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PubMed1976

[Endocardial fibroelastosis (E.F.) and its differential diagnosis].

The endocardial fibroelastosis (EFE) is the most frequent cardiomyopathy. This disease is characterised by endocardial hyperplasia due to proliferation of elastic and collagenous fibres. There are primary and secondary forms. Within the primary form, the infantile form is the most frequent and of greatest importance to the pediatrician. This form is more a syndrom than a distinct disease. It is a reaction of the endocard due to several noxes. Lately a possible viral etiology is being discussed e.g. Parotitis, Coxsackie or other viruses. Clinical criteria for diagnosis are: cardiomegaly, left ventricular hypertrophy seen in 97% in the ECG, the absence of a murmur (or a soft apical mumur) absence of cyanosis and absence of systemic disease. Differential diagnosis is mainly between fibroplastic parietal endocarditis (FPE), cardiovascular collagenosis (CC) and endomyocard fibrosis (EMF). In FPE thrombosis is frequent and typically there is eosinophilia. CC is found in South Africa and is characterised by edema and fibrinoid necrosis. MEF is present mainly in Uganda, Nigeria and South India, characterised by endocardial fibrosis, valve involvement and eosinophilia. The obstructive hypertrophic cardiomyopathy is characterised by a pronounced cardiomegaly, insufficient weight gain as well as dyspnea and cyanosis. Catheterization shows a gradient across one or both of the outflow tracts due to hypertrophic subaortic or subpulmonic stenosis. Therapy of EFE consists in treating the cardiac decompensation and according to the severity of the disease, in steroids.

Cardiomyopathies↗
PubMed2004

Atrial standstill with subnodal conduction defect and diffuse ventricular fibrosis managed with low right atrial pacing.

In patients with congenital heart disease presenting with bradyarrhythmia, many electrophysiological abnormalities are found. This report presents a case of a man with surgically corrected single atrium and pulmonary valve stenosis, atrial standstill, delayed AV node conduction, first-degree intra- and second-degree infra-His block, who was permanently paced from a restricted excitable area of the low right atrium, as the pacing threshold was unacceptable at any ventricular site.

Arrhythmias, Cardiac↗
PubMed1989

[Antihypertensive effect of bopindolol on stroke-prone spontaneously hypertensive rats (SHRSP)].

The antihypertensive effect of bopindolol, a long-acting beta-adrenoceptor blocking agent, was investigated in stroke-prone spontaneously hypertensive rats (SHRSP). One group received tap water during the period of 8 to 32 weeks of age. The average dose of bopindolol administered was calculated from water intake to be approximately 1.4 mg/kg/day. The lowering effect in blood pressure of bopindolol was apparent at the age of 14 weeks, and this continued up to the end of the experiment. Bopindolol significantly reduced the heart rate. Plasma levels of urea nitrogen (BUN), triglyceride, and phospholipid of SHRSP treated with bopindolol were lower than those of the control SHRSP. One of the 8 control SHRSP died, and no rats treated with bopindolol died during the experiment. The histopathological study revealed that three of the control SHRSP had cerebral apoplexy, whereas there was no evidence of cerebral apoplexy in the treated SHRSP. Chronic treatment of bopindolol clearly alleviated myocardial fibrosis and hypertrophic changes in the left ventricular wall of the heart. Decreases in the incidence of proliferative arteritis and malignant nephrosclerosis in the kidney and necrotizing arteritis of the mesenteric arteries were observed in SHRSP treated with bopindolol. The data presented indicate that bopindolol is a powerful antihypertensive agent.

Administration, Oral↗
PubMed1993

Cardiac pathology in patients with end-stage renal disease maintained on hemodialysis.

We report the spectrum of cardiovascular pathology found on autopsy examination in 106 consecutive patients with end-stage renal disease. Cardiovascular pathology was present in nearly all patients, and was the most frequent cause of death (36%), with acute myocardial infarction accounting for 15%. Particularly frequent pathologic findings were left ventricular hypertrophy, coronary and aortic atherosclerosis, pericarditis with effusion, myocardial fibrosis, and valvular dilatation. Cardiovascular death rate was higher during the first year than after the fifth year of dialysis. Nearly all patients had a history of hypertension. The nature of the underlying cause of renal failure and pre-existing cardiovascular disease, specifically diabetes mellitus and hypertension, were the principal predictors of cardiovascular mortality rather than maintenance hemodialysis therapy per se.

