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Biomedical subjects

Tohru Masuyama

Publications and source records attributed to Tohru Masuyama.

At least 19 recordsLinked to original sources
PubMed2007

Therapeutic effects of angiotensin II type 1 receptor blocker at an advanced stage of hypertensive diastolic heart failure.

OBJECTIVE: Angiotensin II type 1 receptor blocker (ARB) is increasingly prescribed for the treatment of systolic heart failure with a growing body of clinical evidence. The roles of ARB, however, remain to be clarified in the treatment of diastolic heart failure (DHF), particularly at its advanced stage. This experimental study investigated the effects of ARB administered at an advanced stage of hypertensive DHF. METHODS: Dahl salt-sensitive rats fed an 8% NaCl diet from age 7 weeks represent overt DHF at age 20 weeks, as noted in previous studies (hypertensive DHF model). The DHF model rats were randomly divided into two groups at age 17 weeks when left ventricular diastolic dysfunction, hypertrophy, fibrosis, macrophage infiltration and reactive oxygen species generation were already augmented; six rats treated for 3 weeks with a subdepressor dose of ARB (olmesartan 0.6 mg/kg per day), and six untreated rats. RESULTS: The 3-week administration of ARB significantly decreased the left ventricular end-diastolic pressure in association with attenuation of left ventricular hypertrophy, fibrosis and diastolic dysfunction. Macrophage infiltration was attenuated with decreased gene expression of transforming growth factor-beta1 and monocyte chemoattractant protein-1 in the left ventricular myocardium of the ARB-treated rats. The production of reactive oxygen species also decreased with NADPH oxidase activity. CONCLUSIONS: ARB provides beneficial effects in hypertensive DHF independent of its antihypertensive effects even if initiated at an advanced stage. The beneficial effects are at least partly attributed to the attenuation of inflammatory changes and oxidative stress through the suppression of cytokine and chemokine production and of NADPH oxidase activity.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

Elevated cardiac tissue level of aldosterone and mineralocorticoid receptor in diastolic heart failure: Beneficial effects of mineralocorticoid receptor blocker.

Cardiac aldosterone levels have not been evaluated in diastolic heart failure (DHF), and its roles in this type of heart failure remain unclear. This study aimed to detect cardiac aldosterone by use of a liquid chromatographic-mass spectrometric method and to assess the effects of mineralocorticoid receptor blockade on hypertensive DHF. Dahl salt-sensitive rats fed 8% NaCl diet from 7 wk (hypertensive DHF model) were divided at 13 wk into three groups: those treated with subdepressor doses of eplerenone (12.5 or 40 mg x kg(-1) x day(-1)) and an untreated group. Dahl salt-sensitive rats fed 0.3% NaCl diet served as controls. Cardiac aldosterone was detected in the DHF rats but not in the control rats, with increased ventricular levels of mineralocorticoid receptor. Cardiac levels of 11-deoxycorticosterone, corticosterone, and 11-dehydrocorticosterone were not different between the control and DHF rats, but the tissue level of corticosterone that has an affinity to mineralocorticoid receptor was 1,000 times as high as that of aldosterone. Aldosterone synthase activity and CYP11B2 mRNA were undetectable in the ventricular tissue of the DHF rats. Administration of eplerenone attenuated ventricular hypertrophy, ventricular fibrosis, myocardial stiffening, and relaxation abnormality, leading to the prevention of overt DHF. In summary, the myocardial aldosterone level increased in the DHF rats. However, its value was extremely low compared with corticosterone, and no evidence for enhancement of intrinsic myocardial aldosterone production was found. The upregulation of mineralocorticoid receptor may play a central role in the pathogenesis of DHF, and blockade of mineralocorticoid receptor is likely an effective therapeutic regimen of DHF.

Aldosterone↗
PubMed2006

Circadian variation of beat-to-beat QT interval variability in patients with prior myocardial infarction and the effect of beta-blocker therapy.

