Interventricular delay interval optimization in cardiac resynchronization therapy guided by echocardiography versus guided by electrocardiographic QRS interval width

Present devices for cardiac resynchronization therapy offer the possibility of tailoring the hemodynamic effect of biventricular pacing by optimization of the interventricular delay (VV) beyond atrioventricular (AV)-interval optimization. It was not yet defined whether a QRS width-based strategy may be a helpful tool for echocardiography for device programming. The aim of the study was to investigate the relation between VV-interval optimization guided by echocardiography and guided by QRS interval width. One hundred six patients with a cardiac resynchronization therapy device for > or =3 months were enrolled. All patients underwent echocardiographic AV and VV delay optimization. The AV interval was optimized according to the E wave-A wave (EA) interval and left ventricular filling time. At the optimal AV delay, VV optimization was performed by measuring the aortic velocity time integral at 5 different settings: simultaneous right and left ventricle output, left ventricle pre-excitation (left ventricle + 40 and 80 ms, respectively), and right ventricle pre-excitation (right ventricle + 40 and 80 ms, respectively). A 12-lead electrocardiogram was recorded and QRS duration was measured in the lead with the greatest QRS width. The electrocardiographic (ECG)-optimized VV interval was defined according to the narrowest achievable QRS interval among 5 VV intervals. The echocardiographic-optimized VV interval was left ventricle + 40 ms in 28 patients, left ventricle + 80 ms in 15 patients, simultaneous in 46 patients, right ventricle + 40 ms in 14 patients, and right ventricle + 80 ms in 3 patients. Significant concordance (kappa = 0.69, p <0.001) was found between the echocardiographic- and ECG-optimized VV interval. In conclusion, significant concordance appeared to exist during biventricular pacing between VV programming based on the shortest QRS interval at 12-lead ECG pacing and echocardiographic-guided VV-interval optimization. A combined ECG- and echocardiographic approach could be a less time-consuming solution in performing this operation.     

Correct allometric analysis is always helpful for scaling flow‐mediated dilation in research and individual patient contexts

McLay et al. (Clin Physiol Funct Imaging (2017); DOI: 10.1111/cpf.12465 ) recently examined whether the allometric scaling of flow‐mediated dilation influenced the mean difference between samples of young and older adults compared with the traditional percentage change approach. They also explored whether a new scaling calculation improved the ability to obtain individually scaled flow‐mediated dilation. In our response to their study, we can demonstrate that McLay et al. (Clin Physiol Funct Imaging, 2017) have (i) managed to formulate a new scaling index which does nothing to remove the dependency of that index on baseline diameter and (ii) suggested, incorrectly, that the original allometric approach cannot be used to derive individually‐adjusted values of flow‐mediated dilation, which can be interpreted in a similar way to a percentage change.     

Contribution of vasoconstriction to the origin of atherosclerosis: a conceptual study

Research during the past century has clearly shown that endothelial injury (EI) and/or endothelial dysfunction (ED) are among the major events determining the onset of atherosclerosis. Included in the events that may elicit endothelial damage, vasoconstriction (VC) has received relatively little attention. This conceptual review attempts to show that in elastic and conduit arteries, VC is not only capable of producing EI/ED, but is also closely associated with many recognized proatherogenic stimuli. Of related interest is the observation that a number of suspected antiatherogenic stimuli oppose VC by their vasodilatory effects, lending further support to this relationship. In addition, recent developments in the knowledge of the molecular basis of VC (including the role of specific inhibitors) are discussed, and their potential for preventing lesion formation and thus becoming novel therapeutic alternatives against the onset of atherosclerosis are highlighted.     

