Effect of Valsalva maneuver on surface electrocardiographic P-wave dispersion in paroxysmal atrial fibrillation

Obesity is a worldwide health problem with epidemic proportions that has been associated with atrial fibrillation (AF). Even though the underlying pathophysiological mechanisms have not been completely elucidated, several experimental and clinical studies implicate obesity in the initiation and perpetuation of AF. Of note, hypertension, diabetes mellitus, metabolic syndrome, coronary artery disease, and obstructive sleep apnea, represent clinical correlates between obesity and AF. In addition, ventricular adaptation, diastolic dysfunction, and epicardial adipose tissue appear to be implicated in atrial electrical and structural remodeling, thereby promoting the arrhythmia in obese subjects. The present article provides a concise overview of the association between obesity and AF, and highlights the underlying pathophysiological mechanisms.

Multiple sclerosis (MS) is one of the most frequent disorders of central nervous system, resulting in autonomic disturbances. Some electrocardiographic changes have been reported in these patients that can lead to arrhythmia. In this study we compared P wave duration and dispersion and QT interval of MS patients to healthy control subjects.

Eighty four multiple sclerosis patients and 84 healthy, age and sex-matched volunteers were included. A 12-lead electrocardiogram was undertaken in order to measure minimal and maximal P wave duration, P wave dispersion (PWD) and QT interval.

In patient group, mean P wave duration, maximum P wave duration and PWD were significantly longer than control group. QT interval was longer in patient group but the difference was not significant.

In this study, P wave duration and P wave dispersion was found to be higher in MS patients than healthy control subjects.

Metabolic syndrome (MS) is an important risk factor for atrial fibrillation. P-wave indices, including P-wave dispersion (PWD) and P-wave duration, can be used as non-invasive markers of heterogeneous atrial conduction. The aim of our study was to evaluate the relationship between P-wave indices and insulin resistance in patients with MS.

Seventy-four patients with MS (44 men, 30 women) and 81 patients without MS (48 men, 33 women) were enrolled in the study. A diagnosis of MS was made as defined by the Adult Treatment Panel III of the National Cholesterol Education Program. Insulin resistance was estimated using the homeostasis model assessment (HOMA) index. P-wave maximum duration (Pmax) and P-wave minimum duration (Pmin) were calculated on a 12-lead electrocardiogram, and the difference between the Pmax and the Pmin was defined as PWD.

Patients with MS had a longer PWD and a higher Pmax compared with patients without MS (PWD, 35.65 ± 4.36 vs. 26.27 ± 4.04, P < 0.001; Pmax, 117.12 ± 10.77 vs. 105.98 ± 9.02, P < 0.001), whereas no difference was found between Pmin values from MS patients and controls (81.47 ± 9.54 vs. 79.70 ± 8.76, P = 0.231). Stepwise multivariate analysis revealed only the HOMA index to be an independent predictor of PWD (β = 3.115, P < 0.001) and Pmax (β = 7.175, P < 0.001).

This study suggests that patients with MS have a prolonged PWD and Pmax. The increase in these parameters may be an indicator for identification of patients at an increased risk for atrial fibrillation.

Le syndrome métabolique (SM) est un facteur de risque important pour la fibrillation auriculaire. Les indices des ondes P, à savoir leurs dispersion et durée, peuvent être utilisés comme marqueurs non invasifs de la conduction auriculaire hétérogène. Le but de notre étude était d’évaluer la relation entre les indices des ondes P et la résistance à l’insuline chez les patients atteints de SM.

Soixante-quatre patients atteints de SM (44 hommes, 30 femmes) et 81 patients non atteints (48 hommes, 33 femmes), ont été inclus dans l’étude. Le diagnostic de MS était défini par le Adult Treatment Panel III du National Cholesterol Education Program. La résistance à l’insuline était estimée au moyen du modèle d’évaluation de l’homéostasie (HOMA). La durée maximale de l’onde P (Pmax) ainsi que sa durée minimale (Pmin) ont été calculées sur un électrocardiogramme à 12 dérivations, et la différence entre la Pmax et la Pmin a été définie comme dispersion de l’onde P (DOP).

Les patients atteints de SM ont une vitesse de dispersion de l’onde P supérieure et une Pmax plus élevée par rapport aux patients sans SM (DOP, 35,65 ± 4,36 vs 26,27 ± 4,04, p < 0,001 ; Pmax, 117,12 ± 10,77 vs 105,98 ± 9,02, p < 0,001), alors qu’aucune différence n’a été observée entre les valeurs Pmin de patients atteints de SM et les témoins (81,47 ± 9,54 vs 8,76 ± 79,70, p = 0,231). L’analyse multivariée pas à pas a révélé que l’indice HOMA était un facteur prédictif indépendant de la DOP (β = 3,115, p < 0,001) et de la Pmax (β = 7,175, p < 0,001).

Cette étude suggère que les patients atteints de sclérose en plaques ont un PH et Pmax prolongés. L’augmentation de ces paramètres peut être un indicateur pour l’identification de patients à un risque accru de fibrillation auriculaire.

