Plasma C-Reactive Protein Is Not Related to Sinus Non-Conversion by Maze Procedure Adjunct to Mitral Valve Surgery

In Framingham cohort study, C-reactive protein was not associated with incident atrial fibrillation (AF) after adjustment for left atrial size. This study examined whether levels of plasma inflammatory markers would be significant risk factors for failed maze procedure for AF. This study enrolled 88 patients with mitral valve disease undergoing valve surgery (n = 32, sinus control group) or concomitant maze procedure for persistent atrial fibrillation (AF) (n = 56, AF group). The mean follow-up in the AF group was 55.0 ± 17.5 months. The AF and sinus control groups did not differ in preoperative levels of C-reactive protein (p = 0.636). In the AF group receiving maze procedure, the sinus conversion (n = 37) and non-conversion (n = 19) groups did not significantly differ in preoperative levels of interleukin-6 (p = 0.607) and tumor necrosis factor-α (p = 0.379). In multivariate analysis after adjustment for preoperative plasma inflammatory markers, independent factors associated with sinus conversion were AF duration (p =0.003), and left atrial area (p = 0.014). In conclusion, plasma inflammatory markers are not associated with sinus non-conversion by radiofrequency maze procedure.     

Preoperative atrial histological changes are not associated with postoperative atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) remains the most common complication of cardiac surgery. Prophylactic therapies have been studied, but their utility has been limited by the inability to accurately identify patients who will develop this complication. Recent studies have suggested that atrial myolysis and lipofuscin pigmentation are associated with post-coronary artery bypass grafting (CABG) AF. We sought to determine whether there is an association between preoperative atrial histology and subsequent post-CABG AF. METHODS: Samples of right atrial appendage were obtained from 94 patients undergoing CABG. Tissue was formalin fixed and paraffin embedded. Sections 4 mum thick were cut, stained with hematoxylin and eosin, and examined for the following parameters: fibrosis, myolysis, inflammation, nuclear size, pericardial exudates, lipofuscin pigment, arteriolar hypertrophy, contraction banding, mesothelial hyperplasia, and atrial diverticula. Results were graded as absent, mild, moderate, or severe by two independent observers who were blinded to the clinical outcomes. Univariate and multivariate analyses were carried out. RESULTS: Thirty-six (38%) patients developed AF. No correlation was found between the 10 features assessed, including myolysis and lipofuscin pigmentation, and the development of AF. CONCLUSION: Simple morphology of right atrial appendages does not predict the development of postoperative AF.     

Atrial fibrillation may be a vascular disease: the role of the pulmonary vein

Recent years have seen an enormous amount of experimental and clinical research into role of the pulmonary veins (PVs) in atrial fibrillation (AF). The PVs contain cardiomyocytes with easily inducible arrhythmogenic activity due to the enhanced automaticity, induction of triggered activity, and genesis of microreentrant circuits. The enhanced automaticity, induced triggered activity, either alone or in combination with the reentrant mechanisms, may play a role in the initiation of PVs AF. Detailed mapping studies suggest that reentry within the PVs is most likely responsible for their arrhythmogenicity. There is no doubt that the PVs represent the most important source of arrhythmogenic activity in patients with paroxysmal AF. In AF patients with risk factors for development of AF, the presence of the pathological situation is important in enhancing the PV arrhythmogenic activity. Coronary sinus or superior vena cava may also be a source of rapid repetitive electrical activity during AF. Thus, AF should be considered a kind of vascular disease. Moreover, in patients with paroxysmal AF originating from the PVs, a wide spectrum of atrial arrhythmias may coexist, including paroxysms of atrial premature, tachycardia, flutter and fibrillation. This kind of arrhythmias should be named as PV atrial arrhythmias. These new views will help understand the mechanism, diagnosis and treatment method for AF.     

