Atrioventricular plane displacement correlates closely to circulatory dimensions but not to ejection fraction in normal young subjects

Aims Mitral atrioventricular plane displacement (AVPD) provides information about left ventricular systolic function. M‐mode of systolic annulus amplitude or tissue Doppler imaging of systolic annulus velocity are the current methods of evaluating AVPD. A correlation to ejection fraction (EF) has been demonstrated in patients with coronary artery disease and left ventricular dysfunction. Our aim was (i) to investigate the mitral AVPD of normal subjects with different physical work capacities and (ii) to further evaluate AVPD as an index of left ventricular systolic function. Methods and results Twenty‐eight healthy men mean age 28 years (20–39) were included: endurance trained (ET) (n=10), strength trained (ST) (n=9) and untrained (UT) (n=9). The systolic AVPD was recorded at four sites, septal, lateral, anterior and posterior, using M‐mode. Left ventricular volumes were calculated according to Simpson’s rule. Systolic AVPD was higher in endurance trained, 16·9 ± 1·5 mm, as compared with both strength trained, 13 ± 1·6 (P<0·001) and untrained, 14 ± 1·6 (P<0·001). Left ventricular systolic AVPD correlated strongly with end‐diastolic volume (r=0·82), stroke volume (r=0·80) and maximal oxygen consumption per body weight (r=0·72). The correlation between AVPD and EF was poor (r=0·22). Conclusion In the subjects studied, with a range of normal cardiac dimensions, AVPD correlated to stroke volume, end‐diastolic volume and maximal oxygen consumption per body weight, but not to EF. On theoretical grounds, it also seems reasonable that a dimension like AVPD is related to other cardiac dimensions and volumes, rather than to a fraction, like EF. AVPD is one parameter that is useful for evaluation of left ventricular systolic function but is not interchangeable with other measurements such as EF.     

Right and left heart dysfunction predict mortality in pulmonary hypertension

In pulmonary hypertension (PH), the right heart dysfunction is a strong predictor of adverse clinical outcome, while the role of the left heart is not fully determined. The aim of this study was to identify predictors of mortality in precapillary PH including measures of both right and left heart function. We studied 34 patients (mean age 64 ± 13, range 31–82 years, 24 females) with precapillary PH, all of whom underwent detailed Doppler echocardiographic examination of the right and left heart function using conventional and speckle-tracking echocardiography. Patients were followed up for up to 8 years (mean 4·2 ± 1·9 years). At follow-up, 16 patients survived. Left ventricular (LV) filling time (P = 0·007), pulmonary artery acceleration time (P = 0·009), right atrial pressure (RAP) (P<0·001) and tricuspid regurgitation (TR) severity (P = 0·007) were worse in the deceased group. RV global longitudinal strain (GLS) (P = 0·001), RAP (P≤0·001), LV filling time (P<0·001) and TR severity (P<0·001) were the most accurate predictors, having the largest AUC (>0·65) and carried the highest risk for mortality (P<0·001 for all). The strongest predictors of mortality in precapillary PH indirectly reflect both left and right heart dysfunction including atrial structure and function disturbances. While an interaction pattern is observed, it needs to be confirmed in a larger cohort.     

Evaluation and simplified measurement of infarct size by myocardial contrast echocardiography in a rat model of myocardial infarction

To test the feasibility and accuracy of myocardial contrast echocardiography (MCE) for predicting infarct size (IS) in a rat model of myocardial infarction (MI) and to compare a simplified single plane-based measurement of IS with the conventional three plane-based approach. Fifty male SD rats underwent left anterior descending artery ligation and were evaluated by MCE 8 h post MI. IS was calculated by the single and three plane-based approaches, compared to that determined by triphenyltetrazolium chloride (TTC) staining method. Simplified single plane-based MCE approach and TTC method showed similar IS values (38.48 ± 16.80% vs. 35.72 ± 15.33%, P > 0.05) and presented a favorable positive correlation (r = 0.851, P < 0.001). IS values derived from simplified single plane-based approach was also highly significantly correlated with that by the conventional MCE method (r = 0.973, P < 0.001). Bland–Altman plots also displayed satisfactory agreement between them. MCE was validated as a novel technique to quantify infarct area in rats with MI. A single measurement at the mid-papillary muscle level may become a simple, efficient and reliable approach for in vivo IS assessment. Xianghui Chen and Kai Cui are co-first authors.     

