Body Mass Index below Obesity Threshold Implies Similar Cardiovascular Risk among Various Polycystic Ovary Syndrome Phenotypes

Objective

The aim of this study was to determine the cardiometabolic risk factors in different polycystic ovary syndrome (PCOS) phenotypes.

Subjects and Methods

This cross-sectional study was performed between 2010 and 2011. Eighty-nine patients with PCOS and 25 age- and weight-matched healthy controls were included in the study. Patients were grouped using the Rotterdam 2003 criteria as: group 1, oligomenorrhea and/or anovulation (ANOV) and hyperandrogenemia (HA) and/or hyperandrogenism (n = 23); group 2, ANOV and polycystic ovaries (PCO; n = 22); group 3, HA and PCO (n = 22); group 4, ANOV, HA and PCO (n = 22); group 5, controls (n = 25). Laboratory blood tests for diagnosis and cardiometabolic risk assessments were performed. Insulin resistance (IR) was calculated in all patients with the homeostasis model assessment of IR (HOMA-IR) formula. An euglycemic hyperinsulinemic clamp test was performed on 5 randomly selected cases in each subgroup, making 25 cases in total, and indicated as the ‘M'' value (mg/kg/min), which is the total body glucose disposal rate.

Results

The mean BMl values of the groups were: group 1, 26.1 ± 5.3; group 2, 27.9 ± 5.2; group 3, 24.3 ± 4.2; group 4, 27.9 ± 7.5; group 5, 24.7 ± 5.2 (p > 0.05). There were no differences in the lipid profile, plasma glucose, HOMA-IR, insulin and M values between the groups (p > 0.05). Phenotypes with oligomenorrhea/anovulation (groups 1, 2 and 4) were more obese than group 3 (p = 0.039).

Conclusions

The cardiometabolic risk profile was similar among the PCOS subgroups. This finding could be attributed to the mean BMl values, which, being below 30, were not within the obesity range. Obesity appeared to be an important determinant of high cardiovascular risk in PCOS.Key Words: Polycystic ovary syndrome, Cardiovascular system, Obesity     

Analysis of the outcomes of cardiopulmonary resuscitation in an emergency department

OBJECTIVE: The aim of this study is to analyse the factors affecting emergency department (ED) cardiopulmonary resuscitation (CPR) outcome. METHODS: A standard CPR protocol was performed in all patients and certain pre and postresuscitation parameters including age, sex, initial arrest rhythm, primary underlying disease, initiation time of advanced cardiac life support, duration of return of spontaneous circulation were recorded. Patients were followed up to determine rates of successful CPR, survival and one-year survival. RESULTS: From December 1999 to May 2001, 80 consecutive adult patients in whom a standard CPR was performed in the ED were prospectively included in the study. The overall rate for successful CPR, survival and one-year survival were found to be 58.8% (47/80), 15% (12/80) and 10% (8/80), respectively. Survival and one-year survival rates were better in patients with an initial arrest rhythm of ventricular fibrillation or pulseless ventricular tachycardia (VF/pVT) than both pulseless electrical activity (pEA) and asystole; survival and one-year survival rates were better in patients with a primary underlying disease of cardiac origin than non-cardiac origin. Acute myocardial infarction had the best prognosis among conditions causing arrest. Presence of sudden death was found to have a better survival and one-year survival rate. CONCLUSION: Initial cardiac rhythm of VF/pVT, cardiac origin as the primary disease causing cardiopulmonary arrest and presence of sudden death were found to be good prognostic factors in CPR.     

Rapid Induction of COOLing in Stroke Patients (iCOOL1): a randomised pilot study comparing cold infusions with nasopharyngeal cooling

Introduction

Induction methods for therapeutic cooling are under investigated. We compared the effectiveness and safety of cold infusions (CI) and nasopharyngeal cooling (NPC) for cooling induction in stroke patients.

Methods

A prospective, open-label, randomised (1:1), single-centre pilot trial with partially blinded safety endpoint assessment was conducted at the neurointensive care unit of Heidelberg University. Intubated stroke patients with an indication for therapeutic cooling and an intracranial pressure (ICP)/temperature brain probe were randomly assigned to CI (4°C, 2L at 4L/h) or NPC (60L/min for 1 h). Previous data suggested a maximum decrease of tympanic temperature for CI (2.1L within 35 min) after 52 min. Therefore the study period was 1 hour (15 min subperiods I-IV). The brain temperature course was the primary endpoint. Secondary measures included continuous monitoring of neurovital parameters and extracerebral temperatures. Statistical analysis based on repeated-measures analysis of variance.

Results

Of 221 patients screened, 20 were randomized within 5 months. Infusion time of 2L CI was 33 ± 4 min in 10 patients and 10 patients received NPC for 60 min. During active treatment (first 30 min), brain temperature decreased faster with CI than during NPC (I: -0.31 ± 0.2 versus -0.12 ± 0.1°C, P = 0.008; II: -1.0 ± 0.3 versus -0.49 ± 0.3°C, P = 0.001). In the CI-group, after the infusion was finished, the intervention no longer decreased brain temperature, which increased after 3.5 ± 3.3 min. Oesophageal temperature correlated best with brain temperature during CI and NPC. Tympanic temperature reacted similarly to relative changes of brain temperature during CI, but absolute values slightly differed. CI provoked three severe adverse events during subperiods II-IV (two systolic arterial pressure (SAP), one shivering) compared with four in the NPC-group, all during subperiod I (three SAP, one ICP). Classified as possibly intervention-related, two cases of ventilator failure occurred during NPC.

