Compared to skeletal muscle cells, cardiac muscle cells are shorter and have fewer nuclei. Cardiac muscle tissue is also striated forming protein bands and contains tubules and gap junctions, unlike skeletal muscle tissue. Due to their continuous rhythmic contraction, cardiomyocytes require a dedicated blood supply to deliver oxygen and nutrients and remove waste products such as carbon dioxide from the cardiac muscle tissue.
This blood supply is provided by the coronary arteries. The inner layer of the heart wall is the endocardium, composed of endothelial cells that provide a smooth, elastic, non-adherent surface for blood collection and pumping. The endocardium may regulate metabolic waste removal from heart tissues and act as a barrier between the blood and the heart muscle, thus controlling the composition of the extracellular fluid in which the cardiomyocytes bathe.
This in turn can affect the contractility of the heart. This tissue also covers the valves of the heart and is histologically continuous with the vascular endothelium of the major blood vessels entering and leaving the heart. The Purkinje fibers are located just beneath the endocardium and send nervous impulses from the SA and AV nodes outside of the heart into the myocardial tissues.
The endocardium can become infected, a serious inflammatory condition called infective endocarditis. This and other potential problems with the endocardium may damage the valves and impair the normal flow of blood through the heart. CRT device configurations that induced the best haemodynamic response at the epicardial and endocardial LV pacing sites.
The main finding of the study is that endocardial biventricular pacing has similar acute haemodynamic effects than pacing at the epicardium in a NICM swine model. LV endocardial and epicardial biventricular pacing induced the best haemodynamic response at the basal regions, as compared with mid or apical positions. Our results are in concordance with those reported by Dzemali et al. These authors observed that both endocardial and epicardial pacing of the lateral wall of the LV led to an improvement in LV function, with no differences between endocardium and epicardium in any of the haemodynamic and echocardiographic parameters analysed.
In the present study we used a swine animal model of dilated NICM and further evaluate all LV epicardial—endocardial representative regions, recording multiple haemodynamic aortic blood flow, intraventricular pressures and electrocardiographic parameters. In contrast, various studies have demonstrated the advantages of LV endocardial pacing over epicardial pacing in canine models of isolated acute left bundle branch block LBBB and heart failure plus acute LBBB.
This study demonstrated the clinical feasibility of endocardial pacing in CRT and, although it was not a comparative study, that the rate of responders to endocardial pacing was similar to the rate of responders to classical CRT. The authors also pointed out that there is a large inconsistence between the results of small and large studies, probably due to publication bias.
It can be hypothesized that the discrepancies observed between the different animal and human studies could be related to differences in the species-specific intrinsic characteristics of the Purkinje system and its functional remodelling under myocardial disease. The distribution of the Purkinje system in dogs is similar to that of healthy humans, being circumscribed to the endocardium, 10 , 12 resulting in faster conduction velocities in the endocardium than in the epicardium.
These differences between dogs, sheep and swine would explain the discordant results of the animal studies evaluating endocardial—epicardial pacing in CRT. Studies in humans with heart failure HF and advanced myocardial disease have demonstrated damage of the distal Purkinje network and conduction remodeling. This has been related to a reduced gradient of conduction velocities between the endocardium and epicardium.
This absence of haemodynamic—ECG correlation occurred both in epicardial as well as to endocardial pacing. To the extent of our knowledge, studies correlating pacing locations with acute haemodynamic response and ECG changes are scarce in the literature and their results are limited.
Spotnitz et al. These authors found a negative correlation improved haemodynamics with shorter QRS only in five of seven patients, although the best haemodynamic response did not correspond to the shortest QRS.
Derval et al. They found that QRS shortening correlated with acute haemodynamic response and that LV pacing location was a primary determinant of paced QRS duration. However, QRS shortening did not predict the maximum haemodynamic response. Porta-Sanchez et al. The response of epicardial and endocardial LV pacing was regional dependent and the best response was obtained at the basal regions. Our observation is in agreement with previous experimental studies.
Similarly, Bordachar et al. Our study extends their results by evaluating all endocardial and epicardial LV representative regions, and corroborates that the region dependency present in epicardial pacing is also observed in endocardial pacing.
In addition, these results fully agree with long term studies in humans that report worse CRT outcomes associated to pacing from apical regions. We found a specific device programming configuration AV and VV interval for each site and animal that induced the best haemodynamic response to biventricular pacing. These results are comparable with clinical observations stressing the need for an individual optimization of the device pacing parameters.
Left ventricular pacing in CRT is generally performed epicardially via the coronary venous system. This study suggests non-inferiority of endocardial versus epicardial LV pacing, and therefore endorses the clinical strategy of endocardial pacing when conventional epicardial pacing is not feasible or for non-responders.
Some limitations of our study should be noted. The LV dilatation and dys-synchrony model did not generate a definitive LBBB pattern but a certain degree of non-specific intraventricular conduction defect. We did not collect data on regional electrical delays due to technical issues related to the experimental setting. However, our pacing results were regional dependent and the best response was obtained at the basal regions, suggesting that the electrical properties of the model are comparable to those of human diseased hearts.
We only analysed the acute haemodynamic and ECG effects of biventricular endocardial and epicardial pacing. Whether acute results correlate to the long-term response to CRT needs further investigation. It is also the standard contractility parameter used in the clinical setting. Additional parameters of contractility like those based on pressure volume loops were not assessed since LV volumes were not measured.
The right ventricular pacing electrode in this study was positioned in the apex. Our findings regarding segmental LV lead position may differ from other right ventricular pacing sites i. However, this should not significantly alter the comparison between LV endocardial and epicardial pacing that was the main aim of the study. Additionally, the use of an electrophysiological endocardial catheter and a plunge epicardial electrode, and the methodology for assuring the correspondence of the endocardial and epicardial sites may arise some concerns.
The plunge electrode was minimally inserted in the epicardium to obtain pure epicardial regional capture.
The radiological approach to position the endocardial catheter facing the plunge electrode and the inter-electrode separation of the catheter seems accurate enough as to allow the capture of the same segment of the heart, allowing direct comparison of paired pacing segments. The study shows that endocardial pacing has similar haemodynamic and electrocardiographic benefit than pacing from the epicardium in a dilated NICM swine model.
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Left ventricular endocardial or triventricular pacing to optimize cardiac resynchronization therapy in a chronic canine model of ischemic heart failure. Endocardial left ventricular pacing improves cardiac resynchronization therapy in chronic asynchronous infarction and heart failure models.
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