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PubMed2004

Incidence of postdischarge symptomatic paroxysmal atrial fibrillation in patients who underwent coronary artery bypass graft: long-term follow-up.

The aim of this retrospective study was to determine the incidence of symptomatic AF of patients who had undergone coronary artery bypass grafting (CABG) during long-term follow-up. The study population included 305 post-CABG patients who were regularly followed in the outpatient clinic. Paroxysmal AF (PAF) was defined as an episode of symptomatic AF when symptoms were prolonged enough for the patient to request medical care. Perioperative AF occurred in 88 (28.9%) patients. Postdischarge symptomatic PAF occurred in 25 (8.2%) patients with an annual incidence of 2% during a mean follow-up of 48 +/- 30 months. Eighteen (20.4%) patients also experienced perioperative AF with an annual incidence of 5.1%, while only 7 (3.2%) of 217 patients, without perioperative AF, had postdischarge AF (P < 0.0003). During long-term follow-up, postdischarge AF has a low incidence and prophylactic antiarrhythmic therapy is not recommended. The method of follow-up and retrospective analysis may understate PAF and even miss some symptomatic episodes. Perioperative AF is a predictor of symptomatic late PAF recurrences, particularly in patients with reduced left ventricular function.

Aged↗
PubMed2006

Event-recorder monitoring in the diagnosis of atrial fibrillation in symptomatic patients: subanalysis of the SOPAT trial.

In the SOPAT (suppression of paroxysmal atrial tachyarrhythmias) trial, a high number of asymptomatic atrial fibrillation (AF) episodes were registered in patients with symptomatic AF. This subanalysis was performed to answer three questions: (1) Does antiarrhythmic therapy influence the ratio of symptomatic to asymptomatic AF? (2) Are symptoms during AF dependent on the heart rate (HR)? (3) Do symptoms correlate with an episode of AF? Within 60 months 1,033 patients with symptomatic AF were randomized to either quinidine plus verapamil (Q+V) 480/240 mg/day, Q+V 320/160 mg/day, sotalol 320 mg/day, or placebo, and followed up by daily and symptom-triggered ECG event recording. Over 188,634 ECGs were analyzed (87% SR, 7% AF). Symptoms were reported in only 46% of AF-ECGs. Quinidine plus verapamil reduced the ratio of symptomatic to asymptomatic AF, whereas sotalol had no effect (median [%] (25/75% quartile): Q+V 480/240: 33 (0/79), Q+V 320/160: 45 (1/82), sotalol: 56 (7/93), placebo: 63 (8/92)). The HR during AF directly correlates with the occurrence of symptoms (P < 0.001) and was significantly lower during asymptomatic AF in all groups (mean +/- SD: sympt.: 113 +/- 27/minute, asympt.: 103 +/- 27/minute, P < 0.001). Both antiarrhythmics reduced the mean HR compared to placebo (P < 0.001). Analyzing all symptom-triggered ECGs, AF was diagnosed in only 37%, whereas the majority were SR. Taken together, in contrast to sotalol, Q+V reduces the ratio of symptomatic to asymptomatic AF compared with placebo, at least in part by decreasing the heart rate. Furthermore, patients' symptoms are not a reliable surrogate parameter for the prevalence of AF.

Anti-Arrhythmia Agents↗
PubMed2006

Endoscopic gallbladder stent placement for treatment of symptomatic cholelithiasis in patients with end-stage liver disease.

OBJECTIVES: Symptomatic cholelithiasis is a common disease in the general population with an increased prevalence in patients with cirrhosis. While cholecystectomy is the procedure of choice for the treatment of symptomatic cholelithiasis, cirrhotics have an increased risk of complications associated with this therapy. We have found that placement of an endoscopic gallbladder stent is an alternative, less invasive treatment for cirrhotic patients with symptomatic gallbladder disease and describe our experience here. METHODS: A retrospective medical record review of 23 patients with cirrhosis who underwent endoscopic retrograde cholangiography with gallbladder stent placement for symptomatic gallbladder disease from July 1994 to August 2004. RESULTS: Indications for stent placement included recurrent biliary colic (56.5%), acute calculous cholecystitis (39%), acalculous cholecystitis (8.6%), and gallstone pancreatitis (8.6%). All patients experienced resolution of their symptoms following stent placement. Twenty patients (87%) were asymptomatic from 5 days to 3 years post-procedure until transplantation, death, or end of study period. Nine patients (39%) underwent liver transplantation, 5 days to 34 months after the procedure. Eleven patients are well, with ten patients awaiting liver transplantation. Three patients developed late complications and were treated successfully with antibiotics. CONCLUSION: Endoscopic stenting of the gallbladder may be a potential treatment for symptomatic gallbladder disease in patients with cirrhosis awaiting liver transplantation, considered to be high-risk for cholecystectomy.

