Increased ambulatory arterial stiffness index and blood pressure load in normotensive obese patients.

OBJECTIVES: It has been shown that blood pressure (BP) values measured in obese subjects are higher than the individuals with normal weight, even in normotensive limits. However, data concerning the Ambulatory Arterial Stiffness Index (AASI) and blood pressure load in normotensive obese subjects is lacking. This study was aimed to compare the ambulatory arterial stiffness index and blood pressure load in normotensive obese and healthy controls. METHODS: One hundred normotensive obese and one hundred normal weight subjects were included in this study. All subjects underwent 24-hour ambulatory blood pressure monitoring. Ambulatory arterial stiffness index was calculated from 24-hour ambulatory blood pressure monitoring records. Ambulatory arterial stiffness index was defined as one minus the regression slope of unedited 24-h diastolic on systolic blood pressures. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) load values were calculated from 24-hour ambulatory blood pressure monitoring analysis. RESULTS: Ambulatory arterial stiffness index of the obese subjects was significantly higher than the healthy controls (0.48±0.2 vs. 0.33±0.11, p<0.001). 24-hours systolic blood pressure and diastolic blood pressure loads were significantly higher in obese subjects. Logistic regression analysis revealed that body mass index (BMI) was an independent predictor for an abnormal ambulatory arterial stiffness index (≥0.50) (OR: 1.137, 95% CI: 0.915-1.001, p=0.004). CONCLUSION: Blood pressure load and ambulatory arterial stiffness index are increased in normotensive obese patients. Moreover, body mass index is an independent predictor for an abnormal ambulatory arterial stiffness index. Our results indicate that obese subjects are at higher risk for future cardiovascular events despite normal office BP levels.

The Usefulness of Admission Plasma NT-pro BNP Level to Predict Left Ventricular Aneurysm Formation after Acute ST-Segment Elevation Myocardial Infarction / Utilidade do Nível de NT-Pro-BNP no Plasma à Internação em Predizer a Formação de Aneurisma do Ventrículo Esquerdo após Infarto Agudo do Miocárdio com Elevação do Segmento ST

Abstract Background: Left ventricular aneurysm (LVA) is an important complication of acute myocardial infarction. In this study, we investigated the role of N- Terminal pro B type natriuretic peptide level to predict the LVA development after acute ST-segment elevation myocardial infarction (STEMI). Methods: We prospectively enrolled 1519 consecutive patients with STEMI. Patients were divided into two groups according to LVA development within the six months after index myocardial infarction. Patients with or without LVAs were examined to determine if a significant relationship existed between the baseline N- Terminal pro B type natriuretic peptide values and clinical characteristics. A p-value < 0.05 was considered statistically significant. Results: LVA was detected in 157 patients (10.3%). The baseline N- Terminal pro- B type natriuretic peptide level was significantly higher in patients who developed LVA after acute MI (523.5 ± 231.1 pg/mL vs. 192.3 ± 176.6 pg/mL, respectively, p < 0.001). Independent predictors of LVA formation after acute myocardial infarction was age > 65 y, smoking, Killip class > 2, previous coronary artery bypass graft, post-myocardial infarction heart failure, left ventricular ejection fraction < 50%, failure of reperfusion, no-reflow phenomenon, peak troponin I and CK-MB and NT-pro BNP > 400 pg/mL at admission. Conclusions: Our findings indicate that plasma N- Terminal pro B type natriuretic peptide level at admission among other variables provides valuable predictive information regarding the development of LVA after acute STEMI.

