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PubMed1988

Quantitation of myocardial fibrosis and its relation to function in essential hypertension and hypertrophic cardiomyopathy.

Myocardial interstitial fibrosis is an important microscopic feature of hypertrophic cardiomyopathy. To determine whether interstitial fibrosis of the myocardium in hypertrophic cardiomyopathy and essential hypertension differ in quality or quantity, and to determine whether fibrosis affects cardiac function directly, we measured the percentage of fibrosis in patients of both categories and compared the severity of fibrosis with several cardiac functions. Left and right ventricular endomyocardial biopsies were performed in 25 patients with essential hypertension and in 19 patients with hypertrophic cardiomyopathy. Interstitial fibrosis was classified into four different microscopic types, and the percentage of total and of each type was calculated using the point-counting method. Although the percentage of total fibrosis was similar between the two groups, the type of fibrosis was different. There was no correlation between the percentage of total fibrosis and the mean size of myocytes in either group. Although there was a significant correlation between the percentage of total fibrosis and the thickness of the interventricular septum in hypertrophic cardiomyopathy, such correlation was lacking in hypertension. There was no correlation between the percentage of total fibrosis and the ejection fraction, cardiac index, or left ventricular end-diastolic pressure in either group. We concluded that the amount of myocardial interstitial fibrosis in hypertrophic cardiomyopathy is no greater than that in essential hypertension, but the type of fibrosis is different. Furthermore, in subjects in whom the ejection fraction is normal or only slightly decreased, fibrosis does not influence global cardiac functions.

Adult↗

PubMed1978

Cardiac amyloidosis in hereditary neuropathic amyloidosis diagnosed by endomyocardial biopsy.

A 57 year old male first developed progressive neuropathy of the lower extremities and then similar involvement in the upper extremities. Two years later he developed dyspnea and then complete atrioventricular block requiring the use of a permanent cardiac pacemaker. An older brother had an almost identical clinical course, including the installation of a permanent pacemaker. Both died of left ventricular failure. An endomyocardial biopsy revealed extensive amyloidosis and fibrosis of the myocardium. This is the first report of a myocardial biopsy showing amyloid on electron microscopy.

Amyloidosis↗

PubMed1992

Late onset renal hypertension in old rats alters left ventricular structure and function.

This study was designed to test the hypothesis that the left ventricle of the senescent rat has a limited compensatory response to late onset hypertension. Data were obtained from middle-aged (15 mo) and senescent (24 mo) Sprague-Dawley rats either 1 or 3 mo after the initiation of one-kidney figure-8 renal wrap (Grollman) hypertension. Peak left ventricular (LV) function assessed during acute volume expansion was not markedly affected 1 mo after induction of hypertension with the exception of a decrement in the acceleration of aortic flow (dF/dt) in the senescent hypertensive group. Three months after the surgery was performed, peak LV function (stroke index, stroke volume/g LV, and dF/dt) was depressed in the senescent hypertensive rats, compared with the controls. In contrast, these indexes in the 15-mo-old rats were similar in the experimental and control groups after either 1 or 3 mo of hypertension. Developed pressure, however, was not compromised by hypertension at either age. Cardiocyte hypertrophy due to pressure overload occurred in both age groups but to a greater extent in the senescent group. This cellular response did not cause an absolute increase in LV mass and was associated with endomyocardial foci of cellular degeneration and fibrosis suggestive of cell loss. Mitochondria-to-myofibril volume ratios were not significantly altered in the experimental groups at either age, thus the cellular hypertrophy in these rats was characterized by uniform organelle growth. These data support two important conclusions regarding late onset hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1994

Strongyloides stercoralis infestation masquerading as steroid resistant asthma.

A 42 year old man presented with steroid resistant asthma of 6 months duration. Serial chest radiographs showed migrating interstitial shadowing. Electrocardiographs showed decreasing R-wave progression in the precordial leads, and endomyocardial biopsy showed eosinophil infiltration with fibrosis. Bronchoscopy revealed inflammatory changes and lavage showed filariform larvae of Strongyloides stercoralis in the washings. This confirms the diagnosis of parasitic infection with eosinophilic cardiomyopathy.

