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PubMed1994

Haemodynamic actions of a novel sino-atrial node function modulator, ZENECA ZD7288, in the anaesthetized dog: a comparison with zatebradine, atenolol and nitrendipine.

1. ZENECA ZD7288 (4-(N-ethyl-N-phenylamino)-1,2-dimethyl-6-(methylamino) pyrimidinium chloride, formerly ICI D7288) is a novel sino-atrial node function modulator which selectively slows sinus node rate. Its effects on haemodynamic function have been studied in pentobarbitone anaesthetized dogs, in comparison with zatebradine, atenolol and nitrendipine. 2. ZD7288 lowered heart rate in the dose-range 0.02 to 1.0 mg kg-1 i.v. from 152 to 77 beats min-1. Myocardial contractile function (measured as both dPLV/dtmax and right ventricular free wall developed force) decreased along with rate. Stroke volume increased as rate decreased. Cardiac output decreased at doses in excess of 0.2 mg kg-1, i.v. 3. These haemodynamic changes were reversed when heart rate reduction was reversed by atrial pacing and are, therefore, considered to be indirect consequences of heart rate changes induced by ZD7288. 4. The effects of zatebradine paralleled those of ZD7288 (heart rate reduced from 149 to 60.5 beats min-1 over the dose-range 0.02 to 1.0 mg kg-1, i.v.), except that dPLV/dtmax did not decrease with heart rate and increased during arial pacing. 5. Neither ZD7288 nor zatebradine had significant effects on atrio-ventricular conduction at intrinsic heart rates, but both significantly and dose-dependently prolonged the atrio-ventricular conduction interval during atrial pacing at 180 beats min-1. 6. The observed effects of atenolol were commensurate with removal of beta-sympathetic cardiac drive. Atrial pacing was found not to restore the pre-atenolol heamodynamic state completely. 7. Nitrendipine up to 0.2 mg kg- i.v. induced changes indicative of direct vasodilatation accompanied by reflex compensation, followed by cardiac depression at higher doses. Atrial pacing failed to compensate for the effects of vasodilatation, but caused atrio-ventricular conduction block at doses above 0.5mgkg-1, i.v.8.data show ZD7288 has marked heart rate slowing properties and that accompanying haemodynamic changes appear to be secondary to the rate changes, being reversed by atrial pacing even in the continued presence of the drug. Heart rate slowing without depression of contractile function should prove to be of benefit in the treatment of myocardial ischaemia, particularly in the presence of myocardial dysfunction.

Animals↗
PubMed2004

Echocardiographic assessment of the right ventricular stress-velocity relationship under normal and chronic overload conditions.

UNLABELLED: The effects of chronic volume or pressure overload on the velocity of right ventricular ejection have not been previously well defined. We hypothesized that, as formerly shown for the left ventricle, there would be a direct relationship between the velocity of ejection and an estimate of systolic wall stress. METHODS: Echocardiograms of asymptomatic patients, not on cardiac medications, with either an isolated secundum atrial septal defect > or = 5 mm in diameter or isolated pulmonic stenosis with a peak instantaneous pressure gradient > or = 20 mmHg, were reviewed. Forty-one patients with an atrial septal defect and 34 with pulmonary stenosis met criteria, and were compared to age-matched normal controls. Total subjects were 127 with ages ranging from 1 day to 54 years. Right ventricular monoplane ejection fraction, ejection time corrected for heart rate (ETc), mean normalized systolic ejection rate (MNSERc) and meridianal peak-systolic wall stress (WSps) were measured. RESULTS: Compared to controls, ejection fractions were not significantly different, but WSps averaged 81% and 110% higher, ETc 8% and 9% longer, and MNSERc 5% and 9% slower in the atrial septal defect and pulmonary stenosis groups, respectively. Among all subjects WSps had a significant linear correlation with ETc (r = 0.61, P < 0.01), MNSERc (r =-0.46, P < 0.01), and ejection fraction (r =-0.19, P < 0.05). CONCLUSIONS: Increases in WSps cause an incremental slowing of MNSERc in the right ventricle, with a relationship that is linear over a wide range of normal and abnormal loading conditions.

Adolescent↗
PubMed2005

Mechanism and mapping of atrial arrhythmia in the modified Fontan circulation.

The Fontan circulation has been a major success in the management of patients with functionally single-ventricle cardiac lesions, although arrhythmia remains one of the major complications in the long term and historically has been difficult to treat. The electrophysiologic substrate within the right atrium is complex, with areas of scarring and/or anatomic structures acting as central barriers to conduction in reentrant circuits, which may be mechanistically and anatomically different from typical atrial flutter. Developments in three-dimensional mapping have improved our understanding of different arrhythmia mechanisms, which is fundamental to developing a better strategy for arrhythmia ablation using percutaneous techniques.

