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PubMed1981

Antithrombin III deficiency appearing as mesenteric vein thrombosis.

Mesenteric vein thrombosis is a relatively uncommon but devastating problem. Absence of any of the generally accepted etiologic factors of mesenteric vein thrombosis has lead to the diagnosis of "primary" mesenteric vein thrombosis in 25-55% of all cases. In this report we identify a young man with antithrombin III deficiency presenting as "primary" mesenteric vein thrombosis with massive bowel infarction. It again raises the possibility that other cases of "primary" mesenteric vein thrombosis may have been associated with this coagulopathy. Factors influencing antithrombin III levels are discussed in relation to diagnosis of the familial deficiency state in a patient with mesenteric vein thrombosis. The association of intra-abdominal venous occlusion and antithrombin III deficiency is emphasized.

Adult↗
PubMedDate not supplied

[Portal thrombosis and liver cirrhosis. Value of ultrasound-guided puncture-biopsy of the thrombus].

OBJECTIVES AND METHODS: Portal vein thrombosis which occurs in the course of cirrhosis, associated or not with hepatocellular carcinoma, can be either cruoric or neoplastic. The aim of this study was to assess the feasibility and the results of ultrasound guided biopsy of portal vein thrombosis in 21 patients with cirrhosis (20 men and 1 woman; mean age 66 +/- 9 years), who were hospitalized between May 1989 and November 1993. Ultrasound guided biopsies of the cirrhotic liver, of the portal vein thrombosis and, when present, of a hepatic nodular lesion were performed. The diagnosis of hepatocellular carcinoma was made if the histological examination of the hepatic and portal biopsy samples were positive or if serum concentrations of alpha-fetoprotein were higher than 500 IU/mL. RESULTS: All portal vein thrombosis biopsies were successfully performed. No side-effects were observed. Before ultrasound guided biopsy of the portal thrombosis, diagnosis of hepatocellular carcinoma was made in 15 cases, and diagnosis of cirrhosis in 6 cases. After histological examination of the portal sample, hepatocellular carcinoma was diagnosed in 19 cases and cirrhosis in 2 cases. Thus, in 19% of cases, ultrasound guided biopsy of the portal thrombus provided a definitive diagnosis. CONCLUSION: Ultrasound guided biopsy of the portal vein thrombosis must be performed before liver transplantation for cirrhosis or hepatocellular carcinoma to exclude the presence of a vascular neoplastic extension.

Adult↗
PubMed1994

Cerebral venous thrombosis in Behçet's disease.

A 20 year-old Turkish patient presented with superior sagittal and lateral sinus thrombosis. The frequency of cerebral venous thrombosis generally is underestimated and may be the first clinical manifestation. In case of intracranial hypertension, cerebral venous thrombosis and Behcet's disease should be taken into consideration, especially in the high risk population from Eastern Mediterranean countries and Japan. CT with enhancement and MRI study with T1- and T2- weighted images were used to detect the thrombosed veins and to evaluate the thrombosis. Treatment with anticoagulation and corticosteroid therapy in cerebral venous thrombosis is well established today. Clinical course and prognosis in cerebral venous thrombosis are generally benign if adequate management is started in time.

Adult↗
PubMed1995

Cost-effectiveness of enoxaparin vs low-dose warfarin in the prevention of deep-vein thrombosis after total hip replacement surgery.