Adult↗
PubMed1981

Early prediction of symptomatic patent ductus arteriosus from perinatal risk factors: a discriminant analysis model.

A scoring system based on discriminant analysis was devised to predict, within 24 hours after birth, whether or not a premature infant will subsequently develop a symptomatic PDA. Five risk factors including birth weight, the diagnosis of hyaline membrane disease, intrauterine growth retardation, acute perinatal stress, and treatment with distending airway pressure were reduced to a discriminant score which separated infants with symptomatic PDA from infants without symptomatic PDA. Based on this score, the likelihood that an individual infant would later develop symptomatic PDA could be expressed as a probability function. When applied prospectively, this score predicted the correct outcome of 80% of infants in a test population. This predictive model should be useful in clinical trials and other applications requiring a quantitative expression of risk for developing symptomatic ductus shunting.

Birth Weight↗
PubMed2002

Immunological responses are not abnormal in symptomatic Gulf War veterans.

The underlying etiology and pathogenesis of Gulf War veterans' illnesses continue to be under intense investigation. Reports have suggested the basis for these illnesses may be an altered immune system, but compelling evidence is lacking. We sought to determine whether in vitro immune responses were abnormal in symptomatic Gulf War veterans relative to matched controls. A randomized case-control study was conducted by blinded comparison of laboratory measures of in vitro immune responses in blood samples obtained from veterans in an outpatient facility of a Veterans Affairs medical center. Symptomatic Gulf War veterans with otherwise undefined illnesses (52 symptomatic subjects), asymptomatic Gulf War veterans (31 asymptomatic controls), and veterans who had applied for disability compensation and had not participated in the Gulf War (21 disability controls) represented the volunteer sample. In vitro cellular and humoral immune responses were measured to detect functional abnormalities in antigen presenting cells (autologous mixed leukocyte reactions and expression of interleukin (IL)-1beta, IL-6, IL-10, and tumor necrosis factor-alpha); T cells (lymphocyte proliferation using the polyclonal T-cell activators phytohemagglutinin and Concanavalin A; primary immune responses in allogeneic mixed leukocyte reactions; secondary immune response using the recall antigens tetanus toxoid, Candida albicans, and anthrax vaccine; and soluble IL-2 receptor expression); type-1 T-helper cells (gamma interferon expression); type-2 T-helper cells (IL-4 and IL-10 expression); and B cells (polyclonal B-cell activator pokeweed mitogen-induced immunoglobulin production). In general, immune response measures did not differ significantly between groups. Heightened responses observed in the disability control group (sporadically greater responses to one mitogen and two antigens) and the Gulf War participation control group (greater recall responses to anthrax vaccine) did not suggest impaired immune cell function in symptomatic veterans when compared with controls. We conclude that in vitro immunological responses are not abnormal in symptomatic Gulf War veterans.

Adult↗
PubMed2005

Evaluation of enzyme-linked immunosorbent assays, an immunofluorescent-antibody test, and two rapid tests (immunochromatographic-dipstick and gel tests) for serological diagnosis of symptomatic and asymptomatic Leishmania infections in dogs.

