Israel Medical Association Journal

Background: Guidelines are frequently under-implemented in older patients with heart failure. Octogenerians are often excluded from clinical trials.

Objectives: To characterize the clinical profile of the oldest-old (age ≥ 80 years) heart failure patients hospitalized in a subacute geriatric hospital and to evaluate their management and 1 year outcome.

Methods: Patient characteristics and in-hospital course were retrospectively collected. Diagnosis of heart failure was based mainly on clinical evaluation in addition to chest X-ray results and echocardiographic findings when available.

Results: The study population comprised 96 consecutive unselected heart failure patients hospitalized from January to June 2003. The patients were predominantly women (67%), aged 85 ± 5 years, fully dependent or frail with a high rate of comorbidities. Adherence to guidelines and recommended heart failure medications was poor. Their 1 year mortality was 57%. According to logistic regression analysis, predictors of 1 year mortality were lower body mass index (odds ratio 0.86, 95% confidence interval 0.78–0.96) and high urea levels (OR[1] 1.04, 95% CI[2] 1.02–1.06).

Conclusions: Our study confirms that the management of oldest-old heart failure patients hospitalized in a subacute geriatric hospital was suboptimal and their mortality was exceptionally high.

Background: Kidney disease and cardiovascular disease seem to be lethally synergistic and both are approaching the epidemic level. A reduced glomerular filtration rate is associated with increased mortality risk in patients with heart failure. Many patients with congestive heart failure are anemic. Anemia is very often associated with chronic kidney disease.

Objectives: To assess – in relation to New York Heart Association class – the prevalence of anemia and chronic kidney disease in patients with normal serum creatinine in a cohort of 526 consecutive patients with coronary artery disease undergoing percutaneous coronary interventions.

Methods: GFR[1] was estimated using the simplified MDRD formula, the Cockcroft-Gault formula, the Jeliffe and the novel CKD-EPI formula.

Results: According to the WHO definition the prevalence of anemia in our study was 21%. We observed a progressive decline in GFR and hemoglobin concentration together with a rise in NYHA[2] class. Significant correlations were observed between eGFR[3] and systolic blood pressure, diastolic blood pressure, age, NYHA class, complications of PCI[4], including bleeding, and major adverse cardiac events.

Conclusions: The prevalence of anemia and chronic kidney disease is high in patients undergoing PCI despite normal serum creatinine, particularly in higher NYHA class. Lower eGFR and hemoglobin are associated with more complications, including bleeding after PCI and higher prevalence of major adverse cardiac events. In patients with risk factors for cardiovascular disease, GFR should be estimated since renal dysfunction and subsequent anemia are important risk factors for cardiovascular morbidity and mortality.

Background: Clinical and epidemiologic features of coronary heart disease may not be explained solely by established risk factors. The role of infectious pathogens in the development and rupture of atherosclerotic plaques remains elusive but an association between Chlamydia pneumoniae, Mycoplasma pneumoniae and CHD[1] has been previously reported

Objectives: To determine whether there is an association between mycoplasmal infections and CHD.

Methods: We conducted a prospective cohort analysis of 150 consecutive hospitalized patients with CHD (85 with acute coronary syndrome and 65 admitted for unrelated reasons) and 98 healthy blood donors. Antibody titers for Mycoplasma pneumoniae, M. fermentans, M. hominis and Ureaplasma urealyticum were measured with the agglutination test or specific enzyme-linked immunosorbent assay in all three groups of patients.

Results: Analysis of the antibody titers did not reveal any significant difference in the presence of mycoplasmal antibodies between the patients with ACS[2], patients with known stable CHD hospitalized for non-CHD reasons, and healthy blood donors.

Conclusions: Determination of specific antibodies did not reveal a significant association among different types of mycoplasmal infection and CHD.





[1] CHD = coronary heart disease

[2] ACS = acute coronary syndrome

Background: The American Academy of Pediatrics recently published recommendations for the red reflex assessment in the newborn period to detect and treat ocular disorders as early as possible, and to prevent lifelong visual impairment and even save lives. The test is technically simple to perform, non-invasive, requires minimal equipment and can detect a variety of ocular pathologies including cataracts and retinal abnormalities. No specific national guidelines exist on this issue.

Objectives: To document the implementation of red reflex examination in routine neonatal care and present the findings.

Methods: Our clinical experience following implementation of the red reflex test into the newborn physical examination in a single center was reviewed. In addition, an electronic mail questionnaire was sent to all neonatology departments in Israel regarding the performance of the red reflex test.

Results: During 2007–2008, five infants were identified with congenital cataracts at days 2–6 of life prior to discharge from hospital. Surgery was performed in one infant at age 2 months and all infants underwent a thorough follow-up. The incidence of congenital cataract in our center was 1:2300. Less than half the neonatology departments have endorsed the AAP[1] recommendation and perform the red reflex test routinely.

Conclusions: Abnormal red reflex test after delivery enables a rapid ophthalmologic diagnosis, intervention and close follow-up. We recommend that red reflex screening be performed as part of the newborn physical examination if abnormal, an urgent ophthalmologic referral should be made. 