Syndecan-4 shedding is involved in the oxidative stress and inflammatory responses in left atrial tissue with valvular atrial fibrillation

Oxidative stress and inflammation play critical roles in the development and maintenance of atrial fibrillation (AF). In addition, syndecan-4 (Synd4) shedding induced by oxidative stress or inflammation plays a role in the migration of inflammatory cells. Therefore, we hypothesized that Synd4 shedding was also involved in the inflammatory response in atrial fibrillation patients with valvular heart disease. To confirm this suppose, left atrial appendages and clinical data were obtained from 65 patients with valvular disease undergoing valve surgery. Ten left atrial appendages obtained from healthy heart donors were used as controls. Analyses including histopathology, western blotting, and enzyme kinetics were performed to assess the oxidative injury, inflammation responses, and Synd4 shedding. The results showed that the inflammatory response and oxidative injury were increased significantly, whereas as levels of the Synd4 ectodomain was decreased significantly in AF patients. Furthermore, Synd4 ectodomain levels were correlated with atrial oxidative and inflammatory markers. The results showed that Synd4 shedding is a molecular pathological alteration in the development and maintenance of inflammation-associated AF.     

Lipomatous hypertrophy of the interatrial septum: an overview

Lipomatous hypertrophy of the interatrial septum is a rare, but increasingly recognized, anomalous developmental or neoplastic lesion of the heart. This entity was first described in 1964 at autopsy and is identified before death based on its distinctive characteristics on echocardiography, computed tomography, and magnetic resonance imaging. Although it is often asymptomatic, the mass has been associated with supraventricular arrhythmias and sudden death. In rare patients who experience intractable symptoms, surgical excision of the lesion may provide relief. Therefore, lipomatous hypertrophy of the interatrial septum is of interest to the pathologist when a cardiac mass is received for evaluation or at autopsy when a patient has experienced sudden death from an unknown cause.     

Diagnosis of cardiac thrombosis in patients with atrial fibrillation in the absence of macroscopically visible thrombi

Summary Cardiac thrombosis due to atrial fibrillation (AF) has been recognized as the most common cause of cerebral embolism. However, sometimes no macroscopic thrombus is found at autopsy in the heart of a victim of this type of cerebral embolism. We investigated morphological changes in the left atrial endocardium of 31 patients (including 21 cases with AF) who had died of cerebral embolism. Rough endocardium (RE) seen macroscopically provided evidence for the existence of atrial thrombosis. The RE that appeared in AF cases was due to a granular and wrinkled appearance of the endocardium associated with oedematous and fibrous thickening. Fibrin-thread deposits were also always distinguishable. Mural thrombi and oedema with neutrophil infiltration in the subendocardium could be seen under the microscope. Small areas of endothelial denudation and thrombotic aggregations were commonly observed by scanning electron microscopy (SEM). These SEM lesions were significantly more frequent in cases with AF than in controls (P< 0.001). The diagnostic success rate for atrial thrombosis among cases with AF increased from 33.3% to 81% when thrombi proven by histological investigation of the areas with RE were added. Left atrial RE may be an anatomically relevant finding for the existence of atrial thrombosis with AF, when the thrombosis cannot be detected upon gross observation at autopsy.     

CLINICAL REPORT OF MODIFIED MAZE PROCEDURE

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Alternative energy sources for surgical treatment of atrial fibrillation in patients undergoing mitral valve surgery: microwave ablation vs cryoablation

The study aim was to compare maze outcomes using microwave ablation or cryoablation in patients with mitral disease and atrial fibrillation (AF). Between 1999 and 2005, 340 patients underwent mitral valve surgery and concomitant maze procedure involving either microwave ablation (n=96, MW group) or cryoablation (n=244, Cryo group). Mean age at operation was 50.0±12.5 yr. Follow-up period was 46.1±28.2 months. The Cryo group showed a longer aortic clamping time than the MW group (P=0.005). There were no differences in operative mortality and morbidity rates. The unadjusted 5-yr AF free rate was 61.3±1.2% in the MW group and 79.9±3.2% in the Cryo group (P=0.089). After adjustment, the MW group only showed a tendency toward more frequent AF recurrence than the Cryo group (Hazard ration 1.66, 95% confidence interval 0.89 to 3.07). Multivariate analysis revealed that older patient age (P<0.001) and greater left atrial size (P<0.001) were independent risk factors for AF recurrence. Although the use of microwave ablation results in shorter aortic clamping time, it has a tendency toward more frequent late AF recurrence than with cryoablation.     