Enzyme-linked immunosorbent assays (ELISAs) based on soluble antigens derived from promastigote or amastigote-like stages of Leishmania infantum and on the recombinant rK39 antigen, each in combination with different conjugates [anti-immunoglobulin G1 [IgG1], anti-IgG2, anti-IgG(gamma), and anti-IgG heavy plus light chains], were compared to an immunofluorescent-antibody test (IFAT) and two commercially available rapid test systems (DiaMed-Vet-IT Leish and ID-PaGIA canine leishmaniasis antibody test) for the detection of specific anti-Leishmania antibodies in symptomatic and asymptomatic dogs with proven L. infantum infections. ELISAs based on soluble promastigote and amastigote antigens had very high sensitivities in symptomatic (n = 30; 100%) and asymptomatic dogs (n = 17; 94.1 to 100%), except when combined with the anti-IgG1 conjugate (41.2 to 82.4%). Specificities were high for all combinations (n = 50; 96 to 100%). The rK39 ELISA detected fewer asymptomatic cases (sensitivities, 52.9 to 64.7%) but was highly specific (96 to 100%). The IFAT was 90% sensitive in symptomatic dogs but was significantly less sensitive in asymptomatic cases (29.4%). However, it had an excellent specificity (100%). Test performances of the rapid tests based on the rK39 antigen were comparable to the ELISAs based on the same antigen. ELISAs based on soluble promastigote or amastigote antigens seem to be most suited for the serological diagnosis of canine Leishmania infections in both symptomatic and asymptomatic dogs. IFAT and the rK39 ELISA lack sensitivity in asymptomatic cases but are highly specific. Rapid tests like the rK39 dipstick test or the ID-PaGIA are helpful for confirming clinically suspected cases because of their high specificities in symptomatic animals.

Animals↗
PubMed1988

Sequence of the fourth gene of human rotaviruses recovered from asymptomatic or symptomatic infections.

The complete nucleotide sequence of the fourth gene of symptomatic (Wa, DS-1, P, and VA70) and asymptomatic (M37, 1076, McN13, and ST3) rotaviruses of serotype 1, 2, 3, or 4 was determined by the dideoxy chain termination method. In each strain, the fourth gene, which encodes the outer capsid protein VP3, is 2,359 base pairs in length and has 5'- and 3'-noncoding regions of 9 and 25 nucleotides, respectively. The gene has a single long open reading frame of 2,325 base pairs that is capable of coding for a protein of 775 amino acids. A total of 14 N-terminal and 12 C-terminal amino acids are completely conserved or almost completely conserved, respectively, among nine human rotavirus VP3 genes that have been sequenced. In addition, there is conservation of arginine at the two trypsin cleavage sites as well as conservation of clusters of amino acids in different regions of the two VP3 cleavage products, VP8 and VP5. Three distinct forms of VP3 were identified among the nine human rotavirus strains analyzed. Three symptomatic rotaviruses (serotypes 1, 3, and 4) possess highly related VP3 genes (92.2 to 97% nucleotide identity). Two symptomatic serotype 2 rotaviruses possess VP3 genes which are even more closely related to each other (98.6% nucleotide identity) and only moderately related to the aforementioned VP3 genes of serotypes 1, 3, and 4 (87.4 to 88.2% nucleotide identity). The four asymptomatic rotaviruses, which constitute the third group, possess highly related VP3 genes (95.5 to 97.5% nucleotide identity) which are distinct from those of the virulent rotaviruses (73 to 74.8% nucleotide identity). At 91 positions in the protein sequence of VP3, an amino acid is conserved among the asymptomatic rotaviruses, while a different amino acid is conserved among the symptomatic rotaviruses. Notably, five regions are conserved among the symptomatic rotaviruses, while a different set of sequences are conserved among the asymptomatic rotaviruses. It is possible that some or all of these regions of sequence dimorphism may be responsible for the difference in virulence of these two groups of human rotaviruses. There are 13 regions in the VP3 protein sequence which exhibit the greatest variability; the majority of these variable regions are observed between amino acids 106 to 192. These regions may represent potential antigenic sites related to heterotypic rotavirus neutralization.

Amino Acid Sequence↗
PubMed1994

Differences in autonomic nerve function in patients with silent and symptomatic myocardial ischaemia.

BACKGROUND: Autonomic neuropathy provides a mechanism for the absence of symptoms in silent myocardial ischaemia, but characterisation of the type of neuropathy is lacking. AIM: To characterise and compare autonomic nerve function in patients with silent and symptomatic myocardial ischaemia. METHODS AND RESULTS: The Valsalva manoeuvre, heart rate variation (HRV) in response to deep breathing and standing, lower body negative pressure, isometric handgrip, and the cold pressor test were performed by patients with silent (n = 25) and symptomatic (n = 25) ambulatory ischaemia and by controls (n = 21). No difference in parasympathetic efferent function between patients with silent and symptomatic ischaemia was recorded, but both had significantly less HRV in response to standing than the controls (p < 0.005 for silent and p < 0.01 for symptomatic). Patients with silent ischaemia showed an increased propensity for peripheral vasodilatation compared with symptomatic patients (p < 0.02) and controls (p < 0.04). Impaired sympathetic function was found in patients with pure silent ischaemia (n = 4) compared with the remaining patients with silent ischaemia whose pain pathways were presumed to be intact. CONCLUSIONS: Patients with silent ischaemia and pain pathways presumed to be intact have an enhanced peripheral vasodilator response, and if this applied to the coronary vasculature it could provide a mechanism for limiting ischaemia to below the pain threshold. Patients with pure silent ischaemia have evidence of sympathetic autonomic dysfunction.

