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PubMed1987

Restrictive cardiomyopathy in children. Ultrastructural findings.

Restrictive cardiomyopathy is usually related to fibrosis of the endocardium or to an infiltrative disorder. However, in few cases, it can be due to isolated pathology of the myocytes but such alterations are not well characterized. This paper reports the disease in two 7 year old patients. There was severe venous congestion and catheterisation revealed increased end diastolic pressure in the ventricles. Both pericardial and myocardial biopsies were performed, as the clinical and haemodynamic data were indistinguishable from constrictive pericarditis. The structure of the pericardium was normal. The endocardium was not thickened. The interstitium of the myocardial tissue was not increased. Electron microscopic examination revealed intracellular masses of disorganized myofilaments. These large deposits may have produced decrease compliance of the myocytes and of the ventricular walls.

Biopsy↗
PubMedDate not supplied

Regional difference of capillary-to-fiber ratio in the heart of monocrotaline-treated rats.

This study was designed to investigate the capillary-to-fiber (CF) ratio, and regional differences in this ratio in the hearts of monocrotaline-induced pulmonary hypertensive rats (MCT rats) as compared with normal rats in an attempt to examine capillary proliferation relative to that of muscle cells responding to the pressure stress on right ventricle (RV). Ten Sprague-Dawley male rats (5 weeks old) were injected with 60 mg/Kg monocrotaline, while eight rats were injected with saline as a control. At the age of 8 weeks they were anesthetized and the heart was excised and immediately frozen. The capillaries were stained enzyme-histochemically by detecting alkaline phosphate and dipeptidylaminopeptidase IV. The main finding in this study was a decrease in the CF ratio of MCT rats in all regions of the heart except in the RV mid-layer and endocardium. The CF ratio in the RV-mid-layer was 1.21 +/- 0.11 (mean +/- SD) in MCT rats and 1.27 +/- 0.12 in control rats (no change), while in the mid-layer of the interventricular septum (IVS) it was 1.13 +/- 0.05 in MCT rats and 1.35 +/- 0.07 in control rats (p < 0.001), and in the left ventricular (LV) mid-layer it was 1.20 +/- 0.06 in MCT rats and 1.40 +/- 0.12 in control rats (p < 0.001). This result indicates that capillary proliferation in the IVS and LV was poor in MCT rats, while in RV capillary proliferation was maintained at the control level. In MCT rats, the CF ratio in the RV endocardium and epicardium was significantly higher than the ratio in the LV epicardium, while in control rats the CF ratio in the LV endo- and mid-cardium was significantly higher than in the RV endo- and epicardium. It was suggested that in the hearts of growing MCT rats capillary proliferation in RV compensated for the suppressed capillary proliferation in the whole heart.

Animals↗
PubMed1994

Endothelial control of vascular and myocardial function in heart failure.

The effect of vascular endothelium, endocardium, and coronary endothelium on vascular tone and myocardial contraction-relaxation sequence in heart failure is discussed. Vascular endothelium affects underlying vascular smooth muscle through paracrine secretion of relaxing and constricting factors. In heart failure, systemic vasoconstriction results not only from neuroendocrine activation, but also from disturbed local endothelial control of vascular tone because of impaired endothelial-dependent vasodilation and because of increased plasma concentration of endothelin. Experimental evidence obtained in isolated cardiac muscle strips established the influence of endocardial endothelium on the duration of myocardial contraction and on the onset of myocardial relaxation. By analogy to vascular endothelium, both diffusible agents that abbreviate (endothelial-derived relaxation factor-like substance) and those that prolong (endocardin) myocardial contraction have been shown to be released from the endocardium. Similar agents are released from the coronary endothelium and, because of the close proximity of capillaries and myocytes, could exert a major effect on myocardial performance. Endothelial dysfunction and concomitant lack of release of myocardial relaxant factors could explain left ventricular relaxation abnormalities observed in the cardiac allograft or in arterial hypertension. Since endothelial-derived relaxation factor or nitric oxide mediates the coronary reactive hyperemic response, a negative inotropic action of nitric oxide could contribute to left ventricular failure when left ventricular wall stress is elevated, as occurs after myocardial infarction in the noninfarcted zone and during left ventricular volume or pressure overload in the absence of adequate hypertrophy.