Association between high grade ventricular arrhythmia and extent of left ventricular hypertrophy in hypertrophic cardiomyopathy.

The association between the extent of left ventricular (LV) hypertrophy and severity of ventricular or atrial arrhythmias are examined. Two-dimensional echocardiography and 24-h Holter electrocardiography monitoring were performed in 60 patients with hypertrophic cardiomyopathy (HCM). According to the distribution of the LV hypertrophy, the patients were divided into three groups: 1. Apical hypertrophy (APH), 2. Septal hypertrophy, and 3. Extensive hypertrophy. Ventricular arrhythmias were found in 82% of the patients and supraventricular arrhythmias were detected in 70% of the patients. Lown grade III and IV arrhythmias occurred significantly more frequently in patients with extensive than with septal hypertrophy. Lown grade III to IV arrhythmias did not occur in patients with APH. Present results show a significant association between the extent of LV hypertrophy and the severity of ventricular arrhythmias in HCM.     

Pulmonary veins and atrial fibrillation: a pathological study of 100 hearts

Pathogenesis of atrial fibrillation (AF), the most common sustained heart arrhythmia, is not yet fully elucidated. Recent electrophysiological studies have shown that in most patients with AF the arrhythmia is triggered by ectopic beats originating from extensions of left atrial myocardium over the pulmonary veins (PVs), so called myocardial sleeves (MSPV). A total of 100 hearts (393 PVs) obtained at autopsy were prospectively studied - 50 from patients with chronic AF (average age 76.9 +/- 7.3 yrs.) and a control group of 50 with a sinus rhythm (aver. age 71.7 +/- 9.5 yrs.). This is a largest study published on this topic so far. It appeared that MSPV frequently harbour pathological lesions, particularly senile atrial amyloid, and scarring. These two pathological changes were evaluated semiquantitatively on a grade 0-3 basis in individual PVs, comparing the results in the AF vs. the control group. Amyloidosis of MSPV was found in 68 % of all hearts and in 55 % of all sleeves. The deposits were most marked in the right superior PV. Amyloidosis was more frequent and more severe in MSPV of patients with AF (58.5 %; average grade 0.89) than of those without AF (51.7 %; aver. grade 0.76); the differences, however, lack statistical significance. Scarring of MSPV was present in all 349 sleeves, more markedly in the left inferior, left superior, and right superior PVs. It was significantly more severe in patients with AF compared to those without the arrhythmia. By an injection metod, we have shown that MSPV are supplied by coronary arteries. However, the degree of scarring of the sleeves did not correlate with the degree of coronary atherosclerosis. We suggest that genesis of the scarring is not postnecrotic but degenerative, due to diffuse hypoxia of the sleeve myocardium. To conclude, amyloidosis and particularly scarring of MSPV appear generally in the elderly population as an arrhythmogenic substrate for AF.     

Lipomatous hypertrophy of the cardiac interatrial septum

Lipomatous hypertrophy of the interatrial septum (LHIS) is a rare lesion of unknown origin usually diagnosed as an incidental finding during autopsy. It can be associated with supraventricular arrhythmias, venous return obstruction and sudden cardiac death. Five necropsy cases (4 females, 1 male) of LHIS were encountered during the last 31 years; only one case from this series was diagnosed ante mortem. The patients' mean age was 68 years; their mean BMI was 28.4. The mean size of the lesion was 31 mm. In three patients the LHIS was asymptomatic, two patients experienced relapsing multifocal atrial tachycardia and sick sinus syndrome, respectively. Histologically, all cases consisted of a mixture of mature and brown adipose tissue with foci of cardiomyocytes. For a pathologist the knowledge of LHIS is important because of an increasing possibility of its ante mortem diagnosis by imaging methods with a following endomyocardial biopsy, and also because it may appear as a cause of sudden cardiac death.     

