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PubMed1990

Sodium intake modulates the development of cardiac hypertrophy in two-kidney, one clip rats.

Sodium homeostasis exerts a powerful influence on the cardiovascular system in normotensive and hypertensive animals. Previous studies indicate that factors other than blood pressure can influence cardiac hypertrophy. In the present experiments, we evaluated the effects of different sodium diets in the two-kidney, one clip hypertension model in the rat. After the renal artery had been clipped, the rats received a normal sodium (177 meq/kg), high sodium (517 meq/kg), and low sodium (7 meq/kg) diet during 4 weeks. The final blood pressure was almost the same in the three groups (normal sodium 170 +/- 12 mm Hg; low sodium 168 +/- 4 mm Hg; and high sodium 162 +/- 7 mm Hg). Sodium restriction significantly reduced the development of cardiac hypertrophy as compared with rats on normal or high sodium diets. Thus, ventricular weight and ventricular weight/body weight ratio were significantly higher in rats subjected to a normal or high sodium diet (p less than 0.01). The hypertrophied hearts of rats on normal and high sodium diets showed a larger increase in the number of cardiac beta-adrenergic receptors than those observed in hearts from low sodium diet, clipped rats. These results show that sodium modulates the development of cardiac hypertrophy in two-kidney, one clip hypertensive rats. Similarly, the cardiac beta-adrenergic receptors appear to be influenced by dietary sodium intake. A possible role of the sympathetic nervous system is suggested.

Animals↗
PubMed2006

Upregulation of TRPC1 in the development of cardiac hypertrophy.

The importance of Ca(2+) entry in the cardiac hypertrophic response is well documented, but the actual Ca(2+) entry channels remain unknown. Transient receptor potential (TRP) proteins are thought to form either homo- or heteromeric Ca(2+) entry channels that are involved in the proliferation and differentiation of various cells. The purpose of this study was to explore the potential involvement of TRP channels in the development of cardiac hypertrophy. The mRNA and protein expression of several TRP channel subunits were evaluated using hearts from abdominal aortic-banded (AAB) rats. Although TRPs C1, C3, C5, and C6 were constitutively expressed, only TRPC1 expression was significantly increased in the hearts of AAB rats compared to sham-operated rats. Using primary cultures of neonatal rat cardiomyocytes, we detected increases in the expression of TRPC1, brain natriuretic peptide (BNP), and atrial natriuretic factor (ANF), as well as increases in store-operated Ca(2+) entry (SOCE) and cell surface area, following endothelin-1 (ET-1) treatment. Silencing of the TRPC1 gene via small interfering RNA (siRNA) attenuated SOCE and prevented ET-1-, angiotensin-II (AT II)-, and phenylephrine (PE)-induced cardiac hypertrophy. In HEK 293T cells, overexpression of TRPC1 augmented SOCE, leading to an increase in nuclear factor of activated T cells (NFAT) promoter activity, while co-transfection with dominant-negative forms of TRPC1 suppressed it. In conclusion, TRPC1 functions in Ca(2+) influx, and its upregulation is involved in the development of cardiac hypertrophy; moreover, it plays an important role in the regulation of the signaling pathways that govern cardiac hypertrophy. These findings establish TRPC1 as a functionally important regulator of cardiac hypertrophy.

Animals↗
PubMed2004

Cardiac and respiratory failure in limb-girdle muscular dystrophy 2I.

Mutations in the gene encoding fukutin-related protein cause limb-girdle muscular dystrophy 2I. In this multicenter retrospective analysis of 38 patients, 55.3% had cardiac abnormalities, of which 24% had developed cardiac failure. Heterozygotes for the common C826A mutation developed cardiac involvement earlier than homozygotes. All patients initially improved while receiving standard therapy. Independent of cardiac status, forced vital capacity was below 75% in 44.4% of the patients. There was no absolute correlation between skeletal muscle weakness and cardiomyopathy or respiratory insufficiency. These complications are a primary part of this specific type of limb-girdle muscular dystrophy, with important implications for management.

Adolescent↗
PubMed2005

Dynamic balance between activation and repression regulates pre-mRNA alternative splicing during heart development.