Conclusions

In intubated stroke patients, brain cooling is faster during CI than during NPC. Importantly, contrary to previous expectations, brain cooling stopped soon after CI cessation. Oesophageal but neither bladder nor rectal temperature is suited as surrogate for brain temperature during CI and NPC. Several severe adverse events in CI and in NPC demand further studying of safety.

Trial registration

ClinicalTrials.gov NCT01573117. Registered 31 March 2012

     

Red blood cell rheological properties in various rat hypertension models

Red blood cell (RBC) properties were proposed to play role in the development of hypertension (HT). This study aimed at investigating the alterations of RBC deformability and aggregation, in various models of HT in rats. The following four models of HT were developed in rats: one kidney-one clip HT (1K-1C HT), two kidney-one clip HT (2K-1C HT), deoxycorticosterone acetate (DOCA) induced HT (15 mg/kg, 2 times/week, sc) and N-nitro L-arginine methyl ester (L-NAME) induced HT (50 mg/kg/day, 10 weeks, ip). The blood samples were obtained from abdominal aorta, under ether anesthesia, after a period of 10 weeks of increased blood pressure. RBC deformability was determined by ektacytometry. RBC aggregation was measured in autologous plasma and 0.5% dextran 500, using a photometric rheoscope. Plasma fibrinogen concentration was determined by Clauss method. The mean blood pressure in all four HT models were about 140 mmHg, on the day of sampling, compared to approximately 110 mmHg in the control group. RBC deformability was found to be significantly decreased in the L-NAME model of HT. RBC aggregation in autologous plasma was significantly higher than control in 2K-1C, L-NAME and DOCA models, DOCA HT model being the most effective in altering the RBC aggregation. Plasma fibrinogen values were found to be higher than control in 2K-1C and L-NAME HT models, but not in DOCA HT. These results confirm that RBC rheological properties might be altered in HT. It can also be suggested that these alternations may not simply be the result of the vascular effects of HT, but may play role in the development of HT, as the alterations in different HT models were not the same, although the length and magnitude of increased blood pressure were similar.     

Increased P wave dispersion: a new finding in patients with syndrome X

The present clinical study was undertaken in patients with syndrome X, namely angina with normal coronary arteries, to investigate the presence of increased P wave dispersion by comparing patients with coronary artery disease (CAD) and healthy control subjects. Three groups were studied - group A, 21 patients (48 6 years) with syndrome X; group B, 16 patients (56 9 years) with CAD; and group C, 16 healthy subjects (49 8 years). Patients with CAD were older than those in groups A and C (P=0.005 and P=0.035, respectively). All groups demonstrated similar PQ, QRS and RR intervals. Group B had a lower minimum P wave duration than group C (P=0.05). P wave dispersion in group A was found to be higher than that in groups B and C (P=0.018 and P=0.0001, respectively). Patients with syndrome X demonstrated increased P wave dispersion compared to patients with CAD and healthy subjects. High sympathetic tone or autonomic imbalance observed in patients with syndrome X may affect intra-atrial and interatrial conduction times, and leave them prone to develop atrial arrhythmias.     

Unusual case of severe late-onset cytomegalovirus-induced hemorrhagic cystitis and ureteritis in a renal transplant patient

Cytomegalovirus (CMV) infection is common in solid organ transplant recipients and accounts for the majority of graft compromise. Major risk factors include primary exposure to CMV infection at the time of transplantation and the use of antilymphocyte agents such as OKT3 (the monoclonal antibody muromonab-CD3) and antithymocyte globulin. It most often develops during the first 6 months after transplantation. Although current prophylactic strategies and antiviral agents have led to decreased occurrence of CMV disease in early posttransplant period, the incidence of late-onset CMV disease ranges from 2% to 7% even in the patients receiving prophylaxis with oral ganciclovir. The most common presentation of CMV disease in transplant patients is CMV pneumonitis followed by gastrointestinal disease. Hemorrhagic cystitis is a common complication following hematopoietic stem cell transplantation. The condition is usually due to cyclophosphamide-based myeloablative regimens and infectious agents. Even in these settings, CMV-induced cases occur only sporadically. Ureteritis and hemorrhagic cystitis due to CMV infection after kidney transplantation is reported very rarely on a case basis in the literature so far. We report here a case of late-onset CMV-induced hemorrhagic cystitis and ureteritis presenting with painful macroscopic hematuria and ureteral obstruction after 4 years of renal transplantation. The diagnosis is pathologically confirmed by the demonstration of immunohistochemical staining specific for CMV in a resected ureteral section. We draw attention to this very particular presentation of CMV hemorrhagic cystitis with ureteral obstruction in order to emphasize atypical presentation of tissue-invasive CMV disease far beyond the timetable for posttransplant CMV infection.