Post‐ischaemic angiogenic therapy using in vivo prevascularized ascorbic acid‐enriched myocardial artificial grafts improves heart function in a rat model

Angiogenesis plays a key role in post‐ischaemic myocardial repair. We hypothesized that epicardial implantation of an ascorbic acid (AA)‐enriched myocardial artificial graft (MAG), which has been prevascularized in the recipients' own body, promotes restoration of the ischaemic heart. Gelatin patches were seeded with GFP–luciferase‐expressing rat cardiomyoblasts and enriched with 5 μm AA. Grafts were prevascularized in vivo for 3 days, using a renal pouch model in rats. The MAG patch was then implanted into the same rat's ischaemic heart following myocardial infarction (MI). MAG‐treated animals (MAG group, n = 6) were compared to untreated infarcted animals as injury controls (MI group, n = 6) and sham‐operated rats as healthy controls (healthy group, n = 7). In vivo bioluminescence imaging indicated a decrease in donor cell survival by 83% during the first week post‐implantation. Echocardiographic and haemodynamic assessment 4 weeks after MI revealed that MAG treatment attenuated left ventricular (LV) remodelling (LV end‐systolic volume, 0.31 ± 0.13 vs 0.81 ± 0.01 ml, p < 0.05; LV end‐diastolic volume 0.79 ± 0.33 vs 1.83 ± 0.26 ml, p < 0.076) and preserved LV wall thickness (0.21 ± 0.03 vs 0.09 ± 0.005 cm, p < 0.05) compared to the MI group. Cardiac output was higher in MAG than MI (51.59 ± 6.5 vs 25.06 ± 4.24 ml/min, p < 0.01) and comparable to healthy rats (47.08 ± 1.9 ml/min). Histology showed decreased fibrosis, and a seven‐fold increase in blood vessel density in the scar area of MAG compared to MI group (15.3 ± 1.1 vs 2.1 ± 0.3 blood vessels/hpf, p < 0.0001). Implantation of AA‐enriched prevascularized grafts enhanced vascularity in ischaemic rat hearts, attenuated LV remodelling and preserved LV function. Copyright © 2011 John Wiley & Sons, Ltd.     

Myocardial perfusion defects in Bartter and Gitelman syndromes

Background Normotensive hypokalaemic tubulopathies (Bartter and Gitelman syndromes (BS/GS)) are genetic diseases that are considered benign. However, QT prolongation, left ventricular dysfunction and reduction of cardiac index upon exercise leading to arrhythmias and sudden cardiac death have been reported in these patients. Hence, we aimed to verifying whether an isometric exercise could represent a useful tool for the identification of patients at risk for future cardiac events. Patients and methods Myocardial function (MF) and perfusion, evaluated as myocardial blood flow (MBF) of 10 BS/GS patients and 10 healthy controls, were investigated at rest and during isometric exercise. MF and MBF were evaluated using quantitative two‐dimensional and myocardial contrast echocardiography. Results BS/GS patients had normal baseline MF and MBF. During exercise in BS/GS patients, corrected QT (QTc) was prolonged to peak value of 494 ± 9·1 ms (P < 0·001). In controls, MF increased from resting to peak exercise (left ventricular ejection fraction: 65 ± 4% to 78 ± 5%, P < 0·003) while in seven BS/GS patients (Group 1) it declined (64 ± 5% to 43 ± 9%, P < 0·001). Myocardial perfusion increased upon exercise in controls as shown by changes of its markers: β (a measure of myocardial flow velocity; 0·89 ± 0·12 vs. 0·99 ± 0·12, P < 0·001) and myocardial blood volume (14·4 ± 2 vs. 20·2 ± 0·25, P < 0·001), while in Group 1 BS/GS it decreased (0·87 ± 0·15 vs. 0·67 ± 0·15, P < 0·001; and 14·5 ± 1·9 vs. 8·3 ± 0·22, P < 0·001, respectively). Conclusions Our results document for the first time that exercise induce coronary microvascular and myocardial defects in BS/GS patients. Therefore, this may challenge the idea that BS/GS are benign diseases. In addition, the diagnostic approach to these syndromes should include an in‐depth cardiac assessment in order to identify patients at higher risk.     

