Impact of metabolic syndrome and C-reactive protein on outcome after coronary stenting.

Metabolic syndrome (MS) identifies cardiovascular risk; however, there is little information regarding the evolution of patients with MS after stent implantation. The aim of this single-center study is to evaluate the possible association between MS and clinical restenosis, after adjustment for highsensitivity C-reactive protein (hs-CRP) and angiographic predictors of restenosis. In a longitudinal study, 159 patients (89 with and 70 without MS) were studied. Criteria for MS were: elevated blood pressure (systolic >or=130 mmHg, diastolic >or=85 mmHg or drug treatment for hypertension; elevated fasting glucose (>100 mg/dl) or drug treatment for elevated glucose; reduced HDL-cholesterol (<40 mg/dl in men and <50 mg/dl in women) or drug treatment for reduced HDL-cholesterol; elevated triglycerides (>or=150 mg/dl) or drug treatment for elevated triglycerides; and obesity (body mass index >28.8 kg/m2). The primary end point was the rate of major adverse clinical events (MACE): cardiovascular death, myocardial infarction, or target lesion revascularization (TLR) during the 12-month follow-up period. The secondary end point was the rate of TLR. MS was neither identified as predictor of MACE [hazard ratio (HR): 0.844; 95% CI: 0.41-1.74; p=0.648], nor TLR (HR: 1.05; 95% CI: 0.44-2.50; p=0.91), even when controlled for hs-CRP levels and angiographic predictors of restenosis. Also, no significant interaction between MS and hs-CRP was found (p=0.135 and p=0.194, for MACE and TLR, respectively). This study shows that patients with MS do not have an additional risk of MACE, even when controlled for angiographic predictors of restenosis and hs-CRP.

Association of the 894G>T polymorphism of the endothelial constitutive nitric oxide synthase gene with unstable angina.

The 894G>T polymorphism of the endothelial constitutive nitric oxide synthase gene consists of the substitution of a guanine base by a thymine at the 894th nucleotide of the gene. An association of this polymorphism with acute coronary syndromes has been described, only when in combination with other polymorphisms of this gene. The aim of the present study was to search for an association between this polymorphism and unstable angina in a southern Brazilian population. In a case-control study, 156 patients (group 1 (N = 83): unstable angina, group 2 (N = 73): stable angina) were genotyped by PCR and digestion of the product. Univariate analysis demonstrated that the minimal luminal diameter and the degree of stenosis of the culprit lesion differed between groups (P = 0.006 and 0.005, respectively). In addition, the frequencies of the T allele and of the T allele carriers (combined TT and TG genotypes) were significantly higher in the group with unstable angina (41.6 vs 28.8%; P = 0.025, Pearson chi-square test, and 73.5 vs 45.2%; P = 0.001, Pearson chi-square test, respectively). Multivariate logistic regression showed that the frequency of the T allele carriers was the only variable with a predictive value for unstable angina, when controlled for the other variables (6.1 (95% CI = 2.55-14.43); P < 0.001). Thus, in a homogenous group of patients, the endothelial constitutive nitric oxide synthase 894G>T polymorphism was associated with unstable angina. We suggest that this polymorphism may be a genetic risk factor for unstable angina.

Association of the 894G>T polymorphism of the endothelial constitutive nitric oxide synthase gene with unstable angina

The 894G>T polymorphism of the endothelial constitutive nitric oxide synthase gene consists of the substitution of a guanine base by a thymine at the 894th nucleotide of the gene. An association of this polymorphism with acute coronary syndromes has been described, only when in combination with other polymorphisms of this gene. The aim of the present study was to search for an association between this polymorphism and unstable angina in a southern Brazilian population. In a case-control study, 156 patients (group 1 (N = 83): unstable angina, group 2 (N = 73): stable angina) were genotyped by PCR and digestion of the product. Univariate analysis demonstrated that the minimal luminal diameter and the degree of stenosis of the culprit lesion differed between groups (P = 0.006 and 0.005, respectively). In addition, the frequencies of the T allele and of the T allele carriers (combined TT and TG genotypes) were significantly higher in the group with unstable angina (41.6 vs 28.8 percent; P = 0.025, Pearson chi-square test, and 73.5 vs 45.2 percent; P = 0.001, Pearson chi-square test, respectively). Multivariate logistic regression showed that the frequency of the T allele carriers was the only variable with a predictive value for unstable angina, when controlled for the other variables (6.1 (95 percent CI = 2.55-14.43); P < 0.001). Thus, in a homogenous group of patients, the endothelial constitutive nitric oxide synthase 894G>T polymorphism was associated with unstable angina. We suggest that this polymorphism may be a genetic risk factor for unstable angina.