Juxtaposition of atrial appendages. Reinterpretation as an accessory appendage or atrial diverticulum

The pathological features of 13 cases with juxtaposition of the atrial appendages in the autopsy files of The Johns Hopkins Hospital were studied. The anomaly occurs most frequently in association with transposition of the great vessels, ventricular septal defect, patent foramen ovale, and obstructive lesions of the tricuspid and pulmonic valves. The malformation complex of tricuspid atresia, atrial and ventricular septal communication, and the transposition of the great vessels seems particularly common with juxtaposition of the atrial appendage. A recent case showed a small accessory right atrial appendage lying in juxtaposition to the left atrial appendage. In addition, a normally situated right atrial appendages in addition to well-formed accessory appendages lying in juxtaposition to the left atrial appendages. It seems that juxtaposition of the atrial appendages should be reinterpreted as an accessory appendage or atrial diverticulum.     

Pathophysiological mechanisms of atrial fibrillation: a translational appraisal

Atrial fibrillation (AF) is an arrhythmia that can occur as the result of numerous different pathophysiological processes in the atria. Some aspects of the morphological and electrophysiological alterations promoting AF have been studied extensively in animal models. Atrial tachycardia or AF itself shortens atrial refractoriness and causes loss of atrial contractility. Aging, neurohumoral activation, and chronic atrial stretch due to structural heart disease activate a variety of signaling pathways leading to histological changes in the atria including myocyte hypertrophy, fibroblast proliferation, and complex alterations of the extracellular matrix including tissue fibrosis. These changes in electrical, contractile, and structural properties of the atria have been called "atrial remodeling." The resulting electrophysiological substrate is characterized by shortening of atrial refractoriness and reentrant wavelength or by local conduction heterogeneities caused by disruption of electrical interconnections between muscle bundles. Under these conditions, ectopic activity originating from the pulmonary veins or other sites is more likely to occur and to trigger longer episodes of AF. Many of these alterations also occur in patients with or at risk for AF, although the direct demonstration of these mechanisms is sometimes challenging. The diversity of etiological factors and electrophysiological mechanisms promoting AF in humans hampers the development of more effective therapy of AF. This review aims to give a translational overview on the biological basis of atrial remodeling and the proarrhythmic mechanisms involved in the fibrillation process. We pay attention to translation of pathophysiological insights gained from in vitro experiments and animal models to patients. Also, suggestions for future research objectives and therapeutical implications are discussed.     

Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy

In patients with hypertension, a pattern of left ventricular hypertrophy on the electrocardiogram is associated with a risk of sudden death in excess of the risk attributable to hypertension alone. We therefore investigated the frequency of complex ventricular arrhythmias by means of 48-hour ambulatory electrocardiographic monitoring in 100 treated hypertensive patients, of whom 50 had electrocardiographic evidence of left ventricular hypertrophy and 50 did not, and in 50 normotensive controls. The groups were matched for age, sex, and smoking habits, and the two hypertensive groups were matched for blood-pressure levels before and after antihypertensive therapy. Nonsustained ventricular tachycardia, defined as greater than or equal to 3 complexes at a rate greater than or equal to 120 beats per minute, occurred in 14 (28 percent) of the 50 patients with an electrocardiographic pattern of left ventricular hypertrophy, in 4 (8 percent) of the 50 patients without hypertrophy (P less than 0.05), and in 1 (2 percent) of the control subjects. Eight of the 50 patients (16 percent) with hypertrophy had episodes of nonsustained ventricular tachycardia longer than 5 complexes, whereas no patients without hypertrophy and no controls had such episodes. The group with nonsustained ventricular tachycardia was characterized by a high left ventricular mass on echocardiography and a high prevalence of ST-T abnormalities on electrocardiography. Ventricular tachycardia was not closely related to blood-pressure levels, nor was it associated with diuretic therapy or hypokalemia. The clinical importance of these arrhythmias is uncertain. Nevertheless, our data suggest that complex ventricular arrhythmias occur commonly in hypertensive patients with left ventricular hypertrophy and may contribute to the higher incidence of sudden death in these patients.     