Infarct transmurality and adjacent segmental function as determinants of wall thickening in revascularized chronic ischemic heart disease

Background: There are many factors which influence regional left ventricular wall thickening (WT) in ischemic heart disease (IHD). We used magnetic resonance imaging (MRI) to explore, in patients with chronic ischemic heart disease (CIHD), how regional WT is affected by both infarct transmurality (IT) and the function of adjacent segments. We also compared these findings with a group of healthy volunteers (controls). Methods: Twenty patients (20 men, mean age 63, range 45–80 years) were imaged with cine MRI for function and delayed enhancement MRI for infarction 6 months after revascularization. Twenty age and sex matched controls underwent cine MRI. Short‐axis images were analysed using a 12‐segment per slice model in four midventricular slices per subject. Results: WT and IT were inversely related (r² = 0·11, P<0·001). WT of non‐infarcted segments in patients was lower than corresponding segments in controls (5·1 versus 4·6 mm, P<0·001). WT in patients decreased with an increasing number of dysfunctional adjacent segments (P<0·001) and increasing IT (P<0·001). WT was more strongly influenced by the number of dysfunctional adjacent segments (t = ?22·93, P<0·001) than by IT (t = ?4·50, P<0·001). Conclusions: The number of dysfunctional adjacent segments is a greater determinant than infarct transmurality on regional wall thickening.     

Forearm skin tissue dielectric constant measured at 300 MHz: effect of changes in skin vascular volume and blood flow

Skin tissue dielectric constant (TDC) values measured via the open‐ended coaxial probe method are useful non‐invasive indices of local skin tissue water. However, the effect of skin blood flow (SBF) or skin blood volume (SBV) on TDC values is unknown. To determine the magnitude of such effects, we decreased forearm SBV via vertical arm raising for 5 min (test 1) and increased SBV by bicep cuff compression to 50 mmHg for 5 min (test 2) in 20 healthy supine subjects (10 men). TDC values were measured to a depth of 1·5 mm on anterior forearm, and SBF was measured with laser‐Doppler system simultaneously on forearm and finger. Results indicate that decreasing vascular volume (test 1) was associated with a small but statistically significant reduction in TDC (3·0 ± 4·3%, P = 0·003) and increasing vascular volume (test 2) was associated with a slight but statistically significant increase in TDC (3·5 ± 3·0%, P<0·001). SBF changes depended on test and measurement site. For forearm, test 1 significantly increased SBF (102·6 ± 156·2%, P<0·001) and test 2 significantly decreased it (39·5 ± 13·1%, P<0·001). In finger, SBF was significantly reduced by both tests: in test 1 by 55·3 ± 32·1%, P<0·001 and in test 2 by 53·3 ± 27·6%, P<0·001. We conclude that the small percentage changes in TDC values (3·0–3·5%) over the wide range of induced SBV and SBF changes suggest a minor effect on clinically determined TDC values because of SBV or SBF changes or differences when comparing TDC longitudinally over time or among individuals of different groups in a research setting.     

Cardiac performance during exercise in patients with Fabry's disease

Background Fatigability and dyspnoea on effort are present in many patients with Fabry's disease. We assessed the determinants of cardiac performance during exercise in patients with Fabry's disease and preserved left ventricular ejection fraction at rest. Materials and methods Sixteen patients with Fabry's disease and 16 control subjects underwent radionuclide angiography at rest and during exercise, tissue Doppler echocardiography and magnetic resonance imaging at rest. Results The exercise‐induced change in stroke volume was +25 ± 14% in controls and +5·8 ± 19% in patients with Fabry's disease (P < 0·001). In 10 patients (group 1), the stroke volume increased (+19 ± 10%), and in 6 patients (group 2) it decreased (–16 ± 9%) with exercise. Patients of group 2 were older, had worse renal function, higher left ventricular mass and impaired diastolic function compared to group 1. The abnormal stroke volume response to exercise in group 2 was associated with a decrease in end‐diastolic volume (P < 0·001) and a lack of reduction of end‐systolic volume (P < 0·01) compared with both controls and group 1. The ratio of peak early‐diastolic velocity from mitral filling to peak early‐diastolic mitral annulus velocity was the only independent predictor of exercise‐induced change in stroke volume (B –0·44; SE 0·119; β–0·70; P < 0·005). Conclusions The majority of patients with Fabry's disease were able to augment stroke volume during exercise by increasing end‐diastolic volume, whereas patients with more advanced cardiac involvement may experience the inability to increase cardiac output by the Frank Starling mechanism.     

