Hyperphosphatemia is associated with cardiac valve calcification in chronic hypoparathyroidism.

PURPOSE: To evaluate the association between metabolic abnormalities and cardiovascular risk factors in patients with chronic hypoparathyroidism (HPP). PATIENTS AND METHODS: Patients 18 years and older, glomerular filtration > 30 mL/min/1.73 m2 and no documented coronary artery disease were selected. Serum calcium, phosphorus, glucose, lipids, PTH, 25(OH)D and FGF23 were measured. Cardiovascular risk was estimated by the European Society of Cardiology (ESC) calculator. Transthoracic echocardiogram and carotid ultrasound were performed to detect carotid plaques (CP), carotid intima-media thickness (IMT), cardiac valve calcification (CVC), and left ventricular hypertrophy (LVH). RESULTS: Thirty-seven patients (94.6% female), aged 56.0 ± 13.5 years and HPP duration 7.0 (4.0; 11.3) years, were included. Fifteen were classified as low cardiovascular risk, 9 as intermediate risk, 9 as high risk and none as very high risk. The prevalence of CP, CVC and LVH was 24.3%, 24.3% and 13.5%, respectively. IMT values were within normal ranges in all cohort. FGF23 were not associated with CP, IMT, CVC or LVH. After logistic regression, phosphorus was the only significant metabolic variable impacting CVC in univariate analysis (OR 2.795; 95% CI 1.132-6.905; p = 0.026), as well as in the multivariate analysis (OR 3.572; 95% CI 1.094-11.665; p = 0.035). Analysis by ROC curve showed serum phosphorus > 5.05 mg/dL (AUC 0.748; CI 0.584-0.877; p = 0.05) as the best cutoff point associated with valve heart calcification (sensitivity 78%; negative predictive value 91.3%). CONCLUSION: Hyperphosphatemia was associated with CVC in HPP patients. Further studies are needed to investigate whether the control of hyperphosphatemia may reduce cardiovascular risk in this population.

Low risk of coronary artery disease in patients with acromegaly.

The aims of this study are to determine the prevalence of coronary atherosclerosis in acromegalic patients and to investigate the relationship between the coronary artery calcium score (CS) and acromegaly status and clinical parameters [Framingham risk score (FRS)]. Fifty-six acromegalic patients and paired non-acromegalic volunteers were stratified according to the FRS into low-, intermediate-, and high-risk groups. CS was assessed using multidetector computed tomography. The patients were considered to have controlled or active acromegaly at the time they were submitted to evaluation. Sixty-six percent of acromegalic patients exhibited arterial hypertension, 36 % had diabetes mellitus, and 34 % had hypercholesterolemia. The median FRS and the median risk for cardiovascular event within the next 10 years were similar in the acromegalics and the controls. The median total CS and CS >75th percentile didn't differ significantly between these groups. In patients with controlled acromegaly, a low, intermediate, or high FRS risk was observed in 86, 14, and 0 %, respectively. In patients with active disease, a low, intermediate, or high FRS risk was verified in 94, 3, and 3 %, respectively, and differences between the controlled and active groups were not significant. Seventy-two percent of the patients had total CS = 0, and there were no differences between the controlled and active groups. The risk of coronary artery disease in acromegalic patients, determined according to FRS and CS, is low despite the high prevalence of metabolic abnormalities.

Radiation dose in cardiac CT angiography: protocols and image quality.

This paper aims to evaluate the radiation dose exposure of patients submitted to cardiac computed tomography angiography. The effective dose was obtained from the product of dose-length product values and the conversion factor established in the European Working Group for Guidelines on Quality Criteria in CT. The image noise and contrast- and signal-to-noise ratios were obtained for all images. Sixty-four- and 256-slice CT angiographies were used in 211 (68.5 %) and 97 (31.5 %) patients, respectively. The calculated mean effective dose with prospective CT angiography was 6.0±1.0 mSv and the retrospective mode was 8.4±1.2 mSv. The mean image noise values were 38.5±9.5 and 21.4 ± 5.3 for prospective and retrospective modes, respectively. It was observed that the image noise increased by 44.4 % using a prospective mode. Prospective CT angiography reduces radiation dose by ∼29 % compared with the retrospective mode, while maintaining diagnostic image quality and the ability to assess obstructions in patients.

Oral complaints related to menopause.

OBJECTIVES: The purpose of the present study was to correlate oral and systemic symptoms of menopause and the oral health and salivary composition and flow rate in a group of women in menopause prior to hormone replacement therapy. METHODS: One-hundred fifty-four women attending a menopause clinic were divided into two groups. Group A, 58 women, without any systemic disease or treatments, and Group B,96 women with diseases and on various medications. They answered a questionnaire on their general health and oral and systemic complaints related to menopause. Fifty-four of the women agreed to have an oral examination and saliva analysis. Whole resting and submandibular (SM-SL) stimulated saliva were analyzed. RESULTS: The oral discomfort complaint was found in 45% in Group A and in 60% in Group B. 74% complained of climacteric symptoms in Group A and 63% in Group B. The odds ratio (OR) between oral discomfort and climacterics complaints of menopause was 8.03 in Group A and 4.08 in Group B. The salivary composition and flow rates did not differ significantly between the groups of menopausal women. However the salivary total protein and IgA concentrations were significantly higher in comparison to healthy young controls. CONCLUSIONS: The present study reports a high prevalence of oral discomfort in the women attending a menopause clinic. A highly significant odds ratio between systemic and oral complaints of menopause was found. The significantly altered salivary composition in these women might point to sympathetic activation due to psychological stress.