Autonomic Nervous System↗
PubMed1999

Time course of symptomatic orthostatic hypotension and urinary incontinence in patients with postmortem confirmed parkinsonian syndromes: a clinicopathological study.

OBJECTIVE: Although both orthostatic hypotension and urinary incontinence have been reported in a number of parkinsonian syndromes, such as Parkinson's disease (PD), multiple system atrophy (MSA), dementia with Lewy bodies (DLB), corticobasal degeneration (CBD), and progressive supranuclear palsy (PSP), differences in the evolution of these features have not been studied systematically in pathologically confirmed cases. METHODS: 77 cases with pathologically confirmed parkinsonian syndromes (PD, n=11; MSA, n=15; DLB, n=14; CBD, n=13; PSP, n=24), collected up to 1994, formed the basis for a multicentre clinicopathological study organised by the NINDS to improve the differential diagnosis of parkinsonian disorders. The present study determined the time course-that is, latency to onset and duration from onset to death, of symptomatic orthostatic hypotension, and urinary incontinence in the NINDS series. Furthermore, the diagnostic validity of a predefined latency to onset within 1 year of disease onset of symptomatic orthostatic hypotension or urinary incontinence was analysed. RESULTS: Significant group differences for latency, but not duration, of symptomatic orthostatic hypotension and urinary incontinence were found. Latencies to onset of either feature were short in patients with MSA, intermediate in patients with DLB, CBD, and PSP, and long in those with PD. Symptomatic orthostatic hypotension occurring within the first year after disease onset predicted MSA in 75% of cases; early urinary incontinence was less predictive for MSA (56%). CONCLUSION: Latency to onset, but not duration, of symptomatic orthostatic hypotension or urinary incontinence differentiates PD from other parkinsonian syndromes, particularly MSA.

Age of Onset↗
PubMed2001

Symptomatic HIV seroconverting illness is associated with more rapid neurological impairment.

OBJECTIVES: To establish whether symptomatic seroconverting illness in HIV infected people is associated with more rapid development of neurological impairment. METHODS: 166 HIV infected subjects with a known date of HIV infection enrolled in a longitudinal study of neurocognitive function were stratified by whether or not they had experienced a symptomatic serconverting illness. RESULTS: 29 of 166 (17.5%) dated HIV seroconverters had a history of symptomatic seroconverting illness. Though baseline neurocognitive function was similar, subjects with a symptomatic seroconverting illness developed clinical neurocognitive impairment significantly more rapidly than their asymptomatic counterparts in a survival analysis model (636 v 1075 days till impaired). CONCLUSION: Symptomatic seroconverting illness predisposes to more rapid neurocognitive impairment.

AIDS Dementia Complex↗
PubMed2000

Elective versus symptomatic antibiotic treatment in cystic fibrosis patients with chronic Pseudomonas infection of the lungs.

BACKGROUND: A previous retrospective study suggested that a policy of regular anti-pseudomonal antibiotic treatment improved pulmonary function and increased survival in patients with cystic fibrosis chronically infected with Pseudomonas species. The results of a prospective multicentre study to compare the effects on pulmonary function and mortality of three monthly elective anti-pseudomonal antibiotic treatment with conventional symptomatic treatment are reported. METHODS: Sixty patients with cystic fibrosis, chronically infected with P aeruginosa, were randomised to the two treatment arms (elective or symptomatic) and followed clinically at yearly reviews. The major end points were changes in forced expiratory volume in one second (FEV(1)) and forced vital capacity (FVC). Survival was a secondary end point. RESULTS: Patients in the symptomatic group received a mean of three antibiotic treatments each year and those in the elective group received four antibiotic treatments during each year of the study. No significant differences in FEV(1) and FVC were found between the two groups after three years. There was a statistically non-significant higher rate of deaths in the elective group (n = 4), three of which were associated with B cepacia infection, compared with the symptomatic group (n = 0). CONCLUSIONS: This study did not demonstrate an advantage of a policy of elective antibiotic treatment over symptomatic treatment in patients with cystic fibrosis chronically infected with Pseudomonas species.