A wearable real-time telemonitoring electrocardiogram device compared with traditional Holter monitoring

Arrhythmias are very common in the healthy populations as well as patients with cardiovascular diseases. Among them, atrial fibrillation (AF) and malignant ventricular arrhythmias are usually associated with some clinical events. Early diagnosis of arrhythmias, particularly AF and ventricular arrhythmias, is very important for the treatment and prognosis of patients. Holter is a gold standard commonly recommended for noninvasive detection of paroxysmal arrhythmia. However, it has some shortcomings such as fixed detection timings, delayed report and inability of remote real-time detection. To deal with such problems, we designed and applied a new wearable 72-hour triple-lead H3-electrocardiogram (ECG) device with a remote cloud-based ECG platform and an expert-supporting system. In this study, 31 patients were recruited and 24-hour synchronous ECG data by H3-ECG and Holter were recorded. In the H3-ECG group, ECG signals were transmitted using remote real-time modes, and confirmed reports were made by doctors in the remote expert-supporting system, while the traditional modes and detection systems were used in the Holter group. The results showed no significant differences between the two groups in 24-hour total heart rate (HR), averaged HR, maximum HR, minimum HR, premature atrial complexes (PACs) and premature ventricular complexes (PVCs) (P>0.05). The sensitivity and specificity of capture and remote automatic cardiac events detection of PACs, PVCs, and AF by H3-ECG were 93% and 99%, 98% and 99%, 94% and 98%, respectively. Therefore, the long-term limb triple-lead H3-ECG device can be utilized for domiciliary ECG self-monitoring and remote management of patients with common arrhythmia under medical supervision.     

Atrial expression of endothelial nitric oxide synthase in patients with and without atrial fibrillation

BackgroundAtrial fibrillation (AF) is associated with oxidative stress within the fibrillating atrial myocardium. Experimental studies suggest that reduced levels of nitric oxide (NO) caused by down-regulation of the NO synthase (eNOS) contribute to the development of prothrombotic endocardial remodeling in AF. This study was designed to determine the endocardial expression of eNOS in atrial tissue samples from patients with and without AF.MethodsTissue microarrays were used to analyze right atrial tissue specimens obtained from 234 patients (38 with AF; 196 with sinus rhythm) for differences in atrial eNOS expression. In selected patients, immunohistological results were confirmed by Western blotting.ResultsImmunohistochemical analyses showed that eNOS is expressed by endocardial cells and myocytes. However, endocardial expression of eNOS was not independently related to AF per se. There was no difference between paroxysmal and persistent AF. Clinical factors like gender (P=.05) and coronary artery disease (P=.06) were associated with down-regulation of eNOS. Interestingly, diabetes mellitus (P=.02) was associated with an up-regulation of endocardial eNOS, whereas other risk factors for thromboembolic events did not influence eNOS levels. Multivariable analysis showed that eNOS expression is influenced by interactions between diabetes mellitus and AF (P=.09) as well as by interactions between gender and AF (P=.04). Lowest levels of eNOS were found in women with AF.ConclusionAF does not independently effect atrial eNOS expression in humans. Due to the nonuniform regulation of endocardial eNOS expression, it appears unlikely that down-regulation of eNOS is a final common pathway for the development of prothrombotic endocardial remodeling, since classical risk factors for thromboembolic events do not reduce endocardial eNOS protein.     

Postmortem findings in morbidly obese individuals dying after gastric bypass procedures

Mortality has been reported to complicate gastric bypass, with common causes of death attributable to anastomotic leaks, sepsis, hemorrhage, and bowel obstruction. We evaluated autopsy reports from 10 patients having undergone gastric bypass. Medical records were reviewed to identify comorbidities. Data of interest included preoperative electrocardiogram (EKG) abnormalities, cause of death, body weight, anastamosis appearance, heart weight, extent of coronary artery disease, ventricular size, liver weight, and gall bladder status. A total of 7 men and 3 women were autopsied. Average age was 40 years (range, 30-49 years), and mean body mass index at autopsy was 60.3 kg/m(2) (range, 33.2-80.9 kg/m(2)). Evidence of anastomotic leaks was present in 7 cases, resulting in 4 deaths. Death was attributed to pulmonary embolism in one case. There were 5 cardiac-related deaths, all attributed to arrhythmias. Microscopic evidence of coronary artery disease was observed in 6. Cardiomegaly was seen in all patients, left ventricular hypertrophy in 8, right ventricular hypertrophy in 3, and hepatomegaly in all 10. Nine patients were status post cholecystectomy. Of the 8 preoperative EKG available, abnormalities were identified in 5. After gastric bypass, death was attributed to cardiac-related causes, pulmonary embolism, and operative complications. A significant proportion of cardiac-related deaths occured in the absence of atherosclerosis. Most patients had preoperative EKG abnormalities. As a high incidence of cardiomegaly was observed, operative stress associated with the procedure may increase the risk of arrhythmia in morbid obesity. Consequently, in morbidly obese patients, a detailed preoperative cardiovascular evaluation is warranted to reduce postoperative mortality.     