Cardiac troponin T (cTNT) exon 5 splicing is developmentally regulated such that it is included in embryonic but not adult heart. CUG-BP and ETR-3-like factor (CELF) proteins promote exon inclusion, whereas polypyrimidine tract binding protein (PTB) and muscleblind-like (MBNL) proteins repress inclusion. In this study, we addressed what happens to these regulatory proteins during heart development to shift the regulatory balance of cTNT alternative splicing. Using dominant-negative proteins, we found that both CELF and PTB activities are required for appropriate splicing in cardiomyocytes. Two CELF proteins, CUG-BP and ETR-3, are nuclear and cytoplasmic in embryonic heart but are down-regulated in adult heart concomitant with loss of exon inclusion. In contrast, PTB and MBNL1 are expressed throughout heart development. The patterns of cTNT splicing and expression of its regulatory factors are conserved between mouse and chicken. Thus, alternative splicing is determined by a balance between positive and negative regulation, and modulation of expression levels of auxiliary splicing regulators may drive developmental splicing changes. ETR-3 and CUG-BP proteins are also down-regulated in other tissues during development, suggesting that CELF proteins play a broad role in developmental splicing regulation.

Aging↗
PubMedDate not supplied

A new endo aortic occlusion balloon for limited access cardiac surgery: development and clinical evaluation.

In recent years, minimally invasive cardiac surgery (MICS), or limited access cardiac surgery, has been presented as a promising operative procedure. We developed a new balloon device that is inserted directly into the ascending aorta to stop the heart during limited access cardiac surgery. The balloon has a three lumen structure: balloon lumen port, cardioplegia/vent lumen port, and aortic root lumen port. This direct EAC balloon catheter, designed to be inserted directly into the ascending aorta, is different from the Heartport system. The Heartport EAC balloon catheter is inserted into the aorta via an artery in the lower limb, making lower limb arterial disease a key concern. Our Direct Endo Aortic Clamp (EAC) balloon overcomes this problem. The device was clinically used in seven cardiac cases. All patients were discharged within 5 postoperative days, confirming the utility of the device.

Aorta↗
PubMed1992

Functional changes in the right and left ventricle during development of cardiac hypertrophy and after its regression.

OBJECTIVE: The aim was to determine left and right ventricular functional reserves and collagen concentration during the development of cardiac hypertrophy and after its regression. METHODS: Two experimental models of cardiac hypertrophy (chronic thyroxine or isoprenaline treatment of adult rats) were compared 24 h and five weeks after the agent was last given. Pressure changes in the left (right) ventricle before and after acute aortic (pulmonary artery) ligation were recorded in open chest anaesthetised animals. The difference in dP/dtmax after and before ligation was regarded as the functional reserve. The total collagen concentration was determined in both ventricles separately by means of hydroxyproline. RESULTS: Left and right ventricular weight increased by 20% and 30% respectively in the two models employed. In the thyroxine treated group, the functional reserve of the left ventricle rose very noticeably, whereas in the isoprenaline treated group it decreased. The right ventricular functional reserve did not differ from that in the controls in either of the two groups. The collagen concentration rose in the left ventricle in the isoprenaline group only. Five weeks after the last administration of the agent, cardiac mass and ventricular function did not differ from the control values in either of the models studied; the only exception was the incomplete regression of left ventricular hypertrophy and persistent structural and functional impairment of the left ventricle in the isoprenaline treated group. CONCLUSIONS: Our results indicate that hearts undergoing a comparable degree of experimental hypertrophy may have different functional and structural properties; significant differences were found between the right and left ventricular response. Regression of hypertrophy together with a reversal of ventricular function usually occurs unless the myocardium has received severe structural damage.

Animals↗
PubMed1992

Altered renal dopamine receptors during development of cardiac hypertrophy.

