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PubMed1994

Screening-detected and symptomatic ductal carcinoma in situ: mammographic features with pathologic correlation.

PURPOSE: To compare the mammographic and pathologic features of screening-detected and symptomatic ductal carcinoma in situ (DCIS). MATERIALS AND METHODS: The mammographic and pathologic features of 54 screening-detected and 77 symptomatic cases of DCIS were compared. Patients were aged 30-76 years (mean, 58 years). RESULTS: Diffuse involvement was seen in 10 patients (13%) with symptoms but in none of the screening-detected group (P < .05). The disease was radiologically more extensive in the symptomatic group. Calcifications in the symptomatic group (n = 48) were less likely to have a ductal distribution than those in the screening-detected group (n = 48) (30 [63%] vs 40 [83%], respectively; P < .05). At histologic examination in some cases, the symptomatic group (n = 76) included eight (11%) patients with cribriform-micropapillary, large-cell tumors (P < .05) and less comedocarcinoma (20 [26%] vs 23 [45%], respectively; P < .05) compared with the screening-detected group (n = 51). CONCLUSION: The results show differences in the radiologic and pathologic features of screening-detected and symptomatic DCIS.

Adult↗
PubMed2000

Characteristics of triangular fibrocartilage defects in symptomatic and contralateral asymptomatic wrists.

PURPOSE: To characterize triangular fibrocartilage (TFC) defects in symptomatic and contralateral asymptomatic wrists. MATERIALS AND METHODS: Communicating and noncommunicating defects of the TFC were depicted on bilateral wrist arthrograms in 56 patients with unilateral wrist pain and without associated lesions of the scapholunate or lunotriquetral ligaments. The exact location of each TFC lesion was noted. RESULTS: Communicating defects were noted in 36 (64%) of 56 symptomatic and in 26 (46%) of 56 asymptomatic wrists. Twenty-five (69%) of 36 communicating defects were bilateral. Except for one defect in each group of symptomatic and asymptomatic wrists, all communicating defects were noted radially. Noncommunicating defects were noted in 28 (50%) of 56 symptomatic wrists and in 15 (27%) of 56 asymptomatic wrists. Eleven (39%) of 28 noncommunicating defects were bilateral. On the symptomatic side, 28 of 36 noncommunicating defects (including eight multiple defects) were located proximally at the ulnar side. On the asymptomatic side, 11 of 17 noncommunicating defects (including two multiple defects) were at or near the ulna. CONCLUSION: Noncommunicating TFC defects, which typically are located on the proximal side of the TFC near its ulnar attachment, have a more reliable association with symptomatic wrists than do communicating defects. Radial-sided communicating defects described in the literature (Palmer type 1A and 1D) as posttraumatic commonly are seen bilaterally and in asymptomatic wrists.

Adolescent↗
PubMed2006

Insulin-like growth factor-I receptors in atherosclerotic plaques of symptomatic and asymptomatic patients with carotid stenosis: effect of IL-12 and IFN-gamma.

The balance between apoptosis and survival of vascular smooth muscle cells (VSMCs) in the fibrous cap appears to best correlate with plaque instability or stability and is controlled by growth factors and cytokines. We recently reported the inhibition of insulin-like growth factor (IGF)-I-induced proliferation and increase in apoptosis of VSMCs by atheroma-associated cytokines. Here we assessed the expression of IGF-I receptor (IGF-IR) in atherosclerotic plaques and in plaque VSMCs of asymptomatic and symptomatic patients with carotid stenosis and examined the effect of IGF-I, IL-12, and IFN-gamma on the expression of IGF-IR and IGF-binding protein (IGFBP)-3 in plaque VSMCs. We observed significantly lower density of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive apoptotic nuclei and increased positive immunoreactivity to IGF-IR and mRNA transcripts of endogenous IGF-I and IGF-IR in asymptomatic than in symptomatic plaque VSMCs. Positive correlation was found between apoptosis and IGF-IR expression in asymptomatic (r(2) = 0.942) and symptomatic (r(2) = 0.908) plaque VSMCs. The specific binding of (125)I-labeled IGF-I was 3.7-fold higher in plaque VSMCs of asymptomatic patients than in symptomatic patients. IGF-I increased both IGF-IR mRNA transcripts and expression of IGFBP-3 in VSMCs of asymptomatic plaques. IL-12 and IFN-gamma decreased IGF-IR mRNA transcripts and further increased the expression of IGFBP-3 in asymptomatic VSMCs but had no effect in symptomatic VSMCs. These data suggest that the decreased expression of IGF-IR mRNA and increased expression of IGFBP-3 in carotid plaques of symptomatic patients could be due to atheroma-associated cytokines and this could result in plaque instability.

