Endomyocardial Fibrosis ; Fibroblasts ; Humans ; Myocardium ; pathology

Cardiomyopathy, Dilated ; Humans ; Hyperplasia ; Myocardium ; pathology

OBJECTIVE: To evaluate the echocardiographic diagnosis for ventricular non-compaction cardiomyopathy (NCCM) in foetus and to analyze the pathologic features of NCCM.
 METHODS: A total of 9 patients with fetal NCCM were examined by prenatal echocardiography from 2004 to 2013, which was compared with postnatal echocardiography or autopsy to analyze the fetal characteristic of myocardial ultrastructure.
 RESULTS: The results of echocardiography displayed an excessive muscle trabecular meshwork and muscle trabecular crypt, and the ventricular myocardium and non-compaction/compaction ratio was ≥2.0. Among the 9 fetuses of NCCM, 6 fetuses were involved in left ventricle, 2 in both left and right ventricles and 1 in right ventricle. Two fetuses were confirmed by postnatal echocardiography, the remaining 7 patients were chosen to terminate their pregnancies, which were confirmed by autopsy later. Muscle biopsies revealed the abnormal myocardial mitochondria, sarcomeres and myocardial fibrosis.
 CONCLUSION It is feasible to accurately diagnose NCCM by prenatal echocardiography. Fetal NCCM most often involves the left ventricle, but it can involve the right ventricle or both, too. The myocardial ultrastructure of fetal NCCM possesses certain unique characteristics, such as the low maturation of the mitochondria, sarcomeres and myocardial fibers.
Cardiomyopathies ; diagnosis ; Echocardiography ; Fetus ; Heart Ventricles ; pathology ; Humans ; Myocardium ; pathology

Cardiomyopathy, Dilated ; etiology ; pathology ; therapy ; Humans ; Myocardium ; pathology

Adult ; Cardiomyopathy, Hypertrophic ; complications ; pathology ; Humans ; Male ; Myocardium ; pathology

OBJECTIVEThe purpose of this study was to observe histopathological changes post cryoablation in canine myocardium, to characterize the specific ablation lesion post cryoablation.

METHODSCryothermal ablation was applied on myocardium (both epicardium and endocardium) of 14 mongrel dogs with different ablation parameters (-25 degrees C x 4 min, -50 degrees C x 4 min, -75 degrees C x 4 min, -75 degrees C x 2 min, -75 degrees C x 6 min, -75 degrees C x 8 min). Lesion dimensions and histopathologic changes were observed.

RESULTSThe discrete, sharply delimited lesions were detected in cryoablated myocardium. Histologically, cryoablation in all temperatures studied induced heterogeneous necrosis of the myocardium. Lesion dimensions are related to freezing time and temperature.

CONCLUSIONCryoablation is a feasible and preferably choice for clinical application due to its controllable myocardium lesions.

Animals ; Catheter Ablation ; Cryosurgery ; Dogs ; Endocardium ; pathology ; Myocardium ; pathology

OBJECTIVEIt is revealed that circulating fibrocytes are elevated in patients/animals with cardiac fibrosis, and this review aims to provide an introduction to circulating fibrocytes and their role in cardiac fibrosis.

DATA SOURCESThis review is based on the data from 1994 to present obtained from PubMed. The search terms were "circulating fibrocytes " and "cardiac fibrosis ".

STUDY SELECTIONArticles and critical reviews, which are related to circulating fibrocytes and cardiac fibrosis, were selected.

RESULTSCirculating fibrocytes, which are derived from hematopoietic stem cells, represent a subset of peripheral blood mononuclear cells exhibiting mixed morphological and molecular characteristics of hematopoietic and mesenchymal cells (CD34+/CD45+/collagen I+). They can produce extracellular matrix and many cytokines. It is shown that circulating fibrocytes participate in many fibrotic diseases, including cardiac fibrosis. Evidence accumulated in recent years shows that aging individuals and patients with hypertension, heart failure, coronary heart disease, and atrial fibrillation have more circulating fibrocytes in peripheral blood and/or heart tissue, and this elevation of circulating fibrocytes is correlated with the degree of fibrosis in the hearts.

CONCLUSIONSCirculating fibrocytes are effector cells in cardiac fibrosis.

Coronary Disease ; pathology ; Fibroblasts ; physiology ; Fibrosis ; pathology ; Heart Failure ; pathology ; Humans ; Hypertension ; pathology ; Myocardium ; pathology

A series of studies demonstrated that myocardial damage and cardiac dysfunction occurs immediately following severe burn, even before significant reduction in blood volume due to increased capillary permeability. Such myocardial damage and cardiac dysfunction leads to cardiac deficiency, and it is a precipitating factor for burn shock and ischemic/hypoxic injury. In recent years, many experimental and clinical studies elucidated the pathogenesis and confirmed the clinical importance of prevention and treatment of"shock heart"in the early stage post severe burn.
Burns ; pathology ; therapy ; Heart ; physiopathology ; Humans ; Hypoxia ; pathology ; Myocardium ; pathology ; Shock ; pathology

Adult ; Carcinosarcoma ; pathology ; Female ; Heart Neoplasms ; pathology ; Humans ; Lung Neoplasms ; pathology ; Myocardium ; pathology

Obesity is an independent risk factor of cardiovascular diseases. Epidemiological studies have shown that obesity induces the production of inflammatory factors and changes in cardiac hemodynamics, remodeling and function, leading to myocardial damage and heart diseases. The positive effect of exercise on the cardiovascular system has been widely confirmed, while the acute cardiovascular stress caused by exercise cannot be ignored. Compared with the general population, obese people were more prone to arrhythmia and have a higher risk of cardiovascular events during exercise, due to their abnormal cardiac function, myocardial pathological remodeling and low tolerance to corresponding stress. Studies have shown that the intervention of exercise preconditioning (EP) can effectively reduce such risks. EP increases myocardial oxygen consumption through short-term exercise, resulting in relative or absolute myocardial ischemia, inducing the intrinsic myocardial protective effect and reducing the continuous ischemia caused by subsequent long-term exercise. This article reviews the obesity-induced abnormal changes of cardiac function and structure, possible exercise- induced risks of cardiovascular events in obese people and the role of EP in reducing exercise-induced risks of cardiovascular events. We summarize the progress on EP models in obese people, EP prevention against adverse cardiovascular events in obese people, with the aim to provide a theoretical basis for the application of EP in obese people.
Humans ; Exercise ; Obesity ; Myocardium/pathology* ; Myocardial Ischemia ; Cardiovascular Diseases