Thallium Scintigraphy in Prediction of Occlusion of Bypass Grafts in Asymptomatic and Symptomatic Patients

ABSTRACT To evaluate thallium scintigraphy in predicting coronary artery bypass graft patency, exercise thallium scintigraphy and selective graft and native vessel angiograms were performed in 22 asymptomatic and 29 symptomatic consecutive patients three months after coronary artery bypass grafting (CABG). Twelve out of 22 asymptomatic patients (55%) had reversible thallium defects on postoperative images; in 10 patients the postoperative scans were normal. The graft patency was significantly lower in asymptomatic patients with abnormal thallium perfusion compared to those with normal perfusion after CABG (68% vs. 91%. p<0.05). The rate of graft patency in symptomatic patients was 66/87 (76%). Thallium scintigraphy was 77% sensitive and 78% specific in detecting one or more stenosed or occluded bypass grafts in patients without angina (accuracy 77%). When data from exercise electrocardiography were combined with scintigraphy, all but one patient with incomplete revascularization could be detected (positive predictive accuracy 92%). In symptomatic patients, thallium scintigraphy accurately predicted the presence or absence of graft occlusion in 24/29 (83%) cases. Thus, abnormal myocardial perfusion due to stenosis or occlusion of bypass grafts is common in both asymptomatic and symptomatic patients after CABG. Thallium scintigraphy together with exercise electrocardiography appear to be useful non-invasive methods in detecting painless myocardial ischemia and in predicting bypass graft occlusion after CABG.     

Paraganglion cells mimicking metastatic clear cell carcinoma

Four patients are presented whom normal paraganglion cells simulated metastases of clear cell carcinomas of the urogenital tract. The cells, located within and near the lumbar sympathetic ganglia, were initially interpreted by the pathologist as metastatic, but a later examination showed them to be normal paraganglion cells. One ganglion was also examined electron microscopically. Normal ganglion cells were seen, as were cells with intracytoplasmic osmophilic neurosecretory granules, confirming their paraganglionic origin. Awareness of the appearance of paraganglion cells in some instances is essential to avoid their misinterpretation as metastases of clear cell carcinomas.     

Complications Related to Permanent Pacemaker Therapy

This study evaluates complications related to permanent endocardial pacing in the era of modern pacemaker therapy. There is only limited information available about the complications related to modern cardiac pacing. Most of the existing data are based on the 1970s and are no longer valid for current practice. The recent reports on pacemaker complications are focused on some specific complication or are restricted to early complications. Thus, there are no reports available providing a comprehensive view of complications related to modern cardiac pacing. Four hundred forty-six patients, who received permanent endocardial pacemakers between January 1990 and December 1995 at Kuopio University Hospital, were reviewed retrospectively using patient records. Attention was paid to the occurrence of any complication during the implantation or follow-up. An early complication was detected in 6.7%, and 4.9% of patients were treated invasively due to the early complication. Late complication developed in 7.2% and reoperation was required in 6.3% of the patients. Complications related to the implantation procedure occurred in 3.1%. Inadequate capture or sensing was observed in 7.4% of the patients. Pacemaker infection was detected in 1.8% and erosion in 0.9% of the patients. An AV block developed in 3.6% (1.6%/year) patients who received an AAI(R)-pacemaker due to sick sinus syndrome. There was no mortality attributable to pacemaker therapy. A great majority (68%) of the complications occurred within the first 3 months after the implantation. Complications associated to modern permanent endocardial pacemaker therapy are not infrequent. Eleven percent of patients needed an invasive procedure due to an early or late complication.     

