Serum osteoprotegerin level is independently related to subclinical left atrial mechanical function in patients with hypertension and diabetes.

OBJECTIVES: Previous studies showed that subclinical abnormal left atrial (LA) function could be diagnosed with LA speckle tracking evaluation long before chamber enlargement. Osteoprotegerin (OPG) is a member of the tumor necrosis factor (TNF) receptor superfamily and was recently found to be an indicator for adverse cardiovascular outcomes and a risk factor for new onset atrial fibrillation. The authors hypothesized that OPG values could predict LA mechanical dysfunction and LA remodeling assessed by two-dimensional speckle tracking echocardiography (2D-STE) in patients with hypertension (HT) and diabetes mellitus (DM). METHODS: A single center study was conducted including consecutive patients presenting to the authors' outpatient clinic. Enrolled patients needed to have been treated for HT and DM for at least 1 year. RESULTS: The study included 80 patients (mean age, 57.5 ± 8.3 years). Patients in the impaired LA strain group were older (p = 0.035), had lower low density lipoprotein (LDL) cholesterol (mg/dl) (p = 0.021), and higher OPG (pmol/l) (p = 0.004) values than patients in the normal LA strain group. Univariate logistic regression analysis demonstrated that age (p = 0.039), LDL cholesterol (mg/dl) (p = 0.025), and OPG (pmol/l) (p = 0.008) values were associated with impaired LA strain. Backward multivariate logistic regression analysis showed that LDL cholesterol (mg/dl) (OR: 0.982, CI 95% 0.964-0.999, p = 0.049) and OPG (pmol/l) (OR: 1.438, CI 95% 1.043-1.983, p = 0.027) were independently associated with impaired LA strain. CONCLUSION: In hypertensive and diabetic patients, higher OPG values were associated with impaired LA function assessed by 2D-STE. In this high-risk patient group, serum OPG can be used as a risk predictor for LA mechanical dysfunction.

Presystolic wave is associated with carotid intima media thickness.

INTRODUCTION: Carotid intima media thickness (CIMT), a direct marker of atherosclerosis, has emerged as a promising means for cardiovascular risk evaluation. Presystolic wave (PSW) is commonly detected by the Doppler interrogation of the left ventricular outflow tract (LVOT). It is thought to be a result of a stiff left ventricle and impaired LV compliance. Herein, we aimed to investigate a possible association between carotid intima media thickness, an atherosclerotic marker, and PSW. METHOD: We prospectively enrolled 282 patients divided into two groups based on the presence of PSW: 221 (89F; mean age: 49.3 ± 11.5 years) had PSW on Doppler examination while 61 patients (32F; mean age: 46.4 ± 10.3 years) did not. Both groups were compared with respect to demographic, clinical properties, and CIMT. RESULTS: Both groups had comparable age, body mass index, and diabetes mellitus, hypertension, dyslipidemia, smoking, and family history for coronary heart disease. PSW-positive group had significantly higher CIMT (PSW-positive: 0.59 ± 0.22 mm vs PSW-negative: 0.42 ± 0.11 mm; P < 0.001) than PSW-negative group. Multivariate analysis showed that the independent predictors of increased CIMT were age (95% CI; 1.044-1.101, P < 0.001), dyslipidemia (95% CI; 0.147-0.664, P = 0.002), and the presence of PSW (95% CI; 2.168-7.836, P < 0.001).Correlation analysis showed that PSW velocity is correlated with increased CIMT in PSW-positive group (r: 0.418, P < 0.001). CONCLUSION: Assessment of PSW on TTE is easy and feasible method. Presence of PSW and increased PSW velocity on TTE might provide information that we should be careful in terms of subclinical atherosclerosis.

Mitral annular calcification is associated with pulse wave velocity but not with augmentation index.

