Rosemeire M. Kanashiro

Performance of two-dimensional Doppler echocardiography for the assessment of infarct size and left ventricular function in rats

Although echocardiography has been used in rats, few studies have determined its efficacy for estimating myocardial infarct size. Our objective was to estimate the myocardial infarct size, and to evaluate anatomic and functional variables of the left ventricle. Myocardial infarction was produced in 43 female Wistar rats by ligature of the left coronary artery. Echocardiography was performed 5 weeks later to measure left ventricular diameter and transverse area (mean of 3 transverse planes), infarct size (percentage of the arc with infarct on 3 transverse planes), systolic function by the change in fractional area, and diastolic function by mitral inflow parameters. The histologic measurement of myocardial infarction size was similar to the echocardiographic method. Myocardial infarct size ranged from 4.8 to 66.6% when determined by histology and from 5 to 69.8% when determined by echocardiography, with good correlation (r = 0.88; P < 0.05; Pearson correlation coefficient). Left ventricular diameter and mean diastolic transverse area correlated with myocardial infarct size by histology (r = 0.57 and r = 0.78; P < 0.0005). The fractional area change ranged from 28.5 +/- 5.6 (large-size myocardial infarction) to 53.1 +/- 1.5% (control) and correlated with myocardial infarct size by echocardiography (r = -0.87; P < 0.00001) and histology (r = -0.78; P < 00001). The E/A wave ratio of mitral inflow velocity for animals with large-size myocardial infarction (5.6 +/- 2.7) was significantly higher than for all others (control: 1.9 +/- 0.1; small-size myocardial infarction: 1.9 +/- 0.4; moderate-size myocardial infarction: 2.8 +/- 2.3). There was good agreement between echocardiographic and histologic estimates of myocardial infarct size in rats.

Structural and functional characteristics of rat hearts with and without myocardial infarct. Initial experience with doppler echocardiography

OBJECTIVE To assess by Doppler echocardiography the structural and functional alterations of rat heart with surgical induced extensive myocardial infarction. METHODS Five weeks after surgical ligature of the left coronary artery, 38 Wistar-EPM rats of both sexes, 10 of them with extensive infarction, undergone anatomical and functional evaluation by Doppler echocardiography and then euthanized for anatomopathological analysis. RESULTS Echocardiography was 100% sensible and specific to anatomopathological confirmed extensive miocardial infarction. Extensive infarction lead to dilatation of left ventricle (diastolic diameter: 0.89 cm vs.0.64 cm; systolic: 0. 72 cm vs. 0.33 cm) and left atrium (0.55 cm vs. 0.33 cm); thinning of left ventricular anterior wall (systolic: 0.14 cm vs. 0.23 cm, diastolic: 0.11 cm vs. 0.14 cm); increased mitral E/ A wave relation (6.45 vs. 1.95). Signals of increased end diastolic ventricle pressure, B point in mitral valve tracing in 62.5% and signs of pulmonary hypertension straightening of pulmonary valve (90%) and notching of pulmonary systolic flow (60%) were observed in animals with extensive infarction. CONCLUSION Doppler echocardiography has a high sensitivity and specificity for detection of chronic extensive infarction. Extensive infarction caused dilatation of left cardiac chambers and showed in Doppler signals of increased end diastolic left ventricular pressure and pulmonary artery pressure.

Myocardial infarction scar plication in the rat: cardiac mechanics in an animal model for surgical procedures

BACKGROUND The immediate effects of surgical reduction of left ventricle cavity on cardiac mechanics have not been well defined. METHODS Cardiac mechanics were analyzed before and after myocardial infarction scar plication in 11 isolated infarcted rat hearts. RESULTS Despite a decrease in myocardial stiffness, an increase in chamber stiffness was noted after myocardial infarction scar plication. Systolic function was favored in more than one way. For the same diastolic pressures, maximal developed pressures were higher after myocardial infarction scar plication, and the slope of the systolic pressure-volume relationship was steeper afterwards as compared with before; this means that Frank-Starling recruitment is accentuated in smaller cavities. In addition, the developed net forces needed to generate these pressures were clearly lower afterward than before, indicating reduced ventricular afterload. CONCLUSIONS The study results show that diastolic function is harmed and systolic function is favored by myocardial infarction scar plication. We suggest that preoperative evaluation of the degree of diastolic dysfunction and impairment of the Frank-Starling mechanism may help to identify patients who may have a poor postoperative outcome due to diastolic or systolic dysfunction.

