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PubMed2004

Randomized trials for selective site pacing: do we know where we are going?

Clinical evidence is accumulating that pacing from traditional right-sided sites (right ventricular apex and right atrial appendage) may be associated with long-term detriment to left ventricular function and promotion of atrial arrhythmias. Large numbers of small studies, some randomized, have addressed the effects of pacing from nontraditional or alternate sites, but the studies have varied in design such that comparison of results is often difficult. Many studies show data from acute studies only, although more recently longer-term data have started to become available; definition and description of pacing site also varies, adding further to the difficulties in comparing data. This article attempts to examine the randomized studies available to date, and to consider how future studies may contribute to our understanding of the effects of pacing from traditional and selected, specific sites on the right side of the heart.

Cardiac Pacing, Artificial↗
PubMed1995

Paradoxical embolism in the presence of right-to-left shunt due to tricuspid occlusion.

The case of a 33-year-old woman suffering from a paradoxical peripheral embolism in the presence of a right-to-left shunt at the level of an ostium secundum defect is presented. A functional stenosis of the tricuspid valve due to obstruction through a thrombotic atrial mass was found to be responsible for the right-to-left shunt. Treatment consisted of peripheral embolectomy, removal of the atrial mass, and closure of the atrial septum defect.

Adult↗
PubMed1995

Time varying loading of the pulmonary circulation: a model to describe hemodynamic observations in the stiff left atrial syndrome.

OBJECTIVE: To develop a mathematical model that could explain the following observations: that right heart failure can develop in association with no other cardiac abnormality than a severe reduction in the compliance of the left atrium; and that patients with this syndrome have systolic pulmonary hypertension with left atrial v waves in the absence of either mitral regurgitation or left ventricular dysfunction. DESIGN: A model of the pulmonary circulation was designed with a time varying terminal hydraulic load, which was varied between a noncompliant left atrium during systole and a compliant left ventricle/left atrium combination during diastole. Using representative parameters and a pulmonary arterial flow wave as input, pressures in the pulmonary artery and left atrium and right ventricular power output were calculated. RESULTS: Pulmonary arterial and left atrial systolic pressures are increased as left atrial compliance is reduced. The time varying change in terminal load results in an increase in systolic pressures, whereas diastolic pressures remain normal. A decrease in left atrial compliance increases both the nonpulsatile and pulsatile components of pulmonary input impedance, whereas only the nonpulsatile component of right ventricular power output is increased. CONCLUSIONS: The time varying pulmonary load model of the pulmonary circulation, in the presence of a reduced left atrial compliance results in pulmonary, and left atrial pressures similar to those observed in patients with the stiff left atrial syndrome. The resulting increase in right ventricular power output could be an important factor in the development of right heart failure.

Aged↗
PubMed1996

The clinical case report: a tool for hypothesis generation.

The clinical case report is generally limited to a description of unusual examples of the complications of disease or responses to therapy. However, it can also be used to present novel hypotheses which have been derived from individual cases. Two examples of this latter genre are presented and updated. These are Syndrome X and the stiff left atrial syndrome. In both instances, general and novel formulations were derived from single cases. With respect to Syndrome X, a hypothesis was generated that the chest pain and ST abnormalities in these patients represent excess activation of adenosine A1 receptors in the absence of myocardial ischemia. With respect to the stiff left atrial syndrome, recognition of the first case led to the recognition of the problem in many others. Now, a variant of the syndrome has been recognized in which mitral regurgitation is also present. In addition, the possibility that tricuspid annuloplasty may rescue patients dying of cardiac cachexia due to right heart failure caused by combined pressure and volume overload of the right ventricle is outlined.

Atrial Function, Left↗
PubMed1990

Determinants of survival after surgery for mitral valve regurgitation in patients with and without coronary artery disease.

Mortality and its determinants were assessed in 181 consecutive patients undergoing primary mitral valve surgery for pure mitral regurgitation with coronary artery disease (MR + CAD, 79 patients) or without (MR no CAD, 102 patients). Early mortality (C10% vs. 3%) and 6-year estimate of survival (55% +/- 7.1% vs. 82% +/- 4.4%) were significantly different. Mortality was not significantly different in patients with CAD + MR of an ischemic (49 patients) or a non-ischemic etiology (30 patients). Multivariate testing using Cox regression models of overall mortality in patients with MR + CAD indicated that preoperative renal dysfunction, high right atrial pressure, ejection fraction less than 45% as well as qualitatively reduced left ventricular function and left ventricular end-diastolic volume index greater than 120 ml/m2 are associated with decreased survival. Multivariate testing in patients with MR no CAD only identified insertion of a mechanical prosthesis and a degenerative etiology of mitral valve disease as independent predictors of survival. Thus, a common denominator of preoperative pathology (renal dysfunction) and indices of right and left ventricular dysfunction determined overall survival of patients with MR + CAD. Survival of patients with MR no CAD was determined by the valve prosthesis and the etiology of valve disease.

