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PubMed1998

Characteristics of wave fronts during ventricular fibrillation in human hearts with dilated cardiomyopathy: role of increased fibrosis in the generation of reentry.

OBJECTIVES: We sought to evaluate the characteristics of wave fronts during ventricular fibrillation (VF) in human hearts with dilated cardiomyopathy (DCM) and to determine the role of increased fibrosis in the generation of reentry during VF. BACKGROUND: The role of increased fibrosis in reentry formation during human VF is unclear. METHODS: Five hearts from transplant recipients with DCM were supported by Langendorff perfusion and were mapped during VF. A plaque electrode array with 477 bipolar electrodes (1.6-mm resolution) was used for epicardial mapping. In heart no. 5, we also used 440 transmural bipolar recordings. Each mapped area was analyzed histologically. RESULTS: Fifteen runs of VF (8 s/run) recorded from the epicardium were analyzed, and 55 episodes of reentry were observed. The life span of reentry was short (one to four cycles), and the mean cycle length was 172 +/- 24 ms. In heart no. 5, transmural scroll waves were demonstrated. The most common mode of initiation of reentry was epicardial breakthrough, followed by a line of conduction block parallel to the epicardial fiber orientation (34 [62%] of 55 episodes). In the areas with lines of block, histologic examination showed significant fibrosis separating the epicardial muscle fibers and bundles along the longitudinal axis of fiber orientation. The mean percent fibrous tissue in these areas (n = 20) was significantly higher than that in the areas without block (n = 28) (24 +/- 7.5% vs. 10 +/- 3.8%, p < 0.0001). CONCLUSIONS: In human hearts with DCM, epicardial reentrant wave fronts and transmural scroll waves were present during VF. Increased fibrosis provides a site for conduction block, leading to the continuous generation of reentry.

Adolescent↗
PubMed1990

The role of late potentials in the assessment of myocardial degeneration in idiopathic dilated cardiomyopathy.

In order to determine whether or not late potentials indicate either a degree of myocardial fibrosis or necrosis, the relationship between late potentials and thallium-201 myocardial perfusion images was studied in 13 patients with idiopathic dilated cardiomyopathy. Late potentials were defined as low-amplitude waveforms having duration of over 20 msec after the end of the QRS complex using a high-resolution ECG (Marquette electronics, MAC 1). In the T1-201 myocardial perfusion image, the segmental perfusion state was assessed by use of a parameter called the uptake index (= normalized sector counts/maximal normalized sector counts) of each of 6 different segments. Segments which showed an uptake index of -2SD less than the normal value were judged to be abnormal. Late potentials were detected in 8 (61.5%) of the 13 patients. All of the patients showing late potentials also had ventricular tachycardia. Among the patients showing no late potential, ventricular tachycardia was observed in only one patient. Seven of the 8 patients showing late potentials and 3 of 5 patients not showing late potentials, however, had both a higher degree and a greater extent of abnormal perfusion images than the patients not showing late potentials. Therefore, late potentials may reflect a degree of myocardial fibrosis or necrosis in patients with dilated cardiomyopathy, those showing abnormal thallium images are apt to show late potentials, and these patients seem to be also at a high risk of suffering from ventricular tachycardia.

Adult↗
PubMed1992

Myocardial fibrosis and the concepts of cardioprotection and cardioreparation.

PURPOSE: To examine the inter-relationship between effector hormones of the renin-angiotensin-aldosterone system and fibrosis, a determinant of abnormal myocardial stiffness, and to determine whether pharmacological interference with these hormones can prevent or regress this pathological structural remodeling. EFFECTS OF ANGIOTENSIN II AND ALDOSTERONE: Two morphological expressions of myocardial fibrosis are evident, a perivascular and interstitial fibrosis, not related to cardiac myocyte necrosis, and microscopic scarring that replaces lost myocytes. The former, a reactive fibrosis, is related to elevations in circulating mineralocorticoids (aldosterone or deoxycorticosterone) with increased dietary sodium, and not to arterial hypertension or ventricular loading. Scarring follows the cytotoxicity associated with elevated plasma angiotensin II levels and the increased K+ excretion that accompanies chronic mineralocorticoid excess. EFFECTS OF PHARMACOLOGICAL INTERFERENCE: Given the association of these hormones with fibrosis, the concept of cardioprotection was evaluated in various prevention trials. Reactive fibrosis was prevented in unilateral renal ischaemia by angiotensin converting enzyme (ACE) inhibition with captopril and in either primary or secondary hyperaldosteronism by antagonism of the aldosterone receptor with spironolactone. Scarring (and cell loss) was prevented in renal ischemia by captopril and by K(+)-sparing diuretics (spironolactone, amiloride) in primary hyperaldosteronism. In treatment trials, where reactive fibrosis was established, lisinopril promoted regression of the fibrosis and therefore was cardioprotective. CONCLUSIONS: Myocardial fibrosis is related to chronic mineralocorticoid excess (with increased dietary sodium), angiotensin II and increased K+ excretion. Cardioprotective and cardioreparative strategies that respectively prevent or regress the development of fibrous tissue have been demonstrated in experimental models and now merit clinical evaluation.

