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At least 19 recordsLinked to original sources
PubMed1997

Histological substrate of atrial biopsies in patients with lone atrial fibrillation.

BACKGROUND: Lone atrial fibrillation (LAF) is a common clinical syndrome, but its origin remains unknown. METHODS AND RESULTS: We performed endomyocardial biopsies of the right atrial septum (2 to 3 per patient; mean, 2.8) and of the two ventricles (6 per patient) in 12 patients (10 men, 2 women; mean age, 32 years) with paroxysmal LAF refractory to conventional antiarrhythmic treatment. As controls, we used endomyocardial biopsies (3 to 5 per patient; mean, 4.4) from the right atrial septum of 11 patients with Wolff-Parkinson-White syndrome (WPW) undergoing resection of the abnormal AV pathway. The weight of the biopsies ranged from 2.8 to 4.5 mg. Biopsy samples were processed for histology and electron microscopy and were read by a pathologist blinded to clinical data. All patients underwent two-dimensional Doppler echocardiography; cardiac catheterization; coronary angiography; and hormonal, virologic, and electrophysiological studies. All tests and WPW biopsies were normal, but all LAF atrial biopsy specimens (average, 2.8 per patient) showed abnormalities (P<.0001). The type of abnormalities varied: Two patients had a severe hypertrophy with vacuolar degeneration of the atrial myocytes and ultrastructural evidence of fibrillolysis occupying >50% of the areas assessed morphometrically (P=.50), 8 had lymphomononuclear infiltrates with necrosis of the adjacent myocytes (5 with fibrosis and 3 without; P<.003), and 2 had only nonspecific patchy fibrosis (P=.50). Biventricular biopsies were abnormal in only 3 patients and showed inflammatory infiltrates similar to those found in atrial biopsies. CONCLUSIONS: Abnormal atrial histology was uniformly found in multiple biopsy specimens in all patients with LAF. It was compatible with a diagnosis of myocarditis in 66% of patients (active in 25%) and of noninflammatory localized cardiomyopathy in 17% and was represented by patchy fibrosis in 17%. The cause of the pathological changes, which were found only in atrial septal biopsies but not in biventricular biopsies, in 75% of patients remains unknown.

Adult↗
PubMed1985

Changes in atrial biopsies in chronic rheumatic heart disease. II: Muscle fibre reaction.

Myocardial fibres were studied in the right atrial biopsies from 32 patients with chronic rheumatic heart disease (RHD). Paraffin and, particularly, araldite sections showed many muscle fibres well preserved, and others with large hyperchromatic nuclei, or with depleted myofibrils and increased mitochondria. With the SDH and ATPase reactions, there was no type difference in the myocardial fibres, and the former showed the reaction predominantly in the centre while the latter showed it mainly at the periphery of the fibres. At electronmicroscopy, fibres with intact myofibrils were found close to "degenerating" fibres with variable degrees of myofibrillar and myofilament disorganisation and loss, mitochondrial proliferation, occasionally with degeneration of cristae, and accumulation of lipofuscin in varying amounts, and irregularly tortuous or loosened intercellular junctions. This study has revealed more severe muscle changes than expected, even in the clinically less affected right atrial chamber in chronic RHD. It is speculated that this might be due to subclinical involvement of the tricuspid valve, known to be frequent in Indian patients, and the resulting "back pressure" on the right atrium might lead to changes in its myofibres.

Adolescent↗
PubMed1985

Changes in atrial biopsies in chronic rheumatic heart disease. I: Cellulo-vascular and mesenchymal reaction.

The cellular, vascular and connective tissue changes were studied in 32 atrial biopsy specimens from patients with chronic rheumatic heart disease (RHD). 15 of these 32 specimens showed some inflammatory reaction, 7 with small mononuclear cells only and 8 with macrophage reaction amidst increased but necrotic collagen, especially in the subepicardial and subendocardial regions. Most cellulonecrotic foci were histologically consistent with a stage of Aschoff nodule. Acid phosphatase activity in frozen sections was seen in the cytoplasm of the macrophages. Fine structural examination showed membrane-bound vacuoles and lipofuscin bodies rather than ingested material in the macrophages. By light and electronmicroscopy, these macrophages were not different from those encountered in other granulomatous or necrotic conditions. There was moderate proliferation of blood vessels, with prominence of endothelial cells and pinocytotic vesicles, or fibrosis of media, or proliferation of basal laminae. The presence of Aschoff nodules in the right atrium, the least affected chamber in RHD, suggests a diffuse and smouldering pathology on the basis of a persistent subclinical cell-mediated immune (CMI) reaction.

Adolescent↗
PubMed1983

Cardioplegia versus topical cooling for cardiac protection during open-heart surgery. An electron microscopic and histochemical study of right atrial biopsies.

