Cardiovascular risk reduction with periodontal treatment in patients on the waiting list for renal transplantation.

BACKGROUND: Cardiovascular mortality is increased in chronic kidney disease, a condition with a high prevalence of periodontal disease. Whether periodontitis treatment improves prognosis is unknown. METHODS: The effect of periodontal treatment on the incidence of cardiovascular events and death in 206 waitlist hemodialysis subjects was compared with that in 203 historical controls who did not undergo treatment. Patients were followed up for 24 months or until death or transplantation. RESULTS: The prevalence of moderate/severe periodontitis was 74%. Coronary artery disease correlated with the severity of periodontal disease (P = .02). Survival free of cardiovascular events (94% vs 83%, log-rank 0.009), coronary events (97% vs 89%, log-rank = 0.009), and cardiovascular death (96% vs 87%, log-rank = 0.037) was higher in the evaluated group. Death by any cause did not differ between groups. Multivariate analysis showed that treatment was associated with reduction in cardiovascular events (HR 0.43; 95% CI 0.22-0.87), coronary events (HR 0.31; 95% CI 0.12-0.83), and cardiovascular deaths (HR 0.43; 95% CI 0.19-0.98). CONCLUSION: Periodontal treatment reduced the 24-month incidence of cardiovascular events and cardiovascular death, suggesting that periodontal treatment may improve cardiovascular outcomes. We suggest that periodontal screening and eventual treatment may be considered in patients with advanced renal disease.

Association between Neutrophil-Lymphocyte and Platelet-Lymphocyte Ratios and Coronary Artery Calcification Score among Asymptomatic Patients: Data from a Cross-Sectional Study.

INTRODUCTION: Atherosclerosis is a low-grade inflammatory disease. Among markers of inflammation, importance has been given to the neutrophil-lymphocyte ratio (NLR) and platelet-lymphocyte ratio (PLR). The objective of this study was to examine the association between these hematological indices of inflammation and coronary atherosclerotic calcification in clinically asymptomatic patients. METHODS: This study had clinical and laboratorial data collected from consecutive asymptomatic patients that underwent computed tomography coronary artery calcium (CAC) scoring. Risk factors, NLR, and PLR were evaluated at different categories of CAC scoring. Statistical tests included chi-square, linear regression, and logistic regression. Patients (N = 247; age 60.4 ± 8.0 years and 60.7% men) were allocated into four categories according to the CAC score. RESULTS: Respective age, sex (male), NLR, and PLR distribution within groups were as follows: CAC = 0 (n = 98; 52.5 ± 13.6 years, 55%, 2.0 ± 1.0, and 121.5 ± 41.5), CAC 1-100 (N = 64; 61.3 ± 11.0 years, 60%, 2.2 ± 1.2, and 125.6 ± 45.6), CAC 101-400 (N = 37; 64.2 ± 11.6 years, 67%, 2.6 ± 1.3, and 125.4 ± 55.9), and CAC > 400 (N = 48; 69.3 ± 11.1 years, 66%, 3.3 ± 2.0, and 430.1 ± 1787.4). The association between risk factors and CAC score was assessed. Hypertension status and smoking status were similar within groups, while the presence of diabetes (P = 0.02) and older age (P ≤ 0.001) was more prevalent in the CAC > 400 group. LDL cholesterol was greater in the higher CAC score groups (P = 0.002). Multivariate logistic regression of the quartile analysis showed that age and NLR were independently associated with CAC > 100 (OR (CI), P value): 2.06 (1.55-2.73, P = 0.00001) and 1.82 (1.33-2.49, P = 0.0002), respectively. CONCLUSION: Within asymptomatic patients, NLR provides additional risk stratification, as an independent association between NLR extent and CAD extent was identified. Moreover, PLR was not an inflammation marker for CAD severity.

Long-term prospective study of the influence of estrone levels on events in postmenopausal women with or at high risk for coronary artery disease.