Aged↗
PubMed1999

Management of symptomatic BPH in France: who is treated and how?

OBJECTIVE: To review the contemporary management of symptomatic benign prostatic hyperplasia (BPH) in France. METHODS: Information was obtained from published scientific articles, IMS market analysis data and community-based surveys among older men. RESULTS: The prevalence of symptomatic BPH in France is relatively high. About 15-20% of men over 50-60 years of age report moderate to severe lower urinary tract symptoms (LUTS: total I-PSS >7). If this is applied to the 5.7 million men aged 60 or over living in France, it seems that 855,000-1,140,000 men have symptomatic BPH. In the AFU-Synthélabo community-based survey, around half of these men (more than 10%) visited a physician because they were bothered by these symptoms interfering with performing daily life activities. This suggests that approximately 600,000 patients have a diagnosis of symptomatic BPH in France. These patients can contact both general practitioners (GPs) and urologists for the management of symptomatic BPH. Approximately one in every four to one in every three men with LUTS visits directly a urologist whereas the other 65-75% initially contacts a GP in France. GPs very often prescribe medical treatment for LUTS related to BPH. Of all medical prescriptions in France, 80% are made by GPs and only 12.5% by urologists. The total market for medical therapy increased substantially since 1994. Since 1998, it grew with 2-3%/year. A total of 640,000 patients received medical therapy for BPH in 1998. The growth in the medical treatment market was mainly due to an increase in the number of patients receiving alpha(1)-adrenoceptor antagonists. Today, this is the most frequently prescribed class of medical therapy (45.3%) followed by plant extracts (37.5%) who's market share decreased slightly since 1996. The market share of finasteride is also still decreasing and represents today 17.2% of all prescriptions. The growth in the alpha(1)-adrenoceptor antagonist segment can mainly be attributed to the introduction of tamsulosin in 1996. The price for medical therapy in France is around 1 Euro/day and is estimated to be around 229 million Euro in 1998. All drugs are reimbursed for 35% by the Social Insurance. The number of prostatectomies has declined in France in the 1990s. A national database includes information from events taking place in all hospitals in France. It appears that a total of 66,431 surgical procedures for the prostate were done in 1997 of which 81% were performed transurethrally and 14% open. Total direct costs involved with these surgical procedures were 229 million Euro. CONCLUSIONS: The costs involved in the management of symptomatic BPH in France are very high. However, there still exist no official guidelines defining for GPs and urologists in a shared care environment how this condition should be diagnosed and in which situations which medical therapies should be prescribed or when surgery is indicated. The French urological association is playing a key role in improving treatment of BPH. Several initiatives are underway to observe real life practice by developing a national database for urology, promote studies to evaluate cost/effectiveness of each therapy, define national guidelines of good practice and develop the shared care concept with GPs. Copyrightz1999S.KargerAG,Basel

Forecasting↗
PubMed1991

Symptomatic patent ductus arteriosus following prophylactic indomethacin. A clinical and biochemical appraisal.