Adult↗
PubMed1992

Visualization of myocardial cellular architecture using acoustic microscopy.

The resolution of an ultrasound transducer depends on its frequency. The resolution improves when higher frequency transducers are used. A 1000 MHz transducer has a resolution of approximately 1 micron. Acoustic microscopy utilizes very high-frequency ultrasound (600 to 1000 MHz) to visualize structures on a microscopic level. Unstained, deparaffinized, 5 microns sections of myocardial biopsy specimens from 10 patients were placed on a slide and imaged using an Olympus UH3 scanning acoustic microscope. To compare with light microscopy, the section used for acoustic microscopy was subsequently stained with hematoxylin and eosin and a serial section from the paraffin block was stained with PTAH stain. Myocytes, myofibrils, and interstitial tissue were accurately imaged. Pathologic phenomena such as cell fallout, interstitial fibrosis, and lymphocytic infiltration were identified by acoustic microscopy. Intramural vessels, nuclei of endothelial cells, and the media were clearly identified by this technique. There was close correlation between findings by acoustic microscopy and light microscopy. Acoustic microscopy permitted the visualization of cardiac cellular detail with a resolution similar to that of light microscopy. Unlike light microscopy, acoustic microscopy requires no staining of the specimen.

Biopsy↗
PubMed2000

Connective tissue and the heart. Functional significance and regulatory mechanisms.

The heart has a three-dimensional extracellular fibrillar collagen scaffolding that normally serves a variety of functions important to tissue integrity and efficiency of muscular systolic pump and diastolic suction pump function (see article by Kovács). An adverse accumulation of extracellular matrix structural protein compromises tissue stiffness and adversely affects myocardial viscoelasticity, this leads to ventricular diastolic and systolic dysfunction. Hormonal factors, such as chronic, inappropriate (relative to dietary salt intake and intravascular volume) elevations in circulating angiotensin II and aldosterone, are accompanied by fibrosis of right and left sides of the heart. Hemodynamic factors regulate cardiac myocyte work and their adaptive hypertrophic growth. The relative contributions of hormonal and hemodynamic factors in regulating growth of muscular and nonmuscular compartments must form the basis for the selection of pharmacologic intervention that will optimize the management of symptomatic heart failure that accompanies hypertensive heart disease and ischemic cardiomyopathy. Cardioprotective strategies that prevent alteration of normal cardiac tissue structure by fibrosis and appearance of abnormal ventricular stiffness (viscoelasticity) are based on negating the generation of these hormones or interfering with their receptor-ligand binding. A regression of established cardiac fibrosis and improvement in abnormal ventricular stiffness is feasible. Experimental and clinical findings with lisinopril in hypertensive heart disease, where cardiac fibrosis and abnormal ventricular stiffness are present, indicate that such cardioreparation should be a targeted objective of pharmacologic intervention. Systematic analysis of this approach using a controlled clinical trial format is warranted. In recognizing the importance of viscoelastic elements in regulating the mechanical behavior of cardiac tissue, and in turn systolic and diastolic ventricular function, a broader tissue compartment based paradigm (ECM versus myocyte) for the management of heart failure emerges.

Collagen↗
PubMed2002

Effects of canrenone on myocardial reactive fibrosis in a rat model of postinfarction heart failure.

BACKGROUND: Spironolactone reduces overall mortality by 30% in advanced congestive heart failure. Nevertheless, few data are available with regard to the effects of mineral corticoid inhibition in postinfarction heart failure. MATERIALS AND METHODS: Experimental myocardial infarction was induced by left coronary ligation in 70 male rats with body weights ranging from 180 to 200 gr. The day after surgery, animals were randomized to either placebo or canrenone-gamma-cyclodestrin 8 mg/kg/die or canrenone-gamma-cyclodestrin 18 mg/kg/die. Twelve animals served as the control group. After two weeks, the rats underwent closed chest left ventricular catheterization. The heart was the rapidly excised for subsequent histological analysis. RESULTS: Compared with controls, infarcted rats had reduced left ventricular systolic pressures (-6%) and higher left ventricular end-diastolic pressures (+600%), associated with a marked increase of mean collagen fraction (+446%) and perivascular fibrosis (+72%). Compared with placebo-infarcted rats, in the group treated with high canrenone dose there was a significant reduction of left ventricular systolic and end-diastolic pressures (-6.5% and -23%, respectively) and an attenuation of interstitial and perivascular fibrosis (-47% and -34%, respectively). The low-dose canrenone group did not show differences compared with the placebo infarcted rats, except for a slight reduction of mean collagen fraction (-21%). CONCLUSIONS: Canrenone attenuates LV interstitial remodeling and reduces filling pressures in rats with postinfarction heart failure.

