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Ventricular tachycardia may lead to haemodynamic deterioration and, in the case of long term persistence, is associated with the development of tachycardiomyopathy. The effect of ventricular tachycardia on haemodynamics in individuals with tachycardiomyopathy, but being in sinus rhythm has not been studied. Rapid ventricular pacing is a model of ventricular tachycardia. The aim of this study was to determine the effect of rapid ventricular pacing on blood pressure in healthy animals and those with tachycardiomyopathy. A total of 66 animals were studied: 32 in the control group and 34 in the study group. The results of two groups of examinations were compared: the first performed in healthy animals (133 examinations) and the second performed in animals paced for at least one month (77 examinations). Blood pressure measurements were taken during chronic pacing - 20 min after onset of general anaesthesia, in baseline conditions (20 min after pacing cessation or 20 min after onset of general anaesthesia in healthy animals) and immediately after short-term rapid pacing. In baseline conditions significantly higher systolic and diastolic blood pressure was found in healthy animals than in those with tachycardiomyopathy. During an event of rapid ventricular pacing, a significant decrease in systolic and diastolic blood pressure was found in both groups of animals. In the group of chronically paced animals the blood pressure was lower just after restarting ventricular pacing than during chronic pacing. Cardiovascular adaptation to ventricular tachycardia develops with the length of its duration. Relapse of ventricular tachycardia leads to a blood pressure decrease more pronounced than during chronic ventricular pacing.
The aim of the study was to assess the atrioventricular conduction in the model of porcine pacing induced tachycardiomyopathy. Fifty-one swine were examined: 27 were paced and 24 served as a control group. Every 4 weeks, the animals were anaesthetised for 1 h and an ECG Holter was performed. Thirty minutes after the onset of anaesthesia, P-R and R-R intervals were measured. Each result was assigned to the subgroup according to the animal's weight and the presence or absence of previous pacing. P-R interval was longer in animals after at least 4 weeks of rapid ventricular stimulation than in adjusted group of the animals according to the body mass. Multivariate analysis has showed that longer P-R interval was related to male gender, higher body mass, slower heart rate, and history of previous pacing. Chronic ventricular pacing led to the slowing of atrioventricular conduction. The presence of differences in the duration of R-R intervals between groups was only found in swine weighing 120-139 kg. The R-R interval was shorter in paced animals, whereas PR interval was longer in that group, indicating that PR prolongation is related to electrical or structural remodelling of the cardiac conductive tissue but not increased sympathetic nervous system activity, which is expected to produce corresponding changes in PR and R-R intervals.
Congestive heart failure is a clinical syndrome whose hallmarks are fatigue and dyspnea. Common pathophysiologic features of heart failure include changes in the structure of the left ventricle of the heart, function, and neurohormonal activation. A recapitulation of the heart failure phenotype in a large animal model can make it possible to translate basic science discoveries into clinical therapies. Models of myocardial infarction/ischemia, ischemic cardiomyopatyhy, ventricular pressure and volume overload and pacing- -induced dilated cardiomyopathy have been created for dogs, pigs and sheep to investigate heart failure and potential therapies. This article presents types of large animal models of heart failure, methods of their development and their clinical usefulness.
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