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PubMed2005

Reduction of ventricular hypertrophy and fibrosis in spontaneously hypertensive rats by L-arginine.

The purpose of this experiment was to explore long-term L-arginine administration on ventricular hypertrophy and cardiac fibrosis in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) rats. Twenty-four rats of each strain at eight wks of age were divided into two groups--one receiving L-arginine and the other vehicle for twelve wks. Arterial pressure (AP) and heart rate were monitored. At 20 wks of age, the rats' rings of thoracic aorta were isolated to record isometric tension. The study measured left ventricular weight (LVW), body weight (BW), left ventricular (LV) contents of cGMP, and collagen volume fraction (LVCVF). Histological examination of the LV tissue determined changes in cardiomyocytes. Administration of L-arginine did not alter the AP change in SHR, but reduced the AP in WKY after six wks. Our results showed a significantly higher LVW/BW ratio and LVCVF in vehicle-treated SHR compared to levels in corresponding WKY, whereas, the LV cGMP and nitrite/nitrate measurements were higher in vehicle-treated WKY than in SHR. L-Arginine treatment decreased LVW/BW ratio and LVCVF, while increasing the levels of LV cGMP and nitrite/nitrate only in SHR, consistent with histopathological examinations that showed L-arginine prevented cardiomyocytes from thickness and hypertrophy. Our results suggested that the mechanism of reduction in ventricular hypertrophy and fibrosis following long-term L-arginine administration in SHR may stem from increased myocardial nitric oxide-cGMP signaling, independent of AP and EDV of thoracic aorta.

Animals↗
PubMed1998

Dependence of temporal variability of ventricular recovery on myocardial fibrosis. Role of mechanoelectric feedback?

OBJECTIVE: The study was aimed at establishing the effect of factors involved in the expression of mechanoelectric feedback in the heart, such as R-R interval and connective tissue, on time dependent changes in ventricular recovery, as determined at the body surface by beat to beat variability of QRST integral maps (BBV-IM). METHODS: We used 15 normal 6-month-old Wistar rats. In each anesthetized animal, we performed a 3-minute continuous recording of 44. The simultaneous chest ECGs. The signals were interactively processed, 1) to determine mean R-R interval and R-R variability throughout the recording period and 2) to compute QRST integral maps from approximately 50 beats belonging to the end of expiration. Then BBV-IM was calculated and expressed as percentage of beats significantly differing from a template. At sacrifice, the amount of myocardial fibrosis was morphometrically evaluated. RESULTS: R-R interval was 149 ms +/- 4, R-R interval variability 0.008 +/- 0.001 and BBV-IM 30.7% +/- 4.4. Myocardial fibrosis expressed as % volume of left ventricular myocardium, numerical density of fibrotic foci and average cross-sectional area of the foci was 3.0% +/- 0.4, 3.8 +/- 0.6 and 4.4 microns(2)/1000 +/- 0.1 respectively, BB-IM was positively correlated to the % volume of fibrosis (r = 0.83, P < 0.0003). Both measurements were positively correlated to R-R interval (BBV-IM: r = 0.83, P < 0.0001; % volume of fibrosis: r = 0.87, P < 0.001) and negatively correlated to cardiac weights (BBV-IM: r = -0.79, P < 0.0005; % volume of fibrosis: r = -0.75, P < 0.001). CONCLUSION: Beat to beat changes in ventricular repolarization attributable to mechanoelectric transduction can be detected at the body surface by means of BBV-IM.

Analysis of Variance↗
PubMed2004

Myocardial necrosis in a captive binturong (Arctictis binturong).

An adult male binturong, Arctictis binturong, which had been anorexic and lethargic for seven days became acutely dyspnoeic and died under anaesthesia. A postmortem examination revealed left ventricular hypertrophy with a thrombus occluding the left ventricular chamber. Histological findings included moderate to severe multifocal, vasculocentric myocardial degeneration and necrosis with fibrosis replacing myocardiocytes. Escherichia coli and Proteus mirabilis were grown on cultures. The animal's serum vitamin E and selenium levels were considered adequate. The aetiology of the chronic myocardial changes could not be determined.

