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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrophysiological and pathological studies have been performed on three patients with recurrent focal swelling of the calf muscles simulating deep venous thrombosis, and in a patient with both cardiomyopathy and skeletal muscle disease. In all patients there were elevated CPK levels, histological evidence of an acute myopathy, heavy alcohol intake prior to the development of symptoms, and improvement in hospital with the cessation of alcohol consumption. These patients illustrate a form of alcoholic muscle disease which may be more common than generally realised.
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PMID:The effect of ethyl alcohol on striated muscle: some clinical and pathological observations. 27 68

We studied 90 patients with congestive myocardial disease documented at cardiac catheterization (46 idiopathic, 39 ischemic, and 5 hypertensive) who underwent M-mode and two-dimensional echocardiograms every 2-3 months for up to 7 years (mean 3.4 +/- 1.6 years, +/- 1 S.D.). All had angiographic evidence of severe left ventricular dysfunction (left ventricular ejection fraction less than 40%), and were on a variety of inotropic, diuretic, and vasodilating drugs. Only 9 were ingesting anticoagulants (5 warfarin and 4 aspirin), those on warfarin had documented pulmonary emboli or deep venous thrombosis. All but 4 patients were in normal sinus rhythm. Only one subject in this group was found to have a myocardial (left ventricular) thrombus. Postmortem examinations of 27 patients confirmed the ultrasound data. Thus, we conclude that cardiac thrombi are unusual in patients with congestive cardiomyopathies and rarely develop over the course of the illness even in the absence of chronic anticoagulation.
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PMID:Serial echocardiograms in patients with congestive cardiomyopathies: lack of evidence for thrombus formation. 670 98

After decades of focus on the effects of cocaine abuse on the central nervous system (CNS), the cardiovascular toxicity of cocaine is just beginning to be appreciated. The most common cardiovascular pathologies associated with cocaine use include: cardiomyopathy, left ventricular dysfunction, myocarditis, arrhythmia, hypertension, myocardial infarction, stroke, arterial thrombosis, deep vein thrombosis, and gastrointestinal, renal, and skeletal muscle ischemia. This article reviews the above pathologies with speculations on the mechanisms by which cocaine produces cardiovascular tissue damage.
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PMID:Cardiovascular and thrombosis pathology associated with cocaine use. 829 12

Thromboembolic (TE) events have been frequently reported in beta-thalassemic patients in association with known risk factors such as diabetes, complex cardiopulmonary abnormalities, hypothyroidism, liver function anomalies, and postsplenectomy thrombocytosis. In a recent survey involving 9 Italian thalassemic centers, we identified 32 patients with TE episodes in a total of 735 subjects, of whom 683 had thalassemia major and 52 thalassemia intermedia, corresponding to 3.95 and 9.61%, respectively. There was a great variation in localization: the main one (16/32) was CNS, with a clinical picture of headache, seizures and hemiparesis. Other localizations were the pulmonary (3 patients), mesenteric (1 patient) and portal (2 patients) sites. There were 6 cases of deep venous thrombosis (2 in the upper limbs, 4 in the lower ones). Intracardiac thrombosis was found in 2 subjects and clinical and laboratory signs of DIC were observed in 2 others during pregnancy. Since our patients with TE events present a statistically significantly higher incidence of associated dysfunction (cardiomyopathy, diabetes, liver function anomalies, hypothyroidism) than those without TE events (50 vs. 13.8%), we suggest close monitoring of those patients who are at higher risk of developing TE events because of the presence of one or more of these predisposing factors.
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PMID:Thromboembolic events in beta thalassemia major: an Italian multicenter study. 985 99