Adolescent↗
PubMed2006

Revascularization compared to medical treatment in patients with silent vs. symptomatic residual ischemia after thrombolyzed myocardial infarction--the DANAMI study.

AIMS: The aim was to compare the effect of revascularization to conservative treatment in patients with residual silent and with residual symptomatic ischemia following acute myocardial infarction (AMI). The study was a subanalysis of the DANAMI (DANish AMI) randomized study of invasive vs. conservative treatment in patients with inducible ischemia after thrombolysis in AMI. METHODS AND RESULTS: One thousand and eight patients were randomized to invasive or conservative treatment, stratified by the type of ischemia: silent, i.e. ST depression during an exercise test prior to discharge in 56%, or symptomatic, i.e. chest pain occurring either spontaneously during admission or during the exercise test, with or without ST changes, in 44%. Compared to a conservative strategy, invasive treatment reduced the incidence of nonfatal reinfarction, after in median 2.4 years, in both symptomatic patients (13.3-7.2%, p < 0.006) and patients with silent ischemia (10.1 vs. 5.7%, p < 0.05), and of admissions with unstable angina in symptomatic (44.5-27.6%, p < 0.0001) and silent ischemia (21.6-13.3%, p < 0.0006). CONCLUSIONS: Compared to conservative strategy, invasive treatment reduces the risk of nonfatal reinfarction and hospital admissions for unstable angina in thrombolyzed post-AMI patients with silent as well as symptomatic exercise-induced ischemia.

Aged↗
PubMed2004

Arterial neovascularization and inflammation in vulnerable patients: early and late signs of symptomatic atherosclerosis.

BACKGROUND: Atherosclerosis is complicated by cardiovascular events such as myocardial infarction, stroke, or peripheral arterial occlusive disease. Inflammation and pathological neovascularization are thought to precipitate plaque rupture or erosion, both causes of arterial thrombosis and cardiovascular events. We tested the hypothesis that arterial inflammation and angiogenic events are increased throughout the arterial tree in vulnerable patients, ie, in patients who suffered from cardiovascular events, compared with patients who never suffered from complications of atherosclerosis. METHODS AND RESULTS: In a postmortem study, we quantified the inflammatory infiltrate and microvascular network in the arterial wall of iliac, carotid, and renal arteries. Tissue microarray technology was adapted to investigate full-thickness arterial sectors. We compared 22 patients with symptomatic atherosclerosis with 27 patients who never had suffered from any cardiovascular event. The absolute intimal macrophage content was 2- to 4-fold higher in vulnerable patients at all 3 arterial sites analyzed (P<0.05). Patients with symptomatic atherosclerosis had a denser network of vasa vasorum than patients with asymptomatic disease (33+/-2 versus 25+/-2 adventitial microvessels per 1 mm2; P=0.008). Hyperplasia of vasa vasorum was an early and macrophage infiltration was a late sign of symptomatic atherosclerosis. CONCLUSIONS: High intimal macrophage content and a hyperplastic network of vasa vasorum characterize vulnerable patients suffering from symptomatic atherosclerosis. These changes are uniformly present in different arterial beds and support the concept of symptomatic atherosclerosis as a panarterial disease.

Aged↗
PubMed2004

Osteoprotegerin and osteopontin are expressed at high concentrations within symptomatic carotid atherosclerosis.