OBJECTIVE: To investigate the possible relationship between mitral annular calcification (MAC) and arterial stiffness. SUBJECTS AND METHODS: Forty-two patients (mean age 68 ± 6 years) with MAC and an age-matched control group of 41 individuals (mean age 66 ± 6 years) were studied. Arterial stiffness and wave reflections of the study population were evaluated by using applanation tonometry (SphygmoCor). Aortic pulse wave velocity (PWV) was measured as an index of aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a composite marker of wave reflections and arterial stiffness. RESULTS: Aortic PWV was significantly higher in patients with MAC (12.2 ± 2.3 m/s) than in controls (10.1 ± 1.3 m/s, p = 0.0001). However, AIx@75 was similar between the groups (28 ± 10 vs. 29 ± 10%, p = 0.59). Multivariate analysis involving the whole population revealed that brachial diastolic blood pressure (ß = 1.87, p = 0.04) and MAC (ß = 0.41, p = 0.0001) were independent determinants of aortic PWV. CONCLUSION: The data showed that MAC was significantly associated with increased arterial stiffness and that it was an independent determinant of aortic PWV.

Anti-TNF-α therapy may not improve arterial stiffness in patients with AS: a 24-week follow-up.

OBJECTIVE: The availability of new-generation drugs has provided significant success reflected by disease activity markers and clinical status in AS, but controversial reports necessitate further assessment of associated increased risk of cardiovascular burden that might persist. Hence this prospective clinical study evaluated the effectiveness of a 24-week anti-TNF-α therapy on vascular stiffness [pulse wave velocity (PWV)] in AS. METHODS: A total of 28 active AS patients (21 males, 7 females) were enrolled before the start of biologic therapy. Demographic and clinical characteristics were recorded. Arterial stiffness was assessed using PWV. Patients were evaluated before and 24 weeks after anti-TNF-α therapy. RESULTS: The mean disease duration was 8.4 (4.9) years. After 24 weeks of anti-TNF-α therapy, despite significant improvements in patients' symptoms and clinical activity parameters, including BASDAI score [4.9 (0.9) vs 1.9 (0.5), P = 0.0001], ESR [35.5 (23.1) vs 13.8 (9.2) mm/h, P = 0.0001) and CRP level [2.1 (1.6) vs 0.4 (0.3) ng/dl, P = 0.0001], no significant change was seen in arterial stiffness parameters [7.9 (1.3) vs 7.7 (1.3) m/s, P = 0.412]. Significant correlation was determined between arterial stiffness and age, systolic blood pressure and high-density lipoprotein cholesterol levels. CONCLUSION: Despite significant improvement in markers of disease activity, anti-TNF-α therapy does not seem to improve arterial stiffness, a significant AS-associated cardiovascular burden. Thus, when treating AS, significant end-points other than DASs should also be considered, and any hidden threat like arterial stiffness should be addressed further.

Left ventricular dyssynchrony and its effects on cardiac function in patients with newly diagnosed hypertension.

OBJECTIVES: Left ventricular (LV) systolic synchrony, defined as simultaneous peak contractions of corresponding cardiac segments, is well documented to be impaired in hypertension but its effect on LV function is not clear. The aim of this study was to assess the impacts of LV systolic dyssynchrony on LV function in newly diagnosed hypertensives. METHODS: Forty-eight newly diagnosed hypertensive patients and 33 controls were enrolled. All study population underwent a comprehensive echocardiographic evaluation including tissue synchrony imaging. The time to regional peak systolic tissue velocity (Ts) in LV by 12 segmental models was measured and two parameters of systolic dyssynchrony were computed. RESULTS: Baseline demographic characteristics were similar in both study groups. Dyssynchrony parameters prolonged in newly diagnosed hypertensive patients compared to controls: the standard deviation (SD) of 12 LV segments Ts (40.2 ± 21 vs. 26.2 ± 13.4, P = 0.003); the maximal difference in Ts between any 2 of 12 LV segments (123.3 ± 61.5 vs. 79.8 ± 37.9, P = 0.001). In multivariable analysis, Ts-SD-12 was found to be an independent predictor for systolic function (ß=-0.29, P = 0.008). But, both diastolic and global functions were not independently related to Ts-SD-12. CONCLUSION: LV synchronization is impaired in newly diagnosed hypertensive patients. LV dyssynchrony is one of the independent predictors of systolic function in hypertensive patients.

Pseudocholinesterase levels are not decreased in grayanotoxin (mad honey) poisoning in most patients.

