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PubMed2003

Quilty lesions are associated with increased expression of vitronectin receptor (alphavbeta3) and subsequent development of coronary vasculopathy.

BACKGROUND: Quilty lesions are common after heart transplantation; however, their relationship to vasculopathy has not been described. We tested the hypothesis that Quilty lesions are associated with increased expression of vitronectin receptor (alphavbeta3) and the subsequent development of coronary vasculopathy. METHODS: A total of 140 heart transplant recipients underwent coronary intravascular ultrasound at baseline and at 1 year after transplantation, and we measured the change in coronary maximal intimal thickness. Endomyocardial biopsy specimens taken within 8 weeks after transplantation showed Quilty lesions in 54 of 140 (39%) patients (Quilty group). We compared these results with the remaining 86 of 140 patients (61%) who had no evidence of Quilty lesions during the same period (control group). We evaluated 10 endomyocardial biopsy specimens from each group for alphavbeta3, using immunohistochemistry staining and immunoblotting. RESULTS: Quilty lesions stained positive for alphavbeta3, and Western blot analysis showed a 1.3-fold (p = 0.004) increase in expression of alphavbeta3. Compared with control, the Quilty group tended to have a greater incidence of post-transplant ischemic injury complicated by fibrosis (54% vs 38%, p = 0.08) and a greater reported incidence of "previous biopsy site" during the first 4 weeks after transplantation (48% vs 32%, p = 0.06). At 1 year, the Quilty group had a significant increase in the change in coronary maximal intimal thickness seen with intravascular ultrasound (0.54 +/- 0.34 vs 0.42 +/- 0.28 mm, p = 0.038). CONCLUSIONS: This is the first report to describe the association of Quilty lesions with coronary vasculopathy and its association with increased alphavbeta3 expression.

Adult↗

PubMed1983

Value of two-dimensional echocardiography in endomyocardial disease with and without eosinophilia. A clinical and pathologic study.

Ten patients (six women and four men) with endomyocardial disease, four with and six without hypereosinophilia, were studied by two-dimensional echocardiography (2-D echo). Eight had biventricular congestive heart failure and two had atypical chest pain with ischemic electrocardiographic changes. The patients were 15-50 years old (mean 40 years) and duration of illness was 2-9 years (mean 4.4 years). Nine had cardiac catheterization and three pathologic examination. Characteristic 2-D echo findings included apical obliteration of one or both ventricles by echogenic material suggestive of fibrosis or thrombosis; bright, specular echoes at the cavity surface of the apical obliteration suggesting patchy calcification; preserved left apical systolic inward motion, which differed significantly from the dyskinetic motion of thrombotic apical obliteration of ischemic or Chagasic origin (p less than 0.001); involvement of the papillary muscles and posterior atrioventricular valve; preserved ventricular contractile function in most patients; and the combination of normal-to-small ventricles with large atria. None of 14 subjects with secondary hypereosinophilia followed for 15.4 months developed similar 2-D echo findings. We conclude that both forms of endomyocardial disease had a 2-D echo pattern useful for noninvasive recognition and differentiation from patients who have valvular heart disease, constrictive pericarditis and cardiomyopathies of other origins.

Adolescent↗

PubMed1990

Pathologic changes in the long-term transplanted heart: a morphometric study of myocardial hypertrophy, vascularity, and fibrosis.