BACKGROUND AND PURPOSE: The aim of this study was to compare the concentration of osteoprotegerin (OPG), receptor activator of nuclear factor kappaB ligand (RANKL), and osteopontin (OPN) in stable (asymptomatic) and unstable (symptomatic) carotid atherosclerosis. In addition, we were interested in the effect of angiotensin II blockade on the secretion of these proteins by unstable atherosclerosis. METHODS: Endarterectomy samples removed from patients with recent (within 6 weeks) or no previous focal neurological symptoms were assessed by immunohistochemistry, Western analysis, and explant culture. Concentrations of OPG, RANKL, and OPN were measured by mean optical density (MOD), densitometry of protein bands, and enzyme-linked immunosorbent assay of supernatants from explant culture, and compared between symptomatic and asymptomatic patients. RESULTS: The concentration of OPG and OPN within the proximal internal carotid (PIC) part of the endarterectomy specimen removed from symptomatic patients was elevated 2- and 4-fold, respectively. Although the concentration of RANKL did not differ according to patients' symptoms, the quantity of OPG secreted by explants of the PIC was greater in explants from symptomatic patients and could be significantly reduced within 48 hours of incubation with the angiotensin II blocker irbesartan. CONCLUSIONS: OPG and OPN are upregulated in symptomatic human carotid atherosclerosis with possible implications for plaque stability. Angiotensin II blockade is able to downregulate OPG secretion in vitro.

Aged↗
PubMed1996

A systematic comparison of the risks of stroke and death due to carotid endarterectomy for symptomatic and asymptomatic stenosis.

BACKGROUND AND PURPOSE: There is some evidence that carotid endarterectomy reduces the risk of ipsilateral carotid territory ischemic stroke in patients with severe asymptomatic carotid stenosis. However, the benefit of endarterectomy is dependent on a low risk of stroke and/or death due to surgery. Whether the low operative risks reported in recent clinical trials and cited in recent guidelines are widely generalizable to clinical practice is unclear. Is endarterectomy for asymptomatic carotid stenosis really safer than surgery for recently symptomatic stenosis? METHODS: We performed a systematic review comparing the risks of stroke and death due to carotid endarterectomy, performed by the same surgeons or in the same institutions, for symptomatic and asymptomatic stenosis in studies published since 1980. RESULTS: Twenty-five studies fulfilled our criteria. Mortality within 30 days of endarterectomy was 1.31% for asymptomatic stenosis and 1.81% for symptomatic stenosis (odds ratio [OR], 0.69; 95% confidence interval [CI], 0.49 to 0.99). The risks of fatal stroke were 0.47% and 0.91%, respectively (OR, 0.57; 95% CI, 0.34 to 0.98). The overall risk of stroke and/or death was 3.35% for asymptomatic and 5.18% for symptomatic stenosis (OR, 0.61; 95% CI, 0.51 to 0.74). CONCLUSIONS: Mortality and the risk of stroke and/or death due to carotid endarterectomy are significantly lower for asymptomatic than symptomatic stenosis. These findings are consistent across virtually all studies and are likely to be widely generalizable.

CD-ROM↗
PubMed2000

Low risk of ischemic stroke in patients with reduced internal carotid artery lumen diameter distal to severe symptomatic carotid stenosis: cerebral protection due to low poststenotic flow? On behalf of the European Carotid Surgery Trialists' Collaborative Group.

BACKGROUND AND PURPOSE: Patients with recently symptomatic severe carotid stenosis have a high risk of ischemic stroke on medical treatment. The main mechanism of stroke appears to be plaque surface thrombus formation and distal embolism. It is unclear to what extent reduction in blood flow across the stenosis, and the consequent reduction in cerebral perfusion pressure, is also important. Angiographic indices of reduced cerebral perfusion may identify patients at a particularly high risk of stroke who require urgent endarterectomy. The most direct angiographic correlate of poststenotic perfusion pressure is the degree of narrowing of the distal internal carotid artery (ICA) lumen. We sought to develop criteria for the definition of poststenotic narrowing of the ICA and to determine the effect of this and other angiographic characteristics likely to be associated with reduced cerebral perfusion on the risk of ipsilateral ischemic stroke in patients with recently symptomatic carotid stenosis. METHODS: We studied the carotid angiograms of 3007 patients in the European Carotid Surgery Trial. Poststenotic narrowing of the ICA was defined with use of the ratio of the lumen diameter of the ICA to that of the common carotid artery (CCA). The normal range of the ICA/CCA ratio was defined in 2966 symptomatic or contralateral carotid arteries with 0% to 49% stenosis. Arteries with 70% to 99% symptomatic stenosis and an ICA/CCA ratio below this range were categorized as narrowed. We related the presence of narrowing and other angiographic characteristics to the risk of ipsilateral ischemic stroke on medical treatment. RESULTS: An assessment of the ICA/CCA ratio had good interobserver reproducibility. Poststenotic narrowing of the ICA was defined as an ICA/CCA ratio of <0.42. The 5-year risk of ipsilateral carotid territory ischemic stroke on medical treatment was 8% in patients with 70% to 99% stenosis and narrowing of the ICA versus 25% in patients without narrowing (log rank test, P=0.02). This difference remained after correction for other clinical and angiographic variables (hazard ratio 0.40, 95% CI 0.17 to 0.94, P=0. 03). The other angiographic characteristics did not predict stroke. CONCLUSIONS: Poststenotic narrowing of the ICA was associated with a low risk of stroke on medical treatment. This suggests that low flow alone is not usually sufficient to cause ischemic stroke distal to symptomatic carotid stenosis. Poststenotic narrowing may be protective because blood flow distal to the stenosis is insufficient to carry emboli to the brain.

