (PVR) at rest and during supine bicycle ergometer exercise, using the validated formula TRV/VTIRVOT x 10 + 0.16, where VTIRVOT is the velocity time integral at the right ventricular outflow tract and TRV is the tricuspid regurgitation velocity. The group was divided into quartiles according to the degree of smoke exposure. Analysis of variance was used to determine the differences in hemodynamic outcomes. RESULTS: Seventy-nine flight attendants were included in our analysis. Baseline characteristics among participants in each quartile of smoke exposure were similar except for history of systemic hypertension, which was more prevalent in the highest quartile. Peak exercise PASP rose to the same degree in all test groups (mean PASP 44 mm Hg, p = 0.25), and PVR increased by approximately 27% in all quartiles. There was no significant difference in pulmonary artery systolic pressure or pulmonary vascular resistance among quartiles of smoke exposure. CONCLUSIONS: We found that remote heavy second-hand smoke exposure from in-flight tobacco is associated with systemic hypertension but does not have demonstrable pulmonary hemodynamic consequences.

Cystatin C, left ventricular hypertrophy, and diastolic dysfunction: data from the Heart and Soul Study.

BACKGROUND: Impaired kidney function, as measured by serum cystatin C, is associated with risk of incident heart failure. Whether cystatin C is associated with preclinical cardiac structural abnormalities is unknown. We evaluate whether cystatin C is associated with left ventricular hypertrophy, diastolic dysfunction, and systolic dysfunction among 818 outpatients with coronary artery disease who were free of clinical heart failure. METHODS AND RESULTS: The 818 study participants were categorized into quartiles based on serum cystatin C concentrations, with < or =0.91 mg/L constituting the lowest quartile (I) and > or =1.28 mg/L constituting the highest (IV). Left ventricular hypertrophy (left ventricular mass index >90 g/m(2) by truncated ellipsoid method), diastolic dysfunction (impaired relaxation, pseudo-normal, or restrictive filling patterns) and systolic dysfunction (left ventricular ejection fraction < or =50%) were determined by echocardiography. Left ventricular hypertrophy was present in 68% of participants in quartile IV, compared with 44% of those in quartile I (adjusted odds ratio [OR] 2.17; 95% confidence interval [CI] 1.34 to 3.52; P = .002). Diastolic dysfunction was present in 52% of participants in quartile IV, compared with 24% of those in quartile I (adjusted OR 1.79; 95% CI 1.04 to 3.11; P = .04). Systolic dysfunction was present in 12% of those in quartile IV, compared with 6% of those in quartile I (adjusted OR 1.83; 95% CI 0.75 to 4.46; P = .15). CONCLUSION: Higher cystatin C concentrations are strongly associated with left ventricular hypertrophy and diastolic dysfunction in outpatients with coronary artery disease and without heart failure.

Impairment of left atrial function predicts post-operative atrial fibrillation after coronary artery bypass graft surgery.

AIMS: Despite the prevalence of atrial fibrillation (AF) occurring after cardiac surgery, its pathophysiology is incompletely understood. Specifically, whether left atrial (LA) structural remodelling occurs, contributing to a decrement in atrial function and AF has not been previously determined. This study sought to determine the relationship between LA function and post-operative AF. METHODS AND RESULTS: Three hundred patients undergoing elective coronary artery bypass graft surgery were monitored with intraoperative transoesophageal echocardiography to determine LA function and dimensions. Post-operative AF was monitored with continuous telemetry until hospital discharge. The relationship between clinical factors versus LA function and dimension was assessed using multi-variate logistic regression. By univariate analysis, patients who subsequently developed post-operative AF had a larger LA area and LA appendage area, and lower LA ejection fraction measured in the pre-bypass period compared to those without subsequent AF. By multivariable analysis, in addition to clinical data including age (odds ratio [OR] 1.11, 95% confidence interval [CI] 1.05-1.16, P<0.0001), body surface area (OR 13.31, 95% CI 1.87-94.5, P=0.0097) and white race, post-bypass atrial systolic function (atrial filling fraction 0.36, OR 2.51, 95% CI 1.03-6.13, P=0.04) and abnormal relaxation of the left ventricle (E duration 270 ms) (OR 2.89, 95% CI 1.34-6.24, P=0.0067) independently increased the risk of post-operative AF. CONCLUSION: These results demonstrate that some of the structural and functional changes in the atria common to chronic AF in the elderly population are also prevalent in surgical patients who develop post-operative AF, suggesting that post-operative and chronic AF may have similar pathophysiology.