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ABSTRACT: BACKGROUND: Metabolic syndrome (MetS) is characterized by obesity, insulin resistance, dyslipidemia, and hypertension. The Retinal Function Imager (RFI) is a new technique for measuring retinal blood-flow velocity. This study aims to compare retinal blood flow velocity between MetS and healthy subjects. METHODS: Twenty eyes of 20 MetS males and 21 eyes of 21 aged-matched healthy males underwent RFI and carotid-femoral pulse wave velocity (PWV) measurement as well as assessment of MetS parameters. The results in MetS and healthy subjects were compared. RESULTS: The average venular velocity in the MetS patients was significantly higher than in the healthy subjects (2.7 ± 0.0 mm/sec versus 2.5 ± 0.0 mm/sec respectively, P = 0.013), following adjustment for age, heart rate and systolic blood pressure. Carotid-femoral PWV was higher in the MetS population than the healthy controls (10.3 ± 1.2 mm/sec versus 9.3 ± 1.5 mm/sec respectively, P = 0.005). The diastolic blood pressure and MAP were correlated strongly with the arterial blood flow velocities in healthy subjects (r = 0.503, P = 0.020 and r = 0.474, P = 0.030 respectively) but not in MetS subjects. CONCLUSIONS: The RFI was able to distinguish between the retinal blood flow of normal and MetS subjects. Higher venular blood flow velocity and the poor correlation between velocity and blood pressure of MetS subjects suggest that MetS causes microvascular damage.
Albrecht von Graæes Archiv für Ophthalmologie 04/2013; · 2.17 Impact Factor
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ABSTRACT: Atherosclerosis is one of the main causes of morbidity and mortality world-wide and specifically in Israel. These guidelines update the previous guidelines of the Israeli Society for Research, Prevention and Treatment of Atherosclerosis, published in 2005. The need for an update is based on new scientific data published in recent years necessitating changes in the recommendations for preventing and treating atherosclerosis. These guidelines were written in collaboration between all the societies outlined here and the content of this statement was approved by the delegates of these societies. The recommendations were written taking into consideration guidelines published by other international medical societies and also the specific needs of the Israeli medical system. Due to limitations of space, in the current paper we present: assessment of cardiovascular risk, smoking cessation and the treatment of dyslipidemia. Other sections including: recommendations to the general population, nutritional and physical activity recommendations, treatment of hypertension, prevention of ischemic stroke and the metabolic syndrome are available at http://www.ima.org.il/harefuah.
Harefuah 05/2012; 151(5):281-8, 319, 318.
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ABSTRACT: To compare retinal blood flow velocity in small vessels of patients with early diabetes mellitus (DM), without any morphologic changes related to diabetic retinopathy, with that in a control group.
The authors used the retinal function imager to measure blood flow velocities, from many small vessels, simultaneously. Twenty-three eyes of 14 patients with early DM and 51 eyes of 31 healthy subjects were enrolled. Differences between the patients and the control group were assessed by mixed linear models.
Venous average velocity significantly increased in the DM group (3.8 ± 1.2 vs. 2.9 ± 0.5 mm/second, P < 0.0001) than in the healthy subjects. Arterial velocity of DM patients was also significantly higher (4.7 ± 1.7 vs. 4.1 ± 0.9 mm/second, P = 0.03). There was no statistically significant difference between groups in age, gender, heart rate, and systolic blood pressure. The diastolic blood pressure in the DM patients was lower than that in the healthy group (P = 0.03).
There was an increase in arterial and venous retinal blood flow velocities of patients with early DM with no diabetic retinopathy. These findings support the notion that abnormalities in vessel function exist in diabetic eyes before the development of structural changes. This noninvasive approach facilitated the assessment of early hemodynamic abnormalities and may assist in screening and monitoring.