BACKGROUND: The link between endogenous estrogen, coronary artery disease (CAD), and death in postmenopausal women is uncertain. We analyzed the association between death and blood levels of estrone in postmenopausal women with known coronary artery disease (CAD) or with a high-risk factor score for CAD. METHODS: 251 postmenopausal women age 50-90 years not on estrogen therapy. Fasting blood for estrone and heart disease risk factors were collected at baseline. Women were grouped according to their estrone levels (<15 and ≥15 pg/mL). Fatal events were recorded after 5.8 ± 1.4 years of followup. RESULTS: The Kaplan-Meier survival curve showed a significant trend (P = 0.039) of greater all-cause mortality in women with low estrone levels (<15 pg/mL). Cox multivariate regression analysis model adjusted for body mass index, diabetes, dyslipidemia, family history, and estrone showed estrone (OR = 0.45; P = 0.038) as the only independent variable for all-cause mortality. Multivariate regression model adjusted for age, body mass index, hypertension, diabetes, dyslipidemia, family history, and estrone showed that only age (OR = 1.06; P = 0.017) was an independent predictor of all-cause mortality. CONCLUSIONS: Postmenopausal women with known CAD or with a high-risk factor score for CAD and low estrone levels (<15 pg/mL) had increased all-cause mortality.

Myocardial scintigraphy and clinical stratification as predictors of events in renal transplant candidates.

BACKGROUND: We tested the hypothesis that the universal application of myocardial scanning with single-photon emission computed tomography (SPECT) would result in better risk stratification in renal transplant candidates (RTC) compared with SPECT being restricted to patients who, in addition to renal disease, had other clinical risk factors. METHODS: RTCs (n=363) underwent SPECT and clinical risk stratification according to the American Society of Transplantation (AST) algorithm and were followed up until a major adverse cardiovascular event (MACE) or death. RESULTS: Of the 363 patients, 79 patients (22%) had an abnormal SPECT scan and 270 (74%) were classified as high risk. Both methods correctly identified patients with increased probability of MACE. However, clinical stratification performed better (sensitivity and negative predictive value 99% and 99% vs. 25% and 87%, respectively). High-risk patients with an abnormal SPECT scan had a modest increased risk of events (log-rank = 0.03; hazard ratio [HR] = 1.37; 95% confidence interval [95% CI], 1.02-1.82). Eighty-six patients underwent coronary angiography, and coronary artery disease (CAD) was found in 60%. High-risk patients with CAD had an increased incidence of events (log-rank = 0.008; HR=3.85; 95% CI, 1.46-13.22), but in those with an abnormal SPECT scan, the incidence of events was not influenced by CAD (log-rank = 0.23). Forty-six patients died. Clinical stratification, but not SPECT, correlated with the probability of death (log-rank = 0.02; HR=3.25; 95% CI, 1.31-10.82). CONCLUSION: SPECT should be restricted to high-risk patients. Moreover, in contrast to SPECT, the AST algorithm was also useful for predicting death by any cause in RTCs and for selecting patients for invasive coronary testing.

Effect of chronic kidney disease in ischemic cardiomyopathy: Long-term follow-up - REVISION-DM2 trial.

A strong association exists between chronic kidney disease (CKD) and coronary artery disease (CAD). The role of CKD in the long-term prognosis of CAD patients with versus those without CKD is unknown. This study investigated whether CKD affects ventricular function.From January 2009 to January 2010, 918 consecutive patients were selected from an outpatient database. Patients had undergone percutaneous, surgical, or clinical treatment and were followed until May 2015.In patients with preserved renal function (n = 405), 73 events (18%) occurred, but 108 events (21.1%) occurred among those with CKD (n = 513) (P < .001). Regarding left ventricular ejection fraction (LVEF) <50%, we found 84 events (21.5%) in CKD patients and 12 (11.8%) in those with preserved renal function (P < .001). The presence of LVEF <50% brought about a modification effect. Death occurred in 22 (5.4%) patients with preserved renal function and in 73 (14.2%) with CKD (P < .001). In subjects with LVEF <50%, 66 deaths (16.9%) occurred in CKD patients and 7 (6.9%) in those with preserved renal function (P = .001). No differences were found in CKD strata regarding events or overall death among those with preserved LVEF. In a multivariate model, creatinine clearance remained an independent predictor of death (P < .001).We found no deleterious effects of CKD in patients with CAD when ventricular function was preserved. However, there was a worse prognosis in patients with CKD and ventricular dysfunction.Resgistry number is ISRCTN17786790 at https://doi.org/10.1186/ISRCTN17786790.

