scholarly journals A novel substrate for arrhythmias in Chagas disease

2021 ◽  
Vol 15 (6) ◽  
pp. e0009421
Author(s):  
Artur Santos-Miranda ◽  
Julliane V. Joviano-Santos ◽  
Jaqueline O. Sarmento ◽  
Alexandre D. Costa ◽  
Allysson T. C. Soares ◽  
...  
Keyword(s):  
Chagas Disease ◽  
Chronic Phase ◽  
Left Ventricular ◽  
Patch Clamp Technique ◽  
Inward Current ◽  
Transient Inward Current ◽  
Whole Cell Patch Clamp ◽  
Open Questions ◽  
Arrhythmogenic Substrate ◽  
Parasite Detection

Background Chagas disease (CD) is a neglected disease that induces heart failure and arrhythmias in approximately 30% of patients during the chronic phase of the disease. Despite major efforts to understand the cellular pathophysiology of CD there are still relevant open questions to be addressed. In the present investigation we aimed to evaluate the contribution of the Na+/Ca2+ exchanger (NCX) in the electrical remodeling of isolated cardiomyocytes from an experimental murine model of chronic CD. Methodology/Principal findings Male C57BL/6 mice were infected with Colombian strain of Trypanosoma cruzi. Experiments were conducted in isolated left ventricular cardiomyocytes from mice 180–200 days post-infection and with age-matched controls. Whole-cell patch-clamp technique was used to measure cellular excitability and Real-time PCR for parasite detection. In current-clamp experiments, we found that action potential (AP) repolarization was prolonged in cardiomyocytes from chagasic mice paced at 0.2 and 1 Hz. After-depolarizations, both subthreshold and with spontaneous APs events, were more evident in the chronic phase of experimental CD. In voltage-clamp experiments, pause-induced spontaneous activity with the presence of diastolic transient inward current was enhanced in chagasic cardiomyocytes. AP waveform disturbances and diastolic transient inward current were largely attenuated in chagasic cardiomyocytes exposed to Ni2+ or SEA0400. Conclusions/Significance The present study is the first to describe NCX as a cellular arrhythmogenic substrate in chagasic cardiomyocytes. Our data suggest that NCX could be relevant to further understanding of arrhythmogenesis in the chronic phase of experimental CD and blocking NCX may be a new therapeutic strategy to treat arrhythmias in this condition.

Abstract 17193: Inhibiting Late Sodium Current Attenuates Isoproterenol-Induced Transient Inward Current and Delayed Afterdepolarizations in Ventricular Myocytes

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Yejia Song ◽  
Nesrine El-Bizri ◽  
Sridharan Rajamani ◽  
Luiz Belardinelli
Keyword(s):  
Ventricular Myocytes ◽  
Sodium Current ◽  
Selective Inhibition ◽  
Adrenergic Stimulation ◽  
Patch Clamp Technique ◽  
Cardiac Tissues ◽  
Inward Current ◽  
Transient Inward Current ◽  
Whole Cell Patch Clamp ◽  
Series Of Experiments