Retina (Philadelphia, Pa.) 07/2011; 32(1):112-9. · 2.93 Impact Factor
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ABSTRACT: The reduction of elevated low-density lipoprotein cholesterol (LDL-c) and mainly dense LDL, is the main target in reducing CHR closely associated with coronary heart disease (CHD). The findings of epidemiological and clinical investigations have, however, revealed that it poses a cardiovascular risk in only half of CHD patients and that a more effective marker is required. Lipoprotein associated phospholipase A2 (Lp-PLA2) is an inflammatory biomarker which provides information on plaque inflammation and stability. It hydrolyzes oxidized phospholipids, resulting in lysophosphatidylcholine, which is pro-inflammatory in a theoretic plaque. It is an enzyme that is expressed in macrophages and foam cells in rupture-prone atherosclerotic plaque. In plasma, 80% of it is attached to LDL and 20% to HDL. Twenty five epidemiological studies have established that Lp-PLA2 is a unique biomarker that is highly vascular-specific and that it is directly related to plaque instability and rupture. The results of a meta-analysis of 20,000 patients established a high relative risk for cardiovascular events in patients with high Lp-PLA2 Levels. Data from epidemiological studies have shown that Lp-PLA2 is a risk factor for primary and secondary ischemic stroke. Studies on drapalib, which is a direct inhibitor of Lp-PLA2, have shown that Lp-PLA2 prevents necrotic core progression and reduces plaque inflammation. Patients who are at moderate or high risk of CHD, and who have high levels of Lp-PLA2, should be considered as high and very high risk, respectively, and receive the appropriate treatment.
Harefuah 02/2011; 150(2):136-40, 205.
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ABSTRACT: The aim of the current study was to evaluate the therapeutic effects of omega-3 plant sterol esters (n-3-PSE) on lipid profile and other coronary heart disease risk factors in subjects with mixed hyperlipidemia.
Ninety-one patients with mixed hyperlipidemia were randomized in a double blind fashion to receive either placebo (corn oil) or n-3-PSE. Twenty four patients dropped out or were excluded from the efficacy analysis due to protocol violation. The primary efficacy endpoint was mean change in plasma low-density lipoprotein cholesterol (LDL-C) levels after 12 weeks of treatment. Other efficacy measures included plasma lipids, lipoproteins, and high-sensitivity C-reactive protein (hsCRP) levels. Participants who completed the double-blind study were given the option to continue into an open-label, 12-weeks follow up phase.
n-3-PSE treatment did not result in a significant change in LDL-C levels. Triglyceride levels were reduced significantly by 19% (51 mg/dL, p < 0.0001) in the n-3-PSE group in comparison with the placebo group (p = 0.025). Diastolic blood pressure and hsCRP were reduced by 7% (5.9 mmHg) and 7.8% (0.6 mg/L), respectively, and were significantly different from the placebo group (p = 0.036 and p = 0.018, respectively).
In patients with mixed hyperlipidemia, n-3-PSE treatment may offer a safe and effective therapy for triglyceride level reduction while avoiding the typical increase in LDL-C levels associated with n-3 fatty acid treatment. The observed reduction in blood pressure and inflammation markers warrants further evaluation. The positive effect of n-3-PSE treatment was preserved at the end of the follow up phase.
Cardiovascular Drugs and Therapy 12/2010; 24(5-6):429-37. · 3.13 Impact Factor
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ABSTRACT: To compare the predictive power of different endothelial progenitor cell (EPC) phenotypic markers for future cardiovascular events.
Peripheral blood was collected from 76 consecutive patients with acute coronary syndromes (ACS) who underwent percutaneous coronary intervention in our institute. The various EPC phenotypes of peripheral blood mononuclear cells were CD34+CD133+, CD34+KDR+, and CD 133+KDR+. The outcome endpoint included cardiovascular mortality, recurrent ACS, and hospitalization for decompensated heart failure during a 24-mo follow-up period.
CD34+CD133+ cells (P = 0.034), but not CD34+KDR+ (P = 0.35) or CD 133+KDR+ cells (P = 0.19), were found to predict recurrent ACS. We found no correlation between EPCs measured by any of the three phenotypic combinations of accepted CD markers and the total combination of these separate outcomes.
The EPC CD34+CD133+ phenotype, but not the CD34+KDR+ or the CD 133+KDR+ phenotypes, is predictive of future adverse cardiovascular outcomes.
World journal of cardiology. 09/2010; 2(9):299-304.
