ABSTRACT: The decrease of insulin sensitivity (IS) during myocardial infarction (MI) is strongly associated with increased morbidity and mortality. Recent data suggest that in individuals under stable conditions, high-density lipoprotein (HDL) may improve IS. To date, the role of HDL in the modulation of IS in acute metabolic stress conditions such as MI remains unknown.
To explore the association between plasma HDL-C and the change in IS during the acute phase of MI.
Consecutive nondiabetic patients with ST-segment elevation MI (n = 22) underwent direct measurement of IS through the euglycemic hyperinsulinemic clamp on the first morning and on the fifth day after onset of MI. Patients were grouped according to HDL-C levels at admission above and below the median value (35 mg/dL).
At admission, there was no significant difference in baseline IS index, clinical, anthropometric, or treatment characteristics between low and high HDL groups. Between admission and fifth day, there was a decrease of 8% in IS index in the low HDL group and an 11% increase in the high HDL group (P = .001 for intragroup and P = .012 for intergroup difference). This difference remained significant after we controlled for the sex, age, waist circumference, triglycerides, baseline IS index, and statin dose during hospitalization.
This is the first study to provide evidence that plasma levels of HDL-C are strongly associated with the recovery rate of IS during the acute phase of MI.
Journal of Clinical Lipidology 01/2013; 7(1):24-8. · 1.58 Impact Factor
ABSTRACT: Besides the time of exposure to the traditional risk factors, new players take the lead in the modulation of atherogenesis in the very elderly, promoting a step increase in the incidence of cardiovascular events. Accordingly, atherosclerotic plaques become more abundant and portray more unstable features, such as increased inflammatory activity and reduction of smooth muscle cells in the very elderly. This new scenario is composed of new potential modulators of atherogenesis such as cellular senescence, immunosenescence, frailty syndrome, sarcopenia and sirtuins, and changes among the traditional cardiovascular risk factors which gain new attributes and new magnitudes of interaction with atherosclerotic disease. Consistent with this concept, mortality from atherosclerotic disease has shown a decrease in individuals younger than 60 years, but no change in incidence in individuals over the age of 60 years. In this review, we present the most recent and relevant pieces of evidence to the peculiarities of traditional cardiovascular risk factors and new aging-related potential modulators of atherosclerotic disease in very elderly.
Atherosclerosis 07/2012; · 3.79 Impact Factor
ABSTRACT: During myocardial infarction (MI), a transient decrease of both insulin sensitivity and secretion triggers stress hyperglycemia, which is followed by a substantial increase in mortality. Recent findings in cellular models indicate that HDL may act on glucose homeostasis by improving insulin sensitivity and secretion. In this study, we explored this potential effect in patients during the acute phase of MI.
Plasma glucose, insulin and C-peptide were measured at admission in the first 24h and on the fifth day after MI with ST-segment elevation in 183 consecutive non-diabetic patients. Patients were divided into HDL-C quartiles for the analyses (Q1: <31, Q2: 31-38, Q3: 38-47 and Q4: >47mg/dL). The Homeostasis Model Assessment version 2 was used to assess insulin sensitivity (HOMA2S) and beta-cell function (HOMA2B).
On admission, no difference was found between the quartiles in glucose (p=0.6), insulin (p=0.6) or C-peptide (p=0.5) levels, HOMA2S (p=0.9) or HOMA2B (p=1.0). On the fifth day there was a reduction in glucose levels whose intensity was directly proportional to the HDL-C quartile (p<0.001). At the same time, there was a reduction in plasma insulin (p<0.001) and C-peptides (p<0.001) whose magnitude was inversely proportional to the HDL-C quartile. Consistently, the increase of HOMA2S (p<0.001) and HOMA2B (p=0.01) were also positively associated with HDL-C levels. Furthermore, plasma HDL-C levels were inversely and independently associated with blood glucose change during the acute phase.
This study demonstrates the association between low plasma HDL-C levels and increased duration of stress hyperglycemia during MI and suggests in humans the interaction between HDL and insulin secretion and sensitivity.
Atherosclerosis 01/2012; 220(1):231-6. · 3.79 Impact Factor
ABSTRACT: The present study aimed to verify the existence of a rebound inflammatory effect after statin withdrawal in the acute phase of myocardial infarction (MI).
In a prospective observational cohort, changes in C-reactive protein (CRP) between the first and the fifth day after MI were evaluated in 249 consecutive patients who were using statins prior to and during MI (SS), statins prior to but not during MI (SN), no statin prior to but during MI (NS), and no statin prior to nor during MI (NN). Data are presented as median (interquartile range).
At baseline, statin users presented a trend to lower CRP values as compared with those without this treatment before the MI (NN: 1.0(0.4-1.5)mg/dL vs. NS: 1.0(0.3-2.8)mg/dL vs. SS: 0.5(0.3-1.0)mg/dL vs. SN: 0.6(0.4-1.0)mg/dL; p=0.08). By the fifth day, median CRP was significantly higher in the SN (18.1(16.1-23.2)mg/dL) group as compared with other groups (NN: 10.5(9.3-13.2)mg/dL vs. NS: 2.9(1.5-4.5)mg/dL vs. SS: 1.1(0.8-2.4)mg/dL; p<0.0001). At the fifth day, the median CRP in the NN group was lower than in the SN group (p<0.0001), but higher than the NS and SS groups (p<0.0001). There was no significant correlation between CRP change and the change of LDL-cholesterol, HDL-cholesterol or triglycerides.
The present study has, for the first time, provided evidence for the existence of a rebound inflammatory effect after statin cessation. This rebound reaction may contribute for the adverse outcome of patients who stop statin treatment during MI.
Atherosclerosis 04/2009; 207(1):191-4. · 3.79 Impact Factor