Sergio Baratta

Clinical value of the tissue Doppler s wave to characterize left ventricular hypertrophy as defined by echocardiography.

Left ventricular hypertrophy (LVH) may be a physiological finding and may also be associated with different disease entities and hence, with different outcomes. Regional myocardial function can be assessed with color Doppler tissue imaging, specifically by the waveform of the isovolumic contraction (IC) period and the regional systolic wave (“s”). Methods and Results: We studied five groups (G): healthy, sedentary young volunteers (G1, n:10); healthy sedentary adult volunteers (G2, n:8); and subjects with LVH (left ventricular mass index >125 g/m2) including: high performance athletes (G3, n:21), subjects with hypertension (G4, n:21), subjects with hypertrophic cardiomyopathy (HCM) (G5, n:18). We measured peak “s” wave velocity (cm/sec) at the basal and mid septum, the IC/s ratio, and basal to mid‐septal velocity difference (BMVD) of the “s” wave. Regional “s” wave values (cm/sec) were G1 = 5.6 ± 1; G2 = 5.4 ± 0.8; G3 = 5.7 ± 0.6; G4 = 5.3 ± 1.1; G5 = 4.2 ± 1.1 (P < 0.0001). The IC/s ratio was G1 = 0.28 ± 0.18; G2 = 0.39 ± 0.21; G3 = 0.23 ± 0.10; G4 = 0.42 ± 0.15; G5 = 0.64 ± 0.15 (P < 0.0001). The BMVD (cm/sec) was G1 = 2 ± 0.51; G2 = 1.71 ± 0.29; G3 = 1.78 ± 0.44; G4 = 1.26 ± 0.96; G5 = 0.45 ± 0.4 (P < 0.0001). IC/s < 0.38 discriminated physiological from pathological forms of hypertrophy (sensitivity 90%; specificity 88%). Peak “s” wave velocity discriminated HCM from other causes of hypertrophy, with a cutoff value of 4.46 cm/sec (sensitivity 72%; specificity 90%). BMVD <0.98 cm/sec detected HCM with 89% sensitivity and 86% specificity. Conclusions: Peak “s” wave velocity and two indices: IC/s and BMDV are novel parameters that may allow to discriminate physiological from pathological forms of hypertrophy as well as different subtypes of hypertrophy. (ECHOCARDIOGRAPHY 2010;27:370‐377)

Loss of dystrophin is associated with increased myocardial stiffness in a model of left ventricular hypertrophy

Transition from compensated to decompensated left ventricular hypertrophy (LVH) is accompanied by functional and structural changes. Here, the aim was to evaluate dystrophin expression in murine models and human subjects with LVH by transverse aortic constriction (TAC) and aortic stenosis (AS), respectively. We determined whether doxycycline (Doxy) prevented dystrophin expression and myocardial stiffness in mice. Additionally, ventricular function recovery was evaluated in patients 1 year after surgery. Mice were subjected to TAC and monitored for 3 weeks. A second group received Doxy treatment after TAC. Patients with AS were stratified by normal left ventricular end-diastolic wall stress (LVEDWS) and high LVEDWS, and groups were compared. In mice, LVH decreased inotropism and increased myocardial stiffness associated with a dystrophin breakdown and a decreased mitochondrial O2 uptake (MitoMVO2). These alterations were attenuated by Doxy. Patients with high LVEDWS showed similar results to those observed in mice. A correlation between dystrophin and myocardial stiffness was observed in both mice and humans. Systolic function at 1 year post-surgery was only recovered in the normal-LVEDWS group. In summary, mice and humans present diastolic dysfunction associated with dystrophin degradation. The recovery of ventricular function was observed only in patients with normal LVEDWS and without dystrophin degradation. In mice, Doxy improved MitoMVO2. Based on our results it is concluded that the LVH with high LVEDWS is associated to a degradation of dystrophin and increase of myocardial stiffness. At least in a murine model these alterations were attenuated after the administration of a matrix metalloprotease inhibitor.

