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• W1981403669 abstract "Background. Recent investigations have focused on the pathogenetic role of disturbances of calcium phosphate metabolism in causing cardiovascular morbidity and mortality in haemodialysis patients. The aim of the present study was to assess left ventricular function and its relationship to phosphate and calcium plasma levels in stable uraemic patients on haemodialysis treatment. Methods. Twenty uraemic patients (mean age 51 ± 13 years) on maintenance haemodialysis and free from overt cardiac dysfunction, and 20 healthy volunteers underwent standard echocardiography, tissue Doppler-derived early (Em) and late (Am) diastolic velocities, tissue characterization with cyclic variations of integrated backscatter (CV-IBS), and serum biochemistry. Results. With respect to tissue Doppler imaging (TDI), uraemic patients showed a lower Em peak, a higher Am peak, and a reduced Em/Am ratio of both interventricular septum and lateral wall (0.01 > P < 0.001) than controls. CV-IBS of both septum and posterior wall was significantly smaller in uraemic patients than in the control subjects (P < 0.001). Moreover, the Em/Am ratio of septum and lateral wall were negatively related to serum phosphorus and to calcium phosphate product (P < 0.001 for all). Accordingly, an inverse relationship was also found between CV-IBS of septum and lateral wall and calcium phosphate product and phosphorus (P < 0.05 for all). Conclusions. These results showed early cardiac impairment of diastolic myocardial function evaluated by TDI and IBS analysis, and a close relationship between these changes and the calcium-phosphate plasma levels. These findings are well in keeping with the important role of hyperphosphataemia as a risk factor for cardiovascular damage, and justify the effort for optimal control of calcium phosphate metabolism in uraemic patients. Chronic uraemic patients on haemodialysis treatment have a high prevalence of heart failure, coronary disease and cardiovascular mortality [1, 2]. Anaemia, hypertension, myocardial hypertrophy, heart failure, uraemic toxins and endothelial dysfunction are some of the factors related to cardiovascular risk in uraemia [3]. Recent investigations have implicated mineral metabolism, in particular secondary hyperparathyroidism, hyperphosphataemia, elevated calcium phosphate product, as risk factors for cardiovascular calcifications, cardiovascular events and mortality in dialysis patients [4-6]. Structural and functional myocardial abnormalities, including fibrosis and calcification, have been detected in haemodialysis patients and associated with hyperphosphataemia and excessive calcium load [7]. To explore this hypothesis, we employed new echocardiographic techniques, such as integrated backscatter (IBS) analysis and tissue Doppler imaging (TDI), which have enhanced the chance to assess textural and functional properties of the myocardium, in a noninvasive manner. TDI provides valuable insight into the evaluation of left ventricular (LV) function [8-11] and seems to be unrelated to preload compensation [10, 11]. However, Ie et al. [12] have recently reported that the volume overload usually present before the start of the haemodialysis session can result in an underestimation of the degree of diastolic dysfunction, as assessed using TDI. Recently, Hayashi et al. [13] showed inverse correlations between plasma levels of phosphate and calcium phosphate product and TDI-derived systolic velocity, thus suggesting a role for high plasma levels of phosphate and increased calcium phosphate product in the impairment of systolic function. The IBS analysis delineates some physiological and pathological morpho-functional changes of the myocardium. For example, there is evidence that normal myocardium shows cardiac cycle-dependent variation of IBS in both animals and humans [14, 15]. Actually, the measurement of cyclic variation in IBS is a method for the identification of abnormalities in myocardial composition [15, 16]. It is a validated procedure that is used for noninvasive assessment of myocardial fibrosis and calcification in chronic haemodialysis patients [17, 18]. The aim of the present study was to assess LV function and myocardial ultrasound features in dialysis patients, and the relationship to calcium phosphate plasma levels. Twenty patients (17 males and three females, mean age 51 ± 13 years) affected by end-stage renal failure on maintenance haemodialysis (for 56.4 ±19.2 months) were recruited from the dialysis unit of our department. We assumed the following exclusion criteria: subjects with a history of coronary disease or myocardial infarction, absence of sinus rhythm, severe mitral valve disease, pericardial effusion, acute or intercurrent acute illness, diabetes and neoplasia were excluded from the study. Some clinical characteristics of the two studied groups are reported in Table 1. Fifteen of the 