Association between -250G/A polymorphism of the hepatic lipase gene promoter and coronary artery disease and HDL-C levels in a Southern Brazilian population.

Hepatic lipase (HL) is a glycoprotein that plays a major role in remodeling high-density lipoprotein (HDL). The effect of the -250G/A promoter polymorphism on coronary artery disease (CAD) and lipid levels was studied in 231 male CAD patients and in a population-based sample of men and women (n = 514). A sample of 140 men was chosen among those included in the population-based sample as controls for the CAD sample. In the total group of CAD patients, the frequency of the -250A allele was somewhat lower (25% in CAD patients and 32% in controls; p = 0.06), but when the control samples were compared only with the CAD(+) sample (more than 60% of luminal stenosis in at least one coronary artery or major branch segment) the -250A allele was significantly less frequent (23% in the patients vs 32% in controls; p = 0.02). A multiple logistic regression analysis showed that this association was independent of classical CAD risk factors [odds ratio (OR) = 1.79, p = 0.025]. Using multiple linear regression analyses, it has been shown that this polymorphism was a significant factor affecting HDL-C levels in men from the population-based sample (p = 0.001), an interaction between -250G/A variant and wine consumption was also detected (p = 0.001). Thus, our results show that the -250G/A polymorphism in the HL gene is associated with significant variations in HDL-C levels and CAD risk in males.

Interaction between SREBP-1a and APOB polymorphisms influences total and low-density lipoprotein cholesterol levels in patients with coronary artery disease.

In this study, we examined the insertion/deletion (Ins/Del) and XbaI polymorphisms of the apolipoprotein B (APOB) gene and the -36delG polymorphism in the sterol regulatory element binding protein-1a (SREBP-1a) gene in 298 patients with non-diabetic angiographically assessed coronary artery disease (CAD), and 188 healthy controls, from a Brazilian population of European descent. Del/X+ haplotype carriers had higher levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) in patients (TC, p = 0.05; LDL-C, p = 0.049) and controls (TC, p = 0.004; LDL-C, p = 0.013). No association was detected between the SREBP-1a-36delG polymorphism and lipid levels, but a significant interaction effect between APOB and SREBP-1a polymorphisms was observed in the patient sample on TC (p = 0.005) and on LDL-C (p = 0.019) levels. Carriers of the APOB Del/X+ haplotype and SREBP-1a G-G- genotype showed the highest levels of these lipid parameters. This effect of interaction was not observed in the control sample. Despite the associations with lipids, these polymorphisms were not associated with CAD risk or severity in this sample.

Does serum ferritin correlate with coronary angiography findings?

BACKGROUND: A number of epidemiological studies have described a positive relationship between serum ferritin levels and coronary heart disease. In this prospective study, we evaluated the association between serum ferritin levels and the angiographic extent of coronary atherosclerosis. METHOD: We studied 307 consecutive patients (60.9% male, age 60.1+/-11.0 years) referred for diagnostic coronary angiography. Risk factors for coronary artery disease, lipids and ferritin levels, as well clinical characteristics were recorded from all patients. Two experienced cardiologists blinded for clinical and laboratory data reviewed the cinefilms. Angiographic significant coronary artery disease (CAD) was defined as any more than a 50% diameter stenosis. RESULTS: From the 307 patients, 196 (63.8%) were found to have angiographic significant CAD. The presence of significant CAD was associated with ferritin levels (P=0.015) as well as patient age (P<0.001), male sex (P<0.001), smoking (P<0.002), and cholesterol levels (P=0.028). By multivariate analysis, however, ferritin level was not an independent risk factor for CAD (P=0.27), while the association with all the other factors remained significant. CONCLUSION: In patients referred for coronary angiography no independent relationship was found between angiographic significant coronary artery disease and serum ferritin levels.

