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PubMed2003

Beneficial effects of phosphodiesterase 5 inhibition in pulmonary hypertension are influenced by natriuretic Peptide activity.

BACKGROUND: Phosphodiesterase type 5 (PDE5) inhibitors (eg, sildenafil) are a novel, orally active approach to the treatment of pulmonary arterial hypertension. The role of natriuretic peptides in the response to sildenafil was examined in mice lacking NPR-A, a guanylyl cyclase-linked natriuretic peptide receptor, in which pulmonary hypertension was induced by hypoxia. METHODS AND RESULTS: Mice homozygous for NPR-A (NPR-A+/+) and null mutants (NPR-A-/-) were studied. Sildenafil inhibited the pressor response to acute hypoxia in the isolated perfused lungs of both genotypes. This effect was greater in the presence of atrial natriuretic peptide in the perfusate in NPR-A+/+ mice but not NPR-A-/- animals. In vivo, NPR-A mutants had higher basal right ventricular (RV) systolic pressures (RVSPs) than did NPR-A+/+ mice, and this was not affected by 3 weeks of treatment with sildenafil (25 mg x kg(-1) x d(-1)). Both genotypes exhibited a rise in RVSP and RV weight with chronic hypoxia (10% O2 for 21 days); RVSP and RV weight were reduced by continuous sildenafil administration in NPR-A+/+ mice, but only RVSP showed evidence of a response to the drug in NPR-A-/- mice. The effect of sildenafil on hypoxia-induced pulmonary vascular muscularization and cyclic GMP levels was also blunted in NPR-A-/- mice. CONCLUSIONS: The natriuretic peptide pathway influences the response to PDE5 inhibition in hypoxia-induced pulmonary hypertension, particularly its effects on RV hypertrophy and vascular remodeling.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1991

Functional and structural impairment in human, rat and guinea-pig atrial muscle in response to in vitro calcium overload: a cytochemical study on cellular calcium distribution.

Critical accumulation of cellular calcium in ischaemic myocardium is involved in irreversible cell damage. In human right atrial trabeculae and in rat and guinea-pig left atria, we investigated whether direct calcium overload by increasing the extracellular calcium concentration, [Ca2+]o, leads to similar impairment of function and ultrastructure as observed after ischaemia. The force of contraction was measured during two consecutive cumulative increases in [Ca2+]o (1-25 mmol/l) separated by 30 min of incubation at low [Ca2+]o. Compared to the first Ca2+ challenge, the positive inotropic effect of increasing [Ca2+]o was depressed during the second one and the after-contractions, and the increase in resting tension developing with high [Ca2+]o tended to be larger. The ultrastructure of the tissue fixed immediately after excision was well preserved. When fixed after the second Ca2+ challenge, half of the cells were severely damaged with various signs of cellular Ca2+ overload similar to those observed after ischaemic damage: the sarcolemma lost its Ca(2+)-binding properties, sarcomeres showed contraction band necrosis, the mitochondria had disrupted cristae and contained either large clusters of Ca2+ precipitate or amorphous densities (Jennings granules). In many cells, calcium precipitates were present in the cytoplasm. The morphological and functional changes were similar in the three species studied. Our results suggest that the deterioration of atrial myocardium after challenge with high [Ca2+]o or after severe ischaemia may be traced back to a common mechanism, i.e. the sarcolemma loses its competence as a permeable barrier for Ca2+ and therefore facilitates excessive Ca2+ entry. However, for the direct demonstration of calcium precipitates as a sign of cytosolic Ca2+ overload, high [Ca2+]o are required with are not normally present in the myocardium.

Animals↗
PubMed1989

Transfer function analysis of autonomic regulation. I. Canine atrial rate response.