Myocyte hypertrophy and myocardial fibrosis have been observed in transplanted human hearts, and both could potentially have an adverse effect on long-term cardiac function. There has been some concern that distant donor heart procurement and cyclosporine treatment increase the risk of these changes, but their incidence and severity have not been documented quantitatively in large numbers of cardiac transplant recipients. We used light microscopic morphometric methods to estimate myocardial collagen volume fraction and myocyte width in right ventricular endomyocardial biopsies from 95 recipients at 3 years posttransplantation, and electron microscopic stereology to estimate myocardial vascularity and myocyte myofibril content in 40 recipients, also at 3 years posttransplantation. We compared those with locally and distantly procured donor hearts (mean ischemic time 160 minutes) and cyclosporine versus noncyclosporine immunosuppression. Controls were pretransplant right ventricular biopsies from 20 donor hearts which were free of heart disease. We found no significant differences in myocardial collagen volume fractions. Myocyte hypertrophy was typical of all the transplant biopsies (mean myocyte width 20.2 microns, SD 3.0 in all transplants versus 11.8 microns, SD 2.2 in controls, P less than 0.001), but distant donor procurement and cyclosporine had no significant effect. There were significant reductions of myofibril volume fraction in the transplants, which raises the possibility of gradual decompensation in some patients. There were no significant differences in myocardial vascularity, although a few patients were well below the control range. We conclude that distant donor heart procurement, with ischemic times averaging less than 3 hours, and cyclosporine treatment are not responsible for significant hypertrophy or fibrosis in most transplants. Hypertrophy is typical of the transplanted heart, and it is possible that associated abnormalities might have an effect on cardiac function in some long-term survivors.

Adult↗

PubMed1991

Cardiac biopsy in patients with "primary" atrial fibrillation. Histologic evidence of occult myocardial diseases.

Fourteen patients (ten men and four women; mean age, 37 years) with lone atrial fibrillation (AF) (1 to 18 months' duration) were evaluated by thyroid function tests, two-dimensional echocardiography, hemodynamics, coronary angiography, and left ventricular endomyocardial biopsy, because of unresponsiveness to the usual antiarrhythmic therapy. The results of the T3, T4, TSH, and TRH tests were normal in all patients; cardiac valves and ventricular and atrial sizes (left atrium less than 40 mm) were within the normal limits; also normal were LVEDP (less than or equal to 10 mm Hg) and EF (greater than 0.50). Histologic findings were abnormal in all cases, with three patients showing cardiomyopathic changes, three other patients showing active myocarditis (lymphocytic in two and eosinophilic in one), and eight patients with nonspecific necrosis or fibrosis or both. Steroids (prednisone; 50 mg/m2 of body surface area daily) used in addition to antiarrhythmic therapy in patients with eosinophilic and lymphocytic active myocarditis were able to cause reversion to sinus rhythm, while the other patients continued to have AF. This study documents that occult myocardial diseases (myocarditis, cardiomyopathy, and nonspecific necrosis or fibrosis) can underlie "primary" AF. The addition of steroids to antiarrhythmic therapy in patients with refractory AF and histologic evidence of active myocarditis seems to be useful in controlling the arrhythmia.

Adult↗

PubMed1990

Histopathologic findings of endomyocardial biopsies in pediatric patients with arrhythmias or conduction disturbances.

Histopathologic findings of endomyocardial biopsy in 23 pediatric patients with arrhythmias or conduction disturbance were analyzed. ECG abnormalities consisted of atrioventricular block (AVB) in 11, ventricular arrhythmia including premature ventricular contractions (PVC) and ventricular tachycardia in 7, sick sinus syndrome (SSS) in 3, and bundle branch block in 2 cases. Biopsy specimens were obtained from the right ventricle in all cases and, additionally, from the right atrium in SSS cases. Biopsy revealed significant pathology in 19 cases (83%). Advanced histologic changes, including myocyte hypertrophy, disarrangement of muscle bundles, and interstitial fibrosis with or without myocyte degeneration, were observed in 7/11 AVB cases and 1/6 PVC cases. SSS cases showed interstitial fibrosis with disarrangement of muscle bundles in the right atrium, but no significant pathologic changes were seen in the right ventricle. There was no clinical evidence of hypertrophic or dilated cardiomyopathy, cardiac defects, or other heart disease in these patients. It is suggested that these cases may fall under the arrhythmia-conduction disturbance type of cardiomyopathy.

Adolescent↗

PubMed1982

Technique, complications, and clinical value of endomyocardial biopsy in patients with heterotopic heart transplants.

