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Current interest in the arterial switch operation for simple transposition of the great arteries (TGA) has led us to evaluate our latest patients who have undergone intra-atrial repair. Right ventricular function and overall results were compared in 32 patients who had undergone the Senning procedure between 1978 and 1983 and 26 patients who had undergone Mustard repair between 1971 and 1978). Deep hypothermia and circulatory arrest were used in all Senning operations and in 18 of 26 Mustard procedures. Cardiac catheterization was performed an average of 1 year after surgery in all patients. Postoperative right ventricular ejection fraction (EF) was below normal (less than 0.49) in 16 of 32 patients who underwent the Senning procedure and averaged 0.48 +/- 0.09. In the patients in this group with abnormal right ventricular EFs after repair there was a fall in the value after surgery (0.51 to 0.40, p less than .001), while in those with normal right ventricular EFs after repair there was no change (0.57 to 0.55, NS). All 32 patients who underwent the Senning procedure were compared with 26 patients who underwent the Mustard operation (13 treated between 1971 and 1974 and 13 treated between 1975 and 1978). An older age at surgery (12 +/- 7 vs 6 +/- 8 months, p less than .006) and a lower preoperative right ventricular EF (0.46 +/- 0.09 vs 0.54 +/- 0.08, p less than .007) characterized the Mustard vs the Senning group.(ABSTRACT TRUNCATED AT 250 WORDS)
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The present study describes the effects of pimobendan on isolated human right atrial strips and on isolated left atria of the rat. Pimobendan induces a positive inotropic effect both in human and rat preparations. The maximal increase (28 +/- 2.0%) obtained with pimobendan in the strips from human right atria was similar to that obtained in left atria of the rat (31 +/- 1.8%). These observations may have some clinical relevance as pimobendan might prove to be an alternative to catecholamines for inotropic support in patients who undergo general anaesthesia.
After cardioversion of chronic atrial fibrillation to sinus rhythm, there is a gradual increase of 56% in cardiac output over 4 weeks. The increase is caused by the gradual return and increasing strength of left atrial mechanical activity as the atrial myopathy of chronic atrial fibrillation subsides. Cardiac output decreases after cardioversion of atrial fibrillation in more than a third of patients, and the decrease may last a week. Acute pulmonary edema is uncommon; 50% of cases occur within 3 hours of cardioversion, with a mortality of 18%. The reduced cardiac performance after cardioversion most likely results from the combination of heart disease and cardiac depressant effects of anesthetic drugs used. Pulmonary and/or coronary artery emboli and the resumption of right atrial mechanical activity before left atrial mechanical activity may be additional factors in the pathogenesis of pulmonary edema after cardioversion. Anticoagulant therapy should be continued for a month or longer after cardioversion in those patients who maintain sinus rhythm to prevent thromboembolism.
OBJECTIVES: We sought to assess the right heart's response to percutaneous device closure of moderate sized atrial septal defects (ASDs) in adults over a one-year follow-up period. BACKGROUND: Percutaneous ASD device closure is a safe and effective means of reducing or eliminating interatrial shunting. The response of the adult's right heart to device closure is incompletely understood. METHODS: Forty consecutive patients had 40 device implantations (32 with the CardioSeal implant and 8 with the Amplatzer device). The patients were assessed with echocardiography, chest radiography and electrocardiography before the procedure and at 1, 6 and 12 months. RESULTS: The mean ASD size was 13+/-4 mm, and the device size ranged from 33 to 40 mm for CardioSeal and 12 to 36 mm for Amplatzer. At one month, heart size (49% vs. 46%), four-chamber right ventricular (RV) size (45 vs. 41 mm), paradoxical septal motion (60% vs. 5%), QRS duration (125 vs. 119 ms), PR interval (181 vs. 155 ms) and echocardiographically determined pulmonary artery systolic pressure decreased significantly and was maintained at 12-month follow-up. At six months, right atrial length decreased from 50 to 47 mm. At one year, 29% of patients had persistent RV enlargement. CONCLUSIONS: Right heart morphology undergoes rapid improvement within one month of defect closure, with associated mechanoelectrical benefit. A small number of patients had persistent RV enlargement or pulmonary hypertension, or both, at one year. Our data support the application of transcatheter methods in achieving excellent hemodynamic and anatomic outcomes.