20 patients studied were on intestinal phosphate binder therapy, namely calcium carbonate [1-3] in 14 patients, and sevelamer (2400–4800 mg) in six patients. Vitamin D preparations were used in four patients. Three patients showed severe hyperparathyroidism (PTH > 700 pg mL−1), seven patients showed serum PTH levels >300 pg ml−1, and other six patients showed serum PTH levels <150 pg ml−1. The patients were given haemodialysis treatment for 210–240 min, three times a week, using high biocompatibility membranes. The Kt/V was 1.51 ± 0.16 and the normalized protein catabolic rate was 1.2 ± 0.3 g kg−1 day−1. The interdialytic weight gain was 2.7 ± 0.8 kg. Clinical signs of overhydration as lower limb oedema, dyspnoea, uncontrolled hypertension or signs of fluid overload at the chest X-ray examination were absent. Twelve patients were receiving anti-hypertensive medications: calcium antagonists were used in 11 patients, angiotensin-converting enzyme inhibitors in three patients, angiotensin II receptor antagonist in three cases, clonidine in five cases, β-adrenergic blockers in two cases and a vasodilator, minoxidil, in one patient. Twenty healthy volunteers (17 males and three females, mean age 53 ± 11 years) were recruited to form the control group. All patients and controls underwent transthoracic echocardiography, TDI and IBS, and blood biochemistry. Serum levels of creatinine, potassium, sodium, calcium, phosphate, magnesium, albumin, prealbumin and parathyroid hormone were determined using the standard methods of our laboratory. In particular, intact PTH serum levels were determined by a solid-phase, two site chemiluminescent enzyme-labelled immunometric assay (Immunolite 2000 Intact PTH; Diagnostic Products Corporation, Los Angeles, CA, USA). The patients underwent the study procedures within ∼30 min prior to the mid-week haemodialysis session; blood samples were drawn by the afferent line before the start of the dialysis procedure. The investigation conforms to the Declaration of Helsinki. The study protocol has been approved by the Ethic's Committee of the Pisa University Hospital. All the subjects studied gave their own informed consent to the study. The echocardiographic studies were performed by a single experienced operator using a Sonos 5500 ultrasound system (Philips Medical Systems, Andover, MA, USA), equipped with pulsed, continuous and colour-flow Doppler capabilities. The echocardiograms were evaluated according to the recommendations suggested by the American Society of Echocardiography [19]. LV mass (LVM) was calculated according to the ‘Penn convention’ [20], and indexed for body surface area (LVMi). A pulsed Doppler transmitral flow velocity profile was obtained from the apical four-chamber view, and the sample volume was positioned just below the mitral valve leaflets. The following parameters were evaluated: peak transmitral flow velocity in early diastole (peak E), peak transmitral flow velocity in late diastole (peak A) and E/A ratio. The isovolumetric relaxation time (IVRT) was quantified via a simultaneous pulsed Doppler recording of LV output flow and mitral valve inflow. Pulsed wave TDI was performed using a special software package available on the Sonos 5500. This method is capable of providing measurements of ventricular wall motion velocity by positioning the sample volume within the myocardium. TDI of diastolic velocities of the basal lateral segment and of the basal interventricular septum in the apical four-chamber view were measured at the end of echocardiographic studies. The Doppler programme was set to the pulsed mode with a sample volume of 4 mm. We performed a pulsed-wave TDI, adjusting the spectral pulsed Doppler signal filters to obtain a Nyquist limit of 15 and 20 cm s−1, and lowest filter and optimal gain settings were used to minimize noise. The sample volumes were placed in the centre of myocardial segments. From the obtained patterns, the systolic velocity (Sm), the early diastolic myocardial velocity (Em), the late diastolic myocardial velocity (Am) at the time of atrial contraction, and the ratio of Em/Am of both the LV walls were determined. In addition, the IVRT of each segment was measured as the interval from the aortic component of the second heart sound to the peak of the early diastolic wave. All parameters were measured during three consecutive cardiac cycles and their mean value calculated. In our series, this technique has an excellent reproducibility with a coefficient of variation <4%. Ultrasonic characterization of LV myocardium was assessed by IBS analysis using a special software package, available as an option of the HP Sonos 5500, as previously described [21]. Briefly, this system is capable of providing IBS images in which the grey level is displayed proportional to the integrated backscattered power. The backscatter can be measured in dB from an operator-defined region of interest (ROI). A maximum of 60 frames displayed