Angiotensin II↗
PubMed1999

Basic fibroblast growth factor increases regional myocardial blood flow and salvages myocardium in the infarct border zone in a rabbit model of acute myocardial infarction.

Basic fibroblast growth factor (bFGF) has been shown by some to promote angiogenesis and myocardial salvage in experimentally induced acute myocardial infarction. Although these findings have spurred much clinical interest, they are not universally observed, and the true efficacy of bFGF remains unclear. The authors used a rabbit model of acute myocardial infarction to further elucidate the effects of bFGF on acutely infarcted myocardium containing few collaterals. Myocardial infarction was evoked by ligation of the left coronary artery. Prior to ligation, either 100 microg of bFGF (bFGF group; n = 15) or physiological saline (control group; n = 22) was injected into the myocardium supplied by the ligated artery. With use of nonradioactive colored microspheres, regional blood flow (Qm) was measured before, immediately after, and 4 weeks after coronary artery ligation. Infarct and border zone sizes were measured in cross-sectional slices of the resected hearts, and the amount of viable myocardium (myocardium score) and the extent of fibrosis were histologically determined in each area. Four weeks after ligation, Qm values in the infarcted area did not significantly differ between the bFGF and control groups (0.54 +/- 0.36 vs 0.48 +/- 0.30 mL/min/g); in the border zone, Qm tended to be higher in the bFGF group (3.39 +/- 2.68 vs 1.47 +/- 0.80 mL/min/g), but the difference was not significant; finally in the noninfarcted area, Qm was significantly (p < 0.05) higher in the bFGF group (6.06 +/- 3.85 vs 2.09 +/- 0.82 mL/min/g). There was no significant difference in the amount of viable myocardium or the extent of fibrosis in the infarcted areas of the two groups. In the border zone, however, the amount of viable myocardium was significantly (p < 0.005) larger in the bFGF group (61.8 +/- 8.5% vs 35.8 +/- 20.3% of the visual field). Likewise, as graded on a scale from 0 to 5, the extent of fibrosis was significantly (p < 0.005) less in the bFGF group (2.1 +/- 0.5 vs 3.3 +/- 0.8). In conclusion, injection of bFGF into acutely infarcted myocardium increased blood flow to the noninfarcted area and salvaged the myocardium in the border zone.

Animals↗
PubMed2000

[Biochemical diagnosis of hypertensive myocardial fibrosis].

A substantial increase in fibrillar collagen has been observed in the left cardiac ventricle of animals and humans with arterial hypertension. Hypertensive myocardial fibrosis is the result of both increased collagen types I and III due to the fact that its synthesis by fibroblasts and myofibroblasts is stimulated and its extracellular collagen degradation unchanged or decreased extracellular collagen degradation. Hemodynamic and non-hemodynamic factors may be involved in the disequilibrium between collagen synthesis and degradation that occurs in hypertension. As shown experimentally and clinically, an exaggerated rise in fibrillar collagen content promotes abnormalities of cardiac function, contributes to the decrease in coronary reserve and facilitates alterations in the electrical activity of the left ventricle. Although microscopic examination of cardiac biopsies is the most reliable method for documenting and measuring myocardial fibrosis, the development of non-invasive methods to indicate the presence of myocardial fibrosis in hypertensive patients would be useful. We have therefore applied a biochemical method based on the measurement of serum peptides derived from the tissue formation when synthesized and degradation of fibrillar collagens to monitor the turnover of these molecules in rats with spontaneous hypertension and patients with essential hypertension.

Endomyocardial Fibrosis↗
PubMed1988

[Occupationally-induced progressive scleroderma and the heart].

