Measuring of the stiffening of arteries and the cardiac muscle

The classical method to measure stiffening of arteries and the cardiac muscle is measurement of pulse wave velocity (PWV). Currently carotid to femoral PWV is considered the gold standard. However, this method is inconvenient and only moderate correlations have been found between measurements from different anatomic areas. Also, obesity status is a strong predictor for an unsuccesfull examination in about 10 % of obese subjects. Maybe the most accurate method to measure stiffening is cardiovascular magnetic resonance examination. It is, however, too expensive for wide use in preventive medicine.

ELECTROCARDIOGRAPHY (ECG) is the most commonly used method for clinical cardiovascular study in the world . Its great advantages are noninvasiveness, low cost, its easy use and easy digital handling of the electronic amplitude measurements. It can be recorded all over the world. However, detection of quantitative precordial ECG amplitudes compared to other human beings (interindividual variability) is not possible because of individual differences in congenital factors like, for instance, skeletal dimensions and others, that cannot be measured noninvasively.

In intraindividual amplitude changes the congenital differences between different individuals, such as differences in skeletal dimensions and possible differences in the conduction system of the heart, play practically no role. However, there is variability also in intraindividual amplitude changes. Intraindividual variability is a hindrance in serial ECG analysis, where ECGs of the same individual, but taken at different points of time, are compared. Two sources of the intraindividual variability can be distinguished as follows: variability related to the technical circumstances during ECG recording and non-pathologic biologic variability. Among the technical sources, variation in the electrode positioning between recordings, especially, in near the heart situated chest leads, is the most confusing.

The most important biological sources are intraindividual weight changes. Therefore, using of a standardized accurate and reproducible electrode placement method, especially in chest leads, and correction of the individual confounding factor´s effect on the amplitude measurements is necessary. To understand the effect of arterial and cardiac muscle stiffening on ECG amplitudes the different genesis of depolarization and repolarization amplitudes must be known. Although the R wave is largely an expression of the ordered, sequential activation of myocardial fibers, the orientation of the T wave is dependent both on the sequence of repolarization and the comparative local durations of this recovery process. Therefore, the blood volume dependent T wave amplitudes change before changes in QRS amplitudes.

It has been known for years that hypertension and age dependent stiffening of arteries and the cardiac muscle result in a change in certain cardiac QRS voltages in. Criterions of left ventricular hypertrophy, like Sokolow-Lyon index and Cornell voltage have been studied most. Both of them increase with developing of hypertension and cardiovascular ageing. Cardiac depolarization dependent QRS amplitudes of ECG have been found to respond to changes in the status of hypertension and cardiovascular ageing by both decreasing and increasing, before the measured blood pressure. So far the significant changes in the voltages have been possible to identify statistically only by using mean values of a large population because of the today`s inaccurate and nonreproducible amplitude measurement methods.

The relation of cardiac repolarization dependent T wave amplitude to the stiffening has not been studied so much as that of QRS amplitudes. However, in the 21st century T wave decrease has been found to indicate prehypertension in many studies. In the most recent reports a correlation has been found also between stiffening of the cardiac muscle in magnetic resonance examination and T wave decreas). The above mentioned T wave amplitude changes are, however, so small that they cannot be measured reliably for an individual using to-day`s routine used methods. The effects of non-living cardiovascular elements, like left ventricular hypertrophy changes in ECG, may take weeks to appear (10). However, the changes of living cardiovascular elements, for instance on left ventricular and blood volume dependent changes in ventricular repolarization, especially T wave amplitude group changes, may be seen in seconds. In the light of the above mentioned, the first amplitude measurements can be compared only to the normal values of the same age group. The most important thing to see is the possible amplitude changes during the follow-up.

ESSENTIAL REFERENCES

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