The characteristics of dopamine receptors were studied in heart and kidney using the radiolabeled receptor assay of [3H]spiperone during the development of cardiac hypertrophy. Male Sprague-Dawley rats (175-200 g) underwent abdominal aortic constriction above the renal arteries and were studied 3, 14, and 28 days thereafter. Sham-operated animals without aortic constriction were used as control. Although the ratio of left ventricular weight to total body weight was significantly increased 14 and 28 days after aortic constriction in animals, [3H]spiperone binding in left ventricular membrane was increased as early as 3 days after aortic constriction. At 14 days, the binding was still elevated and, by 28 days, it returned to control values. In contrast, membranes obtained from kidney cortex showed an elevation of [3H]spiperone binding only at 28 days after aortic constriction; at 3 days the binding values were decreased. A reciprocal correlation was found between the number of dopamine receptors and the activity of Na(+)-K(+)-ATPase at 28 days of aortic constriction; the enzyme activity, as measured by the release of 32Pi from [gamma-32P]ATP, was decreased in kidney cortex. Autoradiographic data also showed an increased number of dopamine receptors in kidney at 28 days after abdominal aortic constriction. These results suggest that the dopamine receptor is increased very early in heart in response to pressure overload as a result of a compensatory response to maintain an optimal left ventricular output. Kidney dopamine receptors are triggered at a later stage possibly to maintain fluid homeostasis secondary to the cardiac hypertrophic process.

Animals↗
PubMed2006

Increased pericardial fluid level of matrix metalloproteinase-9 activity in patients with acute myocardial infarction: possible role in the development of cardiac rupture.

BACKGROUND: In an animal model of acute myocardial infarction (AMI), deletion of matrix metalloproteinase (MMP)-9 results in suppression of the development of cardiac rupture. The present study sought to clarify how myocardial MMP-9 activity is related to the pathophysiologies of AMI and cardiac rupture in humans. METHODS AND RESULTS: Levels of interleukin-8 (IL-8), polymorphonuclear leukocyte (PMN) elastase, monocyte chemotactic protein-1 (MCP-1) and MMP activity were measured in the pericardial fluid obtained from 28 patients with angina pectoris (AP group) and 16 patients with AMI (AMI group) undergoing cardiac surgery. In the AMI group, 5 were complicated with ventricular septal perforation (VSP) and the remaining 11 were not (non-VSP). Levels of IL-8, PMN elastase, MMP-2 and MMP-9 activity were all higher in the AMI group than in the AP group. In the AMI group, all levels other than MMP-2 activity were further elevated in cases with VSP compared with those in the non-VSP group. There was no significant difference in MCP-1 among the groups CONCLUSIONS: Markers of neutrophil activation in the infarcted cardiac tissue seem to be elevated in AMI. Highly elevated levels of MMP-9 activity, which may be derived from neutrophils, and PMN elastase may be related to the pathophysiology of VSP or cardiac rupture in AMI.

Acute Disease↗
PubMed1997

Developing a cardiac catheterization education program.

This article describes the establishment of a coordinated education program for patients having a cardiac catheterization. The article focuses on developing the program content, instructional aids, and the education of the staff doing the actual patient education for this group of patients and their families.

Cardiac Catheterization↗
PubMed1984

Cardiac muscle development in mice exposed to ethanol in utero.

The purpose of the present research was to determine the effect of in utero ethanol exposure on cardiac muscle development. Pregnant albino mice (Swiss strain) at 8 days of gestation were divided into three groups: a normal group fed Purina lab chow for rodents and water ad libitum; an ethanol group fed the liquid diet ENSURE with 20% of the calories derived from ethanol (12.6 +/- 1.2 gm/kg body weight per day); and an isocaloric group pairfed ENSURE with 20% of the calories derived from sucrose. These diets were continued until birth, at which time the litter size, crown to rump length, and weight were recorded. Randomly selected neonatal pups from each litter were decapitated and their hearts immediately processed for transmission electron microscopy. Litter size, crown to rump length, and body weight of the ethanol-treated mice at birth were significantly less than normal but not less than pairfed controls. Ultrastructural evaluation of cardiac muscle from mice treated in utero with ethanol in comparison to that from both normal and pair-fed control animals revealed various degrees of morphological alterations. The most pronounced alterations were in mitochondrial structure and included an increase in mitochondrial volume per cytoplasmic volume and a marked decrease in the amount of inner mitochondrial membrane. Myofibrillar abnormalities were also evident in the ethanol group but not in either control group. These abnormalities included a decrease in the myofibril volume per cytoplasmic volume and a disruption in myofibril organization particularly the Z-bands. The ultrastructural alterations in the cardiac muscle from the ethanol treated group were not a result of malnutrition or dehydration as the pairfed group did not exhibit these changes. It is apparent from this study that exposure of mice in utero to ethanol can cause ultrastructural abnormalities in cardiac muscle cells. Whether these changes result in heart pathophysiology and persist to adulthood are not known.