Introduction: The β-adrenergic agonist isoproterenol (ISO) is known to induce the arrhythmogenic transient inward current (I Ti ) and delayed afterdepolarization (DAD) via a stimulation of L-type Ca 2+ current. Recent studies found that ISO-induced DADs in cardiac tissues are inhibited by GS967, a selective blocker of the late Na + current (I NaL ). Thus, we hypothesize that I NaL contributes to the actions of ISO, and selective inhibition of this current will reduce ISO-induced I Ti and DADs. Methods: Transmembrane currents and action potentials of rabbit and guinea pig (GP) ventricular myocytes were recorded using the whole-cell patch-clamp technique. ISO (0.1 μM), GS967 (1 μM) and the Na + channel blocker tetrodotoxin (TTX, 3 μM) were used in the experiments. Results: In rabbit myocytes, application of ISO caused an increase in the amplitude of I NaL from -0.10±0.03 to -0.32±0.04 pA/pF (n = 17, p < 0.05). The ISO-stimulated I NaL was inhibited by GS967 and TTX. In one series of experiments, ISO increased the I NaL from -0.14±0.04 to -0.35±0.06 pA/pF, and GS967 applied in the presence of ISO reduced the current to -0.14±0.03 pA/pF (n = 9, p < 0.05). In another series of experiments, the amplitude of I NaL was increased by ISO from -0.17±0.08 to -0.41±0.09 pA/pF, and was decreased to -0.09±0.08 pA/pF when TTX was applied with ISO (n = 5, p < 0.05). Application of ISO also induced I Ti and DADs. GS967 applied in the presence of ISO inhibited the amplitude of I Ti by 52±6%, from -1.79±0.30 to -0.87±0.16 pA/pF (n = 8, p < 0.05). Consistent with the inhibition of I Ti , GS967 suppressed the amplitude of ISO-induced DADs by 56±12%, from 6.54±1.59 to 3.22±1.27 mV (n = 5, p < 0.05). Similarly, in GP myocytes ISO-induced I Ti and DADs were decreased by GS967 from -1.14±0.21 to -0.73±0.16 pA/pF (n = 7, p < 0.05) and from 7.16±0.59 to 4.67±0.24 mV (n = 5, p < 0.05), respectively. Conclusions: An increased I NaL is likely to contribute to the proarrhythmic effects of ISO in cardiac myocytes. GS967 significantly attenuated ISO-induced I NaL , I Ti and DADs, suggesting that inhibiting this current could be an effective strategy to antagonize the arrhythmogenic actions of β-adrenergic stimulation.

Mechanisms underlying delayed afterdepolarizations in hypertrophied left ventricular myocytes of rats

2001 ◽  
Vol 281 (2) ◽  
pp. H903-H914 ◽  
Author(s):  
János Mészáros ◽  
Daniel Khananshvili ◽  
George Hart
Keyword(s):  
Ventricular Myocytes ◽  
Pump Current ◽  
Left Ventricular ◽  
Daily Injection ◽  
Nonselective Cation Channel ◽  
Patch Clamp Technique ◽  
Inward Current ◽  
Na Pump ◽  
Whole Cell Patch Clamp ◽  
Delayed Afterdepolarizations

Cardiac hypertrophy was induced in rats by daily injection of isoproterenol (5 mg/kg ip) for 7 days. Membrane voltage and currents were recorded using the whole cell patch-clamp technique in left ventricular myocytes from control and hypertrophied hearts. Ryanodine-sensitive delayed afterdepolarizations (DADs) and transient inward current ( I ti) appeared in hypertrophied cells more often and were of larger amplitude than in control cells. DADs and I ti are carried principally by Na/Ca exchange with smaller contributions from a nonselective cation channel and from a Cl− channel. The latter is expressed only in hypertrophied myocytes. In hypertrophy, the density of caffeine-induced Na/Ca exchange current ( I Na/Ca) was increased by 26%, sarcoplasmic reticulum (SR) Ca2+ content as assessed from the integral of I Na/Ca was increased by 30%, the density of Na-pump current ( I pump) was reduced by 40%, and the intracellular Na+ content, measured by Na+-selective microelectrodes was increased by 55%. The results indicate that DADs and I ti are generated by spontaneous Ca2+ release from an overloaded SR caused by a downregulated Na pump and an upregulated Na/Ca exchange. These findings may explain the propensity for arrhythmias seen in this model of hypertrophy.

scholarly journals Differential Interactions of Na+ Channel Toxins with T-type Ca2+ Channels

2008 ◽  
Vol 132 (1) ◽  
pp. 101-113 ◽  
Author(s):  
Hui Sun ◽  
Diego Varela ◽  
Denis Chartier ◽  
Peter C. Ruben ◽  
Stanley Nattel ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Low Voltage ◽  
Parallel Evolution ◽  
Na Channel ◽  
Patch Clamp Technique ◽  
Hek 293 ◽  
Inward Current ◽  
Whole Cell Patch Clamp ◽  
The Right ◽  
Ca2 Channels