Differences in the inflammatory response between patients with and those without diabetes mellitus after coronary stenting.

BACKGROUND: Patients with diabetes mellitus who undergo coronary stenting are at increased risk of restenosis. It is known that inflammation plays a crucial role in restenosis. OBJECTIVE: We assessed the inflammatory response to elective coronary stent implantation (CSI) in stable diabetic and nondiabetic patients. METHODS: C-reactive protein (CRP), soluble (s) P-selectin, and soluble intercellular adhesion molecule (sICAM)-1 plasma levels were determined in diabetic (n = 51) and nondiabetic (n = 56) patients before and 48 hours and 4 weeks after bare metal stenting (BMS). RESULTS: Diabetic patients presented significantly higher inflammatory marker levels before and after CSI. Nonetheless, diabetic and nondiabetic patients had postintervention peak of markers attained within 48 hours. At baseline, diabetic and nondiabetic patients presented CRP levels of 5.0 +/- 20.1 (P < or = 0.04) and 3.8 +/- 9.4 microg/ml and, at 48 hours postintervention, 22.0 +/- 20.2 (P = 0.001; P = 0.002) and 12.6 +/- 11.3 (P < or = 0.0001) microg/ml. Regarding sP-selectin, diabetic and nondiabetic patients obtained levels of, at baseline, 182 +/- 118 (P < or = 0.04) and 105 +/- 48 ng/ml and, at 48 hours, 455 +/- 290 (P = 0.001; P < or = 0.01) and 215 +/- 120 (P < or = 0.04) ng/ml. For diabetic and nondiabetic patients, sICAM-1 levels were, at baseline, 248 +/- 98 (P < or = 0.04) and 199 +/- 94 ng/ml and, at 48 hours, 601 +/- 201 (P = 0.001; P < or = 0.01) and 283 +/- 220 (P = 0.001) ng/ml. At 4 weeks, for all patients, markers returned to preprocedural levels: versus before PCI: *P = 0.001, (section sign)P < or = 0.0001; versus nondiabetic patients: (#)P < or = 0.04, (paragraph sign)P = 0.002, (Upsilon)P < or = 0.01. CONCLUSIONS: Diabetic and nondiabetic patients exhibited a temporal inflammatory response after an elective BMS. However, diabetic patients present higher preprocedural levels of CRP, sP-selectin, and sICAM-1 and reveal a further exacerbated inflammatory response after intervention. The differences in inflammatory response may have implications in restenosis within these two sets of patients.

Impact of diabetes mellitus on ischemic cardiomyopathy. Five-year follow-up. REVISION-DM trial.

BACKGROUND: Patients with ischemic cardiomyopathy and severe left ventricular dysfunction have a worse survival prognosis than patients with preserved ventricular function. The role of diabetes in the long-term prognosis of this patient group is unknown. This study investigated whether the presence of diabetes has a long-term impact on left ventricular function. METHODS: Patients with coronary artery disease who underwent coronary artery bypass graft surgery, percutaneous coronary intervention, or medical therapy alone were included. All patients had multivessel disease and left ventricular ejection fraction measurements. Overall mortality, nonfatal myocardial infarction, stroke, and additional interventions were investigated. RESULTS: From January 2009 to January 2010, 918 consecutive patients were selected and followed until May 2015. They were separated into 4 groups: G1, 266 patients with diabetes and ventricular dysfunction; G2, 213 patients with diabetes without ventricular dysfunction; G3, 213 patients without diabetes and ventricular dysfunction; and G4, 226 patients without diabetes but with ventricular dysfunction. Groups 1, 2, 3, and 4, respectively, had a mortality rate of 21.6, 6.1, 4.2, and 10.6% (P < .001); nonfatal myocardial infarction of 5.3, .5, 7.0, and 2.6% (P < .001); stroke of .40, .45, .90, and .90% (P = NS); and additional intervention of 3.8, 11.7, 10.3, and 2.6% (P < .001). CONCLUSION: In this sample, regardless of the treatment previously received patients with or without diabetes and preserved ventricular function experienced similar outcomes. However, patients with ventricular dysfunction had a worse prognosis compared with those with normal ventricular function; patients with diabetes had greater mortality than patients without diabetes.Trial registration http://www.controlled-trials.com. Registration Number: ISRCTN66068876.