[Occupational injuries with risk of transmission of blood-borne pathogens. A study of a 2-year material from the Holstebro Central Hospital]. / Arbejdsskade med risiko for transmission af blodbåren smitte. En opgørelse af et toårsmateriale i Holstebro Centralsygehus.

In order to illuminate causes of accidental occupational exposure of the house staff at the Central Hospital of Holstebro (CHH) to the potential hazards of HIV- and HBV-transmission, all cases of reported injuries occurring in 1991-1992 have been analysed. Needleprick lesions were found to account for the great majority of the reported cases (71%). Sixty-six percent of all injuries were self-inflicted during medical procedures, while 34% were caused by another person, either directly (simultaneous contact of two persons with the contaminated sharp object) or indirectly as a result of carelessness or negligence. Seventy-two percent of the analysed exposures could have been avoided if the staff had complied with Universal Precautions recommended since 1988. In order to estimate the amount of unreported cases, all nurses and laboratory technicians currently employed at CHH were asked to complete an anonymous questionnaire reviewing their past (1991-1992) mucocutaneous and percutaneous exposures to blood or body fluids. Only 28% of the injuries recalled by the subjects had been reported. If the risk of occupational transmission of blood-borne diseases is to be minimized, additional effort must be made to clarify the principles of the Universal Precautions policy. It is of great importance that all injuries are reported by way of an easy reporting procedure which is efficient and familiar to the staff at any time.

Noninvasive cardiac output determined with a new method based on gas exchange measurements and carbon dioxide rebreathing: a study in animals/pigs.

A system has been designed to determine cardiac output noninvasively. The system's main component is a closed breathing circuit and it measures oxygen uptake (VO2), carbon dioxide elimination (VCO2), and end-tidal CO2 partial pressure (PET). As an integral part of the system, periods of CO2 rebreathing can be automatically implemented. The CO2 partial pressure of oxygenated mixed venous blood (Pv) is obtained from the measured exponential rise of the PET value during such a CO2 rebreathing maneuver. A new method is described for estimating the pulmonary blood flow, alveolar ventilation, cardiac output (CO), and mixed venous oxygen saturation (SVO2) from PV, PET, VO2, VCO2, tidal volume, and arterial oxygen saturation. The method was evaluated in 6 anesthetized and mechanically ventilated pigs. A wide range of cardiac output, shunt fractions, and dead space to tidal volume ratios were induced by combinations of bronchoalveolar lavage, hypervolemia, hypovolemia, and variable levels of positive end-expiratory pressure (PEEP). The bias between the CO obtained with the noninvasive technique (CO L/min) and the thermodilution CO (Qt L/min) was 0.13 L/min (SD = 0.78 L/min) and the correlation was N = 64; R = 0.92; CO = 0.95*Qt + 0.38. The bias obtained for double determinations with the noninvasive CO technique was 0.3 L/min (SD = 0.5 L/min). The bias between the noninvasive estimates of Svo2 and the directly measured values was 1.1% (SD = 9.3%). For double determination with the noninvasive technique the bias was -0.9% (SD = 4.7%). It is concluded that in mechanically ventilated pigs the proposed method produces good estimates of CO and SVO2 also in the presence of significant ventilation/perfusion mismatch.

Hypoxic pulmonary vasoconstriction in man: effects of hyperventilation.

The pulmonary vasoconstriction response to hypoxia was studied in eight anaesthetized supine subjects. One lung was made hypoxic while the other was ventilated with 100% oxygen. This was achieved by separating the tidal gas-distribution to the lungs by means of a double-lumen tracheal catheter. The hypoxic pulmonary vasoconstriction (HPV) response was estimated from the blood flow diversion away from the hypoxic lung. Blood flow distribution between the lungs was calculated from the regional expired carbon dioxide production, assuming regional carbon dioxide production to be proportional to blood flow. The subjects were studied during six different conditions. Firstly, when ventilated with 100% oxygen to both lungs at a PaCO2 of about 6 kPa. Secondly, with 100% oxygen to the left lung and 5% oxygen in nitrogen to the right (test) lung. The ratio between carbon dioxide output from right and left lung was calculated. These measurements were repeated during two states of hyperventilation (PaCO2 of about 4.5 kPa and 3.5 kPa, respectively) with and without hypoxia (conditions 3-6). During normoventilation, blood flow distribution between the lungs was equal. During hypoxia, blood flow distribution to the hypoxic lung decreased by 35% of the pre-hypoxic value. Furthermore, a decrease in arterial oxygen tension from 51.5 +/- 4.5 to 11.5 +/- 2.1 kPa was observed. During excessive hyperventilation (PaCO2 3.2 +/- 0.2 kPa), blood flow distribution to the hypoxic right lung decreased by only 10% of its pre-hypoxic value. A further decrease in arterial oxygen tension to 8.5 +/- 1.8 kPa was observed. This decrease in PaO2 was possibly due to an increased venous admixture caused by an abolished HPV response. It is concluded that hyperventilation counteracts hypoxic pulmonary vasoconstriction in man.

