Strain Pattern on Electrocardiogram Is Associated with Increased Carotid Intima-Media Thickness in Patients with Aortic Valve Stenosis.

BACKGROUND: Coronary artery disease is present in at least 30% of patients with degenerative aortic stenosis (AS). Atherosclerosis also performs an important role in the progression of AS, because of the similarities of pathological mechanisms in both conditions. The electrocardiogram (EKG) strain pattern is associated with structural myocardial change and subendocardial ischemia and has been worldwide used as a marker of AS severity. We hypothesized that EKG strain pattern would be a marker of atherosclerosis as well in AS patients. The aim of this study was to associate the presence of EKG strain pattern in AS patients with the carotid intima-media thickness (CIMT). METHODS: Fifty-two consecutive patients referred from the cardiology clinic with moderate or severe AS were included in the study and underwent clinical evaluation, EKG, transthoracic echocardiography, and carotid ultrasonography, following statistical analysis of the results. RESULTS: There was a significant association between left ventricular EKG strain and increased CIMT (P = 0.001). The presence of strain increased the odds of abnormal CIMT (P = 0.004, odds ratio 9.7, 95% confidence interval 2.4-45.0), in a model adjusted for age and clinical diagnosis of systemic arterial hypertension. Additionally, EKG strain was associated with the presence of atherosclerotic plaque in at least one carotid artery (P = 0.011). CONCLUSION: Our results suggest that AS patients with EKG strain pattern should be further investigated for the diagnosis of subclinical atherosclerotic disease.

Ventricular systolic reserve in asymptomatic children previously treated with low doses of anthracyclines: a longitudinal, prospective exercise echocardiography study.

BACKGROUND: The time course of mild cardiotoxicity induced by anthracycline remains unknown. The aim of this study was to evaluate the long-term evolution of decreased myocardial reserve in children previously treated with a cumulative dose of anthracycline up to 100 mg/m(2). PATIENTS AND METHODS: Twenty-seven asymptomatic cancer survival patients (25 with lymphoblastic leukemia), in continuous remission and off treatment for >12 months with no alterations in conventional echocardiograms were evaluated by exercise echocardiography at 37 ± 15.4 months (T1) and 101 ± 24 months (T2) after finishing treatment (ADRIA group). This group was compared with 25 healthy individuals (control group) similar to the ADRIA group with respect to age and body surface area (BSA). All individuals underwent treadmill exercise testing according to Bruce protocol. Echocardiograms were performed before and immediately after exercise. RESULTS: The groups were similar regarding cardiac structure and left ventricular (LV) systolic function at rest at T1 and T2. The growth of LV posterior wall thickness related to BSA was lower in the ADRIA group at T2. Post exercise, smaller LV ejection indexes and attenuated changes in the afterload in ADRIA group were observed at T1 and T2. CONCLUSION: The decreased systolic reserve induced by a low dose of anthracycline in asymptomatic children and adolescents remains unaffected over a 5-year period, suggesting that positive outcomes in chronic cardiotoxicity would be expected in patients with mild impairment after anthracycline treatment.

Prevalence and predictors of ventricular remodeling after anterior myocardial infarction in the era of modern medical therapy.

BACKGROUND: The consequences of aggressive therapy following a myocardial infarction (MI) on ventricular remodeling are not well established. Thus, the objective of this study was to analyze the prevalence, clinical characteristics, and predictors of left ventricular remodeling in the era of modern medical therapy. MATERIAL/METHODS: Clinical characteristics and echocardiographic data were analyzed in 66 consecutive patients with anterior infarction at admission and at 6-month follow-up. Ventricular remodeling was defined as an increase of 10% in ventricular end-systolic or end-diastolic diameter. RESULTS: In our study, 58% of patients presented with ventricular remodeling. Patients with remodeling possessed higher total plasma creatine kinase (CPK), MB-fraction (CPK-MB), heart rate, heart failure, shortness of breath, and reperfusion therapy than patients without remodeling. In contrast, patients with remodeling had a smaller ejection fraction, E-Wave deceleration time (EDT), and early (E' Wave) and late (A' Wave) diastolic mitral annulus velocity (average of septal and lateral walls), but a higher E/E' than patients without remodeling. Patients with remodeling used more diuretics, digoxin, oral anticoagulants and aldosterone antagonists than patients without remodeling. In the multivariate analyses, only E' Wave was an independent predictor of ventricular remodeling. Each 1 unit increase in the E' Wave was associated with a 59% increased odds of ventricular remodeling. CONCLUSIONS: In patients with anterior MI, despite contemporary treatment, ventricular remodeling is still a common event. In addition, diastolic function can have an important role as a predictor of remodeling in this scenario.