Administration, Oral↗
PubMed2006

Glycogen synthase kinase 3beta together with 14-3-3 protein regulates diabetic cardiomyopathy: effect of losartan and tempol.

Glycogen synthase kinase (GSK) 3beta is a multifunctional protein that positively regulates myocardial apoptosis and negatively regulates hypertrophy. However, the role of GSK3beta in the diabetic myocardium is largely unknown. We found that GSK3beta became more active (less phosphorylated at serine 9) via decreased Akt phosphorylation, in parallel to c-Jun NH2 terminal kinase activation, which correlated with increased activated caspase 3 and myocardial apoptosis 3 days after streptozotocin (STZ) injection in mice. However, 28 days after STZ injection, GSK3beta became inactive, which correlated with the enhanced protein kinase C beta2 and p38 mitogen activated protein kinase expression, nuclear translocation of nuclear factor of activated T cells c3, cardiac hypertrophy and fibrosis. All of the above parameters were exacerbated in dominant-negative 14-3-3 transgenic mice. Our results suggest that GSK3beta together with 14-3-3 protein plays essential roles in the signaling of diabetic cardiomyopathy, and treatment with either losartan or tempol prevents these changes.

14-3-3 Proteins↗
PubMed1998

Arrhythmic profile, ventricular function, and histomorphometric findings in patients with idiopathic ventricular tachycardia and mitral valve prolapse: clinical and prognostic evaluation.

BACKGROUND: In patients with ventricular tachycardia (VT) and apparently normal hearts, mitral valve prolapse (MVP) is discovered fairly often, raising the question of whether or not it is an occasional finding. HYPOTHESIS: This issue was analyzed in a series of patients with VT and apparently normal hearts in order to define the prevalence of MVP in this condition, the existence of specific diagnostic features suggesting a nonrandom association between idiopathic VT and MVP, and the prognostic implications of this finding. METHODS: We studied 28 consecutive patients with documented VT and no history of heart disease. Two-dimensional (2-D) echocardiogram, cardiac catheterization, morphometric examination of endomyocardial biopsy and arrhythmologic evaluation (24-h Holter monitoring, electrophysiologic study, and signal-averaged electrocardiogram) were performed. Inclusion criteria for all patients were angiographically normal coronary arteries, normal biventricular function, and absence of histologic evidence of myocarditis. Data obtained in patients found to have MVP at 2-D echo were compared with those of the remaining patients. Long-term follow-up data were also collected. RESULTS: The prevalence of MVP in our study group was 25% (7 patients). It was not associated with leaflet dysplasia or significant regurgitation. Biventricular function (ventricular volumes and ejection fraction) was comparable in patients with and without MVP. Patients with MVP had a significantly higher prevalence of ventricular late potentials at signal-averaged electrocardiogram (86 vs. 29%, p = 0.027), more interstitial fibrosis at morphometry (8.5 +/- 3.7 vs. 5.4 +/- 2.7% p = 0.028), and VT of right bundle-branch block morphology (100 vs. 48%; p = 0.044). Other arrhythmologic findings were similar in the two groups. After a mean follow-up of > 5 years, no patient in either group died, and none developed heart failure or severe mitral regurgitation. CONCLUSIONS: Mitral valve prolapse is frequently detected in idiopathic VT. The distinguishing features of this association are (1) VT of right bundle-branch block morphology, (2) high prevalence of ventricular late potentials, and (3) increased fibrosis on endomyocardial biopsy. Ventricular function and other arrhythmologic findings are not specific of this association. Prognosis remains substantially benign, as is true for most cases of idiopathic VT.

Adolescent↗
PubMed2000

Fibrosis and hypertensive heart disease.