Hypoxic pulmonary vasoconstriction in the human lung: the effect of prolonged unilateral hypoxic challenge during anaesthesia.

The influence of time on the pulmonary vasoconstrictor response to hypoxia was studied in six subjects during general anaesthesia and artificial ventilation prior to elective surgery. The lungs were intubated separately with a double-lumen bronchial catheter. After preoxygenation of both lungs for 30 min, the test lung was rendered hypoxic for 60 min by ventilation with 5% O2 in N2, with the control lung still being ventilated with 100% O2. Cardiac output was determined by thermodilution, and the distribution of blood flow between the lungs was assessed from the excretion of a continuously infused poorly soluble gas (SF6). The fractional perfusion of the test lung decreased from 53% to 25% of cardiac output within the first 15 min of unilateral hypoxia. The pulmonary artery mean pressure increased by 14% and the pulmonary vascular resistance (PVR) of the test lung increased by 54%. Venous admixture increased from 21% to 39% of cardiac output, while the "true" shunt was maintained at about 15%. Arterial oxygen tension (Pao2) fell from 45 kPa to 12 kPa. Prolonging the unilateral hypoxic challenge caused no further change in the redistribution of the pulmonary blood flow, but cardiac output and pulmonary artery mean pressure continued to increase to 40%-50% above control values after 1 h of hypoxia. The PVR of the test lung remained unchanged. The findings suggest that there is an immediate vasoconstrictor response to hypoxia in the human lung and that there is no further potentiation or diminution, of the response during a 60-min period of hypoxia.

Esophageal elastance in anesthetized humans.

Esophageal elastance (Ees) was measured in 13 human subjects, awake and anesthetized by halothane, in the supine and left lateral postures. Static esophageal pressure was measured by an esophageal balloon catheter, respiratory volumes by pneumotachography, and functional residual capacity (FRC) by body plethysmography. In the supine awake subject, Ees averaged 3 cmH2O/ml at FRC and increased significantly with lung volume. Ees remained unaltered at FRC during anesthesia in the supine position, but lung volume dependence was no longer observed. In the left lateral position the awake subject displayed the same Ees at FRC as in the supine position and lung volume exerted only a small influence on Ees. The latter was reduced during anesthesia and tended to diminish with increasing lung volume. All variations in Ees caused by posture, anesthesia, and lung volume were small and affected the shape of the pressure-volume curve of the lung to only a minor degree.

Thoracic gas volume measured by body plethysmography during anesthesia and muscle paralysis: description and validation of a method.

A method based on body plethysmography for the assessment of thoracic gas volume (TGV) in the anesthetized, paralyzed subject is presented. The compression of thoracic gas following inflation is detected by measuring the difference between the inflation volume and the "box volume" change caused by the expansion of the chest. Model experiments showed good agreement between true and measured volumes with a residual standard deviation of 2 per cent. In studies on human subjects with healthy lungs during halothane anesthesia, the coefficient of variation of repeated measurements was 5 per cent. Comparative measurements with resting lung volume (FRC) determined by multiple breath nitrogen washout disclosed a larger volume by the box technique, a difference which was reduced but not eliminated by deep breathing during the nitrogen washout. This difference, amounting to 0.2 liters on the average, may be explained by abdominal gas and by the detection of trapped gas by the box technique but not by the nitrogen washout.

Ventilation-perfusion distribution during inhalation anaesthesia. Effects of spontaneous breathing, mechanical ventilation and positive end-expiratory pressure.

Ventilation-perfusion (VA/Q) ratios were studied by means of an inert gas elimination technique in healthy subjects with an average age of 51 years in the supine posture (a) when awake, (b) during inhalational anaesthesia, spontaneously breathing, (c) during mechanical ventilation, and (d) when a positive end-expiratory pressure (PEEP) was applied. In the awake subject a bimodal distribution of VA/Q was recovered in most patients, one mode centered around the ratio of 1 and another, smaller mode, within low VA/Q-regions. Any shunt was less than 3% of cardiac output. With anaesthesia and spontaneous breathing, the low VA/Q mode was reduced and the shunt increased to an average of 6.2%. With mechanical ventilation, the major VA/Q mode was widened while the shunt was further increased in 4 of 10 subjects (mean 8.6%). With PEEP, the shunt was reduced and a new mode within high VA/Q-regions appeared. The shunt and low VA/Q-regions appeared. The shunt and low VA/Q-regions may be explained in terms of airway closure while the high VA/Q mode with PEEP may be attributed to the development of a zone I.