Functional Aspects of the Normal, Hypertrophied, and Failing Heart
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RCM can be associated with several diseases such as amyloidosis AL , hemosiderosis, hypereosinophilia, endocardial fibroelastosis, systemic sclerosis Figure 5 and secondary to radiation therapy and certain medications.
CMR imaging in year-old patient with restrictive cardiomyopathy representing cardiac involvement in Systemic Sclerosis. Short-axis A and four-chambers B views show focal enhancement in the lateral left ventricle wall white arrows. Lesion topography may misinterpreted because subendocardium is affected. However, increasing evidence strongly suggests that this involvement is related to repeated focal ischemic injury causing irreversible myocardial fibrosis.
The underlying mechanism appears to be microcirculatory impairment with abnormal vasoreactivity, with or without structural vascular abnormalities. Clinically evident cardiac involvement is recognized to be a poor prognostic factor in case of Systemic Sclerosis.
The disease is due to amyloid deposit into the myocardium with a preference for the subendocardial layer disturbing contractile function and electrical conduction. Although myocardial biopsy can make the diagnosis, this procedure is invasive and the risk of sampling error limits its application. In routine, the diagnosis is made by ETT associated with an extracardiac biopsy. However, ETT have some limitations, previously discussed, and particularly if hypertrophy from other causes is observed.
Other non-invasive techniques also have limitations such as ECG and scintigraphy with the use of radiolabled serum amyloid P component.
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Those abnormalities of signal are the direct consequences of amyloid deposition. The first consideration depends on the gradient of amyloid deposition between the subendocardial layer and subepicardial layer, with a high prevalence for the inner border.
The exact inversion- time for the perfect dark myocardium is thus unobtainable Figure 6. The second consequence of the presence of the amyloid depositions is the increase of the extracellular space. So, when delayed contrast enhancement sequence after 10 min is acquired, a hyperenhancement as a regular ring is observed into the subendocardial layer. Top row shows the thickening of the LV wall on short-axis T2-weighted image A and on short-axis diastolic cine image B. Still at the top row, short C and four-chambers D delayed-contrast enhancement sequence show a diffuse biventricular concentric subendocardial enhancement.
Bottom row show how the system failed to select the right inversion-time, from E to H image. Fabry disease is an X-linked lysosomal storage disease that is caused by deficient activity of lysosomal enzyme a-galactosidase A.
Functional Aspects of the Normal Hypertrophied and Failing Heart by Abel & Simone
Cardiac involvement is common, and usually develops in the fourth decade of life. In brief, glycosphingolipids accumulate in the lysosomes of numerous cells owing to a-galactosidase A deficiency. This accumulation leads to cells and tissue ischemia and fibrosis. In case of cardiac involvement, the accumulation concerns the cardiomyocytes, the valve and the vascular endothelium. The result is a concentric cardiac hypertrophy, which has to be differentiating of LV hypertrophy.
Gadolinium enhanced cardiovascular magnetic resonance in Anderson-Fabry disease. Schematically two types of disease must be differentiated.
First, the classic haemochromatosis, inherited or not, its diagnosis can be mad on the basis of history, clinical examination, laboratory abnormalities such as elevated serum iron, ETT and CMR showing DCM. Second, cardiac siderosis, encountered later, and where ventricular dimensions may be normal until the late stage of disease. Its principle is based on iron deposition that reduced the relaxation rates of T1- and T2- weighted sequences by introducing local magnetic field inhomogeneities. Now, beside the right ventricular myocardium, which is usually spared, LV and both atrium are more often affected.
CMR could also be used as an indicator of iron chelation therapy efficiency. Both diseases are directly related to the cardiac toxicity of activated eosinophils. There are three stages: necrotic, thrombotic, and fibrotic.
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The acute necrotic stage is often asymptomatic including eosinophils and lymphocytes infiltration within the myocardium, lesions of the subendocardial layer and necrosis. During the intermediate stage, thrombus formation occurs along necrotic endocardium. The latest stage is the fibrotic stage, because of the endomyocardial replacement scarring, the thickening of the LV wall is observed.
A restrictive pattern is typical of the late stage of the disease. CMR imaging enables to distinguish RCM to constrictive pericarditis, which is the main differential diagnosis for clinicians. Its signal is also quiet different, hyperintense on T2-weighted sequence and enhanced after gadolinium. With real-time cine imaging, the early diastolic interventricular septal flattening or inversion the so-called paradoxical septal movement during inspiration can be observed in cases of constrictive pericarditis.