Combined exercise training in asymptomatic elderly with controlled hypertension: effects on functional capacity and cardiac diastolic function.

BACKGROUND: Aging is associated with changes in cardiac structure and function that are associated with left ventricular diastolic dysfunction. Whether diastolic functional alterations during senescence are manifestations of the intrinsic aging process or related to cardiac adaptations to a more sedentary lifestyle is still unsettled. This was a prospective study evaluating the effects of a 6-month combined exercise training period on functional capacity and diastolic function in sedentary elderly patients with controlled arterial hypertension. MATERIAL/METHODS: Functional capacity was assessed by exercise stress test and muscle strength was evaluated by the one-repetition maximum test. Cardiac structures and function were analyzed by transthoracic echocardiography. RESULTS: Fifteen patients, 68±8 years old, completed the training program. Exercise training significantly improved physical capacity (distance walked: 551±92 vs. 630±153 m, P<0.05; work load: 7.2±1.7 vs. 8.5±3.0 METs, P<0.05) and upper and lower extremity muscle strength (P<0.001). Arterial blood pressure significantly decreased after training (systolic blood pressure: 134±9 vs. 128±8 mmHg; diastolic blood pressure: 82±7 vs. 77±6 mmHg; P<0.05). Cardiac structures and left and right systolic and diastolic function did not change after combined training (P>0.05). CONCLUSIONS: Combined and supervised training for a 6-month period increases physical capacity and muscle strength in elderly patients with controlled arterial hypertension without changing resting left ventricular diastolic function.

Higher salt preference in heart failure patients.

Heart failure (HF) is a complex syndrome that involves changes in behavioral, neural and endocrine regulatory systems. Dietary salt restriction along with pharmacotherapy is considered an essential component in the effective management of symptomatic HF patients. However, it is well recognized that HF patients typically have great difficulty in restricting sodium intake. We hypothesized that under HF altered activity in systems that normally function to regulate body fluid and cardiovascular homeostasis could produce an increased preference for the taste of salt. Therefore, this study was conducted to evaluate the perceived palatability (defined as salt preference) of food with different concentrations of added salt in compensated chronically medicated HF patients and comparable control subjects. Healthy volunteers (n=25) and medicated, clinically stable HF patients (n=38, NYHA functional class II or III) were interviewed and given an evaluation to assess their preferences for different amounts of saltiness. Three salt concentrations (0.58, 0.82, and 1.16 g/100 g) of bean soup were presented to the subjects. Salt preference for each concentration was quantified using an adjective scale (unpleasant, fair or delicious). Healthy volunteers preferred the soup with medium salt concentration (p=0.042), HF patients disliked the low concentration (p<0.001) and preferred the high concentration of salted bean soup (p<0.001). When compared to healthy volunteers, HF patients demonstrated a significantly greater preference for the soup with a high salt concentration (p=0.038). It is concluded that medicated, compensated patients under chronic treatment for HF have an increased preference for salt.

Influence of taurine on cardiac remodeling induced by tobacco smoke exposure.