Animals↗
PubMed1988

[Comparison of regional contractile dynamics and pathological findings of the left ventricular wall in patients with hypertrophic cardiomyopathy].

To investigate the relationship between regional contractile dynamics and regional myocardial lesions of the left ventricular wall in patients with hypertrophic cardiomyopathy (HCM), autopsy findings of 11 patients were compared with their ante mortem echocardiographic findings. The regional systolic wall thickenings (%RWT) of the interventricular septum (IVS) and left ventricular posterior wall (LVPW) obtained using M-mode echocardiography were converted into % normalized RWT (%NRWT) by the averaged %RWT in 15 normal subjects. The %NRWT was compared with the wall thickness obtained by echocardiography and/or autopsy, and histological findings, such as the myocardial fibrosis ratio, disarray area ratio, and mean myocyte diameter. 1. There were no significant correlations among wall thickness of the left ventricle, the myocardial fibrosis ratio, the disarray area ratio, and the mean myocyte diameter of each segment. 2. The %NRWT in 22 segments of the 11 patients with HCM was not significantly related to the echocardiographic wall thickness at end-systole, the autopsy wall thickness, the mean myocyte diameter and the disarray area ratio, but that correlated significantly with the echocardiographically-determined wall thickness at end-diastole (r = -0.53, p less than 0.02), and with the myocardial fibrosis ratios (r = -0.59, p less than 0.005). 3. The %NRWT in the IVS was significantly less than that in the LVPW. The %NRWT in all segments of the LVPW was significantly related to the myocardial fibrosis ratios (r = -0.80, p less than 0.005), but was not related to the wall thicknesses or the disarray area ratios.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1970

The role of rubella in the etiology of supravalvular aortic stenosis.

The possibility of an etiological relationship between rubella embryopathy and sporadic forms of supravalvular aortic stenosis is considered. A case is presented of a patient with rubella embryopathy and supravalvular aortic stenosis associated with pulmonary valvular and peripheral pulmonary artery stenosis, bicuspid aortic valve, aortic valve stenosis and subendothelial myocardial fibrosis. A review of the literature revealed many clinical and pathological features common to both syndromes. The hypothesis that rubella virus produced germ-cell mutation and subsequent persistence of rubella in the zygote produced further fetal damage is presented to explain these observations.

Aortic Coarctation↗
PubMed1995

Are mast cells involved in hypertensive heart disease?

OBJECTIVE: To evaluate the potential relationship of mast cells with myocardial fibrosis in the cardiac ventricles of spontaneously hypertensive rats (SHR). DESIGN: Experiments were performed on hearts from 36-week-old SHR with established left ventricular hypertrophy (n = 12) and from 36-week-old normotensive Wistar-Kyoto (WKY) rats (n = 12). Furthermore, to evaluate whether antihypertensive treatment with the angiotensin converting enzyme inhibitor quinapril interferes with the potential relationship between mast cells and fibrosis in SHR, we treated 16-week-old SHR (n = 12) with oral quinapril (10 mg/kg body weight per day) for 20 weeks. METHODS: Mast cells were counted in 25 high-power fields. Toluidine blue-stained sections and avidin staining were used to detect mast cells. The extent of myocardial fibrosis was analysed in samples stained with Masson's trichrome. The amount of collagen was evaluated morphometrically, using an automatic image analyser, and biochemically, using myocardial hydroxyproline concentration. RESULTS: In the left ventricle of untreated SHR compared with age- and sex-matched normotensive WKY rats we found more extensive interstitial and perivascular fibrosis, an increased collagen volume fraction, an increased hydroxyproline concentration and an increased number of mast cells. Similar but less intense abnormalities were observed in the right ventricles of untreated SHR compared with the left ventricles of the same rats. In the left ventricles of quinapril-treated SHR compared with those of untreated SHR we found a marked decrease in fibrosis, a lower collagen volume fraction, a lower hydroxyproline concentration and fewer mast cells. Treatment with quinapril was also accompanied by normalization in the myocardial structure of the right ventricles of SHR. A positive correlation was found between the density of mast cells and the collagen volume fraction in the left ventricles of all of the rats. CONCLUSIONS: The present findings suggest that mast cells can play a part in the development of the myocardial fibrosis that occurs in the cardiac ventricles with hypertensive cardiac hypertrophy. In addition, the present results suggest that the ability of quinapril to interfere with mast cells might be involved in its cardioreparative properties.