A review of 157 consecutive biopsies of donor endomyocardium in patients with heterotopic heart transplants is reported. The technique of percutaneous transvenous endomyocardial biopsy after this operation is described; manipulation of the catheter and bioptome into the junction of the donor superior vena cava and right atrium can be difficult when this anastomotic junction is small, as a result either of operative surgical technique or of subsequent contraction. The complication rate was 4%, but one patient may have died from infection resulting from biopsy when the bioptome had to be introduced at the groin. The histopathological changes seen in the biopsy specimens have been graded according to a scoring system to give the clinician a guide to the severity of rejection. Histopathological assessment was of clinical value in 96% of cases, but was inaccurate on two occasions, once because an opinion was given on what was in retrospect an inadequate sample. In patients undergoing persistent low-grade acute or chronic rejection there was difficulty in detecting or appreciating the true extent of myocardial fibrosis; this led to inadequate immunosuppressive treatment in two patients. Attention is drawn to the fact that ischaemic fibrosis resulting from the vascular changes of chronic rejection may spare the endomyocardium, which is kept viable by intracavitary blood, and that this may lead to a misleading histopathological report.

Biopsy↗

PubMed2000

Left ventricular myocardial remodeling and contractile state in chronic aortic regurgitation.

BACKGROUND: In chronic aortic regurgitation, eccentric hypertrophy, with combined concentric hypertrophy of the left ventricle, is an important adaptive response to volume overload, which in itself is a compensatory mechanism for permitting the ventricle to normalize its afterload and to maintain normal ejection performance (physiologic hypertrophy). However, progressive dilatation of the left ventricle leads to depressed left ventricular (LV) contractility and myocardial structural changes, including cellular hypertrophy and interstitial fibrosis (pathological hypertrophy). HYPOTHESIS: The study was undertaken to determine the relationship between left ventricular myocardial structure and contractile function in 14 patients with chronic aortic regurgitation by cardiac catheterization and endomyocardial biopsies. METHODS: Myocardial cell diameter and percent interstitial fibrosis were obtained from biopsy samples. Contractile function was evaluated from the ratio of end-systolic wall stress to end-systolic volume index (ESS/ESVI) and the ejection fraction-end-systolic stress (EF-ESS) relationship, which was obtained from 30 normal control subjects. RESULTS: Myocardial cell diameter correlated significantly with the ESVI (r = 0.72, p < 0.005), ejection fraction (r = -0.58, p < 0.05), and ESS/ESVI (r = -0.58, p < 0.05). The percent interstitial fibrosis also correlated inversely with ESS/ESVI (r = -0.71, p < 0.005). Compared with very few patients with an ESVI < 70 ml/m2, the majority of patients with ESVI > or = 70 ml/m2 had a cell diameter of > or = 30 microns and a percent interstitial fibrosis of > or = 10%. The nine patients who had depressed contractile function, as assessed from the EF-ESS relationship, had a higher percent interstitial fibrosis (p < 0.05) than five patients showing a normal EF-ESS relationship, despite the fact that there was no significant difference in myocardial cell diameter between them. Thus, advanced cellular hypertrophy and excessive interstitial fibrosis were significantly and independently associated with myocardial contractile dysfunction and appeared to be responsible for ventricular remodeling. CONCLUSION: Our findings suggest that in many patients with aortic regurgitation, eccentric hypertrophy changes its nature from physiologic to nonphysiologic during the earlier stages in the course of the disease rather than during the stage described previously.

Adolescent↗

PubMed1995

Cardiac failure and dysrhythmias 6-19 years after anthracycline therapy: a series of 15 patients.