Arrhythmias, Cardiac↗
PubMed2004

[Risk assessment in acute myocardial infarction].

Despite the appearance in clinical practice of modern treatment modes as thrombolysis and percutaneous coronary intervention, in-hospital mortality from acute myocardial infarction remains an important problem. In this paper we review recently published data concerning risk stratification in the acute phase of myocardial infarction, different factors affecting the prognosis, their dynamics in the course of the disease, and inter-factor relations. We emphasize the prognostic value of three factors: heart rate variability, left ventricular dysfunction and arrhythmias. Changes in heart rate variability are discussed in association to location of myocardial infarction, patency of infarct-related artery, the chosen treatment mode and its timing. Left ventricular diastolic function and right ventricular function are shown to be predictors of morbidity and mortality after myocardial infarction besides left ventricular systolic function. We also present the latest data concerning the prognostic implication of arrhythmias, their relation to left ventricular function and autonomic nervous system balance. Atrial fibrillation and atrial flutter appear to be important factors in predicting mortality after myocardial infarction, especially in the elderly, as well as ventricular arrhythmias - sustained ventricular tachycardia and ventricular fibrillation.

Aged↗
PubMed2002

Electrophysiological abnormalities of the atrial muscle in patients with paroxysmal atrial fibrillation associated with hyperthyroidism.

OBJECTIVE: Atrial fibrillation (AF) is common in patients with hyperthyroidism. Although the choice of an antiarrhythmic agent should be based on its electrophysiological effects and the electrophysiological properties of the arrhythmia in question, the atrial electrophysiological features of AF associated with hyperthyroidism are unknown. The purposes of this study are to clarify the atrial electrophysiological abnormalities of AF with hyperthyroidism, and to propose effective therapies for AF in patients with hyperthyroidism. SUBJECTS AND DESIGN: This study included 117 patients who underwent electrophysiological study and were evaluated for thyroid function: 29 patients without AF or hyperthyroidism (Group I), 78 patients with lone paroxysmal AF (Group II), and 10 patients with paroxysmal AF and hyperthyroidism (Group III). The following electrophysiological parameters were assessed and measured quantitatively: (1) the incidence of abnormal right atrial electrograms during sinus rhythm, indicating areas of altered anatomy and conduction where AF is likely to develop; (2) the atrial effective refractory period (ERP); and (3) the atrial conduction delay (CD), which is induced by early atrial premature beats close to the atrial ERP and is thought to facilitate the occurrence of AF. RESULTS: The incidence of abnormal right atrial electrograms during sinus rhythm was significantly higher in Group II (67.1%) than in Group I (20.0%, P < 0.001) and Group III (22.2%, P = 0.009). The atrial ERP was significantly shorter in Group III (187 +/- 7 ms) than in Group I (215 +/- 36 ms, P = 0.019) and Group II (208 +/- 28 ms, P = 0.022). The atrial CD was observed in Group III as well as in Group II. CONCLUSIONS: Our data indicate that the electrophysiological features of paroxysmal AF associated with hyperthyroidism are essentially different from those of lone paroxysmal AF. In patients with paroxysmal AF and hyperthyroidism, a shortening of the refractory period in association with a facilitation of the atrial CD could be expected to increase the propensity for AF, and a pre-existent arrhythmogenic substrate might not be essential to the genesis of AF. These findings suggest that the agents that prolong the atrial ERP are effective against AF in patients with hyperthyroidism.

Adolescent↗
PubMed1998

Evaluation of right ventricular systolic pressure during incremental exercise by Doppler echocardiography in adults with atrial septal defect.

STUDY OBJECTIVES: Pulmonary hypertension is the most important complication in patients with atrial septal defect (ASD), but its role in limiting exercise has not been examined. This study sought to evaluate exercise performance in adults with ASD and determine the contribution of elevated pulmonary artery pressure in limiting exercise capacity. DESIGN: We used Doppler echocardiography during exercise in 10 adults (aged 34 to 70 years) with isolated ASD (New York Heart Association class I, II) and an equal number of matched control subjects. Incremental exercise was performed on an electrically braked upright cycle ergometer. Expired gases and VE were measured breath-by-breath. Two-dimensional and Doppler echocardiographic images were obtained at rest prior to exercise to determine ASD size, stroke volume (SV), shunt ratio (Qp:Qs), right ventricular outflow tract (RVOT) size, and right ventricular systolic pressure at rest (RVSPr). Doppler echocardiography was repeated at peak exercise to measure right ventricular systolic pressure during exercise (RVSPex). RESULTS: Resting echocardiography revealed that RVOT was larger (21+/-4 vs 35+/-8 mm, mean+/-SD; p=0.0009) and RVSPr tended to be higher (17+/-8 vs 31+/-8 mm Hg; p=0.08) in ASD; however, left ventricular SV was not different (64+/-23 vs 58+/-23 mL; p>0.05), compared with control subjects. Despite normal resting left ventricular function, ASD patients had a significant reduction in maximum oxygen uptake (VO2max) (22.9+/-5.4 vs 17.3+/-4.2 mL/kg/min; p=0.005). RVSPex was higher (19+/-8 vs 51+/-10 mm Hg; p=0.001) and the mean RVSP-VO2 slope (1+/-2 vs 18+/-3 mm Hg/L/min; p=0.003) and intercept (17+/-4 vs 27+/-4 mm Hg; p=0.05) were higher in the ASD group. VO2max correlated inversely with both RVSPr (r=-0.69; p=0.007) and RVSPex (r=-0.67; p=0.01). CONCLUSION: These findings suggest that adults with ASD have reduced exercise performance, which may be associated with an abnormal increase in pulmonary artery pressure during exercise.