Seven of 36 premature infants with birth weight less than 1,250 g who had been randomly assigned to either high-frequency ventilatory ventilation or conventional mechanical ventilation developed symptomatic patent ductus arteriosus (PDA) after receiving prophylactic indomethacin, 0.2 mg/kg, i.v. 24 h after birth. Infants who developed symptomatic PDA were more likely to be white and male and have more severe pulmonary insufficiency than infants who did not develop symptomatic PDA. Serum indomethacin levels were similar in both groups of patients. There was no difference in the degree of suppression or subsequent recovery of endogenous eicosanoid biosynthesis between infants who did and did not develop symptomatic PDA. Compared to conventional mechanical ventilation, high-frequency oscillatory ventilation had no significant effect on endogenous eicosanoid biosynthesis. The susceptibility of white male infants to symptomatic PDA following prophylactic indomethacin may represent the influence of maturational factors on ductus patency. Cyclooxygenase products do not appear to be involved in mediating ductus patency when symptomatic PDA occurs immediately following administration of prophylactic indomethacin.

Dinoprostone↗
PubMed2005

Increased apolipoprotein deposits in early atherosclerotic lesions distinguish symptomatic from asymptomatic patients.

OBJECTIVE: Apolipoprotein E (apoE) and apolipoprotein B100 (apoB) are both involved in receptor-mediated uptake of atherogenic lipoproteins by the liver. Inefficient hepatic clearance of these lipoproteins leads to symptomatic atherosclerosis. Using arterial tissue microarrays, we tested the hypothesis that apoE and apoB accumulation in the arterial wall discriminates between patients with symptomatic atherosclerosis and patients who never experienced cardiovascular events. METHODS AND RESULTS: In a postmortem study involving 49 patients (22 patients with symptomatic atherosclerosis), we quantified apolipoprotein deposits in arterial rings obtained from the left main coronary, the common carotid, the common iliac, and the renal artery applying tissue microarray technology and semiquantitative immunohistochemistry. In early atherosclerotic lesions, even before atheroma appeared, symptomatic patients had significantly more arterial apoE and apoB deposits than patients without cardiovascular events (P<0.001). Among the symptomatic patients, those without diabetes had more intense apolipoprotein deposits than diabetics. Large amounts of apoE and apoB were found in advanced atherosclerotic lesions, regardless of the activity of the disease. CONCLUSIONS: Increased apolipoprotein deposits are an early sign of symptomatic atherosclerosis. They may reflect either enhanced retention of atherogenic lipoproteins or impaired local apolipoprotein degradation. The arterial lipoprotein turnover may be different in diabetic patients.

Aged↗
PubMed1991

Flecainide acetate prevents recurrence of symptomatic paroxysmal supraventricular tachycardia. The Flecainide Supraventricular Tachycardia Study Group.

Oral flecainide acetate was administered to 34 patients with documented symptomatic paroxysmal supraventricular tachycardia (PSVT) with a double-blind, placebo-controlled, 8-week crossover trial design. PSVT was defined as a regular tachycardia of at least 120 beats/min without evidence of atrioventricular dissociation. The study required considerable patient cooperation. Patients first entered a 4-week qualifying phase followed by a 3-week, open label, flecainide dose-ranging phase. They were then randomized in a blind fashion to receive either placebo or tolerated flecainide dose for an 8-week treatment period and then crossed over after four symptomatic documented episodes of PSVT or at the end of the treatment period. By all efficacy parameters analyzed, flecainide was superior to placebo. Flecainide was associated with an actuarial 79% freedom from symptomatic PSVT events compared with only 15% on placebo at 60 days (p less than 0.001). Of the 34 patients, 29 had recurrence of symptomatic PSVT at least once during the placebo phase; only eight patients had a recurrence during the flecainide phase (p less than 0.001). The median time to the first symptomatic PSVT event was 11 days in the placebo group and greater than 55 days in the flecainide group (p less than 0.001). Likewise, the interval between attacks was a median of 12 days on placebo compared with more than 55 days on flecainide (p less than 0.001). Finally, the flecainide slowed symptomatic PSVT heart rates to 143 +/- 12 beats/min from 178 +/- 12 on placebo (p less than 0.02) in the seven patients who had events in the placebo and flecainide treatment phases.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1993

Spontaneous occurrence of symptomatic paroxysmal atrial fibrillation and paroxysmal supraventricular tachycardia in untreated patients.

