Effects of co-fermented Pleurotus eryngii stalk residues and soybean hulls by Aureobasidium pullulans on performance and intestinal morphology in broiler chickens.

Soybean hulls are a by-product of soybean processing for oil and meal production; Pleurotus eryngii stalk residues (PESR) are by-products of the edible portion of the fruiting body enriched in bioactive metabolites. This study evaluated the effects of co-fermented PESR and soybean hulls with Aureobasidium pullulans on performance and intestinal morphology in broiler chickens. The in vitro experimental results showed that xylananse and mannanase activity of solid-state fermented soybean hulls (100% SBH) and soybean hulls partially replaced with PESR (75:25, SHP) reached peak at day 12; solid-state fermentation (SSF) enhanced the total phenolic content and trolox equivalency in both products as well. Additionally, FSHP had higher xylotriose and mannobiose levels than fermented FSBH did. A total of 400 broilers (Ross 308) were assigned randomly into four groups receiving the basal diet (control) or the basal diet supplemented with 0.5% fermented SBH (0.5% FSBH), 0.5% fermented SBHP (0.5% FSHP) and 1.0% fermented SBHP (1.0% FSHP) until 35 d of age, respectively. Results demonstrated that 0.5% FSHP addition increased body weight gain as compared with corresponding normal diet fed control in birds during entire experimental period. Compared with the control group, 0.5% FSHP group significantly increased the ratio of lactic acid bacteria to Clostridium perfringens in ceca as well as ileum villus height and jejunum villus height/crypt depth ratio of 35 d old birds. In conclusion, 0.5% FSHP supplementation in the diet could obtain not only improved body weight gain, but optimal intestinal morphology by exerting its bioactive metabolite properties when fed to broilers.

Hydronephrosis: an unusual complication of neurogenic bowel in a patient with spinal cord injury: a case report.

STUDY DESIGN/METHODS: Case report. OBJECTIVES: In this case report, a consequence of not following proper care of the bowel affecting the genitourinary system is reported and discussed. SETTING: United States. RESULTS/CONCLUSION: Neurogenic bowel and bladder can result from a spinal cord injury. It is necessary for spinal cord injury patients to continually follow recommended bladder and bowel care programs to decrease complications.

A functional variant in the promoter region regulates the C-reactive protein gene and is a potential candidate for increased risk of atrial fibrillation.

OBJECTIVES: In a large population-based cohort, the level of C-reactive protein (CRP) in patients at baseline predicts an increased risk of future development of atrial fibrillation (AF). The mechanism of this increased risk is unknown. Furthermore, both the molecular effects of CRP on atrial myocytes and fibroblasts and whether genetic variants in the CRP gene predispose to AF are also unknown. METHODS: A genetic association study between CRP gene polymorphisms and AF was performed in two independent populations (I: 100 AF patients and 101 controls; II: 348 AF patients and 356 controls), with functional studies to elucidate the mechanism of association. RESULTS: Three polymorphisms (T-861C, A-821G and C-390A/C-390T) were found in the 1-kb promoter of CRP. A triallelic polymorphism (C-390A/C-390T) captured all haplotype information and determined the CRP gene promoter activity and the plasma CRP level, and was in nearly complete linkage disequilibrium with G1059C polymorphism in exon 2. The -390A variant was associated with a higher CRP gene promoter activity, a higher plasma CRP level and a higher risk of AF. Patients with AF also had a higher plasma CRP level than controls. CRP significantly increased the inward L-type calcium current in atrial myocytes with no changes in other ionic currents. CRP did not affect the expressions of type I alpha 1 (COL1A1), type III alpha 1 (COL3A1) and type 1 alpha 2 (COL1A2) procollagens in atrial fibroblasts. CONCLUSION: A CRP gene promoter triallelic polymorphism was associated with CRP gene promoter activity, determined the plasma level of CRP, and predicted the risk of AF. The mechanism of this may be via augmention of calcium influx by CRP in atrial myocytes, but not because of atrial fibrosis.

Gender difference in clinical and genetic characteristics of Brugada syndrome: SADS-TW BrS registry.