We present a useful technique for analyzing the various functional components that comprise the cardiovascular control network. Our approach entails the imposition of a signal with broad frequency content as an input excitation and the computation of a system transfer function using spectral estimation techniques. In this paper, we outline the analytical methods involved and demonstrate the utility of our approach in studying the dynamic behavior of the canine cardiac pacemaker. In particular, we applied frequency-modulated pulse trains to either the right vagus or the cardiac sympathetic nerve and computed transfer functions between nerve stimulation rate and the resulting atrial rate. We found that the sinoatrial node (and associated automatic tissue) responds as a low-pass filter to fluctuations in either sympathetic or parasympathetic tone. For sympathetic fluctuations, however, the filter has a much lower corner frequency than for vagal fluctuations and is coupled with a roughly 1.7-s pure delay. We further found that the filter characteristics, including the location of the corner frequency and rate of roll-off, depend significantly on the mean level of sympathetic or vagal tone imposed.

Algorithms↗
PubMed1996

Radiofrequency ablation of atrial flutter.

Activation mapping in common atrial flutter has shown circular (reentrant) activation of the right atrium around anatomic structures and areas of functional block. The direction of rotation is counterclockwise (in a frontal view), and in the low right atrium the myocardium between the inferior vena cava (IVC) and the tricuspid valve (TV) is critical to close the activation circle. The circuit can be interrupted by radiofrequency ablation of the myocardium between the TV and the IVC, and, in some cases, by ablation between the coronary sinus and TV. Flutter interruption does not mean complete isthmus ablation, as it may remain inducible, requiring further ablation. Despite attaining noninducibility, flutter may recur, and new procedures may be needed for complete ablation. Atrial fibrillation occurs in up to 30% of the cases during follow-up but is generally well controlled with antiarrhythmic drugs that were ineffective in treating flutter before ablation. Some noncommon atrial flutters show circular right atrial activation in a reversed (clockwise) direction, with the same critical areas in the low right atrium, and in these isthmus ablation is effective. Other noncommon flutters have different substrates in the right or left atrium, and mapping has to define specific critical isthmuses as ablation targets in each case. Left atrial flutter circuits remain inaccessible to ablation.

Atrial Fibrillation↗
PubMed1984

The effect of the site of placement of temporary epicardial pacemakers on ventricular function in patients undergoing cardiac surgery.

Temporary epicardial pacing leads are routinely placed in patients after cardiac surgery, but the positioning of ventricular leads and the use of atrial leads is not uniform. We examined the effect of the epicardial pacing site on ventricular function in 18 patients undergoing coronary surgery. Pacing wires were sutured in the right atrium, left ventricular apex, right ventricular apex, and right ventricular outflow tract before cardiopulmonary bypass. After atrial pacing, eight patients were ventricularly paced (group I) and 10 were atrioventricular (AV) sequentially (PR = 0.12 sec) paced (group II) at 100/minute from the three ventricular sites. Comparison of the groups showed that the addition of atrial activation during ventricular pacing resulted in higher cardiac indexes (2.54 +/- 0.61 vs 1.67 +/- 0.45 liters/min/m2;p less than .00005), higher systolic blood pressures (121 +/- 24 vs 89 +/- 26 mm Hg; p = .006), lower central venous pressures (5.5 +/- 3.2 vs 10.2 +/- 2.2 mm Hg; p = .048), and similar pulmonary arterial pressures (19.5 +/- 7.6/10.8 +/- 6.7 vs 24.7 +/- 3.5/15.4 +/- 3.4 mm Hg; p = NS). Cardiac index did not differ among group I patients during pacing from the different ventricular sites. In group II, cardiac index during pacing from the right ventricular apex was higher than during pacing from the right ventricular outflow tract or the left ventricular apex (2.62 +/- 0.57 vs 2.49 +/- 0.54 and 2.51 +/- 0.76 liters/min/m2, respectively; p = .03). Right ventricular outflow tract pacing resulted in higher cardiac indexes than left ventricular apical pacing in patients with stenosis of the left anterior descending coronary artery of 90% or more, while left ventricular apical pacing produced higher cardiac indexes in the absence of such lesions (p = .006).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1979

Valve replacement for Ebstein's anomaly of the tricuspid valve.