BACKGROUND: Ambulatory outpatients (n = 150) with a history of paroxysmal supraventricular arrhythmia were studied to establish the characteristics of the first recurrence of symptomatic tachycardia (time to first recurrence, heart rate during tachycardia, and observed rhythm that was regular versus irregular) when no antiarrhythmic drug was being taken. Baseline variables were examined to assess their impact on time to first recurrence: index arrhythmia (paroxysmal atrial fibrillation [n = 37] versus paroxysmal supraventricular tachycardia [n = 113]), age (mean +/- SD, 43.3 +/- 16.1 years), female sex (n = 71), or presence of other heart or lung disease (n = 53). METHODS AND RESULTS: Transtelephonic monitoring of the ECG was used to document the rhythm during recurrences of symptomatic tachycardia. Time to first recurrence of symptomatic tachycardia and heart rate during tachycardia were measured, the observed rhythm was classified as irregular (consistent with paroxysmal atrial fibrillation) or regular (consistent with paroxysmal supraventricular tachycardia), and the hour of recurrence was recorded. Advancing age was significantly associated with a decreasing time to first recurrence (p < 0.001); the estimated increase in the hazard function was 25% with each 10 years of advancing age. After the effect of age was adjusted for, neither the classification of arrhythmia (p > 0.2), presence of other heart or lung disease (p > 0.8), nor sex (p > 0.9) was significantly associated with time to first recurrence. Among patients with paroxysmal supraventricular tachycardia, 6.5% had atrial fibrillation recorded at the next symptomatic arrhythmia; among patients with paroxysmal atrial fibrillation, 11.8% had a regular tachycardia recorded at the next symptomatic arrhythmia. There was a circadian pattern to the hour of occurrence of paroxysmal supraventricular tachycardia but not paroxysmal atrial fibrillation. CONCLUSIONS: Age is more important than other clinical variables, including the ECG classification of a paroxysmal supraventricular arrhythmia in predicting the occurrence of symptomatic arrhythmias. Arrhythmias documented by ECG during symptoms are often different from the arrhythmia documented at the time of referral, which may confound interpretation of antiarrhythmic drug effects.

Adult↗
PubMed1994

Asymptomatic arrhythmias in patients with symptomatic paroxysmal atrial fibrillation and paroxysmal supraventricular tachycardia.

BACKGROUND: Paroxysmal atrial fibrillation and paroxysmal supraventricular tachycardia are recognized clinically when patients seek treatment for symptoms due to recurrent arrhythmias; atrial fibrillation also increases the risk of stroke. The frequency with which asymptomatic arrhythmias occur in patients with these arrhythmias is unknown. METHODS AND RESULTS: Twenty-two patients with paroxysmal atrial fibrillation (n = 8) or paroxysmal supraventricular tachycardia (n = 14) were studied for 29 days with two different ambulatory ECG-monitoring techniques to measure the relative frequency of asymptomatic and symptomatic arrhythmias. All class I antiarrhythmic drugs, calcium channel blockers, beta-blockers, and digitalis were withheld. Sustained asymptomatic arrhythmia events (defined as lasting at least 30 seconds) were documented using continuous ambulatory ECG monitoring once weekly for a total of 5 of the 29 study days; symptomatic arrhythmia events were documented using transtelephonic ECG monitoring for all 29 days of the study. In the group of patients with paroxysmal atrial fibrillation, asymptomatic arrhythmia events occurred significantly more frequently than symptomatic arrhythmia events; the mean rates, expressed as events/100 d/patient (95% confidence interval), were 62.5 (40.4, 87.3) and 5.2 (2.7, 9.0) (P < .01); the ratio of the mean rates was 12.1 (5.8, 26.4). In contrast, in the group of patients with paroxysmal supraventricular tachycardia, asymptomatic arrhythmia events were significantly less frequent than symptomatic arrhythmia events; the mean rates were 0.0 (0.0, 5.3) and 7.4 (5.0, 10.6) (P = .02). The ratio of the mean rates was 0.0 (0.0, 0.8). CONCLUSIONS: In a group of patients with paroxysmal atrial fibrillation, sustained asymptomatic atrial fibrillation occurs far more frequently than symptomatic atrial fibrillation. However, it is not known whether asymptomatic atrial fibrillation is a potential risk factor for stroke even when patients are not having symptomatic arrhythmias.