Biological Factors↗
PubMed1994

Myofibrillar adaptations during cardiac hypertrophy.

The main purpose of this study was to determine the transmural adaptive changes that occur in cell size, myofibrils, and myosin isoforms from the endocardium (ENDO) to the epicardium (EPI) of the left ventricle (LV) of the rat heart during compensatory hypertrophy. Hypertrophy was induced by supra-renal aortic constriction for periods of 2, 7, 15 and 30 days. Percent left ventricular hypertrophy averaged 63 +/- 9.7% at 30 days following constriction. A significant (p < 0.05) transmural gradient in the V3 myosin isoform (9 +/- 0.7% ENDO vs. 5 +/- 1.8% EPI) was initially observed at 7 days and was still evident by 30 days (25 +/- 3.6% ENDO vs 15 +/- 2.0% EPI). Cell cross-sectional area was also greater (p < 0.05) in the ENDO than in the EPI at 7, 15 and 30 days. MF diameter was determined only at 30 days and was found to be similar to control values in both the hypertrophied ENDO (sham 1.24 +/- 0.05 vs hyp 1.18 +/- 0.09 microns) and EPI (sham 1.17 +/- 0.08 vs hyp 1.06 +/- 0.08 microns). The combined effects of cardiac myocyte hypertrophy with no change in MF diameter resulted in a calculated increase of approximately 70% in the number of myofibrils per myocyte both in the ENDO and EPI. It was concluded that the adaptive strategy of the left ventricular free wall to pressure overload was to initially increase myocyte cross-sectional area and then switch myosin expression from V1 to V3, both of which proceeds transmurally from the sub-endocardium towards the sub-epicardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1979

Effect of noncoronary blood flow upon myocardial mitochondrial function during hypothermic anoxic arrest.

Mongrel dogs (23) were subjected to the experimental study characterizing the effect of noncoronary blood flow upon myocardial mitochondrial respiration. Anoxic arrest for 60 minutes was obtained by cross-clamping of the aorta under hypothermic cardiopulmonary bypass, and heart was reperfused for 10 minutes, then heart was excised to obtain the endocardium, epicardium of the left ventricle and ventricular septum for study of mitochondrial function and myocardial blood flow. Myocardial blood flow was measured with carbonized plastic tracer 46Sc during cross-clamping of the aorta. Noncoronary blood flow showed equal distribution in the left ventricle and septum with flow of 0.16 +/- 0.23 ml/ min/100g (endocardium). Mitochondrial respiratory function following 60 minutes of hypothermic anoxic arrest at 20 degrees C recovered to normal level, and also no correlation was demonstrated between noncoronary blood flow during cross-clamping of the aorta and mitochondrial respiratory function. It was concluded that noncoronary blood flow was negligible with respect to the oxygen demand at 20 degrees C of myocardial temperature, and that noncoronary blood flow during cross-clamping of the aorta was not correlated to mitochondrial protection from ischemia.

Animals↗
PubMed1983

Fourteen cases of left atrial myxoma with emphasis on related histology.

With the availability of diagnostic ultrasonic equipment, there is an increase in the number of diagnosed cases of left atrial myxoma. Fourteen such patients underwent surgical treatment. One major concern was the possible recurrence of the tumor. Histologic examination revealed that the tumor cells did not invade the muscular layer beyond the layer of elastic fiber adjacent to the endocardium, in all cases. We remove the stalk with the Fossa Ovale when the tumor grows on the Fossa Ovale. When the tumor is attached to the muscular septum or free wall, we remove the stalk with the endocardium and a part of the adjacent myocardial layer. The total resection of the muscular septum may not be necessary as far as the myxoma is concerned.

Adolescent↗
PubMed1997

Altered distribution of collagen type I and hyaluronic acid in the cardiac outflow tract of mouse embryos destined to develop transposition of the great arteries.