Lack of a relationship between serum ferritin levels and coronary atherosclerosis evaluated by coronary arteriography.

Many clinical and epidemiological studies have demonstrated the relationship between serum ferritin and ischemic heart disease. In the present study we evaluated the relationship between coronary heart disease (CHD) and serum ferritin levels in patients submitted to coronary arteriography. We evaluated 307 patients (210 (68.7%) males; median age: 60 years) who were submitted to coronary angiography, measurement of serum ferritin and identification of clinical events of ischemic heart disease. Serum ferritin is reported as quartiles. Ninety-six patients (31.27%) had normal coronary angiography (group 1) and 211 (68.73%) had coronary heart disease (group 2). Of the patients with CHD, 61 (28.9%) had serum ferritin levels higher than 194 ng/ml (4th quartile), as opposed to only 14 (14.58%) of those without CHD (P = 0.0067). In the 2nd quartile, 39 patients (18.48%) had CHD, while 35 patients (36.46%) had normal coronary arteries (P = 0.00064). Multivariate analysis of the data showed that the difference between groups was not statistically significant (P = 0.33). We conclude that there is no independent relationship between coronary heart disease and increased levels of serum ferritin.

Lack of a relationship between serum ferritin levels and coronary atherosclerosis evaluated by coronary arteriography

Many clinical and epidemiological studies have demonstrated the relationship between serum ferritin and ischemic heart disease. In the present study we evaluated the relationship between coronary heart disease (CHD) and serum ferritin levels in patients submitted to coronary arteriography. We evaluated 307 patients (210 (68.7 percent) males; median age: 60 years) who were submitted to coronary angiography, measurement of serum ferritin and identification of clinical events of ischemic heart disease. Serum ferritin is reported as quartiles. Ninety-six patients (31.27 percent) had normal coronary angiography (group 1) and 211 (68.73 perce) had coronary heart disease (group 2). Of the patients with CHD, 61 (28.9 percent) had serum ferritin levels higher than 194 ng/ml (4th quartile), as opposed to only 14 (14.58 percent) of those without CHD (P = 0.0067). In the 2nd quartile, 39 patients (18.48 percent) had CHD, while 35 patients (36.46 percent) had normal coronary arteries (P = 0.00064). Multivariate analysis of the data showed that the difference between groups was not statistically significant (P = 0.33). We conclude that there is no independent relationship between coronary heart disease and increased levels of serum ferritin

Are apolipoproteins A and B better than lipoproteins for assessing risk of obstructive coronary heart disease?

OBJECTIVE: To evaluate whether apolipoproteins A-I (Apo A-I) and B (Apo B) have, higher ensitivity (SN), specificity (SP) and positive predictive value (PPV) than lipoproteins (LP), total cholesterol (TC), high density lipoprotein (HDL), low density lipoprotein (LDL), very low density lipoprotein (VLDL), and triglycerides (TGL) in assessing the risk of coronary heart disease (CHD). METHODS: This is a transversal case-control study of 241 patients, who were divided into two groups: 1) 145 patients with CHD, and 2) 96 patients without coronary disease. A model of logistic regression to evaluate the relation between the LPs and CHD was developed in which variables with a p-alpha < 0.1 were included. RESULTS: Apo A-I levels were higher in the patients without CHD, (OR 2.08, CI 1.20-3.57). There were no statistical differences between the values of Apo A-I and the remaining lipid fractions (Apo A-I: 67%; Apo B: 100%; PPV: TC = 71%; TGC = 71%; HDL = 71%; LDL = 71%). The costs of the tests in Reais were as follows: Apo A-I: R$ 56.60; Apo B-100: R$ 56.60; TC: R$ 9.94; HDL: R$ 21.30; LDL: R$ 28.40; TGL: R$ 14.20. CONCLUSION: Levels of Apo A-I and Apo B have no advantage over conventional lipoproteins in predicting the risk of CHD, despite the statistical association between Apo A-I and CHD; in addition, their costs are higher than those of the conventional lipoproteins.

