Heart rate variability in patients suffering from structural heart disease and decreased AV-nodal conduction capacity. Insights into the formation of heart rate variability

METHODS: Time and frequency domain analysis were conducted during a period of 600 s each. We performed a special protocol consisting of five different "pacing" periods: 1) recording of normal sinus rhythm (SR1); 2) atrial pacing with a rate 15% higher than the intrinsic heart rate; 3) ventricular pacing triggered by atrial activation (VAT, with a short AV-delay of 80 ms); 4) AV-sequential pacing with an atrial rate 15% higher than the intrinsic heart rate and a very short AV delay of 80 ms (DDD); 5) normal sinus rhythm (SR2). Only patients with normal AV-nodal conduction or with AV-block I degrees were included. The influence of a structural heart disease as well as a non-sustained VT on Holter ECG and a depressed EF on HRV parameters were analyzed using a multivariate analysis. All patients were lying in a supine position. Blood pressure was measured continuously and the frequency of breathing was controlled. RESULTS: No differences in HRV between the two sinus rhythm periods SR1 versus SR2 could be detected. Neither SR1 vs VAT showed a significant difference for SDNN and r-MSSD. In contrast, HRV during SR1 compared to AAI, and HRV during VAT compared to AAI were significantly different (p < 0.001). When comparing HRV during DDD, which should be zero, and AAI, we found a significantly lower SDNN and r-MSSD (1.2 ms vs 4 ms, p < 0.04). The presence of structural heart disease, a non-sustained ventricular tachycardia, a depressed ejection fraction of less than 0.50 did not reveal a significant influence on the HRV parameters (multivariate analysis). The mean Wenckebach in patients with structural heart disease tended to be greater (437 ms vs 350 ms, p = 0.05); an increase in the Wenckebach was not correlated to a change in HRV parameters (p = ns). CONCLUSION: Heart rate variability derived from consecutive RR-intervals is predominantly caused by periodicity in sinus-node impulse formation. A conduction variability of the AV-node exists, but is very low. The presence of a structural heart disease, a non-sustained ventricular tachycardia on Holter ECG, as well as a depressed ejection fraction of less than 0.50 showed no significant influence on the HRV parameters. Therefore, one can apply the calculation of heart rate variability for risk stratification in patients suffering from structural heart disease and moderate AV-nodal conduction disturbances.Attenuation of the oscillation of the heart rate, i. e. heart rate variability (HRV), is associated with an increased risk for mortality in patients with structural heart disease. Many of these patients also suffer from conduction disturbances, e. g. AV-nodal conduction delays. Whether the calculation of HRV in those patients is recommendable has not been investigated yet. Therefore, we conducted a study consisting of 20 consecutive patients in order to determine the formation of HRV, the influence of structural heart disease, the presence of a nonsustained ventricular tachycardia (VT), and a reduced ejection fraction (EF) on the HRV parameters during an elective electrophysiologic study.     

Prevalence of hepatitis B infection in the southeastern region of Turkey: comparison of risk factors for HBV infection in rural and urban areas

Although hepatitis B has been well studied, there are still aspects of its epidemiology that remain to be clarified. There are many regions with high seroprevalence, particularly in the developing regions of the world, and these regions are known to have different epidemiologic patterns. Nonetheless, there are currently no data on the differences in hepatitis B seroprevalence between urban and rural areas of Turkey. In the present study, therefore, we used 30-cluster sampling to determine and compare the prevalence of hepatitis B in the urban and rural areas of the least developed region of Turkey, the southeastern region. From 2,888 adults living in the region, blood samples were obtained from house visits, and screened for HBsAg, anti-HBs, and anti-HBcIgG. Factors associated with hepatitis B seroprevalence, particularly living in rural areas, were analyzed with multivariate methods. The seroprevalence of HBsAg was 8.2% in the rural and 6.2% in the urban areas. There was a statistically significant difference between urban and rural regions in terms of HBsAg positivity (crude OR: 0.74; 95% CI: 0.55 - 0.98). Exposure to hepatitis B virus (HBV) increased with age both in urban and rural areas. Lower education level was also an important risk factor for hepatitis B seropositivity in urban areas (adjusted OR: 1.66; 95% CI: 1.26 - 2.19) but not in rural ones (adjusted OR: 0.77; 95% CI: 0.36 - 1.69). Familial jaundice history was a statistically significant risk factor for HBsAg positivity in rural areas (adjusted OR: 2.15; 95% CI: 1.30 - 3.56) but not in urban ones (adjusted OR: 1.48; 95% CI: 0.96 - 2.27). This study shows that the prevalence of HBV infection in the southeastern region of Turkey is intermediate among the levels reported for the European region of the World Health Organization.     