Animals↗
PubMed1975

Cardiomyopathy in crowded rabbits.

Rabbits were crowded 4 to a cage for 2 weeks, then released for 1 week, crowded again for 2 weeks, and so on. Of 44 rabbits subjected to intermittent crowding, only 9 survived for longer than 10 months, 20 died during the 1st month, and 15 died between the 2nd and 9th month of the experiment. Histological sections of the myocardium showed myocytolysis, intersititial edema, and an increased amount of acid mucopoly saccharides in rabbits surviving for 2 weeks and more. The accumulations of acid mucopolysaccharides were apparently unrelated to necrotic foci. Long-term survivors frequently showed myocardial fibrosis and endocardial fibroelastosis, as well as basophilic degeneration of myocardial fibers. The lesions observed were similar to those described in idiopathic endomyocardiopathy in Southern Africa. Therefore, the rabbit may be of some value for research in cardiomyopathies.

Animals↗
PubMed1996

Comparative study of 201Tl-scintigraphic image and myocardial pathologic findings in patients with dilated cardiomyopathy.

The objective of the present study was to characterize the production of 201Tl myocardial perfusion defects, the relation between the 201Tl multiple small defects and the myocardial damage indicated by myocardial fibrosis shown histopathologically in patients with dilated cardiomyopathy (DCM). Rest 201Tl scintigraphy was performed in thirty-seven patients with myocardial tissue fibrosis by endomyocardial biopsy, and without stenosis of the coronary artery. 201Tl myocardial SPECT images were visually classified into 4 grades according to the severity of inhomogeneous perfusion defects (IPD), 0: none, 1: slight, 2: moderate, 3: severe. 201Tl uptake, defect regions (DR), and coefficient of variation % (CV%) were also quantified by Bull's eye quantification in nineteen patients. During cardiac catheterization, three biopsy specimens were obtained from the lateral wall to the apical region of the left ventricle and the amount of fibrosis was assessed by means of light microscopic morphometry. The myocardial fibrosis was also classified into 4 grades by a point-counting method. Autopsy study was also assessed in six patients. 201Tl perfusion defects were observed in 35 (94.6%) patients, of whom 29 (78.4%) showed inhomogeneous perfusion defects. Twenty-four (64.9%) showed Stage 0 and 201Tl findings, and 21 (62.2%) had myocardial fibrosis in stage 1. Clinically, the correlation between the grades of the IPD, % 201Tl uptake, DR and CV% of myocardial uptake, which were calculated semiquantitatively by Bull's eye image, and the histological grades of fibrosis were also good (IPD vs. fibrosis: r = 0.7014; % 201Tl uptake vs. fibrosis: r = -0.6542; DR vs. fibrosis: r = 0.7027; CV% vs. fibrosis: r = 0.6985). The 201Tl SPECT findings were in close agreement with the severity of myocardial fibrosis confirmed by autopsy, but the grading of the IPD was not related to the ejection fraction or left ventricular diameter. It showed a higher rate of inhomogeneous 201Tl myocardial perfusion defects (78.4%) in patients with DCM. This result may contribute to the clinical evaluation of DCM or differentiation from other diseases. Furthermore, the grading of 201Tl inhomogeneous perfusion defects related to the myocardial fibrosis of left ventricular myocardium may contribute to speculation of the myocardial degenerative stage in clinical settings.

Adult↗
PubMed1996

Left ventricular echocardiographic and histologic changes: impact of chronic unloading by an implantable ventricular assist device.