Light and electron microscopic features of surgically excised left atrial appendage in rheumatic heart disease patients with atrial fibrillation and sinus rhythm

IntroductionThere are few studies comparing the pathology of the remodeled substrate in patients of rheumatic heart disease with atrial fibrillation (AF) and normal sinus rhythm (NSR).MethodsThe study group comprised 30 patients with rheumatic heart disease undergoing mitral valve replacement. Excised left atrial appendages of these patients [17 with persistent AF and 13 NSR (control group)] were subjected to light and electron microscopic examination.ResultsThe histopathological findings of the myocardium were characterized by cardiomyocyte hypertrophy (CH), nuclear enlargement (NE), perinuclear clearing (PC), sarcoplasmic vacuolation (SV), fibrosis, and inflammation in the patients with AF and NSR. NE (17/17 vs. 4/13; P= .004), PC (17/17 vs. 4/13; P= .004), SV (17/17 vs. 9/13; P= .06), and fibrosis (15/17 vs. 3/13; P= .001) were all significantly more common in patients with AF. Inflammatory cells were observed in 9/17 patients of AF as compared to 1 in NSR patients (9/17 vs. 1/13; P= .02). CH was common in the patients with AF as compared with those in NSR (17/17 vs. 10/13; P= .103).In AF patients, electron microscopy revealed cardiomyocytes with depletion of the contractile elements (Z-bands), glycogen particle accumulation, and an increase in mitochondria. Cells severely affected by AF showed loss of contractile elements with extensive areas of SV, presence of myelin figures, and mitochondrial aggregates. Majority of AF cases showed extensive fibrosis in the form of collagen bundles in the interstitium.ConclusionThe left atrial substrate in AF as compared with NSR, in rheumatic heart disease patients, is associated with significant degenerative remodeling and ongoing inflammation that is associated with extensive fibrosis.     

Atrial fibrillation, blood loss, and transfusion in patients with left ventricular dysfunction: what is the effect of cardiopulmonary bypass?

Despite advancements in surgical technique, intensive care methods and pharmaceutical prophylaxis atrial fibrillation (AF) after on-pump coronary artery bypass remains common. Transfusion, blood loss, and cardiopulmonary bypass (CPB) have been identified as risk factors for AF and adverse outcomes such as early mortality. This study examines outcomes in patients with left ventricular dysfunction after revascularization with and without CPB. A systematic literature review identified 22 studies including 7,454 patients. Meta-analysis through subgroup analysis of the highest-quality studies revealed that the off-pump coronary artery bypass (OPCAB) technique is associated with a significantly lower incidence of blood loss, transfusion requirement, reoperation for bleeding, and length of stay. There was also a reduction in the incidence of AF in the OPCAB group but this was not statistically significant (odds ratio = 0.77, 95% confidence interval 0.58-1.02, p = 0.07). The results strengthen research suggesting that CPB has a damaging effect on hemostasis and subsequent transfusion requirements in this patient group. More research is required to assess the association between OPCAB and AF in patients with ventricular dysfunction.     

Psychiatric symptoms, type A behavior, and arrhythmias following coronary bypass

One hundred four patients undergoing coronary bypass surgery were evaluated for psychiatric symptoms and their association with postoperative arrhythmias occurring within 48 hours after surgery. Patients high in type A behavior had increased risk of ventricular arrhythmias, while those scoring relatively high in depression and anxiety had fewer atrial arrhythmias than patients low in these measures. No significant association was found between postoperative arrhythmias and obesity, heavy tobacco use, or number of bypasses. A history of arrhythmias correlated significantly with postoperative arrhythmias. Anxious or depressed patients who deny their symptoms may be at increased risk for postoperative atrial arrhythmias.