The normal myocardium is composed of a variety of cells: cardiac myocytes and noncardiomyocytes, which include endothelial and vascular smooth muscle cells and fibroblasts. Hypertensive heart disease involves a structural remodeling of muscular and nonmuscular compartments. It is not the quantity but rather the quality of myocardium that accounts for pathologic hypertrophy and predisposes to ventricular dysfunction and arrhythmias, which, in turn, confer increased risk of adverse cardiovascular events. Herein, factors regulating growth of these compartments are reviewed and in particular signals involved in promoting adverse remodeling of intramyocardial coronary arteries and arterioles by fibrous tissue.

Animals↗
PubMed1980

Stroke-prone SHR (SHRSP) as models for clinical and epidemiological studies on hypertension-related cardiac diseases in humans.

Spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) were vectorcardiographically and pathologically studied for myocardial lesions with left ventricular hypertrophy, and findings were compared with those in normotensive Wistar-Kyoto rats (WK). Characteristic vectorcardiogram (VCG) in adult SHR was left superior (posterior) deviation of major QRS portion usually with ST-T changes, which corresponded to the pathological findings such as increased weight of the heart and the left ventricle. In old SHRSP, VCG showed deformity and deviation of QRS loop with prolonged P and QRS durations, and ST-T changes which corresponded to the pathological findings of myocardial degeneration or fibrosis with aggravated left ventricular hypertrophy. Such myocardial lesions were vectorcardiographically followed up in the ageing process and compared with findings in cases of induced, acute myocardial infarction. Vascular or tissue lesions of the brain, the kidney and the heart were clarified to be organ specific and to be related. Vector- or electrocardiogram are parameters for predicting cerebral stroke and/or ischemic heart diseases in humans. Primary prevention and appropriate therapy should be concomitantly considered.

Aging↗
PubMed1995

Chronic mineralocorticoid excess and cardiovascular remodeling.

Chronic mineralocorticoid (MC) excess, whether due to elevated plasma aldosterone (ALDO) or deoxycorticosterone (DOC), is associated with a perivascular fibrosis of systemic and coronary arterioles. This remodeling of resistance vessels contributes to the appearance of hypertension. Chronic MC excess is also accompanied by cardiac myocyte necrosis, secondary to myocardial potassium depletion, and a subsequent reparative fibrosis that appears in the normotensive, nonhypertrophied right and hypertensive, hypertrophied left ventricles. Fibrosis contributes to the appearance of ventricular arrhythmias and dysfunction. Herein, clinical and experimental evidence linking chronic, inappropriate (relative to dietary sodium) elevations in circulating ALDO and DOC with these reactive and reparative forms of fibrous tissue formation in the heart and other tissues is presented.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2003

Effect of endothelin blockade on early cardiovascular remodeling in the one-clip-two-kidney hypertension of the rat.

BACKGROUND: In models of hypertension and of renal failure, pharmacological blockade of the ET(A) receptor has been shown to cause some inconsistent lowering of blood pressure (BP) and lesser left ventricular hypertrophy (LVH). The effects of ET(A) receptor blockade (ET(A)-RB) on vascular remodeling and their potential relation to BP lowering, have not been clarified. DESIGN: The experimental study in male Sprague-Dawley rats was designed to compare four experimental groups: (1) sham-operated controls (sham); (2) untreated rats with one-clip-two-kidney (1C-2K) renovascular hypertension; (3) 1C-2K rats treated with the ACE inhibitor (ACE-i) trandolapril (0.3 mg/kg b.w./day), and (4) 1C-2K rats treated with the ET(A)-RB LU-135252 (50 mg/kg b.w./day). BP was measured weekly by tail plethysmography. After 3 weeks, animals were sacrificed and cardiac, aortic and mesenteric artery morphology was evaluated using morphometric and stereological techniques. RESULTS: Systolic BP was significantly higher in 1C-2K rats compared to sham. BP was not significantly affected by ET(A)-RB, but was significantly lowered by the ACE-i. Despite no significant change in BP, ET(A)-RB treatment led to a significantly less volume density of the cardiac interstitium (sham 1.40 +/- 0.18, 1C-2K 2.66 +/- 0.56, 1C-2K + ACE-i 1.88 +/- 0.38, 1C-2K + ET(A)-RB 2.15 +/- 0.37%). In contrast, ET(A)-RB had no significant effect on left ventricular/body weight ratio (sham 2.85 +/- 0.26, 1C-2K 2.96 +/- 0.33, 1C-2K + ACE-i 2.54 +/- 0.22 and 1C-2K + ET(A)-RB 3.15 +/- 0.44 mg/g) or on wall thickness of intramyocardial arteries. CONCLUSIONS: The ET(A)-RB LU-135252 ameliorated the development of myocardial fibrosis in a short-term hyperreninemic normal salt model of experimental hypertension nearly as effectively as an ACE-i. This effect of LU-135252 is independent of systemic BP. In contrast to findings in other models, ET(A) receptor blockade had no significant effect on LVH or vascular remodeling. Only the ACE-i but not the ET(A)-RB prevented structural changes of small intramyocardial arteries and of the aorta.

