Zur Entstehung intramyokardialer Blutungen

European Journal of Cardio-Thoracic Surgery

Niederer

Stephenson

et al. 2017

Recent morphological studies provide evidence that the ventricular walls are arranged as a 3D meshwork of aggregated cardiomyocyte chains, exhibiting marked local structural variations. In contrary to previous findings, up to two-fifths of the chains are found to have a partially transmural alignment, thus deviating from the prevailing tangential orientation. Upon contraction, they produce, in addition to a tangential force, a radial force component that counteracts ventricular constriction and aids widening of the ventricular cavity. In experimental studies, we have provided evidence for the existence of such forces, which are auxotonic in nature. This is in contrast to the tangentially aligned myocytes that produce constrictive forces, which are unloading in nature. The ventricular myocardium is, therefore, able to function in an antagonistic fashion, with the prevailing constrictive forces acting simultaneously with a dilatory force component. The ratio of constrictive to dilating force varies locally according to the specific mural architecture. Such antagonism acts according to local demands to preserve the ventricular shape, store the elastic energy that drives the fast late systolic dilation and apportion mural motion to facilitate the spiralling nature of intracavitary flow. Intracavitary pressure and flow dynamics are thus governed concurrently by ventricular constrictive and dilative force components. Antagonistic activity, however, increases deleteriously in states of cardiac disease, such as hypertrophy and fibrosis. ß-blockade at low dosage acts selectively to temper the auxotonic forces.

Section: Vi1 Intrinsic Antagonism Requires Beat-to-beat Control Of Fu...mentioning

confidence: 99%

What is the clinical significance of ventricular mural antagonism?

European Journal of Cardio-Thoracic Surgery

Niederer

Stephenson

et al. 2017

“…This mechanism has been reported in terminal situations, when hypovolemia had erroneously been treated with pharmacological sympathoadrenergic stimulation. In this setting, extensive subendocardial and intramural haemorrhages have been described at autopsy [40]. In those who survive such an emergency, arrhythmias may develop, caused by the persisting damage to the subendocardial tissues.…”

Section: The Dualistic Structure and Function Of The Ventricular Wallmentioning

confidence: 99%

The architecture of the ventricular mass and its functional implications for organ-preserving surgery

European Journal of Cardio-Thoracic Surgery

Redmαnn

Anderson

2005

It has generally been accepted that the myocardial fibres within the ventricular mass are arranged in syncytial fashion, precluding the identification of discrete and isolated muscular pathways. Recently, however, an entire hypothesis for surgical treatment has been proposed on the basis of the existence of a 'ventricular myocardial band', suggesting that this arrangement in itself points to detrimental results following partial ventriculectomy. In this review, we re-state the evidence supporting the accepted concept of the ventricular mass being made up of an undefined number of wedge-shaped functional units, each of them exerting its individually programmed contribution to the global activity of the ventricular walls. The wedge-shaped units consist of bundles of individual fibres which are arranged tangentially. An important subset of fibres intrudes into the ventricular wall, thus creating oblique pathways. Their angle of intrusion varies, and can be measured at up to 30 degrees . The steeper the angle of their intrusion, the more efficiently do the fibres counteract the systolic mural thickening. The network of supporting connective tissue, nonetheless, provides the necessary steep angulation towards the endocardium. This fibrous matrix serves as continuous chain for the transmission of forces, including that in the direction from the epicardium towards the endocardium, resulting in a dilating force. We have shown, using needle force probes, that in the hypertrophic heart the dynamic equilibrium of dilating and constricting forces acts at elevated diastolic and systolic levels, because the obliquity of the fibres increases due to the thickening of the wall, and there is a concomitant increase in connective tissue, causing an increase in the forces opposing systolic mural thickening. Then, in a vicious cycle, both populations of myocardial fibres stimulate each other to hypertrophy. Eventually, coronary perfusion becomes critically impaired, with still further deposition of connective tissue. Ultimately, the vector of the dilating force comes to dominate the constricting force, and the ventricle dilates. In this setting, partial left ventriculectomy remains a functionally sound intervention, since it is capable of improving global ventricular function by improving the geometrical state of the remaining anatomic myocardial units.

Die antagonistische Funktion des Herzmuskels

Lunkenheimer¹,

Niederer

et al. 2018

Herz

In the hypertrophic heart the myostructural afterload in the form of endoepicardial networks is predominant, which enhances myocardial hypertrophy. The intrinsic antagonism is derailed. Likewise, the connective tissue scaffold, i.e. the stromatogenic afterload, is enriched in the response to the derailment of antagonism in a hypertrophic heart up to regional captivation of the heart musculature. Due to the selective susceptibility of the auxotonic, contracting oblique transmural myocardial network for low dose negative inotropic medication, this promises to attenuate progress in myocardial hypertrophy. Volume reduction surgery is most effective in reducing wall stress as long as the myocardium is not critically fettered by fibrosis. The use of external mechanical circulatory support is then effective if the heart is supported in its resting mode, which means around a middle width and at minimal amplitude of motion. The takotsubo cardiomyopathy might possibly reflect an isolated, extreme stimulation of the intrinsic antagonism as a response to hormonally induced sensitization of the myocardium to catecholamine. A particular significant conclusion with respect to the diseased heart is that clinical diagnostics need new impulses with a focus on the analysis of local motion patterns and on myocardial stiffness reflecting disease-dependent antagonistic intensity. This would become a relevant diagnostic marker if corresponding (noninvasive) measurement techniques would become available.