The clinical course of late symptomatic anthracycline cardiomyopathy, and resultant changes of cardiac function, were described in 15 patients. They represented a subset of 300 patients who had cardiac evaluations to identify the prevalence of late cardiotoxicity more than 4 years after anthracycline therapy in these patients. The clinical course and all available cardiac evaluations including electrocardiography, continuous taped electrocardiography, echocardiography, radionuclide cardiac angiography, cardiac catheterization, and endomyocardial biopsy, of the 15 patients were reviewed. The patients had received 285-870 (median 540) mg/M2 of daunorubicin and/or doxorubicin 6-19 (median 12) years prior to the onset of late symptoms. Seven patients also had 2,100-4,000 cGy mediastinal radiotherapy. Five patients had required treatment for cardiac symptoms at the end of chemotherapy but 10 patients had no cardiac problems anteceding their late decompensation. Fractional shortening on echocardiogram at late decompensation was 8-20% (median 17%) and radionuclide left ventricular ejection fraction was 8-59% (median 38%). All were treated with digitalis and diuretics and 13/15 with afterload reduction, with at least transient improvement of symptoms. They were followed for 1-9 (median 3) years after late decompensation. One died of uncontrollable cardiac failure. Another underwent successful cardiac transplantation. Conduction abnormalities and dysrhythmias were present in 14/15 patients and 3 died suddenly. Two more had syncope, one requiring an automatic cardiac defibrillator. Endomyocardial biopsy or autopsy revealed hypertrophy and fibrosis in 10/10 patients. Our patients with early cardiac symptoms improved transiently but decompensated later and patients with no early symptoms developed cardiac symptoms more than 10 years after anthracycline therapy. Therefore, patients who have received anthracyclines should have continued cardiac evaluation.

Adolescent↗

PubMed1986

Cardiac function and coronary arteriography in asymptomatic type 1 (insulin-dependent) diabetic patients: evidence for a specific diabetic heart disease.

Cardiac function was examined in 63 asymptomatic Type 1 (insulin-dependent) diabetic patients, aged 30-50 years, using radionuclide ventriculography and exercise electrocardiography to investigate the possible existence of a specific diabetic heart disease. Comparisons were made with 45 age- and sex-matched non-diabetic controls. Radionuclide ventriculography was performed at rest and during the physiological stresses of isometric exercise, cold-pressor testing and dynamic exercise. Scans were technically satisfactory in 56 of the diabetic patients and 38 of the control subjects. The resting left ventricular ejection fractions and the responses to isometric exercise and cold-pressor testing were similar in the diabetic patients and controls. A smaller rise in the left ventricular ejection fraction during dynamic exercise was observed in male diabetic patients compared with male control subjects (9 +/- 1% (mean +/- SEM) vs 14 +/- 1% (p less than 0.005)). A similar trend was observed in female diabetic patients, with a rise of 5 +/- 1% on dynamic exercise compared with a rise of 8 +/- 1% in the control group. Sixteen diabetic patients (29%) demonstrated an abnormal response to dynamic exercise, and 5 of these had an abnormal exercise electrocardiogram. Cardiac catheterisation and coronary arteriography were performed in eight of these 16 patients, and all 8 had normal coronary arteries. Endomyocardial biopsy revealed arteriolar thickening and interstitial fibrosis in 5 patients, and in 2 patients basement membrane thickening was conspicuous. Thus, in diabetic patients cardiac function may be abnormal without evidence of coronary heart disease, and some patients appear to have the histological changes consistent with a diabetic microangiopathy involving the heart.

Adult↗

PubMed1991

Cardiac manifestations of Weber-Christian disease: report and review of the literature.

A patient with chronic systemic Weber-Christian disease who was treated with hydroxychloroquine developed cardiac dilatation with congestive heart failure. Endomyocardial biopsy demonstrated myocyte degeneration and interstitial fibrosis, but no typical features of chloroquine induced cardiomyopathy. Clinical symptoms of congestive heart failure also were recognized in 7 of the 11 reported autopsy cases of Weber-Christian disease having cardiac involvement. This involvement can affect the pericardium and the myocardium.

Adult↗

PubMed1986

[Asymmetric septal hypertrophy of sporadic form with abnormal thallium perfusion and myocardial enzymes].