BACKGROUND: Recent studies have demonstrated that increased QT interval variability (QTV) is associated with a greater susceptibility to ventricular arrhythmias and that patients with prior myocardial infarction (MI) were prone to ventricular arrhythmias during the daytime. The goal of the present study was to investigate the circadian variation of the QTV and to determine whether beta-blocker therapy improves the temporal fluctuation of the ventricular repolarization in patients with MI. METHODS: The study population consisted of 15 MI patients who had not received beta-blocker therapy, 11 MI patients who had received beta-blocker therapy, and 12 healthy subjects. Twenty-four hour Holter monitoring was obtained, and the RR and QT intervals were calculated automatically from 512 consecutive sinus beats for every 2 hours. RESULTS: In the daytime, the QT-SD was significantly greater in the MI group than in the healthy subjects (P<0.01), but there was no difference in the QT-SD when comparing the beta-blocker group to the control group. Moreover, the QT variability index and the QT variance normalized for the mean QT were similar pattern with QT-SD. The heart rate variability did not significantly differ when compared between the three study groups. CONCLUSION: These data indicate that the QTV increases during the daytime in patients with MI and that this circadian effect is prevented by beta-blocker therapy. Thus, beta-blocker therapy may reverse the maladaptation of the ventricular repolarization to the change in the heart rate and may thereby reduce the ventricular arrhythmias and decrease the mortality in patients with MI.

Adrenergic beta-Antagonists↗
PubMed2006

Correlation between beat-to-beat QT interval variability and impaired left ventricular function in patients with previous myocardial infarction.

BACKGROUND: Beat-to-beat QT interval variability (QTV) is associated with sudden cardiac death and New York Heat Association functional class severity. We sought to evaluate the relationship between QTV and left ventricular (LV) function in patients with previous myocardial infarction (MI). METHODS: Fifty-nine patients with previous anterior MI were enrolled. LV ejection fraction (EF), LV end-systolic volume index (LVESVI), and LV end-diastolic volume index (LVEDVI) were measured by LV contrast angiography. QT interval was measured by automated analysis of 512-beat records of 12-lead electrocardiogram. The mean interval, standard deviation and variance in RR and QT intervals, and the QT variability index (QTVI) were calculated for each patient using two leads that corresponded with and without the infarction site. High-frequency power, low-frequency power, total-frequency power, and the ratio of low-frequency to high-frequency power in RR and QT intervals were calculated. RESULTS: While measured indices of RR intervals and indices of QT intervals, which did not correspond with the infarction site, did not correlate with differences in LV function, measured indices of QT intervals, which corresponded with the infarction site, did correlate with differences in LV function. However, there were no correlations between the ratio of low-frequency to high-frequency power in QT intervals and EF or LVEDVI. Correlations between QTVI and LV function were observed, particularly between QTVI and LVESVI (r = 0.712, P < 0.0001). CONCLUSION: In patients with previous anterior MI, there was variability in temporal dispersion of QT interval and a strong correlation between QTV corresponded with the infarcted site and LV function.

Aged↗
PubMed2006

Left ventricular diastolic dysfunction in diabetic patients: pathophysiology and therapeutic implications.

Patients with signs and symptoms of heart failure and a preserved left ventricular (LV) systolic function may have significant abnormalities in diastolic function. This condition is called diastolic heart failure (DHF) and is observed in about 40% of patients with chronic heart failure (CHF). Diabetes mellitus is one of the major risk factors for DHF. Diastolic dysfunction is observed in about 40% of patients with diabetes mellitus and correlates with poor glycemic control. Suggested mechanisms for diastolic dysfunction in the diabetic heart are: (i) abnormalities in high-energy phosphate metabolism; (ii) impaired calcium transport; (iii) interstitial accumulation of advanced glycosylation end products; (iv) imbalance in collagen synthesis and degradation; (v) abnormal microvascular function, (vi) activated cardiac renin-angiotensin system; (vii) decreased adiponectin levels; and (viii) alteration in the metabolism of free fatty acids and glucose. Because most large, randomized clinical trials in CHF have enrolled only patients with systolic dysfunction, the specific management of diastolic dysfunction is largely unknown. The CHARM-Preserved (Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity-Preserved) trial, the only mega trial specific for DHF (LV ejection fraction >40%), showed that the angiotensin II type 1 receptor antagonist (angiotensin receptor blocker [ARB]) candesartan cilexetil reduced hospital admissions for CHF but not cardiovascular death. Currently, the pharmacologic treatment used in systolic heart failure is also recommended in DHF and includes administration of diuretics and nitrates for pulmonary congestion, and long-term management with ACE inhibitors, ARBs, aldosterone antagonists, and beta-adrenoceptor antagonists. Poor glycemic control is associated with a high incidence of heart failure in diabetic patients, but the preferable antihyperglycemic regimen for DHF in patients with diabetes mellitus needs to be determined in further studies.