Complete transposition of the great arteries (TGA) is inducible by treatment with all-trans retinoic acid in the ICR mouse. In this model, hypoplasia and dysplasia of the proximal outflow tract cushion tissue lead to non-spiral septation. In order to evaluate the effect of retinoic acid on the extracellular matrix of the cardiac outflow tract, we examined the distribution of collagen type I and hyaluronic acid, immunohistochemically, on days 8-9 of gestation. In controls, collagen type I fibrils ran mainly in a radial direction, extending towards the endocardium in the cardiac jelly of the proximal outflow tract. Also, a pair of longitudinal fiber bundles were formed stretching to the distal outflow tract. As for hyaluronic acid, intense staining was observed in the submyocardial and intermyocardial space of the outer curvature of the heart. On the other hand, in retinoic acid-treated embryos, the submyocardial radial fibrils or longitudinal fiber bundles of collagen type I were diminished, and irregular and dense deposits of collagen type I were observed along the endocardium. Furthermore, hyaluronic acid showed a loss of differential localization between the outer and inner curvature. Instead, irregular and intense staining was observed uniformly along the outflow myocardium. Thus, retinoic acid appeared to have perturbed the differentiation in the proximal outflow tract causing an altered organization of multiple extracellular matrix molecules, including collagen type I and hyaluronic acid, which led to an abnormal molecular network of the cardiac jelly in the cardiac outflow tract, abnormal septation and, further, to TGA or TGA-type anomalies.

Animals↗
PubMed2006

Primary pulmonary valve papillary fibroelastoma.

Papillary fibroelastoma (PFE) is a rare and benign cardiac tumor typically found on the valvular endocardium. In most cases, PFE is identified incidentally on echocardiography or during cardiac surgery. The patient was a 73-year-old man who had been treated for hepatocellular carcinoma for 5 years. On echocardiography, a 2.5-cm diameter mass was detected in the pulmonary trunk just above the pulmonary valve. Through a transpulmonary arterial approach with cardiopulmonary bypass, the mass identified on the commissure of the right and posterior pulmonary cusp was surgically excised together with the attached endocardium. Despite the benign histology of PFE, lethal embolic events such as stroke, myocardial infarction, and pulmonary embolism are reported in some cases. To prevent such complications, tumor identification and surgical excision are essential.

Aged↗
PubMed2003

Right atrial thrombus formation associated with central venous catheters utilization in hemodialysis patients.

OBJECTIVE: To report five patients on hemodialysis via an indwelling central venous catheter who developed a thrombus located exclusively on the right atrial wall opposing the emptying site of the superior vena cava and to determine the possible cause of this location. DESIGN: Transthoracic echocardiography was performed in four of the patients as work-up for suspected endocarditis or pulmonary embolism and in one patient for syncope evaluation. The right atrial clots were confirmed in all the patients by transesophageal echocardiography. DESIGN AND SETTING: General intensive care unit of a university hospital, tertiary referral center. PATIENTS: Five patients with end-stage chronic renal failure on hemodialysis via subclavian or internal jugular vein catheter. INTERVENTIONS: Three of these patients underwent surgical thrombectomy, and two others were medically treated. MEASUREMENTS AND RESULTS: The clots were 2-4 cm in length and three of them were infected. Two of the three surgically treated patients and one of the two medically treated patients died. All the patients had the catheter tip in the right atrium, in two of them the bent catheter rubbed the atrial endocardium, and in all the cases the clot was located on the atrial free wall facing the superior vena cava emptying. CONCLUSIONS: We postulate that the mechanism of thrombus formation at this location is related to friction of the catheter on the atrial endocardium, and therefore positioning the distal segment of the central venous catheters in the right atrium should be avoided.

Adult↗
PubMed2000

Secondary endocardial fibroelastosis associated with Pompe disease and multicystic dysplastic kidney.

An infant with secondary endocardial fibroelastosis (EFE) associated with glycogen storage disease II (Pompe disease) and multicystic dysplastic kidney (MCDK) is described. She had had refractory heart and renal failure from the early neonatal period. In spite of administration of cathecholamines and diuretics, ventilator support, and peritoneal dialysis, her heart failure due to reduction of left ventricular contractility progressively worsened. She died on the 40th day after admission. Histological examination of a left ventricular autopsy specimen showed prominent thickening of the endocardium due to fibroelastosis, and a lacework-like structure due to accumulation of glycogen in the cardiomyocytes. The EFE was derived from degeneration of the smooth muscle in the endocardium and cardiomyocytes due to glycogen storage. In addition, we supposed that the renal failure due to MCDK made the preload for the ventricles increase and accelerated her heart failure.

Endocardial Fibroelastosis↗
PubMed1998

Evaluation of cardiac structures and function in small experimental animals: transthoracic, transesophageal, and intraventricular echocardiography to assess contractile function in rat heart.