BACKGROUND: The symptoms of mad honey poisoning resemble those of cholinergic toxidromes; however, it is not clear whether they share a common biochemical basis. OBJECTIVES: The aim of this study was to investigate a possible resemblance between mad honey poisoning and cholinergic toxidromes. METHODS: This is a descriptive study performed prospectively in patients presenting to a University Medical Faculty Emergency Medicine Department emergency service with mad honey poisoning over 1 year, from September 2008 to September 2009. Adult patients with clinical findings suggesting mad honey poisoning (i.e., bradycardia, hypotension, syncope, and vertigo) and with a history of honey consumption were enrolled. Pseudocholinesterase levels in blood samples taken from the mad honey-poisoned patients were analyzed to determine whether these were lower than normal pseudocholinesterase levels for adults (5400-13,200 U/L). RESULTS: The most common symptoms of the 30 patients enrolled in the study were vertigo and nausea. Low blood pressure and bradycardia were the most frequently observed physical examination findings. None of the patients enrolled had a history of disease that might cause low pseudocholinesterase. Mean pseudocholinesterase levels in our patients with mad honey poisoning were 7139.30 ± 2316.41 U/L (min-max: 1785-12,835). Blood pseudocholinesterase levels were within normal limits in 90% of patients and below normal in 10%. CONCLUSION: A low pseudocholinesterase level was found in 3 (10%) of our 30 patients. These biochemical data do not support the hypothesis that mad honey poisoning should be regarded as cholinergic poisoning.

Assessment of the relationship between aortic pulse wave velocity and aortic arch calcification.

OBJECTIVES: We aimed to assess arterial stiffness parameters and to investigate the relationship between these parameters and aortic calcification in patients with aortic arch calcification and without symptomatic atherosclerotic disease. STUDY DESIGN: The population of this study consisted of 41 patients with aortic arch calcification verified by chest X-ray (group I, 17 males, mean age 70±5 years) and individuals without aortic arch calcification (group II, 17 males, mean age 68±6 years). Subjects with symptomatic or known vascular disease were excluded from the study. The arterial stiffness parameters of all subjects were measured non-invasively with a SphygmoCor device. Aortic pulse wave velocity (PWV), augmentation pressure (AP), augmentation index (AIx) and heart rate normalized augmentation index (AIx@75) were used as parameters of arterial stiffness. RESULTS: The two groups were compared according to demographic characteristics, medications currently being taken, and levels of serum lipids. There was no significant difference between the groups. AP in group I was significantly higher than that of group II (p=0.002). AIx and AIx@75 were similar in both groups. Aortic PWV of group I was significantly higher than that of group II (p<0.0001). CONCLUSION: According to the results of this study, the presence of aortic calcification, verified by chest radiography, was associated with increased aortic PWV.

The assessment of left ventricular systolic asynchrony in patients with primary hyperparathyroidism.

OBJECTIVES: Primary hyperparathyroidism (PHP) is associated with a variety of cardiovascular disturbances such as left ventricular (LV) hypertrophy, diastolic cardiac dysfunction, and hypertension. LV asynchrony is defined as the loss of the simultaneous peak contraction of corresponding cardiac segments. The objective of this study was to assess systolic asynchrony in patients with overt hyperparthyroidism. METHODS: Asynchrony was evaluated in 22 patients with PHP and 24 controls. All the patients and controls were subjected to a tissue synchronization imaging (TSI). The time to regional peak systolic tissue velocity (Ts) in LV by the six-basal-six-midsegmental model was measured on ejection phase TSI images and four TSI parameters of systolic asynchrony were computed. RESULTS: All TSI parameters of LV asynchrony increased in patients with PHP patients compared to the controls: the standard deviation (SD) of the 12 LV segments Ts (37.3±20.6 vs. 21.5±11.1, P=0.01); the maximal difference in Ts between any 2 of the 12 LV segments (111.2±59.8 vs. 70.2±32.1, P=0.01); the SD of the 6 basal LV segments (42.9±36.4 vs. 18.5±13, P=0.003); and the maximal difference in Ts between any 2 of the 6 basal LV segments (89.6±50.5 vs. 48±31.1, P=0.003). CONCLUSION: Patients with PHP show an evidence of LV asynchrony by TSI. Asynchrony may contribute to the harmful cardiovascular effects of PHP.