The role of valve replacement in the treatment of Ebstein's anomaly of the tricuspid valve remains controversial. Between 1965 and 1977, five patients with Ebstein's anomaly ranging in age from 11 to 57 years (mean 29) underwent tricuspid valve replacement in our institution. All of the patients were cyanotic but one, three were in Functional Class III, and two were in Class IV (New York Heart Association classification). The valve was placed above the coronary sinus. Plication of the atrialized portion of right ventricle was required in only one patient. Four patients had additional closure of an atrial septal defect. There were no deaths. On follow-up (range 1 to 13 years), four patients are in Functional Class I and one is in Class II. None is cyanotic. Four patients are in sinus rhythm and one has a pacemaker because of postoperative complete heart block. We conclude that valve replacement and, when necessary, plication of the atrialized right ventricle produce excellent clinical improvement.

Adolescent↗
PubMed2004

Assessment of left ventricular cardiac output by arterial thermodilution technique via a left atrial catheter in a patient on a right ventricular assist device.

Following heart transplantation (HTx) in a 49-year old male, the patient's haemodynamic situation deteriorated in the early postoperative period despite increasing doses of catecholamines. When transoesophageal echocardiography (TEE) showed a dilated right ventricle, but adequate left ventricular (LV) function, a right ventricular assist device (RVAD) was implanted to support the right ventricle of the failing graft. Evaluation of the resulting cardiac output (CO) of the left ventricle and, thus, assessment of the remaining right ventricular function in patients supported by a RVAD is of great clinical interest. In this situation, continuous measurement of LV function, enabling assessment of the remaining right ventricular function, can be performed by pulse contour analysis following initial calibration of the system by arterial thermodilution CO measurement via a left atrial catheter.

Arteries↗
PubMed2002

Bosentan.

Bosentan is a nonpeptide, specific, competitive, dual antagonist at both endothelin receptor subtypes (ET(A) and ET(B)). Orally administered bosentan effectively prevents endothelin 1-induced vasoconstriction in pulmonary vessels in patients with pulmonary arterial hypertension. Improvement in exercise capacity from baseline was significantly greater with bosentan than with placebo in two phase III trials in patients with WHO functional class III or IV pulmonary arterial hypertension (primary or associated with connective tissue disease) despite treatment with vasodilators, diuretics, anticoagulants, cardiac glycosides, or supplemental oxygen. The beneficial effects of bosentan on exercise capacity were maintained for at least 20 weeks. Compared with placebo, bosentan led to a significantly greater improvement from pretreatment values in secondary efficacy endpoints such as the Borg dyspnea index, WHO functional class, and cardiopulmonary hemodynamic parameters (cardiac index, pulmonary vascular resistance, pulmonary artery pressure, pulmonary capillary wedge pressure, mean right atrial pressure). Bosentan significantly reduced the incidence, and delayed the onset, of clinical worsening of pulmonary arterial hypertension compared with placebo. In published clinical trials, adverse events that occurred with similar or greater frequency with bosentan 125 mg twice daily than with placebo included headache, syncope, flushing and abnormal hepatic function. Those that occurred less frequently with bosentan 125 mg twice daily than with placebo included dizziness, worsening of symptoms of pulmonary arterial hypertension, cough and dyspnea.

Administration, Oral↗
PubMed2006

Right ventricular pacing can induce ventricular dyssynchrony in patients with atrial fibrillation after atrioventricular node ablation.

OBJECTIVES: This study was designed to assess the effects of long-term right ventricular (RV) pacing on left ventricular (LV) dyssynchrony, LV function, and heart failure symptoms. BACKGROUND: Atrioventricular (AV) node ablation and subsequent long-term RV pacing is a well-established treatment option in patients with atrial fibrillation (AF). METHODS: In 55 patients with drug-refractory AF, AV node ablation and implantation of a pacemaker was performed. At baseline and after a mean of 3.8 +/- 1.7 years, LV dyssynchrony (by M-mode echocardiography and tissue Doppler imaging), LV function, and volumes and functional status were assessed. RESULTS: After long-term RV pacing, 27 patients (49%) had developed LV dyssynchrony. Concomitantly, these patients worsened in heart failure symptoms (New York Heart Association functional class increased from 1.8 +/- 0.6 to 2.2 +/- 0.7, p < 0.05), with a decrease in LV ejection fraction (from 48 +/- 7% to 43 +/- 7%, p < 0.05) and an increase in LV end-diastolic volume (from 116 +/- 39 ml to 130 +/- 52 ml, p < 0.05). Conversely, patients without LV dyssynchrony did not deteriorate in heart failure symptoms, LV function, or LV volumes. CONCLUSIONS: Long-term RV pacing can induce LV dyssynchrony in almost 50% of patients treated with AV node ablation for chronic AF. The development of LV dyssynchrony was associated with deterioration in heart failure symptoms, systolic LV function, and LV dilatation.