BACKGROUND: Brugada syndrome (BrS) is a heritable sudden cardiac death (SCD) disease with male predominance. Information on gender difference of BrS remains scarce. AIM: To investigate the gender difference of BrS in Han Chinese. DESIGN: We consecutively enrolled 169 BrS patients (153 males and 16 females) from Han Chinese in Taiwan from 1998 to 2017. METHODS: Clinical characteristics, electrocardiographic parameters and SCN5A mutation status were compared between genders. RESULTS: The percentage of family history of SCD in females was slightly higher (31.3% vs. 15%, P = 0.15). Females exhibited longer QTc (457.8 ± 33.0 vs. 429.5 ± 42.1 ms, P < 0.01). Regarding cumulative event occurrence by age, Mantel-Cox test showed females had earlier age of onset of first cardiac events (SCD or syncope) than males (P = 0.049), which was mainly attributed to syncope (P < 0.01). Males with SCD exhibited longer QRS duration (114.2 ± 26.8 vs. 104.8 ± 15.3 ms, P = 0.02) and QTc (442.5 ± 57.4 vs. 422.9 ± 28.8 ms, P = 0.02). Males with syncope exhibited longer PR interval (181.2 ± 33.7 vs. 165.7 ± 27.1 ms, P = 0.01), whereas females with SCD or syncope had a trend towards slower heart rates (69.1 ± 9.6 vs. 82.2 ± 16.3 bpm, P = 0.10) than female with no or mild symptoms. There was no difference in the percentage of SCN5A mutation between genders. CONCLUSION: Gender difference is present in BrS. Females have longer QTc and suffer from syncope earlier than males. Risk of SCD in males is associated with boarder QRS complex and longer QTc, whereas risk of syncope is associated with longer PR interval in males and slower heart rate in females.

Renin-angiotensin system gene polymorphisms and diastolic heart failure.

BACKGROUND: Diastolic heart failure (DHF) refers to an abnormality of diastolic distensibility, filling or relaxation of the left ventricle. The genetic study of DHF is scarce in the literature. The association of renin-angiotensin system (RAS) and DHF are well known. We hypothesized that RAS genes might be the susceptible genes for DHF and conducted a case-control study to prove the hypothesis. MATERIALS AND METHODS: A total of 1452 consecutive patients were analysed and 148 patients with a diagnosis of DHF confirmed by echocardiography were recruited. We had two control populations. The first controls consisted of 286 normal subjects while the second were 148 matched controls selected on a 1-to-1 basis by age, sex, hypertension, diabetes and medication use. The angiotensin-converting enzyme (ACE) gene insertion/deletion polymorphism; multilocus polymorphisms of the angiotensinogen gene; and the A1166C polymorphisms of the angiotensin II type I receptor (AT(1)R) gene were genotyped. RESULTS: In a single-locus analysis, the odds ratios (ORs) for DHF were significant with the ACE DD genotype and the AT(1)R 1166 CC plus AC genotype. In addition, the concomitant presence of ACE DD and AT(1)R 1166 CC/AC genotypes synergistically increased the predisposition to DHF. CONCLUSIONS: Genetic variants in the RAS genes may determine an individual's risk to develop DHF. There is also a synergistic gene-gene interaction between the RAS genes in the development of DHF.

C-reactive protein gene polymorphism predicts the risk of thromboembolic stroke in patients with atrial fibrillation: a more than 10-year prospective follow-up study.

Essentials We studied the C-reactive protein (CRP) gene on stroke risk in atrial fibrillation (AF) patients. 725 patients with CRP triallelic polymorphism genotype were followed-up for more than 10 years. Patients with the A-390/T-390 allele of the CRP gene were more likely to get ischemic stroke. The triallelic polymorphism of the CRP is related to ischemic stroke in AF patients. SUMMARY: Background Little evidence is available regarding the impact of genetic polymorphisms on the risk of thromboembolic stroke in patients with atrial fibrillation (AF). An increasing body of evidence is demonstrating that inflammatory responses play an important role in the pathophysiology of AF. Objectives To investigate the effect of genetic polymorphisms of the C-reactive protein (CRP) gene on the incidence of thromboembolic stroke in patients with AF. Methods A total of 725 AF patients were longitudinally followed up for > 10 years; this is the largest and longest AF follow-up cohort with genetic data. CRP promoter triallelic polymorphisms (C-390A and C-390T) were genotyped, and CRP levels were divided into four quartiles. Results Patients with higher CRP levels were more likely to develop thromboembolic stroke than those with lower CRP levels (P<0.001, log-rank test for comparison of four quartiles). After adjustment for conventional risk factors, patients with higher CRP levels were more likely to develop thromboembolic stroke than those in the lowest CRP quartile (hazard ratio [HR] 2.27, 95% confidence interval [CI] 1.08-4.81; the lowest CRP quartile was the reference group). Patients carrying the A-390 or T-390 allele had higher CRP levels (3.35 ± 2.71 mg L-1 versus 2.43 ± 2.00 mg L-1 ), and were more likely to develop thromboembolic stroke, even after adjustment for conventional risk factors (HR 2.07, 95% CI 1.23-3.48). Conclusion The CRP triallelic polymorphism and the CRP level are associated with the risk of incident thromboembolic stroke in patients with AF.