[Comparison of coronary arteriosclerosis in patients with myocardial infarction and angina pectoris]. / Comparação da aterosclerose coronária em pacientes com infarto do miocárdio e angina do peito.

PURPOSE: To compare the severity of the coronary heart disease and the presence of coronary risk factors between angina and myocardial infarction (MI) patients. METHODS: We studied 62 patients with MI and 129 with angina through coronary angiography to evaluate occlusion (lesion of 99% or 100%), extent (with a score of 0-5 derived by the number of vessels affected) and severity (3 groups of different stenosis degrees). Two experiment observers blindly interpreted the angiograms. RESULTS: Patients with MI had more occlusions (50% vs 13.2% [p < 0.01]), more severity (79% vs 54.3% with > 90% stenosis [p < 0.02]) and more extent (2.0 vs 0.87; [p < 0.001]), even when controlled for current coronary risk factors and disease duration. Smoking was the only independent risk factor related to MI (p < 0.001). CONCLUSION: Among the studied patients, coronary heart disease extent and severity was greater in the MI group, as well as the prevalence smoking.

Comparação da aterosclerose coronária em pacientes com infarto do miocárdio e angina do peito / Comparison of coronary heart disease extent and severity in patients with myocardial infarction and angina pectoris

OBJETIVO - Comparar a gravidade da doeça coronária e a presença de fatores de risco cardiovasculares entre pacientes com angina e infarto do miocárdio (IM). MÉTODOS - Estudaram-se 62 pacientes com IM e 129 com angina, através de cineangiocoronariografia, avaliando-se a oclusão (lesäo de 99 'por cento' ou 100 'por cento'), a severidade (escore de 0 a 5 de acordo com o número de vasos afetados) e a extensäo (3 grupos com diferentes graus de estenose). Dois observadores experientes interpretaram cegamente os angiogramas. RESULTADOS - Os pacientes com IM tiveram maior oclusão (50 'por cento' vs 13,2 'por cento'[p<0,01]), maior severidade (79 'por cento' vs 54,3 'por cento' com mais de 90 'por cento' de estenose [p<0,02]) e maior extensão (2,0 vs 0,87 [p<0,001]), mesmo quando controlados para os fatores de risco coronários clássicos e para o tempo de doença. O tabagismo foi o único fator de risco independente correlacionado com IM (P<0,01). CONCLUSÄO - Entre os pacientes estudados, a doença coronária foi maior no grupo IM, bem como a prevalência de tabagismo.

Left ventricular function and endomyocardial biopsy in early and advanced dilated cardiomyopathy.

We evaluated left ventricular function and endomyocardial biopsy in 20 patients with early and advanced dilated cardiomyopathy, with the purpose of assessing the correlation between histologic variables and systolic and diastolic filling indexes. Group 1 included 10 patients with no clinical history of heart failure and left ventricular ejection fraction > or = 45% and group 2, 10 patients with a clinical history of heart failure and left ventricular ejection fraction <45%. Group 1 showed lower left ventricular end-systolic and end-diastolic volumes indexes (49+/-14 versus 86+/-23 ml/m2, P<0.001; 98+/-25 versus 127+/-35 ml/m2, P=0.049), higher left ventricular ejection fraction (50+/-4 versus 32+/-4%, P<0.001) and lower coefficient of variation of percentage shortening of left ventricular transverse hemiaxes (0.3+/-0.1 versus 0.5+/-0.1, P=0.001) compared with group 2. Group 1 had higher A wave peak velocity (78+/-18 versus 60+/-20 cm/s, P=0.048), lower E/A ratio (0.9+/-0.3 versus 1.5+/-0.6, P=0.02) and slower E wave deceleration time (204+/-51 versus 155+/-50 ms, P=0.047) compared with group 2. Semiquantitative histologic scores did not differ significantly between groups. There was no significant correlation between histologic variables and left ventricular systolic and diastolic indexes. Thus, dilated cardiomyopathy shows borderline to severe left ventricular systolic impairment and distinct left ventricular diastolic filling abnormalities, according to the clinical stage. This study suggests a marked dissociation between histologic findings and functional abnormalities in early and advanced dilated cardiomyopathy.