Myocardial velocities measured during adenosine, dobutamine and supine bicycle exercise: a tissue Doppler study in healthy volunteers

Background: Dobutamine stress echocardiography (DSE) quantified by tissue Doppler (TVI) have improved the diagnostic capacity of the procedure. Quantification of other stress modalities, e.g. adenosine stress echo (ASE) and exercise stress echocardiography (ESE) are necessary for assessing any pathophysiological differences in different forms of stress. Methods: Ten healthy individuals underwent ASE, DSE, and ESE during a span of 2–5 days. Left ventricular (LV) apical images at rest and peak stress (max) were postprocessed using TVI on a GE System FiVe equipment. ECG‐derived QRS duration (QRSD, ms), heart rate (HR, bpm), TVI‐estimated basal systolic velocities (S2V, cm s^?1), ejection time (S2T, ms) and strain (S, %) were computed off‐line and compared. Longitudinal displacement imaging, tissue tracking, was also made. Results: Data for ASE, DSE and ESE during peak stress were (HR: 84 ± 12***, 142 ± 19, 137 ± 27; P<0·001) (QRSD: 92 ± 18**, 74 ± 13, 79 ± 9; P<0·05), (S2T: 307 ± 34***, 175 ± 53, 192 ± 25; P<0·001) and (S%: 26·0 ± 3·0, 21·2 ± 7·3, 22·1 ± 5·1; P = n.s.) respectively. Velocity response, registered in the LV septum at max, was lowest during ASE (7·4 ± 1·4) highest during DSE (13·0 ± 2·7; P<0·001 versus ASE) and somewhat intermediate during ESE (11·3 ± 3·5; P<0·001 versus ASE). In contrast, strain and displacement did not differ. Conclusion: ASE evokes significantly less LV systolic response compared with both DSE and ESE. Increased velocity (P<0·05 versus rest) and strain (P>0·05) response at a much lower HR indicates that adenosine has minor effects on contraction presumably secondary to vasodilatation. Powerful chronotropic response to DSE and ESE is probably prerequisite for strong velocity response at the expense of strain and displacement. TVI‐assisted stress echocardiography thereby shows different LV systolic response in healthy individuals, depending on stress modality.     

Postoperative volume balance: does stroke volume increase in Trendelenburg's position?

In healthy humans, stroke volume (SV) and cardiac output (CO) do not increase with expansion of the central blood volume by head-down tilt or administration of fluid. Here, we exposed 85 patients to Trendelenburg's position about one hour after surgery while cardiovascular variables were determined non-invasively by Modelflow. In Trendelenburg's position, SV (83 ± 19 versus 89 ± 20 ml) and CO (6·2 ± 1·8 versus 6·8 ± 1·8 l/min; both P<0·05) increased, while heart rate (75 ± 15 versus 76 ± 14 b min⁻¹) and mean arterial pressure were unaffected (84 ± 15 versus 84 ± 16 mmHg). For the 33 patients (39%) with a > 10% increase in SV (from 78 ± 16 to 90 ± 17 ml) corresponding to an increase in CO from 5·9 ± 1·5 to 6·9 ± 1·6 l min⁻¹ (P<0·05) when tilted head-down, administration of 250 ml Ringer's lactate solution increased SV (to 88 ± 18 ml) and CO (to 6·8 ± 1·7 l min⁻¹). In conclusion, determination of SV and/or CO in Trendelenburg's position can be used to evaluate whether a patient is in need of IV fluid as here exemplified after surgery.     