BACKGROUND/AIMS: To investigate the effect of taurine on cardiac remodeling induced by smoking. METHODS: In the first step, rats were allocated into two groups: Group C (n = 14): control; Group T (n = 14): treated with taurine (3% in drinking water), for three months. In the second step, rats were allocated into two groups: Group ETS (n = 9): rats exposed to tobacco smoke; Group ETS-T (n = 9): rats exposed to tobacco smoke and treated with taurine for two months. RESULTS: After three months, taurine presented no effects on morphological or functional variables of normal rats assessed by echocardiogram. On the other hand, after two months, ETS-T group presented higher LV wall thickness (ETS = 1.30 (1.20-1.42); ETS-T = 1.50 (1.40-1.50); p = 0.029), E/A ratio (ETS = 1.13 ± 0.13; ETS-T = 1.37 ± 0.26; p = 0.028), and isovolumetric relaxation time normalized for heart rate (ETS = 53.9 ± 4.33; ETS-T = 72.5 ± 12.0; p < 0.001). The cardiac activity of the lactate dehydrogenase was higher in the ETS-T group (ETS = 204 ± 14 nmol/mg protein; ETS-T = 232 ± 12 nmol/mg protein; p < 0.001). ETS-T group presented lower levels of phospholamban (ETS = 1.00 ± 0.13; ETS-T = 0.82 ± 0.06; p = 0.026), phosphorylated phospholamban at Ser16 (ETS = 1.00 ± 0.14;ETS-T = 0.63 ± 0.10;p = 0.003), and phosphorylated phosfolamban/phospholamban ratio (ETS = 1.01 ± 0.17; ETS-T = 0.77 ± 0.11; p = 0.050). CONCLUSION: In normal rats, taurine produces no effects on cardiac morphological or functional variables. On the other hand, in rats exposed to cigarette smoke, taurine supplementation increases wall thickness and worsens diastolic function, associated with alterations in calcium handling protein and cardiac energy metabolism.

Tobacco smoke induces ventricular remodeling associated with an increase in NADPH oxidase activity.

BACKGROUND: Recent studies have assessed the direct effects of smoking on cardiac remodeling and function. However, the mechanisms of these alterations remain unknown. The aim of this study was to investigate de role of cardiac NADPH oxidase and antioxidant enzyme system on ventricular remodeling induced by tobacco smoke. METHODS: Male Wistar rats that weighed 200-230 g were divided into a control group (C) and an experimental group that was exposed to tobacco smoke for a period of two months (ETS). After the two-month exposure period, morphological, biochemical and functional analyses were performed. RESULTS: The myocyte cross-sectional area and left ventricle end-diastolic dimension was increased 16.2% and 33.7%, respectively, in the ETS group. The interstitial collagen volume fraction was also higher in ETS group compared to the controls. In addition to these morphological changes, the ejection fraction and fractional shortening were decreased in the ETS group. Importantly, these alterations were related to augmented heart oxidative stress, which was characterized by an increase in NADPH oxidase activity, increased levels of lipid hydroperoxide and depletion of antioxidant enzymes (e.g., catalase, superoxide dismutase and glutathione peroxidase). In addition, cardiac levels of IFN-γ, TNF-α and IL-10 were not different between the groups. CONCLUSION: Cardiac alterations that are induced by smoking are associated with increased NADPH oxidase activity, suggesting that this pathway plays a role in the ventricular remodeling induced by exposure to tobacco smoke.

Retinoic acid prevents ventricular remodelling induced by tobacco smoke exposure in rats.

OBJECTIVE: Our objective was to test the hypothesis that retinoic acid supplementation could attenuate ventricular remodelling induced by tobacco smoke exposure in rats. METHODS AND RESULTS: Wistar rats were allocated into three groups: control (C, n = 8); exposed to tobacco smoke (ETS, n = 9); exposed to tobacco smoke and all-trans-retinoic acid (ETS-RA, n = 9). After two months, cardiac function and geometry were assessed by echocardiography, and geometry changes were confirmed by morphometric analysis. Data are expressed as mean +/- SD or medians (including the lower quartile and upper quartile). ETS showed higher normalized left ventricular diastolic diameters than groups C and ETS-RA (C = 18.4 +/- 3.57 mm/kg, ETS = 23.0 +/- 1.8, ETS-RA = 19.5 +/- 0.99; P <0.05) and systolic diameters (C = 8.25 +/- 2.16 mm/kg, ETS = 11.5 +/- 1.31, ETS-RA = 8.25 +/- 0.71 mm/kg; P < 0.05). ETS showed reduced ejection fraction (C= 91 +/- 2.0, ETS = 87 +/- 3.0, ETS-RA = 92 +/- 3.0; P < 0.05) and fractional shortening (C = 55.8 +/- 4.41%, ETS = 49.7 +/- 4.43%, ETS-RA = 57.6 +/- 5.15 %; P= 0.01) compared to C and ETS-RA. ETS had increased myocyte cross-sectional area (C = 294 +/- 21 mm2, ETS = 352 +/-44, ETS-RA = 310 +/- 35; P < 0.05) compared to C and ETS-RA. Considering all variables, there were no differences between groups C and ETS-RA. CONCLUSION: Retinoic acid prevented ventricular remodelling induced by tobacco smoke exposure.

