Prevalence of abdominal aortic aneurysm in patients referred for transthoracic echocardiography.

BACKGROUND: Previous studies have documented the prevalence of abdominal aortic aneurysm (AAA) during transthoracic echocardiography, but the effect of such screening on subsequent vascular interventions remains unclear. AIM: This study aimed to determine the utility of opportunistic selective screening for AAA in a contemporary large series of patients having transthoracic echocardiography. METHODS: Subjects aged 50 years or older having transthoracic echocardiography had scanning of the infrarenal aorta in a consecutive series of 10 403 men and women. RESULTS: The study subjects had a mean age of 70.2 ± 10.7 years, and 54.1% were men. There was a 3.5% (95% confidence interval (CI) 3.2-3.9%) prevalence of AAA with a median diameter of 39 mm (interquartile range 32 mm-48 mm). In males ≥ 65 years the prevalence of newly diagnosed AAA was 6.2% (95% CI 5.5-7.0%). Of those with newly diagnosed AAA, 39.7% underwent AAA repair. Age and male gender were associated with AAA prevalence. After adjustment for age and gender, echocardiographic variables associated with AAA were left ventricular end diastolic dimension (odds ratio (OR) 1.02, 95%CI 1.01-1.04), interventricular septum thickness (OR 1.11, 95% CI 1.06-1.17), left ventricular posterior wall thickness (OR 1.09, 95% CI 1.03-1.15), left atrial diameter (OR 1.04, 95% CI 1.02-1.07) and aortic root diameter (OR 1.09, 95% CI 1.06-1.11). CONCLUSIONS: This study revealed a high prevalence of newly diagnosed AAA in a group of older men having cardiac evaluation. There was a relationship of increasing age with AAA, and a significant proportion of newly diagnosed subjects were not suitable for AAA repair.

Intra-individual changes of active matrix metalloproteinase-9 are associated with clinical in-stent restenosis of bare metal stents.

OBJECTIVES: Increased chronic postprocedural levels of active matrix metalloproteinase-9 (MMP-9) have been associated retrospectively with a history of in-stent restenosis (ISR). This study aimed to determine whether index or post-percutaneous coronary intervention (PCI) plasma levels of active MMP-9 are a predictor of subsequent clinical ISR, in a standard population of patients treated with bare metal coronary stents. METHODS: Four hundred thirty-two patients were prospectively recruited and sampled at index and 3 and 6 months after PCI. Those who developed symptomatic angiographically confirmed ISR were compared to randomly selected, asymptomatic controls, stratified by index presentation in a nested case-control design. Plasma samples were analyzed for the active form of MMP-9. RESULTS: In all, 35 patients (8.1%) developed ISR, and these were compared to 98 controls. The increase in active MMP-9 over 3 months was significantly greater in the ISR group (p = 0.030) and independent of the established risk factors. Index clinical presentation was not associated with acute changes in active MMP-9; however, patients with ST-elevation myocardial infarction had greater increases in active MMP-9 at 3 months. CONCLUSIONS: The change in active MMP-9 over 3 months after bare metal coronary stent placement appears to be independently associated with the development of ISR in a standard PCI population.

The effect of spironolactone on cardiac and renal fibrosis following myocardial infarction in established hypertension in the transgenic Cyp1a1Ren2 rat.