Adult↗

PubMed1991

Primary restrictive cardiomyopathy: clinical and pathologic characteristics.

Twenty-four patients with restrictive cardiomyopathy were identified at St. Thomas' Hospital during a 17-year period. All had endomyocardial biopsy, but in two patients the biopsy specimens were small and nondiagnostic. Seven patients had amyloidosis and five had other specific heart muscle diseases. The remaining 10 patients with primary restrictive cardiomyopathy had myocyte hypertrophy or interstitial fibrosis, or both. Patients with primary restrictive cardiomyopathy presented earlier but survived longer after presentation than did those with amyloidosis. In each group, survival after cardiac catheterization was related to cardiac index but not to filling pressures. Primary restrictive cardiomyopathy was associated with complete heart block in four patients, two of whom had skeletal myopathy. One had a family history of dominantly inherited skeletal myopathy. Primary restrictive cardiomyopathy was present in a mother and daughter. Two other patients had a family history of heart failure, sudden death or complete heart block, alone or in combination, at a young age. Restrictive hemodynamics and complete heart block were present in patients even in the absence of significant fibrosis. The data suggest that primary restrictive cardiomyopathy may be a distinct myopathy with dominant inheritance and incomplete penetrance that is expressed morphologically as myocyte hypertrophy and interstitial fibrosis. Skeletal myopathy may be associated with the cardiomyopathy.

Adolescent↗

PubMed1996

Clinical value of echocardiographic tissue characterization in the diagnosis of myocarditis.

Inflammatory changes in the myocardium have been visually observed as alterations on echocardiograms. The goal of this study was to determine how these myocardial changes affect the texture of echocardiographic images, and how these could be described through quantitative texture analysis. The results of 142 endomyocardial biopsies were compared with those of texture analysis in echocardiograms of 106 patients suspected of having myocarditis. There were 52 cases of biopsy-proven acute myocarditis, 12 of persistent myocarditis, nine of healed myocarditis without fibrosis, 17 of healed myocarditis with fibrosis, and 35 cases of cardiomyopathy. Eight myocardial biopsies exhibited no pathological changes and nine patients had other cardiac problems. The echocardiograms of a control group of 24 healthy subjects were also evaluated by texture analysis. Three texture parameters were able to differentiate between normal and abnormal myocardium. The mean grey value, i.e. average brightness, was appreciably higher in cases of myocarditis than in control subjects, whereas one co-occurrence and one run length feature had markedly decreased. We conclude that myocarditis and fibrosis induce changes in echocardiographic image texture, i.e. increases in brightness, heterogeneity, and contrast. Performing digital image texture analysis of echocardiograms makes it possible to distinguish between myocarditis and normal myocardium.

Adult↗

PubMed2004

Eosinophilic myocarditis in a patient with idiopathic hypereosinophilic syndrome: insights into mechanisms of myocardial cell death.

Idiopathic hypereosinophilic syndrome (HES) consists of a prolonged state of eosinophilia of unknown origin with organ involvement. We describe the case of a patient who developed fatal eosinophilic myocarditis. A 23-year-old woman with an 8-month history of eosinophilia presented with symptoms of myocarditis. Histological evaluation of an endomyocardial biopsy specimen revealed marked endomyocardial eosinophilic infiltration with eosinophil-rich granulomas and areas of myocyte necrosis. A terminal deoxynucleotidil transferase assay revealed apoptosis in several cardiomyocytes and vascular cells, mainly in the myocardial areas with higher eosinophil density. Evaluation of an endomyocardial biopsy specimen obtained after steroid therapy demonstrated that the eosinophils had disappeared, but there was marked myocardiosclerosis and scattered apoptotic cells. The patient slowly developed heart failure and died of sudden arrhythmic death. HES can cause severe myocarditis with extensive myocyte loss, probably due to both necrosis and apoptosis. Myocardial fibrosis may occur despite treatment, and patients may be at risk for fatal arrhythmias.