Primary aldosteronism and hypertensive disease

Recent studies in hypertensive populations that have used the serum aldosterone (SA) to plasma renin activity (PRA) ratio as a screening test have demonstrated a high prevalence of primary aldosteronism (PA). This frequency is higher than that previously described when hypokalemia was used as a screening tool. However, other factors, such as the characteristics of hypertensive disease, could also influence the prevalence of PA. We studied 609 essential hypertensive patients, classified according to the Joint National Committee VI (JNC VI), in 3 different stages depending on the severity of their hypertensive disease. We measured SA and PRA and calculated the SA-PRA ratio for all patients. An SA-PRA ratio >25 was detected in 63 of 609 patients, and the fludrocortisone test confirmed the PA diagnoses in 37 of 609 (6.1%) cases. PA prevalence according to hypertension stage was as follows: stage 1, 6 of 301 cases (1.99%); stage 2, 15 of 187 cases (8.02%); and stage 3, 16 of 121 cases (13.2%). PA patients were slightly younger than the other hypertensive patients (48.4+/-10.5 vs 53.6+/-10.2 years; P<0.05). Serum potassium levels were normal in 36 of 37 PA patients; only 1 patient had minor hypokalemia. Computed tomography scans showed bilateral adrenal enlargement in 7 and an adrenal nodule in 2 cases. In summary, we found a high frequency of PA in essential hypertensives classified in stages 2 and 3 according to the JNC VI. The low frequency of computed tomography scan abnormalities and hypokalemia suggests that the diagnosis for most PA patients corresponds to attenuated forms of the disease.     

The Non‐Motor Symptoms Scale in Parkinson’s disease: Validation and use

The Non‐Motor Symptoms Scale (NMSS) was developed and validated in 2007 as the first instrument for the comprehensive assessment of a range of non‐motor symptoms in Parkinson's disease (PD). Thirteen years have elapsed since its introduction and extensive international validation with good psychometric attributes has been carried out. Here, we review the validation data of the NMSS and its cross‐validity with other scales, and describe the key evidence derived from use of the NMSS in clinical studies. To date, over 100 clinical studies and trials have made use of it as an outcome measure, showing consistent and strong correlations between NMSS burden and health‐related quality of life measures. Moreover, the scale has shown to be capable of detecting longitudinal changes in non‐motor symptoms, where studies have shown differential changes over time of several of the NMSS domains. The scale has become a key outcome in several randomized clinical trials. Highlighting the prevalence and importance of non‐motor symptoms to quality of life in patients with PD, the development of NMSS has also been useful in signposting clinical and biomarker based research addressing non‐motor symptoms in PD.     

Anticipatory synergy adjustments: preparing a quick action in an unknown direction

We studied a mechanism of feed-forward control of a multi-finger action, namely anticipatory synergy adjustments (ASAs), prior to a quick force correction in response to a change in the gain of the visual feedback. Synergies were defined as co-varied across trials adjustments of commands to fingers that stabilized (decreased variance of) the total force. We hypothesized that ASAs would be highly sensitive to prior information about the timing of the action but not to information on its direction, i.e., on whether the gain would go up or down. The subjects produced accurate constant total force by pressing with four fingers on individual force sensors. The feedback signal could change from veridical (the sum of finger forces) to modified, with the middle finger force multiplied by 0.2 or by 1.8. The timing of the gain change and its direction could be known or unknown to the subject in advance. When the timing of the gain change was known, ASA was seen as a drop in the synergy index starting about 250–300 ms prior to the first visible correction of the total force. When the gain change timing was unknown, ASAs started much later, less than 100 ms prior to the total force correction. The magnitude of synergy index changes was significantly larger under the “time known” conditions. Information on the direction of the visual gain change had no effect on the ASA timing, while the ASA magnitude was somewhat larger when this information was not available to the subject. After the total force correction, the synergy index was significantly larger for the force signal computed using the modified gain values as compared to the synergy index value for the actual total force. We conclude that ASAs represent an important feed-forward motor control mechanism that allows preparing for a quick action even when the direction of the action is not known in advance. The results emphasize the subtle control of multi-finger synergies that are specific to the exact contributions of individual fingers to performance variables. The data fit well the central back-coupling hypothesis of synergies and the idea of control with referent body configurations.