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Simon Chakko

Publications and source records attributed to Simon Chakko.

10 recordsLinked to original sources
PubMed2006

Evaluation of comorbidity scores to predict all-cause mortality in patients with established coronary artery disease.

BACKGROUND: To assess the value of scores based on the presence of comorbid conditions for mortality risk-stratification in patients with coronary artery disease (CAD) METHODS: We prospectively followed 305 males with CAD undergoing coronary angiography for 58 months. We correlated the modified Charlson Index (MCI) and the recently proposed CAD-specific index (CSI) with the risk of all-cause mortality. RESULTS: The odds ratio (OR) for death increased by 31% per point increase in the MCI (95% CI=17-46%; p<0.0001). The OR for death increased by 16% per point increase in the CSI (95% CI=8.5-25%; p<0.0001). In logistic regression models that adjusted for age, left ventricular ejection fraction, and the number of vessels involved with CAD, both the MCI and the CSI were the strongest predictors of mortality according to the chi2 value for each term, with the MCI having the highest value. The adjusted OR per point increase in the MCI was 1.32 (95% CI=1.17-1.48; p<0.0001); the corresponding adjusted OR per point increase in the CSI was 1.17 (95% CI=1.09-1.26; p<0.0001). The model including the MCI had a slightly higher chi2 value (45.1 vs. 39.1) and area under the receiver operator characteristic curve (0.742 vs. 0.727) than the model including the CSI. CONCLUSION: The MCI and the newly proposed CSI are powerful tools to predict all-cause mortality in patients with established CAD. Although the CSI was not superior to the MCI, its simplicity might make it useful in populations with a low prevalence of comorbidities not included in this score.

Cause of Death↗
PubMed2006

Endocarditis associated with antineutrophil cytoplasmic antibodies: a case report and review of the literature.

We report a case of subacute bacterial endocarditis associated with small vessel vasculitis and a strongly positive cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA) test. It is important to recognize this cause of positive c-ANCA because infectious endocarditis may closely mimic the clinical manifestations of ANCA-associated vasculitides such as Wegener granulomatosis or microscopic polyangiitis. Furthermore, ANCA-associated vasculitis may result in noninfectious endocarditis, which may be confused with bacterial endocarditis. In this paper, we review reported cases of ANCA-positive bacterial endocarditis and compare them to the reported cases of ANCA-associated idiopathic vasculitis with endocardial compromise.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2006

The relation between mitral annular calcification and mortality in patients undergoing diagnostic coronary angiography.

To determine whether the observed association between mitral annular calcification (MAC) and mortality is independent of the severity of coronary artery disease (CAD), we analyzed data from 134 male veterans (age 63 +/- 10 years) followed for 5 years who had undergone diagnostic coronary angiography and transthoracic echocardiography within 6 months of each other. Echocardiograms were retrospectively reviewed for the presence of MAC. The relation of MAC to all-cause mortality was analyzed using logistic regression, and odds ratios (OR) were calculated. MAC was present in 49 (37%) subjects. Over the 5-year follow-up period, 38 (28%) patients expired. Five-year survival was 80% for subjects without MAC and 56% for subjects with MAC (P = 0.003). MAC (OR = 3.16, 95% confidence interval [CI]= 1.43-6.96, P = 0.003), ejection fraction (OR = 0.76, 95% CI = 0.59-0.97, P = 0.02), and left main CAD (OR = 2.70, 95% CI = 1.11-6.57, P = 0.02) were significantly associated with mortality in univariate analysis. After adjusting for left ventricular ejection fraction, number of obstructed coronary arteries and the presence of left main coronary artery stenosis, MAC significantly predicted death (OR = 2.48, 95% CI = 1.09-5.68, P = 0.03). Similarly, after adjusting for predictors of MAC, including ejection fraction, age, diabetes, peripheral vascular disease, and heart failure, MAC remained a significant predictor of death (OR = 2.38, 95% CI = 1.02-5.58, P = 0.04). MAC also predicted death independent of smoking status, hypertension, serum creatinine, low density lipoprotein cholesterol, high density lipoprotein cholesterol, and C-reactive protein levels (OR = 3.98, 95% CI = 1.68-9.40, P = 0.001). MAC detected by two-dimensional echocardiography independently predicts mortality and may provide an easy-to-perform and inexpensive way to improve risk stratification.