OBJECTIVES: We studied the effects of chronic left ventricular unloading by a ventricular assist device and assessed left ventricular morphologic and histologic changes. BACKGROUND: The implantable left ventricular assist device has been effective as a "bridge" to cardiac transplantation. Although there are reports documenting its circulatory support, little is known about the effects of chronic left ventricular unloading on the heart itself. METHODS: We performed intraoperative transesophageal echocardiography at the insertion and explanation of a HeartMate left ventricular assist device in 19 patients with end-stage heart failure. They were supported by the assist device for 3 to 153 days (mean [+/-SD] 68 +/- 33). Measurements were taken retrospectively to obtain left atrial and ventricular diameters and interventricular septal and posterior wall thicknesses. Histologic examinations were made from the left ventricular myocardial specimens of 15 patients at the times of insertion and explanation for heart transplantation. Insertion and explanation specimens were compared qualitatively (0 to 3 scale) for wavy fibers, contraction band necrosis and fibrosis, with quantitative measurement of minimal myocyte diameter across the nucleus. RESULTS: Left atrial and left ventricular diastolic and systolic diameters decreased immediately after insertion of the left ventricular assist device (from 46 to 35, 63 to 41 and 59 to 36 mm, respectively, all p < 0.001). Left ventricular wall thickness increased from 10 to 14 mm (p < 0.001) for the interventricular septum and from 10 to 13 mm for the posterior wall (p<0.001). No echocardiographic measurements showed significant subsequent changes at the chronic stage. Myocardial histologic findings demonstrated a reduction in myocyte damage (from 1.9 to 0.5, p<0.001, for wavy fiber and from 1.3 to 0.2, p<0.01, for contraction band necrosis) and an increase in fibrosis (from 1.3 to 1.9, p<0.05), but without significant change in myocyte diameter (from 15.6 to 16.8 micrometer, p=0.065). CONCLUSIONS: Left ventricular unloading with the implantable assist device induces an immediate increase in wall thickness, consistent with the reduction in chamber size, thereby decreasing wall stress. Chronic unloading allows myocardial healing and fibrosis without evidence for ongoing myocyte damage or atrophy. Left ventricular assist device insertion may have a role in "resting" the ventricle for selected patients with heart failure.

Adult↗
PubMed1996

Cine-MRI-aided endomyocardectomy in idiopathic hypereosinophilic syndrome.

The idiopathic hypereosinophilic syndrome is a leukoproliferative disorder marked by a predilection to damage specific organs, including the heart. This report describes a patient with extensive endocardial fibrosis accompanying this syndrome. Right ventricular endomyocardectomy with preservation of the tricuspid valve was performed. The procedure was aided by cine-magnetic resonance imaging for preoperative assessment and follow-up of surgical results.

Adult↗
PubMed2001

Simvastatin induces regression of cardiac hypertrophy and fibrosis and improves cardiac function in a transgenic rabbit model of human hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy is a genetic disease characterized by cardiac hypertrophy, myocyte disarray, interstitial fibrosis, and left ventricular (LV) dysfunction. We have proposed that hypertrophy and fibrosis, the major determinants of mortality and morbidity, are potentially reversible. We tested this hypothesis in beta-myosin heavy chain-Q(403) transgenic rabbits. METHODS AND RESULTS: We randomized 24 beta-myosin heavy chain-Q(403) rabbits to treatment with either a placebo or simvastatin (5 mg. kg(-1). d(-1)) for 12 weeks and included 12 nontransgenic controls. We performed 2D and Doppler echocardiography and tissue Doppler imaging before and after treatment. Demographic data were similar among the groups. Baseline mean LV mass and interventricular septal thickness in nontransgenic, placebo, and simvastatin groups were 3.9+/-0.7, 6.2+/-2.0, and 7.5+/-2.1 g (P<0.001) and 2.2+/-0.2, 3.1+/-0.5, and 3.3+/-0.5 mm (P=0.002), respectively. Simvastatin reduced LV mass by 37%, interventricular septal thickness by 21%, and posterior wall thickness by 13%. Doppler indices of LV filling pressure were improved. Collagen volume fraction was reduced by 44% (P<0.001). Disarray was unchanged. Levels of activated extracellular signal-regulated kinase (ERK) 1/2 were increased in the placebo group and were less than normal in the simvastatin group. Levels of activated and total p38, Jun N-terminal kinase, p70S6 kinase, Ras, Rac, and RhoA and the membrane association of Ras, RhoA, and Rac1 were unchanged. CONCLUSIONS: Simvastatin induced the regression of hypertrophy and fibrosis, improved cardiac function, and reduced ERK1/2 activity in the beta-myosin heavy chain-Q(403) rabbits. These findings highlight the need for clinical trials to determine the effects of simvastatin on cardiac hypertrophy, fibrosis, and dysfunction in humans with hypertrophic cardiomyopathy and heart failure.