Two types of voltage-dependent Ca2+ channels have been identified in heart: high (ICaL) and low (ICaT) voltage-activated Ca2+ channels. In guinea pig ventricular myocytes, low voltage–activated inward current consists of ICaT and a tetrodotoxin (TTX)-sensitive ICa component (ICa(TTX)). In this study, we reexamined the nature of low-threshold ICa in dog atrium, as well as whether it is affected by Na+ channel toxins. Ca2+ currents were recorded using the whole-cell patch clamp technique. In the absence of external Na+, a transient inward current activated near −50 mV, peaked at −30 mV, and reversed around +40 mV (HP = −90 mV). It was unaffected by 30 μM TTX or micromolar concentrations of external Na+, but was inhibited by 50 μM Ni2+ (by ∼90%) or 5 μM mibefradil (by ∼50%), consistent with the reported properties of ICaT. Addition of 30 μM TTX in the presence of Ni2+ increased the current approximately fourfold (41% of control), and shifted the dose–response curve of Ni2+ block to the right (IC50 from 7.6 to 30 μM). Saxitoxin (STX) at 1 μM abolished the current left in 50 μM Ni2+. In the absence of Ni2+, STX potently blocked ICaT (EC50 = 185 nM) and modestly reduced ICaL (EC50 = 1.6 μM). While TTX produced no direct effect on ICaT elicited by expression of hCaV3.1 and hCaV3.2 in HEK-293 cells, it significantly attenuated the block of this current by Ni2+ (IC50 increased to 550 μM Ni2+ for CaV3.1 and 15 μM Ni2+ for CaV3.2); in contrast, 30 μM TTX directly inhibited hCaV3.3-induced ICaT and the addition of 750 μM Ni2+ to the TTX-containing medium led to greater block of the current that was not significantly different than that produced by Ni2+ alone. 1 μM STX directly inhibited CaV3.1-, CaV3.2-, and CaV3.3-mediated ICaT but did not enhance the ability of Ni2+ to block these currents. These findings provide important new implications for our understanding of structure–function relationships of ICaT in heart, and further extend the hypothesis of a parallel evolution of Na+ and Ca2+ channels from an ancestor with common structural motifs.

scholarly journals Prospective Analysis of Myocardial Strain Through Evolution of Chagas Disease in the Hamster Animal Model

2021 ◽  
Author(s):  
Fernando F.F. Ribeiro ◽  
Henrique T. Moreira ◽  
Antônio C.L. Barros-Filho ◽  
Denise M Tanaka ◽  
Camila G. Fabricio ◽  
...  
Keyword(s):  
Animal Model ◽  
Chagas Disease ◽  
Myocardial Strain ◽  
Chronic Phase ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Saline Control ◽  
P Value ◽  
Ventricular Ejection Fraction ◽  
Time Interaction

Abstract Background: Speckle tracking echocardiography (STE) enables early diagnosis of myocardial damage by evaluating myocardial strain. We aimed to study sequential changes in structural and functional ventricular parameters during Chagas disease (CD) natural history in an animal model. Methods: 37 Syrian hamsters were inoculated intraperitoneally with Trypanosoma cruzi (Chagas) and 20 with saline (Control). Echocardiography was performed before the infection (baseline), at 1month (acute phase), 4, 6 and 8 months (chronic phase) using Vevo 2100 (Fujifilm Inc.) ultrasound system. Left ventricular end-diastolic diameter (LVEDD), end-systolic diameter (LVESD), left ventricular ejection fraction (LVEF), global longitudinal (GLS), circumferential (GCS) and radial (GRS) strain were evaluated. Tricuspid annular plane systolic excursion (TAPSE) was used to assess right ventricular function. At 8 months, animals were euthanized and LV myocardial samples were analyzed for quantitation of inflammation and fibrosis. Results: LVEF decreased over time in Chagas group and a difference from Control was detected at 6 months (p-value of groups#time interaction = 0.005). There was a pronounced decrease in GLS, GCS and TAPSE in Chagas group (p-value of groups#time interaction = 0.003 for GLS, < 0.001 for GCS and < 0.009 for TAPSE vs Control) since the first month. LVESD, LVEF and GLS were significantly correlated to the number of inflammatory cells (r= 0.41, p=0.046; r= -0.42, p=0.042; r=0.41, p=0.047) but not to fibrosis. Conclusions: In the Syrian hamster model of CD STE parameters (GLS and GCS) showed an early decrease. Changes in LVEF, LVESD and GLS were correlated to myocardial inflammation but not to fibrosis.