Atrial Fibrillation↗
PubMed2004

Symptomatic and asymptomatic retinal embolism have different mechanisms.

PURPOSE: To investigate differences between symptomatic and asymptomatic retinal embolism regarding the frequency and source of cerebral microemboli. METHODS: Thirty-seven patients with transient monocular blindness or retinal infarction and 27 patients (29 eyes) with asymptomatic retinal embolism were prospectively enrolled. Patients underwent a transcranial Doppler study and noninvasive imaging of the cervical internal carotid arteries (ICA). The middle cerebral artery (MCA) ipsilateral to the affected eye was monitored for 30 minutes for microembolic signals (MES), which were saved and analyzed offline. Age-matched controls (n=15) had no history of retinal or brain ischemia, <50% ICA stenosis, and normal ophthalmologic examinations. RESULTS: MES were detected in 0/15 (0%) controls, 11/37 (30%) MCAs in the symptomatic group (P=0.02), and 3/29 (10%) MCAs in the asymptomatic group (P=0.54). Nine of 11 (82%) symptomatic eyes with MES had ipsilateral ICA stenosis of > or =50%, as compared with 0/3 (0%) eyes in the asymptomatic group with MES (P=0.03). Both MES and ICA stenosis of >50% were present in 9/37 (24%) cases in the symptomatic and in 0/29 (0%) cases of the asymptomatic group (P=0.0036). CONCLUSIONS: The frequency and potential source of cerebral microemboli in symptomatic and asymptomatic retinal embolism are different. Cerebral microemboli are more frequent in symptomatic patients and are associated with ICA stenosis.

Aged↗
PubMed2005

Silent myocardial ischemia in patients with symptomatic intracranial atherosclerosis: associated factors.

BACKGROUND AND PURPOSE: Optimization of coronary risk evaluation in stroke patients has been encouraged. The relationship between symptomatic intracranial atherosclerosis and occult coronary artery disease (CAD) has not been evaluated sufficiently. We aimed to investigate the prevalence of silent myocardial ischemia in patients with symptomatic intracranial atherosclerosis and to identify factors associated with its presence. METHODS: From 186 first-ever transient ischemic attack or ischemic stroke patients with intracranial stenoses, 65 fulfilled selection criteria, including angiographic confirmation of a symptomatic atherosclerotic stenosis and absence of known CAD. All patients underwent a maximal-stress myocardial perfusion single-photon emission computed tomography (SPECT). Lipoprotein(a) [Lp(a)], C-reactive protein, and homocysteine (Hcy) levels were determined before SPECT. RESULTS: Stress-rest SPECT detected reversible myocardial perfusion defects in 34 (52%) patients. Vascular risk factors associated with a pathologic SPECT were hypercholesterolemia (P=0.045), presence of >2 risk factors (P=0.004) and high Lp(a) (P=0.023) and Hcy levels (P=0.018). Ninety percent of patients with high Lp(a) and Hcy levels had a positive SPECT. Existence of a stenosed intracranial internal carotid artery (ICA; odds ratio [OR], 7.22, 2.07 to 25.23; P=0.002) and location of the symptomatic stenosis in vertebrobasilar arteries (OR, 4.89, 1.19 to 20.12; P=0.027) were independently associated with silent myocardial ischemia after adjustment by age, sex, and risk factors. CONCLUSIONS: More than 50% of the patients with symptomatic intracranial atherosclerosis and not overt CAD show myocardial perfusion defects on stress-rest SPECT. Stenosed intracranial ICA, symptomatic vertebrobasilar stenosis and presence of high Lp(a) and Hcy levels may characterize the patients at a higher risk for occult CAD.

Aged↗
PubMed1993

Carotid stenosis and perioperative stroke risk in symptomatic and asymptomatic patients undergoing vascular or coronary surgery.