Animals↗
PubMed1998

[Regeneration of the heart muscle after myocardial infarct].

Myocardial infarction is characterized by the loss of contractile cardiomyocytes. This results in an increased load on the spared myocardium. The aim of this article is to describe the response of the non-affected myocardium after infarction. Human hearts were investigated by microscopical, biochemical and cytophotometrical methods. The number of nuclei was calculated from the numerical ratio of connective tissue nuclei/myocyte nuclei, the values of the total DNA amount and the percentage proportion of the various ploidy classes in the myocyte nuclei. After myocardial infarction the DNA concentration as well as the DNA content was increased. Different DNA distribution pattern could be found in infarcted hearts. Percentage proportion of higher ploid nuclei and aneuploid nuclei was increased. Number of connective tissue nuclei was increased in infarcted hearts. And, in spite fibrosis of the necrotic area, number of myocyte nuclei did not change significantly. Beside scarring of the necrotic tissue, hypertrophy and hyperplasia of cardiomyocytes occur after myocardial infarction and may compensate the loss of contractile fibres to guarantee myocardial function.

Cardiomegaly↗
PubMed1991

Myocardial fibrosis: role of ventricular systolic pressure, arterial hypertension, and circulating hormones.

The myocardium contains myocyte and non-myocyte cells. A disproportionate growth of the nonmyocyte cell population can alter myocardial structure and lead to pathologic hypertrophy. Myocardial fibrosis, the result of cardiac fibroblast growth or abnormal accumulation of fibrillar collagen within the interstitial space, can adversely influence myocardial stiffness and ultimately ventricular function. We have examined the relative importance of ventricular systolic and arterial pressures and the effector hormones of the renin-angiotensin--aldosterone system in mediating this reactive fibrous tissue response in the hypertensive left and normotensive right ventricles in various experimental models of arterial hypertension. To date, our findings implicate arterial hypertension, together with an elevation in plasma aldosterone, as being contributory to the fibrosis in renovascular hypertension that creates tissue heterogeneity in either ventricle and impaired diastolic function. The endocrine properties of aldosterone in this nonclassical mineralocorticoid target tissue, the myocardium, requires further investigation.

Aldosterone↗
PubMed1995

Systolic ventricular dysfunction and heart failure due to coronary microangiopathy in hypertensive heart disease.

Left ventricular hypertrophy in arterial hypertension is characterized by myocyte hypertrophy, myocardial fibrosis, and structural changes of the intramural coronary arteries. Hypertensives with or without left ventricular hypertrophy have a reduced coronary vasodilator reserve due to alterations of the coronary microcirculation. The impairment in coronary vasodilator reserve is likely to initiate a process of malperfusion and malnutrition concomitant with increased metabolic demands. Further, malperfusion is supported by an increase in diastolic filling pressure, which will enhance the extravascular component of coronary resistance. The sum of interactions of these structural alterations of myocardium, interstitium, and coronary vasculature are likely to initiate and maintain a process of myocardial malperfusion and malnutrition, which can provoke functional depression of the myocardial performance, a loss of contractile proteins, an increase in interstitial fibrosis, and, not least, an overall decrease in contractile function in long-standing cardiac hypertrophy. Finally, the reversal of these processes by adequate antihypertensive treatment may contribute to renormalization of cardiac function and to prevention of late cardiac failure in hypertensive heart disease.

Antihypertensive Agents↗
PubMed1996

Endocardial endothelial dysfunction and heart failure.

Like vascular endothelium, the EE plays a role in transendothelial transport, in coagulant and thrombotic processes, and in interactions with inflammatory cells. In addition, EE is involved in the modulation of cardiac performance of subjacent myocardium. EE dysfunction includes insufficient as well as excessive performance of any of its multiple functions. Dysfunction can progress from a disturbed modulation of myocardial performance and an imbalance in the release of growth factors to changes in EE cytoskeletal organization, with concomitant changes in transendothelial permeability, and in extreme cases, to loss of endothelial integrity and frank denudation. Structural and functional impairment of EE and of endocardial interstitial cells may be primary or secondary to the disease. Mechanical stress, various hormones and cytokines can initiate EE dysfunction. EE dysfunction may influence the development of cardiac failure in endo(myo)cardial fibrosis (Loeffler's endocarditis and carcinoid syndrome) and in dilated cardiomyopathy. Although Bouillaud, in 1836, was referring to endocarditis when stating: (quote: see text) his statement may presently find a much broader field of applicability in cardiology.