BACKGROUND: Enoxaparin sodium, a low-molecular-weight heparin, was recently approved for use in the United States to prevent deep-vein thrombosis after total hip replacement surgery. Its cost-effectiveness relative to prophylaxis with low-dose warfarin sodium is unknown. METHODS: A decision-analytic model was developed to compare two strategies of prophylaxis for deep-vein thrombosis with a strategy of not using prophylaxis in a hypothetical cohort of 10,000 patients undergoing total hip replacement surgery. For each of these strategies, we estimated the expected number of cases of confirmed deep-vein thrombosis or pulmonary embolism, the expected number of thromboembolic deaths, and the expected costs of venous thromboembolic care, including prophylaxis, diagnosis, and treatment. Data were drawn primarily from the published literature. RESULTS: Compared with no prophylaxis, the use of low-dose warfarin would be expected to reduce the number of cases of confirmed deep-vein thrombosis from about 1000 (per 10,000 patients) to 420 and the number of thromboembolic deaths from about 250 to 110. Expected costs of care related to deep-vein thrombosis also would be reduced from approximately $530 to $330 per patient. Prophylaxis with enoxaparin would be expected to reduce further the number of cases of confirmed deep-vein thrombosis and the number of thromboembolic deaths (to 250 and 70, respectively) but increase costs of care by approximately $50 per patient. The cost-effectiveness of enoxaparin (relative to low-dose warfarin) is estimated to be approximately $12,000 per death averted. CONCLUSION: Although enoxaparin is more costly than low-dose warfarin, its cost-effectiveness in total hip replacement compares favorably with that of other generally accepted medical interventions.

Cost-Benefit Analysis↗
PubMed1995

High risk of thrombosis in patients homozygous for factor V Leiden (activated protein C resistance)

Resistance to activated protein C (APC) is a common inherited risk factor for venous thrombosis, which is associated with a mutation in coagulation factor V (factor V Leiden). We investigated the risk of venous thrombosis in individuals homozygous for this abnormality. We determined the factor V Leiden genotype in 471 consecutive patients aged less than 70 years with a first objectively confirmed deep-vein thrombosis and in 474 healthy controls. We found 85 heterozygous and seven homozygous individuals among the cases with thrombosis and 14 heterozygous individuals among the control subjects. The expected number of homozygous individuals among the controls was calculated from Hardy-Weinberg equilibrium and estimated at 0.107 (allele frequency, 1.5%). Whereas the relative risk was increased sevenfold for heterozygous individuals, it was increased 80-fold for homozygous individuals. These patients experienced their thrombosis at a much younger age (31 v 44 years). The homozygous individuals were predominantly women, most likely due to the effect of oral contraceptives. Because of the increased risk of thrombosis with age, the absolute risk becomes most pronounced in older patients, both for heterozygous and homozygous individuals. For the homozygous individuals, the absolute risk may become several percentage points per year. This implies that most individuals homozygous for factor V Leiden will experience at least one thrombotic event in their lifetime.

Adult↗
PubMed1994

Prevention of deep vein thrombosis and pulmonary embolism in acetabular and pelvic fracture surgery.

In a prospective nonrandomized study, a protocol was examined for prophylaxis of deep venous thrombosis and pulmonary embolism in patients with operative treatment of acetabular and pelvic fractures. There were 197 patients in the study with 203 fractures, including 148 acetabular and 55 pelvic fractures. There were 2 cases of bilateral acetabular fractures and 4 cases with both acetabular and pelvic fractures. The protocol involved preoperative noninvasive screening of the lower extremities, intraoperative and postoperative use of mechanical antithrombotic devices, and chemical prophylaxis with warfarin for 3 weeks following removal of surgical drains. There were 11 cases (6%) of preoperative deep venous thrombosis detected. There were 6 cases of postoperative deep venous thrombosis and 2 cases of pulmonary embolism. The incidence of postoperative venous thrombosis and pulmonary embolism was 3% and 1%, respectively. The protocol was found to be effective for preoperative detection of venous thrombosis and prevention of deep venous thrombosis and pulmonary embolism in trauma patients with minimal bleeding complications and no morbidity from embolic disease.

Acetabulum↗
PubMed1994

Efficacy and safety of heparin anticoagulation for neonatal renal vein thrombosis.