The effectiveness of topical cooling and cold cardioplegia for cardiac protection in the course of open-heart surgery was studied by electron microscopy and fluorescence microscopy of right atrial biopsies. In 20 patients with topical cooling, no changes or minimal changes were observed in 15 cases, more pronounced changes in 3 cases, and severe destruction in 2 cases. In the group of 20 patients with cold cardioplegia the range of the changes was significantly narrower: no specimen remained completely intact; on the other hand, very severe destruction was not observed. Fluorescence microscopy revealed that the neural noradrenaline stores were relatively resistant to ischaemia. Electron microscopy showed certain failure of the protective procedure, resulting in injury of myocardial cells and neural elements. Even "spot-like" destruction noted in the nerve terminals may interfere with the peripheral neuro-neuronal interaction, resulting in nonhomogenous spread of the excitation wave front and electrical instability of the heart. Therefore cardiac nerve damage should also be taken into consideration when evaluating the effectiveness of different methods for cardiac protection.

Aortic Valve↗
PubMed1993

Right atrial mass biopsy guided by transesophageal echocardiography.

A 69-year-old woman was found to have a right atrial mass on transthoracic echocardiogram. Biopsy of the mass was performed using transesophageal echocardiography for visual guidance. Pathologic study revealed an organizing thrombus. This case illustrates the clinical utility of transesophageal echocardiography in the biopsy of right atrial masses.

Aged↗
PubMed1983

Cefonicid concentrations in serum and atrial tissue during open-heart surgery.

Cefonicid was administered intramuscularly 1 h before open-heart surgery to seven patients in doses of 1 g each and to six patients in doses of 2 g each. Cefonicid concentrations were measured in the right atrial biopsy and in serum at onset of surgery, at time of atrial biopsy, 15 min after starting cardiopulmonary bypass, and at completion of cardiopulmonary bypass. Concentrations in the atrial biopsy and in serum at all periods exceeded the minimal inhibitory concentrations for organisms most frequently responsible for postoperative infections.

Aged↗
PubMed2026

Histological Determinants of Atrial Dysfunction in Patients With Atrial Fibrillation.

BACKGROUND: Atrial fibrillation (AF) is associated with diverse histological abnormalities, but their contributions to atrial dysfunction and functional recovery remain unclear. METHODS: In a discovery cohort of 375 patients with nonvalvular AF undergoing catheter ablation, atrial biopsy samples were quantitatively analyzed for fibrosis, intercellular space expansion, myofibrillar loss, myocardial nuclear density, and amyloid deposition. Left atrial reservoir strain (LASr) was assessed as a measure of atrial function during sinus rhythm (Group 1) or AF (Group 2) at the time of echocardiography. Functional recovery was defined as the change in LASr 12 months after ablation. Findings were validated in an independent cohort of 191 patients with AF. A subset of samples was additionally analyzed for DNA damage markers, poly(ADP-ribose), and phosphorylated histone H2A.X. RESULTS: LASr improved significantly after ablation in Group 2 but not in Group 1. Multivariable analyses identified greater fibrosis, reduced myocardial nuclear density, and advanced amyloid deposition as significant determinants of impaired atrial function in both groups and of limited postablation functional recovery in Group 2 (all P<0.01). Amyloid deposition was also significantly associated with adverse clinical outcomes. Decision-tree models incorporating LASr accurately identified advanced amyloid deposition in both cohorts (accuracy, 94%-96%). DNA damage markers were inversely associated with myocardial nuclear density and positively associated with cardiomyocyte hypertrophy. CONCLUSIONS: Fibrosis, DNA damage-associated reduction in myocardial nuclear density, and advanced atrial amyloidosis are key determinants of atrial dysfunction and impaired postablation functional recovery in patients with AF. LASr enables noninvasive identification of advanced atrial amyloidosis.

Humans↗
PubMed2001

Cardiac surgery increases the activity of matrix metalloproteinases and nitric oxide synthase in human hearts.