Adrenal Cortex Hormones↗

PubMed1990

Relation between myocardial histological changes and ventricular tachycardia in cardiomyopathy: a study by 24-hour ECG-monitoring and endomyocardial biopsy.

The relation between myocardial histological changes and ventricular tachycardia (VT) in cardiomyopathy was investigated. Right ventricular endomyocardial biopsy and 24-hour ECG-monitoring were performed in 19 patients with dilated cardiomyopathy (DCM) and 22 with hypertropic cardiomyopathy (HCM). Cardiomyopathy was histologically divided into the following four groups: group A, hypertrophy without disarray of myocytes (3 DCM and 7 HCM); group B, hypertrophy with disarray of myocytes (14 HCM); group C, fibrosis (9 DCM and 1 HCM); and group D, diffuse myocytic degeneration (7 DCM). VT was observed in 20% (2 of 10 patients) of group A, 14% (2 of 14) of group B, 80% (8 of 10) of group C, and 71% (5 of 7) of group D. The degenerating myocytes and/or the irregular distribution of fibrosis may play an important role in the etiology of VT in cardiomyopathy.

Adult↗

PubMed2004

Increased collagen type I synthesis in patients with heart failure of hypertensive origin: relation to myocardial fibrosis.

BACKGROUND: We investigated whether increased collagen type I synthesis and deposition contribute to enhancement of myocardial fibrosis and deterioration of cardiac function in patients with hypertensive heart disease (HHD). METHODS AND RESULTS: We studied 65 hypertensives with left ventricular hypertrophy subdivided into 2 groups: 34 patients without heart failure (HF) and 31 patients with HF. Transvenous endomyocardial biopsies of the interventricular septum were performed to quantify the amount of fibrotic tissue and the extent of collagen type I deposition. The carboxy-terminal propeptide of procollagen type I (PIP), an index of collagen type I synthesis, was measured by radioimmunoassay in serum samples from the coronary sinus and the antecubital vein. Compared with normotensives, the amount of collagen tissue, the extent of collagen type I deposition, and coronary and peripheral PIP were increased (P<0.01) in the 2 groups of hypertensives. These parameters were also increased (P<0.01) in HF hypertensives compared with non-HF hypertensives. Coronary PIP was higher (P<0.01) than peripheral PIP in hypertensives but not in normotensives. The amount of collagen tissue was inversely correlated with the ejection fraction and directly correlated with both coronary and peripheral PIP in all hypertensives. CONCLUSIONS: These findings suggest that an excess of cardiac collagen type I synthesis and deposition may be involved in the enhancement of myocardial fibrosis that accompanies the development of HF in HHD. In addition, our data show that the heart secretes PIP via the coronary sinus into the peripheral circulation in patients with HHD. Thus, PIP determined in peripheral blood can be a useful marker of myocardial fibrosis in these patients.

Biomarkers↗

PubMed1996

Influence of acute or chronic rejection on myocardial collagen density in serial endomyocardial biopsy specimens from cardiac allografts.

BACKGROUND: The knowledge of long-term changes in the transplanted heart is still incomplete. Among these changes that could potentially have an adverse effect on long-term cardiac function, myocardial fibrosis is of great concern. The aim of this study was to investigate the possible influence of acute or chronic rejection on the development of myocardial fibrosis in cardiac allografts. METHODS: We used light microscopic computer-assisted morphometry of collagen density in 200 right ventricular endomyocardial biopsy specimens taken routinely in 21 heart transplant recipients during a mean follow-up period of 36 months (range, 12 to 84). The 21 patients were divided into two groups according to the presence of chronic rejection assessed by coronary angiography. The first group consisted of 11 patients with no chronic rejection; the second group consisted of 10 patients with chronic rejection. Both groups were divided into four subgroups according to the highest grade of acute rejection reached during the follow-up period (subgroup 1, no acute rejection or grade 1A; subgroup 2, grade 1B; subgroup 3, grades 3A or 3B; subgroup 4, grade 4). Patients of both groups were selected on the basis of similarity patterns in clinical characteristics and mean follow-up time. RESULTS: Patients with no chronic rejection had relatively little variation in serial determinations of myocardial collagen density. During the prechronic and chronic phases in patients with chronic rejection, we found no overall increase in myocardial collagen density. In both the chronic rejection and no chronic rejection groups there was no consistent relationship between myocardial collagen density and severity of acute rejection. In both groups there were occasional strikingly elevated myocardial collagen density values that were well above the other serial determinations. These elevated values of collagen density were mainly a result of scars, the sequellae of prior myocyte damage, because neither interstitial nor perivascular fibrosis could be detected. CONCLUSION: During this long-term follow-up study of endomyocardial biopsy samples, we found no significant association between either acute or chronic rejection and the later increase in myocardial collagen density.