PURPOSE: We report on the safety and efficacy of heparin anticoagulation for the treatment of neonatal renal vein thrombosis. PATIENTS AND METHODS: Six consecutive, prospectively identified, critically ill neonates with renal vein thrombosis were studied. Diagnosis of renal vein thrombosis was based on history and examination and confirmed with renal ultrasound. All neonates were treated with continuous i.v. heparin titrated to achieve a therapeutic whole blood clotting time and/or APTT. RESULTS: Renal vein thrombosis was bilateral for three of six neonates. Heparin infusion rates varied from 8 to 40 U/kg/h and were administered for 7-14 days. Two neonates developed hemorrhagic complications; one had disseminated intravascular coagulation but did not hemorrhage until heparin toxicity ensued, and another was well until an umbilical catheter was removed while he was therapeutically heparinized. Renal outcome at 3 months to 6 years showed hypertension in one neonate, atrophic kidneys in two, and both hypertension and an atrophic kidney in one. CONCLUSIONS: Bleeding was a significant complication of heparin therapy for neonatal renal vein thrombosis. Renal dysfunction was not prevented in four of six neonates treated with heparin. Alternative approaches to titrate heparin, alternative anticoagulants, or fibrinolytic therapy should be considered as therapy for neonatal renal vein thrombosis.

Child↗
PubMed1993

Embolic complications of calf thrombosis following total hip arthroplasty.

The incidence of clinically significant pulmonary embolism following total hip arthroplasty is reported in patients with venographically documented deep venous thrombosis. One hundred seventy-four patients who enrolled in a prospective evaluation of deep venous thrombosis prophylaxis underwent contrast venography 7-10 days after operation. Ten patients with proximal and 12 patients with isolated deep calf thrombosis were identified on routine venogram reading and received appropriate anticoagulant therapy, including a 6-12-week course of warfarin. There were no clinically evident embolic events and no bleeding complications in this group. A secondary blinded review of venograms several weeks later identified isolated deep calf thrombi in 13 other patients, none of whom had received warfarin after discharge. Four of the 13 patients (P < .02) subsequently presented with pulmonary embolism at a mean of 33.5 days after operation. Asymptomatic deep calf venous thrombosis following total hip arthroplasty is associated with a significant risk of developing clinically evident pulmonary embolism within the first 8 weeks after operation. Once identified, these thrombi were effectively managed with outpatient warfarin anticoagulation, and both embolic and bleeding complications were avoided. This study documents the need for more prolonged routine prophylaxis against venous thrombosis than has heretofore been the rule, extending beyond the time of discharge from the hospital. Alternatively, the authors' experience supports the use of routine screening venography following total hip arthroplasty to allow detection and selective anticoagulant treatment of deep venous thrombosis in both the thigh and calf.

Hip Prosthesis↗
PubMed1996

[Main antithrombotic drugs in the therapy and prevention of arterial and venous thrombosis].

The author reviews the use of the main antithrombotic drugs (thrombolytics, dicumarol compounds, heparins and anti-platelet drugs) in the treatment and prophylaxis of the main nosographic syndromes of arterial and venous thrombosis. In the context of arterial thrombosis the paper initially reports the results of the main controlled trials on ischemic cardiopathy (treatment of acute infarction, primary and secondary prophylaxis for re-infarction, post-infarction ventricular thrombosis, stable and instable coronary angor, percutaneous angioplasty, aortocoronary by-pass, stent, valve prosthesis, atrial fibrillation). Turning to peripheral arteriopathies the treatment of acute attacks is death with separately from prophylactic treatment (reduction of atheromatous progression, improved vascular perfusion, reduction of concomitant cardiac and cerebral events, behaviour of carotid stenoses). Vascular cerebropathy is examined during the acute (treatment of ictus in early days) and later phases (prophylaxis of recidivation of ictus). With regard to venous thrombosis, the paper separates the treatment of profound thrombosis and pulmonary embolism (often secondary to the former) from prophylaxis of profound thrombosis; the latter is classified into forms occurring during general surgery (abdominal, pelvic, urologic), orthopedic surgery (hip prosthesis, gonopathies) and general medicine. The author ends the review by making a schematic analysis of the areas of elective use of the above antithrombotic drugs with reference to the nosographical forms examined in the paper.

Coronary Artery Disease↗
PubMed1996

[A case with an isolated cortical vein thrombosis].