Obstructive Membrane at the Base of the Left Atrial Appendage, a Multi‐Imaging Approach

The left atrial appendage (LAA) is a small muscular extension that grows from the anterolateral wall of the left atrium, in the proximity of the left pulmonary veins. The presence of a membrane in the LAA is a rare clinical entity whose origin is not known. Its clinical implication in the genesis of atrial arrhythmias and thromboembolic risk remains unknown. We report a case of an obstructive membrane located at the base of the LAA, found incidentally in a young patient who was initially undergoing a transesophageal echocardiogram prior to an invasive treatment for atrial fibrillation.

When prevention is a risk. More is not always better.

In spite of complex interactions between drugs and dietary supplements, which increase with the number of them taken, the medical, or on occasions, the patient’s judgment tends to be fast and dichotomous. Many contexts of clinical practice do not have scientific evidence derived from randomized clinical trials and action is based on physiopathological or simply epidemiological analysis, and in worst cases personal or common beliefs. Karny-Rahkovich et al’s. study [1] evaluated the use of dietary supplements in 149 patients with cardiovascular (CV) disease who consulted an Internal Medicine Ward and an Emergency Cardiology Clinic. Despite being a small sample, high use of dietary supplements (45%) associated with older age, female sex and a physical activity routine was observed. They also identified 16 potential interactions between the prescribed medical treatment and dietary supplements. It would have been interesting to compare the rate of use of dietary supplements with a control group without CV disease. The study repeats the finding that people who carry out physical activity refer greater consumption of potentially harmful supplements of unproven usefulness. The work details the potentially dangerous interactions between drugs and dietary supplements, although the clinical impact is not fully known [1]. In this sense, the association of elevated levels of homocysteine with higher CV risk and the possibility of its descent through the use of folic acid lead many our colleagues to indicate it systematically. The subsequent randomized studies have shown that the administration of folic acid to reduce levels of homocysteine not only does not reduce CV risk, they also showed that the administration of vitamin B caused an increase in mortality [2]. The association between vitamin E intake and lower incidence of CV events was demonstrated following an epidemiological prospective observational study conducted on nurses. This finding generated a large increase in the consumption of antioxidants such as vitamin E, even among American doctors. Subsequently, several randomized clinical trials on large cohorts highlighted the absence of any protective effect on vascular events and even a higher risk if used in high doses [3]. In spite of the benefits of vitamin C on endothelial function and the popular acceptance of its benefits, the systematic administration of a vitamin complex (600 mg vitamin E, 250 mg vitamin C, and 20 mg beta-carotene daily) in a multicenter study dismissed the improvement in the prognosis, yet not causing higher rate of adverse effects [4]. Finally, a meta-analysis that included 68 studies showed that the administration of antioxidants was associated with an increase in mortality: beta-carotene (vitamin B) — RR 1.07 (95% CI 1.02– –1.11), vitamin A — RR 1.16 (95% CI 1.1–1.24), vitamin E — RR 1.04 (95% CI 1.01–1.07) with no defined adverse effects and no clear benefits with vitamin C or selenium supplements [5]. The evidence showing CV benefit from the use of vitamin D is not conclusive in spite of the fact that in epidemiological studies the reduction in vitamin D levels has been linked to an increased risk of developing CV disease. Vitamin D3 seems to decrease the mortality in the elderly, vitamin D2, alfacalcidol and calcitriol do not have statistically significant effects on mortality, vitamin D3 combined with calcium increases the rate of nephrolithiasis and alfacalcidol as well as calcitriol

HUMORAL MARKERS, CONVENTIONAL DOPPLER ECHOCARDIOGRAM AND BIDIMENSIONAL STRAIN IN THE DETECTION OF MYOCARDIAL TOXIC EFFECT SECONDARY TO CHEMOTHERAPY

Aim: Analyze the usefulness of humoral markers (quantitative troponin T (TT), BNP, NT pro-BNP), conventional and the two-dimensional longitudinal strain (LS), and radial strain (RS) in the prediction of ventricular systolic dysfunction in patients treated with cardiotoxic chemotherapy. Thirty six