Acute Disease↗

PubMed2001

Usefulness of serum carboxy-terminal propeptide of procollagen type I in assessment of the cardioreparative ability of antihypertensive treatment in hypertensive patients.

BACKGROUND: We investigated whether serum concentration of carboxy-terminal propeptide of procollagen type I (PIP), a marker of collagen type I synthesis, can be used to assess the ability of antihypertensive treatment to regress myocardial fibrosis in hypertensive patients. METHODS AND RESULTS: The study was performed in 37 patients with essential hypertension and hypertensive heart disease. After randomization, 21 patients were assigned to losartan and 16 patients to amlodipine treatment. At baseline and after 12 months, right septal endomyocardial biopsies were performed to quantify collagen volume fraction (CVF) on picrosirius red-stained sections with an automated image-analysis system. Serum PIP was measured by specific radioimmunoassay. Nineteen patients in the losartan group and 11 in the amlodipine group finished the study. Time-course changes in blood pressure during treatment were similar in the 2 groups of patients. In losartan-treated patients, CVF decreased from 5.65+/-2.03% to 3.96+/-1.46% (P<0.01) and PIP from 127+/-30 to 99+/-26 microgram/L (P<0.01). Neither CVF or PIP changed significantly in amlodipine-treated patients. CVF was directly correlated with PIP (r=0.44, P<0.001) in all hypertensives before and after treatment. CONCLUSIONS: These findings suggest that the ability of antihypertensive treatment to regress fibrosis in hypertensives with biopsy-proven myocardial fibrosis is independent of its antihypertensive efficacy. Our data also suggest that blockade of the angiotensin II type 1 receptor is associated with inhibition of collagen type I synthesis and regression of myocardial fibrosis in hypertensives. Thus, determination of serum PIP may be useful to assess the cardioreparative properties of antihypertensive treatment in hypertensives.

Adult↗

PubMed1990

[Value of endomyocardial biopsy in the assessment of the degree of the changes in myocarditis].

Right ventricular diagnostic biopsy was performed in 25 patients (12 females and 13 males) aged 19-48 (mean 32) with suspicion of acute or subacute myocarditis for definitive diagnosis verification and to determine indications for therapy with corticosteroids or azathioprine. 3-4 specimens taken from different sites of ventricle were estimated under the light microscope according to Dallas classification distinguishing active myocarditis with or without fibrosis from borderline myocarditis with inflammatory infiltration not causing myocytes damage. Routine clinical and laboratory tests, echocardiographic examination, ECG Holter monitoring and nuclear examination to evaluate left ventricular ejection fraction were performed in all patients. 6 patients underwent coronarography to exclude atherosclerotic changes in coronary arteries. Bioptic examination result confirmed myocarditis suspicion in all patients. Active inflammation was stated in 18 patients including 7 with coexisting fibrosis. Borderline myocarditis was stated in 7 cases. Comparison of clinical examination results with those of pathomorphologic study made possible to state, that tachycardia, cardiac murmur, arrhythmias and left ventricular function impairment were frequent observed in the group of active myocarditis. Ejection fraction less than 30% was observed only in patients with active myocarditis and mainly in those with coexisting fibrosis. Based on performed study we consider that myocardial biopsy allows not only to diagnose myocarditis but also is helpful for lesion extent assessment in myocardium with all clinical implications.

