Common medications used by patients with type 2 diabetes mellitus: what are their effects on the lipid profile?

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Abstract

Dyslipidemia is the most fundamental risk factor for atherosclerotic cardiovascular disease (ASCVD). In clinical practice, many commonly prescribed medications can alter the patient’s lipid profile and, potentially, the risk for ASCVD—either favorably or unfavorably. The dyslipidemia observed in type 2 diabetes mellitus (T2DM) can be characterized as both ominous and cryptic, in terms of unrecognized, disproportionately elevated atherogenic cholesterol particle concentrations, in spite of deceptively and relatively lower levels of low-density lipoprotein cholesterol (LDL-C). Several factors, most notably insulin resistance, associated with the unfavorable discordance of elevated triglyceride (TG) levels and low levels of high-density lipoprotein cholesterol (HDL-C), have been shown to correlate with an increased risk/number of ASCVD events in patients with T2DM. This review focuses on known changes in the routine lipid profile (LDL-C, TGs, and HDL-C) observed with commonly prescribed medications for patients with T2DM, including antihyperglycemic agents, antihypertensive agents, weight loss medications, antibiotics, analgesics, oral contraceptives, and hormone replacement therapies. Given that the risk of ASCVD is already elevated for patients with T2DM, the use of polypharmacy may warrant close observation of overall alterations through ongoing lipid-panel monitoring. Ultimately, the goal is to reduce levels of atherogenic cholesterol particles and thus the patient’s absolute risk.

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Most cited references 109

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Inflammation in atherosclerosis: from pathophysiology to practice.

Peter Libby, Paul M Ridker, Göran K Hansson (2009)

Until recently, most envisaged atherosclerosis as a bland arterial collection of cholesterol, complicated by smooth muscle cell accumulation. According to that concept, endothelial denuding injury led to platelet aggregation and release of platelet factors which would trigger the proliferation of smooth muscle cells in the arterial intima. These cells would then elaborate an extracellular matrix that would entrap lipoproteins, forming the nidus of the atherosclerotic plaque. Beyond the vascular smooth muscle cells long recognized in atherosclerotic lesions, subsequent investigations identified immune cells and mediators at work in atheromata, implicating inflammation in this disease. Multiple independent pathways of evidence now pinpoint inflammation as a key regulatory process that links multiple risk factors for atherosclerosis and its complications with altered arterial biology. Knowledge has burgeoned regarding the operation of both innate and adaptive arms of immunity in atherogenesis, their interplay, and the balance of stimulatory and inhibitory pathways that regulate their participation in atheroma formation and complication. This revolution in our thinking about the pathophysiology of atherosclerosis has now begun to provide clinical insight and practical tools that may aid patient management. This review provides an update of the role of inflammation in atherogenesis and highlights how translation of these advances in basic science promises to change clinical practice.

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From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I.

Morteza Naghavi, Peter Libby, Erling Falk … (2003)

Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document focuses on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.

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Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. Heart and Estrogen/progestin Replacement Study (HERS) Research Group.

S Hulley, D Grady, T. Bush … (1998)