scholarly journals Prospective analysis of myocardial strain through the evolution of Chagas disease in the hamster animal model

2021 ◽  
Author(s):  
Fernando Fonseca França Ribeiro ◽  
Henrique Turin Moreira ◽  
Antônio Carlos Leite de Barros-Filho ◽  
Denise M. Tanaka ◽  
Camila G. Fabricio ◽  
...  
Keyword(s):  
Animal Model ◽  
Chagas Disease ◽  
Myocardial Strain ◽  
Chronic Phase ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Saline Control ◽  
P Value ◽  
Ventricular Ejection Fraction ◽  
Time Interaction

AbstractSpeckle tracking echocardiography (STE) enables early diagnosis of myocardial damage by evaluating myocardial strain. We aimed to study sequential changes in structural and ventricular functional parameters during Chagas disease (CD) natural history in an animal model. 37 Syrian hamsters were inoculated intraperitoneally with Trypanosoma cruzi (Chagas) and 20 with saline (Control). Echocardiography was performed before the infection (baseline), at 1 month (acute phase), 4, 6, and 8 months (chronic phase) using Vevo 2100 (Fujifilm Inc.) ultrasound system. Left ventricular end-diastolic diameter, Left ventricular end-systolic diameter (LVESD), Left ventricular ejection fraction (LVEF), Global longitudinal (GLS), circumferential (GCS) and radial (GRS) strain were evaluated. Tricuspid annular plane systolic excursion (TAPSE) was used to assess right ventricular function. At 8 months, animals were euthanized and LV myocardial samples were analyzed for quantitation of inflammation and fibrosis. LVEF decreased over time in Chagas group and a difference from Control was detected at 6 months (p-value of groups#time interaction = 0.005). There was a pronounced decrease in GLS, GCS and TAPSE in Chagas group (p-value of groups#time interaction = 0.003 for GLS, < 0.001 for GCS and < 0.009 for TAPSE vs Control) since the first month. LVESD, LVEF and GLS were significantly correlated to the number of inflammatory cells (r = 0.41, p = 0.046; r = − 0.42, p = 0.042; r = 0.41, p = 0.047) but not to fibrosis. In the Syrian hamster model of CD STE parameters (GLS and GCS) showed an early decrease. Changes in LVEF, LVESD, and GLS were correlated to myocardial inflammation but not to fibrosis.

Comparison of a Ca(2+)-gated conductance and a second-messenger-gated conductance in rat olfactory neurons

2000 ◽  
Vol 203 (3) ◽  
pp. 567-573
Author(s):  
Y. Okada ◽  
R. Fujiyama ◽  
T. Miyamoto ◽  
T. Sato
Keyword(s):  
Outward Current ◽  
Patch Clamp Technique ◽  
External Application ◽  
Olfactory Neurons ◽  
Internal Solution ◽  
Inward Current ◽  
Whole Cell Patch Clamp ◽  
Cation Conductance ◽  
Intracellular Ca ◽  
Sustained Outward Current

The effect of a rise in intracellular Ca(2+) concentration was analyzed in isolated rat olfactory neurons using a whole-cell patch-clamp technique. Intracellular dialysis of 1 mmol l(−)(1) Ca(2+) in a standard-K(+), low-Cl(−) internal solution (E(Cl)=−69 mV) from the patch pipette into the olfactory neurons induced a sustained outward current of 49+/−5 pA (N=13) at −50 mV in all the cells examined. The outward currents were inhibited by external application of 100 micromol l(−)(1) 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB). External application of a Ca(2+) ionophore, 3 micromol l(−)(1) ionomycin, induced an inward current in three of eight cells whose voltages were clamped using the gramicidin-perforated technique, but ionomycin elicited an outward current in the other five cells, suggesting that natural intracellular Cl(−) concentration in the olfactory neurons was heterogeneous. While intracellular dialysis of 50 micromol l(−)(1) inositol 1,4,5-trisphosphate (1,4,5-InsP(3)) in the standard-K(+), low-Cl(−) internal solution induced the NPPB-sensitive outward current in 31 % of cells, and 500 micromol l(−)(1) cAMP induced it in 21 % of cells, a large proportion of the cells displayed an inward current in response to 1,4,5-InsP(3) and cAMP. The results suggest that 1,4,5-InsP(3) and cAMP can elicit Ca(2+)-dependent Cl(−) conductance and Ca(2+)-independent cation conductance in rat olfactory neurons.