Aged↗
PubMed2000

Urokinase cisternal irrigation therapy for prevention of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage: a study of urokinase concentration and the fibrinolytic system.

BACKGROUND AND PURPOSE: Cisternal irrigation therapy with urokinase (UK) was performed in multiple institutions to prevent symptomatic vasospasm. The efficacy and safety of this therapy were evaluated, and the optimal concentration of UK was estimated. METHODS: This therapy was performed in 28 patients who underwent surgery within 72 hours of the onset of severe subarachnoid hemorrhage (Fisher's group 3, CT number [Hounsfield units] >60). After the aneurysm was clipped, irrigation tubes were placed in the Sylvian fissure (inlet) unilaterally and in the prepontine or chiasmatic cistern (outlet). Lactated Ringer's solution with UK (30, 60, or 120 IU/mL) was infused at a rate of 30 mL/h. The presence of symptomatic vasospasm was evaluated by changes in the clinical symptoms and the presence of a new low-density area on CT scan. Drained irrigation fluid and peripheral blood were examined chronologically to evaluate the fibrinolytic system. RESULTS: Symptomatic vasospasm was observed transiently in 3 cases (10.7%) without any low-density area on CT scan. In the 120-IU/mL group, no symptomatic vasospasm occurred. Analysis of drainage fluid suggested that UK 120 IU/mL is effective. The mean values of total drained blood volume for the respective groups were as follows: 58 mL in 30 IU/mL, 106 mL in 60 IU/mL, and 143 mL in 120 IU/mL. No abnormal changes were observed in the coagulative and fibrinolytic systems after UK irrigation. CONCLUSIONS: These results suggest that cisternal irrigation therapy with UK is safe and effective for the prevention of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage.

Biomarkers↗
PubMed2001

The significance of Chlamydia pneumoniae in symptomatic carotid stenosis.

An association between symptomatic carotid stenosis and recent infection with Chlamydia pneumoniae is reported. Thirty-five patients (20 symptomatic and 15 asymptomatic) with carotid stenosis of 70% to 90% underwent carotid endarterectomy. Endarterectomy was performed without patch and shunt; the average occlusion time of the internal carotid artery was 14 +/- 3 min. The atheromatic plaque and a portion of the thyroid artery were examined with polymerase chain reaction and peripheral vein blood was obtained for serologic detection of systematic infection, and IgG and IgM antibodies to C. pneumoniae by enzyme-linked immunosorbent assay. Twenty of 35 patients (57.1%) had increased titers of IgG antibodies to C. pneumoniae. Eight patients revealed IgG plus IgM antibodies; two of the eight had IgG, IgM, and positive findings on polymerase chain reaction. No C. pneumoniae was detected on the thyroid arteries. Sixty-five percent (13/20) of the patients with increased IgG antibodies to C. pneumoniae, 87.5% (7/8) with IgG + IgM, and 100% with IgG + IgM + positive polymerase chain reaction were symptomatic. Plaque morphology in association with symptoms did not reveal a significant correlation between soft plaques and symptoms, whereas the majority of the symptomatic patients had plaques of type III-V. Patients having recent contamination and positive polymerase chain reaction had a significant relationship between C. pneumoniae infection and symptomatic carotid disease. This supports the hypothesis that C. pneumoniae infection can produce a kind of instability of the carotid plaque. The results of this study demonstrate that patients with advanced atherosclerotic carotid disease have an increased incidence of C. pneumoniae infection. Recent infection could be responsible for instability of the carotid plaque, causing cerebral ischemic episodes.

Aged↗