A 60-year-old man with progressive systemic sclerosis (PSS) had worked as underground miner in ore mining for 26 years with intensive exposure to crystalline silica. The PSS was acknowledged as an occupational disease. Parallel to the progress of the PSS there developed disturbances of the conduction system and cardiac rhythm with left heart failure. Despite treatment sudden death set in. A myocardial fibrosis was found histopathologically. This is a consequence of the PSS and therefore the occupational disease is the cause of death. Cardiac involvement means a poor prognosis and necessitates both evaluation of the damage in percent caused by the occupational disease and interdisciplinary teamwork in the dispensary care of patients.

Cardiomyopathies↗
PubMed1996

Ultrasonic myocardial tissue characterization in patients with dilated cardiomyopathy: value in noninvasive assessment of myocardial fibrosis.

Dilated cardiomyopathy (DCM) is usually diagnosed from the left ventricular functional viewpoint by the detection of dilated ventricular cavity and depressed myocardial contractility. Although histologic analysis of the myocardium no doubt provides clinically important information, it is possible only with microscopic examination of biopsy specimen of the myocardium. The objective of this particular study is to clarify the comparative values of the measures of ultrasonic tissue characterization, that is, calibrated myocardial integrated backscatter (IB) and the magnitude of cyclic variation in IB, with conventional echocardiographic parameters in assessing histologic condition of the myocardium. The magnitude of cyclic variation in IB and myocardial IB at end-diastole calibrate with the power of Doppler signals from the blood were measured in addition to conventional echocardiographic parameters in 14 patients with DCM. Calibrated myocardial IB was higher in patients with more fibrosis in the biopsy specimen of the heart tissue, whereas the magnitude of variation in IB or conventional echocardiographic parameters did not significantly correlate with a histologic estimate of myocardial fibrosis. Calibrated myocardial IB provides information about the myocardial fibrosis that cannot be assessable with conventional echocardiographic parameters. Calibrated myocardial IB and the magnitude of cyclic variation of IB are likely to reflect somewhat different acoustic properties of the myocardium.

Adult↗
PubMedDate not supplied

Factors affecting ventricular function and survival after partial left ventriculectomy.

BACKGROUND: Partial left ventriculectomy (PLV) helps some patients but is deleterious in others. Selection of patients who will benefit from PLV, and exclusion of those who will not is necessary for safe and effective application of the procedure. METHODS: Sixty-nine consecutive patients who underwent PLV were monitored with pressure-volume relationship analyses, Doppler echocardiography, and histopathologic studies of excised myocardium. These parameters were correlated with postoperative stroke volume (SV, ml), cardiac output (CO, L/min), ventricular function (improved, no change, or deteriorated), and postoperative course (duration of survival and/or hospital discharge). RESULTS: Positive responders (n = 36) with increased SV at reduced end diastolic pressure had significantly larger preoperative end-systolic dimension, smaller SV, and less stroke work with milder fibrosis than non- or negative responders (n = 33). In multivariate analyses, poor preoperative hemodynamics were associated with increased SV and CO, but these improvements did not lead to improved survival. Postoperative survival was negatively affected by larger preoperative left ventricular end-diastolic volume and larger excised-muscle-weight. Milder fibrosis and thicker excised wall were consistently related to improved ventricular function and survival. CONCLUSION: Although effects of PLV are related to preoperative status, factors affecting postoperative ventricular function and survival were often discordant. While poor preoperative ventricular function was associated with functional improvement without survival benefit, milder fibrosis, thicker excised wall and less myocardial resection were positive contributors to improved ventricular function, discharge, and survival. Preoperative evaluation with more cases and variables are needed to identify patients more likely to benefit from PLV.

Adult↗
PubMed1991

Myocardial fibrosis in aging germ-free and conventional Lobund-Wistar rats: the protective effect of diet restriction.

The influences of diet restriction and germ-free environment on aging were studied in 127 male Lobund-Wistar rats ranging in age from 7 to 48 months. There was an age-related increase in collagen deposition of the heart, particularly involving the left ventricle. The degree of fibrosis was significantly less extensive in middle and old age rats (18 mo, 30 mo, 32+ mo) maintained on a restricted diet. No clear-cut influence of germ-free environment was apparent. No amyloid was detected in 175 tissue sections examined from hearts, lungs, and livers.

Aging↗
PubMed1987

[Relationships between segmental left ventricular wall motion abnormalities and pathological findings in patients with dilated cardiomyopathy].