Acute Disease↗

PubMed2004

Effects of loop diuretics on myocardial fibrosis and collagen type I turnover in chronic heart failure.

OBJECTIVES: This individually randomized, open-label, parallel-group pilot study was designed to test the hypothesis that the ability of loop diuretics to interfere with cardiac fibrosis in chronic heart failure (CHF) may be different between compounds. BACKGROUND: The apparent mortality and cardiac benefits seen in studies comparing torasemide with furosemide in CHF suggest that torasemide may have beneficial effects beyond diuresis (e.g., on the process of cardiac fibrosis). METHODS: Patients with New York Heart Association functional class II to IV CHF received diuretic therapy with either 10 to 20 mg/day oral torasemide (n = 19) or 20 to 40 mg/day oral furosemide (n = 17), in addition to their existing standard CHF therapy for eight months. At baseline and after eight months, right septal endomyocardial biopsies were obtained to quantify collagen volume fraction (CVF) with an automated image analysis system. Serum carboxy-terminal peptide of procollagen type I (PIP) and serum carboxy-terminal telopeptide of collagen type I (CITP), indexes of collagen type I synthesis and degradation, respectively, were measured by specific radioimmunoassays. RESULTS: In torasemide-treated patients, CVF decreased from 7.96 +/- 0.54% to 4.48 +/- 0.26% (p < 0.01), and PIP decreased from 143 +/- 7 to 111 +/- 3 microg/l (p < 0.01). Neither CVF nor PIP changed significantly in furosemide-treated patients. In all patients, CVF was directly correlated with PIP (r = 0.88, p < 0.001) before and after treatment. No changes in CITP were observed with treatment in either group. CONCLUSIONS: These findings suggest that loop diuretics possess different abilities to reverse myocardial fibrosis and reduce collagen type I synthesis in patients with CHF.

Collagen Type I↗

PubMedDate not supplied

[Histological and ultrastructural characteristics of the recipients' myocardium 7-14 years after orthotopic transplantation of the heart (according to endomyocardial biopsy)].

Light optic and electron microscopic studies were made of endomyocardial biopsies from the right ventricle of 8 patients who had undergone orthotopic transplantation of the heart 7-14 years ago. For this period rejection reaction was not typical, more marked were changes related to transplantation coronary disease and microcirculatory disorders: hibernation of cardiomyocytes (CMC), their apoptosis, interstitial fibrosis, dystrophic alterations of CMC. The results show the CMC pool may be resupplied with pluripotent (stem) cells as well as hibernating CMC which take part in the myocardial activity after myocardial circulation recovery by means of angioplasty and plasmapheresis.

Apoptosis↗

PubMed1997

Role of endomyocardial biopsy in the diagnosis of chronic rejection in human heart transplantation.

To assess the pathologic findings observed in the setting of post-transplant graft atherosclerosis, we have studied 18 endomyocardial biopsies (EMB) from 18 heart-transplanted patients collected at the same time that a coronary angiography (CA) showed changes consistent with graft atherosclerosis. Twenty-two EMB from patients with heart transplant with normal CA were used as controls. In spite of the small size of the sample, the number of acute rejection (AR) episodes correlated with the appearance of graft atherosclerosis (p < 0.001). Heart biopsies in graft atherosclerosis showed myointimal proliferation, thickening and folding of the wall of precapillary arteries, myocyte hypertrophy, and interstitial and perivascular fibrosis. Type III and type IV collagen, laminin, and fibronectin were increased in areas of interstitial and perivascular fibrosis, as well as in the vessel's wall. Fibronectin accumulation was more evident in the subendothelium and inner media of affected vessels. These changes were never found all together in control biopsies. Even though the inespecificity of some of those findings, we conclude that chronic graft atherosclerosis in a heart transplant may be suspected by endomyocardial biopsy when most of these alterations are seen together, especially if small precapillary arteries are present in the specimen.