Exercise-Based Cardiac Rehabilitation Has a Strong Relationship with Mean Platelet Volume Reduction. / Reabilitação Cardíaca Baseada em Exercícios Fortemente Relacionada com Redução do Volume Plaquetário Médio.

BACKGROUND: Mean platelet volume (MPV), which is a simple measure of platelet activation, has recently become an interesting topic in cardiovascular research. Exercise-based cardiac rehabilitation (CR) is a comprehensive intervention that decreases mortality-morbidity in patients with coronary artery disease (CAD). Studies on the effects of exercise on platelet activation have yielded conflicting results. OBJECTIVE: The purpose of this study was to determine the effect of an exercise-based CR programs on MPV in patients with stable CAD. METHODS: The sample was composed of 300 consecutive stable CAD patients. The patients were divided into two groups: CR group (n = 97) and non-CR group (n = 203). Blood analysis was performed. Point-Biserial correlation measures were performed to show correlation between MPV change and CR. A p value of <0.05 was considered statistically significant. RESULTS: The decrease in MPV was greater in the CR group than in the non-CR group [(-1.10(-1.40-(-0.90)) vs. (-0.10 (-2.00-0.00)); p< 0.001]. ΔMPV had a positive correlation with Δ neutrophil (r = 0.326, p < 0.001), ΔTG (r = 0.439, p < 0.001), ΔLDL-c (r = 0.478, p < 0.001), ΔWBC (r = 0.412, p < 0.001), and ΔCRP (r = 0.572, p < 0.001). A significant correlation was found between ΔMPV% and CR (r=0.750, p<0.001). CONCLUSIONS: We were able to show that exercise-based CR has a strong relationship with MPV reduction in patients with CAD. We consider that decreased platelet activation with exercise-based CR might play an important role in reducing thrombotic risk in patients with stable CAD. (Arq Bras Cardiol. 2020; [online].ahead print, PP.0-0).

FUNDAMENTO: O volume plaquetário médio (VPM), uma medida simples de ativação plaquetária, tornou-se recentemente um tópico interessante no campo da pesquisa cardiovascular. A reabilitação cardíaca (RC) baseada em exercícios é uma intervenção abrangente que diminui a morbidade-mortalidade em pacientes com doença arterial coronariana (DAC). Estudos sobre os efeitos do exercício físico na ativação plaquetária têm produzido resultados conflitantes. OBJETIVO: O objetivo deste estudo foi determinar o efeito de um programa de RC baseado em exercícios sobre o VPM em pacientes com DAC estável. MÉTODOS: A amostra foi composta por 300 pacientes consecutivos com DAC estável. Os pacientes foram divididos em dois grupos: grupo RC (n = 97) e grupo não RC (n = 203). Foi feito um hemograma. As medidas de correlação ponto-bisserial foram tiradas para mostrar a correlação entre a alteração do VPM e a RC. Valor de p<0,05 foi considerado estatisticamente significativo. RESULTADOS: A diminuição do VPM foi maior no grupo CR do que no grupo não CR [(-1,10 (-1,40-(-0,90)) vs. (-0,10 (-2,00-0,00)); p<0,001]. ΔVPM teve correlação positiva com Δ neutrófilos (r = 0,326, p<0,001), ΔTG (r = 0,439, p<0,001), ΔLDL-c (r = 0,478, p<0,001), ΔGB (r = 0,412, p<0,001) e ΔPCR (r = 0,572, p <0,001). Foi encontrada uma correlação significativa entre ΔVPM% e CR (r = 0,750, p <0,001). CONCLUSÕES: Pudemos mostrar que a RC baseada em exercícios tem forte relação com a redução do VPM em pacientes com DAC. Consideramos que a diminuição da ativação plaquetária com RC baseada em exercícios pode desempenhar um papel importante na redução do risco trombótico em pacientes com DAC estável. (Arq Bras Cardiol. 2020; [online].ahead print, PP.0-0).

Epicardial adipose tissue is associated with increased systolic pulmonary artery pressure in patients with chronic obstructive pulmonary disease.