OBJECTIVES: Heart function is variably impaired after cardiopulmonary bypass. We hypothesized that, similar to other myocardial injury states, cardiopulmonary bypass leads to enhanced activity of nitric oxide synthase and matrix metalloproteinases. METHODS: We obtained right atrial biopsy specimens and plasma samples at the onset and termination of cardiopulmonary bypass in 10 patients. Biopsy specimens were analyzed for nitric oxide synthase activity by using a citrulline assay, whereas plasma and tissue were analyzed for matrix metalloproteinase-9 and matrix metalloproteinase-2 activity by using zymography. Tissue inhibitor of metalloproteinase-4 was analyzed by means of Western blotting. The cellular expression of inducible nitric oxide, endothelial nitric oxide synthase, matrix metalloproteinase-2, and matrix metalloproteinase-9 was determined in right atrial biopsy samples from 3 additional patients by using the appropriate conjugated antibodies. RESULTS: Nitric oxide synthase activity increased from the beginning to the end of bypass (4.46 +/- 1.07 vs 16.77 +/- 4.86 pmol citrulline/mg of protein per minute, respectively; P =.018). Pro-matrix metalloproteinase-9 activity increased in hearts (199 +/- 41 vs 660 +/- 177 density units/mg protein; P =.008) and plasma (14.1 +/- 4.6 vs 52.2 +/- 5.9 density units/mg protein; P =.008). Pro-matrix metalloproteinase-2 activity increased in the heart (201 +/- 23 vs 310 +/- 35 density units/mg protein, P <.05) but not in plasma. Tissue inhibitor of metalloproteinase-4 expression in the heart decreased (1574 +/- 280 vs 864 +/- 153 density units, P =.014). CONCLUSIONS: Cardiopulmonary bypass activates enzymes mediating acute inflammation and organ injury (ie, nitric oxide synthase, matrix metalloproteinase-9, and matrix metalloproteinase-2). Decreased tissue inhibitor of metalloproteinase-4 expression allows relatively unopposed increases in matrix metalloproteinase tissue activity. We postulate that these changes play a role in the pathogenesis of heart dysfunction after bypass surgery.

Aged↗
PubMed2004

Preconditioning with sevoflurane decreases PECAM-1 expression and improves one-year cardiovascular outcome in coronary artery bypass graft surgery.

BACKGROUND: Cardiac preconditioning is thought to be involved in the observed decreased coronary artery reocclusion rate in patients with angina preceding myocardial infarction. We prospectively examined whether preconditioning by sevoflurane would decrease late cardiac events in patients undergoing coronary artery bypass graft (CABG) surgery. METHODS: Seventy-two patients scheduled for elective CABG surgery were randomized to preconditioning by sevoflurane (10 min at 4 vol%) or placebo. For all patients, follow-up of adverse cardiac events was obtained 6 and 12 months after surgery. Transcript levels for platelet-endothelial cell adhesion molecule-1 (PECAM-1/CD31), catalase and heat shock protein 70 (Hsp70) were determined in atrial biopsies after sevoflurane preconditioning. RESULTS: Pharmacological preconditioning by sevoflurane reduced the incidence of late cardiac events during the first year after CABG surgery (sevoflurane 3% vs 17% in the placebo group, log-rank test, P=0.038). One patient in the sevoflurane group and three patients in the placebo group experienced new episodes of congestive heart failure and three additional patients had coronary artery reocclusion. Perioperative peak concentrations for myocardial injury markers were higher in patients with subsequent late cardiac events [NTproBNP, 9031 (4125) vs 3049 (1906) ng litre(-1), P<0.001; cTnT, 1.31 (0.88) vs 0.46 (0.29) microg litre(-1), P<0.001]. Transcript levels were reduced for PECAM-1 and increased for catalase but unchanged for Hsp70 in atrial biopsies after sevoflurane preconditioning. CONCLUSIONS: This prospective randomized clinical study provides evidence of a protective role for pharmacological preconditioning by sevoflurane in late cardiac events in CABG patients, which may be related to favourable transcriptional changes in pro- and antiprotective proteins.

Adult↗
PubMed1981

Histamine release from human right atrium.

Histamine release has been detected biologically after exposure of human right atrial biopsy samples to compound 48/80. Human right atrial samples contain large quantities of histamine, 1035 +/- 65 ng/g fresh weight. Exposure of untreated electrically paced atrial strips to compound 84/80, 300 micro/ml, caused an increase in the force of atrial contraction similar to that caused by histamine. Pretreatment of strips with cimetidine, 3.16 x 10(-5) M, prevented the inotropic response to compound 48/80. It is concluded that mast cell degranulation in human atrial tissue can cause sufficient release of histamine to modify the function of the heart.

Heart Atria↗
PubMed1993

Acetylcholinesterase changes in hearts with sinus rhythm and atrial fibrillation.

1. Clinical and experimental evidence suggest that changes in the autonomic tone play a role in the pathogenesis of atrial fibrillation. 2. We have studied the distribution of molecular forms of acetylcholinesterase (AChE) in atrial biopsies obtained from individuals without arrhythmias and in patients with atrial fibrillation. 3. Analysis of the distribution of globular and asymmetric AChE forms, showed a decrease in the amount of the globular forms of biopsies taken from atria during fibrillation. 4. This study is the first attempt to characterize the molecular forms of AChE in the human heart of patients with sinus rhythm and chronic atrial fibrillation.

Acetylcholinesterase↗
PubMed1998

Effect of L-carnitine on myocardial metabolism: results of a balanced, placebo-controlled, double-blind study in patients undergoing open heart surgery.