BACKGROUND AND PURPOSE: The management of asymptomatic carotid stenosis found before vascular or coronary surgery is unclear from the literature. We aimed to define the relation of carotid stenosis to perioperative stroke in all patients, symptomatic and asymptomatic, and so determine a policy for the management of asymptomatic carotid stenosis in patients requiring major surgery. METHODS: We conducted a prospective clinical and Duplex ultrasound study of 358 consecutive noncarotid major vascular or coronary artery bypass operations, with a moratorium on endarterectomy for asymptomatic carotid stenosis. RESULTS: There were 145 vascular and 213 coronary bypass operations. Ten of the 49 cases with prior symptoms of cerebral ischemia (38 carotid, 11 vertebrobasilar) had symptomatic stenosis of 50% or greater or occlusion, and 3 of these (30%) had ipsilateral perioperative cerebral infarction (95% confidence interval, 6.67% to 65.25%). Two of these occurred ipsilateral to symptomatic carotid occlusions, and 1 occurred ipsilateral to an 80% symptomatic stenosis. One symptomatic patient with bilateral 30% stenosis had a perioperative infarct in the asymptomatic hemisphere. Among the 309 asymptomatic patients, 1 perioperative infarct occurred ipsilateral to carotid stenosis of 30%. In all there were 5 (1.4%) perioperative (within 72 hours) and 2 late (after 18 days) strokes. All strokes were hemisphere infarcts confirmed by computed tomography. There were 53 cases with 50% or greater asymptomatic carotid stenosis or occlusion, including 28 with 80% or greater stenosis or occlusion. None had an ipsilateral perioperative stroke (95% confidence interval, 0% to 6.72%). CONCLUSIONS: We conclude that the risk of perioperative stroke related to symptomatic carotid stenosis may be high, but for asymptomatic carotid stenosis the risk is low and does not justify preoperative prophylactic carotid endarterectomy.

Aged↗
PubMed1996

Transcranial Doppler assessment of cerebrovascular reactivity in symptomatic and asymptomatic severe carotid stenosis.

BACKGROUND AND PURPOSE: Some studies have suggested a link between impaired cerebral hemodynamics and stroke in patients with carotid stenosis. The aim of this study was to assess the effects of severe carotid stenosis on cerebrovascular reactivity and the possible changes after endarterectomy. METHODS: Using bilateral transcranial Doppler ultrasound, we studied the changes of flow velocity after hypercapnia in the middle cerebral arteries of 10 control subjects and 24 patients (13 symptomatic and 11 asymptomatic) with unilateral severe carotid stenosis before and after endarterectomy. Cerebrovascular reactivity was evaluated with the breath-holding index (BHI). RESULTS: Before endarterectomy, BHI (mean value +/- SD) was significantly lower (P < .001) in the stenotic side of symptomatic patients (0.40 +/- 0.2) than in control subjects (1.12 +/- 0.3), the stenotic side of asymptomatic patients (0.80 +/- 0.4), and the normal side of both symptomatic (0.93 +/- 0.3) and asymptomatic ultrasonics (1.03 +/- 0.2) patients. On the other hand, no significant difference in BHI was detected in control subjects, on the normal side of symptomatic and asymptomatic patients, and the stenotic side of asymptomatic patients. After endarterectomy, BHI significantly increased (P < .0001) on the stenotic side of symptomatic patients (1.06 +/- 0.2) while remaining substantially stable on the normal side of both symptomatic and asymptomatic patients and on the stenotic side of asymptomatic patients. CONCLUSIONS: These findings suggest that the study of cerebrovascular reactivity to hypercapnia may be relevant in evaluating the functional effects of carotid stenosis. Further investigations are needed to confirm the reliability of the breath-holding method in the selection of patients who might benefit most from carotid endarterectomy.

Aged↗
PubMed2000

The symptomatic carotid plaque.

