Hagar Paz

Aldosterone Synthase Gene Polymorphism as a Determinant of Atrial Fibrillation in Patients With Heart Failure

We analyzed the possible association between aldosterone synthase (CYP11B2) T-344C polymorphism, which is associated with increased aldosterone activity, and the prevalence of atrial fibrillation (AF) in 196 consecutive patients who had symptomatic systolic heart failure (HF; left ventricular ejection fraction <40%) for > or =3 months before recruitment. Genomic DNA was extracted from peripheral blood leukocytes using a standard protocol. Subjects were genotyped for the CYP11B2 polymorphism using the polymerase chain reaction/restriction fragment length polymorphism approach. AF was present in 63 patients (33%) with HF. We found the -344 CC genotype to be a strong independent marker for AF. Almost 1/2 (45%) of patients with this genotype had AF compared with 1/4 (27%) with -344 TT and TC genotypes (p = 0.01). A multivariate stepwise logistic regression model that included age, gender, New York Heart Association class, CYP11B2 -344CC genotype, and echocardiographic measurements of left ventricular ejection fraction, left atrial dimension, left ventricular end-diastolic diameter, and mitral regurgitation severity showed that the CYP11B2 CC genotype (adjusted for age and left atrial size) was an independent predictor of AF (adjusted odds ratio 2.35, 95% confidence interval 1.57 to 3.51, p = 0.03). In conclusion, CYP11B2 T-344C promoter polymorphism predisposes to clinical AF in patients with HF.

Serum Oxidative Stress Level Correlates with Clinical Parameters in Chronic Systolic Heart Failure Patients

Serum oxidative stress (OS) level has an important role in the inflammatory process of heart failure.

Implications of Cheyne-Stokes Breathing in Advanced Systolic Heart Failure

Cheyne‐Stokes breathing (CSB) has been associated with heart failure (HF) patients for many years; however, its true prevalence and its prognostic implications are still obscure.

Mortality rates and modes of death in heart failure patients with reduced versus preserved systolic function

BACKGROUND There are conflicting reports regarding the characteristics and mortality rates of heart failure patients with preserved (HFPSF) vs. reduced systolic left ventricular function (SHF). METHODS We evaluated the clinical profiles, mortality rates and modes of death in 481 consecutive symptomatic heart failure patients. In 317(66%) patients LVEF was <40% (SHF), and in 164(34%) LVEF≥40% (HFPSF). RESULTS Compared to the HFPSF group, SHF patients were predominantly younger males with ischemic etiology and less cardiovascular comorbidities such as obesity, hypertension, diabetes mellitus and atrial fibrillation. Over a mean follow-up period of 2 years, 148(31%) patients died. Overall mortality was similar between the two groups: 53(32%) HFPSF patients and 95(30%) SHF patients died (p=0.6), even after adjusting for baseline variables, including age, gender and comorbidities (hazard ratio 1.09; 95% confidence interval 0.74-1.61; p=0.67). In contrast to the similar mortality rates, the modes of death were different. SHF patients had higher death rates due to pump failure compared to the HFPSF group {32/95(34%) vs. 9/53(17%) patients, p=0.03}. A trend towards higher rate of non-cardiac death was observed in HFPSF group {33/53(62%) patients vs. 45/95(47%) patients, respectively, p=0.08}. The prevalence of arrhythmic death was similar in both groups {17/95(18%) vs. 10/53(19%) patients, p=0.9}. CONCLUSIONS Although the characteristics of HFPSF and SHF patients are distinctively different, the mortality rates are similar. The mode of death is different among the two groups of patients, as pump failure death is significantly higher in SHF patients, while non-cardiac mortality is more prevalent in HFPSF patients.

Risk Score Model for Predicting Mortality in Advanced Heart Failure Patients Followed in a Heart Failure Clinic

The prevalence of heart failure (HF) in the population is increasing, concomitant with high incidence of rehospitalizations and mortality. The aim of this study was to characterize a prognostic risk score model for patients with chronic HF. A total of 500 patients followed at the HF clinic were evaluated by clinical, functional, laboratory, imaging, and therapeutic variables that were correlated to mortality during a follow-up period of 25 months. Risk stratification was carried out by applying a risk score model based on multivariate analysis. Predictors correlated with mortality during follow-up were systolic blood pressure <110 mm Hg, male sex, age older than 70 years, 6-minute walk distance <300 m, lack of β-blocker therapy, hyperuricemia (>7.5 mg/dL), hyponatremia, and prolonged QTc interval (>450 ms). Based on these variables, a risk score model (score 0-55) was established and included low risk, score <21 (9% mortality during 2-year follow-up); moderate risk, 21 to 29 (22%); high risk, 30 to 35 (35%), and very high risk: ≥36 points (62% 2-year mortality). The risk model had good discrimination ability (concordance index 0.75), which was better than the performance of the Seattle Heart Failure Model on our cohort (0.69). Simple noninvasive characteristics examined during the initial admission to the HF clinic can serve as prognostic markers for mortality and may help in the process of therapeutic decision-making in patients with HF.

Relation between AT1R gene polymorphism and long-term outcome in patients with heart failure.

Objectives: Angiotensin II plays a key role in the pathophysiology of heart failure (HF). This study examined the angiotensin II type 1 receptor (AT1R) polymorphism in patients with systolic HF and its relation to clinical manifestations and patient outcome. Methods: We genotyped 134 patients with HF and reduced systolic function for the AT1R A1166C genotype using polymerase chain reaction and restriction fragment length polymorphism. We analyzed the relationship between the AT1R A1166C polymorphism and clinical, electrocardiographic, echocardiographic and laboratory parameters in patients with ischemic and non-ischemic etiology and examined the relation between the AT1R genotype and long-term (30 months) patient survival. Results: In HF patients, frequency of the AT1R 1166C allele and specifically the CC genotype was similar to the general population, but associated with an ischemic and not a non-ischemic etiology (p = 0.02). The CC genotype was associated with more advanced disease and more severe abnormalities of renal function (p = 0.008). Survival analysis showed that AT1R CC homozygous patients had significantly higher mortality (p = 0.008; adjusted odds ratio for mortality 6.35, 95% confidence interval 1.49–11.21, p = 0.01). Conclusion: The CC AT1R genotype was associated with poor prognostic markers and increased mortality. The findings support the principle of genome-based therapies in the future treatment of HF patients.