Asymmetric septal hypertrophy with abnormal thallium scintigram and elevated cardiac enzymes were observed in five patients and were studied with special reference to the clinical significance of their clinicopathological features. They were not familial cardiomyopathy patients. Two of the five patients (Cases 1 and 2) exhibited the clinical features characteristic of hypertrophic cardiomyopathy without abnormal thallium perfusion and serum cardiac enzyme levels. A right endomyocardial biopsy for Case 1 disclosed myocardial fibrosis in addition to hypertrophy and disarray of myocardial fibers. The left ventricular cavities of two other patients (Cases 4 and 5) tended to be dilated with signs of impaired systolic function and asymmetric septal hypertrophy. A regional area of reduced thickness was observed in the medial portion of the left ventricular posterior wall of Case 4. The remaining case (Case 3) exhibited left ventricular dilatation and reduced left ventricular systolic function, disproportionate hypertrophy, and had clinical signs of congestive heart failure. Necropsy disclosed massive fibrosis and diffuse disarray of myocardial fibers. Some patients with familial hypertrophic cardiomyopathy progress to exhibit clinical features of dilated cardiomyopathy in the terminal stages, and have massive fibrosis of the myocardium histologically. Thallium scintigraphic abnormalities and elevated serum levels of cardiac enzymes, especially the LDH1 isoenzyme, in patients with hypertrophic cardiomyopathy may be a meaningful indicator of such progression in its early stages. The five patients in the present study exhibited a variety of clinical and histological features which may comprise a spectrum of clinical conditions during the progression from hypertrophic cardiomyopathy to a condition like dilated cardiomyopathy, similar to that in familial patients. This progression and the factors promoting it should be studied further in the near future.

Adult↗

PubMed1995

Sex-dependent differences in left ventricular function and structure in chronic pressure overload.

To evaluate gender-related differences in left ventricular (LV) structure and function in aortic stenosis, LV biplane cineangiography, micromanometry and endomyocardial biopsies were carried out in 56 patients with aortic stenosis and normal coronary arteries. Patients were divided into males (M: n = 35), and females (F: n = 21). Sixteen normal subjects 8 M, 8 F) served as haemodynamic controls. Control biopsy data were obtained from six pre-transplantation donor hearts (3 M and 3 F). LV systolic function was evaluated by ejection fraction and its relationship to mean systolic circumferential wall stress, diastolic function by the time constant of LV pressure decay, peak filling rates and passive myocardial stiffness constant. Biopsy samples were evaluated for interstitial fibrosis, muscle fibre diameter and volume fraction of myofibrils. In a subset of 27 consecutive patients, biopsy samples were evaluated with a morphometric-morphological method, for total collagen volume fraction, endocardial fibrosis and the extension and thickness of orthogonal collagen fibres (cross-hatching). In patients with aortic stenosis, aortic valve area, aortic valve resistance and mean aortic pressure gradient were comparable in males and females, whereas end-systolic and end-diastolic volumes were larger in males than females. Ejection fraction was lower (56%) in males than females (64%) (P < 0.05); 20 of 35 males and four of 21 females had depressed systolic contractility when assessed with regard to the relationship ejection fraction-mean systolic stress (P < 0.01). Myocardial stiffness constant was higher in males than in females (P < 0.01). Nine of 14 males and two of 13 females had endocardial fibrosis (P < 0.009), whereas increased cross-hatching (> 1.5 grade) was present in 11 males and four females with aortic stenosis (P < 0.01). An abnormal collagen architecture was present in 13/14 males and 5/13 females (P < 0.002). In aortic stenosis, males have a depressed systolic function and abnormal passive elastic properties when compared to females with valve lesions of similar severity. Changes in collagen architecture may account, at least in part, for these differences.

Adolescent↗

PubMed1990

Reactive and reparative fibrillar collagen remodelling in the hypertrophied rat left ventricle: two experimental models of myocardial fibrosis.