Tissue vitamin A insufficiency results in adverse ventricular remodeling after experimental myocardial infarction.

BACKGROUND/AIMS: The role of tissue vitamin-A insufficiency on post-infarction ventricular remodeling is unknown. We tested the hypothesis that cardiac vitamin A insufficiency on post-infarction is associated with adverse myocardial remodeling. METHODS: After infarction, rats were allocated into two groups: C (controls, n=25); VA (dietary vitamin A restriction, n= 26). After 3 months, the animals were submitted to echocardiogram, morphometric and biochemical analysis. RESULTS: Rats fed the vitamin-A-deficient diet had lower heart and liver retinol concentration and normal plasma retinol. There were no differences in infarct size between the groups. VA showed higher diastolic left ventricular area normalised by body weight (C= 1.81 ± 0.4 cm2/kg, VA= 2.15 ± 0.3 cm2/kg; p=0.03), left ventricular diameter (C= 9.4 ± 1.4 mm, VA= 10.5 ± 1.2 mm; p=0.04), but similar systolic ventricular fractional area change (C= 33.0 ± 10.0 %, VA= 32.1 ± 8.7 %; p=0.82). VA showed decreased isovolumetric relaxation time normalised by heart rate (C= 68.8 ± 11.4 ms, VA= 56.3 ± 16.8 ms; p=0.04). VA showed higher interstitial collagen fraction (C= 2.8 ± 0.9 %, VA= 3.7 ± 1.1 %; p=0.05). There were no differences in myosin heavy chain expression, metalloproteinase 2 and 9 activation, or IFN-γ and TNF-α cardiac levels. CONCLUSION: Local tissue vitamin A insufficiency intensified ventricular remodeling after MI, worsening diastolic dysfunction.

Ventricular remodeling induced by tissue vitamin A deficiency in rats.

BACKGROUND/AIMS: Experimental studies suggest that vitamin A plays a role in regulating cardiac structure and function. We tested the hypothesis that cardiac vitamin A deficiency is associated with adverse myocardial remodeling in young adult rats. METHODS: Two groups of young female rats, control (C - n = 29) and tissue vitamin A deficient (RVA - n = 31), were subjected to transthoracic echocardiography exam, isolated rat heart study and biochemical study. RESULTS: The RVA rats showed a reduced total vitamin A concentration in both the liver and heart [vitamin A in heart, micromol/kg (C = 0.95 +/- 0.44 and RVA = 0.24 +/- 0.16, p = 0.01)] with the same serum retinol levels (C = 0.73 +/- 0.29 micromol/L e RVA = 0.62 +/- 0.17 micromol/L, p = 0.34). The RVA rats showed higher left ventricular diameters and reduced systolic function. The RVA rats also demonstrated increased lipid hydroperoxide/total antioxidant capacity ratio and cardiac levels of IFN-gamma and TNF-alpha but not of metalloproteinase (MMP)-2 and -9 activity. On the other hand, the RVA rats had decreased levels of beta-hydroxyacylcoenzyme A dehydrogenase and lactate dehydrogenase. CONCLUSIONS: Tissue vitamin A deficiency stimulated cardiac remodeling and ventricular dysfunction. Additionally, the data support the involvement of oxidative stress, energy metabolism, and cytokine production in this remodeling process.

Influence of lisinopril on cardiac remodeling induced by tobacco smoke exposure.