Intravenous sotalol decreases transthoracic cardioversion energy requirement for chronic atrial fibrillation in humans: assessment of the electrophysiological effects by biatrial basket electrodes.

OBJECTIVES: This study was undertaken to assess the effects of sotalol on the transthoracic cardioversion energy requirement for chronic atrial fibrillation (AF) and on the atrial electrograms during AF recorded by two basket electrodes. BACKGROUND: The effects of sotalol infusion on transthoracic electrical cardioversion for chronic atrial fibrillation in humans have not been well investigated. METHODS: We included 18 patients with persistent AF for more than three months. Atrial electrograms were recorded by two basket electrodes positioned in each atrium respectively. Transthoracic cardioversion was performed before and after sotalol 1.5 mg/kg i.v. infusion. RESULTS: In the 14 patients whose AF could be terminated by cardioversion before sotalol infusion, the atrial defibrillation energy was significantly reduced after sotalol infusion (236 +/- 74 jules [J] vs. 186 +/- 77 J; p < 0.01). Atrial fibrillation was refractory to cardioversion in four patients at baseline and was converted to sinus rhythm by cardioversion after sotalol infusion in two of them. We further divided the patients into two groups. Group A consisted of 10 patients in whom the energy requirement was decreased by sotalol while group B consisted of eight patients in whom the energy requirement was not decreased. The mean A-A (atrial local electrogram) intervals during AF were significantly increased after sotalol infusion in both groups, but the increment of A-A interval was significantly larger in group A than it was in group B patients (36 +/- 13 ms vs. 22 +/- 8 ms for the right atrium; 19 +/- 7 ms vs. 9 +/- 7 ms for the left atrium; both p < 0.05). The spatial and temporal dispersions of A-A intervals were not significantly changed after sotalol infusion in both atria in both groups. CONCLUSIONS: Sotalol decreases the atrial defibrillation energy requirement by increasing atrial refractoriness but not by decreasing the dispersion of refractoriness.

Global distribution of atrial ectopic foci triggering recurrence of atrial tachyarrhythmia after electrical cardioversion of long-standing atrial fibrillation: a bi-atrial basket mapping study.

OBJECTIVES: The objective of this study was to assess the spatial distribution of atrial ectopic foci potentially triggering recurrent atrial tachyarrhythmias after electrical cardioversion of long-standing atrial fibrillation (AF). BACKGROUND: It remains unknown whether targeted ablation of atrial ectopic foci concentrated in the pulmonary veins is feasible in patients with long-standin

Down-regulation of L-type calcium channel and sarcoplasmic reticular Ca(2+)-ATPase mRNA in human atrial fibrillation without significant change in the mRNA of ryanodine receptor, calsequestrin and phospholamban: an insight into the mechanism of atrial electrical remodeling.