Radial pressure waveform dP/dt max is a poor indicator of left ventricular systolic function

Background The first derivative of left ventricular (LV) pressure over time (dP/dt max) is a marker of LV systolic function that can be assessed during cardiac catheterization and echocardiography. Radial artery dP/dt max has been proposed as a possible marker of LV systolic function and we sought to test this hypothesis. Materials and methods We compared simultaneously recorded radial dP/dt max (by high‐fidelity tonometry) with LV dP/dt max (by high‐fidelity catheter and echocardiography parameters analogous to LV dP/dt max). In study 1, beat‐to‐beat radial dP/dt max and LV dP/dt max were recorded at rest and during supine exercise in 12 males (aged 61 ± 12 years) undergoing cardiac catheterization. In study 2, 2D‐echocardiography and radial dP/dt max were recorded in 54 patients (separate to study 1; 39 men; aged 64 ± 10 years) at baseline and peak dobutamine‐induced stress. Three basal septum measures were taken as being analogous to LV dP/dt max: 1. Peak systolic strain rate; 2. Strain rate (SR‐dP/dt max) during isovolumic contraction (IVCT) and; 3. Tissue velocity during IVCT. Results In study 1 there was a significant difference between resting LV dP/dt max (1461 ± 383 mmHg s⁻¹) and radial dP/dt max (1182 ± 319 mmHg s⁻¹; P < 0·001), and a poor, but statistically significant, correlation between the variables (R² = 0·006; P < 0·05). Similar results were observed during exercise. In study 2 there were weak (R² = −0·12; P = 0·01) to non‐significant associations between radial dP/dt max and all echocardiographic measures analogous to LV dP/dt max at rest or peak stress. Conclusion Radial pressure waveform dP/dt max is not a reliable marker of LV systolic function.     

Adaptative or maladaptative hypertrophy,different spatial distribution of myocardial contraction

Background: Left ventricular hypertrophy (LVH) may be an adaptative remodelling process induced by physical training, or result from pathological stimuli. We hypothesized that different LVH aetiology could lead to dissimilar spatial distribution left ventricular (LV) contraction, and compared different components of LV contraction using 2‐dimensional (2‐D) speckle tracking derived strain in subjects with adaptative hypertrophy (endurance athletes), maladaptative hypertrophy (hypertensive patients) and healthy controls. Method: We enrolled 22 patients with essential hypertension, 50 endurance athletes and 24 healthy controls. All subjects underwent traditional echocardiography and 2‐D strain evaluation of LV longitudinal, circumferential and radial function. LV basal and apical rotation and their net difference, defined as LV torsion, were evaluated. Results: LV wall thicknesses, LV mass and left atrium diameter were comparable between hypertensive group and athletes. LV longitudinal strain was reduced only in hypertensive patients (P < 0·05). LV apex circumferential strain was higher in hypertensive patients than in other groups (P < 0·001), LV basal circumferential strain, although slightly increased, did not reach significant difference. Hypertensive patients showed significantly increased rotation and torsion (P < 0·001), while no differences were observed between athletes and control. Conclusion: In patients with pathological LVH, LV longitudinal strain was reduced, while circumferential deformation and torsion were increased. No differences were observed in LV contractile function between subjects with adaptative LVH and controls. In pathological LVH, increasing torsion could be considered a compensatory mechanism to counterbalance contraction and relaxation abnormalities to maintain a normal LV output.     

Cardiac power output and its response to exercise in athletes and non‐athletes

Cardiac power output (CPO) is an integrative measure of overall cardiac function as it accounts for both, flow‐ and pressure‐generating capacities of the heart. The purpose of the present study was twofold: (i) to assess cardiac power output and its response to exercise in athletes and non‐athletes and (ii) to determine the relationship between cardiac power output and reserve and selected measures of cardiac function and structure. Twenty male athletes and 32 age‐ and gender‐matched healthy sedentary controls participated in this study. CPO was calculated as the product of cardiac output and mean arterial pressure, expressed in watts. Measures of hemodynamic status, cardiac structure and pumping capability were assessed by echocardiography. CPO was assessed at rest and after peak bicycle exercise. At rest, the two groups had similar values of cardiac power output (1·08 ± 0·2 W versus 1·1 ± 0·24 W, P>0·05), but the athletes demonstrated lower systolic blood pressure (109·5 ± 6·2 mmHg versus 117·2 ± 8·2 mmHg, P<0·05) and thicker posterior wall of the left ventricle (9·8 ± 1 mm versus 9 ± 1·1 mm, P<0·05). Peak CPO was higher in athletes (5·87 ± 0·75 W versus 5·4 ± 0·69 W, P<0·05) as was cardiac reserve (4·92 ± 0·66 W versus 4·26 ± 0·61 W, P<0·05), respectively. Peak exercise CPO and reserve were only moderately correlated with end‐diastolic volume (r = 0·54; r = 0·46, P<0·05) and end‐diastolic left ventricular internal diameter (r = 0·48; r = 0·42, P<0·05), respectively. Athletes demonstrated greater maximal cardiac pumping capability and reserve than non‐athletes. The study provides new evidence that resting measures of cardiac structure and function need to be considered with caution in interpretation of maximal cardiac performance.     