OBJECTIVES: Pulmonary hypertension (PHT) is one of the essential predictors of mortality in chronic obstructive pulmonary disease (COPD). It is thought that PHT is due to vasoconstriction secondary to hypoxia caused by airway obstruction in COPD patients; however, loss of capillary bed with emphysema, inflammation, and endothelial dysfunction may also play a role in the development of PHT. Epicardial adipose tissue (EAT) has a role as a metabolically active endocrine organ and secretes various proinflammatory cytokines. We hypothesized that EAT thickness in COPD patients might be associated with the systolic pulmonary arterial pressure (PAPs) level, and we aimed to test it. METHODS: The present study included 129 consecutive patients with the diagnosis of COPD. All patients underwent transthoracic echocardiographic evaluation. The relationship between PAPs and EAT thickness was evaluated. RESULTS: Positive correlations with PAPs were reported with age, EAT, white blood cell (WBC) and GOLD grade score (range 0.197-0.275, P values 0.026 to 0.002), negative correlations with body-mass index (BMI), hyperlipidemia, FEV1 (% predicted) and pO2 (range -0.216 to -0.340, P values .014 to <.001). In stepwise linear regression analysis, BMI (P = .003), EAT (P = .002), WBC (P = .001), and FEV1 (% predicted) (P = .010), were independently associated with PAPs. CONCLUSION: EAT thickness in COPD patients with preserved left ventricular systolic function is associated with increased PAPs, and this association is independent of the parameters indicating the severity of COPD.

The relationship between endothelial damage and aortic augmentation index.

Augmentation index (AIx), a measure of wave reflection, is regulated by a number of factors, including endothelial function and vascular smooth muscle tone. The relationship between local endothelium-derived factors and AIx is well known; however, association between endothelial damage markers and AIx has not been sufficiently studied. This study investigates whether endothelial damage markers-von Willebrand factor (vWF) soluble thrombomodulin (sTM)--are associated with wave reflections. We studied 46 (48.5 +/- 10.6, years) never-treated patients with hypertension (HT) and an age-matched control group of 40 (47 +/- 8.6, years) normotensive individuals. von Willebrand factor and sTM levels were determined in all subjects. We evaluated the aortic AIx of the study population using applanation tonometry (Sphygmocor, AtCor Medical, Sydney, Australia). The heart rate-corrected augmentation index (AIx@75) was estimated as a marker of wave reflections. Endothelial damage markers and AIx@75 were significantly higher in hypertensive patients than in controls. In the whole population, the vWF level (beta = 0.24, p = 0.01) was an independent determinant of AIx@75 in multivariate analysis. However, the sTM level was not associated with AIx@75. We found that the vWF level was an independent determinant of AIx@75. Our results suggest that increased an vWF level contributes significantly to increased wave reflections.

Effects of prehypertension on arterial stiffness and wave reflections.

The Seventh Report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure classifies blood pressure (BP) as normal, prehypertension, and hypertension. Although it has been shown that there is a relationship between hypertension and arterial stiffness, there is not sufficient data about arterial stiffness in patients with prehypertension. The present study was designed to evaluate arterial stiffness and wave reflections in subjects with prehypertension. We evaluated arterial stiffness and wave reflections of 45 subjects with prehypertension and an age-matched control group of 40 normotensive individuals, using applanation tonometry (Sphygmocor, AtCor Medical, Sydney, Australia). Aortic pulse wave velocity (PWV) was measured as indices of elastic-type aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a composite marker of wave reflections and arterial stiffness. Aortic PWV (10 +/- 2.5 vs. 8.6 +/- 1.7, m/s, p = 0.004) and AIx@75 (21 +/- 8.3 vs. 10 +/- 9.1, %, p = 0.0001) were significantly higher in subjects with prehypertension than in the control group. In multiple linear regression analysis, we found that the presence of the prehypertension was a significant predictor of aortic PWV (beta = 0.26, p = 0.009) and AIx@75 (beta = 0.46, p = 0.0001). Our results suggest that arterial functions were impaired even at the prehypertensive stage.

Low total antioxidative capacity levels are associated with augmentation index but not pulse-wave velocity.