Resumo Fundamento: O aneurisma do ventrículo esquerdo (AVE) é uma importante complicação do infarto agudo do miocárdio (IAM). Objetivo: Investigar o papel da porção N-terminal do pró-hormônio do peptídeo natriurético do tipo B (NT-proBNP) para predizer o desenvolvimento de AVE após infarto agudo do miocárdio com supradesnivelamento do segmento ST (IAMCST). Métodos: Incluímos prospectivamente 1519 pacientes consecutivos com IAMCST. Os pacientes foram divididos em dois grupos de acordo com o desenvolvimento de AVE nos seis meses após o infarto do miocárdio. Os pacientes com ou sem AVE foram examinados para determinar se existia uma relação significativa entre os valores basais do NT-proBNP e as características clínicas. Um valor de p < 0,05 foi considerado estatisticamente significativo. Resultados: O AVE foi detectado em 157 pacientes (10,3%). O nível basal do NT-proBNP foi significativamente maior em pacientes que desenvolveram AVE após IAM (523,5 ± 231,1 pg/mL vs. 192,3 ± 176,6 pg/mL, respectivamente, p < 0,001). Os preditores independentes da formação de AVE após IAM foram idade > 65 anos, tabagismo, classe Killip > 2, cirurgia de revascularização miocárdica anterior, insuficiência cardíaca pós-infarto do miocárdio, fração de ejeção do ventrículo esquerdo < 50%, falha de reperfusão, fenômeno de no-reflow, pico de troponina I e CK-MB e NT-proBNP > 400 pg/mL na internação. Conclusões: Nossos achados indicam que o nível plasmático do fragmento N-terminal do peptídeo natriurético tipo B na admissão, entre outras variáveis, fornece informações preditivas valiosas sobre o desenvolvimento de AVE após o IAMCST agudo.

The Usefulness of Admission Plasma NT-pro BNP Level to Predict Left Ventricular Aneurysm Formation after Acute ST-Segment Elevation Myocardial Infarction.

BACKGROUND: Left ventricular aneurysm (LVA) is an important complication of acute myocardial infarction. In this study, we investigated the role of N- Terminal pro B type natriuretic peptide level to predict the LVA development after acute ST-segment elevation myocardial infarction (STEMI). METHODS: We prospectively enrolled 1519 consecutive patients with STEMI. Patients were divided into two groups according to LVA development within the six months after index myocardial infarction. Patients with or without LVAs were examined to determine if a significant relationship existed between the baseline N- Terminal pro B type natriuretic peptide values and clinical characteristics. A p-value < 0.05 was considered statistically significant. RESULTS: LVA was detected in 157 patients (10.3%). The baseline N- Terminal pro- B type natriuretic peptide level was significantly higher in patients who developed LVA after acute MI (523.5 ± 231.1 pg/mL vs. 192.3 ± 176.6 pg/mL, respectively, p < 0.001). Independent predictors of LVA formation after acute myocardial infarction was age > 65 y, smoking, Killip class > 2, previous coronary artery bypass graft, post-myocardial infarction heart failure, left ventricular ejection fraction < 50%, failure of reperfusion, no-reflow phenomenon, peak troponin I and CK-MB and NT-pro BNP > 400 pg/mL at admission. CONCLUSIONS: Our findings indicate that plasma N- Terminal pro B type natriuretic peptide level at admission among other variables provides valuable predictive information regarding the development of LVA after acute STEMI.

Platelet to lymphocyte ratio predicts all-cause mortality in patients with carotid arterial disease.

BACKGROUND: Platelet to lymphocyte ratio (PLR) has been demonstrated as a risk and prognostic marker in many of cardiovascular diseases. A relationship between PLR and severity of carotid stenosis has been shown. The aim of our study was to investigate the relationship between PLR and all cause mortality in patients with carotid arterial disease. METHODS: This retrospective study included 146 patients who had been performed selective carotid angiography. Carotid stenosis were graded by the North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria. Platelet to lymphocyte ratio was calculated as the ratio of platelets to lymphocytes. The end point of the study was all-cause mortality. RESULTS: During median follow-up of 16 months (0-65 months) 15 (10.3%) patients suffered all-cause mortality. 50 patients (34.2%) underwent carotid endarterectomy and 69 patients (47.3%) had non-carotid cardiac surgery. 38 patients (26.02%) had cerebrovascular events (stroke/transient ischemic attack) at admission. NASCET grades were not different between survivors and non-survivors. Non-survivors had significantly lower hemoglobin (Hb) levels (12.7 ± 1.6 g/dL vs. 13.7 ± 1.7 g/dL, p = 0.031) and they were older than survivors (74.2 ± 8.4 years vs. 68.6 ± 8.5 years, p = 0.029). Non-survivors had significantly higher PLR values compared with survivors (190.3 ± 85.6 and 126.8 ± 53.8, p = 0.017). In multivariate analysis, only PLR predicted all-cause mortality in patients with carotid artery stenosis. CONCLUSION: In our study, higher PLR was associated with increased all-cause mortality.