Coronary Disease↗
PubMed2000

Atypical atrial flutter originating in the right atrial free wall.

BACKGROUND: Data from experimental models of atrial flutter indicate that macro-reentrant circuits may be confined by anatomic and functional barriers remote from the tricuspid annulus-eustachian ridge atrial isthmus. Data characterizing the various forms of atypical atrial flutter in humans are limited. METHODS AND RESULTS: In 6 of 160 consecutive patients referred for ablation of counterclockwise and/or clockwise typical atrial flutter, an additional atypical atrial flutter was mapped to the right atrial free wall. Five patients had no prior cardiac surgery. Incisional atrial tachycardia was excluded in the remaining patient. High-density electroanatomic maps of the reentrant circuit were obtained in 3 patients. Radiofrequency energy application from a discrete midlateral right atrial central line of conduction block to the inferior vena cava terminated and prevented the reinduction of atypical atrial flutter in each patient. Atrial flutter has not recurred in any patient (follow-up, 18+/-17 months; range, 3 to 40 months). CONCLUSIONS: Atrial flutter can arise in the right atrial free wall. This form of atypical atrial flutter could account for spontaneous or inducible atrial flutter observed in patients referred for ablation and is eliminated with linear ablation directed at the inferolateral right atrium.

Aged↗
PubMed1989

Cocaine depresses the canine myocardium.

The effects of cocaine hydrochloride infusion on left ventricular function in the anesthetized dog were observed under controlled heart rate and blood pressure conditions. In every case an immediate decrease in performance, as evidenced by maximal + rate of change of ventricular pressure (dP/dt), occurred and was a linear function of cumulative dose. Maximal (-) dP/dt also declined, indicating a decreased rate of ventricular relaxation. Right atrial and left ventricular end diastolic pressure increased, with no change in cardiac output or cardiac work, whereas coronary flow decreased slightly. This small decrease in coronary flow was probably related to the decrease in contractile vigor rather than a direct effect of cocaine on vascular tone. Although plasma norepinephrine concentration initially increased, ventricular function did not increase and continued to decline with cumulative cocaine dose. Tissue norepinephrine levels measured in isolated heart-lung preparations were not depleted. These findings indicate a direct toxic action of cocaine on the myocardium, decreasing both contractile performance and relaxation state. Plasma cocaine levels were constant during continuous infusion of the drug, indicating that the progressive toxicity observed did not result from increased circulating cocaine.

Animals↗
PubMed1990

[Opening of a foramen ovale during liver transplantation. The value of transesophageal echocardiography].

A case is reported of a foramen ovale becoming patent during orthotopic liver transplantation (OLT). The patient had a hepatoma secondary to post-hepatitis cirrhosis. Monitoring included transesophageal echocardiography (TEE). A veno-venous shunt between the right femoral, portal and left axillary veins was used so as to maintain the venous return during portal and caval clamping. The patient's haemodynamic state remained quite stable throughout this period, and no vasoactive drug was required. Five min after graft reperfusion, pulmonary arterial pressure increased suddenly (mean PAP: 27 mmHg). TEE revealed paradoxical movements of the atrial septum. Colour coded Doppler ultrasound showed blood flowing from the right to the left atrium through a patent foramen ovale. Fifteen min later, mean PAP decreased (18 mmHg) and TEE no longer showed any flow between the two atria. Several studies have reported transient pulmonary hypertension after unclamping when the donor liver is reperfused. This could induce right ventricular failure, with transient inversion of the atrial pressure gradient, which, in turn, could result in a right-to-left shunt through a patent foramen ovale. TEE can monitor regional and overall left ventricular function as well as the atrial septum. This technique might therefore to be useful for cardiac monitoring during OLT.

Cardiomyopathies↗
PubMed1976

Effects of varying pacemaker sites on left ventricular performance.

