Homocysteine increase after acute myocardial infarction--can it explain the differences between case-control and cohort studies?

Several case-control studies agree that elevated homocysteinemia (HC) is a risk factor for cardiovascular disease, particularly for acute myocardial infarction (AMI). However, this agreement does not extend to prospective studies--some of which confirm and others (MRFIT and Karelia) reject this relation. After an AMI there are significant changes in biochemical and laboratory parameters, including a decrease in cholesterolemia, which takes several months to return to baseline levels. The evolution of HC after AMI is still unknown. In this work we set out to evaluate the evolution of homocysteinemia values after acute myocardial infarction. We evaluated fasting homocysteinemia in 34 sequential patients after admission to the Intensive Care Unit and after confirmation of acute myocardial infarction (26 male; mean age 63.8 +/- 13.9 years) in the first 36 hours, between the 3rd and 6th day, and one month after AMI. Simultaneously, we studied traditional risk factors and performed routine laboratory tests. The mean values found for HC were 13.85 +/- 5.46 mol/l in the first 36 hours after AMI, 16.16 +/- 6.63 mol/l between the 3rd and the 6th day, and 16.27 +/- 7.27 mol/l one month after myocardial infarction. The difference between the first and the second, and between the first and the third measurements, was significant (p < 0.05). The HC values found 3-6 days and one month after myocardial infarction were similar (p = 0.88). A highly significant correlation was found between HC values assessed in the first and second (correlation coefficient [CC] = 0.62) and in the second and third measurements (CC = 0.57), both with p = 0.001. We can conclude that HC levels increase significantly 36 hours after an acute myocardial infarction, an increase of around 20%, which is maintained until at least one month after the infarction. In these circumstances the difference in the vascular risk of HC found between case-control and prospective studies may be explained, at least partially, by the HC increase after AMI.

Tissue Doppler imaging and long axis left ventricular function: hypertrophic cardiomyopathy versus athlete's heart.

BACKGROUND: The different diagnosis between hypertrophic cardiomyopathy and athlete's heart has important clinical implications. The assessment of long axis left ventricular function with tissue Doppler imaging in hypertrophic cardiomyopathy (showing systolic and diastolic dysfunction with heterogeneity and asynchrony), may be useful in the differentiation of these situations. AIM: To study, with tissue Doppler imaging, long axis left ventricular function in a population of athletes (rowers) and to compare it with a population of non-obstructive hypertrophic cardiomyopathy patients. METHODS: In 24 patients with non-obstructive hypertrophic cardiomyopathy and in 20 competitive rowers with similar age, blood pressure and heart rate, we analyzed mitral annulus motion with pulsed tissue Doppler imaging in the 4 sides of the annulus (septal, lateral, inferior, anterior), in apical views. In each wave (systolic, rapid filling and atrial contraction) we measured velocities, time intervals and velocity-time integrals, and calculated heterogeneity and asynchrony indices. Data were compared between the groups, between the different sides in each group ("parallel analysis") and with conventional indices of global function. RESULTS: Hypertrophic cardiomyopathy patients showed: systolic function: lower velocities and integrals, shorter ejection time and shorter systolic time. These abnormalities occurred even in annular sites contiguous to walls without hypertrophy. DIASTOLIC FUNCTION: Much lower rapid filling velocities and integrals, lower atrial contraction velocities and integrals, lower e/a, longer isovolumic relaxation time and time to peak rapid filling wave. These abnormalities occurred even in annular sites adjacent to walls without hypertrophy. In the athletes group, the e/a ratio was never < 1, in any annular site. In hypertrophic cardiomyopathy patients this ratio was < 1 in 27% of the sites. CONCLUSIONS: 1--Systolic and diastolic long axis left ventricular function is different in hypertrophic cardiomyopathy and in athletes, in all mitral annulus sides. 2--The presence of these abnormalities in annular sites contiguous to walls without hypertrophy suggests that this technique may be useful in the differential diagnosis between these groups, particularly in the "gray zone" of Maron.