The response of intravascular (PBV) and extravascular (EVLW) pulmonary fluid volume was examined using double-indicator techniques (thermal-green dye) in 11 open-chest anesthetized dogs during the production of sustained left atrial (LA) hypertension by a LA balloon over a period of 195 min. In 6 of these animals data were also acquired after the intravenous administration of furosemide (1 mg/kg). The renal effects of the diuretic were blocked by tying off the ureters and the vascular supply of both kidneys. Left atrial pressure (N = 11) was abruptly increased from 2.2 +/- 2.1 mm Hg to 30.2 +/- 4.0 mm Hg (P less than 0.01) and maintained at that level for 120 min. Data were obtained prior to pressure elevation, immediately upon pressure elevation, and then every 60 min for a total of 120 min. At that point EVLW had increased (8.1 +/- 0.8 cc/kg at control to 21.7 +/- 2.0 cc/kg at 120 min, P less than 0.001), as had PBV (6.2 +/- 2.1 cc/kg to 9.1 +/- 3.1 cc/kg P less than 0.01). After furosemide injection (N = 6), LA pressure declined (mean peak reduction of approximately 6 mm Hg at 60-75 min, P less than 0.01), aortic and pulmonary arterial pressure both declined (P less than 0.01). However, EVLW remained unchanged, though PBV decreased significantly (peak decrease at 75 min after furosemide administration of 2.0 +/- 0.4 cc/kg, P less than 0.01). In the untreated dogs, EVLW continued to climb (P less than 0.05 vs treated dogs at 75 min postfurosemide).(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: A paucity of data exists as to the relation of mean right atrial pressure (RAP) to Doppler parameters of right atrial and ventricular filling. Furthermore, whether echocardiographic parameters of right atrial and right ventricular function and inferior vena cava improve the relation of Doppler filling dynamics with RAP has not been explored. METHODS AND RESULTS: Doppler and echocardiographic studies were performed simultaneously with measurements of mean RAP in consecutive patients who either had a central venous catheter in the Intensive Care Unit or underwent catheterization of the right side of the heart. The initial population consisted of 35 patients with a mean age (+/-SD) of 60+/-15 years; 34% were on mechanical ventilation. Mean RAP averaged 9+/-5.7 mm Hg (range, 2 to 28 mm Hg). Among tricuspid inflow parameters, the strongest relation with RAP was observed with the ratio of early to late velocity (r=.66). For hepatic venous flow, systolic filling wave indexes had the best relation with atrial pressure, the highest being for systolic filling fraction (r=-.86). Weaker relations were noted with the use of right atrial volumes, right ventricular function, and inferior vena caval diameters. The addition of any of these variables did not improve the relation of systolic filling fraction with RAP. The regression equation (RAP=21.6-24 systolic filling fraction) was tested prospectively in the estimation of atrial pressure 50 patients. The correlation coefficient was .89 in the prospective group and .88 in the total group of 85 patients. The mean difference between predicted and actual pressures in the whole population was -0.2+/-2.6 mm Hg. The sensitivity and specificity for mean RAP>8 mm Hg were 86% and 92%, respectively. CONCLUSIONS: Among echocardiographic and Doppler parameters of right atrial and right ventricular function, hepatic venous flow dynamics relate best to mean atrial pressure and can be used clinically to estimate mean RAP.