OBJECTIVES: We investigated the gene expression of calcium-handling genes including L-type calcium channel, sarcoplasmic reticular calcium adenosine triphosphatase (Ca(2+)-ATPase), ryanodine receptor, calsequestrin and phospholamban in human atrial fibrillation. BACKGROUND: Recent studies have demonstrated that atrial electrical remodeling in atrial fibrillation is associated with intracellular calcium overload. However, the changes of calcium-handling proteins remain unclear. METHODS: A total of 34 patients undergoing open heart surgery were included. Atrial tissue was obtained from the right atrial free wall, right atrial appendage, left atrial free wall and left atrial appendage, respectively. The messenger ribonucleic acid (mRNA) amount of the genes was measured by reverse transcription-polymerase chain reaction and normalized to the mRNA levels of glyceraldehyde 3-phosphate dehydrogenase. RESULTS: The mRNA of L-type calcium channel and of Ca(2+)-ATPase was significantly decreased in patients with persistent atrial fibrillation for more than 3 months (0.36+/-0.26 vs. 0.90+/-0.88 for L-type calcium channel; 0.69+/-0.42 vs. 1.21+/-0.68 for Ca(2+)-ATPase; both p < 0.05, all data in arbitrary unit). We further demonstrated that there was no spatial dispersion of the gene expression among the four atrial tissue sampling sites. Age, gender and underlying cardiac disease had no significant effects on the gene expression. In contrast, the mRNA levels of ryanodine receptor, calsequestrin and phospholamban showed no significant change in atrial fibrillation. CONCLUSIONS: L-type calcium channel and the sarcoplasmic reticular Ca(2+)-ATPase gene were down-regulated in atrial fibrillation. These changes may be a consequence of, as well as a contributory factor for, atrial fibrillation.

Supraventricular tachycardia in patients with right atrial isomerism.

OBJECTIVES: To clarify the prevalence and mechanism of supraventricular tachycardia in patients with right atrial isomerism. BACKGROUND: Paired SA and dual atrioventricular (AV) nodes have been described in patients with right atrial isomerism. However, the clinical significance remains unclear. METHODS: From 1987 to 1996, a total of 101 patients (61 male, 40 female) and four fetuses were identified with right atrial isomerism. The diagnosis of supraventricular tachycardia exclude the tachycardia with prolonged QRS duration or AV dissociation, and primary atrial tachycardia. RESULTS: The median follow-up duration was 38 months (range 0.2-270 months). Supraventricular tachycardia was documented in 25 patients (24.8%) and one fetus (25%) (onset age ranged from prenatal to 14 years old; median 4 years old). Actuarial Kaplan-Meier analysis revealed that the probability of being free from tachycardia was 67% and 50% at 6 and 10 years of age, respectively. These tachycardias could be converted by vagal maneuvers in one, verapamil in seven, propranolol in four, digoxin in two, procainamide in one, and rapid pacing in five. Spontaneous conversion was noted in six (including the fetus). Seven cases had received electrophysiological studies. Reciprocating AV tachycardia could be induced in five and echo beats in one. The tachycardia in three patients was documented as incorporating a posterior AV node (antegrade) and an anterior or a lateral AV node (retrograde). Two of them received radiofrequency ablation. Successful ablation in both was obtained by delivering energy during tachycardia, aimed at the earliest retrograde atrial activity and accompanied by junctional ectopic rhythm. The patient with echo beats developed tachycardia soon after operation. CONCLUSIONS: Supraventricular tachycardia is common in patients with right atrial isomerism and can occur during the prenatal stage. Drugs to slow conduction through the AV node may help to terminate the tachycardia. Radiofrequency ablation is a safe and effective treatment alternative to eliminate tachycardia.

Clinical and electrophysiologic characteristics and long-term efficacy of slow-pathway catheter ablation in patients with spontaneous supraventricular tachycardia and dual atrioventricular node pathways without inducible tachycardia.

OBJECTIVES: We sought to investigate the long-term efficacy of slow-pathway catheter ablation in patients with spontaneous, documented paroxysmal supraventricular tachycardia (PSVT) and dual atrioventricular (AV) node pathways but without inducible tachycardia. BACKGROUND: The lack of reproduction of clinical PSVT by programmed electrical stimulation, which is not uncommon in AV node reentrant tachycardia (AVNRT), is a dilemma in making the decision of the therapeutic end point of radiofrequency catheter ablation. METHODS: Twenty-seven patients (group A) with documented but noninducible PSVT and with dual AV node pathways were prospectively studied. Programmed electrical stimulation could induce a single AV node echo beat in 12 patients, double echo beats in 4 patients and none in 11 patients at baseline or during isoproterenol infusion. Of the patients in group A, 16 underwent slow-pathway catheter ablation and 11 did not. The clinical and electrophysiologic characteristics of the 27 patients were compared with those of patients with dual AV node pathways and inducible AVNRT (group B, n = 55) and patients with dual AV node pathways alone without clinical PSVT (group C, n = 47). RESULTS: During 23+/-13 months of follow-up, none of the 16 patients with slow-pathway catheter ablation had recurrence of PSVT. However, 7 of the 11 patients without ablation had PSVT recurrence at 13+/-14 months of follow-up (p < 0.03 by Kaplan-Meier analysis). Compared with groups B and C, group A consisted predominantly of men who had better retrograde AV node conduction and a narrower zone for anterograde slow-pathway conduction. CONCLUSIONS: Slow-pathway catheter ablation is highly effective in eliminating spontaneous PSVT in which the tachycardia is not inducible despite the presence of dual AV node pathways.