Slow coronary flow (SCF) is defined as late opacification at the epicardial coronary arteries without stenosis, in this study we search the effect of isolated CSF on P-wave and QT-interval dispersion.

Thirty five patients with CSF (group 1), and 30 control subjects (group II) matched in sex and age. Both groups underwent a standard 12-lead surface electrocardiogram. Maximal (P max), minimal P-wave durations (P min), P dispersion (PD), and QT dispersion were measured. All patients underwent selective coronary angiography. Coronary flow rates were documented by Thrombolysis in Myocardial Infarction (TIMI) frame count.

CSF patients had more P maximum, P dispersion, C QT duration, QT dispersion, and C QT dispersion. TIMl frame counts of CSF patients were significantly higher than those of the control group for all three coronary vessels (P 0.0001). PD was positively correlated with LAD TIMI frame count (r = 0.42; P: 0.01); LCx TIMI frame count (r = 0.40; P: 0.01); and mean TIMI frame count (r = 0.44; P: 0.007), while weak correlated with RCA TIMI frame count (r = 0.22; and not statistically significant P: 0.18), C QT dispersion was positively correlated with LAD TIMI frame count (r = 0.54; P: 0.001); LCx TIMI frame count (r = 0.70; P: 0.001); and mean TIMI frame count (r = 0.50; P: 0.002), while weak correlated with RCA TIMI frame count (r = 0.24; and not statistically significant P: 0.15).

CSF was found to be associated with prolonged dispersion of P-wave and QT-interval.

Electroconvulsive therapy (ECT) consists of controlled convulsive seizure by electric stimulation of the brain. Although various electrocardiographic (ECG) changes have been reported during ECT, atrial conduction has not been studied extensively. The aim of the present study was to assess the effects of ECT on systemic arterial blood pressure and ECG parameters (P wave duration, P wave dispersion and heart rate).

Thirty depressive patients undergoing ECT were included. Echocardiographic examination was performed on all patients before ECT sessions to exclude systolic heart failure and diastolic dysfunction which may affect P wave duration and dispersion. Twelve-lead ECG records were obtained before the first ECT and after the third session of ECT. Blood pressure was measured before and after convulsive therapy session.

Compared to baseline values, maximum P wave duration (99.3±14.6 to 111.3±8.2 ms, P=.001), P wave dispersion (50±14.8 to 63.3±10.3 ms, P=.001), and systolic (110.7±12 to 116±12.2 mmHg, P=.043) and diastolic blood pressures (70.7±9.4 to 75.3±8.2 mmHg, P=.028) were significantly increased after convulsive therapy session.

We proposed that ECT alone or in combination with atypical antipsychotics or antidepressants may influence atrial conduction as evidenced by the significantly prolonged maximum P wave duration and P wave dispersion. Longer-term follow-up of patients undergoing ECT may be appropriate to evaluate the possible long-term outcomes of our short-term results.

Migraine patients can exhibit autonomic dysregulation, in turn leading to cardiac conduction and repolarization abnormalities. This systematic review and meta-analysis evaluated the electrocardiographic changes in migraineurs.

PubMed and Embase databases were searched for human studies using the search terms ‘migraine’ and ‘electrocardiogram’ until 15th December 2018, identifying 108 and 131 studies.

Thirteen studies involving 667 migraineurs and 208 normal subjects included (mean age = 30.7, total male percentage = 19.8%) were included. A longer mean QTc interval (standard mean difference = 7.89, 95% confidence interval = [3.29, 12.49], p = 0.0008) and higher frequency of QTc prolongation (risk ratio [RR] = 6.23, [2.86–13.58], p < 0.00001), but no difference in PR-interval (SMD = 4.33, [−3.90–12.56], p = 0.30) were observed during migraine attacks compared to pain-free periods. P-wave dispersion was higher in migraine patients compared to controls (mean difference = 3.62, [1.03–6.21], p = 0.006). RR-interval were statistically indistinguishable between migraine patients and controls (SMD = 0.08, [−0.65–0.81], p = 0.83), or between migraineurs with and without aura (SMD = −0.03, [−0.44–0.38], p = 0.89). Deep breathing ratio was significantly lower in migraineurs compared to controls (SMD = −0.27, 95% CI = [−0.46, −0.08], p = 0.006) but similar between migraineurs with and without aura (SMD = −0.04, [−0.27–0.19], p = 0.74). No significant difference in Valsalva ratio is found between migraineurs and controls (SMD = 0.10, [−0.32–0.53], p = 0.63) or between migraineurs with and without aura (SMD = −0.17, [−0.40–0.06], p = 0.14). Root mean square of successive differences (RMSSD) (SMD = −0.07, [−1.10–0.95], p = 0.89) and standard deviation of NN intervals (SDNN) (SMD = −0.10, [−0.61–0.41], p = 0.71) did not significantly differ between migraine patients and controls.

Electrocardiographic alterations are observed in migraine patients compared to controls, especially during migraine attacks.