Exercising muscle hypoperfusion stimulates afferents (metaboreceptors) involved in the regulation of ventilation. Atrial fibrillation (AF), particularly when combined with diseases causing endothelial (ED) impairment, such as hypertension (HP) and diabetes mellitus (DM), depresses the ED activity and enhances exercise hyperventilation. The relationship between these two functions and the underlying mechanisms have not been explored previously. In lone AF or AF associated with HP or DM (12 subjects in each cohort), we investigated the brachial artery flow-mediated dilatation (ED function) and ventilation during the recovery phase of handgrip (metaboreflex) exercise for subjects receiving placebo or oral vitamin C (double-blind crossover), both before and after cardioversion (CV) to sinus rhythm. Baseline ED impairment was increasingly more severe and the ergoreflex activity more pronounced in AF + HP and AF + DM compared with lone AF. Vitamin C and CV significantly improved both flow-mediated dilatation and metaboreflex activity in lone AF and AF + HP, and vitamin C did not produce any additive effect when administered after CV. In AF + DM, neither vitamin C nor CV was effective. This study provides the following information: AF generates oxidative injury, which is less when the arrhythmia is lone AF and greater when the arrhythmia is associated with HP. In DM, the oxidative injury generated by AF is refractory to a rather weak antioxidant, like vitamin C, or the baseline damage is such as to prevent any additive influence of AF. In AF, a cause-effect link exists between ED dysfunction and metaboreflex activity. Ventilatory advantages of CV seem to be inversely related with the extension of the underlying ED oxidative impairment.
To study the assessment of cardiac function in acute myocardial infarction (AMI), we measured left atrial diameter, left ventricular end-diastolic pressure (LVEDP), pulmonary capillary wedge pressure (PCWP), ejection fraction (EF) in 20 patients with acute myocardial infarction. Left atrial diameter was measured using echocardiography and was expressed as left atrial index (LAI, mm/m2) dividing by body surface area. LAI in AMI was 21.3 +/- 2.7 mm/m2 and significantly larger than LAI in normal subject (19.9 +/- 2.0 mm/m2) (p less than 0.05), In AMI, LVEDP was 13.3 +/- 3.4 mmHg, PCWP was 9.0 +/- 2.8 mmHg and EF was 52.3 +/- 14.8%, Relationship (r value) between LAI and LVEDP (r = 0.70, p less than 0.001, y = 0.87 x-5.4 x; LAI, y; LVEDP) was greater than PCWP and LVEDP (r = 0.60, p less than 0.01). LVEDP calculated from LAI using this method was directly measured LVEDP directly measured +/- 2.4 mmHg. In 9 patients, LAI was larger than 20.9 mm/m2, in 8 patients of them LVEDP was higher than 13 mmHg. In 11 patients LAI was smaller than 20.9 mmHg, only in 2 of them LVEDP was lower than 13 mmHg. It concluded that sensitivity was 88.9%, specificity was 81.8%, accuracy was 85.0%. Relationship between LAI and PCWP (r = 0.30), LAI and EF (r = -0.36) were not significant. We can measure LAI repeatedly in AMI non-invasively, and predict LVEDP. Thus, the measurement of LAI is useful in treatment of AMI.
The cellular mechanisms responsible for contractile dysfunction associated with atrial fibrillation (AF) are still poorly understood. Atrial fibrillation is often preceded by atrial dilatation. This study aimed to explain contractile alterations associated with AF and their relation to atrial dilatation, by studying the relationships between atrial dimensions, contractile protein composition, force production and Ca(2+)-sensitivity. Force development was determined in mechanically isolated single skinned cardiomyocytes from right atrial appendages from patients with sinus rhythm without (SR;n=9), or with atrial dilation (SR+AD;n=11) or atrial fibrillation (AF;n=16). Echocardiography showed that, compared to the SR group, mean right atrial dimensions were increased by 18% and 35% in the SR+AD and AF group, respectively (P<0.05). Protein composition was determined by 1- and 2-dimensional gel electrophoresis. Compared to the SR group, the AF group exhibited: a reduction in the kinetics of force redevelopment (K(tr)) in isolated atrial cardiomyocytes, enhanced protein expression of the slow myosin heavy chain isoform (beta-MHC), an increase in troponin T (TnT) phosphorylation and a marked increase (70%) of the cytoskeletal protein desmin. Significant correlations were observed between the right atrial major axis (RA(major)) and beta-MHC expression as well as the desmin/actin ratio. Our findings indicate that dilatation may influence cardiomyocyte stability through altered desmin expression, but that it does not predispose to the alterations in contractile function observed in AF.