Automatic Atrial Threshold Measurement and Adjustment in Pediatric Patients

Background: Automatic threshold measurement and output adjustment are used as default settings in modern pacemakers. The purpose of the study was to assess Atrial Capture Management (ACM) of Medtronic pacemakers in pediatric patients. Methods: Forty children were enrolled in two centers. Median age was 9.8 years (range 0.8–17.5 years). Half had undergone surgery for congenital heart defects; 45% of patients had an epicardial atrial lead. The pacing indication was atrioventricular block in 82% of patients and sinus node disease in 18%. Manually determined atrial thresholds and ACM measurements were compared. Results: ACM measurements were within the expected variation in 37/40 (93%) of the patients. In one patient the threshold was 0.625‐V lower manually than with ACM. One patient had too high an intrinsic atrial rate for ACM to be able to measure threshold. The mean threshold at 0.4 ms was 0.69 ± 0.32 V manually and 0.68 ± 0.35 V with ACM (two‐tailed paired t‐test, P = 0.52) in all patients. The mean difference was 0.012 V (95% confidence interval: ?0.027, 0.053). The mean endocardial threshold was 0.70 ± 0.36 V manually and 0.69 ± 0.38 V with ACM; epicardial threshold was 0.67 ± 0.27 V manually and 0.68 ± 0.32 V with ACM. The difference between the measurements was 0.012 V for endocardial and 0.014 V for epicardial leads. No atrial arrhythmias due to ACM measurements were observed. Conclusions: ACM measures atrial thresholds reliably in pediatric patients with both endocardial and epicardial leads, allowing its use in both. Constant high intrinsic atrial rate may prevent automatic threshold measurement in young children. (PACE 2010; 33:309–313)     

Characterization of fibrin(ogen) fragments in gingival crevicular fluid

Abstract— Crevicular fluid (CF) samples were collected by paper strips from healthy and diseased sites. The molecular distribution of fibrin and fibronectin in CF and plasma samples was investigated using SDS-polyacrylamide gel electrophoresis and specific immunoglobulins. Intact fibrin was found in all CF samples. In addition several bands with both lower and higher molecular weights than intact fibrin were seen. These bands were not present in the plasma samples. The low molecular weight bands are suggested to represent degradation products of fibrin. The high molecular bands could be fibrin-fibronectin complexes or fragments of large fibrin polymers. Fibronectin degradation products, but not intact fibronectin, were seen in both healthy and diseased samples.     

The activation of the inflammatory cytokines in overweight patients with mild obstructive sleep apnoea

It is widely accepted that obstructive sleep apnoea (OSA) is linked with cardiovascular diseases. The relationship is complex and remains still poorly understood. The presence of chronic systemic inflammation has been connected with pathogenesis of both OSA and cardiovascular diseases. While atherogenesis is believed to be a process of many years, little is known about the potential impact of the largest OSA subgroup, mild OSA, on the development of cardiovascular diseases. The aim of the present study was to assess whether untreated mild OSA is associated with an activation of inflammatory cytokine system. The adult study population consisted of two groups: 84 patients with mild OSA [apnoea–hypopnoea index (AHI) 5–15 h^?1] and 40 controls (AHI <5 h^?1). Serum concentrations of pro‐ and anti‐inflammatory cytokines were measured before any interventions. After adjustments for age, sex, body mass index, fat percentage, most important cardiometabolic and inflammatory diseases, and non‐steroidal anti‐inflammatory medication, the mean level of tumour necrosis factor‐α was significantly elevated (1.54 versus 1.17 pg mL^?1, P = 0.004), whereas the level of interleukin‐1β (IL‐1β) was reduced (0.19 versus 0.23 pg mL^?1, P = 0.004) in patients with mild OSA compared with controls. The concentrations of the protective anti‐inflammatory cytokines, interleukin‐10 (1.28 versus 0.70 pg mL^?1, P < 0.001) and interleukin‐1 receptor antagonist (478 versus 330 pg mL^?1, P = 0.003) were elevated in the OSA group. The concentrations of C‐reactive protein increased, but IL‐1β decreased along with the increase of AHI. Mild OSA was found to be associated not only with the activation of the pro‐inflammatory, but also with the anti‐inflammatory systems.     

ASSOCIATION OF SMOKING WITH LOWER URINARY TRACT SYMPTOMS

Purpose

We studied the association of smoking with lower urinary tract symptoms.

Materials and Methods

In 1994 we performed a population based study by mailing a questionnaire to all 3,143 men born in 1924, 1934 or 1944 who resided in Tampere, or in 11 rural or semirural municipalities in the same county. Of this population 68% were ultimately included in the study. A modified Danish Prostate Symptom Score-1 was used to assess urinary symptoms and associated bothersomeness. A symptom index was created by multiplying the symptom and bothersomeness scores of hesitancy, incomplete emptying, urge, urge incontinence, nocturia and daytime frequency, and totaling the products. The index for lower urinary tract symptoms was defined as positive when it reached 7 points. Subjects were also asked whether they had smoked for at least a year, and they were defined as smoking currently, formerly and never according to the response.