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ABSTRACT: The incidence of heart failure (HF) is constantly increasing in the Western world. Treatment with statins is well established for the primary and secondary prevention of cardiac events by lowering low-density lipoprotein (LDL) cholesterol levels. There are conflicting reports on the role of LDL cholesterol as an adverse prognostic predictor in patients with advanced HF. The aim of this study was to investigate the association between LDL cholesterol levels and clinical outcomes in 297 patients with severe HF (average New York Heart Association class 2.8). The mean follow-up period was 3.7 years (range 8 months to 11.5 years), and 37% of the patients died during follow-up. The mean time to first hospital admission for HF was 25 +/- 17 months. The study group was divided according to plasma LDL level < or =89, >89 to < or =115, >115 mg/dl. Patients with the highest baseline LDL cholesterol levels had significantly improved outcomes, whereas those with the lowest LDL cholesterol levels had the highest mortality. When analyzed with respect to statin use, it emerged that the negative association between LDL cholesterol level and mortality was present only in the patients with HF who were treated with statins. In conclusion, lower LDL cholesterol levels appear to predict less favorable outcomes in patients with HF, particularly those taking statins, raising questions about the need for aggressive LDL cholesterol-lowering strategy in patients with HF, regardless of its cause.
The American journal of cardiology 01/2010; 105(1):100-4. · 3.58 Impact Factor
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ABSTRACT: Oxidative stress appears to play a significant role in the pathogenesis of heart failure (HF). Antibodies to oxidized low-density lipoprotein (Ox LDL Abs) reflect an immune response to LDL over a prolonged period and may thus represent oxidative stress over an extended time. Ox LDL Abs have been shown to correlate with clinical control in HF patients. We evaluated the predictive power of Ox LDL Abs on the outcome in patients with HF.
Baseline levels of Ox LDL Abs were determined by enzyme-linked immunosorbent assay in 284 consecutive outpatients with severe chronic HF who were being treated in the cardiology services of our medical center. Their mean New York Heart Association (NYHA) Class was 2.8. The mean follow-up for the group was 3.7 years, during which 107 (37%) died. The mean time from symptom onset to first hospital admission from HF was 25.8 months. Ox LDL Abs were found to predict morbidity and mortality as evaluated by a Cox multivariate regression analysis with a hazard ration of 1.013 (P < .013), whereas N-terminal pro-B-type natriuretic peptide (NT pro-BNP) levels achieved a HR of 1.028 (P < .099).
Ox LDL Abs level maybe a useful parameter for monitoring and planning better management of patients with HF. It was superior to pro-BNP as a predictor of clinical course as expressed by time to hospitalization.
Journal of cardiac failure 11/2009; 15(9):770-4. · 3.25 Impact Factor
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ABSTRACT: Lymphocytes play an important role in the progression of atherosclerosis. Recently, hypoxia inducible factor-1 (HIF-1) was found to attenuate inflammation by regulating T cell activation and cytokine production. We studied the effects of overexpression of HIF-1alpha in ApoE knockout murine lymphocytes, on experimental atherosclerosis.
ApoE-/- mice were submitted to intravenous hydrodynamic injection of empty plasmid or HIF-1alphaP564A (HIF-1alpha mutated stabilized construct). Robust expression of HIF-1alpha was evident in spleen cells of recipient animals. Increased expression of IL-10 as well as decreased expression of IFN-gamma was measured in splenocytes of HIF-1alpha-treated mice by RT-PCR. One week postinjection, antibody array analysis revealed a pattern consistent with a T helper 1 to T helper 2 shift. On sacrifice, assessment of aortic sinus lesions revealed a significant reduction in plaque size in HIF-1alpha injected mice. A reduced expression of IFN-gamma was evident in CD4+ spleen-derived lymphocytes and aortas of HIF-1alpha-injected mice.
HIF-1alpha expression in mouse lymphocytes is associated with a reduced IFN-gamma expression and attenuation of experimental atherosclerosis.
Arteriosclerosis Thrombosis and Vascular Biology 03/2009; 29(5):665-70. · 6.37 Impact Factor
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ABSTRACT: Clopidogrel is a widely used anti-thrombotic for the prevention of stent thrombosis and cardiovascular events in patients with coronary atherosclerosis. Clopidogrel has been shown to exhibit anti-inflammatory effects that are related to the attenuated activation of platelets. Atherosclerosis is a complex process in which the immune system and the endothelium appear to play a prominent role. Herein, we tested the hypothesis that clopidogrel will influence plaque size and composition in the atherosclerosis prone apolipoprotein E knockout (apoE KO) mouse model.