AIMS: The renin-angiotensin-aldosterone axis plays a key role in mediating cardiac and kidney injury. Mineralocorticoid receptor antagonism has beneficial effects on cardiac dysfunction, but effects are less well quantified in the cardiorenal syndrome. This study investigated cardiac and kidney pathophysiology following permanent surgical ligation to induce myocardial infarction (MI) in hypertensive animals with or without mineralocorticoid receptor antagonism. METHODS: Hypertension was induced in adult male Cyp1a1Ren2 rats. Hypertensive animals underwent MI surgery (n = 6), and were then treated daily with spironolactone for 28 days with serial systolic blood pressure measurements, echocardiograms and collection of urine and serum biochemical data. They were compared to hypertensive animals (n = 4), hypertensive animals treated with spironolactone (n = 4), and hypertensive plus MI without spironolactone (n = 6). Cardiac and kidney tissue was examined for histological and immunohistochemical analysis. RESULTS: MI superimposed on hypertension resulted in an increase in interstitial cardiac fibrosis (p<0.001), renal cortical interstitial fibrosis (p<0.01) and glomerulosclerosis (p<0.01). Increased fibrosis was accompanied by myofibroblast and macrophage infiltration in the heart and the kidney. Spironolactone post-MI, diminished the progressive fibrosis (p<0.001) and inflammation (myofibroblasts (p<0.05); macrophages (p<0.01)) in both the heart and the kidney, despite persistently elevated SBP (182±19 mmHg). Despite the reduction in inflammation and fibrosis, spironolactone did not modify ejection fraction, proteinuria, or renal function when compared to untreated animals post MI. CONCLUSION: This model of progressive cardiorenal dysfunction more closely replicates the clinical setting. Mineralocorticoid receptor blockade at a clinically relevant dose, blunted progression of cardiac and kidney fibrosis with reduction in cardiac and kidney inflammatory myofibroblast and macrophage infiltration. Further studies are underway to investigate the combined actions of angiotensin blockade with mineralocorticoid receptor blockade.

Eimeria praecox infection ameliorates effects of Eimeria maxima infection in chickens.

The effect of Eimeria praecox on concurrent Eimeria maxima infection was studied in susceptible chickens. Clinical signs of coccidiosis were assessed in single E. praecox or E. maxima infections and compared to dual infection with both Eimeria species. Groups infected solely with 10(4)E. maxima oocysts displayed weight gains that were 48% of weight gain in uninfected controls. Weight gain in chickens infected only with 10(4)E. praecox oocysts was 90% of uninfected controls. Average weight gain in chickens infected with both E. maxima and E. praecox was 79% of controls, and showed no significant difference (P>0.05) from weight gain in E. praecox-infected chickens. Feed utilization (feed conversion ratio, FCR) in chickens infected with both species showed no significant difference (P>0.05) from FCR in non-infected controls or chickens infected with E. praecox alone; all showing a significant difference (P<0.05) from FCR in chickens infected solely with E. maxima. Although E. praecox did not appear to have a negative effect on weight gain and FCR, it did cause a significant decrease in serum carotenoids. Analysis of oocysts excreted by chickens during dual infection showed little effect of E. praecox on E. maxima oocyst production.

Development and validation of a patient symptom questionnaire to facilitate early diagnosis of thyroid-associated orbitopathy in graves' disease.

BACKGROUND: To construct a patient-based symptom questionnaire to facilitate early referral of thyroid-associated orbitopathy (TAO) in Graves' hyperthyroidism (GH). METHODS: Phase I of our study involved developing a symptomatology-based questionnaire for the self-reporting of TAO symptoms in patients recently diagnosed with GH. Phase II involved administering the questionnaire along with a standard ophthalmic examination to a screening cohort of patients newly diagnosed with GH. Symptoms highly associated with the clinical diagnosis of TAO were used to construct a tool with the highest possible sensitivity. Phase III involved validation of this tool in a new cohort of patients recently diagnosed with GH. For each patient, the diagnosis of TAO was made by both a standardized orbital ophthalmic exam and the questionnaire. Results from the questionnaire were then compared to the clinical examination. RESULTS: The questionnaire was compared to the standardized examination and found to have a sensitivity of 0.76 and a specificity of 0.82 in the validation phase of the study. INTERPRETATION: This questionnaire may be a useful tool in clinical practice to allow identification of patients with TAO secondary to GH. Future studies using this questionnaire are needed to determine whether earlier identification and management of these patients is associated with reduced morbidity from TAO.

Elevated plasma active matrix metalloproteinase-9 level is associated with coronary artery in-stent restenosis.