Animals↗
PubMed1996

Epithelial-mesenchymal transformations in early avian heart development.

Cardiac morphogenesis proceeds from a sequential series of epithelial-mesenchymal transitions which begins by establishing bipotential heart-forming cells and later their segregation into endocardial and myocardial lineages. Cells within each lineage integrate to form two concentric epithelia which inductively interact to transform cells of the inner epithelium, the endocardium, into mesenchymal or 'cushion' cells. Noncardiogenic epithelia (dorsal mesocardium, epicardium, neural ectoderm and coelomic mesothelium) undergo transition into populations of extracardiac mesenchyme that combine over time with cushion tissue to remodel the simple tubular heart into a four-chambered organ. Model systems are described for studying the mechanisms of cardiac-related transformations including primary cultures of precardiac epithelia and a differentiation-inducible, avian stem cell line called QCE-6. Focus is centered on the molecular mechanism by which endocardial epithelium transforms into cushion mesenchyme. Experimental findings are reviewed and interpreted in the context of a hypothetical model that seeks to answer why only some cells within an epithelium transform and whether the transformation process is regulated by intrinsic or extrinsic mechanisms. The model proposes that epithelial cells competent to transform to mesenchyme express characteristic markers including receptors for extrinsic signals secreted by stimulator cells (e.g. myocardium). Candidate extrinsic signals include multicomponent complexes called adherons. If applied directly to cultured endocardium, myocardial adherons but not those secreted by L6 myoblasts, induce changes in gene expression within target endocardial cells for proteases and cell:cell and cell:matrix adhesion molecules that accompanied transformation to mesenchyme. A main component of myocardial adherons has been identified as ES antigens, one of which, ES/130, has been cloned, found to have a novel sequence and in culture assays shown to be required for endocardium to transform to mesenchyme. The spatiotemporal pattern of ES protein expression within the embryo suggests that common mechanisms may exist for embryonic epithelial-mesenchymal transformations.

Animals↗
PubMed2006

Development and cardiac contractility: cardiac troponin T isoforms and cytosolic calcium in rabbit.

Cardiac contractility depends on calcium sensitivity of the myofilaments and cytosolic free calcium concentration ([Ca(2+)](i)) during activation. During development, the cardiac troponin T isoform cTnT(1) is replaced by shorter cTnT isoforms, including cTnT(4), and changes occur in other myofibrillar proteins and in calcium regulation. We expressed rabbit recombinant (r)cTnT(1) and rcTnT(4) in Spodoptera frugiperda cells and determined their effect on calcium binding to TnC in solution and on the calcium sensitivity of myofilaments in skinned rabbit ventricular fibers in vitro. We measured [Ca(2+)](i) and L-type calcium current (I(Ca)) in ventricular myocytes from 3-wk-old and adult rabbits. The dissociation constant (K(d)) of Ca-Tn(cTnT1) in solution was smaller than that of Ca-Tn(cTnT4) (mean +/- SE: 0.52 +/- 0.08 mumol/L versus 0.83 +/- 0.09 mumol/L). The Ca(2+) sensitivity of force development was greater in fibers reconstituted with rcTnT(1) (pCa(50) 6.07 +/- 0.04) than those reconstituted with rcTnT(4) (pCa(50) 5.75 +/- 0.07). Systolic [Ca](i) was lower in 3-wk-old than adult cells (443 +/- 35 nmol/L versus 882 +/- 88 nmol/L) as was I(Ca) (5.8 +/- 0.9 pA/pF versus 14.2 +/- 1.6 pA/pF). The higher calcium sensitivity of Tn-Ca binding and of force development conferred by rcTnT(1) suggest that higher neonatal cTnT(1) expression may partially compensate for the lower systolic [Ca(2+)](i).