OBJECTIVES: The efficacy of three different echocardiographic techniques to assess cardiac structures and function in the rat heart was studied. BACKGROUND: With increasing costs for large animal studies there is need for improved assessment of ventricular function in small animal models. METHODS: Transthoracic, transesophageal, or intracavitary echocardiography was performed in 138 rats using either a pediatric or an intravascular ultrasound transducer in control, infarcted, and obese rats. Left ventricular dimensions and wall thickness were measured. RESULTS: Transthoracic echocardiography allows qualitative and quantitative estimation of cardiac dimensions and ventricular function. End-diastolic and end-systolic diameters were 0.53 +/- 0.08 and 0.26 +/- 0.05 cm in controls, 0.63 +/- 0.08 and 0.41 +/- 0.07 cm in infarcted (p < 0.001 vs controls), and 0.66 +/- 0.1 and 0.21 +/- 0.07 cm in obese rats (p < 0.01 vs controls). Fractional shortening was 52 +/- 6% in controls, 36 +/- 5% in infarcted (p < 0.001), and 68 +/- 9% in obese rats (p < 0.001). Wall thickness was increased in obese rats. Transesophageal echocardiography allows a qualitative rather than quantitative assessment. Intracavitary ultrasound enabled visualization of the endocardium. Following coronary occlusion, fractional shortening and ejection fraction were decreased (30.8 +/- 4.5 vs 44.4 +/- 4.7%, p < 0.005, and 46.7 +/- 8.5 vs 63.4 +/- 5.4%, p < 0.005, respectively). CONCLUSIONS: Transthoracic echocardiography is a non-invasive technique to sufficiently provide information about cardiac structures and function, while transesophageal echocardiography allows rather a qualitative estimation of the rat heart. Intracavitary ultrasound can be used to assess the endocardium, ventricular function, and dimensions in open-chest studies in rats.

Animals↗
PubMed1998

Immunoreactivity of the ets-1 transcription factor correlates with areas of epithelial-mesenchymal transition in the developing avian heart.

Cardiac morphogenesis involves substantial remodeling processes that include cell transdifferentiation and migration. The c-ets-1 protooncogene codes for a transcription factor that can transactivate a number of genes involved in developmental processes such as degradation of extracellular matrices and cell migration. We have immunolocated the ets-1 protein in the heart of quail and chick embryos between the Hamburger and Hamilton stages HH16 and HH37. In HH16-17 embryos, the ets-1 transcription factor was only detected in some endocardial cells and in most mesothelial and mesenchymal cells of the proepicardium. Ets-1 immunoreactivity increased markedly in the developing endocardial cushions, myocardium, epicardium and early subepicardial mesenchyme of HH18-19 embryos. By HH20-24 the immunoreactivity was found throughout the heart, with a stronger intensity in the areas of epithelial-mesenchymal transition of the endocardium and epicardium. In embryos between HH26 and HH33, ets-1 immunoreactivity increased in the cushion mesenchyme, atrioventricular endocardium, ventricular epicardium and subepicardial mesenchyme cells, but not in other areas of the heart. The immunoreactivity declined in the innermost part of the endocardial cushions. The subepicardial mesenchyme was particularly immunoreactive in these stages, coinciding with the development of the subepicardial vascular network. In fact, ets-1 colocalized with the quail vascular marker QH1 in the subepicardial mesenchymal cells. Ets-1-negative cells were abundant in the subepicardium and valvuloseptal tissue of the HH37 embryos. The results suggest that ets-1, probably through transactivation of genes such as urokinase-type plasminogen activator and matrix metalloproteinases, might play a crucial role in the differentiation of the cushion and subepicardial mesenchyme, the formation of the intratrabecular sinusoids and the early development of the cardiac vessels.

Animals↗
PubMed2000

Oxidized low-density lipoprotein is localized in the ventricles of hearts from patients with coronary heart disease.