Postangioplasty restenosis: a practical model in the porcine carotid artery

Transluminal coronary angioplasty is a routine therapeutic intervention in coronary heart disease. Despite the high rate of primary success, restenosis continues to be its major limitation. Porcine models have been considered to be the most adequate experimental models for studying restenosis. One limitation of porcine models is the need for radiological guidance and the expenses involved. The objective of the present study was to adapt an experimental model of angioplasty in the porcine carotid artery that does not require radiological equipment. Eight animals were used to develop the technique of balloon injury to the common carotid artery by dissection without radiological guidance. This technique was then employed in six other animals. Under anesthesia, the left common carotid artery was dissected and incised at the carotid sinus for insertion of an over-the-wire angioplasty balloon towards the aorta. Overstretch injury of the carotid artery was performed under direct visualization. After 30 days, the arteries were excised and pressure-fixated. Uninjured carotid arteries from 3 additional animals were used as controls. A decreased luminal area associated with intimal hyperplasia and medial reaction was observed in all injured arteries. Immunohistochemistry identified the intimal hyperplastic cells as smooth muscle cells. Computerized morphometry of the ballooned segments revealed the following mean areas: lumen 2.12mm2 (+ 1.09), intima 0.22mm2 (+ 0.08), media 3.47mm2 (+ 0.67), and adventitia 1.11mm2 (+ 0.34). Our experimental model of porcine carotid angioplasty without radiological guidance induced a vascular wall reaction and permitted the quantification of this response. This porcine model may facilitate the study of vascular injury and its response to pharmacological interventions.

[Thrombolytic therapy in deep venous thrombosis. Initial clinical experience]. / Terapia trombolítica em trombose venosa profunda. Experiência clínica inicial.

Four cases of proximal deep venous thrombosis treated with streptokinase and tissue plasminogen activator are reported. Therapy monitorization was performed by ultrasonography with color Doppler and thrombolytic agents were used by venous infusion. There was complete lysis in two cases, and the mean rate of venous recanalization was 88%. Reversible hemorrhagic complications were observed in two patients, and late ultrasonographic control (after six months) demonstrated venous insufficiency in one case.

Postangioplasty restenosis: a practical model in the porcine carotid artery.

Transluminal coronary angioplasty is a routine therapeutic intervention in coronary heart disease. Despite the high rate of primary success, restenosis continues to be its major limitation. Porcine models have been considered to be the most adequate experimental models for studying restenosis. One limitation of porcine models is the need for radiological guidance and the expenses involved. The objective of the present study was to adapt an experimental model of angioplasty in the porcine carotid artery that does not require radiological equipment. Eight animals were used to develop the technique of balloon injury to the common carotid artery by dissection without radiological guidance. This technique was then employed in six other animals. Under anesthesia, the left common carotid artery was dissected and incised at the carotid sinus for insertion of an over-the-wire angioplasty balloon towards the aorta. Overstretch injury of the carotid artery was performed under direct visualization. After 30 days, the arteries were excised and pressure-fixated. Uninjured carotid arteries from 3 additional animals were used as controls. A decreased luminal area associated with intimal hyperplasia and medial reaction was observed in all injured arteries. Immunohistochemistry identified the intimal hyperplastic cells as smooth muscle cells. Computerized morphometry of the ballooned segments revealed the following mean areas: lumen 2.12 mm2 (+/- 1.09), intima 0.22 mm2 (+/- 0.08), media 3.47 mm2 (+/- 0.67), and adventitia 1.11 mm2 (+/- 0.34). Our experimental model of porcine carotid angioplasty without radiological guidance induced a vascular wall reaction and permitted the quantification of this response. This porcine model may facilitate the study of vascular injury and its response to pharmacological interventions.