Electrocardiogram Derived QRS Duration >120 ms is Associated With Elevated Plasma Homocysteine Levels in a Rural Australian Cross-Sectional Population

Abstract

Homocysteine levels in the low to moderate range for cardiovascular risk have been previously associated with left ventricular cardiac hypertrophy (LVH). Electrocardiogram (ECG) derived QRS duration has also been used as an epidemiological screening marker for cardiac hypertrophy risk. QRS duration cut offs have not been previously modeled to assess homocysteine levels in community populations. Our aims are to determine if QRS duration is associated with an elevated homocysteine level in a cross-sectional Australian aging rural population.A retrospective study design utilizing a rural health diabetic screening clinic database containing observational data from the period January 9, 2002 till September 25, 2012. One hundred seventy-eight individuals (>21 years of age) from the database were included in the study. Inclusion criteria included being nondiabetic and having both a QRS duration measure and a matching homocysteine level within the same subject. All participants were from the Albury-Wodonga area, with a mean age of >64 years for both sexes.Mean population homocysteine plasma levels were 10.4 μmol/L (SD = 3.6). The mean QRS duration was 101.8 ms (SD = 17.4). Groups were stratified on the basis of QRS duration (≤120 ms [n = 157] and >120 ms [n = 21]). QRS duration subgroup (≤120 ms vs >120 ms) mean differences across homocysteine levels were 10.1 μmol/L (SD = 3.3) and 12.2 μmol/L (SD = 4.7), respectively (P = 0.016). Other ECG parameters (PQ interval, QTc interval, and QT dispersion) measurements were not significantly associated with differences in plasma homocysteine (P = not significant).We conclude that in community populations homocysteine may be moderately elevated when QRS durations are >120 ms. Small additional increases in homocysteine levels may suggest a risk factor for ECG diagnosis of LVH.

Plasma homocysteine levels associated with a corrected QT interval

“…Acampa found that, in OHT patients, plasma Hcy levels significantly correlated with PWD, whereas no correlation was found with the QTc interval [13]. Lee Yin Leng et al concluded that in community populations, homocysteine was moderately elevated when QRS durations were >120 ms, but QTc intervals were not significantly associated with plasma homocysteine [26]. In our study, Linear regression and multiple logistic regression analyses results showed an association between QTc interval and Hcy levels.…”

“…The QT interval is measured from the earliest detection of depolarization in any lead to the latest detection of repolarization in any lead. Since the QT interval is influenced by heart rate, it is necessary to adjust heart rate for QT correction [26]. In this study, the QTc interval was corrected for the heart rate using the Bazett formula, which is the most common method [27–29].…”

Electrocardiogram derived QRS duration associations with elevated central aortic systolic pressure (CASP) in a rural Australian population

“…Resting 12-lead electrocardiograms were obtained from each subject using a Welch Allyn PC-Based ECG system as previously described [ 4 ]. This permitted automated QRS duration calculation from a 10 s ECG trace.…”

“…Electrocardiogram (ECG) derived QRS durations >100 msec and >120 msec have been both associated with hypertension induced increases in left ventricular (LV) mass [ 1 – 4 ]. Myocardial hypertrophy can alter LV tissue repolarisation and slowing of transmural conduction velocity [ 5 , 6 ].…”

Systolic blood pressure but not electrocardiogram QRS duration is associated with heart rate variability (HRV): a cross-sectional study in rural Australian non-diabetics

“…Our main findings do not support the hypothesis that R-R derived HRV parameters are associated with increasing QRS duration in non-diabetics. The QRS duration cut offs that we modeled would reflect both normal and underlying conduction disturbances observed in rural communities [ 6 , 16 ]. QRS duration greater than 120 msec in our cohort were most likely due to pre-existing cardiovascular disease, age related aortic stiffening, remodeling and or conduction slowing [ 6 ].…”