Screening for significant coronary artery disease in high-risk renal transplant candidates.

BACKGROUND: Renal transplant candidates are at an increased risk for coronary artery disease (CAD), a strong predictor of cardiovascular events [major adverse coronary events (MACE)]. Coronary angiography is a costly, risky, invasive procedure. We sought to determine clinical predictors of significant CAD (stenosis > or =70%) in high-risk renal transplant candidates. METHODS: Clinical evaluation and coronary angiography were performed in 301 patients (57+/-8 years, 73% men) on hemodialysis for 32 months (median). Patients were followed-up for 22 months (median). Inclusion criteria were diabetes (type 1 or 2), evidence of cardiovascular disease, or age > or =50 years. Risk factors included hypertension (93.7%), overweight/obesity (54.3%), dyslipidemia (44.9%), diabetes (42.1%), and smoking (24.3%). Cardiovascular disease was found as follows: peripheral arterial disease (PAD) (31.2%), angina (28.1%), stroke (12.9%), myocardial infarction (MI) (10.3%), and heart failure (9.3%). RESULTS: Significant CAD was found in 136 individuals (45.2%). Diabetes [odds ratio (OR)=1.82; 95% confidence interval (CI)=1.08-3.07], PAD (OR=2.50; 95% CI=1.44-4.37), and previous MI (OR=7.75; 95% CI=3.03-23.98) were associated with significant CAD. The prevalence of significant CAD increased with the number of clinical predictors from 26% (none) to 100% (all present) (P<0.0001). The incidence of fatal/nonfatal MACE increased two, four, and sixfold in those with diabetes, PAD, or previous MI, respectively (P<0.0001). CONCLUSIONS: In high-risk patients with end-stage renal disease, the prevalence of CAD and the incidence of MACE were high. Significant CAD or cardiovascular complications were not related to the majority of classic risk factors. Patients with diabetes, PAD, or previous MI are at higher risk of CAD, MACE, or both and, thus, must be referred for invasive diagnostic procedures.

Repercussions of cardiac resynchronization therapy on the ventricular repolarization of heart failure patients as assessed by body surface potential mapping.

OBJECTIVE: Cardiac resynchronization therapy (CRT) is an adjunct treatment for heart failure (HF) which associates with left bundle-branch block (LBBB) and is refractory to medical therapy. However, nearly 1/3 of the patients still do not respond, the reasons for which have yet to be determined. Additionally, experimental studies proved that epicardial left ventricle (LV) pacing yields reversed electrical activation sequence, increasing QT interval duration and dispersion of the ventricular repolarization, and leaving patients at greater risk for ventricular arrhythmias. METHODS: In this study, a series of 60 patients (61.7% male, mean age 59.2+/-11.54 years) in NYHA functional class III-IV heart failure and LBBB, who received CRT through implantation of atrial-biventricular pacemakers, were assessed by 87-lead body surface potential mapping (BSPM). The BSPM, noninvasive technique with semi-automatic readings, allowed analysis of variables associated with the cardiac ventricular repolarization QT intervals, maximal, minimum and mean Tpeak-end, and QT dispersion (QTmax - min), in addition to transmural dispersion of repolarization (Tpeak-end max - Tpeak-end min), in two different moments: baseline rhythm and during atrial-biventricular pacing. RESULTS: QT dispersion showed a significant 19.6% reduction (p=0.0009) under CRT, as compared with baseline measurements (85.58+/-26.63 msec vs. 68.83+/-25.16 msec). The transmural dispersion of repolarization (Tpeak-end max - Tpeak-end min) showed smaller statistical significance (p=0.0343); however, its values were similarly decreased (55.50+/-15.45 msec vs 49.41+/-14.11 msec) during CRT. CONCLUSION: These results may corroborate findings from major randomized clinical trials. We consider that the electrocardiographic variables obtained with the use of the BSPM, namely, the QT and Tpeak-end intervals, are appropriate for analysis and study of the effects of cardiac resynchronization therapy on the improved electrical dispersion as characterizing the improvement of homogeneity of cardiac ventricular repolarization.

Effectiveness of the maze procedure using cooled-tip radiofrequency ablation in patients with permanent atrial fibrillation and rheumatic mitral valve disease.