Animals↗
PubMed2000

Alterations in cardiac function and gene expression during autoimmune myocarditis in mice.

Although myocarditis has been implicated in the pathogenesis of heart failure, a definitive relationship between myocardial inflammation, cardiac dysfunction, and changes in myocyte gene expression has not been established. In this study, we examined the hypothesis that myocardial inflammation and replacement fibrosis following an autoimmune response can progress to cardiac dysfunction and may result in progression to the heart failure phenotype. SWXJ mice were immunized with cardiac myosin on day 0 and day 7, in order to induce an autoimmune response to the myosin protein. Cardiac catheterization via the right carotid artery was performed on days 14, 21, 28, 35, and 42, using a 1.4F Millar transducer-tipped catheter. Hearts were weighed, and cross-sections were cut and stained with either haematoxylin and eosin or Masson's trichrome, in order to identify areas of inflammation and/or fibrosis. Myocardial gene expression was determined by Northern blot analysis. In mice with histological evidence of myocarditis, the heart weight/body weight ratio increased beginning on day 14, and cardiac function decreased beginning on day 21. Myocardial inflammation was accompanied by significant fibrosis beginning on day 21. Quantitation of mRNA showed expression of ventricular atrial naturietic factor, as well as a decrease in myosin heavy chain alpha, beginning on day 21. These data demonstrate that autoimmune inflammation of the heart results in significant cardiac dysfunction, leading to phenotypic alterations similar to those demonstrated in human heart failure and animal models of heart failure.

Animals↗
PubMed2005

[Morphological changes of cardiovascular system at experimental hypertension, caused by no inhibition in condition of the laser irradiation of low-frequency].

The aim of our study was the investigation of the morphological changes of cardiovascular system, caused by NO inhibition during the laser irradiation of low-frequency. On reception of L NAME and a low-frequency laser irradiation arterial pressure during all experiment remains within the norm. At slight increase of phonic arterial pressure the laser irradiation proved to be less effective, while on a background of high arterial pressure the irradiation does not interfere the further development of hypertension and persistency. Immediately after reception of L NAME and at a low-frequency laser irradiation, the fibrosis and inflammatory changes of myocardium have not been observed; on the background of the slight enhancement of arterial pressure, laser irradiation causes insignificantly expressed fibrosis, inflammatory changes in myocardium; while on the background of increased arterial pressure a laser irradiation doesn't interfere development of fibrosis, myocardium and inflammatory changes in it. Immediately after reception L NAME and at a laser irradiation of low-frequency from the third day, a damage of cardiovascular walls, inflammatory changes, perivascular fibrosis have not been developed, while on the background of increased arterial pressure the irritation doesn't interfere the development of the above mentioned changes. Thus, the irradiation of a low-frequency laser might be recommended to prevent the development of hypertension and to avoid the complications of pre-clinical phase of hypertension. Though, the analogous recommendations are not foreseen for involvement in algorithm of the treatment of hypertension and correction of clinical evidence of the disease.

Animals↗
PubMed1998

Cardiac remodelling by fibrous tissue: role of local factors and circulating hormones.

Following myocardial infarction (MI), extensive fibrosis appears at and remote to the MI and is associated with diastolic dysfunction. Both circulating and tissue hormones contribute to the adverse structural remodelling of the myocardium and thereby influence the progressive nature of heart failure. In this review, factors contributing to the appearance of fibrous tissue will be considered, with special emphasis on the role of peptides produced within the diseased myocardium and on the circulating hormones of the renin-angiotensin-aldosterone system.