Polymorphism of the gene encoding a human minimal potassium ion channel (minK).

A gene (minK) that encodes a minimal potassium channel has been cloned recently. We describe in this paper a human minK sequence which differs from the original sequence with a single A-->G at position 112. This resulted in a change from a Ser codon (AGT) to a Gly codon (GGT) and created a new MspAI restriction site. Of the 32 alleles from 16 subjects studied, 25 had this newly discovered sequence and 7 had the previously described sequence.

Usefulness of pulmonary venous flow pattern and maximal mosaic jet area detected by transesophageal echocardiography in assessing the severity of mitral regurgitation.

Pulmonary venous flow pattern detected by transesophageal echocardiography (TEE) has been reported to be a good marker of mitral regurgitation (MR) severity. In 89 patients with MR detected by TEE, both pulmonary venous flow pattern and maximal mosaic jet area were recorded for evaluating the severity of MR. Cardiac catheterization was performed in all patients for grading the severity of MR. Systolic reversed flow in pulmonary veins was a good marker for angiographic grade 3 or 4 MR with a sensitivity of 97% (33 of 34) and specificity of 95% (52 of 55). Maximal mosaic jet area had a good correlation with the grading of MR (r = 0.79). When a maximal mosaic jet area of > 6 cm2 was used to detect grade 3 or 4 MR, the sensitivity and specificity were lower than those of the systolic reversed flow (sensitivity 82 vs 97%, p = 0.073; specificity 80 vs 95%, p = 0.013). The accuracy of systolic reversed flow was not influenced by the cardiac rhythm or jet eccentricity. However, the sensitivity of maximal mosaic jet area was lower in patients with an eccentric jet than in patients with a central jet (67 vs 95%, p = 0.046). In conclusion, systolic reversed flow in pulmonary veins detected by TEE is better than the maximal mosaic jet area in detecting grade 3 or 4 MR, especially in patients with eccentric jet.

Low-serum, high-density lipoprotein cholesterol concentration is an important coronary risk factor in Chinese patients with low serum levels of total cholesterol and triglyceride.

The significance of low-serum high-density lipoprotein concentrations (<35 mg/dl) with respect to coronary atherogenesis in Chinese patients with low levels of total serum cholesterol (<200 mg/dl) and triglycerides (<250 mg/dl) was assessed. Persons with such a lipid profile pattern were still at high risk, and high-density lipoprotein. like smoking, appeared to be the most predictive independent coronary risk factor.

Diagnostic accuracy of transesophageal echocardiography for detecting patent ductus arteriosus in adolescents and adults.

To compare the accuracy of transesophageal echocardiography (TEE) with that of transthoracic echocardiography (TTE) in the detection of patent ductus arteriosus (PDA) in the adolescent and the adult, 40 patients with PDA and 50 patients with other congenital heart diseases were studied. All echocardiograms were recorded before cardiac catheterization and surgery. The echocardiographic diagnosis of PDA was made by direct visualization of a shunt flow in the duct. A mosaic flow in the pulmonary artery without direct visualization of the duct was considered possible but not definitely diagnostic of PDA. TEE showed greater sensitivity and negative predictive value than TTE (97% vs 42%, and 98% vs 68%, respectively; p < 0.001) in confirming the diagnosis of PDA. The specificity and positive predictive value in establishing the diagnosis of PDA were the same for both techniques. In the subgroup of patients with Eisenmenger's syndrome, the sensitivity of TEE and TTE in confirming diagnosis of PDA was 100% and 12% (p < 0.01), respectively. The sensitivity of monoplane and biplane TEE in the diagnosis of PDA was comparable (95% and 100%, respectively; p = NS). In conclusion, TEE was highly sensitive and specific in detecting PDA in adolescents and adults. It was also highly valuable for detecting the cause of pulmonary hypertension in patients with Eisenmenger's syndrome.