BACKGROUND: To investigate the effect of lisinopril on cardiac remodeling induced by smoking. MATERIAL/METHODS: Rats were allocated into 3 groups: group CON (n=8): control; group CSE (n=8): cigarette smoke exposure; group CSE-LIS (n=8): exposed to tobacco smoke and treated with lisinopril. RESULTS: After 2 months, the tail systolic pressure was lower in CSE-LIS (CON=116 +/-27 mm Hg, CSE=126+/-16, CSE-LIS=89+/-12; P<.001). CSE animals showed higher left ventricular systolic diameter (CON=8.25+/-2.16 mm/kg, CSE=11.5+/-1.3, CSE-LIS=9.27+/-2.00; P=.009) and myocyte cross-sectional area (CON=245+/-8 microm2, CSE=260+/-17, CSE-LIS=238+/-12; P=.01) than CON and CSE-LIS. The ejection fraction (CON =0.91+/-0.02, CSE=0.86+/-0.02, CSE-LIS=0.92+/-0.03; P=.002) and fractional shortening (CON=55.7+/-4.41%, CSE=48.7+/-3.43, CSE-LI=58.2+/-7.63; P=.006) were lower in CSE group than CON and CSE-LIS. CSE and CSE-LIS animals showed higher collagen amounts (CON=3.49+/-0.95%, CSE= 5.01+/-1.58, CSE-LIS=5.27+/-0.62; P=.009) than CON. CON group showed a higher connexin 43 amount in the intercalated disc (CON=3.70+/-0.38, CSE=2.13+/-0.53; CSE-LIS=2.17+/-0.73; P=.004) than CSE and CSE-LIS. There were no differences in IFN-gamma or TNF-alpha cardiac levels among the groups. CONCLUSIONS: Lisinopril attenuated both morphologic and functional abnormalities induced by exposure to tobacco smoke. In addition, this effect was associated with diminished blood pressure, but not alterations in connexin 43 distribution, cytokine production or collagen amount.

Tobacco smoke-induced left ventricular remodelling is not associated with metalloproteinase-2 or -9 activation.

AIM: To investigate the role of MMP-2 and MMP-9 in cardiac remodelling induced by tobacco smoke exposure in rats. METHODS: Rats were allocated into two groups: C (n=9): control animals; ETS (n=9): exposed to tobacco smoke. After 4months, the animals underwent echocardiography, morphometric study and determination of MMP-2 and MMP-9 activity. RESULTS: ETS rats had larger diastolic (C=15.6 +/-1.2 mm/kg, ETS=18.0+/-0.9 mm/kg; p < 0.001) and systolic (C=7.3+/-1.2 mm/kg, ETS=9.2+/-0.9 mm/kg; p=0.001) ventricular diameters adjusted for body weight. Fractional shortening (C=53+/-4.8%, ETS=48+/- 3.3%; p=0.031) and ejection fraction (C=0.89+/-0.03, ETS=0.86+/-0.02; p=0.030) were smaller in the ETS group. Myocyte cross-sectional area (C=245+/-8 microm2, ETS=253+/-8 microm2; p=0.028) was higher in ETS rats. There were no differences in MMP-2 (C=50+/-14%; ETS=43+/-11%, p=0.228) or MMP-9 (C=0.36+/-0.3%; ETS=0.62+/-0.3%, p=0.630) activity between the groups. CONCLUSION: MMP-2 and MMP-9 did not participate in the remodelling process induced by tobacco smoke exposure.

Association between atherosclerotic aortic plaques and left ventricular hypertrophy in patients with cerebrovascular events.

BACKGROUND AND PURPOSE: The purpose of this research was to evaluate whether an association exists between the presence of atherosclerotic plaque in the thoracic aorta and left ventricular hypertrophy (LVH) in patients with a cerebrovascular event. METHODS: We included 116 consecutive patients (79 men; mean age, 62+/-12.4 years) with previous history of stroke or transient ischemic attack in a cross-sectional study. Transthoracic echocardiogram was performed to diagnose LVH and transesophageal echocardiogram for the detection of atheromas of the thoracic aorta. Continuous variables were analyzed by Student t or Mann-Whitney tests and categorized variables by Goodman test. From the significant association of LVH and age with atheromatous disease of the aorta, an adjustment to the multivariate logistic model was made using high blood pressure history or age as covariates. All of the statistical tests were carried out at a level of 5% significance. RESULTS: Almost half of the patients (43.1%) presented atherosclerotic lesions in the aorta. LVH was present in 90.0% of patients with plaque and in only 30.3% of patients without plaque. Using high blood pressure as a covariate, the risk of patients with LVH presenting atherosclerotic plaque in the aorta was 18.23-fold greater than the risk for patients without LVH (95% CI, 5.68 to 58.54; P<0.0001). Adding age into the model, the risk increased to 26.36 (95% CI, 7.14 to 97.30; P<0.0001). CONCLUSIONS: LVH detected by conventional echocardiogram is associated with high risk of atherosclerotic plaque in the aorta and would be used as a criterion for indication of transesophageal echocardiography in patients with previous stroke or transient ischemic attack LVH.