Adrenergic beta-Antagonists↗
PubMed2005

Different effects of long- and short-acting loop diuretics on survival rate in Dahl high-salt heart failure model rats.

OBJECTIVES: We compared therapeutic effects of furosemide, a short-acting loop diuretic, and azosemide, a long-acting one, in hypertensive heart failure rats to test the hypothesis that long-acting diuretics are superior to short-acting types in heart failure. METHODS: Dahl salt-sensitive rats fed an 8% NaCl diet from age 8 weeks were divided at age 21 weeks (compensated hypertrophic stage) into three groups: rats treated with furosemide (40 mg/kg/day), those treated with azosemide (80 mg/kg/day) and untreated rats. Rats fed a 0.3% NaCl diet served as controls. RESULTS: Both medications prevented left ventricular systolic dysfunction and enlargement at age 31 weeks, and attenuated macrophage infiltration, reactive oxygen species generation, and gelatinolytic activity to the same degree. Azosemide suppressed left ventricular fibrosis to the control level, but furosemide did not. Azosemide ameliorated myocardial catecholamine depletion and improved survival rate. Furosemide increased plasma norepinephrine levels and did not exert such beneficial effects. CONCLUSIONS: Azosemide provided better prognosis in heart failure rats compared with furosemide, partly through attenuation of the reflex increase in cardiac sympathetic neuronal activity caused by the development of heart failure. The current findings suggest a need for clinical trials examining whether long- and short-acting diuretics provide a different prognosis in patients with heart failure.

Animals↗
PubMed2005

ACE inhibitor and angiotensin II type 1 receptor blocker differently regulate ventricular fibrosis in hypertensive diastolic heart failure.

BACKGROUND: Promoted myocardial stiffening has a crucial role in the transition to overt diastolic heart failure (DHF) in hypertensive hearts and is attributed to progressive ventricular fibrosis. Previous studies revealed the effects of an angiotensin II type 1 receptor blocker (ARB) and an angiotensin-converting enzyme inhibitor (ACEI) on the synthesis and degradation of collagens in the other phenotype of heart failure, systolic heart failure, which has a different pathophysiology; however, little is known about their effects in DHF. OBJECTIVE: To investigate effects of an ACEI and an ARB on the regulatory system of ventricular fibrosis in hypertensive DHF. DESIGN AND METHODS: Dahl salt-sensitive rats fed a diet containing 8% NaCl from age 7 weeks (DHF model) were divided into three groups: six untreated rats, six rats treated with a subdepressor dose of an ARB, candesartan cilexetil (1 mg/kg per day), from age 8 weeks, and six rats treated with a subdepress or dose of an ACEI, temocapril hydrochloride (0.2 mg/kg per day), from age 8 weeks. Six Dahl salt-sensitive rats fed on normal chow served as controls. Data were collected when animals were aged 20 weeks. RESULTS: The administration of an ARB or an ACEI inhibited ventricular fibrosis to the same degree. The ACEI decreased the level of type I collagen mRNA, but the decrease was less than that induced by the ARB. The difference in collagen synthesis was probably cancelled out by that in degradation: both in-vitro and in-situ zymography showed that gelatinase activity was greater in the rats treated with the ACEI than in those treated with the ARB. CONCLUSIONS: An ARB and an ACEI inhibited ventricular fibrosis through different mechanisms in hypertensive DHF.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2005

Plasma interleukin-18 concentration: a novel marker of myocardial ischemia rather than necrosis in humans.

OBJECTIVE: Myocardial ischemia contributes to cytokine expression in the myocardium in animals; therefore, plasma interleukin-18 concentration may be a good marker of myocardial ischemia/injury in patients with possible acute coronary syndrome. We sought to determine whether increases in plasma interleukin-18 concentrations might be indicative of myocardial ischemia in patients with acute coronary syndrome. METHODS: Plasma interleukin-18 concentrations were assessed in 27 acute coronary syndrome patients in whom creatine kinase activity was within normal range on admission, in addition to 10 controls. Myocardial infarction was retrospectively evidenced in 15 of the 27 patients. All patients with acute coronary syndrome were treated by emergent coronary interventions just after admission. Blood sampling was done immediately after admission to determine plasma IL-18 concentration and biochemical markers of myocardial infarction. RESULTS: An increase in plasma interleukin-18 concentration was observed in acute coronary syndrome patients on admission, regardless of the retrospective evidence of myocardial necrosis. Plasma interleukin-18 elevation preceded creatine kinase-MB elevation in myocardial infarction patients. Plasma interleukin-18 concentrations on admission did not correlate with peak creatine kinase-MB (r=0.38, P=n.s.) or with left ventricular ejection fraction (r=-0.14, P=n.s.). CONCLUSIONS: Plasma interleukin-18 concentration elevates quickly after severe myocardial ischemic event regardless of evolving myocardial necrosis. Thus, plasma interleukin-18 concentration may be a good and early marker to identify whether the symptom is due to myocardial ischemia, and therefore, may be used in deciding the therapeutic strategy in individual patients with possible acute coronary syndrome.