Acute infarct selective MRI contrast agent

To determine the infarct affinity of a low molecular weight contrast agent, Gd(ABE-DTTA), during the subacute phase of myocardial infarct (MI). Dogs (n = 7) were examined, using a closed-chest, reperfused MI model. MI was generated by occluding for 180 min the Left Anterior Descending (LAD) coronary artery with an angioplasty balloon. DE-MRI images with Gd(ABE-DTTA) were obtained on days 4, 14, and 28 after MI. Control DE-MRI by Gd(DTPA) was carried out on day 27. T2-TSE images were acquired on day 3, 13 and 27. Triphenyltetrazolium chloride (TTC) histomorphometry validated postmortem the existence of infarct. Gd(ABE-DTTA) highlighted the infarct on day 4, but not at all on day 14 or on day 28, following MI. On day 4, the mean ± SD signal intensity (SI) of infarcted myocardium in the presence of Gd(ABE-DTTA) significantly differed from that of healthy myocardium (45 ± 6.0 vs. 10 ± 5.0, P < 0.05), but it did not on day 14 (11 ± 9.4 vs. 10 ± 5.7, P = NS), nor on day 28 (7 ± 1.5 vs. 7 ± 2.4, P = NS). The mean ± SD signal intensity enhancement (SIE) induced by Gd(ABE-DTTA) was 386 ± 165% on day 4, significantly different from mean SIE on day 14 (9 ± 20%), and from mean SIE on day 28 (12 ± 18%), following MI (P < 0.05). The last two mean values did not differ significantly (P = NS) from each other. As control, Gd(DTPA) was used and it did highlight the infarct on day 27, inducing a mean SIE value of 312 ± 40%. The mean SIE on day 3, 13, or 27 did not vary significantly (P = NS) on the T2-TSE images (114 ± 41%, 123 ± 41%, and 150 ± 79%, respectively). Post mortem, the existence of infarcts was confirmed by TTC staining. The infarct affinity of Gd(ABE-DTTA) vanishes in the subacute phase of scar healing, allowing its use for infarct age differentiation early on, immediately following the acute phase.     

Regional contribution to ventricular stroke volume is affected on the left side,but not on the right in patients with pulmonary hypertension

To develop more sensitive measures of impaired cardiac function in patients with pulmonary hypertension (PH), since detection of impaired right ventricular (RV) function is important in these patients. With the hypothesis that a change in septal function in patients with PH is associated with altered longitudinal and lateral function of both ventricles, as a compensatory mechanism, we quantified the contributions of these parameters to stroke volume (SV) in both ventricles using cardiac magnetic resonance (CMR). Seventeen patients (10 females) evaluated for PH underwent right heart catheterization (RHC) and CMR. CMR from 33 healthy adults (13 females) were used as controls. Left ventricular (LV) atrioventricular plane displacement (AVPD) and corresponding longitudinal contribution to LVSV was lower in patients (10.8?±?3.2 mm and 51?±?12?%) compared to controls (16.6?±?1.9 mm and 59?±?9?%, p?<?0.0001 and p?<?0.01, respectively). This decrease did not differ in patient with ejection fraction (EF) >50?% and <50?% (p?=?0.5) and was compensated for by increased LV lateral contribution to LVSV in patients (49?±?13?% vs. 37?±?7?%, p?=?0.001). Septal motion contributed less to LVSV in patients (5?±?8?%) compared to controls (8?±?4?%, p?=?0.05). RV AVPD was lower in patients (12.0?±?3.6 mm vs. 21.8?±?2.2 mm, p?<?0.0001) but longitudinal and lateral contribution to RVSV did not differ between patients (78?±?17?% and 29?±?16?%) and controls (79?±?9?% and 31?±?6?% p?=?0.7 for both) explained by increased RV cross sectional area in patients. LV function is affected in patients with PH despite preserved global LV function. The decreased longitudinal contribution and increased lateral contribution to LVSV was not seen in the RV, contrary to previous findings in patients with volume loaded RVs.     

