Rebound hyperlipemia following intravenous heparin

1. 1. Lipemia is more severe in a group of subjects with coronary artery disease than in normal subjects. The degree of difference is accentuated after a fat load test in three and five hour specimens.

2. 2. Heparin, given intravenously, causes a distinct clearing of lipemic turbidity in both groups.

3. 3. Heparin, given intravenously, in an attempt to prevent the expected hyperlipemia following a fat load test, was found to be associated with rebound hyperlipemia.

4. 4. Possible implications of this rebound hyperlipemia are discussed in relation to fat transport.

     

Effect of single injections of heparin on postprandial hyperlipemia

1. 1. An attempt was made to determine and compare the duration of clearing effect of single doses of heparin administered intramuscularly, intravenously and subcutaneously after a fat meal.

2. 2. The doses of heparin and routes of injection as employed in this study do not alter to any significant extent the degree of postprandial hyperlipemia.

3. 3. “Rebound hyperlipemia” following intravenous heparin is again demonstrated.

4. 4. “Rebound hyperlipemia” occurs even though in vitro studies show continued lipoprotein lipase activity for several more hours.

5. 5. Benefit of multiple injections of heparin over a single dose is discussed.

     

Effect of heparin on blood lipids under conditions of endo- and exogenous hyperlipemia]

In 15 patients suffering from ischemic heart disease and in 5 healthy individuals (controls) the dynamics of the blood lipids content (NEFA, triglycerides and atherogenic lipoproteins) was followed up on an empty stomach, during a 18-hour fasting, after carbohydrate and fat loadings, before and after intravenous administration of heparin. Data on a quick and abrupt rise of the NEFA level and a falling triglycerides concentration, and also on a certain decline in the content of atherogenic lipoproteins following administration of heparin were obtained. In atherosclerotic patients the development of hypertriglyceridemia in response to introduction of glucose and a prolonged rise in the level of triglycerides following a fat loading were recorded. Intravenous administration of heparin with carbohydrates and fat loads contributes in atherosclerotic patients to a rapid fall of the blood plasma tryglycerides concentration.     

低分子肝素对伴高脂血症急性坏死性胰腺炎大鼠PAF、ET-1/NO的影响

目的:研究低分子肝素(LMWH)治疗伴高脂血症性急性胰腺炎(HL-AP)大鼠微循环障碍的作用.方法:SD大鼠80只,高脂饲料喂养4wk建立高脂血症模型后,随机分成3组:假手术(S)组,n=16;NS对照(N)组,n=32;低分子肝素(L)组,n=32.N组与L组大鼠建立ANP模型,S组大鼠仅开腹翻动胰腺.L组造模后分别于0h,6h,12h及18h开始使用LMWH皮下注射.N、S组同时点同方法用生理盐水对照,24h后抽门静脉检测血小板活化因子(PAF)、内皮素-1(ET-1)/一氧化氮(NO)浓度并行电镜观察胰腺组织微循环结构.结果:L组PAF、ET-1/NO浓度分别为5.9250mmol/L±0.6113mmol/L及3.5368±0.26;N组为7.4059mmol/L±0.4281mmol/L及4.1697±0.08;SO组为4.4950mmol/L±0.2628mmol/L及2.5133±0.20;L组PAF、ET-1/NO浓度均低于N组但高于SO组,有统计学意义;L组中0h及6h开始用LMWH的大鼠PAF、ET-1/NO浓度低于12h及18h组,有统计学意义.电镜观察L组胰腺病变程度轻于N组.结论:高脂血症急性胰腺炎大鼠存在胰腺微循环障碍;LMWH可以改善高脂血症大鼠SAP胰腺微循环障碍,并且早期应用优于晚期应用.     

Etiology of thrombocytopenia in all patients treated with heparin products

Abstract:  Purpose : To characterize the cause of thrombocytopenia in all patients treated with heparin products, to determine the incidence of heparin-induced thrombocytopenia (HIT) in unselected hospitalized patients, and to have modern data of the magnitude of this problem. Methods : Retrospective hospital-based cohort study. During a random 2-month period, we reviewed the medical records of all patients treated with heparin agents, screened them for thrombocytopenia, and determined the cause of it. Results : Out of 674 patients who received heparin products, 110 (16%) had thrombocytopenia. The most common causes included cancer chemotherapy, surgery, sepsis, and medications. Three patients met the clinical criteria for HIT. One had antibodies for heparin-platelet factor-4, and received a direct thrombin inhibitor. The other two individuals had a clinical syndrome that resembled immune HIT, but were not tested for HIT antibodies. One suffered a thrombotic episode that led to the death of her fetus. The other died of a possible thromboembolism. Conclusions : This study provides evidence-based data for the differential diagnosis of thrombocytopenia after treatment with heparin products. Our findings suggest that increased awareness of the HIT syndrome might reduce morbidity and mortality. Patients exposed to heparin products, who develop thrombocytopenia, should not be overlooked.     

Essential thrombocythemia and acute myocardial infarction treated with rescue coronary angioplasty

A 48-year-old man with essential thrombocythemia suffered an extensive anterior acute myocardial infarction; this is a rare association. A pharmacological thrombolysis was performed, without success. He subsequently underwent successful rescue coronary angioplasty. To our knowledge, there is no other report in the literature relating the triad of essential thrombocythemia, acute myocardial infarction and rescue coronary angioplasty.     

Incidence and prognostic significance of thrombocytopenia in patients treated with prolonged heparin therapy

BACKGROUND: Despite widespread heparin use in clinical practice, the associated development of thrombocytopenia is an underrecognized and undertreated complication. METHODS: We analyzed data from consecutive hospitalized patients treated with heparin (unfractionated or low molecular weight) for 4 days or longer to determine the incidence, predictors, prognostic significance, and management of "thrombocytopenia," defined as a platelet count less than 150 x 10(9)/L, reduction in platelet count of 50% or more from the admission level, or both. RESULTS: We enrolled 2420 patients (median age, 65.2 years; 43.8% women) in 48 US hospitals. Thrombocytopenia occurred in 881 patients (36.4%; 95% confidence interval [CI], 34.5%-38.3%). Of those who developed thrombocytopenia, 5.1% died, compared with 1.6% of those without thrombocytopenia (odds ratio [OR], 3.4; 95% CI, 2.1-5.6; P< .001). Thrombocytopenia was also associated with greater risk of myocardial infarction (OR, 2.1; 95% CI, 1.5-2.8; P< .001) and congestive heart failure (OR, 1.3; 95% CI, 1.1-1.6; P= .01). After adjustment for important covariates, thrombocytopenia remained an independent predictor of thrombotic and hemorrhagic events. A relative reduction in platelet count of more than 70% was the strongest independent predictor of death (OR, 13.4; 95% CI, 6.5-27.6; P< .001), followed by a relative reduction in platelet count of 50% to 70%, worse Killip class, occurrence of thromboembolic complications, older age, and longer duration of heparin therapy. CONCLUSIONS: Thrombocytopenia occurs frequently after prolonged heparin therapy and is strongly associated with worse short-term clinical outcome. The relative reduction in platelet count is a powerful independent predictor of all-cause mortality in hospitalized patients.     

Post-transplant IVC occlusion and thrombosis treated with tPA, heparin, and sharp recanalization

Complete inferior vena cava (IVC) thrombosis can be a lethal complication in a liver transplant recipient. The case of a 52-year-old liver transplant recipient, who developed complete IVC as well as left iliofemoral thrombosis, is reported. After treatment with combined tissue plasminogen activator (tPA) and heparin, the IVC was successfully recanalized with sharp dissection, balloon dilatation, and stent placement.