Clinical implications of left atrial appendage flow patterns in nonrheumatic atrial fibrillation.

Left atrial appendage (LAA) function and flow patterns in 29 patients with chronic nonrheumatic atrial fibrillation were studied by transesophageal echocardiography. These 29 patients (16 men and 13 women; mean age, 63.8 years; range, 38 to 77 years) were classified into two groups according to different LAA flow patterns. Seventeen patients (group 1) had well-defined LAA emptying and filling Doppler flow signals, and the other 12 patients (group 2) had very low LAA flow signals. No significant differences were found in age, sex, mean duration of atrial fibrillation, left ventricular end diastolic dimension, and left ventricular ejection fraction between the two groups. However, group 2 patients had larger left atrial diameter (42.8 +/- 4.2 mm vs 36.6 +/- 8.8 mm; p < 0.05), lower LAA ejection fraction (26.4 +/- 15.2 percent vs 42.6 +/- 14.1 percent; p < 0.05), and lower LAA peak emptying velocity (0.13 +/- 0.03 m/s vs 0.36 +/- 0.16 m/s; p < 0.001). Higher incidence of LAA spontaneous echocardiographic contrast formation in group 2 patients (8/12 vs 1/17; p < 0.001) was noted. In conclusion, a subset of patients with nonrheumatic atrial fibrillation were found to have lower LAA blood flow and poorer LAA function. These patients had higher incidence of left atrial or LAA spontaneous echo contrast formation which had been proved previously to be a marker for future systemic thromboembolism.

Differential changes of myocardial beta-adrenoceptor subtypes and G-proteins in dogs with right-sided congestive heart failure.

We have shown previously in dogs with right heart failure that the reduction of myocardial beta-adrenoceptor density occurs only in the failing right ventricle, while cardiac inotropic responses to beta-adrenergic stimulation are reduced in both the right and left ventricles. The purpose of the present study was to determine whether a post-receptor defect in the guanine nucleotide-binding regulatory proteins (G-proteins) existed which would explain, at least in part, the adrenergic subsensitivity in both ventricles of the heart failure dogs. Using both immunoblotting technique and the bacterial toxin-mediated ADP ribosylation assays, we found that the stimulatory G-protein (Gs) was reduced in both ventricles of the heart failure dogs. In contrast, there were no changes in the inhibitory G-protein (Gi). In addition, receptor subtype analysis showed that only beta(1)-adrenoceptors were reduced in the failing right ventricle of the heart failure animals. This study demonstrated that the reduction of beta-adrenoceptors in right heart failure was chamber-specific whereas the reduction of Gs was non-selective, occurring in both ventricles of right heart failure dogs. The findings further suggest that the reduction of Gs probably was caused by systemic neurohormonal activation, independent of local ventricular stress.

Elevated myocardial interstitial norepinephrine concentration contributes to the regulation of Na+,K(+)-ATPase in heart failure.

Myocardial Na+,K(+)-ATPase is reduced in congestive heart failure. To study the regulation of Na+,K(+)-ATPase in congestive heart failure, we performed Western and Northern blot analyses of ventricular myocardium of dogs with pacing-induced congestive heart failure and chronic norepinephrine infusion, using isoform-specific antibodies and cDNA probes. Congestive heart failure and norepinephrine infusion caused similar increases in myocardial interstitial norepinephrine concentration and reductions of myocardial Na+,K(+)-ATPase alpha 3-subunit protein, but differed in their effects on myocardial Na+,K(+)-ATPase alpha 3-subunit gene expression. Chronic norepinephrine infusion produced no changes in the steady-state mRNA level for the alpha 3-subunit of Na+,K(+)-ATPase, suggesting that the changes in Na+,K(+)-ATPase protein were induced via a post-transcriptional mechanism. In contrast, down-regulation of the Na+,K(+)-ATPase alpha 3-subunit in the failing heart was accompanied by a decreased alpha 3-subunit mRNA level, indicating the presence of a transcriptional event. The alpha 1-subunit protein content and mRNA level were not affected by either norepinephrine infusion or rapid ventricular pacing. We conclude that, while elevated myocardial interstitial norepinephrine levels may contribute substantially to the down-regulation of the Na+,K(+)-ATPase alpha 3-subunit in the failing myocardium, additional regulatory factors are responsible for the decreased myocardial alpha 3-subunit mRNA expression in congestive heart failure.