Ultrasound measurements of carotid intima–media thickness by two semi‐automated analysis systems

Increased carotid intima–media thickness (cIMT) is associated with an increased risk of cardiac events and stroke. Several semi‐automated edge‐detection techniques for measuring cIMT are used for research and in clinical practice. Our aim was to compare two currently available semi‐automated techniques for the measurement of cIMT. Carotid ultrasound recordings were obtained from 99 subjects (mean age 54·4 ± 8·9 years, range 33–69) without known cardiovascular diseases using a General Electric (GE) Vivid 7 ultrasound scanner, 8‐MHz transducer. The far‐wall cIMT was evaluated 1–2 cm proximal to the carotid bulb. Three diastolic images (ECG R‐wave) from the left and three images from the right common carotid arteries were analysed using GE and Artery Measurement System (AMS) semi‐automated softwares. Mean systolic and diastolic blood pressures were 120 ± 13 and 76 ± 8 mmHg, respectively. The cIMT_mean (left + right)/2 by GE and cIMT_mean (left + right)/2 AMS were highly correlated (r = 0·92, P<0·001). Higher values were measured by GE (0·72 ± 0·12 mm) compared with AMS (0·69 ± 0·12 mm), and this was significant (P<0·001). The coefficients of variation for the intra‐observer variability of cIMT_mean (left + right)/2 were 1·0% (GE) and 2·2% (AMS). cIMT_mean measured by GE's semi‐automated edge‐detection method correlated well with that measured by AMS. However, there were small but significant systematic differences between the cIMT_mean values measured by the two techniques. Thus, the use of only one type of measurement program seems favourable in follow‐up studies and when evaluating treatment effects.     

Patients with Parkinson disease present high ambulatory blood pressure variability

Patients with Parkinson disease (PD) present blunted nocturnal blood pressure fall and similar ambulatory blood pressure variability (ABPV) measured by standard deviation (SD) and coefficient of variation (CV) compared with healthy subjects. However, these classical indices of ABPV have limited validity in individuals with circadian blood pressure alterations. New indices, such as the average of daytime and night‐time standard deviation weighted by the duration of the daytime and night‐time intervals (SD_dn) and the average real variability (ARV), remove the influence of the daytime and the night‐time periods on ABPV. This study assessed ABPV by SD_dn and ARV in PD. Twenty‐one patients with PD (11 men, 66 ± 2 years, stages 2–3 of modified Hoehn & Yahr) and 21 matched controls without Parkinson disease (9 men, 64 ± 1 years old) underwent blood pressure monitoring for 24 h. ABPV was analysed by 24 h, daytime and night‐time SD and CV, and by the SD_dn and ARV. Systolic/diastolic 24‐h and night‐time SD and CV were similar between the patients with PD and the controls. The patients with PD presented higher daytime systolic/diastolic CV and SD than the controls (10·4 ± 0·9/12·3 ± 0·8 versus 7·0 ± 0·3/9·9 ± 0·5%, P<0·05; 12·6 ± 1·0/9·1 ± 0·5 versus 8·6 ± 0·4/7·5 ± 0·3 mmHg, P<0·05, respectively) as well as higher systolic/diastolic SD_dn (10·9 ± 0·8/8·2 ± 0·5 versus 8·2 ± 0·3/7·1 ± 0·2 mmHg, P<0·05, respectively) and ARV (8·8 ± 0·6/6·9 ± 0·3 versus 7·2 ± 0·2/6·0 ± 0·2 mmHg, P<0·05, respectively). In conclusion, patients with PD have higher ABPV than control subjects as assessed by SD_d, CV_d, SD_dn and AVR.     

