Alfonso Roberto Martiniello

Atrial Myocardial Deformation Properties Predict Maintenance of Sinus Rhythm After External Cardioversion of Recent-Onset Lone Atrial Fibrillation A Color Doppler Myocardial Imaging and Transthoracic and Transesophageal Echocardiographic Study

Background—Accurate echocardiographic parameters to predict maintenance of sinus rhythm in patients with atrial fibrillation (AF) are poorly defined. This study was conducted to assess the atrial myocardial properties during AF through myocardial velocity, strain rate, and strain and to compare their prognostic value in maintaining sinus rhythm in patients with lone AF with standard transthoracic (TTE) and transesophageal echocardiography (TEE). Methods and Results—Sixty-five consecutive patients with lone AF for ≤3 months underwent TTE, TEE, and myocardial velocity and strain and strain rate imaging examinations before successful external cardioversion. Maintenance of sinus rhythm was assessed during a 9-month follow-up. Atrial myocardial velocity, strain, and strain rate values in AF patients were compared with those of age- and sex-matched referents. Moreover, clinical and echocardiographic parameters of patients with maintenance of sinus rhythm (MSR patients) over the 9-month follow-up period (n=25) were compared with those from patients with AF recurrence (AFR patients; n=40). Atrial myocardial properties assessed by myocardial velocity, strain rate, and strain were significantly reduced (P<0.0001) in patients (velocity, 3.2±1.4 cm/s; strain, 23.3±19%; strain rate, 2±0.9 seconds−1) compared with referents (velocity, 5.7±1.3 cm/s; strain, 92±26%; strain rate, 4.2±1.8 seconds−1). The individual predictors of sinus rhythm maintenance were atrial appendage flow velocity (MSR patients, 39±12 cm/s; AFR patients, 32±15 cm/s; P<0.01) assessed by TEE and atrial strain (MSR patients, 33±27%; AFR patients, 17±9%; P=0.0007) and strain rate (MSR patients, 2.7±1 seconds−1; AFR patients, 1.6±0.6 seconds−1; P<0.0001) peak systolic values. Atrial strain (P<0.0001; coefficient, 0.015; SE, 0.003) and strain rate (P<0.0001; coefficient, 0.372; SE, 0.075) parameters alone were confirmed as independent predictors of sinus rhythm maintenance by multivariable analysis. Conclusions—Patients with higher atrial strain and strain rate appear to have a greater likelihood of staying in sinus rhythm. If the current data are verified in future studies, then additional pharmacological therapy and maintenance of anticoagulants for a longer period may need to be considered in those with lower atrial strain and strain rate measurements.

Atrial reservoir function by strain rate imaging in asymptomatic mitral stenosis: prognostic value at 3 year follow-up

AIMS Assessment of left and right systolic atrial reservoir function in asymptomatic mitral stenosis (MS) by strain and strain rate imaging (SRI) and their prognostic power at 3 year follow-up was the purpose of this study. There is clear indication to treat (by surgery or percutaneous valvotomy) symptomatic patients with MS, whereas for the asymptomatic ones, the question is much debated. So, we need new echocardiographic parameters helpful for the management of asymtomatic patients. Atrial reservoir function by SRI could help in evaluation of these patients. METHODS AND RESULTS Fifty-three asymptomatic patients with MS and 53 healthy controls were evaluated by the standard echo-Doppler study [mitral valve (MV) area, mean gradient, systolic pulmonary pressure, left atrial (LA) width, LA volumes, LA compliance index] and by Doppler myocardial imaging (velocity, strain, and SR of both atria). The endpoint at 3 year follow-up was symptoms, hospitalization for cardiac cause, atrial fibrillation, thrombo-embolic events, valvular surgery, or percutaneous commissurotomy. LA width, volumes, and systolic pulmonary pressure were significantly increased in MS patients (P < 0.001). Atrial myocardial velocities and deformation indices were significantly compromised in MS patients (P < 0.0001). Significant correlation was found between atrial myocardial velocity and MV area (by pressure half-time method: P = 0.019, R = 0.41; by planimetric method: P = 0.016, R = 0.43). Peak systolic LA myocardial strain and SR were significantly correlated with atrial volumes (strain: P = 0.03, R = -0.28; SR: P = 0.0008, R = -0.42), with atrial compliance index (strain: P = 0.04, R = 0.26; SR: P = 0.04, R = 0.16), with atrial ejection fraction (strain: P < 0.0001, R = 0.56; SR: P = 0.03, R = 0.43). At 3 year follow-up, 22 (41%) patients had events. Comparing the MS patients who had events during the 3 year follow-up with those who did not, the former had bigger LA volumes, although these parameters did not reached a significant value, whereas atrial myocardial systolic SR was significantly impaired in patients with events. In multivariate analysis, the best predictor of adverse events was LA peak systolic SR average (P = 0.04; coefficient: 0.113; SE: 0.055; cut-off value of 1.69 s(-1) for LA peak systolic SR average) with a sensitivity of 88%, specificity of 80.6%, area under the receiver operating characteristic curve of 0.852 (SE: 0.048; 95% CI: 0.74-0.93, P = 0.0001). CONCLUSION Atrial myocardial deformation properties, assessed by SRI, are abnormal in asymptomatic patients with rheumatic MS. The degree of this impairment is predictor of events in a 3 year follow-up. SRI could be helpful in decision-making of asymtomatic patients with MS.