Relationships between segmental left ventricular wall motion abnormalities and myocardial fibrosis at autopsy were examined in 12 patients who died of dilated cardiomyopathy. In each case, wall motion abnormalities were assessed by two-dimensional echocardiograms for 11 segments, and semiquantitatively evaluated as normokinesis (N) to hypokinesis (H), severe hypokinesis (SH) or akinesis (A). From the necropsy specimens, the myocardial fibrosis ratio was histologically quantitated using a point-counting method in each segment corresponding to the echocardiographic segment. Wall motion abnormalities and the fibrosis ratio correlated significantly in a total of 132 segments of the 12 patients, but there were some discordances. The cases were then categorized in uniform and non-uniform groups based on the patterns of myocardial fibrosis. Wall motion abnormalities correlated much better with the fibrosis ratio in a total of 44 segments among four cases with non-uniform fibrosis, whereas no significant correlation was found in a total of 88 segments in eight cases with uniform fibrosis. The latter group had more severe segmental wall motion abnormalities in the interventricular septum than in the left ventricular free wall; and in the apical portion rather than in the basal portion, although no significant difference was observed in the fibrosis ratio among these regions. Patients with non-uniform fibrosis had higher incidences of chest pain and sudden deaths and a significantly larger left ventricular end-diastolic dimension on M-mode echocardiogram as compared to those with uniform fibrosis. Pathologically, in the former group, the heart was heavier, the mean left ventricular fibrosis ratio was significantly higher, and there was a greater incidence of infiltration of the myocardium by mononuclear cells, but there was no difference in the mean left ventricular wall thickness. These results suggest that myocardial fibrosis mainly contributes to the wall motion abnormalities in cases with non-uniform fibrosis which may be caused by chronic myocarditis, but not in cases with uniform fibrosis. In the latter group, other factors such as reduced contractility of the myocardial cells or lack of a compensatory mechanism for wall stress seem to play important roles in causing left ventricular wall motion abnormalities.

Adult↗
PubMed1997

[Spironolactone: renaissance of anti-aldosterone therapy in heart failure?].

Mortality of patients with severe congestive heart failure (CHF) is still high despite combined treatment with angiotensin-converting enzyme (ACE) inhibitors, diuretics, and digitalis. Further therapeutic regimens are needed which include reversal of adverse myocardial remodeling and subsequent ventricular dysfunction. One third of all patients with CHF have diastolic left ventricular (LV) dysfunction with preserved systolic function. In these patients myocardial collagen matrix is the major determinant of myocardial stiffness and therefore diastolic function. Cardiac fibroblasts, expressing mRNA for types I and III collagens which are the major fibrillar proteins of the myocardial collagen network and for matrix metalloproteinase (MMP) 1 which is the key enzyme for interstitial collagen degradation, are controlled by the renin-angiotensin-aldosterone (RAAS) system irrespective of hemodynamics and cardiac myocyte growth. In the rat with primary or secondary hyperaldosteronism, myocardial fibrosis occurs in the pressure overloaded, hypertrophied left and in the normotensive, nonhypertrophic right ventricle. In contrast, no fibrosis is found in either ventricle of rats with infrarenal aortic banding, when the RAAS is not activated, despite comparable systemic hypertension and LV hypertrophy. In cultured cardiac fibroblasts, either effector hormone of the RAAS, angiotensin (Ang) II and aldosterone (Aldo) stimulate collagen synthesis measured by 3H-proline incorporation under serum-free conditions. Aldo is able to stimulate collagen synthesis normalized per total protein synthesis in a dose-dependent manner and at concentrations (10(-9) M) which are comparable to stimulated states in vivo (e.g., CHF). While Aldo does not affect collagen degradation AngII significantly inhibits, MMP 1 activity that would lead to further accumulation of collagen in the myocardium. Specific AngII type I or Aldo receptor antagonists are able to abolish the AngII or Aldo-mediated increase in collagen synthesis, respectively. In vivo in rats with primary or secondary hyperaldosteronism, the Aldo antagonist spironolactone has been shown to prevent myocardial fibrosis in both ventricles irrespective of the development of LV hypertrophy and hypertension. Thus, in vivo and in vitro evidence could be provided that the mineralocorticoid. Aldo, plays a pivotal role in promoting myocardial fibrosis and can be antagonized by its competitive receptor blocker, spironolactone. This may be of particular clinical relevance in treating patients with CHF where the RAAS is activated leading to myocardial fibrosis with subsequent deterioration of myocardial function. Clinical trials are needed to confirm these experimental data. If the ongoing RALES mortality study will prove that survival and/or morbidity of patients with CHF are improved by combined ACE inhibitor/spironolactone treatment a renaissance of anti-aldosterone therapy in patients with CHF would occur.