A 45-year-old man was admitted to our hospital because of generalized seizure. He had epilepsy and mental retardation since age of two. On admission temperature was 37.9 degrees C but, nuchal rigidity and Kernig's sign were not present. There were no other abnormal findings on physical examination. Neurological examination revealed consciousness disturbance, generalized seizure and mental retardation. Right hemiparesis gradually developed after generalized seizure. Laboratory data did not show any abnormalites to induce cerebral venous thrombosis. A brain MRI revealed hyperintensity on T2-weighted images and slightly enhanced on T1-weighted images in the left frontal lobe, using Gd-DTPA. An increased signal was also noted in the superior sagittal sinus on T1-weighted images. The superior sagittal sinus was patent but the cortical vein in the left frontal lobe was not demonstrated on cerebral angiography. A diagnosis of an isolated cortical vein thrombosis was made by exploratory craniotomy. Anticoagulation with heparin was started. Although the cortical vein thrombosis usually co-exsists with dural sinus thrombosis, an isolated cortical vein thrombosis like this case was rather rare. A case with cerebral venous thrombosis localized only in the left frontal cortical vein is reported, but definitive etiology is not known.

Cerebral Cortex↗
PubMed1997

Use of magnetic resonance imaging and magnetic resonance angiography in diagnosis of sigmoid sinus thrombosis.

Magnetic resonance angiography is an established radiologic technique which is rapidly becoming useful in imaging the head and neck. Currently, this imaging modality is important in the diagnosis of sigmoid sinus thrombosis caused by otologic disease. Since the introduction of antibiotic therapy, the percentage of deaths attributed to intracranial complications from otitic disease has decreased from 2.5 to approximately 0.25% of documented deaths. Also, the incidence of sinus thrombosis within this group has decreased, but it is still a serious and potentially lethal condition. Sinus thrombosis is suspected clinically when mastoid disease progresses, with picket fence fever pattern, chills, headaches and signs of papilledema. Definitive diagnosis is necessary before surgical treatment. The Queckenstedt test is unreliable, computed tomography is better suited for demonstrating thrombosis of the sagittal sinus rather than the sigmoid sinus, and conventional angiography (although it provides excellent visualization) has the hazard of ionizing radiation and requires vessel puncture and the use of intraarterial contrast agents. We present two cases of thrombosis of the sigmoid sinus as an intracranial otologic complication which were diagnosed definitively with magnetic resonance imaging and magnetic resonance angiography. The combination of magnetic resonance imaging, which showed the thrombosis displaying abnormal signal intensity, and magnetic resonance angiography, which demonstrated the absence of flow in the sinus, was an ideal diagnostic tool. For both patients, treatment consisted of mastoidectomy, sigmoid sinus decompression and antibiotics.

Adolescent↗
PubMed1997

Anticardiolipin, anti-beta(2)-glycoprotein I, antiprothrombin antibodies, and lupus anticoagulant in patients with systemic lupus erythematosus with a history of thrombosis.

OBJECTIVE: To determine the clinical importance of anticardiolipin (aCL), anti-beta(2)-glycoprotein I (a beta(2)-GPI), antiprothrombin (aPT), and lupus anticoagulant (LAC) antibodies in patients with systemic lupus erythematosis (SLE) with and without a history of thrombosis. METHODS: We studied 100 patients with SLE (32 with a history of thrombosis), 27 patients with a lupus-like disease (9 with a history of thrombosis), and 41 healthy volunteers, IgG and IgM aCL, antibodies to the protein cofactors (a beta(2)-GPI and aPT) were determined by ELISA. Eighty-six of 127 patients were also tested for LAC. RESULTS: IgG aCL and LAC were associated with thrombosis but sensitivity (63 and 61%) and specificity (66 and 66%, respectively) of these tests were low. IgG and IgM a beta(2)-GPI were, respectively, 85 and 86% specific for a thrombotic history, but sensitivity was very low (32 and 29%). High IgG aCL were associated with the presence of a beta(2)-GPI and were 85% specific for thrombosis. There was no significant association between IgG or IgM aPT and thrombosis. CONCLUSION: Only high levels of IgG aCL and presence of LAC and/or a beta(2)-GPI are relevant in defining a thrombotic subset of patients with SLE. Longitudinal prospective studies are needed to investigate the predictive value of the different antiphospholipid and protein cofactor antibodies.