Phase encoded flow velocity imaging is helpful in order to measure constrictive inflow patterns in the caval veins. However this sequence is time consuming and not use in routine. With RCM, others anatomical MR findings can be observed, normal ventricular size with or without wall thickening and bi-atrial enlargement, with systolic function almost preserved. Journal page Archives Sommaire.
Article Article Outline. Access to the text HTML. Access to the PDF text If you experience reading problems with Firefox, please follow this procedure. Recommend this article. Save as favorites. Free Article! Cardiomyopathies hypertrophy and failure : What can offer cardiac magnetic resonance imaging? Outline Masquer le plan. Hypertrophic Cardiomyopathy. Endomyocardial disease and hypereosinophilic syndrome.
Disclosure of interest. Cardiac CT: Practical approach to integrate appropriate indications in daily practice. Cardiac magnetic resonance imaging and ischaemic cardiomyopathies: what are the indications? Wright Brisbane Australia and J.
Left ventricular hypertrophy - Symptoms and causes - Mayo Clinic
Bogaert Leuven, Belgium. Cardiomyopathies hypertrophy and failure : what can offer cardiac magnetic resonance imaging?
Management of peripheral arterial disease: role of computed tomography angiography and magnetic resonance angiography. Top of the page - Article Outline. Figure 1. Hypertrophic Cardiomyoathy.
Figure 2. Pheochromocytoma-related cardiomyopathy. The focal hyperenhancement observed in the mid-myocardium of the lateral left ventricle wall is highly suggestive of adrenergic myocarditis Zoom. Figure 3. Ischaemic dilated cardiomyopathy. Further, the thinning in the anterior wall and apex is related to scarring fibrosis Zoom. Figure 4.
Figure 5. Clinically evident cardiac involvement is recognized to be a poor prognostic factor in case of Systemic Sclerosis Zoom. Subsequent fashioning of the developing heart is determined by an intricate interplay between genetic programs and mechanical forces. The fetal four-chambered mammalian heart attains an adult structural configuration in the second trimester, but continues to enlarge to maintain circulatory support for the growing embryo and juvenile. Growth of the left ventricle exceeds that of the right ventricle during the early postnatal period as the mammalian heart transitions from the fetal- to adult-type circulation.
Thereafter, the heart undergoes a six-fold increase in mass. The heart-to-body weight ratio then remains relatively constant throughout adolescence and adulthood. In the adult, increases in cardiac mass are produced largely by an increase in size of fully differentiated cardiomyocytes.
Adult cardiomyocytes have long been viewed as terminally differentiated—that is, incapable of reentering the cell cycle—and there is little evidence that they are capable of cell division under normal conditions after the early postnatal period. However, there is emerging evidence suggesting that a small subpopulation of cardiomyocytes can reenter the cell cycle and proliferate, 3, 7 although the clinical significance of this finding is currently uncertain. One recent study has demonstrated that the growth factor neuregulin-1 can induce mononucleate adult cardiomyocytes to proliferate in a mouse and thereby promote myocardial regeneration after infarction.
In response to stimuli such as chronic endurance exercise or pregnancy, the heart hypertrophies without alterations in structure and function. Indeed, the association of intense athletic conditioning with cardiac hypertrophy has been recognized for more than a century. This form of cardiac growth is not associated with altered excitation-contraction coupling, metabolic dysregulation, cardiac fibrosis, or arrhythmia susceptibility. In humans, physiologic hypertrophy has been best studied in high-performance endurance athletes.
Even in the most conditioned athletes, LV wall thickness of greater than 1. Thus it is important clinically to distinguish physiologic hypertrophy resulting from physical training from other forms of cardiomyopathy.
Physiologic hypertrophy can regress to baseline levels after cessation of intense training 11 or in the postpartum period. In both humans and animal models, ventricular cardiomyocytes undergoing pathologic hypertrophy reinduce a subset of genes that are normally expressed at high levels during fetal life.
An established geometric classification scheme describes cardiac hypertrophy as occurring in a concentric or eccentric pattern. Concentric hypertrophy is typically triggered by pressure overload eg, chronic hypertension , which results in significantly elevated systolic wall stress. At the organ level, concentric hypertrophy is characterized by an increase in relative wall thickness and cardiac mass with little or no change in chamber volume.
At the cellular level there is increased cardiomyocyte cross-sectional area with addition of sarcomeres in parallel, thereby causing predominantly lateral growth of individual cells. Eccentric hypertrophy is typically triggered by volume overload as occurs in chronic valvular regurgitation , which results in increased diastolic and systolic wall stress. Regional hypertrophy that develops in viable myocardium after a myocardial infarction also occurs in an eccentric pattern. At the organ level, eccentric hypertrophy is characterized by an increase in cardiac mass with increased chamber volume.