The hemodynamic effects of the site of the artificial cardiac stimulation were studied in 17 open chest dogs. The right atrium and five ventricular sites (the inflow and outflow tracts and apex of the right ventricle, apex and lateral wall of the left ventricle) were stimulated electronically at a given rate, ranging from 130 to 190 per min. When cardiac performance during ventricular pacing was compared with those during right atrial pacing, the former uniformly caused a diminution of cardiac output and systemic blood pressure, without reduction of left ventricular end-diastolic pressure. Ventricular function curves, in which left ventricular stroke work was related to left ventricular end-diastolic pressure, shifted downwards and to the right during ventricular pacing. Stimulation frequency did not alter these variables. It was considered that the left ventricular dysfunction in ventricular pacing resulted from the absence of atrial contribution to ventricular filling, mitral regurgitation present and asynchronous ventricular contraction. No significant difference of cardiac performance was demonstrated by changing the site of ventricular pacing, suggesting that the mode of ventricular depolarization itself was not relevant to a decrease in cardiac performance.

Animals↗
PubMed1990

Single-lead VDD pacing system.

A single pass ventricular lead with a dual chamber electrode system, designed for VDD pacing, was implanted in 17 patients (11 men, 6 women, aged 53 to 86 years, mean 74) for symptomatic bradycardia due to second-or third-degree AV block and normal sinus node function. Bipolar atrial electrodes, diagonally displaced along the lead axis and positioned within the right atrial cavity, are used to detect atrial activity that is then differentially processed within the pacemaker. P wave amplitude (amp) derived from a PSA-DAA device at implant was 1.38 +/- 0.28 mV. P wave signal amp derived from telemetered atrial electrograms was 1.29 +/- 0.22 mV at predischarge (n = 17), 1.31 +/- 0.24 mV at 3 months (n = 15), 1.30 +/- 0.24 mV at 6 months (n = 8), 1.51 +/- 0.34 mV at 9 months (n = 4), and 1.35 +/- 0.35 mV at 12 months (n = 2); and the far-field QRS signal measured at predischarge was of negligible voltage (0.17 +/- 0.07 mV). The susceptibility of the atrial sensor system to interference was noted with chest wall stimulation and only at higher sensitivities (0.1 to 0.3 mV) and not with isometric arm exercise. Intact VDD pacing function at rest and during exercise was established using Holter and periodic ECG monitoring. Postoperative complications included one lead displacement and one pocket hematoma. Three patients died postimplant of causes unrelated to pacemaker function. Advantages of the single-lead VDD pacing include: (1) elimination of second atrial sensing lead; (2) superior atrial sensing performance; (3) effective resistance to myopotential and far-field signal interference; and (4) stability of postimplant atrial signal amplitude.

Aged↗
PubMed1993

Isolated lung transplantation for patients with Eisenmenger's syndrome.

BACKGROUND: Eisenmenger's syndrome remains one of the greatest challenges in lung transplantation. METHODS AND RESULTS: Since October 1990, seven such patients with Eisenmenger's syndrome received isolated pulmonary grafts (six double lungs and one single lung). Mean patient age was 32 +/- 6 years (two men and five women). The preoperative mean pulmonary arterial pressure was 90.7 +/- 31.2 mm Hg, and the ventriculoscintigram showed markedly enlarged right ventricle and normal left ventricular function with ejection fraction of 0.660 +/- 0.115. Three atrial septal defects and four patent ducti arteriosus were repaired concomitantly. Excised lung histology showed plexogenic pulmonary arteriopathy with Heath-Edwards' grade 4 through 6. One double lung patient who had preexisting systemic vascular collapse died intraoperatively. The other six patients tolerated transplantation, and on the first operative day, mean pulmonary artery pressure decreased to 22.4 +/- 7.3 mm Hg (P < .002) and gas exchange was acceptable with an arterial/alveolar oxygen tension ratio of 0.47 +/- 0.15. Two patients died of mediastinal and pulmonary infection. The follow-up for the four survivors ranged from 13 to 25 months after transplantation. CONCLUSIONS: Our preliminary experience shows that concomitant isolated lung transplantation with cardiac repair could be a viable therapeutic option for patients with Eisenmenger's syndrome and normal left ventricular function. Dynamic right ventricular outflow obstruction is a potential hemodynamic problem in these pulmonary recipients.

Adult↗
PubMed1984

Effects of atropine on atrial refractoriness and its dispersion in humans.

To evaluate the influence of atropine on atrial refractoriness and its dispersion, we studied ten subjects with sinus bradycardia who were otherwise healthy. Effective and functional refractory periods were measured at three sites of the right atrium (high, middle, and low in the lateral wall), in sinus rhythm and during atrial pacing (120/min), before and after i.v. administration of 0.04 mg/kg of atropine. Both before and after administration, dispersion of atrial refractoriness was determined from the range of refractory periods measured at the three atrial sites as the longest minus the shortest refractory period. Our data indicate that atropine was able to significantly reduce refractoriness and its dispersion. The study protocol allowed us to exclude the possibility that cycle length played a role. The antivagal effect of atropine seemed to explain our findings, even if the possibility that the drug had a direct effect could not be excluded.