Animals↗
PubMed1990

Diastolic function in left ventricular hypertrophy: clinical and experimental relationships.

The evaluation of patients with left ventricular hypertrophy and the clinical syndrome of congestive heart failure requires the ability to distinguish between the etiologies of abnormal systolic contractile function and abnormalities of diastolic relaxation and filling. In patients with left ventricular hypertrophy and congestive heart failure, predominant diastolic dysfunction should be suspected when elevation of left ventricular diastolic pressure is detected in the presence of normal diastolic chamber volume or dimensions and preserved systolic shortening. The mechanisms which account for diastolic dysfunction in the presence of cardiac hypertrophy are controversial and are likely to be multiple. These mechanisms may include changes in left ventricular geometry, per se, changes in the composition of the left ventricular wall (fibrosis or alteration in collagen), and dynamic factors which modulate diastolic force inactivation (loading conditions, cytosolic calcium handling, cyclic AMP availability). In addition, recent studies suggest that hypertrophied cardiac muscle may be particularly susceptible to develop diastolic dysfunction in response to the stress of hypoxia or ischaemia.

Cardiac Volume↗
PubMed1993

[Histopathological analysis of cellular infiltration in 42 autopsied cases of dilated cardiomyopathy].

Myocarditis is a possible cause of dilated cardiomyopathy (DCM), but criteria for cell infiltration in autopsy cases have not been established. The significance of cell infiltration was evaluated in 42 autopsied cases of DCM which met the diagnostic criteria of the Ministry of Health and Welfare, among 1,700 serial autopsy cases at the National Cardiovascular Center, using the W.D. Edwards and Dallas criteria. Microscopic examinations used sections of the heart along the short axis at the upper one-third and lower one-third levels. Infiltration of small round cells was divided into 3 layers: the epicardial layer, myocardial layer and endocardial layer. Three types of fibrosis were classified: interstitial, focal (less than 1 cm in greatest diameter), and massive (equal to or exceeding 1 cm in greatest diameter). The mean age at death was 50.3 years, but female patients died earlier than male patients. The period of congestive heart failure was 5 years; with a family history of cardiomyopathy in 10% of all patients. The subgroup which fulfilled both criteria consisted of 12 patients (28.6%; positive group). The other subgroup consisted of 30 patients (71.4%; negative group). Cell infiltration tended to be greater in the epicardial layer and less in the endocardial layer. This trend was more prominent in the positive group. Interstitial fibrosis was seen in 73.8% of all patients. Clinically, the positive group was younger at death with higher serum LDH values and lower % fractional shortening on echocardiograms, all statistically significant. Other trends were thinner left ventricular walls, smaller left ventricular cavities and lower cardiac weights in the positive group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Myocardial necrosis and cocaine. A quantitative morphologic study in 26 cocaine-associated deaths.

A quantification of different forms of acute myocardial necrosis, myocardial leukocytic infiltrates and myocardial fibrosis was accomplished in 26 chronic cocaine abusers who died of cocaine intoxication and compared to 45 normal subjects who died from head trauma and 38 who died of acquired immunodeficiency syndrome. The findings were: absence of infarct necrosis, a similar frequency and extent of coagulative myocytolysis (contraction band necrosis) and leukocytic infiltrates in cocaine abusers and normal controls, and an absence of myocardial fibrosis in cocaine abusers. These findings question both the acute and chronic cardiotoxicity of cocaine. The infarct-like pattern in some predisposed subjects may be due to an excess of catecholamine release induced by the drug resulting in coagulative myocytolysis and platelet thrombi.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[The heart and diabetes. An anatomo-clinical study].

We performed a retrospective study in 72 autopsies of diabetic patients (DMP) selected out of 2,239 adult autopsies, comprehending the period between 1966 to 1982. In order to analyse the possible Diabetic Cardiomyopathy, the DMP were divided into 8 groups according to the presence or the absence of Myocardial Fibrosis (MF) and Congestive Heart Failure (CHF). The Diabetes Mellitus (DM) incidence according to the race, sex, age and the presence of Kimmestiel-Wilson (KW) were in agreement with the literature data. The majority of the deaths occurred after the sixth-decade and we did not find any DMP with Malignant Hypertension. Hypertension and Coronary Artery Disease (CAD) increased the frequency of anatomical cardiac alterations, as follows: 1. MF was more associated with CAD, 2. Hypertension was more frequent in DMP with KW in the nodular form; 3. Hypertension increased the frequency of left ventricular hypertrophy; 4. Myocardial Infarction occurred in the absence of occlusive vascular phenomena. The Myocardial Fibrosis (MF) observed in DMP without ACD and without hypertension may be final anatomic demonstration of a gradual metabolic-functional process, and not the basic mechanism of the CHF in the possible Diabetic Cardiomyopathy.