Aged↗
PubMed2005

Discordant repolarization alternans-induced atrial fibrillation is suppressed by verapamil.

BACKGROUND: Ventricular alternans of repolarization produces serious ventricular arrhythmias in experimental models. The present study investigated the role of alternans of atrial repolarization in patients with atrial fibrillation (AF). METHODS AND RESULTS: Electrophysiological studies were performed in 19 patients without structural heart disease. Monophasic action potentials (MAP) were recorded with 2 Franz catheters during steady state pacing, starting at a cycle length (CL) of 400 ms with subsequent decrements of 10 ms. Duration from the onset of upstroke to 90% repolarization of the MAP were measured. If discordant alternans (DA) was present during pacing, verapamil was administrated, and MAP measurements were repeated. Rapid pacing resulted in concordant alternans to DA in 13 of 19 (68%) patients. AF was initiated after the induction of DA in 8 of 13 patients (p=0.012). Verapamil treatment resulted in a significant decrease in the longest pacing CL at which DA was induced (207+/-19 vs 178+/-17 ms, p<0.0001). CONCLUSIONS: Rapid atrial pacing induced DA and was associated with initiation of AF. Furthermore, induction of DA was suppressed by verapamil. Reducing the spatiotemporal repolarization heterogeneity may be how the calcium-channel blockade prevents initiation of AF.

Action Potentials↗
PubMed2005

Long-term effect of spironolactone on cardiac structure as assessed by analysis of ultrasonic radio-frequency signals in patients with ventricular hypertrophy.

BACKGROUND: An effect of aldosterone on ventricular fibrosis has been demonstrated in animals, but remains unclear in human patients. This study aimed to investigate (1) the relationship between left ventricular (LV) fibrosis and myocardial ultrasonic texture as assessed with myocardial radio-frequency (RF) signals analyzed from the viewpoint of their waveform with chaos theory in animals and (2) serial changes in myocardial ultrasonic texture following long-term aldosterone blockade in patients with LV hypertrophy. METHODS AND RESULTS: In an animal study, Sprague-Dawley rats were divided into 2 groups with and without adriamycin administration, and the relationship between the RF signals and LV fibrosis was assessed. In a clinical study, effects of 12-month-administration of spironolactone were assessed in patients with LV hypertrophy. The animal study revealed that the correlation dimension (CD) calculated from the RF signals inversely correlated with the area of fibrosis. The clinical study demonstrated an increase in CD following 6-month administration of spironolactone. The changes in CD positively correlated with those in the serum carboxy-terminal telopeptide of collagen type I. CONCLUSION: Myocardial RF signals analyzed with chaos theory reflect the severity of LV fibrosis. Aldosterone blockade may alter myocardial ultrasonic texture with regression of LV fibrosis, at least partly through enhanced collagen degradation.

Adult↗
PubMed2004

Prediction of the no-reflow phenomenon with ultrasonic tissue characterization in patients with anterior wall acute myocardial infarction.

The no-reflow phenomenon after acute myocardial infarction seems to be related to ischemic injury before reperfusion. Analyzing cardiac cycle-dependent variation of integrated backscatter (IBS) is a unique method to assess myocardial viability. In this study, the ability of ultrasonic tissue characterization with IBS to predict the no-reflow phenomenon was investigated in 90 patients with first anterior wall infarction who underwent successful primary percutaneous coronary intervention. IBS images were recorded on admission (before reperfusion), and the magnitude of the cyclic variation of IBS within the infarct zone was expressed as phase-corrected magnitude (PCM) by giving positive and negative values when it showed synchronous and asynchronous contraction, respectively. Myocardial contrast echocardiography was performed soon after reperfusion, and 21 patients showed substantial no-reflow. They had smaller PCM before reperfusion than patients without no-reflow (-1.6 +/- 1.9 vs 0.7 +/- 2.7 dB, respectively; p = 0.0002). Multivariate logistic regression analysis revealed that PCM before reperfusion and the number of Q waves were the independent predictors of no reflow. Using -1.0 dB as the cut-off point, PCM predicted no reflow with 66.7% sensitivity and 81.2% specificity. These results indicate that the analysis of myocardial IBS could predict the no-reflow phenomenon before reperfusion.