OBJECTIVE: This study aimed to determine whether the plasma levels of matrix metalloproteinase-9 (MMP-9) or tissue inhibitor of metalloproteinases-1 (TIMP-1) were altered in patients with a history of symptomatic in-stent restenosis (ISR). METHODS AND RESULTS: A group of 158 patients with a history of ISR were compared with 128 symptom-free patients. Plasma samples and a detailed risk factor history were collected. Plasma samples were analyzed for pro-MMP-9 and latent MMP-9 and active MMP-9, latent MMP-3, and TIMP-1. Several variables were associated with ISR, including index coronary disease extent and severity (number of diseased vessels and American College of Cardiology/American Heart Association lesion classification), number, diameter, and total length of stent(s) inserted, and plasma high-density lipoprotein cholesterol. Plasma active MMP-9 (odds ratio, 1.96; 95% CI, 1.43 to 2.69) showed independent risk association with ISR. Patients with multiple sites of ISR had significantly higher levels of active MMP-9 compared with patients with only a single ISR lesion or no ISR. CONCLUSIONS: Plasma active MMP-9 levels may be a useful independent predictor of bare metal stent ISR.

Hemithyroidectomy: the preferred initial surgical approach for management of Hurthle cell neoplasm.

BACKGROUND: The objective of this study was to evaluate the cancer risk of patient clinicopathologic characteristics to determine the optimal approach for the surgical management of individuals with Hurthle cell neoplasm (HN) diagnosed by cytology. METHODS: Patient clinicopathologic characteristics evaluated included age, sex, tumor size, and ipsilateral thyroid lobe nodularity. The association of these characteristics with a pathologic cancer diagnosis was evaluated using Fisher's exact test and Student t test. RESULTS: Of the 422 patients undergoing thyroidectomy, 27 presented with a fine-needle aspiration biopsy diagnosis of HN, and by pathologic assessment 7 HN patients (25.9%) had a cancer diagnosis. Although none of the clinicopathologic characteristics evaluated were able to reliably differentiate benign from malignant tumors, large tumor size and male sex were significantly associated with a pathologic diagnosis of Hurthle cell carcinoma (P < .05). CONCLUSIONS: Hemithyroidectomy represents the preferred initial surgical approach for the management of individuals presenting with nodular thyroid disease and a cytologic diagnosis of HN.

The effects of free radical scavengers on the oxidation of low-density lipoproteins by macrophages.

Oxidised LDL has been implicated in the pathogenesis of atherosclerosis. Macrophages can oxidatively modify low-density lipoprotein (LDL) in vitro. The mechanisms of this oxidation process are presently unclear. In this study, we have investigated the effects of compounds and enzymes widely used to quench or scavenge active oxygen species to try to identify the oxidative species involved in this process. The data obtained suggest that hydrogen peroxide may possibly play a role in LDL oxidation by macrophages, whereas singlet oxygen and hydroxyl radicals may not. The role of superoxide anions was uncertain because copper-zinc superoxide dismutase (Cu/Zn-SOD) and manganese SOD (Mn-SOD), widely used to determine superoxide-dependency in other systems may be unsuitable in this particular system. Cu/Zn-SOD at high concentrations displayed a variability in its effects, sometimes augmenting LDL oxidation and sometimes inhibiting it. In the experiments in which Cu/Zn-SOD augmented LDL oxidation, heat inactivation of the enzyme decreased the augmentation; in the experiments in which Cu/Zn-SOD inhibited LDL oxidation, it retained its inhibitory effect after heat inactivation. Mn-SOD always inhibited modification even after heat inactivation. We have therefore concluded that superoxide involvement in LDL oxidation by macrophages is still uncertain and the uncertainty will remain until a suitable probe is found.

The effect of inhibitors of free radical generating-enzymes on low-density lipoprotein oxidation by macrophages.