Adolescent↗
PubMed1994

[AIDS and heart disease].

This article reviews cardiac manifestations of AIDS in terms of etiology, pathogenesis, pathoanatomic lesions and heart function. Hypothetically the prevalence of myocarditis and disperse fibrosis of the myocardium are correlated to increasing rates of dilated cardiomyopathy and cardiac insufficiency. Echocardiography has proved to be of value in detecting early abnormalities and should be recommended on broad indications, though aggressive therapy of cardiac abnormalities is of importance to ensure quality of life and surveillance for the patients.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Angiotensin II type 2 receptor is upregulated in human heart with interstitial fibrosis, and cardiac fibroblasts are the major cell type for its expression.

The expression pattern of angiotensin (Ang) II type 2 receptor (AT2-R) in the remodeling process of human left ventricles (LVs) remains poorly defined. We analyzed its expression at protein, mRNA, and cellular levels using autopsy, biopsy, or operation LV samples from patients with failing hearts caused by acute (AMI) or old (OMI) myocardial infarction and idiopathic dilated cardiomyopathy (DCM) and also examined functional biochemical responses of failing hearts to Ang II. In autopsy samples from the nonfailing heart group, the ratio of AT1-R and AT2-R was 59% and 41%, respectively. The expression of AT2-R was markedly increased in DCM hearts at protein (3.5-fold) and mRNA (3.1-fold) levels compared with AMI or OMI. AT1-R protein and mRNA levels in AMI hearts showed 1.5- and 2.1-fold increases, respectively, whereas in OMI and DCM hearts, AT1-R expression was significantly downregulated. AT1-R-mediated response in inositol phosphate production was significantly attenuated in LV homogenate from failing hearts compared with nonfailing hearts. AT2-R sites were highly localized in the interstitial region in either nonfailing or failing heart, whereas AT1-R was evenly distributed over myocardium at lower densities. Mitogen-activated protein kinase (MAPK) activation by Ang II was significantly decreased in fibroblast compartment from the failing hearts, and pretreatment with AT2-R antagonist caused an additional significant increase in Ang II-induced MAPK activity (36%). Cardiac hypertrophy suggested by atrial and brain natriuretic peptide levels was comparably increased in OMI and DCM, whereas accumulation of matrix proteins such as collagen type 1 and fibronectin was much more prominent in DCM than in OMI. These findings demonstrate that (1) AT2-R expression is upregulated in failing hearts, and fibroblasts present in the interstitial regions are the major cell type responsible for its expression, (2) AT2-R present in the fibroblasts exerts an inhibitory effect on Ang II-induced mitogen signals, and (3) AT1-R in atrial and LV tissues was downregulated during chronic heart failure, and AT1-R-mediated functional biochemical responsiveness was decreased in the failing hearts. Thus, the expression level of AT2-R is likely determined by the extent of interstitial fibrosis associated with heart failure, and the expression and function of AT1-R and AT2-R are differentially regulated in failing human hearts.

Adult↗
PubMed1996

Cytokine production in hearts of Trypanosoma cruzi-infected CBA mice: Do cytokine patterns in chronic stage reflect the establishment of myocardial pathology?

The authors analysed cytokine production in hearts of Trypanosoma cruzi-infected CBA-J mice by in situ immunocytochemical staining. Cellular infiltrates were recorded in hearts from both acute and chronic stages, but were not apparent in control hearts. In the acute heart, CD8 cells predominated, with associated production of IL-4, IL-6 and TNF-alpha. Cytokine production was characterized by IL-4, IL-5, IL-6 and TNF-alpha in the chronic heart, and numbers of CD4 and CD8 cells were more equal. At this stage, calcified infarctions and associated fibrosis were apparent, mimicking chronic human Chagas' heart pathology. The authors consider the CBA mouse an appropriate model of chronic T. cruzi infection, and suggest that local cytokine production reflects establishment of heart pathology.

Acute Disease↗