Function of remote non-infarcted myocardium after STEMI: analysis with cardiovascular magnetic resonance

To evaluate remote myocardial function after ST-elevation myocardial infarction (STEMI) and the impact of infarct size (IS) using cardiovascular magnetic resonance (CMR). 161 patients and 15 controls underwent CMR at 1st week and 6th month after STEMI. Using the 17-segments model, segments were categorized into infarcted, adjacent and remote myocardium. Relative systolic wall thickening (SWT, %) was assessed using the centerline method. IS (% of left ventricular mass) was determined in late enhancement imaging. Overall, in remote myocardium, SWT was comparable (83 ± 32) to controls (77 ± 25, P = .5) and did not increase significantly (P = .2) at the 6th month (88 ± 35, P = .3 vs. control). When IS was categorized into tertiles (<13.6%, (n = 49), 13.7–28.2%, (n = 60), >28.2%, (n = 52)), SWT in the remote area at the 1st week was not different from controls, regardless of infarct size (p between .2 and .8 for all tertiles). At 6 months, SWT was larger compared to controls only in small infarctions (98 ± 34 vs. 77 ± 25, P = .03). In medium and large infarctions there was no difference in SWT of the remote area compared to controls (87 ± 33 and 79 ± 34, P = .3 and P = .09) and there was no significant increase at 6 months (P between .2 and .9). In remote myocardium there was no difference in contractility compared to controls after STEMI. After 6 month a slight hypercontractility can only be observed in small infarctions. In medium and large infarctions no difference of SWT in remote myocardium compared to controls can be observed.     

Effects of trimetazidine,a partial inhibitor of fatty acid oxidation,on ventricular function and survival after myocardial infarction and reperfusion in the rat

Trimetazidine (TMZ), a partial inhibitor of fatty acid oxidation, has been effective in treating chronic angina, but its effects on the development of post‐myocardial infarction (MI) left ventricular remodeling are not defined. In this study, we tested whether chronic pre‐MI administration of TMZ would be beneficial during and after acute MI. Two‐hundred male Wistar rats were studied in four groups: sham + TMZ diet (n = 20), sham + control diet (n = 20), MI + TMZ diet (n = 80), and MI + control diet (n = 80) splitted into one short‐term and one long‐term experiments. Sham surgery consisted of a thoracotomy without coronary ligation. MI was induced by coronary occlusion followed by reperfusion. Left ventricle (LV) function and remodeling were assessed by serial echocardiography throughout a 24‐week post‐MI period. LV remodeling was also assessed by quantitative histological analysis of post‐MI scar formation at 24 weeks post‐MI. During the short‐term experiment, 10/80 rats died after MI, with no difference between groups (MI + control = 7/40, MI + TMZ = 3/40, P = 0.3). In the long‐term experiment, the deaths occurred irregularly over the 24 weeks with no difference between groups (MI + control = 16% mortality, MI + TMZ = 17%, P = 0.8). There was no difference between groups as regard to LV ejection fraction (MI + control = 36 ± 13%, MI + TMZ = 35 ± 13%, P = 0.6). In this experimental model, TMZ had no effects on the post‐MI occurrence of LV dysfunction or remodeling. Further investigations are warranted to assess whether the partial inhibition of fatty acid oxidation may limit the ability of the heart to respond to acute severe stress.     

Muscular adaptations to fatiguing exercise with and without blood flow restriction

The purpose of this study was to determine the muscular adaptations to low‐load resistance training performed to fatigue with and without blood flow restriction (BFR). Middle‐aged (42–62 years) men (n = 12) and women (n = 6) completed 18 sessions of unilateral knee extensor resistance training to volitional fatigue over 6 weeks. One limb trained under BFR, and the contralateral limb trained without BFR [free flow (FF)]. Before and after the training, measures of anterior and lateral quadriceps muscle thickness (MTh), strength, power and endurance were assessed on each limb. The total exercise training volume was significantly greater for the FF limb compared with the BFR limb (P<0·001). Anterior quadriceps thickness and muscle function increased following the training in each limb with no differences between limbs. Lateral quadriceps MTh increased significantly more (P<0·05) in the limb trained under BFR (BFR: 3·50 ± 0·61 to 3·67 ± 0·62 cm; FF: 3·49 ± 0·73 to 3·56 ± 0·70 cm). Low‐load resistance training to volitional fatigue both with and without BFR is viable options for improving muscle function in middle‐aged individuals. However, BFR enhanced the hypertrophic effect of low‐load training and reduced the volume of exercise needed to elicit increases in muscle function.