BACKGROUND: The natural histories of equally severe symptomatic and asymptomatic carotid stenoses are very different, which suggests dichotomy in plaque behavior. The vascular biology of the symptomatic carotid plaque is presented in this review. SUMMARY OF REVIEW: Histology studies comparing asymptomatic and symptomatic plaques were identified from MEDLINE. Reports in which stenosis severity was not stated or not similar for symptomatic and asymptomatic patients were excluded. In vitro studies and reports from the coronary circulation were reviewed with regard to the vascular biology of the plaque. Histology studies comparing carotid plaques removed from symptomatic and asymptomatic patients reveal characteristic features of unstable plaques: surface ulceration and plaque rupture (48% of symptomatic compared with 31% of asymptomatic, P<0.001), thinning of the fibrous cap, and infiltration of the cap by greater numbers of macrophages and T cells. In vitro studies suggest that macrophages and T cells release cytokines and proteinase, which stimulate breakdown of cap collagen and smooth muscle cell apoptosis and thereby promote plaque rupture. CONCLUSIONS: Infiltration of inflammatory cells to the surface of carotid plaques may be a critical step in promoting plaque rupture and resultant embolization or carotid occlusion. Further understanding of cell recruitment and behavior in carotid atherosclerosis may allow better detection of unstable plaques and therapeutic methods of plaque stabilization.

Carotid Arteries↗
PubMed2001

Presence of Chlamydia pneumoniae in human symptomatic and asymptomatic carotid atherosclerotic plaque.

BACKGROUND: Chlamydia pneumoniae has been identified in atherosclerotic plaques of patients with cerebrovascular and cardiovascular disease. However, the direct causative effect of C pneumoniae infection in the activation of atherosclerotic plaque to a prothrombotic state remains to be established. The aim of the present study is to examine the correlation between intraplaque presence of chlamydiae and symptomatic carotid disease in humans. METHODS: Plaques from 37 symptomatic and 57 asymptomatic consenting patients undergoing carotid endarterectomy were snap-frozen, and the tissue was prepared for polymerase chain reaction analysis for Chlamydia pneumoniae per Institutional Review Board-approved protocol. Blood was drawn from each patient at the time of surgery for serological analysis. RESULTS: The overall rate of plaques positive for C pneumoniae was 14.82%, with 5 of 37 (13.5%) plaques from symptomatic patients and 9 of 57 (15.8%) from asymptomatic patients, which revealed a definitive presence of the organism. No association existed between C pneumoniae presence and symptomatic disease (P:=1.0). Also, no association existed between presence of C pneumoniae and severity of stenosis. Finally, seropositivity for anti-chlamydial IgG, IgA, and IgM anti-chlamydial antibodies did not correlate with identification of C pneumoniae in the plaques. However, high-serum anti-chlamydial IgA levels (>/=1:128) were associated with occurrence of symptomatic disease (P=0.03; odds ratio, 2.86; 95% CI, 1.12 to 7.28). CONCLUSIONS: Presence of C pneumoniae as a single factor does not appear to be sufficient to explain the occurrence of cerebrovascular symptoms. Low sensitivity of seropositivity for IgG, IgA, or IgM associated with PCR-identified C pneumoniae presence in the plaque makes it unlikely to be valuable as the single determining factor for actively infected plaque. Association of high-level anti-chlamydial IgA with symptomatic disease suggests that chronic or acute chlamydial infection anywhere in the body could play a role in atherosclerotic plaque activation and be used as a marker to target populations in future stroke prevention trials.

Aged↗
PubMed2001

Overexpression of functionally coupled cyclooxygenase-2 and prostaglandin E synthase in symptomatic atherosclerotic plaques as a basis of prostaglandin E(2)-dependent plaque instability.