Eight week old mice were fed daily with either PBS, 1 mg or 2 mg of clopidogrel for 10 weeks. Plaque size was evaluated in the aortic sinus and cellular and humoral responses were studied as well as splenic and bone marrow endothelial progenitors by FACS. Treatment with either 1 mg and 2 mg of clopidogrel significantly reduced plaque size and augmented its stability by increasing atheromatous fibrous area. Whereas antigen specific oxLDL immune response was not influenced by clopidogrel feeding, the number of atheroprotective regulatory CD4+CD25+ T cells was significantly increased. Moreover, clopidogrel treatment resulted in a prominent rise in splenic but not bone marrow derived Sca-1+/flk-1+ endothelial progenitors.
Clopidogrel significantly reduces atheroma burden and stabilizes aortic sinus plaques in apoE KO mice. These effects may partially be mediated by upregulation of the regulatory T cell pool and splenic endothelial progenitor cells. These findings may expand the potential applications of clopidogrel in human subjects.
Microvascular Research 02/2009; 77(3):364-9. · 2.83 Impact Factor
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ABSTRACT: Myeloperoxidase levels were shown to reflect endothelial dysfunction, inflammation, atherosclerosis and oxidative stress.
To examine the role of circulating myeloperoxidase, a leukocyte-derived enzyme, as a predictor of mortality in patients with congestive heart failure.
Baseline serum MPO levels were measured in 285 consecutive CHF patients and 35 healthy volunteers. N-terminal pro-brain natriuretic peptide and high sensitivity C-reactive protein concentrations were also measured. The primary outcome endpoint was overall mortality.
MPO levels were significantly elevated in patients with CHF compared to healthy volunteers (P = 0.01). During a mean follow-up of 40.9 +/- 11.3 months there were 106 deaths. On a univariate Cox regression analysis MPO levels were of marginal value (P = 0.07) whereas NT-proBNP was of considerable value (P < 0.0001) in predicting all-cause mortality. By dividing our cohort according to NT-proBNP levels into high, intermediate and low risk groups a clear difference in mortality was shown. By further dividing the patient cohort according to MPO levels above or below the median (122.5 ng/ml), mortality prediction improved in the patients with intermediate NT-proBNP values.
MPO levels are elevated in CHF and correlate with disease severity. MPO has an additive predictive value on mortality in patients with intermediate NT-proBNP levels.
The Israel Medical Association journal: IMAJ 12/2008; 10(12):884-8. · 1.02 Impact Factor
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ABSTRACT: Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are in widespread use due to their LDL reducing properties and concomitant improvement of clinical outcome in patients with and without preexisting atherosclerosis. Considerable evidence suggests that immune mediated mechanisms play a dominant role in the beneficial effects of statins. Naturally occurring CD4(+)CD25(+) regulatory T cells (Tregs) have a key role in the prevention of various inflammatory and autoimmune disorders by suppressing immune responses. We tested the hypothesis that statins influence the circulating number and the functional properties of Tregs. We studied the effects of in vivo and in vitro statin treatment of human and murine mononuclear cells on the number of Tregs and the expression level of their master transcription regulator, Foxp3. Atorvastatin, but not mevastatin nor pravastatin, treatment of human peripheral blood mononuclear cells (PBMCs) increased the number of CD4(+)CD25(high) cells, and CD4(+)CD25(+)Foxp3(+) cells. These Tregs, induced by atorvastatin, expressed high levels of Foxp3, which correlated with an increased regulatory potential. Furthermore, co-culture studies revealed that atorvastatin induced CD4(+)CD25(+)Foxp3(+) Tregs were derived from peripheral CD4(+)CD25(-)Foxp3(-) cells. Simvastatin and pravastatin treatment in hyperlipidemic subjects increased the number of Tregs. In C57BL/6 mice however, no effect of statins on Tregs was evident. In conclusion, statins appear to significantly influence the peripheral pool of Tregs in humans. This finding may shed light on the mechanisms governing the plaque stabilizing properties of statins.