Aldosterone↗
PubMed1989

Toxicological evaluation of the cardiotonic isomazole in the dog.

Acute, subchronic, and chronic toxicity studies were conducted in dogs with the new vasodilator/cardiotonic drug isomazole (IMZ) to support, in part, clinical investigations of this agent in humans. Single oral doses of IMZ of 25, 50, or 100 mg/kg given to English pointer dogs (2/dose) caused a marked drop in systemic blood pressure and reflex-induced increases in heart rate to values well over 200 beats per minute. These responses were maintained for 12 to 22 hr depending on the dose given. One of the dogs receiving 100 mg/kg died at 4.5 hr postdose. Results of subchronic (3 months) and chronic (1 year) studies in beagle dogs (4/sex/dose group), in which measurable plasma levels of the drug and its metabolites were found, indicated that IMZ did not produce any discernible adverse findings when given in doses up to 16 mg/kg, other than expected cardiotoxic effects. The plasma t1/2 of IMZ at 16 mg/kg increased to between 4 and 8 hr from 2 hr noted at lower doses. In the 1-year study, at all doses and in both sexes, plasma levels of IMZ declined over the first month, stabilizing (at the 2 and 6 mg/kg doses) thereafter for the duration of the study. At the high dose of 16 mg/kg, after 1 year plasma levels of IMZ exceeded (females) or equaled (males) the 1-month values. At peak plasma levels of IMZ (2 hr postdose), plasma levels of parent drug increased linearly with the dose. The cardiotoxic effects consisted of substantial postdose increases in heart rate throughout the course of treatment (5 mg/kg and above), significant increases in heart weight (6 mg/kg and above), and multifocal myocardial fibrosis (6 mg/kg and above). There was a decline in basal heart rate at doses of 12.5 mg/kg and higher. The results of these studies demonstrated that repeated IMZ administration, as expected, was cardiotoxic to the dog, a species relatively sensitive to the pharmacological activity and hemodynamic changes induced by vasodilator/cardiotonic drugs. The no-effect dose level for cardiotoxicity in the repeated dose studies was considered to be 2 mg/kg, the lowest dose tested.

Animals↗
PubMed1994

Structural basis of end-stage failure in ischemic cardiomyopathy in humans.

BACKGROUND: Ischemic cardiomyopathy is characterized by myocyte loss, reactive cellular hypertrophy, and ventricular scarring. However, the relative contribution of these tissue and cellular processes to late failure remains to be determined. METHODS AND RESULTS: Ten hearts were obtained from individuals undergoing cardiac transplantation as a result of chronic coronary artery disease in its terminal stage. An identical number of control hearts were collected at autopsy from patients who died from causes other than cardiovascular disease, and morphometric methodologies were applied to the analysis of the left and right ventricular myocardium. Left ventricular hypertrophy evaluated as a change in organ weight, aggregate myocyte mass, and myocyte cell volume per nucleus showed increases of 85%, 47%, and 103%, respectively. Corresponding increases in the right ventricle were 75%, 74%, and 112%. Myocyte loss, which accounted for 28% and 30% in the left and right ventricles, was responsible for the difference in the assessment of myocyte hypertrophy at the ventricular, tissue, and cellular levels. Left ventricular muscle cell hypertrophy was accomplished through a 16% and 51% increase in myocyte diameter and length, whereas right ventricular myocyte hypertrophy was the consequence of a 13% and 67% increase in these linear dimensions, respectively. Moreover, a 36% reduction in the number of myocytes included in the thickness of the left ventricular wall was found. Collagen accumulation in the form of segmental, replacement, and interstitial fibrosis comprised an average 28% and 13% of the left and right ventricular myocardia, respectively. The combination of cell loss and myocardial fibrosis, myocyte lengthening, and mural slippage of cells resulted in 4.6-fold expansion of left ventricular cavitary volume and a 56% reduction in the ventricular mass-to-chamber volume ratio. CONCLUSIONS: These results are consistent with the contention that both myocyte and collagen compartments participate in the development of decompensated eccentric ventricular hypertrophy in the cardiomyopathic heart of ischemic origin.

Cardiomyopathy, Dilated↗