UNLABELLED: Atrial fibrillation (AF) was described to be associated with an adverse prognosis in several studies of heart failure (HF). However, it is not clear whether it directly increased mortality or is only a marker for severity of HF. AIMS: To determine the influence of AF on mortality of HF patients distinguishing between patients with preserved and deteriorated systolic function (SF). METHOD AND RESULTS: 1636 patients who, between 1991 and 2002 had been hospitalized in a Cardiology Service for HF, were studied. Survival (SV) data (mean follow-up time: 3.14 years) has shown that there was no difference in SV between patients with (540 patients of the whole group) and without AF in the group with preserved SF (presented in 38.7% of cases), however, in the group of patients with deteriorated SF (AF presented in 31.0% of cases), SV time was significantly (p=0.01) shorter among patients with AF, this association being independent of age, sex, aetiology, risk factors, clinical signs and pharmacological treatment; relative risk: 1.831(1.120-2.994). CONCLUSION: AF is more prevalent among HF patients with preserved SF than among those with deteriorated SF, but only increases the risk of death among the latter.
We present the case of a 14-year-old boy who had secondary hyperkalemic periodic paralysis caused by Gordon's syndrome. This syndrome consists of hypertension, tubular acidosis, and hyperkalemia with normal glomerular filtration rate. The pathophysiological mechanism is still unknown. Pathophysiological studies suggest that in this disorder the kidney lacks sensitivity to atrial natriuretic peptide. After treatment with hydrochlorothiazide, serum potassium and plasma aldosterone values, plasma renin activity, and blood pressure became normal and the attacks of periodic paralysis disappeared.
The present study was undertaken: 1) to localize and characterize atrial natriuretic peptide (ANP) receptors in the rat mammary gland; and 2) to elucidate ANP-induced cellular formation of cyclic GMP (cGMP) and alterations in alveolar morphology during both early and late lactation. Receptor autoradiography, employing rat-specific [125I]ANP as radioligand, demonstrated binding sites in the secretory tissue and larger blood vessels of the mammary gland. Binding of [125I]rANP to membrane fractions was completely displaced by unlabeled ANP and brain natriuretic peptide. C-type natriuretic peptide and cANP(4-23) revealed limited competition with radiolabeled ANP only during early lactation, indicating a more heterogeneous receptor population at that time. Systemically administered ANP induced cGMP formation in the alveolar epithelium, as shown with immunohistochemistry, and increased mammary tissue cGMP concentrations in vivo throughout the lactation period. Image analysis revealed enlargement of alveolar (but not epithelial) cell area after ANP stimulation in late lactation, suggesting altered alveolar filling or myoepithelial cell relaxation. These results indicate that ANP induces biological effects in the rat mammary gland through specific ANP-A receptor interaction with subsequent intracellular cGMP formation. ANP may therefore play a regulatory role in the control of mammary gland blood supply and secretory function.