Aged↗
PubMed1993

Cardiac noradrenergic nerve terminal abnormalities in dogs with experimental congestive heart failure.

BACKGROUND: We have shown previously that norepinephrine (NE) uptake activity is reduced in the failing right ventricle of animals with right heart failure (RHF) produced by tricuspid avulsion and progressive pulmonary constriction. However, it is unknown whether this defect in neuronal NE uptake is related to reduction of noradrenergic nerve terminals or whether these changes also occur in animals with left heart failure (LHF). It is also unknown whether increased NE release in heart failure contributes to the noradrenergic nerve abnormalities. METHODS AND RESULTS: We measured myocardial NE content. NE uptake function, and noradrenergic nerve profiles in dogs with either RHF or LHF induced by rapid ventricular pacing. NE uptake activity was measured using [3H]NE, and noradrenergic nerve profiles were visualized by glyoxylic acid (SPG)-induced histofluorescence and tyrosine hydroxylase immunocytochemical staining. To study the effects of excess NE, we exposed normal dogs to 8 weeks of chronic NE infusion using subcutaneous osmotic minipumps. RHF and LHF animals exhibited reduced myocardial contractile function and congestive heart failure, as evidence by reduced cardiac output and elevated right atrial pressure. However, unlike that in LHF, left atrial pressure was not increased in RHF. The animals also showed an increase in plasma NE and a decrease in cardiac NE. In addition, SPG-induced histofluorescence correlated significantly with NE uptake activity (r = .712, P < .001) and tyrosine hydroxylase immunoreactive profiles (r = .569, P < .001) in the right ventricles of RHF dogs and in both ventricles of LHF dogs. The numbers of catecholaminergic profiles and tyrosine hydroxylase profiles significantly correlated with cardiac filling pressures. Chronic infusion of NE decreased heart rate in normal dogs but had no effect on either mean aortic pressure or left atrial pressure; like heart failure, it resulted in significant decreases in myocardial NE uptake activity and numbers of SPG-induced catecholaminergic histofluorescence and immunoreactive tyrosine hydroxylase profiles. CONCLUSIONS: Myocardial NE uptake activity was reduced only in the failing ventricles with elevated filling pressure in RHF and LHF. These changes probably were caused by loss of noradrenergic nerve terminals in the failing ventricles, as evidenced by the reductions of catecholaminergic histofluorescence and tyrosine hydroxylase immunostained profiles. Furthermore, since similar reductions of myocardial NE uptake and noradrenergic nerve profiles could be produced by chronic NE infusion in normal dogs, elevated NE levels may play a role in the development of cardiac noradrenergic nerve abnormalities in congestive heart failure.

Animals↗
PubMed2003

The effects of right ventricular apical pacing on left ventricular function. Stimulation of the right ventricular apex: should it still be the gold standard?

Current pacing practice is undergoing continuous and substantial changes. Initially pacing had an exclusively palliative role, since it was reserved for patients developing complete heart block or severe symptomatic bradycardia. With the appearance of novel pacing indications such as pacing for heart failure and atrial fibrillation, the effect of pacing site on cardiac function has become a critically important issue and a subject for consideration. It seems that the classical pacing site in the right ventricular apex is no longer the gold standard because of possible disadvantageous effects on cardiac function. The aim of this review article is to discuss the effect of right ventricular apical pacing on cardiac function including cellular and hemodynamic changes. We also aim to discuss the role of alternative pacing sites in the light of cardiac function.

Journal Article↗
PubMed1989

[Clinical significance of right ventricular ejection fraction in cases with atrial septal defect].

Right ventricular ejection fraction (RVEF) assessed by cardiac radionuclide angiography has been applied to evaluate right ventricular function such as ischemic, valvular and congenital heart disease. Using this modality, previous reports also suggest that there is good correlation between RVEF and mean pulmonary arterial pressure (mPA) from catheterization findings in mitral valvular disease and chronic obstructive lung disease. In this study, cardiac RI angiography were performed on 33 adult patients with atrial septal defect (ASD), RVEF is not so good correlation (r = -0.42) with mPA, but in cases within pulmonary to systemic ratio (Qp/Qs) less than 2.0 limits, there is good correlation between RVEF and mPA (n = 9, r = -0.71). As a conclusion, in ASD, both afterload assessed by mPA and preload assessed by Qp/Qs decrease RVEF.

Adult↗