Ultrasound imaging versus morphopathology in cardiovascular diseases: the heart failure

Abstract

This review article summarizes the results of histopathological studies to assess heart failure in humans. Different histopathological features underlying the clinical manifestations of heart failure are reviewed. In addition, the present role of echocardiographic techniques in assessing the failing heart is briefly summarized.

Figure 1

Stretched, i.e. elongation of sarcomeres and nuclei in viable myocardial cells in an old aneurysm of the left ventricular wall with dense fibrosis [A]. Dense and compact fibrosis as end result of a repair process of an infarct. The collagen fibers are straight and closed together [B]. In contrast in hearts with congestive heart failure the myocardial fibrosis is very mild [C, D] showing a corkscrew aspect of the collagen fibers [E]. This means an adaptation of the collagenogenesis to the contraction cycle without any capability to reduce or stop the latter. Furthermore, the fibrous tissue may metaplasize in adipose tissue which substitutes large fibrous area [F, G]. A fact to have in mind when quantifying the size of a scar or measuring by nuclear method the myocardial viability.

Figure 2

Weight/size paradox in congestive heart failure. The slippage of myocardial cell to explain a normal wall and myocellular size despite a heavy cardiac weight [A], does not consider the myofibrillar bridging between myocells and fibrillar collagen connections. Slippage of myocells, capable to reduce for instance a 3 cm cardiac wall in 1.5 one, should imply an extensive destruction of all interstitial structures [vessels, including lymphatics, and nerves] and consequent widespread tissue damage never seen in this condition. Even a neogenesis of the myocardial cell was never observed. Only once in an endomyocardial biopsy at a previous site of sampling in a transplanted heart, we had the opportunity to see new myocells forming a focus of small elements assuming the aspect of atrio-ventricular node [B, C]. Just to emphasize that a neogenesis when exists can be seen, apparently without integration in the functioning myocardium.

Figure 3

Colliquative myocytolysis. Progressive disappearance of myofibrils [A], with intramyocardial edema [B] resulting in empty sarcolemmal tube seen in longitudinal [C] and transverse section [D]. Note the absence of any type of reaction. E, ultrastructural view of an edematous myocell filled by mitochondria and few contracted myofibrils in contrast with a normal contracted myocell [F] of the same case with congestive heart failure.

Figure 4

Endomyoelastofibrosis of the endocardium. Thickening of the endocardium is considered consequent to intracavitary thrombi organization. The latter is a relatively rare event. The majority of endocardial thickening is due to the formation of smooth muscle cell bundles [A] with hyperelastosis [B] ending in fibrous replacement [C]. A process similar to that shown in the early pathogenesis of an atherosclerotic plaque, to keep in mind in relation to antithrombotic therapy.