BACKGROUND: Although the Cox-Maze III procedure is effective for treating permanent atrial fibrillation (AF), its high complexity limits its use. The Saline-Irrigated Cooled-tip Radiofrequency Ablation (SICTRA) System is an alternative source of energy used to ablate AF. The aim of this study was to evaluate the effectiveness of the SICTRA for the treatment of permanent AF in patients with rheumatic mitral valve (MV) disease. METHODS AND RESULTS: Between February 2002 and April 2003, 70 patients with permanent AF and rheumatic MV disease were randomly assigned to undergo a modified Maze III procedure using SICTRA associated with MV surgery (group A) or MV surgery alone (group B). Groups A and B were similar in terms of baseline characteristics. The in-hospital mortality rate was 2.3% (1 death) in group A versus 0% (no deaths) in group B (P>0.99). The additional time required for the left-sided radiofrequency ablation in group A was 14.2+/-5.1 minutes and for right-sided ablation was 12.3+/-4.2 minutes. The mean postoperative follow-up periods were 13.8+/-3.4 and 11.5+/-7.3 months, respectively, in groups A and B. The overall mid-term survival rate was 95.1% in group A and 92.8% in group B (P>0.99). The cumulative rates of sinus rhythm were 79.4% in group A and 26.9% in group B (P=0.001). Doppler echocardiography documented biatrial transport function in 90.3% of group A patients in sinus rhythm. CONCLUSIONS: The SICTRA is effective for treating permanent AF associated with rheumatic MV disease.

[Monocytosis is an independent risk marker for coronary artery disease]. / Monocitose é um marcador de risco independente para a doença arterial coronariana.

OBJECTIVES: Inflammation and activation of immune system cells play an important role in the pathogenesis of atherosclerosis. This study analyzes the white blood count, including neutrophils, eosinophils, lymphocytes, monocytes and basophils, of patients with chronic coronary artery disease (CAD) and acute myocardial infarction (AMI). METHODS: The white blood cell count was analyzed in 232 patients without diabetes between the ages of 15 and 88. One hundred and forty-two patients were angiographically diagnosed with CAD (57 with stable CAD and 85 with AMI) and compared to 90 control individuals. The control and CAD groups were similar in respect to age, body mass index, family history, smoking habits, hypertension, HDL and LDL (all variables with p > 0.25). RESULTS: The univariate analysis revealed a higher prevalence of leukocytosis in the CAD group, which in turn was higher in the AMI patients than the stable CAD patients. The same trend was observed for monocytes. However, the distribution of all other cells in the complete blood count (CBC) was similar. Multivariate analysis using the logistic regression method with the stepwise (all variables) and backward models (p < 0.25), showed that monocytosis was an independent variable for CAD and AMI. CONCLUSION: The number of monocytes, one of the most important components of the inflammatory process in the atherosclerosis plaque was an independent risk marker for CAD and AMI.

Ten-year clinical laboratory follow-up after application of a symptom-based therapeutic strategy to patients with severe chronic aortic regurgitation of predominant rheumatic etiology.

OBJECTIVES: This study was designed to assess the feasibility and the long-term results of a symptom-based strategy of aortic valve replacement in a Brazilian population with predominant rheumatic etiology. BACKGROUND: Optimal criteria for valve replacement in aortic regurgitation (AR) are still not entirely clear. The appearance of symptoms is an indication for surgery, but may be associated with myocardial damage. Although cardiac imaging data have provided a safer guide for such decisions, the use of symptom-based surgical indication has not been validated and might conceivably be better in populations with predominant rheumatic etiology and younger age. METHODS: Echocardiography and rest-exercise radionuclide ventriculography were performed in 75 patients with severe AR, age 28 +/- 9 years, over a period of 10 +/- 0.69 years. Thirty-seven patients developed symptoms and underwent aortic valve replacement surgery within six months. Thirty-eight patients remained asymptomatic and were managed medically. RESULTS: Survival was 100% in asymptomatic patients and 82% in symptomatic. Surgical treatment caused marked ventricular remodeling, with ventricular diameter involution and an improvement of rest-exercise ejection fraction percent variation. Multivariate analysis showed that the probability of developing symptoms within 10 years was 58% for a patient with a left ventricular end-diastolic diameter > or =70 mm and 76% for a patient with left ventricular end-systolic (LVESD) > or =50 mm. Logistic regression identified LVESD and age as the most predictive and specific, but not sensitive, indicators of symptom development. CONCLUSIONS: Application of a standardized therapeutic strategy to patients with severe AR and predominant rheumatic etiology resulted in 90.6% survival after 10 years of follow-up.

