Relation of atrial electromechanical delay to P-wave dispersion on surface ECG using vector velocity imaging in patients with hypertrophic cardiomyopathy.

OBJECTIVES: Heterogeneity of structural and electrophysiologic properties of atrial myocardium is common characteristic in hypertrophic cardiomyopathy (HCM). We assessed the dispersion of atrial refractoriness on surface ECG using P-wave dispersion (PWD) and its relation to atrial electromechanical functions using vector velocity imaging (VVI) in HCM population. METHODS: Seventy-nine HCM patients (mean age: 43.7 ± 13 years, 67% male) were compared with 25 healthy individuals as control. P-wave durations, Pmax and Pmin , P-wave dispersion (PWD), and P terminal force (PTF) were measured from 12-lead ECG. LA segmental delay (TTP-d) and dispersion (TTP-SD) of electromechanical activation were derived from atrial strain rate curves. RESULTS: HCM patients had longer PR interval, PW duration, higher PWD, PTF, QTc compared to control (p < .001). HCM patients were classified according to presence of PWD into two groups, group I with PWD > 46 ms (n = 25) and group II PWD ≤ 46 ms (n = 54). Group I showed higher prevalence of female gender, higher PTF, QTc interval, left ventricular outflow tract (LVOT) obstruction, p < .01, LVOT gradient (p < .001), LV mass index (p < .01), E/E' (p < .01), and severe mitral regurgitation (p < .001). Moreover, PWD was associated with increased atrial electromechanical delay (TTP-d) and LA mechanical dyssynchrony (TTP-SD), p < .001. LA segmental delay and dispersion of electromechanical activation were distinctly higher among HCM patient. CONCLUSION: PWD is simple ECG criterion, and it is associated with more severe HCM phenotype and LA electromechanical delay while PTF is linked only to atrial remodeling.

Asynchrony of left ventricular systolic performance after the first acute myocardial infarction in patients with narrow QRS complexes: Doppler tissue imaging study.

BACKGROUND: Left ventricular (LV) electromechanical delay results in asynchronized contraction. However, it is not known if the presence of cardiac diseases without QRS prolongation may result in interventricular or intraventricular asynchrony. Doppler tissue imaging is now established for detecting regional contractile abnormalities and asynchrony in the LV. OBJECTIVES: The aim of the study was to assess the degree of LV asynchrony after the first acute myocardial infarction (AMI) in patients with a narrow QRS complex using Doppler tissue imaging and correlate this with the site and extent of the infarction. METHODS: Echocardiography with Doppler tissue imaging was performed within 1 week of AMI in 155 patients and compared with 50 age- and sex-matched healthy volunteers. Regional myocardial velocities were assessed at the 4 mitral annular sites, and the corresponding systolic velocity (Sm), early diastolic velocity (Em), time to peak Sm (Ts), and time to peak Em (Te) were measured. To assess LV synchronicity, SDs of Ts (Ts-SD) and Te (Te-SD) of all the 4 mitral annular sites were computed. Location and size of infarct were confirmed by echocardiographic wall-motion score index. RESULTS: QRS complex duration was normal in all patients. Wall-motion score index was significantly higher in patients with anterior than inferior AMI (2.02 +/- 0.34 vs 1.24 +/- 0.21, P < .001). Ts-SD was significantly higher in patient than control group, and in patients with anterior than inferior AMI (38.21 +/- 2.59 vs 21.06 +/- 0.52 milliseconds and 43.18 +/- 3.77 vs 33.24 +/- 1.4 milliseconds, respectively, P < .001 for each), whereas Te-SD did not differ significantly among these groups (20.35 +/- 1.77 vs 18.17 +/- 1.14 milliseconds and 21.6 +/- 1.35 vs 19.1 +/- 1.11 milliseconds, respectively, P > .05 for each). A strong positive correlation was detected between LV systolic asynchrony (Ts-SD) and wall-motion score index (r = .77), LV mass (r = .67), LV end-systolic dimension (r = .65), and LV end-diastolic dimension (r = .5). The correlation was negative with LV ejection fraction (r = -.70) and Sm (r = -.6); the correlation was weak with Em (r = -.33) (P < .001 for all). In multivariate logistic regression analysis, infarct size was found to be the most independent predictor for systolic asynchrony (odds ratio 3.59, 95% confidence interval [1.43-9.33], P < .001). CONCLUSION: AMI has a significant impact on regional myocardial contractility and LV systolic (but not diastolic) synchronicity early in the course even in the absence of QRS widening or bundle branch block. The degree of LV systolic asynchrony is greater with anterior than inferior AMI and mainly determined by infarct size.

Impact of type 2 diabetes mellitus on aortic elastic properties in normotensive diabetes: Doppler tissue imaging study.

OBJECTIVES: The stiffening of aorta and other central arteries is a potential risk factor for increased cardiovascular morbidity and mortality. The association of hypertension with type 2 diabetes may obscure the degree to which diabetes alone contributes to impaired arterial function. This study examined whether the presence of type 2 diabetes alone is associated with an impaired aortic mechanical function in patients with or without coronary artery disease (CAD). METHODS: In all, 154 patients were recruited and assigned to groups A (n = 46, type 2 diabetes with no CAD), B (n = 64, nondiabetic CAD), or C (n = 44, diabetes with CAD) and 20 age- and sex-matched healthy participants were enrolled in a control group. Patients were recruited from those sent for coronary angiography. CAD was excluded for group A. Pulse pressure, aortic strain, and distensibility were calculated from the aortic diameters measured by echocardiography and blood pressure obtained by sphygmomanometer. Aortic wall systolic velocity was measured using pulsed wave Doppler tissue imaging. RESULTS: Pulse pressure was significantly higher in patient groups A, B, and C in comparison with control group (40.2 +/- 9, 40.1 +/- 11, and 50.2 +/- 13 vs 35.5 +/- 9 mm Hg [P < .01], respectively). The pulsatile change in the aortic diameter and distensibility were less in the patient groups than in the control group (11 +/- 4%, 8 +/- 5%, and 8 +/- 4% vs 17 +/- 9% [P<.001], and 6 +/- 2, 6 +/- 1, and 3 +/- 2 vs 10 cm(2)/dyne/10(3), respectively). In addition, the aortic wall systolic velocity was significantly lower in patient groups compared with control group (6 +/- 2, 6.1 +/- 1, and 5.1 +/- 1 vs 8.5 +/- 1.5 cm/s [P < .01], respectively). Although aortic function parameters were very declined for group C, there was no significant difference between groups A and B that reflected equivalent risk. In diabetic groups A and C, aortic strain, distensibility, and aortic wall systolic velocity showed strong negative correlation with the duration of diabetes (r = -.53, r = -.68, and r = -.56, respectively) and glycosylated hemoglobin (HBA(1)) (r=-.64 [P < .01], r = -.77 [P < .001], and r = -.57 [P < .01], respectively). CONCLUSION: The increased aortic stiffness that affects patients with type 2 diabetes seems to be an early event that may explain why patients with diabetes have a particularly high risk of developing cardiovascular complications. Poor glycemic control and duration have detrimental effect on aortic elastic properties.