at a real-time frame rate of 30 Hz (30 frames s−1) are captured into cine-loop memory and subsequently stored on optical disk in a digital format with the same resolution as the scan converter memory (512 × 512, 8 bits). This system has the possibility to display the transmit power, log compression and time-gain compensation values on a screen; this permits to adjust the system to the same values at every examination. The two-dimensional backscatter images were acquired into cine-loop memory and stored on an optical disk. The image preprocessing, transmit power, focus, and time-gain compensation settings were adjusted to yield optimal images, and the system controls were unchanged for measurements of all subjects. For an analysis of the image data, the IBS images were retrieved from disk into the system memory. The IBS was measured by placing an elliptic ROI at the centre of the mid-anterior septum and of the mid-posterior wall, and time–intensity curves of backscatter were derived. The largest possible ROI (21 × 21 to 41 × 41 pixels) was used, avoiding bright, specular echoes from the endocardium and epicardium. Location of the site was manually adjusted frame by frame to keep the ROI within myocardial midwall throughout a cardiac cycle. The average power of the IBS signal contained within the ROI was measured and displayed in dB for a total of 60 time frames. Calibrated IBS for both septum and posterior wall was calculated by subtracting average pericardial IBS intensity from average myocardial IBS intensity, obtained at the septum and posterior wall levels. The magnitude of the cyclic variations of IBS (CV-IBS) was calculated as the average in three consecutive cardiac cycles of the difference between the end-diastolic IBS value, coinciding with the peak of the R wave at ECG, and the value at end-systole, typically corresponding to the end of the T wave. The intra-observer and inter-observer variability of CV-IBS were both <5%. The results were expressed as mean ± standard deviation (SD). Differences were assessed by one-way analysis of variance (anova) and analysis of covariance (ancova). Univariate correlational analyses were performed to determine relationships between variables of interest. Differences were considered significant when P < 0.05. Standard echocardiography, TDI and IBS data are given in Tables 2 and 3. LV end-diastolic diameter, septal and posterior wall thicknesses, and LVMi were significantly higher in uraemic patients than in control subjects. The indices of LV diastolic function were significantly deteriorated in uraemic patients with respect to controls (peak E, 58.8 ± 6.5 vs. 86.6 ± 6.3 cm s−1, P < 0.001; E/A ratio, 0.87 ± 0.12 vs. 1.53 ± 0.16, P < 0.001), whilst indices of LV systolic function (ejection fraction and fractional shortening) were within normal range and quite similar to the normal controls (Table 2). Regarding TDI measures, the uraemic patients exhibited a lower Sm peak, a lower Em peak, a higher Am peak, and a reduced Em/Am ratio of both interventricular septum and lateral wall than controls (Table 2). Calibrated IBS values of both septum and posterior wall were significantly higher in uraemic patients than in controls (septal: −26.8 ± 9.2 dB vs. −33 ± 6 dB, P < 0.001; posterior wall −28.4 ± 8.2 dB vs. −45.6 dB, P < 0.001). Moreover, in uraemic patients CV-IBS was significantly lower than that of controls, at both septum (4.9 ± 1.6 dB vs. 9.2 ± 1.2 dB, P < 0.001) and posterior wall level (7.3 ± 1.9 dB vs. 11.4 ± 2.3 dB, P < 0.001). In uraemic patients, the Em/Am ratio of both septum and lateral wall was inversely related to serum phosphorus (r = −0.65, P = 0.005 and r = −0.82, P < 0.0001 respectively) and calcium phosphate product (r = −0.55, P = 0.02 and r = −0.78, P < 0.0002 respectively) (Fig. 1). Accordingly, an inverse relationship was found also between CV-IBS of both septum (r = −0.61, P = 0.008 and r = −0.49, P < 0.05) and posterior wall (r = −0.57, P = 0.02 and r = −0.51, P = 0.04) and calcium phosphate product and phosphorus (Fig. 2). No correlation was found between TDI-derived diastolic velocities and the calcium-containing phosphate-binder dose. Interestingly, Em/Am ratio of both septum and lateral wall was positively related to dialysis duration (r = 0.59, P = 0.0004 and r = 0.68, P < 0.001). We performed multiple linear regression analysis to partial out the effect of age and BMI on those relations. After controlling for age (r = 0.64, P = 0.02 and r = 0.65, P = 0.02) and BMI (r = 0.59, P = 0.04 and r = 0.65, P = 0.01), the effect of dialysis duration on Em/Am ratio remained statistically significant. No correlation was found between TDI parameters or IBS values and age, BMI, PTH, Kt/V, haematocrit and dietary protein intake. Correlation analysis between septal (upper panels) and lateral Em/Am ratio (lower panels) and phosphorus (left) and calcium phosphorus (right) plasma levels in uraemic patients. Correlation analysis between