Interleukin-6 and flow-mediated dilatation as markers of increased vascular inflammation in women receiving hormone therapy.

OBJECTIVE: The lack of a beneficial long-term cardiovascular effect of hormone therapy and the early incidence of cardiovascular adverse events observed in recent randomized studies have been related to a heightened inflammatory effect of hormone therapy. DESIGN: We evaluated the effect of different postmenopause therapies on inflammatory markers and endothelial function in 205 postmenopausal women before and after therapy. RESULTS: all postmenopausal women, estrogens alone increased plasma levels of C-reactive protein (CRP) but decreased all other markers of inflammation including interleukin-6 (IL-6) (CRP: +75% +/- 11%, intracellular adhesion molecule: -21% +/- 4%, vascular cell adhesion molecule: -15% +/- 6%, E-selectin: -18% +/- 4%, s-thrombomodulin -10.5% +/- 3.7%, IL-6 -14% +/- 6%; percent changes, P < 0.01 compared with baseline). Raloxifene and tibolone did not significantly affect the overall inflammatory milieu. In a minority of patients, estrogen-progestogen associations and tibolone increased IL-6 levels and induced unfavorable changes on inflammation markers (CRP: +93% +/- 8%, intracellular adhesion molecule: -3% +/- 2%, vascular cell adhesion molecule: -5% +/- 2%, E-selectin: +6% +/- 2%, s-thrombomodulin: +5% +/- 2%, IL-6: +12% +/- 4%; percent changes compared with baseline). Patients with increased IL-6 levels were older and had a longer time since menopause. In all patients except those with increased IL-6 levels, hormone therapy improved endothelial function, whereas tibolone and raloxifene did not significantly change endothelial function compared with baseline. A worsening of endothelial function was detected in patients with increased IL-6 levels during therapy. CONCLUSIONS: Postmenopausal hormone therapy is associated with decreased vascular inflammation; however, in patients with a longer time since menopause, postmenopause hormone therapy may increase inflammation and worsen endothelial function. These unfavorable vascular effects may be detected by an elevation in IL-6 levels and by a lack of improvement in endothelial function.

Genetic polymorphisms of estrogen receptors in patients with premature coronary artery disease.

BACKGROUND: Estrogen protects against atherosclerosis through its genomic/nongenomic effects. Estrogen receptors (ESR) alpha (1) and beta (2) mediate much estrogen action. Both receptors exist in the arterial wall, but the extent of their distribution in arterial layers is unknown. Allelic variants of the gene encoding ESR1 and ESR2 may alter their expression and function, resulting in genetic variability. METHODS: In the present age-adjusted, case-control study, the prevalence of four mutations in estrogen receptors was analyzed in patients with premature CAD and controls. RESULTS: Mutation in the ESR1 (PvuII) was more prevalent in the controls (18 vs. 11%; p=0.062) than in CAD patients, and the mutation identified by the XbaI enzyme in the same receptor was associated with reduced apolipoprotein B levels and low body mass index. Mutation of the ESR2 (AluI) was more prevalent in CAD patients (0.6 vs. 18%; p=0.008). Homozygosis for this mutation involved increased body mass index, elevated serum triglycerides and apolipoprotein B, and reduced HDL-cholesterol. Multivariate logistic regression analysis showed dyslipidemia, low serum HDL levels, and ESR2 polymorphism (AluI) [OR=1.89 (95% CI: 1.08-3.34); p=0.034] to be independent risk factors for CAD. CONCLUSIONS: Our data suggest that mutation of the ESR2 is an independent risk marker for premature CAD.

Platelet and leukocyte adhesion and activation in unstable angina and post-PTCA.