scholarly journals In SituExpression of Regulatory Cytokines by Heart Inflammatory Cells in Chagas' Disease Patients with Heart Failure

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Denise Bertulucci Rocha Rodrigues ◽  
Marlene Antonia dos Reis ◽  
Audrey Romano ◽  
Sanívia Aparecida de Lima Pereira ◽  
Vicente de Paula Antunes Teixeira ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chagas Disease ◽  
Chronic Phase ◽  
Protozoan Parasite ◽  
Parasite Load ◽  
Inflammatory Cells ◽  
Left Ventricular ◽  
Inflammatory Cell Infiltrate ◽  
Heart Cells ◽  
Th1 Immune Responses

Chagas' disease is caused by the protozoan parasiteTrypanosoma cruzi. The immune system plays an important role in the reduction of parasite load, but may also contribute to the development of lesions observed during the chronic phase of the disease. We analyzed cytokines produced by inflammatory heart cells in 21 autopsy samples obtained from patients with Chagas' disease divided according to the presence or absence of heart failure (HF). Left ventricular sections were analyzed by immunohistochemistry using antibodies against human IL-4, IFN-γ, TGF-β, TNF-α, and NOS2.In situmRNA expression was quantified by a Low Density Array. The number of IFN-γ-positive cells was significantly higher than IL-4 positive cells. TNF-α, TGF-βand NOS2 were detected in 65%, 62% and 94% of samples respectively. There was an association between TNF-α-producing cells and the presence of HF. Subjects with HF presented higher levels of STAT4 mRNA, whereas FoxP3 and STAT6 levels were similar in the two groups. A Th1 cytokine pattern predominated in the cardiac inflammatory cell infiltrate of Chagas’ disease patients associated with HF. High degree of fibrosis was associated with low NOS2 expression. These results support the idea that Th1 immune responses are involved in heart lesions of Chagas' disease patients.

GABA-Mediated Inhibition of Glutamate Release During Ischemia in Substantia Gelatinosa of the Adult Rat

2003 ◽  
Vol 89 (1) ◽  
pp. 257-264 ◽  
Author(s):  
Noriaki Matsumoto ◽  
Eiichi Kumamoto ◽  
Hidemasa Furue ◽  
Megumu Yoshimura
Keyword(s):  
Glutamate Release ◽  
Control Level ◽  
Outward Current ◽  
Substantia Gelatinosa ◽  
Slow Inward Current ◽  
Patch Clamp Technique ◽  
Inward Current ◽  
Adult Rat ◽  
Whole Cell Patch Clamp ◽  
Inward Currents

An ischemia-induced change in glutamatergic transmission was investigated in substantia gelatinosa (SG) neurons of adult rat spinal cord slices by use of the whole cell patch-clamp technique; the ischemia was simulated by superfusing an oxygen- and glucose-free medium (ISM). Following ISM superfusion, 21 of 37 SG neurons tested produced an outward current (23 ± 4 pA at a holding potential of −70 mV), which was followed by a slow and subsequent rapid inward current; the remaining neurons had only inward currents. During such a change in holding currents, spontaneous excitatory postsynaptic currents (EPSCs) were remarkably decreased in a frequency with time (half-decay time of the frequency: about 65 s). The frequency of spontaneous EPSCs was reduced to 28 ± 13% ( n = 37) of the control level during the generation of the slow inward current (about 4 min after the beginning of ISM superfusion) without a change in the amplitude of spontaneous EPSCs. When ISM was superfused together with either bicuculline (10 μM) or CGP35348 (20 μM; GABAA and GABAB receptor antagonists, respectively), spontaneous EPSC frequency reduced by ISM recovered to the control level and then the frequency markedly increased [by 325 ± 120% ( n = 22) and 326 ± 91% ( n = 17), respectively, 4 min after ISM superfusion]; this alteration in the frequency was not accompanied by a change in spontaneous EPSC amplitude. Superfusing TTX (1 μM)-containing ISM resulted in a similar recovery of spontaneous EPSC frequency and following increase (by 328 ± 26%, n = 12) in the frequency; strychnine (1 μM) did not affect ISM-induced changes in spontaneous EPSC frequency ( n = 5). It is concluded that the ischemic simulation inhibits excitatory transmission to SG neurons, whose action is in part mediated by the activation of presynaptic GABAAand GABAB receptors, probably due to GABA released from interneurons as a result of an ischemia-induced increase in neuronal activities. This action might protect SG neurons from an excessive excitation mediated by l-glutamate during ischemia.