A routine electrocardiogram cannot be used to determine the size of myocardial infarction in the rat

Nine lead electrocardiograms of non-infarcted (N = 61) and infarcted (N = 71) female Wistar rats (200-250 g) were analyzed in order to distinguish left ventricle myocardial infarction (MI) larger than 40% (LMI) from MI smaller than 40% (SMI). MI larger than 40% clearly caused a deviation of AQRS and AT from normal values of 270-360 degrees to 90-270 degrees. Infarcted rats showed Q wave in D1 larger than 1 mm with 94% sensitivity and 100% specificity. The sum of QRS positivity in V1, V2 and V6 lower than 10 mm identified MI with 82% sensitivity and 100% specificity. The data showed that MI can be easily and reliably diagnosed by electrocardiogram in the rat. However, contradicting what is frequently believed, when specificity and sensitivity were analyzed focusing on MI size, none of these current electrocardiographic indices of MI size adequately discriminates LMI from SMI.

A novel inexpensive murine model of oral chronic digitalization

1. A novel inexpensive murine model of oral administration of digitoxin (100 µg/kg per day) added to routine chow is described.

Incidence of heart failure in infarcted rats that die spontaneously

The present study reports for the first time the incidence of congestive heart failure (CHF) in previously infarcted rats that died spontaneously. Previously, pulmonary (PWC) and hepatic (HWC) water contents were determined in normal rats: 14 control animals were evaluated immediately after sacrifice, 8 placed in a refrigerator for 24 h, and 10 left at room temperature for 24 h. In the infarcted group, 9 rats died before (acute) and 28 died 48 h after (chronic) myocardial infarction. Thirteen chronic animals were submitted only to autopsy (N = 13), whereas PWC and HWC were also determined in the others (N = 15). Seven rats survived 48 h and died during anesthesia. Notably, PWC differed in normal rats: ambient (75.7 +/- 1.3%) < control (77.5 +/- 0.7%) < refrigerator (79.1 +/- 1.4%) and there were no differences with respect to HWC. No clinical signs of CHF (dyspnea, lethargy or foot edema) were observed in infarcted rats before death. PWC was elevated in all chronic and anesthetized rats. HWC was increased in 48% of chronic and in all anesthetized rats. Our data showed that PWC needs to be evaluated before 24 h post mortem and that CHF is the rule in chronic infarcted rats suffering natural death. The congestive syndrome cannot be diagnosed correctly in rats by clinical signs alone, as previously proposed.

A redução do ventrículo esquerdo não apenas diminui a pós-carga

A proposta, aparentemente insolita, de retirada de fatiado miocardio para tratamento de cardiopatias com disfuncaocontratil avancada, lastreia-se em principio fisiologico irre-futavel: a reducao da cavidade ventricular resultante facilitaa ejecao ventricular.Como ocorre com todos os musculos, o miocardio temas funcoes precipuas de desenvolver forca e encurtar. Es-tas duas funcoes guardam sempre uma relacao inversa, istoe, quando o miocardio e exigido a desenvolver maior forca,o encurtamento e prejudicado. Inversamente, quando me-nos solicitado no desenvolvimento de forca, o montante deencurtamento miocardico se acentua. Este principio rege aacentuacao do desague ventricular que acompanha as dimi-nuicoes da pos-carga.No coracao, em funcao da distribuicao espacial domiocardio acabar compondo uma cavidade, circunstancial-mente, a forca desenvolvida pelo musculo e convertida empressao, que e a variavel que regula fluxo e, portanto, regu-la a ejecao ventricular. As relacoes entre a forca desenvolvi-da pelo musculo e a pressao gerada no interior da cavidadesao definidas pela lei de Laplace: a forca miocardica e direta-mente proporcional a pressao intraventricular e ao raio dacavidade e, inversamente proporcional a espessura da pare-de (F = P x R / 2h). Deriva que, para desenvolver uma deter-minada pressao de ejecao, a forca a ser gerada pelo miocar-dio e diretamente proporcional a relacao raio da cavidade/espessura da parede, frequentemente considerada como arelacao volume/massa. Reduzindo-se o volume da cavida-de, sera menor a forca a ser gerada pelo miocardio para de-senvolver a mesma pressao de ejecao, configurando a dimi-nuicao da pos-carga.A aplicacao destes conceitos as miocardiopatias - econsequente indicacao de cirurgia para reducao da cavida-de - gerou expressivo interesse de grupos cirurgicos inter-nacionais, visando estabelecer o merito da proposta. Se-guindo-se periodo inicial de otimismo, e perceptivel a exis-tencia atual de descrenca nos resultados da reducao doventriculo esquerdo como estrategia de tratamento das mio-cardiopatias