Cardiac fluid dynamics anticipates heart adaptation

Hemodynamic forces represent an epigenetic factor during heart development and are supposed to influence the pathology of the grown heart. Cardiac blood motion is characterized by a vortical dynamics, and it is common belief that the cardiac vortex has a role in disease progressions or regression. Here we provide a preliminary demonstration about the relevance of maladaptive intra-cardiac vortex dynamics in the geometrical adaptation of the dysfunctional heart. We employed an in vivo model of patients who present a stable normal heart function in virtue of the cardiac resynchronization therapy (CRT, bi-ventricular pace-maker) and who are expected to develop left ventricle remodeling if pace-maker was switched off. Intra-ventricular fluid dynamics is analyzed by echocardiography (Echo-PIV). Under normal conditions, the flow presents a longitudinal alignment of the intraventricular hemodynamic forces. When pacing is temporarily switched off, flow forces develop a misalignment hammering onto lateral walls, despite no other electro-mechanical change is noticed. Hemodynamic forces result to be the first event that evokes a physiological activity anticipating cardiac changes and could help in the prediction of longer term heart adaptations.

Noninvasive Evaluation of Arterial Abnormalities in Young Patients with Neurofibromatosis Type 1

Neurofibromatosis regroups at least two different autosomal dominant genetic disorders: neurofibromatosis type 1 (NF1) and neurofibromatosis type 2 (NF2). Vascular disease is an underestimated complication of NF1. Few studies are available on this, all based on case reports. Neurofibromin, NF1 protein product, has also been detected in aortic smooth muscle. The purpose of this study was to evaluate the physical properties of the vessels, by measuring the carotid-femoral pulse wave velocity (PWV). This parameter was assessed by the Complior®, a new noninvasive, validated device, used to screen a large population. The authors studied 64 neurofibromatosis patients (34 boys and 30 girls) with a mean age of 12 years (range 5-25 years). To investigate the presence of vascular lesions, aortic stiffness was evaluated by carotid-femoral PWV by using an automatic processor (Complior®). They compared data from the PWV with a control group (30 healthy children, 17 boys and 13 girls, mean age 11 years, range 5-23 years). The calculated mean PWV in the control group was 6.5 ±1.15 m/s. The mean PWV of the 64 young patients with NF1 was 6.3 ±1.02 m/s. There was no difference between the two groups (p=0.39). Nevertheless, analysis of the linear regression has shown a linear relationship between systolic blood pressure (SBP) and PWV in the control group, while in NF1 patients this relationship is not present. The authors suggest that the coexistence of different factors, such as intimal proliferation, thinning media, fragmentation of the elastic tissue, irregularity, stenosis and tortuosity of the vessels, dysplasia of the small vessels, that counterbalance PWV, normalize the mean value. They emphasize the impor tance of a careful vascular evaluation, using noninvasive method, such as Complior®. This device is well accepted by NF1 patients.

Effects of volume loading on strain rate and tissue Doppler velocity imaging in patients with idiopathic dilated cardiomyopathy.