It is well known the relationship between oxidative stress and vascular function. However, association between total antioxidative capacity and arterial stiffness was not studied in patients with hypertension (HT). This study investigated whether total antioxidative capacity is associated with arterial stiffness and wave reflections. We studied 46 (age 48.5 +/- 10.6 years) never treated patients with HT and age-matched control group of 40 (age 47 +/- 8.6 years) normotensive individuals. Total antioxidative capacity level was determined in all subjects. We evaluated arterial stiffness and wave reflections of the study population, using applanation tonometry (SphygmoCor). Carotid-femoral pulse-wave velocity (PWV) was measured as index of aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a composite marker of wave reflections and arterial stiffness. Carotid-femoral PWV (10.5 +/- 2.2 vs 8.7 +/- 1.6, m/s, P = 0.0001) and AIx@75 (22.7 +/- 9.5 vs 15 +/- 11, %, P = 0.001) were significantly higher in patients with HT compared with age-matched control subjects. Total antioxidative capacity level (274 +/- 70 vs 321 +/- 56 micromol/l, P = 0.001) was significantly lower in hypertensive patients than controls. In the whole population, total antioxidative capacity level negatively correlated with AIx@75 (r = -0.24, P = 0.02) in univariable analysis, but not with carotid-femoral PWV (r = -0.08, P = 0.43). Also, we found that total antioxidative capacity level (beta = -0.21, P = 0.03) was an independent determinant of AIx@75 in multivariable analysis. Our results suggest that the decrease in the ability of antioxidant defenses contributes significantly to increased wave reflections.

Circulating levels of relaxin and its relation to cardiovascular function in patients with hypertension.

BACKGROUND: The role of endogenous relaxin on hypertensive cardiovascular damage remains unknown. We investigated the relaxin level and its relation to cardiovascular function in patients with never treated hypertension (HT). METHODS: We studied 42 (47.8+/-10 years) never treated patients with HT and 40 age-matched (47+/-8.6 years) normotensive individuals. Serum relaxin levels were determined in all subjects using enzyme-linked immunosorbent assay. Left ventricular (LV) diameters were evaluated by transthoracic echocardiography. Ejection fraction and LV mass index were measured. Diastolic functions were evaluated with both conventional and tissue Doppler echocardiography. We evaluated central aortic pressures, heart rate-corrected augmentation index (AIx@75), a marker of wave reflections, and aortic pulse wave velocity (PWV) as indices of elastic-type aortic stiffness of the study population using applanation tonometry (SphygmoCor). RESULTS: Relaxin levels were significantly lower in hypertensive patients as compared with controls (36.5+/-7.3 vs 49.7+/-39.8 pg/ml, p=0.03). The relaxin level was negatively correlated with brachial and central aortic pressure. However, serum relaxin was not significantly associated with LV diameters, ejection fraction, LV mass index, LV diastolic function, AIx@75 or aortic PWV in our study. CONCLUSION: Serum relaxin is decreased in patients with HT. However, low endogenous relaxin is not related to cardiovascular function.

Assessment of left ventricular systolic synchronization in patients with chronic kidney disease and narrow QRS complexes.

OBJECTIVE: The evidence of structural and functional cardiac abnormalities has been demonstrated by echocardiography in patients with chronic kidney disease (CKD). This study investigated whether left ventricular (LV) asynchrony is present in patients with CKD and normal QRS duration. METHODS: Tissue synchronization imaging (TSI) was performed in 25 (56 +/- 14 years) patients with CKD and narrow QRS complexes and 25 (51 +/- 12 years) control subjects. LV asynchrony was identified on TSI images and the time to regional peak systolic velocity (Ts) in LV was measured by the six-basal-six-midsegmental model. Four TSI parameters of systolic asynchrony were computed when Ts was measured in ejection phase. RESULTS: The standard deviation of Ts of 12 LV segments (33.6 +/- 17.8 vs 16.7 +/- 10 ms, P = 0.0001), standard deviation of Ts of the six basal LV segments (30 +/- 20 vs 17.6 +/- 9.6 ms, P = 0.008), maximal difference in Ts between any two of the 12 LV segments (102 +/- 45 vs 54 +/- 32 ms, P = 0.0001), and maximal difference in Ts between any two of the six basal LV segments (78 +/- 50 vs 46 +/- 22 ms, P = 0.007) were prolonged in patients with CKD compared with controls. The prevalence of LV systolic asynchrony was significantly higher in patients with CKD compared with controls (44% vs 12%, P = 0.01). The standard deviation of Ts of 12 LV segments were significantly associated with LV diameters, LV volumes, LV mass, blood pressure levels, and renal functions in univariate analysis. CONCLUSION: The results of this study indicate that LV systolic asynchrony may develop in patients with CKD.