The effects of L-carnitine on cardiac performance after open heart surgery were evaluated in a balanced, placebo-controlled, double-blind study in 38 patients. Preoperative haemodynamic status was good in all of them. Seventeen subjects underwent mitral valve replacement and 19 patients coronary artery bypass grafting. Five grams L-carnitine were given intravenously over 2 h, twice daily for 5 consecutive days; moreover, 10 g L-carnitine in 1500 ml cardioplegia were administered through the aortic root after aortic cross-clamping. Surgery was always planned on treatment day 3. The post-ischaemic functional recovery of the heart was assessed by clinical parameters, as well as by biochemical and ultrastructure evaluations on biopsy specimens. No differences were found between the control and the treatment group with respect to all clinical parameters of cardiac performance after cardiopulmonary bypass. At anaesthesia induction, serum carnitine was significantly increased in treated patients, but carnitine concentrations in the right atrial biopsy obtained just before aortic declamping were similar in the two groups. In patients with mitral valve replacement, L-carnitine therapy was associated with significantly higher concentrations of pyruvate, ATP and creatine phosphate in papillary muscle. Glycogen levels were also higher in the treated group, but the difference was not statistically significant. Myocardial ultrastructure on septal biopsies, obtained within 5 min from weaning from extracorporeal circulation, showed better preservation scores for all considered parameters (nucleus, sarcoplasmic reticulum, mitochondria and cellular oedema) in the treated subjects, although the difference reached statistical significance only for nuclei. When biochemical and ultrastructural data are considered, these findings suggest that L-carnitine improves myocardial metabolism. However, it cannot be concluded that L-carnitine provides an advantageous support therapy for well-compensated patients requiring cardiac surgery. In contrast, the positive effects of L-carnitine on cardiac recovery after bypass might become clinically relevant in the surgical setting for haemodynamically compromised patients, in which further investigations are required.

Aged↗
PubMed1987

Some aspects of the mitochondrial oxidative metabolism in human atrial tissue during cardiopulmonary by-pass.

Following previous research on the hypoxic cell in human circulatory shock, the present work has investigated some mitochondrial oxidative aspects in atrial biopsies taken during cardiopulmonary by-pass. Cardioplegic solution and hypothermia were administered to 10 patients and the atrial samples were collected before and after aortic clamping. The results show a cellular protective effect of cardioplegia and hypothermia on the electron-transport chain, even if the enzymes with high KmO2 appear to be more sensitive to ischaemia. The results suggest a metabolic injury rather than an oxidative damage due to the induced ischaemia, alterations to fatty-acid beta-oxidation being especially notable. Because of the unchanged oxidative capacities, the oxyradical generation and the peroxidative damage appear to be irrelevant in the ischaemic period and during the course of reperfusion. Further studies are needed to elucidate the metabolic damage and the therapeutic implications due to the induced ischaemia in the myocardial cell during the aortic clamping.

Adult↗
PubMed2000

Changes in ultrastructural calcium distribution in goat atria during atrial fibrillation.

It has been suggested that Ca(2+)content of atrial cardiomyocytes is increased at the onset of atrial fibrillation (AF). Whether this phenomenon is transient is currently unknown. Therefore, in this study the time-related changes in Ca(2+)location in atrial myocytes from goats with chronic AF have been investigated. The distribution of calcium was assessed with the electron microscope using the cytochemical phosphate-pyroantimonate and oxalate-pyroantimonate methods in atrial biopsies from goats in sinus rhythm and goats with 1-16 weeks of burst-pacing-induced AF. In atrial myocytes from control goats in sinus rhythm, a normal Ca(2+)distribution was observed, with regular deposits along the sarcolemma (an average of 3.4 deposits per microm at a regular distance). The number of sarcolemma-bound Ca(2+)deposits substantially increased after 1 and 2 weeks of atrial fibrillation. After this period the amount of Ca(2+)precipitate decreased at 4 and 8 weeks, and became below control level at 16 weeks. A similar time-related redistribution of Ca(2+)occurred in mitochondria. Whereas mitochondria from control goats displayed very few Ca(2+)deposits (average 4.0 deposits per micro m(2)), their number markedly increased after 1 and 2 weeks of atrial fibrillation, which indicates cellular Ca(2+)overload. From 4 weeks, Ca(2+)deposits reached control levels and were below control level after 16 weeks of atrial fibrillation (2.5 deposits per microm(2)). Our findings are consistent with the previously observed Ca(2+)overload early after the onset of atrial fibrillation. The present study shows that this overload persists for at least 2 weeks, after which the cardiomyocytes apparently adapt to a new Ca(2+)homeostasis, thereby avoiding Ca(2+)overload. This protection against Ca(2+)overload co-occurs with dedifferentiation like cellular remodeling.

Animals↗