Atrial Fibrillation↗
PubMed1996

Pulmonary hypertension after transjugular intrahepatic portosystemic shunt: effects on right ventricular function.

The short- and mid-term hemodynamic effects of transjugular intrahepatic portosystemic shunt (TIPS) were studied in 16 sedated cirrhotic patients. Indications included relapsing variceal bleeding (n = 10) and refractory ascites (n = 6). The decrease of porto-atrial pressure gradient (from 20.4 +/- 4.2 mm Hg to 10.1 +/- 2.4 mmHg; P < .05) was associated with an increase of mean pulmonary artery pressure (MPAP) (from 12.3 +/- 3.0 mm Hg to 20.3 +/- 5.3 mm Hg; P < .05) and of right atrial pressure (RAP) from 3.4 +/- 2.6 mm Hg to 8.3 +/- 3.7 mm Hg; P < .05), whereas right ventricular end-diastolic volume (RVEDVI) remained unchanged. The significant increase of cardiac index (CI) (from 4.5 +/- 1.2 L/min/m2 to 5.0 +/- 1.1 L/min/m2; P < .05) was essentially attributable to an increase of heart rate (HR) (from 81 +/- 11 to 88 +/- 10 beats/min; P < .05). Systemic vascular resistance (SVR) decreased (from 812 +/- 281 to 666 +/- 191 dynes/sec/cm5; P < .05), whereas pulmonary vascular resistance (PVR) increased (from 60.6 +/- 29.6 to 82.0 +/- 34.6 dynes/sec/cm5; P < .05). After transient shunt occlusion with a balloon catheter, all of the hemodynamic parameters returned to baseline values, except pulmonary artery pressure, which also decreased but remained significantly increased. One month after TIPS, pulmonary pressure remained elevated, and CI further increased. It is concluded that increased PVR is the major hemodynamic alteration occurring after TIPS placement. It correlates with the decrease of porto-atrial gradient and is probably mediated by both mechanical and neurohumoral factors.

Adult↗
PubMed1993

[Atrial activity and its effects].

The initiation of cardiac impulse is located in the sinus node, in the upper anterior part of the right atrium. The importance of the atrium is not only linked to the regulation of heart rate, but also to its haemodynamic function. Indeed, atrial depolarization leads to atrial contraction which can be responsible for up to 30% of cardiac output by way of ventricular filling. Supraventricular arrhythmias are related to one of the following mechanisms: abnormal automaticity, triggered activity, and reentry. Most of supraventricular tachycardias are due to a reentrant phenomenon (intranodal reentrant tachycardia, orthodromic circusmovement tachycardia, atrial flutter and atrial fibrillation). At the onset of a supraventricular tachycardia, the loss of efficacious atrial contraction as well as the increased heart rate may abruptly decrease ventricular filling. As a consequence, stroke volume is reduced, leading to a decrease in cardiac output and in arterial blood pressure, explaining that the patient may experience syncope. Usually, blood pressure reduction resumes within 30 seconds after activation of the autonomic adrenergic nervous system. In case of an underlying heart disease, the supraventricular tachycardia may lead to acute cardiac failure. When reentry is concerned, the tachycardia is going around a specific circuit. The existence of such a circuit in most of supraventricular tachycardias has led to the development of ablation therapy, the goal of which is to destroy a critical portion of the circuit hence making the recurrence of reentrant tachycardia impossible.