Assessment of left ventricular function and Tei index by tissue Doppler imaging in patients with slow coronary flow.

BACKGROUND: The aim of this study was to assess left ventricular (LV) function and the Tei index by tissue Doppler imaging (TDI), and also to evaluate the relationship of thrombolysis in myocardial infarction (TIMI) frame count (TFC) with the Tei index and LV function in patients with slow coronary flow (SCF). METHODS: We prospectively evaluated 50 patients with SCF and 27 control subjects. Diagnosis of SCF was made by TFC. LV systolic and diastolic function was assessed by conventional echocardiography and TDI. RESULTS: Early diastolic mitral annular velocity (Em), Em/Am, and peak systolic mitral annular velocity (Sm) were lower in patients with SCF than those in controls (13+/-2.8 cm/sec vs 15.2+/-2.8 cm/sec, P = 0.002; 0.88+/-0.22 vs 1+/-0.23, P = 0.03; and 14.1+/-3.51 vs 16.5+/-3.31, P = 0.005, respectively). In patients with SCF, the Tei index was significantly higher than that in controls (0.34+/-9.6 vs 0.29+/-9.5, P = 0.02, respectively). Mean TFC and RCA TFC were positively correlated with the Tei index (r = 0.3, P = 0.02 and r = 0.329, P = 0.02). Left circumflex (LCX) TFC was negatively correlated with Em/Am (r =-0.310, P = 0.03) only in patients with SCF. CONCLUSION: LV systolic and diastolic function is impaired in patients with SCF. TDI analysis of mitral annular velocities such as the Tei index, Em, Em/Am, and Sm is useful to assess LV systolic and diastolic dysfunction in patients with SCF. Mean TFC and RCA TFC were positively correlated with the Tei index and LCX TFC was negatively correlated with Em/Am. TDI may be better than conventional echocardiography in assessing LV function in patients with SCF.

Relationship between arterial stiffness and myocardial damage in patients with newly diagnosed essential hypertension.

BACKGROUND: Arterial stiffness increases in hypertensive individuals. Arterial stiffness is associated with impairment of systolic and diastolic myocardial function in hypertension (HT). However, the relationship between arterial stiffness and serum heart-type fatty acid-binding protein (H-FABP) levels, a sensitive marker of myocardial damage, has not been previously examined in patients with HT. We investigate the relationship between serum H-FABP levels and arterial stiffness in patients with newly diagnosed HT. METHODS: We studied 46 (48.5 +/- 10.6, years) never-treated patients with HT and age-matched control group of 40 (47 +/- 8.6, years) normotensive individuals. H-FABP levels were determined in all subjects. We evaluated arterial stiffness and wave reflections of study population, using applanation tonometry (Sphygmocor). Carotid-femoral pulse wave velocity (PWV) was measured as indices of elastic-type, aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a marker of wave reflections. RESULTS: Carotid-femoral PWV (10.5 +/- 2.2 vs. 8.7 +/- 1.6, m/s, P = 0.0001) and AIx@75 (22.7 +/- 9.5 vs. 15 +/- 11, %, P = 0.001) were significantly higher in patients with HT than control group. H-FABP levels were increased in hypertensive patients compared with control group (21.1 +/- 14.8 vs. 12.9 +/- 8.5, ng/ml, P = 0.002). In multiple linear regression analysis, we found that the body mass index (beta = 0.42, P = 0.0001) and carotid-femoral PWV (beta = 0.23, P = 0.03) were significant determinants of H-FABP levels. CONCLUSION: Arterial stiffness is associated with serum H-FABP levels, a sensitive marker of myocardial damage, in patients with newly diagnosed HT.

Aortic pulse wave velocity in subjects with aortic valve sclerosis.