Animals↗
PubMedDate not supplied

The value of SPECT-thallium scanning in screening for myocardial contusion.

In this prospective study of 40 patients sustaining blunt chest trauma, the value of single-photon-emission computed tomography (SPECT)-thallium scanning in the prediction of morbidity due to cardiac contusion was examined. Twelve patients developed cardiac complications--arrhythmias, ventricular conduction defects, and pericarditis. The sensitivity of SPECT-thallium scans was 55.6%, and the specificity was 32.1%, with an accuracy of 37.8%. Accuracy of the initial electrocardiogram (ECG) was 85%, with a sensitivity of 91.7% and a specificity of 82.1%. Patients with a normal ECG on admission rarely developed cardiac complications. It is concluded that SPECT-thallium is not a useful screening tool in this patient population.

Adolescent↗
PubMed1998

Efficient inhibition of the development of cardiac remodeling by a long-acting calcium antagonist amlodipine.

The purpose of the present study was to examine the effects of a long-acting calcium antagonist, amlodipine, on the development of cardiac remodeling. Dihydropyridine calcium antagonists have been used widely for many years in the treatment of hypertension and angina pectoris. It has been reported, however, that a prototype of dihydropyridines, nifedipine, does not reduce mortality of patients with ischemic heart disease, possibly because of reflex stimulation of the sympathetic nervous system. A calcium antagonist, amlodipine, has been reported to have potential benefits by virtue of a gradual onset of action and a long duration of effects. Amlodipine (8 mg/kg per day, once a day) or nifedipine (24 mg/kg per day, three times a day) was administered to spontaneously hypertensive 12-week-old rats for 12 weeks. Left ventricular wall thickness was measured by echocardiography, and relative amounts of myosin heavy chain isoforms were assessed by pyrophosphate gels. Expressions of "fetal type" genes and type 1 collagen gene were examined by Northern blot analysis. Amlodipine and nifedipine both markedly reduced systolic blood pressure. However, the decrease in systolic blood pressure caused by nifedipine continued for no more than 8 hours, whereas the blood pressure-lowering effect of amlodipine continued for more than 16 hours post dose. Amlodipine markedly reduced left ventricular wall thickness, whereas nifedipine only weakly attenuated an increase in the wall thickness. Amlodipine, but not nifedipine, prevented an increase in the relative amount of V3 myosin heavy chain isoform and suppressed an increase in mRNA levels of beta-myosin heavy chain, skeletal alpha-actin, and type 1 collagen. Unlike nifedipine, amlodipine effectively prevented cardiac remodeling secondary to high blood pressure at biochemical levels and morphological levels. These results suggest that a long-acting calcium antagonist is more effective than a short-acting one in preventing organ injury in hypertensive subjects.

Amlodipine↗
PubMed1976

[Importance of myocardial asynergy zones in the development of cardiac insufficiency].

The paper presents the results of an examination of 62 patients with postinfarction cardiosclerosis by means of echocardiography and ultrasonic scanning. The impact of the asynergy zone on the development of cardiac insufficiency was studied with reference to the area of myocardial lesion. Myocardial hyperkinesia is characterized, its compensatory effect in postinfarction cardiosclerosis and arterial hypertension is discussed. The effect of Inderal and Ildomen on both the zones of hyperkinesia, and on the indices of cardiac haemodynamics as a whole is described.

Adaptation, Physiological↗
PubMed2001

Genetic variation in angiotensin-converting enzyme does not prevent development of cardiac hypertrophy or upregulation of angiotensin II in response to aortocaval fistula.