The present study was designed to investigate whether oxidized low-density lipoprotein is accumulated in the left and right ventricular walls of patients with coronary heart disease (n=10) compared with patients with dilated cardiomyopathy (n=9) or healthy heart donors (controls, n=5). Sections from both ventricles of explanted hearts and coronary arteries of the same patients were analyzed by semiquantitative immunohistochemistry for the presence of oxidized low-density lipoprotein. Oxidized low-density lipoprotein was enriched in the left and right ventricular walls from coronary heart disease patients compared with patients with dilated cardiomyopathy (P=0.0012 for left ventricle and P=0.103 for right ventricle) or controls (P=0.0012 for the left ventricle and P<0.05 for the right ventricle). The accumulation of oxidized low-density lipoprotein was higher in the left than in the right ventricles in all three groups. Positive immunoreactivity for oxidized low-density lipoprotein was mainly identified in the endocardium and the subendocardial areas of the ventricles and co-localized with macrophages. Accumulation of oxidized low-density lipoprotein in the ventricles significantly correlated with the enrichment in the respective coronary arteries, whereas only poor correlations were observed between various hemodynamic parameters and ventricular oxidized low-density lipoprotein accumulation. Ventricular accumulation of oxidized low-density lipoprotein seems to be a generalized pathophysiological process which does not exclusively involve the coronary arteries. Higher oxidative stress in combination with impaired oxygen supply in the endocardium could have favored low-density lipoprotein deposition and oxidation.

Adult↗
PubMed1983

Contrasting effects of nifedipine and verapamil on myocardium and vascular smooth muscle at two levels of coronary occlusion in the dog.

The calcium flux inhibitors nifedipine and verapamil have recently been used in the setting of both classical Heberden's and variant angina. It has also been suggested that these agents may preserve function and viability of threatened myocardium. The effects of these agents on the relationship between myocardial blood flow and contraction in the setting of partial coronary occlusion is unknown. Thus 39 open-chest dogs underwent partial coronary occlusion to diastolic perfusion pressures of 25 or 40 mm Hg. The dogs then received intracoronary infusions of 10 micrograms nifedipine or 100 micrograms verapamil. Myocardial blood flow was measured with tracer microspheres and myocardial shortening was assessed with ultrasonic crystals. At 25 mm Hg nifedipine improved myocardial shortening while blood flow did not change. In contrast, verapamil caused shortening to be abolished but also did not change blood flow. At 40 mm Hg nifedipine, while not affecting shortening, caused a "redistribution" of blood flow from endocardium to epicardium; in contrast, verapamil again caused shortening to be abolished, but only increased epicardial blood flow leaving endocardial flow intact. Thus verapamil and nifedipine have differing effects. Nifedipine is a potent vasodilator at doses having no negative inotropic effects. In addition, nifedipine can cause a transmural "redistribution" of blood flow from endocardium to epicardium. In contrast, verapamil is also a potent vasodilator, but has profound negative inotropic effects.

Animals↗
PubMed1991

Endocardial monophasic action potential recordings for the detection of myocardial ischemia in man: a study using atrial pacing stress and myocardial perfusion scintigraphy.

In a study designed to appraise the use of monophasic action potentials (MAPs) to detect myocardial ischemia in endocardial recordings, changes in steady-state MAP duration were compared in recordings between normal and ischemic areas of myocardium identified by the use of a radionuclide tracer simultaneously with the MAP recording procedure. Single-site recordings were made from the left or right ventricular endocardium or both in 26 patients (32 recording sites) during atrial pacing up to angina threshold. Pacing was maintained for 2 minutes at each increment in heart rate and MAPs were recorded at the end of each 2-minute period. Perfusion defects produced by atrial pacing stress were detected using technetium-99m hexakis-2-methoxy-2-methylpropyl-isonitrile injected at peak pacing stress. In 18 recordings from normally perfused areas of endocardium, MAP duration at 70% and 90% repolarization shortened by a mean (+/- SD) of 20.9 (3.7) msec and 22.0 (4.8 msec, respectively, for every 100 msec change in cycle length. This is in keeping with the effect of cycle length changes on the action potential duration. The extent of shortening was significantly greater (p less than 0.01) for 14 recordings from ischemic areas, being 32.0 (8.6) and 33.8 (9.7) msec, respectively, indicating the additional effect of localized myocardial ischemia. These results validate the applicability of the endocardially recorded MAPs for the detection of ischemia. Such methodology may provide a means of assessing therapeutic interventions aimed at the early phase of ischemia.

Action Potentials↗
PubMed1995

Quantitative Doppler tissue imaging of the left ventricular myocardium: validation in normal subjects.