Contrast Media↗
PubMed2004

Myocardial contrast echocardiography with a new calibration method can estimate myocardial viability in patients with myocardial infarction.

OBJECTIVES: We have developed a novel calibration technique applicable for myocardial contrast echocardiography (MCE). We assessed the value of this technique in the recognition of myocardial infarction (MI) and its spatial extent, and we also performed a validation study in normal subjects. BACKGROUND: The heterogeneity of contrast intensity (CI) among myocardial segments limits the clinical use of MCE. METHODS: We performed MCE with a slow-bolus injection of Levovist and recorded end-systolic harmonic power Doppler images at intervals of four heart beats in 15 normal volunteers and 30 patients with MI. We divided the left ventricular (LV) wall into 12 segments and placed the region of interest in the subendocardial region in each segment and in the adjacent LV cavity. We measured calibrated CI (dB) by subtracting the cavity CI from myocardial CI. RESULTS: The mean intersegmental difference in myocardial CI was 15.8 dB at baseline, whereas it was reduced to 6.3 dB after calibration (p < 0.01). Calibrated CI was higher in the kinetic segments than in the akinetic segments (-14.5 +/- 2.3 dB [range -18.7 to -9.9 dB] vs. -22.5 +/- 2.6 dB [-27.8 to -17.7 dB], p < 0.001), and -18.0 dB was the optimal cutoff point to discriminate these from each other. Color-coded mapping of calibrated CI may identify the spatial extent of persistently akinetic myocardium as areas of calibrated CI of <or=-18.0 dB. CONCLUSIONS: This new calibration method reduces the intersegmental difference in CI in normal subjects. Calibrated CI provides an estimate of persistently akinetic myocardium in patients with MI, and its color-coded mapping is comprehensive and identifies the spatial extent of MI.

Adult↗
PubMed2004

Usefulness of impairment of coronary microcirculation in predicting left ventricular dilation after acute myocardial infarction.

The goals of this study were to assess the serial change in coronary blood flow velocity (CBFV) patterns with transthoracic Doppler echocardiography and to decide optimal timing to predict left ventricular (LV) remodeling in patients with anterior acute myocardial infarction. We recorded CBFV of the left anterior descending (LAD) coronary artery with transthoracic Doppler echocardiography and measured diastolic deceleration time (DDT, measured in milliseconds) on days 2, 7, and 21 in 52 patients with anterior acute myocardial infarction treated with primary coronary angioplasty. On day 2, DDT was >/=600 ms in 21 patients (group A) and <600 ms in the other 31 patients (group B). In group B, DDT increased to >/=600 ms in 12 patients on day 7 (group B1), and DDT was still <600 ms in the other 19 patients (group B2). However, DDT became comparable among 3 groups on day 21. Group B2 patients had significant chronic LV dilation (LV end-diastolic volume index in groups A, B1, and B2 at 6 months: 74 +/- 16 vs 81 +/- 17 vs 100 +/- 22. ml/m(2), respectively; p <0.05 vs other groups). Multivariate analysis revealed that DDT <600 ms on day 7 was the only independent variable related to LV remodeling. In conclusion, the CBFV pattern changed toward normalization with time in patients with acute myocardial infarction. Time taken for normalization varied among patients. Persistence of microvascular dysfunction up to 7 days after reperfusion predicted LV remodeling.

Blood Flow Velocity↗
PubMed2004

Activation of matrix metalloproteinases precedes left ventricular remodeling in hypertensive heart failure rats: its inhibition as a primary effect of Angiotensin-converting enzyme inhibitor.