Radiofrequency (RF) ablation is a new modality of pennanently curing patients with various tachycardias using radiofrequency energy, a technique evolved in the past decade. RF ablation was performed on 913 patients with different tachyarrhythmias from April, 1994 to July, 1999. There were 491 men and 422 females aged 42 +/- 34 years (range 1 to 76 years). Supraventricular tachycardia (SVT) was present in 462 patients, accessory pathway mediated atrioventricular re-entrant tachycardia (AVRT) in 355 patients (377 accessory pathways) and idiopathic ventricular tachycardia (VT) in 96 patients. Amongst the patients with SVT, 402 had atrioventricular nodal re-entrant tachycardia (AVNRT), 22 had atrial flutter, 20 had ectopic atrial tachycardia and 18 had atrial fibrillation. RF successfully abolished the tachycardia in 400/402 patients (99.5%) with AVNRT, 330/377 (87.5%) accessory pathways in patients with AVRT, 14/22 patients (63.6%) of atrial flutter, 18/20 patients (90%) of atrial tachycardia and 79/96 patients (82.3%) with idiopathicVT. Successful AV nodal ablation with pacemaker implantation was done in 10/18 patients with chronic atrial fibrillation with fast ventricular rate and tachycardia induced cardiomyopathy. AV nodal modulation for atrial fibrillation was tried in the remaining 8 patients and was successful in 4 (4/8). The overall success rate for all arrhythmias was 93.6%, and there was no mortality. At a follow-up of 6.8 +/- 5.4 months, there was a recurrence in 34/420 patients (8%), in whom successful re-ablation was performed. One patient with AVNRT and another with a parahisian pathway developed complete heart block and were given pacemakers. One patient developed inferior wall infarction on the next day post RF. There were 4 patients who had pericardial tamponade necessitating pericardiocentesis and 2 patients developed deep vein thrombosis, which was treated conservatively. Thus RF ablation is an effective, safe and curative therapy for various arrhythmias.
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PMID:Radiofrequency ablation: a cure for tachyarrhythmias. 1126 97

Although heart failure is a procoagulant state, the incidence of arterial thromboembolism (peripheral arterial emboli and strokes) is relatively low in the outpatient setting and seems to be higher in those with concomitant atrial fibrillation or recent large anterior myocardial infarction, especially in the presence of a dyskinetic apex. Hospitalized heart failure patients, on the other hand, have an extremely high rate of deep venous thrombosis and pulmonary emboli. Outpatients with heart failure should receive anticoagulation only in the presence of atrial fibrillation or if they have experienced a prior embolic event. Patients with recent large anterior infarction or recent infarction with documented thrombus should be treated with anticoagulation for the initial 3 months after the infarct, whereas those with evidence of a mural thrombus should receive anticoagulation at least until the thrombus has resolved. Heart failure patients with ischemic cardiomyopathy should receive antiplatelet agents for the prevention of myocardial infarction, stroke, or death. Antiplatelet agents should not be prescribed for heart failure patients with nonischemic cardiomyopathy or without other evidence of atherosclerotic vascular disease. All hospitalized heart failure patients who are not taking oral anticoagulants should receive prophylaxis with low molecular weight heparins or factor Xa inhibitors.
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PMID:Thromboembolic risk in the patient with heart failure. 1776 Nov 16

Anticardiolipin antibodies are associated with arterial and venous thrombosis, and repetitive miscarriages. The involvement of the heart has been described frequently and can evolve into cardiomyopathy. It has been known for some decades that chronic alcoholism can lead to alcoholic cardiomyopathy (ACM). The objective of this study was to evaluate whether anticardiolipin antibodies represent a worse prognosis for patients with ACM. The authors present a case of a chronic alcoholic patient (30 y of alcoholism) who died at 44 y of age, and who was considered positive for anticardiolipin antibodies. The patient developed deep vein thrombosis, and peripheral arterial and pulmonary embolism. The presence of another risk factor seems to represent a worse prognosis for patients with ACM.
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PMID:Anticardiolipin antibodies associated with alcoholic cardiomyopathy. 1866 84