Adult↗
PubMed1997

[A longitudinal study on left atrial thrombosis in patients with non-rheumatic atrial fibrillation treated with anticoagulants].

BACKGROUND: Although atrial thrombosis is common in patients with non-rheumatic atrial fibrillation (NRAF) (6-27%), there are no studies about the effect that anticoagulant or antiplatelet drugs have on it. AIM OF THE STUDY: We have investigated the role of anticoagulant therapy, followed by family physicians, on left atrial thrombosis detected via transesophageal echocardiography (TEE) in patients with NRAF. METHODS: Sixty patients enrolled in the TASAF (Trieste Area Study on non-rheumatic Atrial Fibrillation) (60% males, mean age 72 +/- 7 years, 17% with lone atrial fibrillation, duration of arrhythmia 111 +/- 79 months), in whom we found a left atrial and/or left atrial appendage thrombus via TEE, were anticoagulated. The thrombus was in the left atrial appendage in 57 patients and in the left atrium in the others. In 28 of them it was mobile and in 50, the left atrial appendage flow was low or absent. Lastly, in 46 patients we found spontaneous echocontrast and a bilobate appendage was present in 8 of them. At follow-up, we repeated the TEE to evaluate the effect of the therapy on the atrial thrombosis. RESULTS: Only 53 patients received anticoagulant therapy (45 correctly), while 7 were treated with antiplatelet drugs by their family physicians. After a mean follow-up of 16 months, all patients underwent a repeat TEE and the thrombus was no longer evident in 35 cases (58%). The thrombosis disappeared in 26 (58%) of the 45 patients who correctly took anticoagulant therapy and in 5 of the 8 who were not adequately anticoagulated. Moreover, we didn't observe the thrombus in 4 of the 7 patients who were treated with antiplatelet drugs. There was no significant statistical difference between the benefits of anticoagulants and antiplatelet therapy in dissolving left atrial thrombosis. During follow-up, we recorded only one embolic event in the retina. None of the patients on antiplatelet drugs complained of any side effects, whereas in 5 of the 53 on anticoagulant therapy, we recorded one fatal intracranial hemorrhage, one gastric hemorrhage and three minor complications. CONCLUSIONS: Left atrial thrombosis in NRAF disappears in anticoagulated patients in an high percentage of cases (the therapy probably acts on more recent thrombi). Moreover, this therapy decreases the incidence of embolic events, although it increases the risk of hemorrages. Since the management of this preventive treatment in general medicine is very difficult, we hope that our health organization will establish Anticoagulation Clinics for the centralized management of this therapy.

Aged↗
PubMed1998

Tributary venosinus occlusion and septic cavernous sinus thrombosis: CT and MR findings.

PURPOSE: In autopsy reports of patients who died of septic cavernous sinus thrombosis, tributary venosinus occlusion has been a common finding related to intracranial inflammatory complications. The purpose of this article is to illustrate the MR and CT appearance of septic cavernous sinus thrombosis and tributary venous occlusion. METHODS: Over a period of 7 years, eight patients with septic cavernous sinus thrombosis were examined by contrast-enhanced thin-section CT. The CT scans of these eight patients and those of 30 healthy control subjects were assessed independently and subjectively by two blinded readers to ascertain the presence, size, and density of areas of nonopacification within the cavernous sinus and the presence of filling defects and dilation of tributary veins and venous sinuses. In six subjects, MR images supplemented by a contrast-enhanced spoiled gradient-recalled acquisition in the steady state (SPGR) sequence were assessed with respect to the presence of filling defects, expansion, and signal abnormalities within the cavernous sinus and tributary veins and sinuses. The MR and CT findings were compared. RESULTS: The CT studies of the eight patients were consistently differentiated from those of the control subjects by the two readers. Contrast-enhanced CT findings in patients included areas of nonopacification that were present within the cavernous sinus bilaterally in six cases and unilaterally in two. The size of the filling defects exceeded 7 mm in 76% of thrombosed cavernous sinuses compared with 9% of control subjects. The mean density of filling defects in patients differed significantly from those in control subjects. Comparison of the MR and CT findings in six cases showed the contrast-enhanced SPGR sequence to be equivalent to CT with respect to delineation of filling defects. CONCLUSION: Contrast-enhanced high-resolution CT findings indicate that venosinus thrombosis associated with septic cavernous sinus thrombosis is not restricted to the superior ophthalmic vein and is more common than previously assumed. A contrast-enhanced SPGR MR sequence may be used as a reliable alternative to establish the diagnosis of cavernous sinus and tributary venosinus thrombosis.