Increased expression of the G gamma and A gamma globin genes associated with a mutation in the A gamma enhancer

We have previously described a unique type of delta beta-thalassemia in a Chinese family characterized by increased expression of the G gamma and A gamma fetal globin genes in the absence of a large deletion in the beta-globlin gene cluster. Our earlier study of the beta-globin gene on this delta beta-thalassemia chromosome showed a promoter mutation in the TATA box. In this report, we describe the results of our study of the fetal globin domain of this delta beta-thalassemia chromosome. We have cloned a 13-kb DNA fragment that includes the G gamma and the A gamma genes and the 3' A gamma enhancer element of this delta beta-thalassemia chromosome. DNA sequence analysis of the G gamma and A gamma-globin genes including their promoters did not show any mutations, but analysis of the putative enhancer element downstream from the A gamma-globin gene showed a C to T substitution 2,401 nucleotides downstream from the A gamma cap site. We performed DNA linkage analysis to determine if this mutation is unique to this chromosome or represents a common polymorphism. Our linkage analysis showed that this mutation is not a common polymorphism and that it is also not an intrinsic part of the haplotype of the chromosome on which it was found. We also studied the interaction of nuclear proteins from erythroid and nonerythroid cells with the DNA sequences surrounding this mutation. We have shown by in vitro DNase I footprinting that this mutation falls within a region that is occupied by a novel DNA-binding protein that binds to this site in nuclear extracts from erythroid, but not nonerythroid cells. The binding of this nuclear protein to DNA appears to be dependent on GATA-1 binding to an adjacent GATA-1 site. We have also developed a new functional assay to compare the activity of the normal and mutant A gamma enhancer elements in erythroid cells. Analysis of the activity of the mutant enhancer shows that the mutation completely eliminates all enhancer activity in this assay. These findings suggest that this mutation of the A gamma enhancer on a chromosome that carries a partially inactivated beta-globin gene may be responsible for the increased expression of both gamma-globin genes seen in this condition.     

Effectiveness of a multidimensional approach for prevention of ventilator-associated pneumonia in 11 adult intensive care units from 10 cities of Turkey: findings of the International Nosocomial Infection Control Consortium (INICC)

Purpose

To evaluate the impact of the International Nosocomial Infection Control Consortium (INICC) multidimensional approach on the reduction of ventilator-associated pneumonia (VAP) in adult patients hospitalized in 11 intensive care units (ICUs), from 10 hospitals, members of the INICC, in 10 cities of Turkey.

Methods

A prospective active before-after surveillance study was conducted to determine the effect of the INICC multidimensional approach in the VAP rate. The study was divided into two phases. In phase 1, active prospective surveillance of VAP was conducted using the definitions of the Centers for Disease Control and Prevention National Health Safety Network, and the INICC methods. In phase 2, we implemented the multidimensional approach for VAP. The INICC multidimensional approach included the following measures: (1) bundle of infection control interventions, (2) education, (3) outcome surveillance, (4) process surveillance, (5) feedback of VAP rates, and (6) performance feedback of infection control practices. We compared the rates of VAP obtained in each phase. A time series analysis was performed to assess the impact of our approach.

Results

In phase 1, we recorded 2,376 mechanical ventilator (MV)-days, and in phase 2, after implementing the multidimensional approach, we recorded 28,181 MV-days. The rate of VAP was 31.14 per 1,000 MV-days during phase 1, and 16.82 per 1,000 MV-days during phase 2, amounting to a 46 % VAP rate reduction (RR, 0.54; 95 % CI, 0.42–0.7; P value, 0.0001.)

Conclusions

The INICC multidimensional approach was associated with a significant reduction in the VAP rate in these adult ICUs of Turkey.     

Accuracy of serum c-reactive protein measurements in diagnosis of acute appendicitis compared with surgeon's clinical impression

Diagnosis of acute appendicitis is established generally by the surgeon's clinical impression. Today, negative laparotomy rate because of clinical diagnosis is still 15 to 25 percent. PURPOSE: This study was designed to determine the accuracy of C-reactive protein (CRP) measurements in the diagnosis of acute appendicitis and to compare it with the surgeon's clinical diagnosis. METHODS: One hundred eight consecutive patients were studied prospectively. Depending on results of the examination by a surgeon, patients underwent surgery for acute appendicitis. Serum CRP measurements were performed before the operations but were not taken into account for the decision of laparotomy to compare it with the surgeon's clinical diagnosis. RESULTS: Histopathologic findings confirmed acute appendicitis in 90 patients. Normal appendixes were removed in the remaining 18 patients. Mean serum CRP value was 5 (range, 0–12.6) mg/l in patients with normal appendix, 33.8 (range, 5–85.1) mg/l in patients with nonperforated appendicitis, and 128.5 (range, 79.2–230) mg/l in patients with perforated appendixes. These differences were highly significant (P <10^–6). Serum CRP levels were normal in three patients with acute appendicitis. Thus, the false-negative rate of CRP was 3 percent. Of 18 patients with normal appendectomy serum CRP levels were slightly elevated in two patients. We determined, therefore, a false-positive rate of CRP as 11 percent. CRP levels were false-negative in three patients and false-positive in two patients. Thus, CRP levels were true (positive or negative) in the remaining 103 patients. On the other hand, the diagnosis depending on surgeon's clinical impression was true in 90 patients and false in 18 patients. This difference was statistically significant (P = 0.0035). In the present study the sensitivity, specificity, and accuracy of serum CRP measurements were calculated as 93.5, 80, and 91 percent, respectively. CONCLUSION: We found that elevated serum CRP levels support surgeon's clinical diagnosis. We recommend CRP measurement as a routine laboratory test in patients with suspected diagnosis of acute appendicitis.     

Ictal singing due to left mesial temporal sclerosis.

Simple ictal or interictal automatisms are commonly seen in epilepsy, whereas complex automatisms are rare. Simple ictal vocalizations or appendicular automatisms have been reported to be due to mesial temporal lobe epilepsy. However, seizure-associated singing and dancing is very rare. We report a seventeen-year-old patient with ictal singing and rhythmic swinging of the arms as a dancing gesture. The video-EEG recording showed ictal left temporal lateralization and neuropathology confirmed left mesial temporal sclerosis.