BACKGROUND: Experimental and clinical evidence suggests that angiotensin II may be an important mediator of cardiac hypertrophy in response to hemodynamic stress. We investigated the effect of genetic variation in angiotensin-converting enzyme (ACE) on the development of cardiac hypertrophy and left ventricular (LV) dysfunction in response to volume overload. METHODS AND RESULTS: Male heterozygous ACE knockout (1/0) and wild-type (1/1) mice were studied 4 weeks after the creation of an aortocaval fistula (ACF). The LV weight/body weight ratio increased 74% in ACF versus sham-operated control mice but did not differ between genotypes. Echocardiographic circumferential stress versus rate-corrected velocity of circumferential shortening curves demonstrated depressed LV function in ACF versus sham-operated mice but no difference between genotypes. LV ACE activity was higher in 1/1 versus 1/0 mice and in ACF versus sham-operated mice, and it increased significantly more in the 1/1 versus the 1/0 mice after ACF (P<0.001 for effect of genotype, ACF/sham operation, and interaction term). LV angiotensin II was higher in ACF versus sham-operated mice but did not differ between genotypes, despite 3-fold higher LV ACE activity in ACF 1/1 versus ACF 1/0 mice. CONCLUSIONS: ACE underexpression does not prevent cardiac hypertrophy or LV dysfunction in response to volume overload. LV angiotensin II is unaffected by ACE genotype, both at baseline and after volume overload, indicating that the heart can maintain angiotensin II levels across a broad range of genetic ACE variation under both physiological and pathophysiological conditions.

Angiotensin II↗
PubMed1996

Fetal surgical interventions and the development of the heart in congenital diaphragmatic hernia.

Selective left ventricular hypoplasia is a recognized feature of congenital diaphragmatic hernia (CDH). It is speculated that the herniated viscera act as a space occupying lesion that inhibit normal cardiac development. The purpose of this study was to determine the effect of two separate fetal surgical interventions on subsequent cardiac development in CDH. CDH lambs were created at 80 days gestation and underwent either tracheal ligation (CDH + TL) or diaphragmatic repair (CDH + repair) at 110 days gestation. At term (141 days gestation) the hearts were harvested and fixed in 4% paraformaldehyde solution. Anatomic dissections were performed and component heart weights determined. Fresh specimens were analyzed for DNA and protein content. All weights are expressed in grams/kilogram body weight and all data as mean +/- SEM. All measurements are compared to control and CDH tissues. There were seven CDH lambs, five control lambs, five CDH + TL lambs, and five CDH + repair lambs. There were no differences in body weight (kg) between CDH, CDH + TL, CDH + repair, and control littermates. CDH lambs have significantly decreased total heart (4.88 +/- .25* vs 6.75 +/- .49, P < 0.05), left ventricular (1.65 +/- .11* vs 2.15 +/- .19, P < 0.05), septal (1.29 +/- .11* vs 1.99 +/- .21, P < 0.05), and combined atrial (0.68 +/- .06* vs 1.14 +/- .15, P < 0.05) weights (g/kg lamb) without differences in RV weights (1.26 +/- .07 vs 1.57 +/- .17, P = NS) when compared to littermate controls. No differences were found in total heart (4.82 +/- 0.38 vs 4.88 +/- 0.25), left ventricular (1.48 +/- 0.13 vs 1.65 +/- 0.11), septal (1.26 +/- 0.17 vs 1.29 +/- 0.11), combined atrial weights (0.56 +/- 0.07 vs 0.68 +/- 0.06), and right ventricular (1.52 +/- 0.12 vs 1.26 +/- 0.07) between CDH + TL and CDH lambs. There were no differences in total heart (6.60 +/- 0.29 vs 6.75 +/- 0.49), left ventricular (2.10 +/- 0.15 vs 2.15 +/- 0.19), septal (1.97 +/- 0.18 vs 1.99 +/- 0.21), combined atrial (1.10 +/- 0.10 vs 1.14 +/- 0.15), or right ventricular (1.52 +/- 0.12 vs 1.57 +/- 0.17) weights between CDH + repair and control lambs. LV and RV wall thicknesses (cm), as well as total protein and DNA content, and DNA/total protein ratios were identical in all groups. CDH lambs have a significant reduction in total heart weights mainly caused by hypoplasia of the left ventricle (left ventricular "smallness") and the interventricular septum. Removal of the herniated viscera and repair of the diaphragmatic defect correct this abnormality, but tracheal ligation does not. We speculate that although tracheal ligation reverses pulmonary hypoplasia, the enlarging lungs act as space occupying lesions that adversely affect cardiac development. Further investigations are necessary to determine the functional significance of these findings.

Animals↗