BACKGROUND: Aortic stiffness is an independent risk factor for cardiovascular events and mortality. The measurement of pulse-wave velocity (PWV) is the most simple, noninvasive, and robust method to determine aortic stiffness. Whether aortic stiffness contributes to aortic valve sclerosis (AVS) remains unknown. The aim of the present study was to examine the relationship between PWV and AVS in subjects free of clinically evident atherosclerotic disease. METHODS: We enrolled 62 patients (48 men; age 65 +/- 8 years) diagnosed with AVS and an additional 62 age-, hypertension-, diabetes mellitus-, and history of smoking-matched subjects without AVS. Applanation tonometry was applied to assess the augmentation index and aortic PWV. The subjects with symptomatic vascular disease were excluded from the study. AVS was defined by echocardiography as thickening and calcification of the normal trileaflet aortic valve without obstruction to the left ventricular outflow. RESULTS: There was no significant difference between the two groups regarding the aortic PWV and augmentation index (11.7+/-3.3 vs 11.8+/-3.7, P=0.85; 28.0+/-9.4 vs 25.0+/-8.6, P=0. 17, respectively). The presence of AVS was significantly correlated with ejection fraction (r=0.211, P=0.011), male gender (r=0.362, P=0.0001), and age (r=0.200, P=0.026). CONCLUSIONS: The lack of an association between the aortic PWV and AVS suggests that AVS is a complex phenomenon consisting of several distinct processes, related to both atherosclerotic and nonatherosclerotic processes.

Psychiatric comorbidity in patients with chest pain without a cardiac etiology.

OBJECTIVE: Throughout the world and among different cultural groups, physical symptoms are the most common expressions of social problems and distress; chest pain is one of the most widely seen, medically unexplained physical symptoms. Most of the time, chest pain cases in which an organic etiology cannot be determined over time and in those presenting with atypical features should be evaluated as a component or an accompanying symptom of various specific psychiatric disorders, primarily such as panic disorder and depression. The aim of this study was to determine the psychiatric comorbidity rate in patients with chest pain without a cardiac etiology. METHOD: Seventy patients admitted to the cardiology clinic with a complaint of chest pain but without any detectable cardiac etiology were included in the study. All patients were evaluated using a Sociodemographic Data Collection Form and Structured Clinical Interview for DSM-IV. RESULTS: Panic disorder was diagnosed in 47.1% of the non-cardiac chest pain group, depressive disorders in 21.4%, generalized anxiety disorder in 5.7%, anxiety disorders not otherwise specified in 5.7%, obsessive compulsive disorder in 5.7%, and undifferentiated somatoform disorder in 2.9%. Two psychiatric diagnoses were established in 12.9% of the patients and no psychiatric diagnosis in 24.3%. CONCLUSION: Psychiatric disorder rates are quite high in patients with chest pain that cannot be explained cardiologically. These results show the importance of psychiatric evaluations in patients with non-cardiac chest pain or unexplained chest pain (UCP). In addition, understanding the psychiatric symptom profile of these patients will make an important contribution to the treatment of non-cardiac chest pain.

Carotid intima-media thickness in patients with isolated coronary artery ectasia.

OBJECTIVE: Carotid artery intima-media thickness (IMT) is now widely used as a surrogate marker for atherosclerotic disease. Carotid IMT measured by ultrasound has been shown to be correlated with coronary artery disease as defined by angiography. However, the relation between carotid IMT and isolated coronary artery ectasia (CAE) has not been investigated. The aim of our study was to assess this relation. METHODS: Twenty-five patients with isolated CAE without stenosis and 25 control subjects with angiographically normal coronary arteries were included in this study. These were examined by B-mode ultrasound to measure the IMT at the far wall of the common carotid artery. RESULTS: Patients with isolated CAE had significantly higher carotid IMT compared to control subjects with angiographically normal coronary arteries (0.95+/-0.12 versus 0.71+/-0.10mm respectively, p<0.0001). In addition, we detected a significant positive correlation between the presence of CAE and carotid IMT (r=0.748, p<0.001). CONCLUSION: We have shown for the first time an association between increased carotid IMT and isolated CAE, suggesting that atherosclerosis may be involved in the pathogenesis of isolated CAE in the adult population.