Electrophysiological determinant for induction of isthmus dependent counterclockwise and clockwise atrial flutter in humans.

OBJECTIVE: To investigate the electrophysiological determinant underlying the electrical induction of counterclockwise and clockwise isthmus dependent atrial flutter. PATIENTS AND METHODS: The isthmus bordered by the inferior vena caval orifice-tricuspid annulus-coronary sinus ostium (IVCO-TA-CSO) has been assumed to be the site of both slow conduction and unidirectional block critical to the initiation of atrial flutter. Trans-isthmus and the global atrial conduction were studied in 25 patients with isthmus dependent atrial flutter (group A) and in 21 patients without atrial flutter (group B), by pacing at the coronary sinus ostium and the low lateral right atrium (LLRA) and mapping with a 20 pole Halo catheter in the right atrium. RESULTS: Mean (SD) fluoroscopic isthmus length between the coronary sinus ostium and LLRA sites was 28.1 (4.0) mm in group A and 28.0 (3.9) mm in group B (p = 0.95), but the trans-isthmus conduction velocity of both directions at various pacing cycle lengths was nearly halved in group A compared with group B (mean 0.39-0.46 m/s v 0.83-0.89 m/s, p < 0.0001). Pacing at coronary sinus ostium directly induced counterclockwise atrial flutter in 14 patients and pacing at LLRA induced clockwise atrial flutter in 11 patients, following abrupt unidirectional trans-isthmus block. Transient atrial tachyarrhythmias preceded the onset of atrial flutter in 10 counterclockwise and six clockwise cases of atrial flutter. None of the group B patients had inducible atrial flutter even in the presence of trans-isthmus block. The intra- and interatrial conduction times, as well as the conduction velocities at the right atrial free wall and the septum, were similar and largely within the normal range in both groups. CONCLUSIONS: Critical slowing of the trans-IVCO-TA-CSO isthmus conduction, but not the unidirectional block or the global atrial performance, is the electrophysiological determinant of the induction of counterclockwise and clockwise isthmus dependent atrial flutter in man.

New electrocardiographic criteria for the differentiation between counterclockwise and clockwise atrial flutter: correlation with electrophysiological study and radiofrequency catheter ablation.

OBJECTIVE: To develop new electrocardiographic (ECG) criteria for the differentiation between counterclockwise and clockwise atrial flutters. BACKGROUND: Traditionally, the ECG differentiation between counterclockwise and clockwise atrial flutters is based on the flutter wave polarity in the inferior leads. However, determination of flutter wave polarity is subjective and sometimes difficult, especially in flutter waves of undulating pattern. PATIENTS: The study comprised 37 consecutive patients with drug resistant atrial flutter; 30 had counterclockwise and 17 had clockwise atrial flutter (10 had both forms of atrial flutter). The isthmus dependence was confirmed by entrainment study and catheter ablation. The ECG patterns of both types of atrial flutter were compared and the flutter wave polarity in the inferior leads was determined by four independent cardiologists. RESULTS: The flutter wave polarity in the inferior leads appeared negative in 24, positive in one, and equivocal in five of the counterclockwise atrial flutters; polarity appeared negative in one, positive in 10, and equivocal in six of the clockwise atrial flutters. However, the aVF/lead I flutter wave amplitude ratio was > 2.5 in all counterclockwise but < 2.5 in all clockwise atrial flutters. The flutter wave nadirs in the inferior leads corresponded to the upstrokes in V1 in all counterclockwise atrial flutters, but corresponded to the downstrokes in V1 in all clockwise atrial flutters. CONCLUSIONS: The flutter wave polarity in the inferior leads does not correlate well with the flutter wave rotating direction. However, counterclockwise and clockwise atrial flutters can be differentiated by new ECG criteria with high accuracy.