Animal – ABC CARDIOL

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Editorial

Applicability of Body Surface Potential Mapping Through Exercise in Small Animals

The electrical potentials of the heart have been recorded for over a hundred years to represent the distribution of these internal electrical events on the torso surface. Such recordings that started with Waller tried to establish a resultant vector from a bipolar source, the “heart vector,” assuming that this distribution of potentials would act as if an electrical bipole was inserted inside the thorax and applied to the body surface, with a third electrode adding the sagittal component of the vector. The three would be enough to supply all the electrocardiogram (ECG) information extracted from measurements from the body surface. It was not until the 1930s and 1940s that the number of electrodes on the chest surface was tentatively increased to detect events occurring in cardiac areas near the precordial leads. Finally, after 1950 some studies demonstrated that the complexity of the electrical information generated inside the heart was far greater than that generated by a sole bipole, with multiple wavefronts in the ventricles creating currents that flow into and from the heart in several places; the potentials, therefore, would exhibit maximum and minimum distributions varying with time, usually located in areas unexplored by the conventional electrocardiogram.

New methodologies complementing the ECG and vectorcardiogram (ECG) added new electrodes (dorsal and right precordial leads), and, since Wilson, the 12-lead ECG started to have three bipolar and three unipolar modified leads in the frontal plane, in addition to six unipolar (precordial) leads on the anterior chest, which can record most of the information about electrical events in the heart. However, the myocardial electrical activity global expression cannot be captured without a larger number of simultaneously recorded leads.

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Editorial

Preconditioning in Ischemia-Reperfusion Lesion

Mariana Gatto et al. Gustavo Augusto Ferreira Mota Luana Urbano Pagan Mariana Janini Gomes Marina Politi Okoshi

Ischemic heart disease is characterized by a decrease in myocardial blood flow, which reduces the relationship between oxygen supply and demand. The condition has attracted the attention of the scientific community due to its high incidence, elevated morbidity and mortality, and high therapeutic cost. The treatment primarily relies on myocardial revascularization. Paradoxically, reperfusion and restoration of blood flow can cause additional damage, called myocardial ischemia-reperfusion (IR) injury. Several mechanisms are involved in the IR injury, such as ionic homeostasis change, intracellular calcium transient alteration, metabolic and mitochondrial dysfunction, inflammation, and reactive oxygen species increase.^, These factors may contribute to an increase in the myocardial necrosis size, post-ischemia heart failure, and death.

First identified in the mid-1980s, ischemic preconditioning is a process whereby repeated application of short periods of ischemia alternating with reperfusion protect the myocardium from longer ischemic insults, therefore reducing the infarction size.^, The beneficial effect of ischemic preconditioning was shown in angina patients; when evolving to myocardial infarction, they had a smaller infarcted area and a better clinical prognosis than previously asymptomatic patients.^, Additionally, preconditioning of rats with acute physical stress prior to the IR insult reduced infarct size and improved hemodynamic parameters.

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Original Article

Cardiac implications after myocardial infarction in rats previously undergoing physical exercise

Eduardo Carvalho de Arruda Veiga et al. Leslie Andrews Portes Danilo Sales Bocalini Ednei Luiz Antonio … Alexandra Alberta dos Santos Marília Higuchi Santos Flavio André Silva Paulo José Ferreira Tucci

BACKGROUND: Few studies have analyzed the cardiac effects of exercise prior to coronary occlusion. OBJECTIVE: To evaluate the effects of myocardial infarction in rats undergoing physical exercise. METHODS: Female rats underwent swimming exercise or were kept sedentary for eight weeks and were randomized to coronary occlusion or sham surgery, in one of the following four groups: Sedentary (S), exercise (E), Sedentary myocardial infarction (SMI) and Exercise myocardial infarction (EMI). After six weeks, their biometrics, Doppler echocardiography, hemodynamics and myocardial mechanics were analyzed. RESULTS: No cardioprotection was observed in EMI animals and there was no difference in infarct size (%LV) between EMI (38.50 ± 4.60%) and SMI (36.58 ± 4.11%). Water content of the lung (%) of SMI (80 ± 0.59) and EMI (80 ± 0.57) was higher than that of S (78 ± 0.15) and E (78 ± 0.57) groups. Left ventricular systolic pressure (mmHg) (S: 130 ± 5, E: 118 ± 8; SMI: 91 ± 3; EMI: 98 ± 3) and the first positive time derivative (mmHg) positive pressure (S: 8216 ± 385; E: 8437 ± 572; SMI: 4674 ± 455; EMI: 5080 ± 412) of S and E were higher than those of SMI and EMI. The transverse fractional shortening (%) of SMI (27 ± 2) and EMI (25 ± 2) were similar and lower than that of E (65 ± 2) and S (69 ± 2). The E/A ratio was higher in SMI (5.14 ± 0.61) and EMI (4.73 ± 0.57) compared to S (2.96 ± 0.24) and E (2.83 ± 0 21). In studies of isolated papillary muscle, depression of the contractile capacity observed was similar to that of SMI and EMI, and there was no change in myocardial stiffness. CONCLUSION: Previous training by swimming did not attenuate cardiac implications due to myocardial infarction.

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Applicability of Body Surface Potential Mapping Through Exercise in Small Animals

Preconditioning in Ischemia-Reperfusion Lesion

Cardiac implications after myocardial infarction in rats previously undergoing physical exercise

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