Adolescent↗
PubMed1998

Attenuation of tissue thrombosis and hemorrhage by ala-TFPI does not account for its protection against E. coli--a comparative study of treated and untreated non-surviving baboons challenged with LD100 E. coli.

This study was designed to determine the effect of a delayed infusion (T+120 min) of alanyl tissue factor pathway inhibitor (ala-TFPI) on the response to LD100 E. coli. We hypothesized that baboons treated with a low dose of TFPI (5 mg/kg) which did not survive would exhibit thrombosis, infarction and hemorrhage of target tissues such as that seen in untreated animals infused with LD100 E. coli. Eight baboons were infused with 5 mg/kg of ala-TFPI over a 10 h period beginning immediately after a 2 h infusion of LD100 E. coli (experimental group). Four baboons were infused with E. coli followed by a 10 h infusion of saline (control group). Of the 12 baboons, the 11 non-survivors (TFPI = 7 out of 8; controls = 4 out of 4) were evaluated for the extent of thrombosis, necrosis, hemorrhage, and congestion of target tissues and for changes in clinical chemical parameters. We expected that failure to protect would correlate with failure to inhibit thrombosis of target tissue (8). Surprisingly ala-TFPI significantly inhibited thrombosis, hemorrhage and necrosis of adrenal and renal tissues and attenuated the rise in creatinine in the 7 treated non-survivors. The lungs of these non-survivors, however, exhibited intra-alveolar fibrin and a mild degree of hemorrhage and edema. We concluded that low doses of ala-TFPI begun as late as T+120 in minutes failed to protect against the lethal effects of LD100 E. coli in spite of completely preventing thrombosis and hemorrhage in target organs, and that thrombosis, infarction and hemorrhage of adrenal and renal tissue are not part of the lethal chain of events in this IV model of E. coli sepsis.

Animals↗
PubMedDate not supplied

Peritoneal dialysis is not a risk factor for primary vascular graft thrombosis after renal transplantation.

OBJECTIVE: To find out if patients undergoing peritoneal dialysis (PD) have an increased risk of primary vascular thrombosis of the renal allograft, compared with patients on hemodialysis (HD). DESIGN: Observational, retrospective cohort study. SETTING: Tertiary care hospital, covering an approximate population of 2,000,000. Extensive use of suboptimal donors for renal transplantation. PATIENTS AND METHODS: The study included 827 patients receiving a cadaveric renal transplantation (RTx) in our center between 1988 and 1997 (700 on HD and 127 on PD). We searched for a potential difference in the incidence of graft thrombosis, according to the pretransplant dialysis modality and taking into consideration the main reported risk factors for this complication of RTx. RESULTS: The accumulated incidence of primary graft thrombosis was 4.7% in PD patients, and 6.1% in HD patients (NS). Arterial and venous thrombosis were also similar in both groups. Logistic regression analysis demonstrated that extremes of age of the donor, use of the right kidney, protracted cold ischemia, delayed graft function, and transplantation to a hypersensitized recipient independently predicted graft thrombosis. Peritoneal dialysis was not independently associated with the complication under study (adjusted odds ratio HD/PD = 2.5, 95% CI = 0.8-7.7). CONCLUSIONS: Peritoneal dialysis is not associated with an increased risk of primary vascular thrombosis of the renal allograft.