Acute Disease↗

PubMed2002

Aldosterone synthase (CYP11B2) expression and myocardial fibrosis in the failing human heart.

The pathway of tissue aldosterone production may exist in the heart, and may be an important contributory factor to myocardial fibrosis and cardiac remodelling in the failing heart. CYP11B2 (aldosterone synthase) catalyses the final step of aldosterone production. The aim of the present study was to determine whether CYP11B2 and CYP11B1 (11beta-hydroxylase) are expressed in myocardial tissues, and whether these enzymes contribute to collagen accumulation and myocardial dysfunction in the failing human heart. Endomyocardial tissues were obtained from 23 patients with chronic heart failure (CHF) and 10 controls. CYP11B2 and CYP11B1 mRNA levels were measured by real-time quantitative reverse transcriptase-PCR. The myocardial collagen volume fraction (CVF) was determined by digital planimetry. CYP11B2 mRNA expression was greater in the CHF group than in the controls (P<0.05), while CYP11B1 mRNA was barely expressed in either group. There was a positive correlation between CYP11B2 mRNA levels and CVF (r=0.64, P=0.001). CYP11B2 mRNA was particularly highly expressed in subgroups of CHF patients with a large left ventricular end-systolic diameter (>55 mm) or a low left ventricular ejection fraction (<30%). CYP11B2 mRNA expression and CVF were lower in a CHF subgroup treated with a combination of spironolactone and angiotensin-converting enzyme inhibitors (ACEIs) than in a subgroup not treated with these drugs. In conclusion, this study has shown that increased myocardial expression of CYP11B2 mRNA is associated with increased myocardial fibrosis and with the severity of left ventricular dysfunction in human CHF. In addition, CYP11B2 expression and cardiac fibrosis are found to be decreased in CHF patients on drug therapy comprising spironolactone combined with ACEIs.

Adult↗

PubMed1979

[Endomyocardial biopsy results and left ventricular function in primary myocardiopathies (author's transl)].

Endomyocardial biopsies (EMB) of the left ventricle (LV) were performed during cardiac catheterization in 27 patients with apparently primary myocardiopathies (PMC). The results of optical and electron microscopy were compared with ventricular performance indices calculated from hemodynamic and cinematographic data from the left ventricle. The telediastolic pressure of the LV increases with the spread of fibrosis (r = 0.68) suggesting that it disturbs the filling of this cavity. Systolic effort is reduced as this fibrosis increases (r = 0.56), and it contributes to the changes in the pumping function of the LV, but the contractile power of the LV is altered in a less evident and less constant manner. The association of cell and fibro-elastic tissue degeneration is always accompanied by a drop in ventricular performance (p less than 0.0001). Apart from its diagnostic role, which is limited but may be of great value, the EMB can help to clarify the physiopathology of PMC and to formulate a prognosis based on more solid grounds.

Biopsy↗

PubMed1983

Echocardiographic features of tropical endomyocardial disease in South India.

Fifteen patients with tropical endomyocardial disease which had been proved angiographically were studied using M-mode and cross-sectional echocardiography to determine the extent to which specific features of this disease could be recognised by these non-invasive methods. Tethering of the posterior mitral valve leaflet to the ventricular wall in combination with areas of echo-dense material in the posterior left ventricular wall and associated papillary muscle appeared to be a constant diagnostic feature of this disease. Colour coding of regional echo amplitude showed high intensity echoes in a distribution corresponding closely to that of the fibrosis known to occur in this condition. Though M-mode echocardiography did not contribute diagnostic information, it was useful in defining the functional consequences of myocardial or mitral valve disease. Digitisation of records allowed a restrictive pattern of left ventricular filling to be observed. It was concluded that cross-sectional echocardiography, particularly when supplemented by colour coded amplitude processing, can make a confident non-invasive diagnosis of tropical endomyocardial disease and so could be useful in assessing its progression or response to treatment.

Adolescent↗