BACKGROUND: Unstable atherosclerotic plaques activate blood cells which may adhere to the coronary endothelium causing vessel occlusion. However, it is unknown if different clinical syndromes associated with plaque rupture induce similar blood cell activation and adhesion to the endothelium. METHODS: We studied changes in adhesion molecule expression of platelets (GPIIb/IIIa), neutrophils--CD18, CD11b and L-selectin--and monocytes (CD14) after interaction with active lesions of patients with stable angina subjected to PTCA and patients with unstable angina (UA). Generation of superoxide (SO) radicals from PMNs and PMN sequestration in the coronary circulation were also assessed. Blood samples were collected from the aorta (Ao) and coronary sinus (CS) before and 15 min after PTCA (n=13) and within the first 48 h of UA (n=12). RESULTS: PTCA induced a marked up-regulation of CD18, CD11b, CD14 and GPIIb/IIIa with L-selectin shedding and reduced SO formation, whereas only minor L-selectin down-regulation and decreased SO production indicated activation in UA. However, a significant decrease in neutrophil count in the CS compared to the Ao was only observed in UA. CONCLUSIONS: The magnitude of cellular activation depends on the underlying clinical setting and just partially contributes to cell adhesion to the endothelium which might be modulated by different extent of vascular occlusion and shear forces.

Postmenopausal hormone replacement therapy increases plasmatic thromboxane beta 2.

OBJECTIVE: This study shows the effect of hormone replacement therapy (HRT), using oral estrogen exclusively or in combination with progestin, on platelet activation in healthy menopaused women. BACKGROUND: Recent evidence from studies of postmenopausal HRT in healthy women demonstrated a short-time increased risk of coronary heart disease. Platelet activation, which generates vasoconstrictory thromboxane A(2) (TxA(2)), has been related to the risk of cardiovascular diseases. METHODS: By means of a placebo-controlled study twenty-seven postmenopausal patients were continuously orally administered estrogen in combination with progestin or estrogen exclusively for an 8-week period. Platelet activation was evaluated by flow cytometric P-selectin expression and by enzyme immunoassay plasmatic TxA(2) (TxB(2)) concentrations. RESULTS: P-selectin binding index changed from 6.3+/-3.6 to 7.0+/-3 in the placebo group (n=10); from 5.9+2.2 to 7.9+/-3.3 in the E+P group (n=8) and from 6.4+2.7 to 7.1+/-1.9 in the E group (n=9). Plasma concentrations of TxB(2) before and after intervention, changed from 1.2+1.2 to 1.5+1.4 (pg/well) in the placebo group; significantly (p=0.005) in the E+P group (n=8), from 0.9+0.3 to 6.1+6.5 (pg/well), and from 1.3+1.5 to 0.8+0.4 (pg/well) in the E group (n=8; mean+standard deviation, basal x therapy, p<0.05). CONCLUSIONS: Healthy menopaused women who were administered estradiol in association with norethisterone continuously had an increase of plasmatic thromboxane, possibly determined by platelet activation, which indicates a higher short-term thrombotic risk. P-selectin expression analyses failed to demonstrate the impact of HRT on platelets.

[Left ventricular pseudoaneurysm associated to severe mitral insufficiency, complicating inferolaterodorsal acute myocardial infarction]. / Pseudoaneurisma de ventrículo esquerdo associado a insuficiência mitral grave complicando infarto agudo do miocárdio ínfero-látero-dorsal.

We described a case of left ventricular pseudoaneurysm associated to a severe mitral regurgitation, complicating a inferolaterodorsal acute myocardial infarction. The lesion was found in a routine echocardiogram during the in-hospital follow-up. The well-succeeded surgical strategy and the good clinical evolution of the patient were distinguished.

Role of Trimetazidine in Ischemic Preconditioning in Patients With Symptomatic Coronary Artery Disease.