Adult↗
PubMed1998

[Deep venous thrombosis in pregnant women].

The main risk factors for deep vein thrombosis in pregnancy and after delivery are preeclampsia, operative delivery, adiposity, prolonged bed rest, and haemostatic defects (antithrombin, protein C and protein S deficiencies), activated protein C resistance, lupus anticoagulant/antiphospholipid antibodies. Hyperhomocystinaemia is a general risk factor for deep vein thrombosis. The clinical diagnosis of deep vein thrombosis is difficult and must be confirmed by imaging techniques. Positive D-dimer has high sensitivity, but low specificity to detect acute thrombosis. Standard treatment is unfractionated heparin intravenously for 7-10 days, followed by subcutaneous injections. Anticoagulant treatment is prolonged for 6-12 weeks after delivery, usually with warfarin. During pregnancies associated with high risk of thrombosis, low molecular heparin prophylaxis is given during pregnancy and 6-12 weeks after delivery. Thrombosis in pregnancy must be followed by adequate investigation for an underlying thrombotic predisposition.

Disease Susceptibility↗
PubMed1998

High prevalence of hypercoagulable states in patients with recurrent thrombosis of mechanical heart valves.

BACKGROUND AND AIMS OF THE STUDY: Thrombosis is one of the most feared and life-threatening complications of mechanical heart valves (MHV), with an incidence of 1-3 per 100 patient-years. Hypercoagulable states are highly prevalent in the general population and can predispose MHV to thrombus formation. Thus, we conducted a study to investigate the frequency of hypercoagulable states in patients with MHV who had recurrent thrombosis at least twice after valve implantation. METHODS: Fifteen patients (mean age 42 +/- 11 years; range: 18 to 55 years) with recurrent thrombosis of MHV (2.4 +/- 0.8 recurrences/patient) (group 1) and 15 matched patients (mean age 40 +/- 12 years; range: 18 to 55 years) with MHV without thrombosis (group 2) were followed up with transthoracic and transesophageal echocardiography. Patients' sera were monitored for antibodies to cardiolipin (ACLA-IgG and ACLA-IgM), phosphatidylserine (APSA), lupus-type anticoagulant (LA) and lipoprotein(a) (LP(a)). RESULTS: Average values for group 1 versus group 2 were: ACLA-IgG (normal range < 15 GPLU/ml) 24.7 +/- 14.6 versus 6.2 +/- 2.7 (p < 0.001); ACLA-IgM (< 12.5 MPLU/ml) 7.9 +/- 5.0 versus 3.3 +/- 1.7 (u = 185; p < 0.001); APSA (< 12 RLU/ml) 4.8 +/- 5.7 and 2.9 +/- 1.2 (p = 0.56); and LP(a) (< 30 mg/dl) 36.5 +/- 26.5 and 13.4 +/- 7.1 (p < 0.001). The frequency of LA-positive cases was 4/15 in group 1 and 0/15 in group 2 (p > 0.05). The frequency of abnormally high levels of ACLA-IgG was 9/15 in group 1 and 0/15 in group 2 (p < 0.001); of ACLA-IgM, 2/15 in group 1 and 0/15 in group 2 (p > 0.05); of APSA, 1/15 in group 1 and 0/15 in group 2 (p > 0.05); and of LP(a), 5/15 in group 1 and 0/15 in group 2 (p < 0.05). At least one of the factors included in this study was abnormal in 14 of 15 (93%) patients (p < 0.0001). CONCLUSIONS: Hypercoagulable states are highly prevalent in patients with recurrent thrombosis of MHV. All patients evaluated for therapy of obstructive thrombosis of MHV should be investigated for hypercoagulable state. Moreover, in high-risk patients, surgical replacement of the MHV with a bioprosthesis should be considered.

Adolescent↗