Rats with high left ventricular end-diastolic pressure can be identified by Doppler echocardiography one week after myocardial infarction

Saraiva, R.M.; Kanashiro‐Takeuchi, Rosemeire M.; Antônio, Ednei Luiz; Campos, O.; Tucci, Paulo José Ferreira; Moisés, Valdir Ambrósio

doi:10.1590/s0100-879x2006005000178

Cited by 7 publications

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“…The electrocardiogram 2 and the echocardiogram [3][4][5][6][7][8][9][10][11][12][13][14][15] are noninvasive methods capable of identifying the area of necrosis or scarring. Although it identifies the presence of an MI-dependent electrically inactive area, the ECG is not a method that can quantify the infarction area 2 .…”

Section: Introductionmentioning

confidence: 99%

“…In many rats of our series, AE ratio mean values ± SD oscillated around 2.0. In the group of HF rats analyzed, AE ratio values higher than 2.7 identified an LVDP higher than 12 mmHg, with 90% of sensibility, and 80% of specificity 15 . In more recent series, the study showed AE ratio values of 2.15 ± 0.44, in 44 normal rats.…”

mentioning

confidence: 96%

“…Although it identifies the presence of an MI-dependent electrically inactive area, the ECG is not a method that can quantify the infarction area 2 . The echocardiogram can determine the presence and the size of the MI with very good sensitivity [3][4][5][6][7][8][9][10][11][12][13][14][15] , even in periods as early as two days after necrosis, and it also provides information about deviant atrial and ventricular function. The best method for post-mortem diagnosis of MI depends on the stage in which the autopsy occurs.…”

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confidence: 99%

“…The DE assessment offers valuable information for the serial follow-up of the animals, because it shows a reduction in atrial emptying due to an increased LVDP. Both AE ratio and tissue Doppler analysis (E/Em ratio) can identify an increased LVDP 15 . Curiously, in rats, the initial pattern of impaired atrial emptying analyzed by mitral valve flow (AE ratio reduction) is not observed, whereas the restrictive pattern of DE is identified (AE ratio increase).…”

mentioning

confidence: 99%

“…In animals with MI ≥ 40% of the LV, it is common to observe mean values higher than 4.0. This seems to be the most dependable noninvasive indicator that the LVDP is high 15 and, therefore, the subject has CHF. It should be emphasized that DE can reveal clinically hidden ventricular dysfunctions by determining the ratios between systolic and diastolic ventricular measurements (diameter, area, volume) 11 .…”

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confidence: 99%

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Características fisiopatológicas do modelo de insuficiência cardíaca pós-infarto do miocárdio no rato

Tucci¹

2011

Arq. Bras. Cardiol.

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Congestive heart failure (CHF) caused by myocardial infarction in rats is the most commonly used experimental model to study the congestive heart failure syndrome. Following myocardial necrosis, the manifestations observed in rats very satisfactorily reproduce the findings in humans with cardiac decompensation and substantiate the study of CHF pathogenesis, pathophysiology, and treatment. Two features are inadequate in the model: the high mortality rate in the first 24 hours after coronary occlusion, and the considerable diversity of myocardial infarct sizes. In this review we described methodological and pathophysiological aspects of the model, concluding with a reference to an alternative technique, which uses radio frequency electric current to produce myocardial necrosis, and evolves with low mortality rates and homogeneous infarct sizes.For years, congestive heart failure (CHF) has been among the most investigated topics in cardiology. Besides the information obtained in humans, contribution made by the research conducted in laboratory animals is also noteworthy. Among the several experimental models available, the most used is that which promotes a congestive heart syndrome by the induction of myocardial necrosis in rats. Its current popularity and the foreseen increased interest in this model stress the importance of describing the pathophysiological characteristics after myocardial infarction (MI) in rats. Recently, a valuable literature review on the rat myocardial infarction model was published in the Arquivos Brasileiros de Cardiologia 1 .Although useful for the assessment of the congestive syndrome and the myocardial remodeling that occurs in the remaining cardiac muscle, the pathophysiological process established in rats after coronary artery ligation is not analogous to what happens in human coronary syndromes. The model lacks the arterial lesions that determine the distinctive clinical profile of human coronary artery disease: arrhythmias, transient ischemia, and recurrence of coronary occlusion, which are absent in laboratory animals.Occlusion of the anterior interventricular coronary artery is the strategy most frequently used for the induction of MI.The electrocardiogram 2 and the echocardiogram [3][4][5][6][7][8][9][10][11][12][13][14][15] are noninvasive methods capable of identifying the area of necrosis or scarring. Although it identifies the presence of an MI-dependent electrically inactive area, the ECG is not a method that can quantify the infarction area 2 . The echocardiogram can determine the presence and the size of the MI with very good sensitivity [3][4][5][6][7][8][9][10][11][12][13][14][15] , even in periods as early as two days after necrosis, and it also provides information about deviant atrial and ventricular function. The best method for post-mortem diagnosis of MI depends on the stage in which the autopsy occurs. In the first days after myocardial necrosis, the histopathologic exam may be inconclusive as to the limits of the necrotic area. For this phase, the triphe...

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