 |
International Journal of Bioelectromagnetism Vol. 5, No. 1, pp. 199-200, 2003. |
 |
 |
www.ijbem.org |
|
IIM QRS in Concentric Left Ventricular Hypertrophy Katarína Kozlíkováa,
Juraj Martinkaa, Ján Murínb aInstitute of Medical Physics and Biophysics, Comenius University, Medical
Faculty, Correspondence: K Kozlíková, Institute of Medical Physics
and Biophysics, Comenius University, Medical Faculty, Abstract. When
left ventricular hypertrophy (LVH) is evaluated by electrocardiographic means,
amplitude and time criteria are used assuming increased voltage and prolonged
duration. We tested whether there is increased time integral in chest leads
when using isointegral body surface mapping for detection of concentric LVH.
Mean isointegral maps of QRS complex (IIM QRS) and its thirds were constructed
using the lead system after Barr in 12 patients with concentric LVH based
on echocardiographic examination and in 22 controls. Values of map extrema
were analysed. Extreme values of patients’ maps tended to be lower than in
controls. There were significant differences concerning minima and peak-to-peak
values. Concentric LVH caused preferably voltage decrease in IIM QRS and its
parts in accordance with model studies and published standard electrocardiograms.
No published mapping data concerning IIM QRS with strictly defined concentric
LVH have been found yet.
Keywords: Left Ventricular Hypertrophy; Electrocardiography; Body Surface Mapping; Isointegral Maps 1. Introduction One way how to diagnose left ventricular (LV) hypertrophy (LVH) is the use of electrocardiographic criteria resulting from the 12-lead electrocardiogram. Increased voltage during QRS complex in single leads and their combination is considered (Milliken et al., 1989). Papers using the voltage-duration products of QRS complex or the more precise time integrals in chest and limb leads were also published (Okin et al., 1995; Jerm, 1997). Spatial analogy of single leads time integral is the isointegral map (IIM) when using electrocardiographic body surface mapping. We wanted to find out whether the hypothesis of increased time integrals holds in patients with concentric LVH when using IIM QRS. 2. Material and Methods Thirty-three patients with hypertension (20 men) were examined for LVH. It was considered as present if the LV mass (LVM) over the body surface area (BSA [m2]), represented by the LVM index LVMI [g/m2], exceeded the borderline value (LVMI > 125 g/m2, Bulas et al., 1998). Echocardiographic examination of ventricular walls and chamber were done during diastole using the M mode (Devereux, 1987). A group with concentric LVH was chosen (12 patients, 55 ± 12 years old, 7 men) according to the relative wall thickness RWT > 0.45 and without LV dilation (men: LVIDd Ł 5.9 cm, women: LVIDd Ł 5.4 cm, Bulas et al., 1998). The control group involved 22 subjects, 32 ± 14 years old (14 men), with no history of any cardiovascular disease and normal 12-lead ECG findings. We used the limited 24-lead system after Barr implanted in the mapping system ProCardio for the body surface mapping of the electric heart field (Rosík et al., 1997). The onset and offset of the QRS complex was established manually from the root mean square signal (Kozlíková, 1997). We constructed the IIM of the whole QRS complex (IIM QRS) and its thirds of equal duration – the initial third (IIM QRS1/3), the middle third (IIM QRS2/3) and the terminal third (IIM QRS3/3). We assumed that the initial third of QRS complex displays mainly the activation of septum, the middle third mainly the apical part of ventricles and the terminal third the free ventricular walls and their basal parts. Analysis of variance, unpaired t-test and Mann-Whitney test for medians were used for statistical evaluation. Value p < 0.05 or less was considered statistically significant. 