Oxidised low-density lipoprotein (LDL) produced by the action of arterial cells, including macrophages, has been implicated in atherosclerosis. We have investigated the effect of inhibitors of various cellular free-radical generating enzymes on macrophage-mediated LDL oxidation. Xanthine oxidase and nitric oxide synthase are not responsible for LDL modification by resident mouse peritoneal macrophages. Eicosatetraynoic acid, a lipoxygenase inhibitor, produced a dose-dependent irreversible inhibition of macrophage modification of LDL, but at concentrations rather close to those toxic to the cells. Diphenyl and diphenylene iodonium, NADPH oxidase and mitochondrial electron transport inhibitors, inhibited macrophage oxidation of LDL, at concentrations that were not obviously toxic. This suggests that NADPH oxidase, or some other flavin nucleotide-dependent process, may be involved in LDL oxidation by macrophages. Wortmannin and thiopropionic acid dilauryl ester did not inhibit LDL oxidation, suggesting that inhibition of NADPH oxidase may not be the means by which the iodonium compounds inhibit LDL oxidation. Macrophages from C3H/HeJ mice, which lack receptors for lipopolysaccharide, modified LDL normally, suggesting that the inadvertent priming of resident macrophages by traces of lipopolysaccharide bound to LDL was not involved in LDL oxidation.

Association between activity at onset of symptoms and outcome of acute myocardial infarction.

OBJECTIVES: This study sought to compare the clinical features and outcome of a first myocardial infarction with onset of symptoms during or within 30 min of exercise, at rest and in bed. BACKGROUND: It is not known whether activity at onset influences outcome of acute myocardial infarction. METHODS: Information collected using a standard questionnaire was used to relate activity at the onset of symptoms to in-hospital outcome in 2,468 consecutive patients admitted to a coronary care unit with a first myocardial infarction between 1975 and 1993. RESULTS: Patients with exercise-related onset were more likely to be younger and male. Those with onset in bed were more likely to be older and have a history of stable or unstable angina. Compared with patients whose symptoms began at rest, those with exercise-related onset had a lower in-hospital mortality rate after adjusting for age, gender and year of admission (odds ratio [OR] 0.60, 95% confidence interval [CI] 0.40 to 0.89), and patients with onset in bed had a higher mortality rate (OR 1.38, 95% CI 1.03 to 1.85). The incidence of cardiac failure requiring diuretic therapy was also lower for exercise-related onset (OR 0.83, 95% CI 0.67 to 1.04) and higher when onset was in bed (OR 1.36, 95% CI 1.11 to 1.66). CONCLUSIONS: There is an association between activity at onset and outcome of acute myocardial infarction. Differences in pathophysiology or in the population at risk could explain this observation.

A new echocardiographic model for quantifying three-dimensional endocardial surface area.

A new technique for quantitatively mapping the three-dimensional left ventricular endocardial surface was developed, using measurements from standard cross-sectional echocardiographic images. To validate the accuracy of this echocardiographic mapping technique in an animal model, the endocardial areas of 15 excised canine ventricles were calculated using measurements made from echocardiographic studies of the hearts and compared with areas determined with latex casts of the same ventricles. Close correlation (r = 0.87, p less than 0.001) between these two measures of endocardial area provided preliminary confirmation of the accuracy of the maps. To further characterize the mapping algorithm, it was translated into computer format and used to map the surfaces of idealized hemiellipsoids. Areas measured with this mapping technique closely approximated the actual areas of idealized surfaces with a wide spectrum of shapes; maps were particularly accurate for ellipsoids with shapes similar to those of undistorted human ventricles. Also, the accuracies of area calculations were relatively insensitive to deviation from the assumed positions of the echocardiographic short-axis planes. Finally, although the accuracy of the mapping technique improved as data from more transverse planes were added, the procedure proved reliable for estimating surface areas when data from only three planes were used. These studies confirm the accuracy of the echocardiographic mapping technique, and they suggest that the resulting planar plots might be useful as templates for localizing and quantifying the overall extent of abnormal wall motion.

An echocardiographic technique for quantifying and displaying the extent of regional left ventricular dyssynergy.