Age Factors↗
PubMed2005

Ability of serum to decrease cellular acylCoA:cholesterol acyl transferase activity predicts cardiovascular outcomes.

BACKGROUND: We evaluated whether cholesterol efflux activity of serum is associated with the presence of angiographic coronary artery disease (CAD) and the risk of major adverse cardiovascular events (MACE) and death. METHODS AND RESULTS: We studied 168 men undergoing coronary angiography. Cholesterol efflux activity was measured in vitro by incubation of patient serum with human skin fibroblasts and defined as the ability of serum to decrease the pool of cholesterol available for esterification by the acylCoA:cholesterol acyl transferase (ACAT) reaction. We evaluated whether this activity was associated with the presence of CAD and the risk of MACE and death during a 4.5-year follow-up. Serum-induced changes in ACAT activity did not correlate with HDL levels or the presence of CAD. Patients in the highest tertile of change in ACAT activity had a significantly higher risk for MACE (HR, 2.15; 95% CI, 1.36 to 3.39; P=0.001) and death (HR, 2.23; 95% CI, 1.17 to 4.26; P=0.01). These correlations were independent of other risk markers including LDL, HDL, and C-reactive protein levels. CONCLUSIONS: Serum-induced depletion of cellular cholesterol available for esterification by ACAT was a strong, independent predictor of MACE and death. We speculate that the ability of serum to decrease ACAT activity depends on ATP binding cassette transporter A1 (ABCA1)-mediated efflux. Furthermore, serum samples that induce larger changes in ACAT activity contain increased levels of HDL particles that preferentially interact with ABCA1 and that these particles accumulate in the serum of patients because of low activity of ABCA1 in vivo preventing or limiting the extent of apoA-I lipidation.

Aged↗
PubMed2005

Relation between ascending aortic pressures and outcomes in patients with angiographically demonstrated coronary artery disease.

We prospectively followed 324 men, who underwent coronary angiography, for 1,161 +/- 418 days. We analyzed the association between ascending aortic pressures measured during cardiac catheterization and the risk of all-cause mortality and a combined end point of major adverse cardiovascular events (MACEs), including unstable angina pectoris, myocardial infarction, coronary revascularization, stroke, or death. Pulse pressure significantly predicted MACEs (hazard ratio [HR] per 10 mm Hg increase 1.09, 95% confidence interval [CI] 1.002 to 1.17, p = 0.04). Diastolic blood pressure (BP) inversely correlated with the risk of MACEs (HR per 10 mm Hg increase 0.85, 95% CI 0.74 to 0.98, p = 0.02). These correlations remained significant after adjusting for other predictors and potential confounders. The association between lower diastolic BP with the risk of MACEs was more pronounced in patients with triple-vessel coronary artery disease (p for interaction = 0.03). Peripheral diastolic BP (but not pulse pressure) correlated inversely with the risk of MACEs (HR 0.87 per 10 mm Hg increase, 95% CI 0.75 to 0.998, p = 0.047). Aortic pulse pressure significantly predicted death (HR per 10 mm Hg increase 1.18, 95% CI 1.05 to 1.33, p = 0.004), and aortic diastolic BP correlated inversely with the risk of death (HR 0.76, 95% CI 0.62 to 0.94, p = 0.01).

Aorta↗
PubMed2005

Aortic pressure augmentation predicts adverse cardiovascular events in patients with established coronary artery disease.