OBJECTIVE: The authors analyzed the clinical results during the first 8 1/2 years' experience with the Maze procedure for the surgical treatment of atrial fibrillation. SUMMARY BACKGROUND DATA: Atrial fibrillation occurs in 0.4% to 2% of the general population and in approximately 10% of patients older than 60 years of age. It is associated with significant morbidity and mortality. The irregular heartbeat causes discomfort, the loss of synchronous atrioventricular contraction compromises hemodynamics and the stasis of blood flow increases the vulnerability to thromboembolism. METHODS: From September 25, 1987 to March 1, 1996, 178 patients underwent the Maze procedure. Thirty-two patients underwent the Maze-I procedure, 15 underwent the Maze-II procedure, and 118 underwent the Maze-III procedure. Patients were analyzed for recurrence of atrial flutter and atrial fibrillation between 3 months and 8 1/2 years after surgery (n = 164). Patients were analyzed for atrial transport function, sinus nodule function, and postoperative pacemaker requirements. RESULTS: Ninety-three percent of all patients were arrhythmia free without any antiarrhythmic medication. Of the remaining patients with arrhythmia recurrence, all were converted to sinus rhythm with medical therapy. All patients were documented to have atrial transport function by either direct visualization, transesophageal echocardiography, or atrioventricular versus ventricular pacing at the same rate. Ninety-eight percent had documented right atrial function, and 94% had left atrial function. Of the 107 patients in this series who were documented to have a normal sinus node preoperatively, only 1 patient required a permanent pacemaker. CONCLUSION: The Maze procedure is an effective treatment for medically refractory atrial fibrillation in properly selected patients.
The present study was designed to determine the factors governing the ability of premature beats at various atrial sites to initiate atrial fibrillation (AF) and the determinants of the duration of AF in dogs at 1-10 Hz. The site of atrial extrasystoles determined their ability to induce AF. Regional differences in AF inducibility were due to differences in local refractoriness. Premature beats initiated AF by blocking in regions of greater refractoriness, causing macroreentrant activation with subsequent disorganization producing fibrillation. The atrial refractory period and wavelength during rapid 1:1 atrial pacing were weak predictors of AF duration (r = 0.24 and 0.23, respectively), which depended strongly on variability in regional refractoriness measured by the standard deviation in local refractory periods (r = 0.80, P < 0.001) and on the heterogeneity of activation during AF (r = 0.74, P < 0.001). Thus, premature beats cause AF by initiating a single macroreentrant cycle that degenerates into multiple wavefronts, regional refractoriness is the primary determinant of AF induction by premature beats, and variability in refractoriness may be an important determinant of the ability of AF to sustain itself.
BACKGROUND: Surgery for atrial fibrillation (AF) is performed with the aim of restoring sinus rhythm and atrial transport function, and preventing thromboembolism. The radial incision approach (RIA), in which the atrial incisions radiate from the sinus node toward the atrioventricular annular margins and parallel the coronary arteries, was developed as an outgrowth of and an alternative to the maze procedure in order to preserve a more physiological activation sequence and the atrial transport function. METHODS: To determine whether the RIA is a promising procedure for AF, 23 patients who had undergone the RIA (n = 10) or the maze procedure (n = 13) for chronic AF associated with valvular heart disease were examined in terms of the postoperative cardiac rhythm and atrial transport function. RESULTS: AF was cured in 90% of RIA patients and 92.3% of maze patients (not significant). One patient in each group required pacemaker implantation for an insufficient sinus rate postoperatively. The RIA was technically easier than the maze procedure, because the incisions were more linear and there was no isolation incision or "T-shape" incision in the left atrium. The left atrial transport function, assessed by transthoracic Doppler echocardiography, was greater after the RIA than after the maze procedure, while the right atrial transport function was equally preserved by both procedures. The peak atrial filling/early filling waves of the flow-velocity spectra across the mitral valve was significantly larger after the RIA than after the maze procedure (0.58+/-0.17 vs. 0.25+/-0.07, p<0.005). The left atrial filling fraction was significantly larger after the RIA than after the maze procedure (28.5%+/-5.0% vs. 15.1%+/-4.0%, p<0.001). CONCLUSIONS: RIA provides a greater atrial transport function, and thus may represent a physiological alternative to the maze procedure as a surgical procedure for AF.