[1] AAP = American Academy of Pediatrics

Background: Obesity has become a major public health problem worldwide.

Objectives: To examine the effect of orlistat in promoting weight loss and its specific effect on the visceral adipose tissue and subcutaneous adipose tissue as evaluated by computed tomography.

Methods: A prospective case series study of 10 obese subjects was conducted. The 6 women and 4 men, age 50–67 years (mean 59 ± 8 years), had a mean body mass index of 34.1 ± 3.2 kg/m². All subjects were prescribed a mildly hypocaloric diet (600 kcal/day deficit). In addition, all subjects were treated with orlistat 120 mg 3 times a day for 20.1 ± 7 weeks.

Results: The subjects had lost approximately 8.2 kg each, or 8.4% of their initial body weight. Mean body weight decreased from 98 ± 13 to 89.8 ± 13.6 kg at the last follow-up visit (P = 0.0001) mean BMI[1] decreased from 34.1 ± 3.2 to 30.3 ± 3.9 kg/m² (P = 0.0001), and mean waist circumference from 113.8 ± 11.4 to 107.6 ± 10 cm (P = 0.0006). Mean total abdominal adipose tissue volume, evaluated by computed tomography, decreased from 426 ± 104.3 to 369.8 ± 99.6 mm³ (P = 0.0001). Mean abdominal SAT[2] volume decreased from 251.1 ± 78.8 to 224 ± 81.1 mm³ (P = 0.006), and mean abdominal VAT[3] volume decreased from 176 ± 76.7 to 141.6 ± 67 mm³ (P = 0.0001). Thus, the total abdominal adipose tissue volume for the whole group decreased by 15.4%, and most of this decrease was attributable to the reduction in VAT (24.8%) as opposed to SAT (only 12% reduction) (P = 0.03). The weight reduction that occurred during the study was accompanied by a statistically significant reduction in levels of total cholesterol, low density lipoprotein-cholesterol, triglycerides, and fasting blood glucose.

Conclusions: Our results demonstrate the effect of orlistat in reducing human visceral adipose tissue as evaluated by CT. The benefit of the treatment is further supported by the statistically significant reduction in cardiovascular risk factors.

 
[1] BMI = body mass index

[2] SAT = subcutaneous adipose tissue

[3] VAT = visceral adipose tissue

 

Background: Pathologic breast conditions are rare in childhood and adolescence. The spectrum of breast disease in the pediatric age group is different from that in adults, and most lesions are benign

Objectives: To describe the causes and characteristics of breast asymmetry in adolescents with normal endocrine profiles and sexual development.

Methods: The files of patients with a diagnosis of breast asymmetry referred to a tertiary pediatric center from 1990 to 2007 were reviewed for history and findings on physical examination with or without imaging, treatment and outcome.

Results: Eleven patients aged 12.5 to 18 years were identified. The cause of the breast asymmetry was traced to unpreventable medical factors in eight patients (physiologic, Poland anomaly, scleroderma), preventable/iatrogenic factors in two patients (chest tissue biopsy, thoracic drain), and possible combined medical-iatrogenic factors in one patient (scoliosis treated by a body brace). All patients were referred for breast reconstruction after full breast development.

Conclusions: Severe breast asymmetry in adolescence may be due to congenital factors, diseases involving the breast tissue, or to the effects of medical treatment, and may have severe adverse psychological and social implications. To prevent iatrogenic breast asymmetry, physicians should be made aware of the sensitivity of the breast tissue and should avoid unnecessary tests/procedures that involve the chest wall. In most cases a precise medical history and physical examination can differentiate between physiologic and non-physiologic causes.

Background: Interleukin-10 is an anti-inflammatory cytokine and consequently is considered by many to have a protective role in heart failure, as opposed to the notorious tumor necrosis factor-alpha.

Objectives: To test the hypothesis of the possible beneficial impact of IL-10[1] on mortality in systolic heart failure patients in relation to their circulating TNFα[2] levels.

Methods: We measured circulating levels of IL-10 and TNFα in 67 ambulatory systolic heart failure patients (age 65 ± 13 years).

Results: Mortality was or tended to be higher in patients with higher levels (above median level) of circulating TNFα (9/23, 39% vs. 6/44, 14%; P = 0.02) or IL-10 (10/34, 30% vs. 5/33, 15%; P = 0.10). However, mortality was highest in the subset of patients with elevation of both markers above median (7/16, 44% vs. 8/51, 16%; P = 0.019). Elevation of both markers was associated with more than a threefold hazard ratio for mortality (HR[3] 3.67, 95% confidence interval 1.14–11.78).

Conclusions: Elevated circulating IL-10 levels in systolic heart failure patients do not have a protective counterbalance effect on mortality. Moreover, patients with elevated IL-10 and TNFα had significantly higher mortality, suggesting that the possible interaction in the complex inflammatory and anti-inflammatory network may need further study.