Left atrial peak systolic strain as an indicator pathway of diastolic dysfunction of the left ventricle.

BACKGROUND: Left atrial peak systolic strain (LA-PSS) imaging is an emerging index of LA function, and it was shown to be decreased in heart failure with preserved ejection fraction. We aimed to determine whether LA-PSS could be used as an additional diagnostic parameter to current existing guidelines for the presence of left ventricle diastolic dysfunction (LVDD). MATERIALS AND METHODS: A total of 190 consecutive adult patients with cardiovascular risk factors and normal LV ejection fraction with no prior history of heart failure were included in the study. Speckle tracking software was used to study ventricular parietal deformity, left ventricle global longitudinal systolic strain (LV-GLS), and LA-PSS. RESULTS: The median LV-GLS was -19%, with a significant difference (p<0.001) between patients with normal diastolic function vs those with LVDD. The median LA-PSS was 33% (30 to 38%) (p<0.001). Most patients (61%) had grade 1 atrial dysfunction based on PSS (range 24% to 35%). The analysis of the area under the ROC curve of the LA-PSS as a potential indicator pathway of LVDD was 67% (95% CI 62-72), and 75% (95% CI 70-80), when the indeterminate pattern was included. The decreased LA-PSS made it possible to reclassify patients with an indeterminate pattern of diastolic function in 96% of cases. CONCLUSION: These results support the potential role of LA-PSS as an additional parameter for the diagnosis of LVDD in patients with normal ejection fraction, and may be integrated into the guidelines for routine evaluation of patients.

Role of the Electrocardiographic MVP Risk Score (Morphology-Voltage-P Wave Duration) in Predicting the Development of Atrial Fibrillation in Patients With Systemic Arterial Hypertension.

BACKGROUND: There is a global tendency to emphasize the prevention and early diagnosis of diseases that have a great impact on public health. Atrial fibrillation (AF) has a prevalence affecting 1.5-2% of the general population. Certain variables of the P wave allow us to identify and stratify patients at risk of developing AF. MATERIALS AND METHODS: This is an observational, descriptive, and longitudinal study to determine the applicability of the electrocardiographic (ECG) morphology, voltage, and P wave duration (MVP) risk score to predict the development of AF in consecutive patients with systemic hypertension (SH) in an initial follow-up of 12 months. RESULTS: Initially, 104 patients were included, of whom 12 died during follow-up and 17 did not attend subsequent checkups during the COVID-19 pandemic; therefore, they were excluded. The study patients were 75, of whom AF was detected in 25 patients (33%). The average duration of the P wave was 120 ± 26 ms, the average voltage was 0.1 ± 0.5 Mv. The high-risk MVP ECG score had an [area under the curve, 0.69; 95% confidence intervals (CI), 0.59-0.79] and demonstrated a specificity and a positive predictive value of 100%, a negative predictive value of 76%, and a sensitivity of 40% for predicting the development of AF. CONCLUSIONS: The present study establishes for the first time that SH patients who possess a high-risk MVP ECG score have a significantly higher incidence of developing AF. The high-risk MVP Score has a specificity and a positive predictive value of 100% and a high negative predictive value with a moderate sensitivity for the prediction of the development of AF in SH patients.

Correlation of connexin43 expression and late ventricular potentials in nonischemic dilated cardiomyopathy.

Nonischemic dilated cardiomyopathy (DCM) is associated with a high risk of sudden cardiac death. Signal-averaged electrocardiography (SAECG) is a useful clinical tool for detecting late ventricular potentials (LP). Gap junction alterations have recently been shown to be involved in the pathogenesis of ventricular arrhythmias in DCM; however, the possible relationship between gap junctional connexin43 (C x 43) expression and SAECG has not yet been evaluated. In the present study 16 patients (47+/-13 years) with DCM who had undergone SAECG testing were evaluated. In each patient, the expression of C x 43 proteins was qualitatively and quantitatively determined using immunoconfocal microscopy and right ventricular biopsy specimens. The level of expression of C x 43 protein was defined as the proportion of tissue area occupied by C x 43 (percent tissue area) in each test area. The abundance and distribution of the C x 43 signal was assessed in relation to LP. Late ventricular potentials were positive in 5 patients (LP (+) group) and negative in 11 patients (LP (-) group). The incidence of sustained ventricular tachycardia in the LP (+) group was higher than that in the LP (-) group (80% vs 18%, p=0.04). The percent tissue area of C x 43 in the LP (+) group was significantly lower than that in the LP (-) group (p=0.02). Furthermore, C x 43 protein in the LP (+) group was distributed more heterogeneously than that in the LP (-) group (p=0.001). The heterogeneous expression of C x 43 protein may contribute to impaired ventricular conduction, which may be related to the LP detected on SAECG.

Comparative usefulness of beat-to-beat QT dispersion and QT interval fluctuations for identifying patients with organic heart disease at risk for ventricular arrhythmias.

The comparative usefulness of 10 min of beat-to-beat 12-lead QT dispersion (QTd) and QT interval variability index (QTVI) analysis for identifying patients with organic heart disease (OHD) at risk for ventricular arrhythmias was assessed in 86 subjects: 54 had OHD without a history of ventricular arrhythmias, 15 had OHD with documented ventricular tachycardia, and there were 17 controls. The following parameters were analyzed among the groups: (1) the average QTd (mean QTd), (2) the difference between the maximum and minimum QTd observed over the recording time (QTd variation), (3) the maximum difference of QTd between consecutive beats (QTd maximum), (4) the QTd standard deviation (QTd variability), and (5) QTVI, calculated in lead I or II according to an established formula: log 10 [(QTv/QTm2) / (HRv/HRm2)]. All the analyzed parameters were significantly increased in the patients with and without ventricular tachycardia when compared with the controls. QTd variation, QTd maximum and QTd variability were the only variables that remained significantly increased in the group of patients with documented ventricular tachycardia, compared with those without arrhythmia. Thus, beat-to-beat fluctuations of both the QT interval and QTd may be markers of temporal electrical instability in patients with OHD.

Heterogeneous loss of connexin43 protein in nonischemic dilated cardiomyopathy with ventricular tachycardia.

INTRODUCTION: Gap junction alterations recently have been implicated in chronic heart failure, but direct evidence between gap junction manifestation in nonischemic dilated cardiomyopathy (DCM) is lacking. The current study examines whether qualitative changes or altered distribution of gap junctional connexin43 (Cx43) are related to global ventricular function and ventricular arrhythmia in DCM. METHODS AND RESULTS: We investigated 31 DCM patients (52 +/- 15 years) and 5 control subjects (55 +/- 10 years). Expression of Cx43 proteins was qualitatively and quantitatively determined using immunoconfocal microscopy in right ventricular biopsy specimens from each patient. The expression level of Cx43 protein was defined as the proportion of tissue area occupied by Cx43 (percent tissue area) in each test area. Cx43 immunoreactive signal expressed as percent tissue area was not correlated with the change in left ventricular ejection fraction (P = 0.17). Of 31 DCM patients, 23% subsequently developed sustained ventricular tachycardia (VT), which allowed retrospective division of the samples into two groups: non-VT and VT. Left ventricular ejection fraction was comparable in both groups, but the percent tissue area in the VT groups was significantly decreased compared with that of the non-VT groups (P = 0.03). Furthermore, Cx43 protein was distributed heterogeneously in the VT groups (P < 0.0001). CONCLUSION: Heterogeneous reduction of Cx43 protein may result in development of malignant ventricular arrhythmia in DCM.