STUDY OBJECTIVE: The aim was to compare the temporal sequence and structural relationship between perivascular and interstitial fibrosis and microscopic scarring seen in the left ventricle in response to either a transient or sustained stimulus to fibrosis. DESIGN: In 72 male Wistar rats (250-350 g) the transient stimulus model was based on the administration of isoprenaline (500 micrograms.kg-1) while the sustained stimulus model was produced by abdominal aortic banding with right renal artery constriction. Serial sections of myocardium were examined and compared at 4 and 12 weeks in each model and to corresponding controls. EXPERIMENTAL MATERIAL: The collagen specific stain, Sirius Red F3BA, was used to determine collagen volume fraction and the fibrillar nature of the fibrous tissue response seen by light microscopy. MEASUREMENTS AND MAIN RESULTS: Following isoprenaline a stable reparative fibrosis of the endomyocardium and increase in collagen volume fraction was seen without an interstitial or perivascular fibrosis of the non-involved myocardium. In unilateral renal ischemia, on the other hand, a progressive perivascular fibrosis was evident throughout the myocardium and from which fibrillar collagen extended into the extracellular space between muscle bundles creating an interstitial fibrosis; microscopic scarring of the endomyocardium became evident at 12 weeks. CONCLUSIONS: The reactive perivascular fibrosis of intramyocardial coronary arteries seen in renovascular hypertension is a progressive process that leads to an interstitial fibrosis and eventual microscopic scarring. In contrast, the endomyocardial scarring that follows isoprenaline induced myocyte necrosis is stable and intramural vessels in remote regions are not involved.

Animals↗

PubMed1999

Ultrastructural characteristics of myocardial and coronary microvascular lesions in Kawasaki disease.

Kawasaki disease (KD) is an acute febrile mucocutaneous lymph node syndrome with multisystemic vasculitis affecting mainly infants and children. Although several studies on cardiovascular lesions in KD have been done at the light microscopic level, the ultrastructural characteristics and incidences of these lesions have not been well defined. In order to investigate the myocardial and coronary microvascular sequelae in KD, we performed an ultrastructural study on endomyocardial biopsy specimens obtained during follow-up from 54 patients who had typical clinical manifestations of KD, of whom 47 had associated coronary aneurysms as demonstrated by coronary arteriography (CAG) or two-dimensional echocardiography in the acute or healed stage. The average age of onset was 2.2 years old and the duration of illness was from 2 months to 23 years. Follow-up CAG showed that the coronary aneurysms persisted in 33 of the 47 patients (8 with associated stenosis) and resolved in the remaining 14 patients. Ultrastructurally, the myocardial changes revealed hypertrophy, various degrees of degeneration, proliferation and abnormality of mitochondria, infiltration of a small number of lymphocytes, and fibrosis. The coronary microvascular lesion was characterized by microvascular dilatation, endothelial cell injury, platelet aggregation with thrombosis, and stenotic lumen with thickened walls in the small arterioles. It persisted after convalescent stage even up to 23 years and closely correlated with the myocardial sequelae. Moreover, significantly increased incidences of myocardial and coronary microvascular lesions were found in patients with coronary artery lesion. These findings suggest the coronary microvascular lesion as a possible underlying factor of persistent sequelae in KD.

Adolescent↗

PubMed1986

[Right ventricular endomyocardial biopsy findings in idiopathic mitral valve prolapse: comparison with clinical findings].

Right ventricular endomyocardial biopsies were performed in nine patients with mitral valve prolapse (MVP), and the histological features were compared with the clinical findings. All of them had atypical anterior chest pain and/or dangerous ventricular arrhythmias, but the grade of MVP was mild. Five patients had non-specific ST-T changes on resting 12 leads ECG, four had ischemic ST depression on treadmill exercise ECG, and five had dangerous arrhythmias on 24 hour Holter monitoring ECG. Resting echocardiography showed normal left ventricular function in all, but exercise echocardiography revealed reduced increment of % fractional shortening (delta % FS) in five patients. Right ventricular endomyocardial biopsy findings disclosed endocardial thickening and interstitial myocardial fibrosis in eight patients, myocardial hypertrophy in two, myocardial degeneration in five, and myocardial disarray in five, although these changes were mild. These results suggest that in patients with MVP, there is a subgroup with endomyocardial abnormalities, and these might have some relations to the variety of clinical findings in MVP.

Adolescent↗

PubMed1999

Global biventricular dysfunction in patients with asymptomatic coronary artery disease may be caused by myocarditis.