Pulse pressure (PP), a marker of arterial stiffness, predicts cardiovascular risk. We aimed to determine whether augmentation pressure (AP) derived from the aortic pressure waveform predicts major adverse cardiovascular events (MACE) and death independently of PP in patients with established coronary artery disease (CAD). We prospectively followed-up 297 males undergoing coronary angiography for 1186+/-424 days. Ascending aortic pressure tracings obtained during catheterization were used to calculate AP (difference between the second and the first systolic peak). Augmentation index (AIx) was defined as AP as a percentage of PP. We evaluated whether AP and AIx can predict the risk of MACE (unstable angina, acute myocardial infarction, coronary revascularization, stroke, or death) and death using Cox regression. All models evaluating AP included PP to assess whether AP adds to the information already provided by PP. Both AP and AIx significantly predicted MACE. The hazard ratio (HR) per 10 mm Hg increase in AP was 1.20 (95% confidence interval [CI], 1.08 to 1.34; P<0.001); the HR for each 10% increase in AIx was 1.28 (95% CI, 1.11 to 1.48; P=0.004). After adjusting for other univariate predictors of MACE, age, and other potential confounders, AP remained a significant predictor of MACE (HR per 10 mm Hg increase=1.19; 95% CI, 1.06 to 1.34; P=0.002), as did AIx (adjusted HR, 1.28; 95% CI, 1.09 to 1.50; P=0.003). AP was a significant predictor of death (HR per 10 mm Hg increase=1.18; 95% CI, 1.02 to 1.39; P=0.03). Higher AIx was associated with a trend toward increased mortality (HR=1.22; 95% CI, 0.98 to 1.52; P=0.056). Aortic AP predicts adverse outcomes in patients with CAD independently of PP and other risk markers.

Aged↗
PubMed2005

Usefulness of C-reactive protein as an independent predictor of death in patients with ischemic cardiomyopathy.

The usefulness of serum C-reactive protein, an inflammatory marker, to predict mortality risk in patients who have ischemic cardiomyopathy was investigated. C-reactive protein was measured in 123 men who underwent cardiac catheterization and were noted to have left ventricular ejection fraction <or=45% and significant angiographic coronary artery disease. They were prospectively followed for 3 years. Higher levels of C-reactive protein were associated with increased mortality rate. This correlation was independent of other prognostic factors, such as age, ejection fraction, symptoms of severe congestive heart failure, use of angiotensin-converting enzyme inhibitors, and use of beta blockers.

Biomarkers↗
PubMed2004

Severe volume depletion leading to mitral insufficiency.

We report a patient with profound hypovolemia who developed dynamic left ventricular outflow tract obstruction and severe mitral regurgitation. Both the outflow tract obstruction and mitral regurgitation resolved with volume replacement. Unlike previous reports of dynamic left ventricular outflow obstruction and mitral regurgitation, the degree of mitral regurgitation was severe. Possible mechanisms are discussed.

Acute Disease↗
PubMed2002

Effects of carvedilol on heart rate dynamics in patients with congestive heart failure.

BACKGROUND: Patients with congestive heart failure (CHF) have alterations in the traditional and nonlinear indices of heart rate (HR) dynamics, which have been associated with an increased risk of mortality. This study was designed to test the effects of carvedilol, a nonselective beta-blocker with alpha-1 blocking properties, on HR dynamics in patients with CHF. METHODS: We studied 15 patients with CHF secondary to ischemic or idiopathic cardiomyopathy who met the following inclusion criteria: NYHA functional class II-III, optimal conventional medical therapy, normal sinus rhythm, left ventricular ejection fraction (LVEF) of < 40%, and resting systolic blood pressure greater than 100 mmHg. The 6-minute corridor walk test, estimation of LVEF, and 24-hour Holter recording were performed at baseline and after 12 weeks of therapy with carvedilol. Traditional time and frequency domain measures and short-term fractal scaling exponent of HR dynamics were analyzed. RESULTS: After 12 weeks of therapy with carvedilol, the mean LVEF improved significantly (from 0.27 +/- 0.08 to 0.38 +/- 0.08, P < 0.001). The average HR decreased significantly (from 86 +/- 11 to 70 +/- 8 beats/min, P < 0.001). The mean distance traveled in the 6-minute walk test increased significantly (from 177 +/- 44 to 273 +/- 55 m, P < 0.01). The frequency-domain indices (HF and LF), the time domain indices (rMSSD and PNN5 ), and the short-term fractal scaling exponent increased significantly. The scaling exponent increased particularly among the patients with the lowest initial values (< 1.0), and the change in the fractal scaling exponent correlated with the change in ejection fraction (r = 0.63, P < 0.01). CONCLUSION: Carvedilol improves time and frequency domain indices of HR variability and corrects the altered scaling properties of HR dynamics in patients with CHF. It also improves LVEF and functional capacity. These specific changes in HR behavior caused by carvedilol treatment may reflect the normalization of impaired cardiovascular neural regulation of patients with CHF.

Adrenergic beta-Antagonists↗