Beta-carotene supplementation attenuates cardiac remodeling induced by one-month tobacco-smoke exposure in rats.

OBJECTIVE: The objectives were to analyze the cardiac effects of exposure to tobacco smoke (ETS), for a period of 30 days, alone and in combination with beta-carotene supplementation (BC). RESEARCH METHODS AND PROCEDURES: Rats were allocated into: Air (control, n = 13); Air + BC (n = 11); ETS (n = 11); and BC + ETS (n = 9). In Air + BC and BC + ETS, 500 mg of BC were added to the diet. After three months of randomization, cardiac structure and function were assessed by echocardiogram. After that, animals were euthanized and morphological data were analyzed post-mortem. One-way and two-way ANOVA were used to assess the effects of ETS, BC and the interaction between ETS and BC on the variables. RESULTS: ETS presented smaller cardiac output (0.087 +/- 0.001 vs. 0.105 +/- 0.004 l/min; p = 0.007), higher left ventricular diastolic diameter (19.6 +/- 0.5 vs. 18.0 +/- 0.5 mm/kg; p = 0.024), higher left ventricular (2.02 +/- 0.05 vs. 1.70 +/- 0.03 g/kg; p < 0.001) and atrium (0.24 +/- 0.01 vs. 0.19 +/- 0.01 g/kg; p = 0.003) weight, adjusted to body weight of animals, and higher values of hepatic lipid hydroperoxide (5.32 +/- 0.1 vs. 4.84 +/- 0.1 nmol/g tissue; p = 0.031) than Air. However, considering those variables, there were no differences between Air and BC + ETS (0.099 +/- 0.004 l/min; 19.0 +/- 0.5 mm/kg; 1.83 +/- 0.04 g/kg; 0.19 +/- 0.01 g/kg; 4.88 +/- 0.1 nmol/g tissue, respectively; p > 0.05). Ultrastructural alterations were found in ETS: disorganization or loss of myofilaments, plasmatic membrane infolding, sarcoplasm reticulum dilatation, polymorphic mitochondria with swelling and decreased cristae. In BC + ETS, most fibers showed normal morphological aspects. CONCLUSION: One-month tobacco-smoke exposure induces functional and morphological cardiac alterations and BC supplementation attenuates this ventricular remodeling process.

Beta-carotene supplementation results in adverse ventricular remodeling after acute myocardial infarction.

OBJECTIVE: We studied the effects of beta-carotene (BC) on ventricular remodeling after myocardial infarction. METHODS: Myocardial infarction was induced in Wistar rats that were then treated with a BC diet (500 mg/kg of diet per day; MI-BC; n = 27) or a regular diet (MI; n = 27). Hearts were analyzed in vivo and in vitro after 6 mo. RESULTS: BC caused decreased left ventricular wall thickness (MI = 1.49 +/- 0.3 mm, MI-BC = 1.23 +/- 0.2 mm, P = 0.027) and increased diastolic (MI = 0.83 +/- 0.15 cm2, MI-BC = 0.98 +/- 0.14 cm2, P = 0.020) and systolic (MI = 0.56 +/- 0.12 cm2, MI-BC = 0.75 +/- 0.13 cm2, P = 0.002) left ventricular chamber areas. With respect to systolic function, the BC group presented less change in fractional area than did controls (MI = 32.35 +/- 6.67, MI-BC = 23.77 +/- 6.06, P = 0.004). There was no difference in transmitral diastolic flow velocities between groups. In vitro results showed decreased maximal isovolumetric systolic pressure (MI = 125.5 +/- 24.1 mmHg, MI-BC = 95.2 +/- 28.4 mmHg, P = 0.019) and increased interstitial myocardial collagen concentration (MI = 3.3 +/- 1.2%, MI-BC = 5.8 +/- 1.7%, P = 0.004) in BC-treated animals. Infarct sizes were similar between groups (MI = 45.0 +/- 6.6%, MI-BC = 48.0 +/- 5.8%, P = 0.246). CONCLUSION: Taken together, these data suggest that BC has adverse effects on ventricular remodeling after myocardial infarction.