A convenient noninvasive method of mapping the left ventricular endocardial surface has been developed that can be used to display regional dysfunction and calculate the total area of abnormal endocardial excursion from data obtained in two orthogonal apical and three or more short-axis cross-sectional echocardiographic images. Visually identified regions of abnormal systolic function are plotted on end-diastolic, planar endocardial surface maps, and the extent of dysfunction can be expressed either as an absolute area or as a fraction of the total endocardial surface area involved. The extent of the left ventricular surface moving abnormally, calculated with this echocardiographic mapping technique, was compared with two histochemical measures of infarct size in a series of 11 closed chest dogs with acute circumflex coronary artery occlusions. Overall extent of abnormally moving left ventricular wall correlated closely with both the fraction of the endocardial area overlying infarct (r = 0.92, p less than or equal to 0.001) and the fraction of the myocardial volume infarcted (r = 0.86, p less than or equal to 0.001). This suggests that the echocardiographic mapping technique can be used to accurately quantify the global extent of abnormal systolic function in the presence of regional wall motion abnormalities.

Impaired endothelial function following a meal rich in used cooking fat.

OBJECTIVES: The purpose of this study was to test the hypothesis that intake of used cooking fat is associated with impaired endothelial function. BACKGROUND: Diets containing high levels of lipid oxidation products may accelerate atherogenesis, but the effect on endothelial function is unknown. METHODS: Flow-mediated endothelium-dependent dilation and glyceryl trinitrate-induced endothelium-independent dilation of the brachial artery were investigated in 10 men. Subjects had arterial studies before and 4 h after three test meals: 1) a meal (fat 64.4 g) rich in cooking fat that had been used for deep frying in a fast food restaurant; 2) the same meal (fat 64.4 g) rich in unused cooking fat, and 3) a corresponding low fat meal (fat 18.4 g) without added fat. RESULTS: Endothelium-dependent dilation decreased between fasting and postprandial studies after the used fat meal (5.9 +/- 2.3% vs. 0.8 +/- 2.2%, p = 0.0003), but there was no significant change after the unused fat meal (5.3 +/- 2.1% vs. 6.0 +/- 2.5%) or low fat meal (5.3 +/- 2.3% vs. 5.4 +/- 3.3%). There was no significant difference in endothelium-independent dilation after any of the meals. Plasma free fatty acid concentration did not change significantly during any of the meals. The level of postprandial hypertriglyceridemia was not associated with change in endothelial function. CONCLUSIONS: Ingestion of a meal rich in fat previously used for deep frying in a commercial fast food restaurant resulted in impaired arterial endothelial function. These findings suggest that intake of degradation products of heated fat contribute to endothelial dysfunction.

Responsiveness of plasma atrial natriuretic factor to short-term changes in left atrial hemodynamics after percutaneous balloon mitral valvuloplasty.

To assess the effect of short-term alteration of left atrial pressure and volume on the circulating plasma level of atrial natriuretic factor, 11 patients with left atrial hypertension due to mitral stenosis were studied at the time of percutaneous balloon mitral valvuloplasty. Hemodynamic measurements and plasma atrial natriuretic factor levels were obtained before, immediately (5 to 10 min) after and 24 h after valvuloplasty, and echocardiographic left atrial size was determined before and 24 h after valvuloplasty. Immediately after valvuloplasty, left atrial pressure decreased from 28 +/- 2 to 10 +/- 1 mm Hg (p less than 0.0005), mitral pressure gradient decreased from 20 +/- 2 to 7 +/- 1 mm Hg (p less than 0.0005), mitral valve area increased from 0.8 +/- 0.1 to 1.9 +/- 0.2 cm2 (p less than 0.0005) and plasma atrial natriuretic factor level rose from 249 +/- 42 to 348 +/- 50 pg/ml (p less than 0.01). This short-term rise in atrial natriuretic factor level may reflect a transient increase in left atrial pressure associated with balloon occlusion of the mitral valve.(ABSTRACT TRUNCATED AT 250 WORDS)

Mitral regurgitation after percutaneous balloon mitral valvuloplasty in adults: evaluation by pulsed Doppler echocardiography.