Arrhythmias, Cardiac↗
PubMed2004

Mice with cardiac-restricted angiotensin-converting enzyme (ACE) have atrial enlargement, cardiac arrhythmia, and sudden death.

To investigate the local effects of angiotensin II on the heart, we created a mouse model with 100-fold normal cardiac angiotensin-converting enzyme (ACE), but no ACE expression in kidney or vascular endothelium. This was achieved by placing the endogenous ACE gene under the control of the alpha-myosin heavy chain promoter using targeted homologous recombination. These mice, called ACE 8/8, have cardiac angiotensin II levels that are 4.3-fold those of wild-type mice. Despite near normal blood pressure and a normal renal function, ACE 8/8 mice have a high incidence of sudden death. Both histological analysis and in vivo catheterization of the heart showed normal ventricular size and function. In contrast, both the left and right atria were three times normal size. ECG analysis showed atrial fibrillation and cardiac block. In conclusion, increased local production of angiotensin II in the heart is not sufficient to induce ventricular hypertrophy or fibrosis. Instead, it leads to atrial morphological changes, cardiac arrhythmia, and sudden death.

Angiotensin II↗
PubMedDate not supplied

Doppler echocardiographic evaluation of right ventricular diastolic function in children.

Right ventricular diastolic function was evaluated by flow velocity pattern in the right ventricular inflow tract by means of pulsed Doppler echocardiography. Traditionally used to evaluate this function are peak velocities obtained during early diastole (peak E wave) and during atrial contraction (peak A wave), their ratio (peak E/A ratio), and the deceleration half-time. We conducted pulsed Doppler echocardiographic studies of right ventricular inflow and outflow patterns in 171 children (105 normal children and 66 children who were undergoing total surgical repair of congenital heart defects without sequelae). Results showed that summation flow was present in the right ventricular inflow tract in 43 (25%) of the 171 subjects, which made it difficult to separate the peak E wave from the peak A wave. We noted the presence of antegrade late diastolic flow (DW) in the right ventricular outflow tract of all subjects. DW, measured in 121 subjects in whom both E and A waves were detected in the right ventricular inflow tract, showed a highly significant correlation (p < 0.0001) with A waves in the right ventricular inflow tract. The ratio of DW to right ventricular outflow tract velocities during systole (SW) showed a highly significant (p < 0.0001) correlation with E/A ratio. When evaluating right ventricular diastolic function by pulsed Doppler, especially in children, the analysis of right ventricular outflow tract patterns is helpful in addition to that of inflow tract patterns. The DW and DW/SW ratio may present good alternatives to traditional parameters in children.

Blood Flow Velocity↗
PubMed1998

Evidence for an influence of mechanical restitution on beat-to-beat variations in haemodynamics during chronic atrial fibrillation in patients.

OBJECTIVE: We tested the hypothesis that beat-to-beat changes in haemodynamics during atrial fibrillation include an effect of each preceding R-R interval through the interval-strength relationship (mechanical restitution). BACKGROUND: The variation in stroke volume and pulse pressure characteristic of atrial fibrillation is usually ascribed to time dependent ventricular filling. METHODS: We measured the maximum rate of rise of left ventricular pressure (LVdP/dtmax), and aortic blood velocity and its integral in patients with atrial fibrillation undergoing cardiac catheterisation. The contractile response of isometric human myocardial trabeculae to sequences of atrial fibrillation was also studied, using the recorded ECGs as stimuli. The trabeculae were obtained from the resected right ventricular outflow tracts of patients with Fallot's tetralogy undergoing operative correction. RESULTS: Beat-to-beat variations in contractile function during atrial fibrillation in the patients were recorded as LVdP/dtmax and left ventricular ejection (ascending aortic) velocity integral (proportional to stroke volume). Both these indices correlated well with the response to the same ECG (R wave) sequences in the isometric model measured as the maximum rate of rise of force, dF/dtmax, r = 0.72 to 0.81, p, 0.0001. When short pre-preceding intervals were excluded (minimizing the effect of post-extrasystolic potentiation), these variables showed a positive curvilinear relationship to preceding interval typical of mechanical restitution. CONCLUSIONS: Mechanical restitution, which causes beat-to-beat changes in inotropic state, accounts in part for the changes in stroke volume in atrial fibrillation.