Adult↗
PubMed1995

Does ischemic preconditioning in the human involve protein kinase C and the ATP-dependent K+ channel? Studies of contractile function after simulated ischemia in an atrial in vitro model.

Protein kinase C (PKC) and the ATP-dependent K+ channel (KATP channel) have been implicated in the mechanism of ischemic preconditioning in animal models. This study investigated the role of KATP channels and PKC in preconditioning in human myocardium and whether KATP channels are activated via a PKC-dependent pathway. Right atrial trabeculae were superfused with Tyrode's solution and paced at 1 Hz. After stabilization, muscles underwent one of nine different protocols, followed by simulated ischemia (SI) consisting of 90 minutes of hypoxic substrate-free superfusion paced at 3 Hz and then by 120 minutes of reperfusion. Preconditioning consisted of 3 minutes of SI and 7 minutes of reperfusion. The experimental end point was recovery of contractile function after SI, presented here as percentage recovery (%Rec) of baseline function. %Rec was significantly improved by preconditioning by the KATP channel opener cromakalim (CK), and by the PKC activator 1,2-dioctanoyl-sn-glycerol (DOG) compared with nonpreconditioned controls when these treatments were given before the SI insult (control group, 29.5 +/- 3.6%; preconditioned group, 63.5 +/- 5.4%, CK-treated group, 52.9 +/- 3.1%; and DOG-treated group, 48.0 +/- 3.5%; P < .01). The effects of CK could be blocked by the KATP channel blocker glibenclamide (%Rec, 17.8 +/- 3.5%). Preconditioning could be blocked by the PKC antagonist chelerythrine (%Rec, 24.1 +/- 5.0%) and the KATP blocker glibenclamide (%Rec, 24.8 +/- 3.1%). The effects of DOG could also be blocked by glibenclamide (%Rec, 23.1 +/- 2.3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1984

Left ventricular volumes and function during atrial pacing in coronary artery disease: a radionuclide angiographic study.

This study set out to determine the pathophysiologic changes in the left ventricle during atrial pacing in 22 patients with coronary artery disease. Graduated right atrial pacing to a rate of 160 beats/min, or the induction of angina pectoris or significant ST depression was undertaken. Ventricular volumes were measured at rest and at rates of 100, 120, 140 and 160 beats/min using radionuclide angiography. The volumes at a pacing rate of 100 beats/min were used as a reference standard (100%). In the 22 patients with coronary artery disease, left ventricular end-diastolic volume decreased from 118 +/- 3% at rest to 80 +/- 5% at a rate of 160 beats/min; stroke volume from 121 +/- 3% to 54 +/- 5%; and ejection fraction (EF) from 49 +/- 3% to 37 +/- 5%. End-systolic volume decreased from 118 +/- 4% at rest, reached its minimal value of 94 +/- 5% at a rate of 120 beats/min and then increased slightly to 106 +/- 9% at 160 beats/min. Cardiac output and blood pressure did not change significantly. Compared to the control group of 10 normal subjects, the patients had a significantly smaller decrease in end-diastolic volume and end-systolic volume than in normal control subjects. EF in the normal subjects did not change. Blood pressure, cardiac output and stroke volume were similar in both groups. Atrial pacing tachycardia induced reversible ventricular dysfunction with a decrease in EF. Stroke volume was maintained because of relative ventricular dilatation.

Adult↗
PubMed1987

Primary pulmonary hypertension. A national prospective study.

