Danaparoid is not a low-molecular-weight heparin.
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Biomedical subjects
Publications and source records attributed to M J Cziraky.
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OBJECTIVE: To review the structure and physiologic function of lipoprotein(a) [Lp(a)], review the association of Lp(a) with the development of atherosclerosis, and to critically evaluate the current literature regarding the effects of lipid-lowering drug therapy on Lp(a) serum concentrations. DATA SOURCES: English language clinical and animal studies, abstracts, and review articles pertaining to Lp(a). STUDY SELECTION AND DATA EXTRACTION: Relevant human and animal studies examining Lp(a)'s role in atherosclerosis and the effect of drug therapy on Lp(a) serum concentrations. DATA SYNTHESIS: Possible physiologic functions and potential atherogenic mechanisms of Lp(a) are discussed. Evidence supporting the association of Lp(a) with atherosclerosis is presented. Studies evaluating the effects of lipid-lowering drug therapy on Lp(a) concentrations are reviewed and critiqued. CONCLUSIONS: Lp(a) concentrations are correlated with the risk of atherosclerotic vascular disease (AVD) in both animals models and human studies. Drug therapies that have produced a consistent reduction in Lp(a) concentration include niacin alone or in combination with a bile acid sequestrant or neomycin. However, additional, larger studies are needed to evaluate the ability of drug therapies to specifically reduce elevated Lp(a) concentrations. Preliminary information suggests that reduction in Lp(a) concentrations may be associated with atherosclerotic plaque regression. Although drugs are available to lower Lp(a), one cannot conclude that lowering of Lp(a) is warranted until clinical trials demonstrating beneficial effects have been published.
The pharmacologic characteristics of low-molecular-weight (LMW) heparins and unfractionated heparin are reviewed, and clinical trials comparing LMW heparins with unfractionated heparin for the initial treatment of deep-vein thrombosis (DVT) are described. LMW heparins are derived from native heparin and range in mass from 3000 to 8000 daltons. All LMW heparins contain the antithrombin III-specific pentasaccharide unit found on unfractionated heparin. LMW heparins are stronger inhibitors of factor Xa than unfractionated heparin, but their mechanisms of action, like that of unfractionated heparin, is predominantly the inhibition of thrombin. The efficacy of LMW heparins in the prophylaxis of DVT is not correlated with activated partial thromboplastin time (APTT); monitoring of APTT or anti-factor Xa may not be necessary. Compared with unfractionated heparin, LMW heparins have a lower affinity for heparin cofactor II, platelet factor 4, von Willebrand factor, and vascular epithelium. Subcutaneously administered LMW heparins are more bioavailable than s.c. unfractionated heparin. In clinical trials in patients with DVT, LMW heparins (dalteparin, enoxaparin, nadroparin, and tinzaparin) have resulted in venography scores similar to those obtained with unfractionated heparin. Frequencies of recurrent thromboembolism and bleeding complications were also similar. Dalteparin and logiparin were effective when administered in single daily subcutaneous doses; this could lead to lower treatment costs. Additional studies are needed to compare LMW heparins and unfractionated heparin with respect to efficacy, bleeding complications, mortality, and cost. LMW heparins may be valuable alternatives to unfractionated heparin for the treatment of DVT.
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OBJECTIVE: To demonstrate that pharmacists, working collaboratively with patients and physicians and having immediate access to objective point-of-care patient data, promote patient persistence and compliance with prescribed dyslipidemic therapy that enables patients to achieve their National Cholesterol Education Program (NCEP) goals. DESIGN: Observational study. PARTICIPANTS: 26 community-based ambulatory care pharmacies: independent, chain-professional, chain-grocery store, home health/home infusion, clinic, health maintenance organization/managed care. MAIN OUTCOME MEASURES: Rates of patient persistence and compliance with medication therapy and achievement of target therapeutic goals. RESULTS: In a population of 397 patients over an average period of 24.6 months, observed rates for persistence and compliance with medication therapy were 93.6% and 90.1%, respectively, and 62.5% of patients had reached and were maintained at their NCEP lipid goal at the end of the project. CONCLUSION: Working collaboratively with patients, physicians, and other health care providers, pharmacists who have ready access to objective clinical data, and who have the necessary knowledge, skills, and resources, can provide an advanced level of care that results in successful management of dyslipidemia.
Office blood pressure measurement is the standard for assessing blood pressure control. Many patients, however, take their antihypertensive medication in the morning, so they are likely to have their office blood pressure measured during the maximal antihypertensive effect. It is therefore unknown whether patients deemed by office blood pressure to be controlled do in fact have 24h blood pressure control. The objectives of this study were to determine blood pressure control, including blood pressure control while the patients were awake and during the first 6 hours after awakening, by ambulatory blood pressure monitoring (ABPM) in treated hypertensive patients deemed by office blood pressure measurements to be controlled. A total of 103 patients on a stable antihypertensive regimen and deemed to be controlled in terms of office blood pressure values (mean office blood pressure <140/90mmHg) were enrolled. Patients were stratified by cardiovascular risk status and the number of antihypertensive medications that they were taking. Seventy-eight out of 103 participants successfully completed ABPM. The mean ambulatory blood pressure was greater than 135/85mmHg and 140/90mmHg while awake for 37% (95% confidence interval [CI] 26-48%) and 23% (95% CI 14-32%) of all patients respectively. Forty-eight per cent (95% CI 33-63%) of patients taking monotherapy versus 25% (95% CI 11-39%) of patients on multiple antihypertensive medications were uncontrolled (P=0.039) using 135/85mmHg as the reference value. Thirty-one per cent (95% CI, 17-44%) of patients on monotherapy versus 14% (95% CI 3-25%) of patients on multiple antihypertensive medication were uncontrolled (P=0.064) using 140/90mmHg instead. These results demonstrate that a high number of patients deemed by office blood pressure to be under control do not have adequate blood pressure control based on ABPM.
OBJECTIVE: To review the pathophysiology of hypertension and complications in patients with diabetes mellitus, specifically focusing on diabetic nephropathy; to evaluate the current clinical literature regarding the appropriate management of hypertension in this patient group; and to offer treatment recommendations. DATA SOURCES: A MEDLINE search of applicable English-language clinical studies, abstracts, and review articles pertaining to hypertension, diabetes, and diabetic nephropathy. STUDY SELECTION: Relevant studies on humans, examining hypertension, diabetes, and diabetic nephropathy, and the effects of drug therapy on these interrelated disease states. DATA SYNTHESIS: Pathophysiology of hypertension in the patient with diabetes mellitus and the pathophysiology of diabetic nephropathy are discussed. Studies evaluating the therapeutic effect of certain antihypertensive agents, their effect on glucose control and insulin sensitivity, and the progression of diabetic nephropathy are reviewed. Recommendations on the treatment of the patient with diabetes and hypertension are given. CONCLUSIONS: The treatment of the patient with diabetes mellitus and hypertension remains complex. Interventions in this patient population should not only decrease blood pressure, but also reduce the risk of both vascular and nonvascular complications. Data support the theory that by controlling a patient's hypertension, the incidence of albuminuria and the progression of diabetic nephropathy are slowed. Additionally, data are available to support the use of pharmacologic interventions in nonhypertensive patients with diabetes and proteinuria. Drug therapies that have produced reductions in proteinuria in this patient population include angiotension-converting enzyme inhibitors and nondihydropyridine calcium-channel antagonists. Additional information is needed to better differentiate the individual agents within each of the antihypertensive drug classes regarding their individual effects on the patient with diabetes and hypertension, specifically effects on diabetic nephropathy and its progression to endstage renal disease.