Observational studies have found lower rates of coronary heart disease (CHD) in postmenopausal women who take estrogen than in women who do not, but this potential benefit has not been confirmed in clinical trials. To determine if estrogen plus progestin therapy alters the risk for CHD events in postmenopausal women with established coronary disease. Randomized, blinded, placebo-controlled secondary prevention trial. Outpatient and community settings at 20 US clinical centers. A total of 2763 women with coronary disease, younger than 80 years, and postmenopausal with an intact uterus. Mean age was 66.7 years. Either 0.625 mg of conjugated equine estrogens plus 2.5 mg of medroxyprogesterone acetate in 1 tablet daily (n = 1380) or a placebo of identical appearance (n = 1383). Follow-up averaged 4.1 years; 82% of those assigned to hormone treatment were taking it at the end of 1 year, and 75% at the end of 3 years. The primary outcome was the occurrence of nonfatal myocardial infarction (MI) or CHD death. Secondary cardiovascular outcomes included coronary revascularization, unstable angina, congestive heart failure, resuscitated cardiac arrest, stroke or transient ischemic attack, and peripheral arterial disease. All-cause mortality was also considered. Overall, there were no significant differences between groups in the primary outcome or in any of the secondary cardiovascular outcomes: 172 women in the hormone group and 176 women in the placebo group had MI or CHD death (relative hazard [RH], 0.99; 95% confidence interval [CI], 0.80-1.22). The lack of an overall effect occurred despite a net 11% lower low-density lipoprotein cholesterol level and 10% higher high-density lipoprotein cholesterol level in the hormone group compared with the placebo group (each P<.001). Within the overall null effect, there was a statistically significant time trend, with more CHD events in the hormone group than in the placebo group in year 1 and fewer in years 4 and 5. More women in the hormone group than in the placebo group experienced venous thromboembolic events (34 vs 12; RH, 2.89; 95% CI, 1.50-5.58) and gallbladder disease (84 vs 62; RH, 1.38; 95% CI, 1.00-1.92). There were no significant differences in several other end points for which power was limited, including fracture, cancer, and total mortality (131 vs 123 deaths; RH, 1.08; 95% CI, 0.84-1.38). During an average follow-up of 4.1 years, treatment with oral conjugated equine estrogen plus medroxyprogesterone acetate did not reduce the overall rate of CHD events in postmenopausal women with established coronary disease. The treatment did increase the rate of thromboembolic events and gallbladder disease. Based on the finding of no overall cardiovascular benefit and a pattern of early increase in risk of CHD events, we do not recommend starting this treatment for the purpose of secondary prevention of CHD. However, given the favorable pattern of CHD events after several years of therapy, it could be appropriate for women already receiving this treatment to continue.

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Author and article information

Contributors

Paul D. Rosenblit: 714-375-5575 , pdrosenblit@yahoo.com

Journal

Journal ID (nlm-ta): Cardiovasc Diabetol

Journal ID (iso-abbrev): Cardiovasc Diabetol

Title: Cardiovascular Diabetology

Publisher: BioMed Central (London )

ISSN (Electronic): 1475-2840

Publication date (Electronic): 14 July 2016

Publication date PMC-release: 14 July 2016

Publication date Collection: 2016

Volume: 15

Electronic Location Identifier: 95

Affiliations

[ ]Diabetes/Lipid Management & Research Center, 18821 Delaware St, Suite 202, Huntington Beach, CA 92648 USA

[ ]Division of Endocrinology, Diabetes, Metabolism, Department of Medicine, University of California, Irvine (UCI) School of Medicine, Irvine, CA USA

Article

Publisher ID: 412

DOI: 10.1186/s12933-016-0412-7

PMC ID: 4946113

PubMed ID: 27417914

SO-VID: 687468a8-be48-4a93-8313-77d5ee2534b6

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 17 March 2016

Date accepted : 14 June 2016

Funding

Funded by: Janssen Scientific Affairs, LLC

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ScienceOpen disciplines: Endocrinology & Diabetes

Keywords: atherosclerosis,dyslipidemia,hdl cholesterol,ldl cholesterol,triglycerides,type 2 diabetes mellitus,cardiovascular risk factors,polypharmacy

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ScienceOpen disciplines: Endocrinology & Diabetes

Keywords: atherosclerosis, dyslipidemia, hdl cholesterol, ldl cholesterol, triglycerides, type 2 diabetes mellitus, cardiovascular risk factors, polypharmacy

Common medications used by patients with type 2 diabetes mellitus: what are their effects on the lipid profile?

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Abstract

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Journal of the ASEAN Federation of Endocrine Societies

Most cited references 109

Inflammation in atherosclerosis: from pathophysiology to practice.

From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I.

Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. Heart and Estrogen/progestin Replacement Study (HERS) Research Group.

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