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AIMS: The prognostic role of inflammation in peripheral arterial disease (PAD) remains to be conclusively established. Accordingly, in these patients we investigated the impact of myeloperoxidase (MPOx) and C-reactive protein on the incidence of myocardial infarction and stroke. METHODS AND RESULTS: Of 156 PAD patients, 10 had a myocardial infarction and seven a stroke, during follow-up. We used the receiver operating characteristic curve analysis and the bootstrap approach to identify the MPOx, C-reactive protein, and ankle brachial index (ABI) threshold levels that provided the best cut-off to predict the outcome. For MPOx a cut-off > or =183.7 pM was independently associated with a poor outcome (HR = 6.80, 95% CI 1.20-38.69, P = 0.031). The result remained unmodified when MPOx was used as a continuous variable (HR = 1.03, 95% CI 1.01-1.05, P = 0.031). Conversely, C-reactive protein was not a prognostic determinant in our series (HR = 0.88, 95% CI 0.60-1.29, P = 0.514). Kaplan-Meier curves for the four groups of patients delineated according to ABI and MPOx values identified using the bootstrap approach showed that the addition of MPOx measurement to ABI improved the ability to identify patients at risk for myocardial infarction and stroke. CONCLUSION: In PAD, MPOx, but not C-reactive protein, predicts an increased risk of major cardiovascular events, and adds to the prognostic value of ABI, currently the most powerful prognostic indicator in these patients.

The effects of vigorous training on left ventricular structure and function were evaluated in 15 top level rowers using electrocardiography, Doppler echocardiography and radionuclide angiography. All subjects were studied after 1 month of deconditioning and again after 5 months of vigorous training. After training there was an increase in the ventricular hypertrophy voltage criteria proposed by Sokolow-Lyon and by Friedman but not in that proposed by Casale; T wave amplitude in leads V5 and V6 increased in nine subjects, was unchanged in one and decreased in five; the mean values were also unchanged. Training induced a significant increase in left ventricular end-diastolic and end-systolic diameter and in left ventricular mass index, while peak systolic stress and mean wall stress index decreased. No change was detected after training in the mean values of Doppler echocardiographic and radionuclide angiographic data; nevertheless a significant relationship was found between changes in T wave height in V5 or V6 and in peak filling rate, and between changes in T wave height and ejection fraction. Our study confirms that the effect of vigorous training on left ventricular mass and dimensions does not include changes in mean values of systolic and diastolic function. The relationship between change in T wave amplitude and in peak filling rate values suggests that some metabolic or neurohumoral derangement occurs in the subset of athletes with T wave flattening, that is responsible for the slight reduction in peak filling rate and ejection fraction.

The presence and the characteristics of left ventricular diastolic dysfunction in mild to moderate systemic hypertension were evaluated in 13 normotensive subjects (Group I), in 12 hypertensive subjects without (Group II) and 28 with (Group III) LV hypertrophy who underwent two-dimensional Doppler echocardiographic study. Among Group III patients, a subset (n = 12) with a dilated left ventricle was identified. Diastolic filling parameters were impaired in Group III patients while, in Group II, they were intermediate between Groups I and III. In all Group III patients normalized peak filling rate (nPFR) correlated directly with mean velocity of circumferential fibre shortening (mVCF) (r = 0.55; P less than 0.001) and inversely with left ventricular mass index (LVM) (r = -0.60; P less than 0.001), left ventricular end-diastolic diameter (LVIDd) (r = -0.63; P less than 0.001), LV peak systolic stress (LVWST) (r = -0.64; P less than 0.01). A separate analysis showed that these correlations were also present in patients without left ventricular dilation; in the subset with left ventricular dilation nPFR correlated only with LVWST (r = -0.73; P less than 0.01), but not with LVM, mVCF, LVIDd. Thus, left ventricular hypertrophy is one of the major determinants of diastolic dysfunction in hypertensives; other factors influence nPFR values in hypertensive patients when the left ventricle dilates.