[Cigarette smoke exposure intensifies ventricular remodeling process following myocardial infarction]. / A exposição à fumaça de cigarro intensifica a remodelação ventricular após o infarto agudo do miocárdio.

OBJECTIVE: To evaluate the role of cigarette smoke exposure (CSE) on ventricular remodeling following acute myocardial infarction (AMI). METHODS: Rats were submitted to myocardial infarction and divided into two groups: C (control, n = 31) and F (CSE: 40 cigarettes/day, n = 22). After 6 months, the survivors were submitted to echocardiogram, functional study with isolated heart, and morphometric analysis. For comparison purposes, we used the t test (mean +/- standard deviation) or the Mann-Whitney test (with median and 25th and 75th percentiles). RESULTS: The CSE animals tended to have larger diastolic (C = 1.5 +/- 0.4 mm2, F = 1.9 +/- 0.4 mm2; p = 0.08) and systolic (C = 1.05 +/- 0.3 mm2, F = 1.32 +/- 0.4 mm2; p = 0.08) left ventricular(LV) areas. The systolic function of the LV, assessed according to the fractional area change, tended to be impaired in CSE animals (C = 31.9 +/- 9.3%, F = 25.5 +/- 7.6%; p = 0.08). The dp/dt values for CSE animals were statistically lower (C = 1474 +/- 397 mmHg, F = 916 +/- 261 mmHg; p = 0.02) than for control animals. The CSE animals presented higher right ventricle (RV) weight adjusted for body weight (C = 0.8 +/- 0.3 mg/g, F = 1.3 +/- 0.4 mg/g; p = 0.01), higher content of water in lungs (C = 4.8 (4.3-4.8)%, F = 5.4 (5.1-5.5); p = 0.03), and larger LV myocyte cross-sectional areas (C = 239.8 +/- 5.8 microm2, F = 253.9 +/- 7.9 microm2; p = 0.01). CONCLUSION: Cigarette smoke exposure intensifies ventricular remodeling following acute myocardial infarction.

[Diastolic dysfunction in diabetic normotensive patients, regardless of the presence of microangiopathy]. / Disfunção diastólica em pacientes diabéticos normotensos, independente da presença de microangiopatia.

OBJECTIVE: To assess the Doppler-echocardiographic changes in normotensive patients with type II diabetes mellitus, in the presence or absence of signs of microangiopathy. METHODS: Patients with type II diabetes mellitus were submitted to funduscopy contrasted with fluorescein and dosage of microalbuminuria for diagnose of microangiopathy and divided into two groups: DMII (patients without microangiopathy, n=19) and DM+A (patients with microangiopathy, n=13). All of them were submitted to a Doppler-echocardiography and the results were compared with normotensive patients of same sex and age (group C, n=20), by using the ANOVA, followed by the test of Tukey. In all comparisons the significance level p<0.05 was adopted. RESULTS: There were no differences among the groups regarding the systolic function indicators or left ventricular mass. Differences compatible with diastolic dysfunction in the two groups of diabetic were observed, regardless of the presence of microangiopathy, which showed significantly higher values of the times of isovolumetric relaxation of the left ventricle (TIRLV, ms): (DMII= 97+/-22.2; DM+A= 107+/-28.2 and C= 80+/-10.7; p<0.05), and lower values of the maximum speeds of the wave of fast ventricular filling (E, cm/s): (DMII= 69+/-17.5; DM+A= 75+/-19.7 and C= 84+/-14.5, p<0.05 between DMII and C). There was no difference among the groups concerning the E/A rate. CONCLUSION: Normotensive patients with type II diabetes mellitus and without clinical signs of cardiovascular compromising showed signs of diastolic dysfunction, non-associated to the presence of microangiopathy.

[Chronic cigarette smoke exposure results in cardiac remodeling and impaired ventricular function in rats]. / A exposição crônica à fumaça do cigarro resulta em remodelação cardíaca e prejuízo da função ventricular em ratos.