BACKGROUND: Matrix metalloproteinases (MMPs) are activated in dilated failing hearts, and angiotensin-converting enzyme (ACE) inhibition prevents left ventricular (LV) dilatation. However, it remains unclear whether activation of MMPs precedes or is secondary to LV remodeling, and an effect of ACE inhibition on MMPs is unknown. METHODS AND RESULTS: Dahl salt-sensitive rats fed a high-salt diet from 8 weeks served as the hypertensive heart failure (HF) model. LV echo, histological study, measurement of mRNA levels, and gelatin zymography were performed before (at 23 weeks) and after (at 26 weeks) the development of LV dilatation and pulmonary edema. The same procedures were conducted in the HF model rats treated with a subdepressor dose of ACE inhibitor (enalapril 5 mg x kg(-1) x d(-1)) from 9 weeks. Rats fed on normal chow served as age-matched controls. In the untreated HF model rats, gene expression of MMP-2 and MMP-9 and tissue gelatinase activity were elevated at 23 weeks without LV dilatation. LV dilatation, LV systolic dysfunction, and pulmonary edema occurred at 26 weeks, with further enhancement of the expression and activity of MMPs. ACE inhibition prevented such geometrical and functional deterioration. The gene expression and activity of MMPs were suppressed by ACE inhibition at 23 weeks without a decrease in blood pressure, and the suppressive effects continued at 26 weeks. CONCLUSIONS: MMPs are likely to trigger and promote LV remodeling, and ACE inhibition directly exerts inhibitory effect on MMPs, leading to the prevention of LV remodeling and dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

AT1 receptor blocker added to ACE inhibitor provides benefits at advanced stage of hypertensive diastolic heart failure.

Diastolic heart failure (DHF) has become a social burden; however, evidences leading to its therapeutic strategy are lacking. This study investigated effects of addition of angiotensin II type 1 receptor blocker (ARB) to angiotensin-converting enzyme inhibitor (ACEI) at advanced stage of DHF in hypertensive rats. Dahl salt-sensitive rats fed 8% NaCl diet from age 7 weeks served as DHF model, and those fed a normal chow served as control. The DHF model rats were arbitrarily assigned to 3 treatment regimens at age 17 weeks: ACEI (temocapril 0.4 mg/kg per day), combination of ACEI (temocapril 0.2 mg/kg per day) with ARB (olmesartan 0.3 mg/kg per day), or placebo. At age 17 weeks, this model represents progressive ventricular hypertrophy and fibrosis, relaxation abnormality, and myocardial stiffening. Data were collected at age 20 weeks. As compared with the monotherapy with ACEI, the addition of ARB induced more prominent suppression of ventricular hypertrophy and fibrosis, leading to suppression of myocardial stiffening, improvement of relaxation, and inhibition of hemodynamic deterioration. Such benefits were associated with greater decreases in reactive oxygen species (ROS) generation, macrophage infiltration, and gene expression of transforming growth factor (TGF)-beta(1) and interleukin (IL)-1beta, but not with changes in gene expression of monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-alpha. Thus, ARB added to ACEI provides more benefits as compared with ACEI alone in DHF when initiated at an advanced stage. The additive effects are likely provided through more prominent suppression of ROS generation and inflammatory changes without effects on expression of MCP-1 and TNF-alpha.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2004

Higher levels of interleukin-6 are associated with lower echogenicity of carotid artery plaques.

BACKGROUND AND PURPOSE: Echo-lucent carotid plaques can be fragile and vulnerable to rupture, representing a risk factor for ischemic stroke. Given the studies showing that elevated levels of circulating inflammatory markers are predictive of cardiovascular events, we sought to determine whether higher levels of serum interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hsCRP) are associated with lower echogenicity of carotid plaques. METHODS: The study comprised 246 patients who had carotid atherosclerotic plaques as evidenced by ultrasound. Using acoustic densitometry, we quantified the echogenicity of the largest plaque in each patient by integrated backscatter analysis. Serum IL-6 and hsCRP levels were determined in all patients. RESULTS: Both log-transformed IL-6 and hsCRP concentrations were negatively correlated with carotid plaque echogenicity (r=-0.28, P<0.001, and r=-0.14, P<0.05, respectively). When traditional atherosclerotic risk factors, plaque thickness, and medication use were controlled for, IL-6 levels were inversely associated with plaque echogenicity (beta=-0.21, P<0.01), whereas such an association was of borderline significance for hsCRP (beta=-0.12, P=0.06). CONCLUSIONS: Higher IL-6 levels, in addition to hsCRP levels, appear to be associated with lower echogenicity of carotid plaques, suggesting a link between inflammation and potential risk of plaques.

Aged↗