BackgroundStrain rate is a promising echocardiographic technique which adds further information to that obtained with two-dimensional echocardiography and tissue Doppler imaging (TDI). The present study aimed to evaluate the effects of acute isotonic volume expansion on left ventricular function in patients with idiopathic dilated cardiomyopathy (DCM) utilizing TDI and strain rate measurements. MethodsTen patients with DCM and a left ventricular ejection fraction (LVEF) ≤ 40% underwent two-dimensional echocardiography during volume expansion (0.9% NaCl; 0.25 ml/kg/min for 120 min). Peak systolic tissue velocity and peak systolic strain rate were measured at baseline and at the end of volume loading. ResultsMean LVEF was 32 ± 9% at baseline and remained unchanged after volume loading. Similarly, peak systolic velocity was 2.21 cm/s at baseline and remained unchanged after volume expansion. By contrast, peak systolic strain rate significantly reduced from −1.08 ± 0.37/s to −0.76 ± 0.12/s (P < 0.05). ConclusionsIn patients with DCM, peak systolic strain rate significantly reduces with volume loading in the absence of change in LVEF or peak systolic velocities at TDI. Because strain rate is a relative load-independent index of systolic function, the reduction observed is probably related to the decrease in left ventricular systolic performance that follows volume loading in heart failure patients. Thus, peak systolic strain rate appears to be more useful than TDI velocities to evaluate left ventricular dynamics during volume loading in patients with depressed left ventricular function.

Changes in electrical activation modify the orientation of left ventricular flow momentum: novel observations using echocardiographic particle image velocimetry

AIMS Changes in electrical activation sequence are known to affect the timing of cardiac mechanical events. We aim to demonstrate that these also modify global properties of the intraventricular blood flow pattern. We also explore whether such global changes present a relationship with clinical outcome. METHODS AND RESULTS We investigated 30 heart failure patients followed up after cardiac resynchronization therapy (CRT). All subjects underwent echocardiography before implant and at follow-up after 6+ months. Left ventricular mechanics was investigated at follow-up during active CRT and was repeated after a temporary interruption <5 min later. Strain analysis, performed by speckle tracking, was used to assess the entity of contraction (global longitudinal strain) and its synchronicity (standard deviation of time to peak of radial strain). Intraventricular fluid dynamics, by echographic particle image velocimetry, was used to evaluate the directional distribution of global momentum associated with blood motion. The discontinuation of CRT pacing reflects into a reduction of deformation synchrony and into the deviation of blood flow momentum from the base-apex orientation with the development of transversal flow-mediated haemodynamic forces. The deviation of flow momentum presents a significant correlation with the degree of volumetric reduction after CRT. CONCLUSION Changes in electrical activation alter the orientation of blood flow momentum. The long-term CRT outcome correlates with the degree of re-alignment of haemodynamic forces. These preliminary results suggest that flow orientation could be used for optimizing the biventricular pacing setting. However, larger prospective studies are needed to confirm this hypothesis.

Recoordination of opposing walls drives the response to cardiac resynchronization therapy: a longitudinal study using a strain discoordination index.

Background and aims Intraventricular dyssynchrony has traditionally been studied by means of contraction delays between different myocardial segments. Recently, the discoordination of opposing wall contraction throughout the cardiac cycle has been proposed as a more faithful predictor of response. Aim of the current study was to evaluate which parameters – mechanical dyssynchrony or discoordination – normalize with left ventricular response to cardiac resynchronization therapy (CRT). Methods Cardiac mechanics were analysed before and after 6 months of CRT in 53 patients with left bundle branch block and advanced heart failure. Discoordination was quantified by means of the transverse strain discoordination index (TSDI) at basal and mid-ventricular segments; this index takes into account the percentage of time in the cardiac cycle in which cardiac deformation (transverse strain) of the two opposing walls occurs in noncoordinated directions. Dyssynchrony indices included septal to lateral peak-to-peak transverse strain delay and the standard deviation of time to peak tissue velocity in 12 mid-basal segments (Yu index). Results Around 63% of patients met the response criteria. Several baseline indices were predictive of reverse remodelling; TSDI at the mid-ventricular level demonstrated the best accuracy. Time from Q to peak velocity and strain tended to increase in all explored myocardial segments; despite a trend towards a decrease in septal-to-lateral strain delay, the latter decreased equally in responders and in nonresponding patients. Yu index decreased in responders more than in nonresponders, with borderline significance. Basal and medium TSDI remained unchanged in nonresponders and consistently normalized in patients who responded to CRT. The changes in TSDI were significantly correlated with improvements in left ventricular end-systolic volume and ejection fraction; the strongest correlation was observed for changes in TSDI measured at the mid-ventricular level. Conclusion Left ventricular reverse remodelling after CRT is accompanied by the recoordination of opposite-wall contraction, as testified by changes in mid-ventricular TSDI, which also reveals as a very good predictor of response. On the contrary, changes of segmental peak-to-peak delays (dyssynchrony indices) fail to capture the complex nature of left ventricular response to CRT.