3. Results Mean IIM of the control group showed smooth dipolar distributions of time integrals on the chest in all parts of the QRS complex. Both IIM QRS2/3 and IIM QRS revealed negative potentials over the right upper chest and back, positive potentials over the precordium and lower parts of chest with horizontally oriented zero line. In the IIM QRS1/3, the positivity covered almost the whole anterior chest and the negativity the back with zero lines oriented vertically. Distribution of potentials in IIM QRS3/3 had opposite polarity with dominating negativity. Mean IIM in concentric LVH showed smooth dipolar distributions. The IIM QRS1/3 and IIM QRS3/3 map patterns resembled the corresponding maps of control group. IIM QRS2/3 and IIM QRS displayed ventricular orientation of zero line and negativities over the left chest with more separated maxima and minima. Extremes of mean maps in LVH were always smaller (in absolute value) than those of control group except for the IIM QRS3/3 maximum. We found lower minima (less negative) in concentric LVH IIM compared to the controls’ IIM. Significant differences were in the terminal third and the whole QRS complex (IIM QRS3/3, IIM QRS). Similar trend was seen in the case of peak-to-peak values where patients’ values were lower than were those of the control group. Significant differences were found in the middle third and the whole QRS complex (IIM QRS2/3, IIM QRS). 4. Discussion and Conclusions Our results are supported by model studies, in which it was found that concentric (“centripetal”) hypertrophy results in a decrease of resultant cardiac vector magnitudes during the first half of ventricular activation followed only by a slight increase (Szathmáry et al., 1994). Another model study based on concentric spheres showed that if wall thickness increases completely at the expense of intracavitary space, i.e. the blood mass is reduced, surface potential falls despite the increase in LV muscle mass (Rudy, 1987). This may be due not only to decreased Brody effect but also due to cancellation effects mainly if we consider the whole QRS complex. The activation fronts in the walls spread in opposite directions and we can assume that there is no change in the heart – chest geometry. Our results and mentioned model studies are in accordance with a clinical study that compared the heart geometry and LV mass obtained from LV cineangiograms with electrocardiographic appearance of LVH based on voltage criteria in limb and chest leads (Antman et al., 1979). It was found that wall thickening sufficient to result in an increased LVM did not result in LVH on the ECG unless sufficient concurrent chamber dilation was present. But a normal wall thickness could produce LVH on the ECG in a patient with increase in ventricular volume sufficient to increase the total LVM. No mapping data concerning IIM QRS with strictly geometrically defined concentric LVH have been published yet. References Antman EM, Green LH, Grossman W, Physiologic determinants of the electrocardiographic diagnosis of left ventricular hypertrophy. Circulation 1979; 60(2): 386-396 Bulas J, Murín J, Kozlíková K, Echocardiographic characteristics of left ventricular hypertrophy. Kardiológia/Cardioogy. 1998; 7(2): 92-98 (in Slovak) Devereux RB, Detection of left ventricular hypertrophy by M-mode echocardiography. Anatomic validation, standardization and comparison to other methods. Hypertension 1987; 9( suppl. II): II19-II26 Jern S, Assessment of left ventricular hypertrophy in patients with essential hypertension. Blood Pressure 1997; 2: 16-23 Kozlíková K, Body surface integral maps, their characteristics and methods of quantitative analysis. Bratislava Medical Journal 1990; 91(11): 815-823 (in Slovak) Milliken JA, Macfarlane PW, Veitch Lawrie TD, Enlargement and hypertrophy. In: Macfarlane PW, Veitch Lawrie TD, eds. Comprehensive Electrocardiology. New York: Pergamon Press, 1989: 631-670 Okin PM, Roman MJ, Devereux RB, Kligfield P, Electrocardiographic identification of left ventricular mass by simple voltage-duration products. Journal of the American College of Cardiology 1995; 25: 417-423 Rosík V, Tyšler M, Turzová M, Portable device for ECG mapping. In: Frollo I, Plačková A, eds. Measurement’97. Proceedings, International conference of measurement. Bratislava: SAS, 1997: 367-370 Rudy Y, The effects of the thoracic volume conductor (inhomogeneities) on the electrocardiogram. In: Liebman J, Plonsey R, Rudy Y, eds. Pediatric and fundamental electrocardiography. Boston: Martinus Nijhoff Publishing, 1987: 49-73 Szathmáry V, Ruttkay-Nedecký I, Osvald R, Computer simulation of propagated activation in different types of left ventricular enlargement. Computer Methods and Programs in Biomedicine 1994; 44(2): 85-91
© International Society for Bioelectromagnetism
|