OBJECTIVE: To determine the cardiac structural and functional alterations caused by cigarette smoke exposure in rats. METHODS: The animals were randomly distributed into the following 2 groups: 1) smokers (S), comprising 10 animals exposed to cigarette smoke at a rate of 40 cigarettes/day; and 2) control (C), comprising 10 animals not exposed to cigarette smoke. After 4 months, the animals underwent morphological and functional study with echocardiography. The variables studied were analyzed by use of the t test or the Mann-Whitney test. RESULTS: The smoking rats had a greater left atrium (S=4.2+/-0.7 mm; C=3.5+/-0.6 mm; P<0.05), and greater left ventricular diastolic (S=7.9+/-0.7 mm; C=7.2+/-0.5 mm; P<0.05) and systolic (S=4.1+/-0.5; C=3.4+/-0.5; P<0.05) diameters. The left ventricular mass index was greater in the smoking animals (S=1.5 mg/kg+/-0.2; C=1.3 mg/kg+/-0.2; P<0.05), and the ejection fraction (S=0.85+/-0.03; C=0.89+/-0.03; P<0.05) and the shortening fraction (S=47.8%+/-3.7; C=52.7%+/-4.6; P<0.05) were greater in the control group. No differences were observed in the diastolic transmitral flow variables (E wave, A wave, and E/A ratio). CONCLUSION: Chronic cigarette smoke exposure results in cardiac remodeling with a decrease in ventricular functional capacity.

Doppler echocardiographic assessment of pregnant women with chronic arterial hypertension.

OBJECTIVE: To assess structural and functional cardiac changes in asymptomatic pregnant women with chronic arterial hypertension (CAH). METHODS: One hundred pregnant women with CAH underwent conventional Doppler echocardiography. The Student t test was used to compare them with 29 normotensive pregnant women (NT) in their third gestational trimester. RESULTS: Systolic (SBP; mmHg) and diastolic (DBP; mmHg) blood pressure values were higher (p<0.001) in the CAH pregnant women (SBP: 139+/-19 and DBP: 92+/- 18) as compared with those of the NT group (SBP: 112+/-10 and DBP: 74+/-9). A significant enlargement of the left atrium (4.10+/-0.48 cm vs 3.6+/-0.3 cm; p<0.001) and of the left ventricular normalized mass (59.6+/-19.7 g/cm2,7 vs 41.9+/-3.4 g/cm2,7; p<0.001) was observed. Cardiac output (CO, L/min) and systolic volume (SV, mL) were significantly higher in the CAH group (CO: 6.0+/-1.54 vs 4.9+/-2.1, p<0.01; SV: 77.3+/-19.8 vs 56.5+/-25.8, p<0.001). CONCLUSION: Chronic hypertensive pregnant women have structural and functional cardiac changes that justify routine cardiologic assessment, even in the absence of cardiopulmonary symptoms.

Infarct size as predictor of systolic functional recovery after myocardial infarction.

BACKGROUND: The effects of modern therapy on functional recovery after acute myocardial infarction (AMI) are unknown. OBJECTIVES: To evaluate the predictors of systolic functional recovery after anterior wall AMI in patients undergoing modern therapy (reperfusion, aggressive platelet antiaggregant therapy, angiotensin-converting enzyme inhibitors and beta-blockers). METHODS: A total of 94 consecutive patients with AMI with ST-segment elevation were enrolled. Echocardiograms were performed during the in-hospital phase and after 6 months. Systolic dysfunction was defined as ejection fraction value < 50%. RESULTS: In the initial echocardiogram, 64% of patients had systolic dysfunction. Patients with ventricular dysfunction had greater infarct size, assessed by the measurement of total and isoenzyme MB creatine kinase enzymes, than patients without dysfunction. Additionally, 24.5% of patients that initially had systolic dysfunction showed recovery within 6 months after AMI. Patients who recovered ventricular function had smaller infarct sizes, but larger values of ejection fraction and E-wave deceleration time than patients without recovery. At the multivariate analysis, it can be observed that infarct size was the only independent predictor of functional recovery after 6 months of AMI when adjusted for age, gender, ejection fraction and E-wave deceleration time. CONCLUSION: In spite of aggressive treatment, systolic ventricular dysfunction remains a frequent event after the anterior wall myocardial infarction. Additionally, 25% of patients show functional recovery. Finally, infarct size was the only significant predictor of functional recovery after six months of acute myocardial infarction.