Doppler tissue imaging (DTI) is a new echocardiographic imaging technique from which quantitative data regarding myocardial velocity can be extracted. The purpose of this study was to compare endocardial velocities determined from DTI with those determined from M-mode echocardiography and to assess the range of myocardial velocities in normal subjects. Nineteen subjects were evaluated by M-mode echocardiography and quantitative DTI for maximal systolic velocities of the anteroseptal and inferoposterior walls. Mid-myocardial and epicardial velocities were also measured by DTI for each wall. Maximal systolic velocities of the anteroseptal and inferoposterior endocardium determined by DTI correlated significantly with those derived from M-mode echocardiography (r = 0.87). The velocity of the inferoposterior wall by DTI (27.3 +/- 4.8 mm/sec) was greater than that of the anteroseptum (20.8 +/- 4.1 mm/sec) by a mean difference of 7.0 +/- 5.7 mm/sec (p < 0.001). A peak velocity gradient of 5.9 +/- 3.5 mm/sec (p < 0.001) between the epicardium to endocardium was detected. These data confirm that (1) regional myocardial velocities may be quantified with DTI in human beings; (2) the high resolution of DTI allows velocities to be determined at different levels within the myocardium; and (3) heterogeneity of myocardial velocities may be demonstrated in normal subjects.

Adult↗
PubMed1976

The heart in the Hurler syndrome: gross, histologic and ultrastructural observations in five necropsy cases.

Clinical and morphologic features of the cardiovascular system are described in five necropsy patients with the Hurler syndrome. In all five patients the coronary arteries, four cardiac valves, mural endocardium of all four chambers, myocardial walls and aorta were affected in a characteristic manner. All of these sites contained large clear cells known as Hurler cells (readily visible by light microscopy). In addition, granular cells were observed in semi-thin (1 mu) sections and by electron microscopy in the coronary arteries, atrioventricular (A-V) valves and in myocardial interstitium. These latter cells appear to produce collagen in an abnormal way and are probably responsible for the heavy deposits of collagen in the cardiovascular system of patients with the Hurler syndrome. In the cardiac muscle cells, in smooth muscle cells of the coronary arteries and in fibroblasts, wherever located, deposits of acid mucopolysaccharides and glycolipids usually were also observed. The acid mucopolysaccharide deposits were observed easily with light microscopy except in the cardiac muscle cells where they were seen only with electron microscopy. The glycolipid depositis, observed only on examination of 1 mu thick sections or with electron microscopy, have not previously been observed in coronary arteries or in myocardial cells. The infiltration into the heart by these cells and deposits in all five patients resulted in severe narrowing of the extramural coronary arteries, considerable thickening of the cardiac valves (the left-sided more than the right-sided valves), generalized thickening of mural endocardium and "stiffening" of the myocardial walls. Thus, the cardiovascular lesions in the Hurler syndrome are specific and life-threatening.

Adolescent↗
PubMed1986

Extent of myocardial fibrosis and cellular hypertrophy in dilated cardiomyopathy.

The distribution of fibrosis and cellular hypertrophy was studied in the hearts of patients with dilated cardiomyopathy (DC). Transmural sections were removed from the left and right ventricular free walls and the ventricular septum of 9 patients with heart failure and 6 control subjects. These sections were stained with hematoxylin-eosin (to determine cell size) and trichrome (to determine percent fibrosis). The sections were separated into equal areas from epicardium to endocardium in the free walls and right to left across the septum. Percent fibrosis was greater in patients with DC (20 +/- 4%) than control subjects (4 +/- 1%, p = 0.0001). A pattern of increasing fibrosis in the left ventricular free wall from epicardium (14 +/- 6%) to endocardium (22 +/- 9%, p less than 0.05) was documented. Fibrosis was greater on the left (21 +/- 12%) than the right (15 +/- 6%, p less than 0.05) side of the septum. No pattern was evident in the right ventricular free wall or in the control group. Myocardial cell diameter was greater in the heart failure group (22 +/- 5 micron) than the control group (17 +/- 2 micron, p less than 0.05), but no pattern of hypertrophy across the walls was seen. The increased fibrosis, the pattern of fibrosis and the increased cell diameter in patients with DC help to characterize DC.

Adult↗