Although heparin-dependent antibodies (HDAs) typically manifest with thrombocytopenia as in heparin-induced thrombocytopenia (HIT), they may also manifest with preserved platelet counts. We describe a 35-year-old woman who developed severe thrombotic complications due to heparinization and unrecognized HDAs. She had received subcutaneous heparin as prophylaxis for deep vein thrombosis during a 5-day hospitalization for postpartum cardiomyopathy. Five days after discharge (day 1), she developed bilateral lower extremity arterial thrombi and underwent heparinization and successful lower extremity thrombectomies. A pulmonary embolus and hepatic and renal infarcts were then found. On days 2-6, the patient experienced a myocardial infarction, ischemic cerebrovascular accident, recurrent lower extremity arterial thrombus, and splenic infarct. On day 7, blood obtained on day 4 was found to be strongly positive for HDAs. In the interim, the patient had been transitioned to warfarin. Her platelet counts were never less than 75% of baseline and were consistently above 200 x 10(3)/mm(3). Hypercoagulability studies were negative. The patient's score on the Naranjo adverse drug reaction probability scale indicated that the relationship between this adverse reaction and heparin was probable. An extensive MEDLINE search located 22 other reports of patients who developed HDAs, sometimes associated with thrombosis, but whose platelet counts did not decrease. As with our patient, many of these case reports described clinicians who overlooked thrombosis due to HDAs because the patients did not have HIT. Clinicians should be cognizant of this possibility and consider a diagnosis of HDAs in patients with ongoing thrombosis who are receiving heparin therapy. It is strongly recommended that heparin be substituted with another anticoagulant in such cases until the presence of HDAs can be definitively ruled out.
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PMID:Heparin-dependent antibodies and thrombosis without heparin-induced thrombocytopenia. 1895

Isolated ventricular non-compaction (IVNC) is a rare, congenital, unclassified cardiomyopathy characterized by prominent trabecular meshwork and deep recesses. Major clinical manifestations of IVNC are heart failure, atrial and ventricular arrhythmias, and thrombo-embolic events. We describe a case of a 69-year-old woman in whom the diagnosis of IVNC was discovered late, whereas former echocardiographic examinations were considered normal. She was known for systolic left ventricular dysfunction for 3 years and then became symptomatic (NYHA III). In the past, she suffered from multiple episodes of deep vein thrombosis and pulmonary embolism. Electrocardiogram revealed a wide QRS complex, and transthoracic echocardiography showed typical apical thickening of the left and right ventricular myocardial wall with two distinct layers. The ratio of non-compacted to compacted myocardium was >2:1. Cardiac MRI confirmed the echocardiographic images. Cerebral MRI revealed multiple ischaemic sequellae. In view of the persistent refractory, heart failure in medical treatment of patients with classical criteria for cardiac re-synchronization therapy, as well as the ventricular arrhythmias, a biventricular automatic intracardiac defibrillator (biventricular ICD) was implanted. The 2-year follow-up period was characterized by improvement of NYHA functional class from III to I and increasing in left ventricular function. We hereby present a case of IVNC with favourable outcome after biventricular ICD implantation. Cardiac re-synchronization therapy could be considered in the management of this pathology.
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PMID:Cardiac re-synchronization therapy in a patient with isolated ventricular non-compaction: a case report. 1940 40

The puerperium is the period from the end of labour to the appearance of the first menstruation. The possible pathologies that can occur in this period of time are the most frequent cause of maternal mortality even in our setting. The pathology of lactation includes failure of breastfeeding, cracks in the nipple, mammary ingurgitation and puerperal mastitis. Puerperal infection is a frequent obstetric complication although clinical guidelines for prophylaxis have considerably reduced its incidence. The vascular pathology of the puerperium includes clinical features of great seriousness, representing one of the main causes of maternal mortality. These include deep vein thrombosis, of which pulmonary thromboembolism is the most serious complication. It does not appear that a psychiatric pathology is more frequent in the puerperium than in other periods of life, but the clinical features related to this period are described, such as "blues", puerperal depression and puerperal psychosis. Finally, other clinical features which although infrequent can constitute a medical emergency in the puerperium are: Sheehan's syndrome, peripartum cardiomyopathy and postpartum thyroids.
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PMID:[Puerperal pathology]. 1943 48


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