Animals↗
PubMed1996

Causal relationship between occlusive lesions of the coronary artery and myocardial fibrosis in arteriosclerotic rabbits--differences between cholesterol-fed and heritable hyperlipidemic rabbits.

To investigate the causal relationship between lesions of either the proximal large or the distal small coronary arteries and myocardial fibrosis, the hearts and the aortas of 99 cholesterol-fed rabbits with either intermittent or continuous hyperlipidemia for 8 months or more, 44 Watanabe-heritable hyperlipidemic (WHHL) rabbits and 20 normal rabbits were studied histologically. The size and location of the myocardial fibrosis correlated closely with the almost completely occlusive distal small coronary artery which mainly consisted of macrophages, necrosis and calcification but did not correlate with the maximum % stenosis of the large proximal subepicardial coronary arteries in the cholesterol-fed-rabbits. Myocardial fibrosis and almost completely occlusive lesions of the distal small coronary arteries were very rare in the WHHL rabbits, and the maximum % stenosis of the proximal coronary artery and aortic lesions in the WHHL rabbits tended to be greater than those in the cholesterol-fed rabbits. Thus, we are still not certain as to whether or not, the organic stenosis of the subepicardial coronary artery is responsible for myocardial fibrosis in WHHL-rabbits. In conclusion, a causal relationship was observed between myocardial fibrosis and the occlusive lesions of the distal small coronary arteries in cholesterol-fed rabbits, while the arteriosclerotic lesions of the small coronary artery in cholesterol-fed rabbits completely differed from those observed in WHHL-rabbit.

Animals↗
PubMed1995

Aldosterone escape during ACE inhibitor therapy in chronic heart failure.

In the setting of chronic heart failure (CHF), therapy with angiotensin converting enzyme (ACE) inhibitors generally reduces serum aldosterone levels acutely. However, long-term ACE inhibition is associated with aldosterone suppression that is weak, variable, and unsustained, i.e. aldosterone 'escape'. Magnesium loss caused by aldosterone and by diuretics can contribute to coronary artery spasm and arrhythmias. Aldosterone can block noradrenaline uptake by the myocardium; extracellular catecholamines may lead to arrhythmias and ischaemia. Aldosterone has been shown to have an acute arrhythmogenic effect as well as a potential detrimental effect on baroreflex function, a marker of prognosis in CHF. Both angiotensin II and aldosterone may stimulate myocardial fibrosis, which is associated with a higher incidence of malignant ventricular arrhythmias. ACE inhibition initiated early in the progression of CHF may prevent development of patchy myocardial fibrosis and its inherent arrhythmias and thus reduce the incidence of sudden death. Spironolactone therapy added to the regimen of an ACE inhibitor and diuretic can induce natriuresis and magnesium retention, increase myocardial noradrenaline uptake, and reduce the incidence of arrhythmias.

Aldosterone↗
PubMed2005

Imaging the renin-angiotensin- aldosterone system in the heart.

The influence of the renin-angiotensin system (RAS) is recognized in cardiac and vascular injury. An extrinsic RAS has been known for decades, and an equally important intrinsic RAS has been discovered recently. The latter leads to pathologic tissue alterations in the absence of systemic stimuli and may be the main source of local tissue effects of RAS. A new radiotracer fluorobenzoyl-lisinopril was synthesized by radiolabeling benzoic acid active ester with 18F and reacting that with the epsilon-amino group of lisinopril. The presence of angiotensin-converting enzyme (ACE) activity and angiotensin II receptors was examined in relation to myocardial fibrosis. This tissue-specific radioligand represents the first study of ACE in the human heart. This article presents preliminary data on imaging the RAS in the human cardiac tissue and discusses the potential for clinical application of these imaging techniques to human patients.

Animals↗