Percutaneous balloon mitral valvuloplasty is a new technique used in the treatment of adult patients with mitral stenosis. To evaluate the occurrence and severity of mitral regurgitation after balloon valvuloplasty, 24 patients (20 women and 4 men, mean age 57 years) were studied using two-dimensional and Doppler echocardiography before and less than 24 h after this procedure. Mitral valve area increased after valvuloplasty in all patients, from 0.89 +/- 0.07 to 1.61 +/- 0.09 cm2 (p less than 0.001). Before valvuloplasty, 10 patients had no mitral regurgitation, 4 had 1+, 4 had 2+ and 6 had 3+ mitral regurgitation. After valvuloplasty, new mitral regurgitation occurred in six patients. Regurgitation grade did not change in 13 patients (54%), increased by one grade in 8 patients (33%) and by two grades in 3 patients (13%). Left atrial volume decreased in all except one patient from 100 +/- 12 to 83 +/- 12 cm3 (p less than 0.001). Neither age, sex, cardiac rhythm, initial mitral valve area, increase in mitral valve area, morphologic characteristics of the valvular and subvalvular apparatus, previous mitral commissurotomy nor effective balloon dilating area discriminated between those patients with and without an increase in mitral regurgitation after valvuloplasty. Thus, mitral balloon valvuloplasty is frequently associated with an increase in mitral regurgitation. However, in this series, no patient developed severe mitral regurgitation, and left atrial volume decreased in nearly all patients. An increase in mitral regurgitation could not be predicted from any features of the valve or subvalvular apparatus, clinical characteristics of the patients or technical aspects of the procedure.

Echocardiographic evaluation of mitral valve structure and function in patients followed for at least 6 months after percutaneous balloon mitral valvuloplasty.

Although beneficial results have been reported immediately after percutaneous mitral balloon valvuloplasty, little information is available concerning the longer-term outcome of this procedure. The anatomic and functional results of percutaneous mitral valvuloplasty were assessed in 20 patients, in whom two-dimensional and Doppler echocardiographic examination could be obtained both immediately and 6 to 11 months (mean 7.5 +/- 2.0) after balloon dilation. Mean valve area measured by planimetry decreased slightly but significantly from 1.90 +/- 0.59 cm2 immediately after valvuloplasty to 1.62 +/- 0.55 cm2 (p less than 0.001) at follow-up. Individual changes in valve area were variable, and in four patients valve area decreased by greater than 25%. Echocardiographic scores of valvular morphology were obtained by assigning scores of 0 to 4 (with increasing abnormality) to each of four morphologic characteristics of the valve, namely, leaflet mobility, thickening, calcification and subvalvular thickening. This score was higher in the four patients with a decrease in valve area greater than 25% at follow-up than in the other patients (11 +/- 2 versus 7 +/- 2, p less than 0.002). Multiple regression analysis of several hemodynamic and echocardiographic factors identify first the echocardiographic score and second the valve area postvalvuloplasty as the only significant predictors of the percent decrease in valve area (r = 0.70, p less than 0.006). Mitral regurgitation graded by pulsed Doppler ultrasound decreased from 1.9 +/- 1.2 immediately after valvuloplasty to 1.0 +/- 0.9 (p less than 0.003) at follow-up, whereas there was no change in mean transmitral pressure gradient by Doppler echocardiography (5 +/- 2 versus 6 +/- 3 mm Hg, p = NS) and left atrial volume (74 +/- 34 versus 72 +/- 27 cm3, p = NS). Thus, 6 to 11 months after balloon mitral valvuloplasty, mean mitral valve area decreases slightly. Individual changes in valve area, however, are variable. Valvular morphology assessed by two-dimensional echocardiography may be useful for identifying those patients who have an increased likelihood of developing valvular restenosis.

Unusual sequelae after percutaneous mitral valvuloplasty: a Doppler echocardiographic study.