[Levosimendan and dobutamine have a similar profile for potential risk for cardiac arrhythmias during 24-hour infusion in patients with acute decompensated heart failure]. / Levosimendan ve dobutamin akut dekompanse kalp yetersizliginde 24 saatlik infüzyon sirasinda benzer aritmi potansiyeli göstermektedir.

OBJECTIVES: Unlike traditional inotropic agents, levosimendan is thought to have a lower potential to induce arrhythmias because it does not increase intracellular calcium levels and myocardial oxygen consumption. We compared the potential effect of levosimendan and dobutamine to induce cardiac arrhythmias in patients with decompensated heart failure. STUDY DESIGN: Fifty patients with acute decompensated heart failure (NYHA class III-IV, ejection fraction <35%) who were in need of inotropic support were randomized to dobutamine (n=25; mean age 69±10 years) or levosimendan (n=25; mean age 67.5±11.5 years) and underwent 24-hour Holter monitoring before and during inotropic infusion. Holter recordings were analyzed with respect to heart rate (HR), ventricular premature contraction (VPC), couplets of VPC, supraventricular premature contraction (SVPC), paroxysmal atrial fibrillation (PAF), and nonsustained ventricular tachycardia (NSVT). RESULTS: Before infusions, the two groups were similar with respect to HR, VPC, couplets of VPC, SVPC, and PAF episodes, but the number of NSVT episodes was significantly higher in the levosimendan group. Heart rate and the number of VPCs increased significantly during infusions of levosimendan (p=0.036 and p<0.001, respectively) and dobutamine (for both p<0.001). Increase in couplets of VPC was significant only with dobutamine (p=0.012). The episodes of NSVT and PAF increased with levosimendan, without reaching significance. Levosimendan and dobutamine groups were similar in terms of percentage changes in arrhythmias (55±224% vs. 11±16% for VPC; 2±2.7% vs. 12±9% for couplets of VPC; 3.4±5.8% vs. 16±39% for SVPC, 0.4±2.8% vs. -2±0% for NSVT) and percentage change in total arrhythmias (41±190% vs. 18±35.4%), and the mean HR, VPC, couplets of VPC, SVPC, and episodes of NSVT and PAF (p>0.05). CONCLUSION: Our findings suggest that levosimendan and dobutamine have a similar profile for potential risk for cardiac arrhythmias.

Both levosimendan and dobutamine treatments result in significant reduction of NT-proBNP levels, but levosimendan has better and prolonged neurohormonal effects than dobutamine.

Levosimendan and dobutamine are comparable inotropic drugs as regards their hemodynamic effects and clinical outcomes in decompensated heart failure (HF). The aim of this study was to compare the effects of levosimendan and dobutamine treatment on NT-proBNP levels in patients with decompensated HF. Forty-four patients with decompensated HF and ejection fraction <35% received either a 24-h infusion of levosimendan (n=26) or dobutamine (n=18). NT-proBNP was measured at baseline and 12 h, 24 h and 48 h after the initiation of drug infusion. NT-proBNP levels at baseline, 12 h, 24 h and 48 h were 16,879+/-2437, 16,004+/-2635, 12,881+/-2305 and 11,078+/-2092 pg/ml, respectively, in the levosimendan group and 16,031+/-3463, 15,908+/-3806, 12,271+/-3299 and 14,840+/-4009 pg/ml, respectively, in the dobutamine group. NT-proBNP decreased significantly at 24 h in response to both levosimendan and dobutamine treatment (p<0.01 and p<0.05, respectively) with no significant difference among the treatment groups. In the dobutamine group, NT-proBNP increased at 48 h (p=n.s. vs. baseline), in contrast, NT-proBNP reduction continued for up to 48 h in the levosimendan group (p<0.001 vs. baseline). Although not statistically different, a greater percentage of NT-proBNP reduction was observed with levosimendan treatment at both 24 h (-25+/-7% vs. -20+/-10%) and 48 h (-32+/-7% vs. -20+/-11%) compared to dobutamine. Both levosimendan and dobutamine treatments result in significant reduction of NT-proBNP levels at the end of the 24-h infusion. However, compared to dobutamine, levosimendan has better and prolonged effects on NT-proBNP levels in decompensated HF.