Dual effect of phosphatase inhibitors on calcium channels in intestinal smooth muscle cells

1993 ◽  
Vol 264 (2) ◽  
pp. C296-C301 ◽  
Author(s):  
K. Obara ◽  
H. Yabu
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Patch Clamp Technique ◽  
Pipette Solution ◽  
Phosphatase Inhibitors ◽  
Inward Current ◽  
Whole Cell Patch Clamp ◽  
Voltage Dependent ◽  
High Concentrations

The effects of okadaic acid (OA) and calyculin A (CL-A), potent inhibitors of protein phosphatases type 1 (PP1) and type 2A (PP2A), on inward current carried by Ba2+ through voltage-dependent Ca2+ channel in guinea pig teniae coli smooth muscle cells were investigated using whole-cell patch-clamp technique. High concentrations of OA (5 x 10(-8)-5 x 10(-6) M) and CL-A (10(-9)-10(-7) M) dose dependently increased the inward current. The concentration producing apparent half-maximum enhancing effect values for OA and CL-A were 1.12 x 10(-7) and 1.78 x 10(-9) M, respectively. CL-A appeared to be approximately 100-fold more potent in increasing the inward current than OA. Lower concentrations of OA (10(-10)-2 x 10(-8) M) and CL-A (10(-11)-10(-9) M) decreased the inward current. The maximum inhibitory effects of OA and CL-A were observed at 10(-8) M OA and 5 x 10(-10) M CL-A, respectively. CL-A is approximately 100 times more effective inhibitor of PP1 than OA, and lower concentrations of OA and CL-A used in the present study inhibit PP2A activity, but they have no or little effect on PP1 activity (Ishihara, H., B. L. Martin, D. L. Brautigan, H. Karaki, H. Ozaki, Y. Kato, N. Fusetani, S. Watabe, K. Hashimoto, D. Uemura and D. J. Hartshorne. Biochem. Biophys. Res. Commun. 159: 871-877, 1989). In the absence of ATP in pipette solution, OA and CL-A did not affect the inward current.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Resting and Dynamic Electrocardiography in Dogs with Experimental Chagas Cardiomyopathy

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
R. Oliveira Alves ◽  
A. A. Camacho ◽  
D. P. Junior
Keyword(s):  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Acute Phase ◽  
Sinus Tachycardia ◽  
Chronic Phase ◽  
Left Ventricular ◽  
Sinus Arrest ◽  
Chagas Cardiomyopathy ◽  
Electrocardiographic Monitoring ◽  
Electrocardiographic Changes

In the present protocol, adult dogs were infected with Trypanosoma cruzi, Bolivian strain, in order to show electrocardiographic changes by means of resting and dynamic (Holter) methods during acute and chronic phases of Chagas disease. In the acute phase there were sinus tachycardia, atrial and left ventricular overload, millivoltage suppression, electric alternance, and episodes of sinus arrest. At the parasitemia peak, atrium-ventricular block, junctional escape complexes, and atrium-ventricular dissociation were observed. Dogs that presented the most serious arrhythmias died suddenly. The increase in supraventricular and ventricular arrhythmic events, concentrated in the 4th postinoculation week, was visible at electrocardiographic monitoring. In the chronic phase, the events were restricted to first-degree atrium-ventricular blocks, premature ventricular complexes, ventricular bigeminy, and electrical alternation. It was concluded that the computerized and dynamic electrocardiography allowed to diagnose transient arrhythmia and to observe that the main tachyarrhythmic changes are concentrated at the acute phase concomitantly to the parasitemia peak.

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