Aged↗
PubMed2002

Prenatal role of the ductus arteriosus in absent pulmonary valve syndrome.

Absent pulmonary valve with ventricular septal defect is associated with ductal agenesis and markedly dilated main and branch pulmonary arteries. The less common variant with intact ventricular septum generally exhibits a patent ductus and smaller branch pulmonary arteries, and may be associated with tricuspid atresia. We identified 7 patients with the prenatal diagnosis of absent pulmonary valve, 5 with ventricular septal defect (Group 1) and 2 with an intact ventricular septum (Group 2). Imaging, color Doppler, and pulsed-Doppler recordings were analyzed. The branch and main pulmonary arteries were measured and expressed as a ratio with the descending aorta. Pulmonary regurgitation time (PRT) and diastolic acceleration time (DAT) were derived, and DAT/PRT was calculated to characterize diastolic pulmonary flow. Group 1 patients all had a large ventricular septal defect, normal biventricular size and function, and dilated main and branch pulmonary arteries. Group 2 patients had dilated main but smaller branch pulmonary arteries, moderate right ventricular dilation with severe dysfunction, and limited or absent tricuspid inflow. Group 1 demonstrated shorter acceleration time and earlier peak velocity, resulting in a smaller DAT/RT ratio. We speculate that free communication between the fetal aorta and the ventricles may limit atrial inflow and elevate diastolic pressure, affecting cardiac output, ventricular function, and atrioventricular valve development. With an intact ventricular septum, these physiologic and anatomic repercussions are limited to the right ventricle, but with a ventricular septal defect, both ventricles would experience similar consequences and cardiac performance could be critically impaired.

Ductus Arteriosus, Patent↗
PubMed1977

[The relation between the electrophysiological parameters of the right atrium and the AV-node conduction (author's transl)].

40 patients were examined with the extrastimulus method at 3 different driving rates (80, 100 and 120/min). It was found that the atrial conduction velocity during the relative refractory period sometimes explains a paradoxical conduction of a premature atrial beat. The AV-node conduction is mainly determined by the correlation between the functional refractory period of the right atrium (FRPRA) and the effective retractory period of the AV-node (ERPAVN). With increasing driving rate the FRPRA shortened while ERPAVN lengthened. This explains why in this study the number of patients in which the ERPAVN could be reached progressively increased from 23 at a driving rate of 80/min to 31 and 33, respectively, at the driving rates of 100 and 120/min.

Adolescent↗
PubMed2003

The role of Pitx2 during cardiac development. Linking left-right signaling and congenital heart diseases.

Pitx2 is a bicoid-related homeodomain transcription factor that plays a critical role in directing cardiac asymmetric morphogenesis. Ectopic Pitx2c expression in the developing myocardium correlates with double outlet right ventricle (DORV) in laterality mutants. Pitx2 loss of function experiments cause severe cardiovascular defects, such as atrial isomerism (AI), double inlet left ventricle, transposition of the great arteries (TGA), persistent truncus arteriosus (PTA), and abnormal aortic arch (AAA) remodeling. Current studies suggest that Pitx2-mediated signaling during cardiogenesis is conducted within three different cell types: the myocardium, the cardiac neural crest (CNC) cells, and the pharyngeal arch mesenchyme. Impaired Pitx2 function in discrete myocardial regions seems to lead to DORV, AI, and possibly TGA. On the other hand, impaired Pitx2 expression in the CNC leads preferentially to PTA. AAA remodeling is likely to occur owing to impaired cross-talk of the CNC cells with the pharyngeal arch mesenchyme. Thus, Pitx2 appears to be directing left-right identity to the cardiac venous components (e.g., the atria), whereas it appears to be modeling the morphologic arrangement of distinct myocardial components in the arterial pole. These data suggest that altered left-right signaling underlies the etiology of several common congenital cardiac malformations.

Animals↗