Ischemic preconditioning (IP) is a powerful cardioprotective cellular mechanism that has been related to the "warm-up phenomenon" or "walk-through" angina, and has been documented through the use of sequential exercise tests (ETs). It is known that several drugs, for example, cromokalim, pinacidil, adenosine, and nicorandil, can interfere with the cellular pathways of IP. The purpose of this article is to report the effect of the anti-ischemic agent trimetazidine (TMZ) on IP in symptomatic coronary artery disease (CAD) patients.We conducted a prospective study evaluating IP by the analysis of ischemic parameters in 2 sequential ETs. In phase I, without TMZ, patients underwent ET1 and ET2 with a 30-minute interval between them. In phase II, after 1 week of TMZ 35 mg twice daily, all patients underwent 2 consecutive ETs (ET3 and ET4). IP was considered present when the time to 1.0-mm segment ST on electrocardiogram deviation (T-1.0 mm) and rate pressure product (RPP) were greater in the second of 2 tests. The improvement in T-1.0 mm and RPP were compared in the 2 phases: without TMZ and after 1-week TMZ to assess the action of such drug in myocardial protective mechanisms. ETs were analyzed by 2 independent cardiologists.From 135 CAD patients screened, 96 met inclusion criteria and 62 completed the study protocol. Forty patients manifested IP by demonstrating an improvement in T-1.0 mm in ET2 compared with ET1, without the use of any drugs (phase I). In phase II, after 1-week TMZ, 26 patients (65%) did not show any incremental result in ischemic parameters in ET4 compared with ET3. Furthermore, of these patients, 8 (20%) had IP blockage.In this study, TMZ did not add any benefit to IP in patients with stable symptomatic CAD.

Atorvastatin reduces proinflammatory markers in hypercholesterolemic patients.

BACKGROUND: Reduction in cardiovascular events with statins has been in part attributed to their anti-inflammatory properties. OBJECTIVE: Evaluate the effects of atorvastatin on levels of inflammatory markers, such as tumor necrosis factor-alpha (TNF), interleukins (IL-1 and IL-6), soluble intercellular adhesion molecule-1 (sICAM-1) and C-reactive protein (CRP) in hypercholesterolemic patients (LDL-cholesterol >160 mg/dL). METHODS AND RESULTS: Two lipid-lowering regimens were taken for 8 weeks. One set of patients (n=45, 26 men, average 50 +/- 2 years of age) was subjected to atorvastatin treatment (20-40 mg/day), plus diet recommendation. Another set of patients (n=23, 12 men, average 53 +/- 3 years of age) went through diet recommendation alone. Both groups were recommended to perform standard physical activity. Plasma samples were collected after overnight fasting at baseline and after 8 weeks for ELISA. The use of atorvastatin when compared to diet alone, resulted in significant (P <0.0001) reductions for: LDL-cholesterol (39.9% versus 4.4%), TNF (21.4% versus 2.9%), IL-6 (22.1% versus 2.0%), IL-1 (16.4% versus 2.7%) and sICAM-1 (9.6% versus 0.1%), respectively. The percentage of patients with CRP levels >3 mg/dL in the atorvastatin group fell from 25.0 to 6.7% (P <0.0001) while in the diet group the reduction was not significant. CONCLUSION: In hypercholesterolemic patients, atorvastatin, compared to diet alone resulted in significant reductions in levels of proinflammatory cytokines (TNF, IL-1 and IL-6) as well as in sICAM-1 and CRP. Thus, statin-induced inhibition of inflammatory markers may play an important role in the pharmacological and clinical effects of statins seen in cardiovascular diseases.

The role of gender in the long-term prognosis of patients with myocardial infarction submitted to fibrinolytic treatment.

PURPOSE: To determine the role of gender in short- and long-term survival after a thrombolytic-treated myocardial infarction. METHODS: A total of 686 consecutive patients with ST-elevation acute myocardial infarction, admitted to a single center and treated with intravenous streptokinase, were studied prospectively and consecutively. Assessment of clinical and in-hospital variables permitted comparison of baseline characteristics and both in-hospital and long-term survival between men and women. RESULTS: A significantly (odds ratio=0.48, P=0.009) lower 14-day mortality rate for males (8.5%) relative to females (16%) was noted. However, this difference became non-significant after adjustment for age (odds-ratio male/female=0.62, P=0.097) or age and other variables (odds ratio=0.71, P=0.17). At the end of the follow-up (up to 12 years), survival rates for the whole population were 59.6% and 54.4% for men and women, respectively (chi-square=1.4, P=0.24); excluding in-hospital deaths, the rates were 65.1% and 64.8%, respectively (chi-square=0.21, P=0.65). CONCLUSIONS: In the short-term follow-up, women have a significantly higher mortality relative to men in an unadjusted analysis. This difference became non-significant after adjusting for age, or age and other variables. In the long-term follow-up, sex was not correlated with prognosis.