Atherosclerosis 05/2008; 197(2):829-39. · 3.79 Impact Factor
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ABSTRACT: Atherosclerosis is one of the principal causes of morbidity and mortality worldwide. The recent decades have witnessed great advances both in the identification of risk factors for the development of atherosclerosis and the treatment of its complications. This effort was rewarded with the reduction of mortality rates from cardiovascular diseases. The need for an update of the recommendations for the prevention of atherosclerosis and cardiovascular diseases stems from a large body of recently published trials, leading to fundamental changes in the way we treat patients with various levels of risk. The second part of the guidelines deals with the treatment of diabetes mellitus, dyslipidemia and the prevention of stroke.
Harefuah 10/2005; 144(9):647-54, 675.
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ABSTRACT: Atherosclerosis is one of the principal causes of morbidity and mortality worldwide. The recent decades have witnessed great advances both in the identification of risk factors for the development of atherosclerosis and the treatment of its complications. This effort was rewarded with the reduction of mortality rates from cardiovascular diseases. The need for an update of the recommendations for the prevention of atherosclerosis and cardiovascular diseases stems from a large body of recently published trials, leading to fundamental changes in the way we treat patients with various levels of risk. The first part of the guidelines deals with general recommendations, applicable to the population as a whole, at all levels of risk, together with recommendations for the treatment of hypertension.
Harefuah 08/2005; 144(7):506-12, 525.
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ABSTRACT: Patients with diabetes mellitus have a 2- to 4-fold increased risk of atherosclerotic cardiovascular, peripheral vascular, and cerebrovascular disease, which are the leading causes of morbidity and mortality in this population. Several epidemiological studies have shown an association between diabetic dyslipidemia, which is characterized by hypertriglyceridemia, low levels of high density lipoprotein-cholesterol, postprandial lipemia and small, dense low density lipoprotein-cholesterol (LDL-C) particles, and the occurrence of cardiovascular disease. Other studies have established the beneficial effects of lipid lowering on the reduction of major coronary events in diabetic patients. The recent National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) guidelines emphasize diabetes as a coronary heart disease risk equivalent. The NCEP ATP III states that elevated LDL-C is a major risk factor for coronary heart disease, and the primary goal of risk-reduction therapy is the reduction of LDL-C levels to 100 mg/dL. This article defines and describes diabetic dyslipidemia and its etiology and pathogenesis, as well as reviewing guidelines and recommendations for treatment of this disorder. Treatment of diabetic dyslipidemia includes 1) lifestyle modifications: physical activity and a diet low in saturated fats and cholesterol and high in complex carbohydrates and fiber; and 2) pharmacological treatment with (i) oral antihyperglycemic agents: metformin and thiazolidinediones; (ii) weight reduction drugs: orlistat and sibutramine and; (iii) lipid-lowering drugs: HMG-CoA reductase inhibitors, fibric acid derivatives, nicotinic acid, and bile acid sequestrants.
Treatments in Endocrinology 02/2003; 2(4):231-45.
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Rivka Rotstein,
Tali Landau,
Abraham Twig, Ardon Rubinstein,
Michael Koffler,
Daniel Justo,
Doron Constantiner,
David Zeltser,
Itzhak Shapira,
Tamar Mardi,
Yelena Goldin,
Shlomo Berliner
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ABSTRACT: Multiple acute phase proteins and atherosclerotic risk factors increase the aggregability of erythrocytes.
We used a simple slide test and image analysis to determine the degree of erythrocyte adhesiveness/aggregation in the peripheral blood of 222 women and 221 men with no, one, two or more atherosclerotic risk factors. The degree of erythrocyte adhesiveness/aggregation correlated significantly with the concentration of commonly used variables of the acute phase response. We also showed that individuals with low erythrocyte adhesiveness/aggregation tend to be younger and to have fewer risk factors for atherosclerosis, including diabetes mellitus, hypertension, hyperlipidemia and smoking.
The association between increased erythrocyte adhesiveness/aggregation, higher concentrations of acute phase proteins, and increased atherosclerotic risk factors points to a possible clinical applicability of the erythrocyte adhesiveness/aggregation test (EAAT) to reveal the presence of both low-grade subclinical smoldering inflammation and morbid biology in individuals with risk factors for atherosclerosis.
