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Determination of myocardial energetic output for cardiac rhythm pacing.

ABSTRACT: This research is aimed to the determination of the changes in the cardiac energetic output for three different modes of cardiac rhythm pacing. The clinical investigation of thirteen patients with the permanent dual-chamber pacemaker implantation was carried out. The patients were taken to echocardiography examination conducted by way of three pacing modes (AAI, VVI and DDD). The myocardial energetic parameters-the stroke work index (SWI) and the myocardial oxygen consumption (MVO2) are not directly measurable, however, their values can be determined using the numerical model of the human cardiovascular system. The 24-segment hemodynamical model (pulsating type) of the human cardiovascular system was used for the numerical simulation of the changes of myocardial workload for cardiac rhythm pacing. The model was fitted by well-measurable parameters for each patient. The calculated parameters were compared using the two-tailed Student's test. The differences of SWI and MVO2 between the modes AAI and VVI and the modes DDD and VVI are statistically significant (P<0.05). On the other hand, the hemodynamic effects for the stimulation modes DDD and AAI are almost identical, i.e. the differences are statistically insignificant (P>0.05).

SUBMITTER: Herman D

PROVIDER: S-EPMC2137944 | biostudies-other | 2007 Dec

REPOSITORIES: biostudies-other

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Project description:BackgroundInflammation process is an important determinant for subsequent changes in cardiac function and remodeling after acute myocardial infarction (MI). Recent studies have implicated that ALK4 haplodeficiency improves cardiac function after MI. However, it remains unknown if the beneficial effects are partly attributed to ALK4 haplodeficiency-induced modulation on inflammatory response in the inflammatory phase of MI. In this research, we aimed to explore the mechanism of ALK4 haplodeficiency in the inflammatory stage of MI.MethodsALK4, CD16, and CD14 were detected in peripheral blood mononuclear cells (PBMCs) isolated from MI patients and healthy volunteers. ALK4 haplodeficiency (ALK4+/-) mice and wild-type (WT) littermates were randomly divided into the sham group and the MI group. Inflammation cytokines and chemokines were measured. Echocardiography and intracardiac electrophysiological recordings were performed on the 3rd day and the 7th day after MI operation. ALK4 expression and inflammation cytokines were also detected in LPS- or IL-4-stimulated bone marrow-derived macrophages (BMDM) from the ALK4+/- mice and WT littermates.ResultsALK4 gene expression in circulating monocytes of MI patients was higher than that in those of healthy volunteers. Cardiac inflammation and vulnerability of ventricular arrhythmia after acute myocardial injury are significantly alleviated in ALK4+/- mice as compared to WT littermates. On the 3rd day post-MI, the level of M1 macrophages were decreased in ALK4+/- mice as compared to WT littermates, while the level of M2 macrophages were increased on the 7th day post-MI. BMDM isolated from ALK4+/- mice displayed reduced secretion of pro-inflammation cytokines after stimulation by LPS in hypoxic condition and increased secretion of anti-inflammation cytokines after stimulation by IL-4. As a result, the haplodeficiency of ALK4 might be responsible for reduced inflammation response in the post-MI stage.ConclusionsALK4 haplodeficiency reduces cardiac inflammation, improves cardiac function, and finally reduces the vulnerability of ventricular arrhythmia in the inflammatory stage after MI.

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Determination of myocardial energetic output for cardiac rhythm pacing.

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