BackgroundChronic Chagas cardiomyopathy in humans is characterized by segmental left ventricular wall motion abnormalities (WMA), mainly in the early stages of disease. This study aimed at investigating the detection of WMA and its correlation with the underlying histopathological changes in a chronic Chagas cardiomyopathy model in hamsters.Methods and ResultsFemale Syrian hamsters (n=34) infected with 3.5×104 or 105 blood trypomastigote Trypanosoma cruzi (Y strain) forms and an uninfected control group (n=7) were investigated. After 6 or 10 months after the infection, the animals were submitted to in vivo evaluation of global and segmental left ventricular systolic function by echocardiography, followed by euthanasia and histological analysis for quantitative assessment of fibrosis and inflammation with tissue sampling in locations coinciding with the left ventricular wall segmentation employed at the in vivo echocardiographic evaluation. Ten of the 34 infected animals (29%) showed reduced left ventricular ejection fraction (<73%). Left ventricular ejection fraction was more negatively correlated with the intensity of inflammation (r=−0.63; P<0.0001) than with the extent of fibrosis (r=−0.36; P=0.036). Among the 24 animals with preserved left ventricular ejection fraction (82.9±5.5%), 8 (33%) showed segmental WMA predominating in the apical, inferior, and posterolateral segments. The segments exhibiting WMA, in comparison to those with normal wall motion, showed a greater extent of fibrosis (9.3±5.7% and 7±6.3%, P<0.0001) and an even greater intensity of inflammation (218.0±111.6 and 124.5±84.8 nuclei/mm², P<0.0001).ConclusionsIsolated WMA with preserved global systolic left ventricular function is frequently found in Syrian hamsters with experimental chronic Chagas cardiomyopathy whose underlying histopathological features are mainly inflammatory.

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Patients with CHF and SA present a reduced and blunted cardiac autonomic modulation across the 24-hour period. These findings may help to explain the increased cardiovascular risk in patients with CHF and SA.

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Quantifying complexity from heart rate variability (HRV) series is a challenging task, and multiscale entropy (MSE), along with its variants, has been demonstrated to be one of the most robust approaches to achieve this goal. Although physical training is known to be beneficial, there is little information about the long-term complexity changes induced by the physical conditioning. The present study aimed to quantify the changes in physiological complexity elicited by physical training through multiscale entropy-based complexity measurements. Rats were subject to a protocol of medium intensity training (n = 13) or a sedentary protocol (n = 12). One-hour HRV series were obtained from all conscious rats five days after the experimental protocol. We estimated MSE, multiscale dispersion entropy (MDE) and multiscale SDiff q from HRV series. Multiscale SDiff q is a recent approach that accounts for entropy differences between a given time series and its shuffled dynamics. From SDiff q , three attributes (q-attributes) were derived, namely SDiff q max , q max and q zero. MSE, MDE and multiscale q-attributes presented similar profiles, except for SDiff q max. q max showed significant differences between trained and sedentary groups on Time Scales 6 to 20. Results suggest that physical training increases the system complexity and that multiscale q-attributes provide valuable information about the physiological complexity.

The present study investigated morpho-functional relations of the aortic depressor nerve (ADN) 5, 15 and 120 days after the onset of streptozotocin-induced diabetes in rats. Time control animals received vehicle. Under pentobarbital anesthesia, ADN activity was recorded simultaneously with arterial pressure. After the recordings, nerves were prepared for light microscopy study and morphometry. ADN function was accessed by means of pressure-nerve activity curve (fitted by sigmoidal regression) and cross-spectral analysis between mean arterial pressure (MAP) and ADN activity. The relation between morphological (myelinated fibers number and density, total myelin area, total fiber area and percentage of occupancy) and functional (gain, signal/noise relation, frequency) parameters were accessed by linear regression analysis and correlation coefficient calculations. Functional parameters obtained by means of the sigmoidal regression curve as well as by cross-spectral analysis were similar in diabetic and control rats. Morphometric parameters of the ADN were similar between groups 5 days after the onset of diabetes. Average myelin area and myelinated fiber area were significantly smaller on diabetic rats 15 and 120 days after the onset of diabetes, being the myelinated fiber and respective axons area and diameter also smaller on 120 days group. Nevertheless, G ratio (ratio between axon and fiber diameter) was nearly 0.6 and not different between groups or experimental times. No significant relationship between morphological and functional parameters was detected in all experimental groups. The present study suggests that ADN diabetic neuropathy was time-dependent, with damage to myelinated fibers to be the primary event, not evidenced by physiological methods.