septal (upper panels) and posterior cyclic variations of integrated backscatter (CV-IBS) (lower panels) and phosphorus (left) and calcium phosphorus (right) plasma levels in uraemic patients. The results of the present study suggest that in chronic uraemic patients on haemodialysis treatment, structural and functional myocardial changes are associated with calcium–phosphorus disturbances. The data of this study confirm that both the conventional mitral inflow Doppler and the TDI examination show an impairment of the LV diastolic function in the absence of overt clinical signs of heart failure. In particular, TDI findings, characterized by a progressive decline in peak Em velocity and Em/Am ratio, are correlated with elevated phosphorous plasma levels and calcium phosphate product. The correlation we found between TDI-derived diastolic velocities and the plasma levels of phosphate and calcium phosphate product suggest a relationship between high plasma levels of phosphate and increased calcium phosphate product and impaired diastolic function. Our results differ to those obtained by Hayashi et al. [13], who recently reported an inverse correlation between TDI-derived systolic velocity and plasma levels of phosphate and calcium phosphate product. Actually, it is quite difficult to discern the discrepancy with our data showing an impairment of diastolic function instead of systolic function. However, TDI-diastolic velocities are considered more sensitive markers of myocardial dysfunction because diastolic dysfunction usually precedes systolic dysfunction. Therefore, a possible explanation could be an overall lower cardiac impairment in our series. These LV diastolic function abnormalities in uraemic patients may be related to changes in myocardial wall structural properties, like atrophy of the myocardial fibres and increased myocardial fibrosis [22]. Although we have no myocardial histopathology data, an increased myocardial collagen content and interstitial calcium salts deposition [23, 24] in our patients might explain the alterations in the myocardium contractile properties. Myocardial fibre degeneration, interstitial calcium deposits and dense interstitial fibrosis are predominantly confirmed by most autopsies with lesions containing large irregular calcium deposits [25]. Our patients showed a high calibrated IBS value, that is an increased myocardial ultrasound reflectivity, in keeping with the presence of increased connective tissue and myocardial fibrosis [26], which can cause an impaired diastolic compliance. This feature was found using CV-IBS at the interventricular septum and the posterior wall, in the absence of abnormalities at the standard echocardiography examination. Different degrees of fibre disarray, fibrosis and regional asymmetry in the contractile process have also been proposed to explain the reduction in CV-IBS [27]. Recent investigations have focused on calcium phosphate abnormalities as an emerging risk factor for vascular calcification, cardiovascular disease and mortality in dialysis patients. Our results indicate that the higher is phosphataemia and calcium phosphate product, the more severe is heart damage in terms of diastolic dysfunction and myocardial ultrasound hyper-reflectivity, which is a possible expression of myocardial fibrosis [22-24]. All these data are in line with previous studies showing a relationship between serum calcium and phosphate level with coronary, myocardial and valvular calcifications in uraemics [28, 29]. Moreover some authors showed that elevated serum phosphataemia and elevated calcium phosphate product may contribute to increased mortality in uraemic patients [4, 5]. It is speculated that elevated phosphataemia may aggravate the effects of coronary atherosclerosis through increased vascular calcification and smooth muscle proliferation [30]. It has also been suggested that calcification, a consequence of elevated phosphataemia, may alter microcirculatory haemodynamics through increased extravascular resistance and further compromise myocardial perfusion [31]. In conclusion, this study confirms that uraemic patients on haemodialysis have an impairment of the LV function. In particular, the sub-clinical abnormalities of diastolic function are related to hyperphosphataemia and increased calcium phosphate product. This is in accordance with the important role of changes of calcium phosphate homeostasis on cardiovascular damage. This is one more reason for making any effort to achieve an optimal control of phosphate balance, phosphataemia and of calcium phosphate product, with the aim of reducing the risk of cardiovascular events and heart failure in uraemic patients. No conflict of interest was declared." @default.
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• W1981403669 title "Left ventricular function and calcium phosphate plasma levels in uraemic patients" @default.
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