BACKGROUND: Studies have implicated a role for prostaglandin (PG) E(2)-dependent matrix metalloproteinase (MMP) biosynthesis in the rupture of atherosclerotic plaque. Cyclooxygenase-2 (COX-2) and PGE synthase (PGES) are coregulated in nucleated cells by inflammatory stimuli. The aim of this study was to characterize the expression of COX-2 and PGES in carotid plaques and to correlate it with the extent of inflammatory infiltration and MMP activity and with clinical features of patients' presentation. METHODS AND RESULTS: Plaques were obtained from 50 patients undergoing carotid endarterectomy and divided into 2 groups (symptomatic and asymptomatic) according to clinical evidence of recent transient ischemic attack or stroke. Plaques were analyzed for COX-2, PGES, MMP-2, and MMP-9 by immunocytochemistry and Western blot, whereas zymography was used to detect MMP activity. Immunocytochemistry was used to identify CD68+ macrophages, CD3+ T lymphocytes, and HLA-DR+ cells. The percentage of macrophage-rich areas was larger (P<0.0001) in symptomatic plaques. COX-2, PGES, and MMPs were detected in all specimens; enzyme concentration, however, was significantly higher in symptomatic plaques. COX-2, PGES, and MMPs were especially noted in shoulders of symptomatic plaques, colocalizing with HLA-DR+ macrophages. All symptomatic plaques contained activated forms of MMPs. Finally, inhibition of COX-2 by NS-398 was accompanied by decreased production of MMPs that was reversed by PGE(2). CONCLUSIONS: This study demonstrates the colocalization of COX-2 and PGES in symptomatic lesions and provides evidence that synthesis of COX-2 and PGES by activated macrophages is associated with acute ischemic syndromes, possibly through metalloproteinase-induced plaque rupture.

Aged↗
PubMed1999

The relationship of skin test positivity, high serum total IgE levels, and peripheral blood eosinophilia to symptomatic and asymptomatic airway hyperresponsiveness.

The relationships of skin test positivity, high serum total IgE levels (> 100 kU/L), and peripheral blood eosinophilia (>/= 275 cells/microliter) to symptomatic (either chronic cough, chronic phlegm, bronchitis episodes, dyspnea, wheeze, or asthma) and asymptomatic bronchial hyperresponsiveness (BHR) were studied cross-sectionally in 620 adult subjects who participated in the Vlagtwedde-Vlaardingen Study of 1989 and 1990. Eosinophilia (OR = 2.06, 95% CI = 1.28 to 3.31) and skin test positivity (OR = 1.66, 95% CI = 1.02 to 2.71) were both significantly associated with BHR independent of age, sex, smoking, and urban area of residence. High serum total IgE levels were not associated with BHR (OR = 1.29, 95% CI = 0.81 to 2.03). Separate analyses for symptomatic and asymptomatic subjects showed that the higher risk of BHR with skin test positivity applied only to symptomatic subjects (OR = 5.78, 95% CI = 1.63 to 20.51), independent of eosinophilia and high serum total IgE levels. The higher risk of BHR with eosinophilia was not different between symptomatic and asymptomatic subjects, and independent of skin test positivity and high serum total IgE levels. The results of this study show that, in the general adult population, eosinophilia is associated with BHR both in symptomatic and asymptomatic persons, whereas skin test positivity is associated with BHR only in symptomatic subjects.

Adult↗
PubMed1992

Acute health effects of PM10 pollution on symptomatic and asymptomatic children.

This study assessed the association between daily changes in respiratory health and respirable particulate pollution (PM10) in Utah Valley during the winter of 1990-1991. During the study period, 24-h PM10 concentrations ranged from 7 to 251 micrograms/m3. Participants included symptomatic and asymptomatic samples of fifth- and sixth-grade students. Relatively small but statistically significant (p less than 0.01) negative associations between peak expiratory flow (PEF) and PM10 were observed for both the symptomatic and asymptomatic samples. The association was strongest for the symptomatic children. Large associations between the incidence of respiratory symptoms, especially cough, and PM10 pollution were also observed for both samples. Again the association was strongest for the symptomatic sample. Immediate and delayed PM10 effects were observed. Respiratory symptoms and PEF changes were more closely associated with 5-day moving-average PM10 levels than with concurrent-day levels. These associations were also observed at PM10 levels below the 24-h standard of 150 micrograms/m3. This study indicates that both symptomatic and asymptomatic children may suffer acute health effects of respirable particulate pollution, with symptomatic children suffering the most.

Air Pollution↗