Percutaneous mitral valvuloplasty is a promising new technique for the treatment of mitral stenosis, with a relatively low complication rate reported to date. To assess the sequelae of this procedure, Doppler echocardiographic studies were prospectively performed before and after percutaneous mitral valvuloplasty in a series of 172 patients (mean age 53 +/- 17 years). After balloon dilation, mitral valve area increased from 0.9 +/- 0.3 to 2 +/- 0.8 cm2 (p less than 0.0001), mean gradient decreased from 16 +/- 6 to 6 +/- 3 mm Hg (p less than 0.0001) and mean left atrial pressure decreased from 24 +/- 7 to 14 +/- 6 mm Hg (p less than 0.0001). Although most patients were symptomatically improved, six (4%) were identified who had unusual sequelae evident on Doppler echocardiographic examination immediately after percutaneous mitral valvuloplasty. These included rupture of a posterior mitral valve leaflet, producing a flail distal leaflet portion with severe mitral regurgitation detected on Doppler color flow mapping (n = 1); asymptomatic rupture of the chordae tendineae attached to the anterior mitral valve leaflet with systolic anterior motion of the ruptured chordae into the left ventricular outflow tract (n = 1); a double-orifice mitral valve (n = 1); and evidence of a tear in the anterior mitral valve leaflet (n = 3), producing on both pulsed Doppler ultrasound and color flow mapping a second discrete jet of mitral regurgitation in addition to regurgitation through the main mitral valve orifice. All six patients made a satisfactory recovery and none has required mitral valve replacement.(ABSTRACT TRUNCATED AT 250 WORDS)

Complications of intra-aortic balloon pump use: does the final position of the IABP tip matter?

We report results of a retrospective review of intra-aortic balloon pump (IABP) use in two Australasian centres and evaluate the effect of final IABP tip position on outcome. Indications for counterpulsation, patient demographics and in-hospital outcomes and complications were retrospectively collected. The chest X-ray reports provided the 'final' position of the IABP tip. The position was defined as acceptable (tip was seen just below the aortic arch, at T2-T5 vertebrae), malpositioned (tip > 5 cm below aortic arch or at T5-T6) or severely malpositioned (tip > 10 cm below aortic arch or at T7 or below).?Major complications were considered a composite of death secondary to IABP, major limb ischaemia, major IABP malfunction, balloon rupture or haemorrhage, severe renal dysfunction (rise in creatinine > 200 µmol/l), stroke and mesenteric ischaemia. Six hundred and forty-five cases were reviewed. The overall major complication rate was 26.2% and 24.3%. Severe renal impairment was the most common complication (16.6%), and second, severe catheter dysfunction (5.4%). ?Final IABP position was acceptable in 39.9%, malpositioned in 11.1%,?severely malpositioned in 6.7% and unavailable for 42.4%. Logistic regression analysis showed IABP tip malposition (compared with satisfactory position odds ratio=3.9 [95% confidence interval=2.0-7.6, P < 0.001] and severely malpositioned odds ratio=13.0 [95% confidence interval 5.3-31.7, P < 0.001]) was associated with major complications more than the presence of shock (odds ratio=3.8, confidence interval=2.1-6.8 P < 0.001). The acceptance of a less-than-ideal final position was highly predictive of morbidity directly related to IABP device therapy.

Oncogenic osteomalacia: evidence for a humoral phosphaturic factor.

Oncogenic osteomalacia is a syndrome characterized by phosphaturia, hypophosphatemia, reduced vitamin D levels, and osteomalacia. The cause is not known, but all patients have had a tumor; usually of mesenchymal origin. Removal of the tumor reverses the metabolic abnormalities. We report a patient with osteomalacia, severe hypophosphatemia, elevated alkaline phosphatase, low 1,25-dihydroxyvitamin D3, and phosphaturia. A tumor was identified in the infratemporal fossa. The tumor was removed, and all of the biochemical abnormalities resolved over the subsequent 8 months. The bone density returned to normal values. The tumor had the appearance of a paraganglioma and was used to establish a cell culture line called JH-55. Electron microscopy of the original tumor and the JH-55 cells demonstrated the presence of neurosecretory granules. A bioassay using opossum kidney cells was used to evaluate phosphate transport. Conditioned medium from the JH-55 cells inhibited phosphate reabsorption by the kidney tubular cells. Maximal inhibition required a 24-h incubation period and was not altered by the presence of an inhibitor of protein synthesis (10 micrograms/mL cycloheximide). Immunoassays revealed no detectable PTH-related peptide or intact PTH in the JH-55 medium. The cause of this paraneoplastic syndrome is not known, but all of the evidence is consistent with the action of a hormone that produces phosphaturia. This putative factor is distinct from other hormones that cause phosphaturia.