The aim of the present study was to investigate the effects of converting enzyme inhibition by captopril on ECG parameters in aged rats. Four-month-old male rats received captopril dissolved in tap water (0.5 mg/l) or tap water for 2 or 20 months. At the end of treatment, under anesthesia, RR and PR interval, P wave and QRS duration, QT and corrected QT interval were measured in all animals. On the following day, chronic ECG (lead II) recordings were performed to quantify supraventricular (SVPB) or ventricular premature beats (VPB). After sacrifice, the hearts were removed and weighed. RR interval was similar in young and untreated aged rats, but significantly larger in aged rats treated with captopril. P wave and QRS length did not differ among groups. PR interval was significantly larger in old than in young rats and was not affected by captopril. Corrected QT interval was larger in aged than in young rats (117 ± 4 vs 64 ± 6 ms, P<0.05) and was reduced by captopril (71 ± 6 ms, P<0.05). VPB were absent in young rats and highly frequent in untreated old animals (8.4 ± 3.0/30 min). Captopril significantly reduced VPB in old rats (0.3 ± 0.1/30 min, P<0.05). The cardiac hypertrophy found in untreated aged rats was prevented by captopril (3.44 ± 0.14 vs 3.07 ± 0.10 mg/g, P<0.05). The beneficial effects of angiotensin converting enzyme inhibition on the rat heart during the aging process are remarkable.

Although spectral analysis has been widely used to assess the autonomic control of the heart, several issues are still in debate about its interpretation, especially in experimental animals such as rats and mice. A nonlinear alternative method, namely symbolic dynamics, was proposed and has been reported to be very useful to represent sympathetic and parasympathetic modulation to the heart. However, studies evaluating the validity of symbolic dynamics in experimental models still lack. Conscious male Wistar rats, under continuous recording of electrocardiogram (ECG) or arterial pressure (AP), were subjected to autonomic imbalance by two protocols: pharmacological blockade of adrenergic or cholinergic muscarinic receptors administration (atenolol 4 mg/kg or methylatropine 2 mg/kg, iv, N=9 in each group) and reflex changes in sympatho‐vagal balance by AP changes elicited by phenylephrine (PHE, N=9) or sodium nitroprusside (NPS, N=9). Beat by beat series of cardiac interval (CI) were generated from ECG or AP recordings and both spectral analysis and symbolic dynamics were calculated for each animal. Spectra of CI series were calculated by FFT and integrated in low‐ (LF: 0.2–0.8Hz) and high‐frequency bands (HF: 0.8–3Hz). For symbolic analysis, symbols were attributed to CI values and sequences of 3 symbols were classified as 0, 1 or 2V according to the number of variations showed. Percentage of 0V and 2V are associated to sympathetic and vagal cardiac modulation, respectively. Hypertensive response caused by PHE (33 ± 3 mmHg) led to a reflex bradycardia (−45 ± 3 bpm) while hypotension due to NPS (−15 ± 1 mmHg) was accompanied by tachycardia (46 ± 6 bpm). The administration of atenolol and atropine led to a reduction and an increase in HR, respectively (−19 ± 6 and 70 ± 8 bpm). All drugs used reduced the total variability (standard deviation) of the CI series. The results of the spectral and symbolic analysis are showed in the table at the end. The symbolic dynamics proved to be more robust than the spectral analysis for the evaluation of the autonomic control in rats. The 1V family patterns, hitherto unknown, have been shown to be linked to sympathetic modulation in the rat and should be considered in future studies.Support or Funding InformationFapesp basal atenolol basal atropine basal NPS basal PHE LF (nu) 35±2 23±4* 40±4 28±4* 9.8±2.1 14±4 11±2 9.3±2.0 HF (ms2) 6.0±0.8 2.7±0.9* 4.3±0.4 0.2±0.03* 10±2 6.3±1.5* 4.2±1.0 25±6* 0V (%) 27±2 16±3* 27±3 29±4 7.7±1.4 9.1±1.7 9.0±1.4 5.6±1.2 1V (%) 44±1 38±2* 42±1 46±2 35±2 40±1* 45±2 33±2* 2UV (%) 25±2 37±4* 26±2 19±1* 50±3 43±2* 39±3 51±4* P<0.05 compared to basal.