Atherosclerosis 01/2003; 165(2):343-51. · 3.79 Impact Factor
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Galit Fusman,
Tamar Mardi,
Daniel Justo,
Meirav Rozenblat,
Rivka Rotstein,
David Zeltser, Ardon Rubinstein,
Michael Koffler,
Esther Shabtai,
Shlomo Berliner,
Itzhak Shapira
The American Journal of Cardiology 10/2002; 90(5):561-3. · 3.37 Impact Factor
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The Israel Medical Association journal: IMAJ 07/2002; 4(6):456-7. · 1.02 Impact Factor
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ABSTRACT: The aim of this study was to investigate the effect of interferon alpha-2a, an angiogenesis inhibitor, on eyes with active neovascularization after complete laser panretinal photocoagulation treatment.
Eight patients with active neovascularization persisting for 6 months or more after completion of full panretinal photocoagulation were included in the study. All patients were treated with subcutaneous injections of 6 million international units of interferon alpha-2a, 3 times a week, for an average period of 10 months. Visual acuity, contrast sensitivity, blood tests, fundus photographs, fluorescein angiography, and physical examination were performed periodically. The main outcome measures were visual acuity and extent of neovascularization as assessed by fundus photography and fluorescein angiography.
The 5 men and 3 women (mean age, 60 years) had a mean duration of diabetes of 19 years. The average study follow-up was 42.2 +/- 8.7 weeks. Visual acuity and extent of neovascularization improved or remained stable in 7 patients. In none of the patients was there progression of neovascularization, but in 1 patient it could not be assessed due to vitreous hemorrhage. Most patients had malaise during the first weeks of treatment, but none of the patients suffered from nonreversible side effects associated with interferon alpha-2a.
This pilot study provides evidence that interferon alpha-2a might have a role in the regression of proliferative diabetic retinopathy and that further investigation is warranted.
Ophthalmic Surgery Lasers and Imaging 35(1):16-22. · 0.62 Impact Factor
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ABSTRACT: Although a low plasma high-density lipoprotein cholesterol (HDL-C) level is a well-accepted risk factor for coronary artery disease (CAD), it is unclear whether pharmacologic agents can effectively increase HDL-C levels and/or reduce the incidence of CAD in patients with isolated low HDL-C levels. An important determinant of HDL levels is the efficiency of postprandial lipoprotein catabolism. The purpose of the present study was to evaluate the efficacy of bezafibrate therapy in increasing HDL-C levels in these patients and to examine its effect on postprandial lipoprotein levels. Fasting and postprandial lipid and lipoprotein levels were studied in 23 patients with isolated low HDL-C levels before and during 3 and 6 months of bezafibrate treatment. Postprandial lipoprotein levels were evaluated using the vitamin A—fat loading test, in which these intestinally derived lipoproteins are specifically labeled with retinyl palmitate (RP). Patients with isolated low HDL had significantly higher levels of chylomicron RP than a control group of 19 normolipidemic subjects. The area below the chylomicron RP curve was 17,773 ± 6,821 versus 13,936 ± 6,217 μg/L · h, respectively (P < .005). No differences were found in chylomicron remnant levels between the groups. Bezafibrate therapy reduced the chylomicron RP area by 27%, from 17,773 ± 6,821 to 12,895 ± 2,576, and the nonchylomicron RP area by 25%, from 6,059 ± 3,310 to 4,430 ± 1,963 (P < .0001). It increased fasting HDL-C levels from 35 ± 3 to 38 ± 1.4 mg/dL after 3 months (P < .001) and to 40 ± 2.2 mg/dL after 6 months (P < .001). A highly significant inverse correlation (r = .8885, P < .001) was found between fasting HDL-C and postprandial chylomicron RP levels. The patients did not respond to therapy as a homogenous group. That is, eight patients did not respond to bezafibrate either by reducing postprandial lipoprotein levels or by increasing HDL-C levels, bezafibrate in these patients did significantly reduce low-density lipoprotein cholesterol (LDL-C) levels from 138 ± 4.8 to 125 ± 5.9 mg/dL (P < .0001) while the patients were on a strict low-fat, low-cholesterol diet. In conclusion, most patients with isolated low HDL-C levels also have a defect in postprandial lipoprotein metabolism. Bezafibrate therapy has a dual effect: it reduces the level of these possibly atherogenic lipoproteins and increases HDL-C levels. These findings support the use of bezafibrate therapy in high-risk patients with isolated low HDL-C levels.
Metabolism.