Results

Compared with respondents who never smoked age adjusted odds ratios were 1.47 (95% confidence interval 1.09 to 1.98) and 1.38 (1.08 to 1.78), respectively, for those who currently and formerly smoked. After further adjusting for alcohol consumption, body mass index, previous prostate surgery, pelvic area surgery, prostate cancer and bladder cancer, the odds ratios for current and former smokers were 1.39 (95% confidence interval 1.02 to 1.93) and 1.34 (1.03 to 1.75), respectively.

Conclusions

Smoking increases the prevalence of lower urinary tract symptoms. The similarity in the odds ratios of these symptoms between current and former smokers suggests that changes caused by smoking occur long term or the pathological process resulting in symptoms starts early in smokers. The decreased risk of lower urinary tract symptoms after the cessation of smoking suggests that the process is reversible but recovery is a long-term process.     

THE USE OF IMMUNOHISTOCHEMISTRY TO IMPROVE SENSITIVITY AND SPECIFICITY IN THE DIAGNOSIS OF SYSTEMIC MYCOSES IN PATIENTS WITH HAEMATOLOGICAL MALIGNANCIES

The original histomorphological diagnoses in a series of 34 mycotic lesions from 23 patients with haematological malignancies were re-evaluated by immunohistochemistry. A panel of antibodies was used to identify the agents of aspergillosis, candidosis, fusariosis, scedosporiosis (pseudallescheriosis), and zygomycosis. Apart from improving the diagnosis of aspergillosis, candidosis, and zygomycosis, the application of immunohistochemistry also disclosed three lesions of aspergillosis which had been overlooked during the original screening. It is concluded that the use of immunohistochemistry for the diagnosis of common opportunistic mycoses will not only increase diagnostic specificity, but will also reveal more tissue infections than the conventional histomorphological examination of traditionally stained sections. © 1997 by John Wiley & Sons, Ltd.     

Analgesics and Risk of Coronary and other Death in Middle-aged Men in Eastern Finland

Abstract The association between oral analgesics and the risk of death from ischaemic heart disease (IHD), cardiovascular disease, disease other than IHD, and any disease was studied in a cohort of 3 551 men aged 30–59 years, based on a random sample from the population of eastern Finland. A number of potential coronary risk factors were allowed for in multiple logistic models. On the basis of these data, a regular use of oral analgesics is associated with a decreased risk of death from IHD. The relative risk was 0.6 with 95 % confidence interval (CI) of 0.2–0.9 for IHD death and 0.6 (95 % CI = 0.4–0.9) for cardiovascular death. No significant association was found between oral analgesics and the risk of death from diseases other than IHD.     

Postmyocardial Infarction Patients Susceptible to Ventricular Tachycardia Show Increased T Wave Dispersion Independent of Delayed Ventricular Conduction

Arrhythmia Markers After Myocardial Infarction. Introduction: Experimentally, both delayed ventricular conduction and nonhomogeneous ventricular repolarization contribute to reentrant arrhythmias. We tested the hypothesis that increased T wave dispersion is independent of delayed ventricular conduction associated with arrhythmia vulnerability in postmyocardial infarction (post-MI) patients.
Methods and Results: We studied 32 post-MI patients with clinical or inducible monomorphic ventricular tachycardia (VT group), 28 post-MI patients without arrhythmias (MI group), and 13 healthy controls, using magnetocardiographic (MCG) mapping with signal averaging. Twelve-lead ECG was the reference. Filtered QRS duration (fQRS) and T wave peak to T wave end interval (TPE) were used as measures of ventricular conduction and nonhomogeneity in ventricular repolarization, respectively. In MCG, the VT group showed the longest fQRS (  135 ± 34  msec vs  114 ± 22  msec in the MI group;  P = 0.012  ). Mean TPE and maximum TPE in VT versus MI groups were  78 ± 9  msec versus  70 ± 6  msec (  P < 0.001  ) and  117 ± 23  msec versus  104 ± 19  msec (  P = 0.020  ), respectively. Maximum TPE did not correlate with fQRS in the VT group (  r = 0.063; P = NS  ) but did correlate in the MI group (  r = 0.396; P = 0.037  ). For identification of post-MI patients prone to VT, selection of cutoff values for fQRS > 140 msec and mean TPE > 81 msec gave sensitivity and specificity of 41% and 89%, and 31% and 96%, respectively. Their combination increased sensitivity to 63% while maintaining 89% specificity.
Conclusion: Post-MI patients susceptible to VT show increased T wave dispersion independent of delayed ventricular conduction.