BACKGROUND: The causal role of asymptomatic critical coronary artery obstruction in patients presenting with severe global biventricular dysfunction but no evidence of myocardial infarction is uncertain. METHODS AND RESULTS: Among 291 patients aged >40 years undergoing a noninvasive (2-dimensional echocardiography) and invasive (catheterization, coronary angiography, and biventricular endomyocardial biopsy, 6 to 8 samples/patient) cardiac study because of progressive heart failure (New York Heart Association functional class III or IV) with global biventricular dysfunction and no history of myocardial ischemic events, 7 patients (2.4%; 7 men; mean age, 49+/-6.9 years) had severe coronary artery disease (3 vessels in 4 patients; 2 vessels in 1 patient, proximal occlusion of left anterior descending coronary artery in 2 patients). Left ventricular end-diastolic diameter and ejection fraction by 2-dimensional echocardiography were 73+/-10.5 mm and 23+/-6.5%, respectively, and right ventricular end-diastolic diameter and ejection fraction were 39+/-7 mm and 29+/-7.2%, respectively. Biopsy specimens showed extensive lymphocytic infiltrates with focal myocytolysis meeting the Dallas criteria for myocarditis in all patients (in 5 patients with and 2 patients without fibrosis). Cardiac autoantibodies were detected with indirect immunofluorescence in the serum of 2 patients with active myocarditis. The 2 patients with active inflammation received prednisone (1 mg. kg-1. d-1 for 4 weeks followed by 0.33 mg. kg-1. d-1 for 5 months) and azathioprine (2 mg. kg-1. d-1 for 5 months) in addition to conventional drug therapy for heart failure. At 8-month overall follow-up, cardiac volume and function improved considerably in immunosuppressed patients but remained unchanged in conventionally treated patients, of whom 1 died. CONCLUSIONS: Global biventricular dysfunction in patients with severe asymptomatic coronary artery disease and no evidence of previous myocardial infarction may be caused by myocarditis. Histologic findings may influence the treatment.

Adult↗

PubMed2006

Serum cardiac troponin T in cardiac amyloidosis: serial observations in five patients.

The most common cause of death of patients suffering from amyloidosis is heart failure and sudden death, and cardiac troponin T (cTnT), a highly specific and sensitive biomarker of myocardial injury, has been reported to be a prognostic marker at presentation. But the relationship between serial measurements of serum cTnT and clinical course of the disease has not been described. An illustrative case was a 55-year-old man with normal renal function presenting with congestive heart failure (CHF), whose initial concentration of cTnT was 0.72 ng/ml. Eight samples of initial endomyocardial biopsy specimens showed the presence of myocyte degeneration and interstitial fibrosis with a small amount of amyloid infiltration. However, the cTnT values remained at 0.69 ng/ml after successful management of CHF, and four months later, a second endomyocardial biopsy revealed diffuse massive amyloid protein deposition. He died of CHF, 9 months after initial presentation. In addition, we present 4 cases of amyloidosis with increased serum cTnT levels. We therefore propose that serial measurements of serum cTnT might be helpful for early diagnosis and prediction of prognosis of patients with amyloidosis.

Aged↗

PubMed1992

The conduction system in transplanted hearts.

This is a serial section examination of the conduction system (CS) in six patients who died seven months, 11 months, two years four months, four years two months, 11 years, and 16 years eight months following cardiac transplantation. The heart was hypertrophied and enlarged in all. There was myocarditis of varying degree in all cases with arteriosclerosis and arteriolosclerosis. These findings were more dominant in the atria than in the ventricles. In the CS, myocarditis with fibrosis was found in all in the approaches to the sinoatrial (SA) node, the SA node, the atria, the atrioventricular (AV) node, and the bundle and bundle branches, to a varying degree. When compared with the endomyocardial biopsy findings, the autopsied cases revealed more myocarditis and fibrosis than those estimated to be present in the biopsy specimen. In summary, this study demonstrates that there are fibrotic changes in the CS with the persistence of inflammatory phenomena of the myocardium and the CS to a varying degree in transplanted hearts. This is accompanied by the ubiquitous coronary artery disease affecting not only the large coronaries but also the small vessels. The pathologic changes in and around the CS may be responsible for arrhythmias and sudden death in some cases of cardiac transplantation.

Adolescent↗