A national registry was begun in 1981 to collect data from 32 centers on patients diagnosed by uniform criteria as having primary pulmonary hypertension. Entered into the registry were 187 patients with a mean age (+/- SD) of 36 +/- 15 years (range, 1 to 81), and a female-to-male ratio of 1.7:1 overall. The mean interval from onset of symptoms to diagnosis was 2 years. The most frequent presenting symptoms included dyspnea (60%), fatigue (19%), and syncope (or near syncope) (13%). Raynaud phenomenon was present in 10% (95% of whom were female) and a positive antinuclear antibody test, in 29% (69% female). Pulmonary function studies showed mild restriction (forced vital capacity [FVC], 82% of predicted) with a reduced diffusing capacity for carbon monoxide (DLCO), and hypoxemia with hypocapnia. The mean (+/- SD) right atrial pressure was 9.7 +/- 6 mm Hg; mean pulmonary artery pressure, 60 +/- 18 mm Hg; cardiac index, 2.3 +/- 0.9 L/min X m2; and pulmonary vascular resistance index, 26 +/- 14 mm Hg/L/min X m2 for the group. Although no deaths or sustained morbid events occurred during the diagnostic evaluation of the patients, the typically long interval from initial symptoms to diagnosis emphasizes the need to develop strategies to make the diagnosis earlier.

Adolescent↗
PubMed1989

Electrophysiologic assessment of the effects of enflurane, halothane, and isoflurane on properties affecting supraventricular re-entry in chronically instrumented dogs.

Most paroxysmal forms of clinical supraventricular tachycardia (SVT) are likely due to re-entrant excitation. Electrophysiologically demonstrated mechanisms for re-entrant SVT include, in descending order of importance, atrioventricular (AV) node, AV node and accessory (AV bypass) pathway, sinus node, or atrial re-entry. Except for sinus node re-entry, none of these mechanisms for re-entrant SVT can be reliably reproduced in animal models. The authors suspected, however, that anesthetic effects on atrial and AV nodal electrophysiologic properties might be used to predict their actions against suspected re-entrant SVT. Awake-to-anesthetized (1.2 and 1.6 MAC) comparisons for the effects of enflurane (ENF), halothane (HAL), and isoflurane (ISO) on atrial and AV nodal electrophysiologic properties were made in ten chronically instrumented dogs. Studies were carried out with and without pharmacologic autonomic blockade with atropine, propranolol, and hexamethonium. By ANOVA, significant (P less than 0.05) effects of the anesthetics included: prolongation of AV nodal conduction time and the Wenckebach point in dogs with autonomic blockade (ENF, HAL, ISO); increased atrial effective and functional refractory periods in dogs without autonomic blockade (ENF, ISO); increased atrial functional refractory period in dogs without autonomic blockade (HAL); increased AV nodal functional refractory period in dogs with and without autonomic blockade (ENF, ISO), or with autonomic blockade (HAL). Sinus node re-entry, manifest by atrial echo beats during high right atrial stimulation, could be demonstrated in several dogs of each anesthetic test group during awake electrophysiologic testing. All anesthetics, with or without autonomic blockade and autonomic blockade in awake dogs, invariably abolished such re-entry. It is concluded that any anesthetic that increases atrial and AV nodal refractoriness should not be conducive to SVT caused by AV node or atrial re-entry. All of the anesthetics tested also appear effective against sinus node re-entry in dogs in which this mechanism can be demonstrated. Finally, no conclusions can be reached concerning anesthetic effects on re-entry requiring participation of both AV node and AV bypass pathways, since anesthetic effects on AV bypass pathways were not tested.

Animals↗
PubMed1999

Morphologic spectrum of Ebstein's malformation: revisitation relative to surgical repair.

OBJECTIVE: Our aim was to elucidate the morphologic spectrum of Ebstein's malformation of the tricuspid valve with regard to diagnosis and the feasibility of surgical repair, in the light of the currently favored reconstructive techniques. METHODS: We examined 23 autopsied hearts. Taking the displacement of the septal and mural leaflets of the abnormal tricuspid valve as our diagnostic criterion, we focused subsequently on the location of the distorted valvular orifice and the attachment and formation of the anterosuperior leaflet. We also assessed the dimensions of the components of the right ventricle relative to the plane of the displaced valvular orifice. RESULTS: In all hearts, the septal and mural leaflets were hinged at various points within the inlet of the right ventricle. In many cases, however, these leaflets were virtually absent. The plane of the effective tricuspid valvular orifice was displaced anterosuperiorly to varying degrees. In the most severe forms, the valvular mechanism took the form of a 1-leaflet valve. The length of the functional right ventricle when compared with the left ventricle ranged proportionally from 0.6 to 1. 1 (mean, 0.9). CONCLUSIONS: Ebstein's malformation is much more than simple "downward displacement" of the leaflets. In essence, the valvular orifice is formed within the ventricular cavity at the junction of the atrialized inlet and functional ventricular components. When surgical intervention becomes necessary, it is essential to make a detailed assessment of both valvular and ventricular abnormalities.

Adolescent↗
PubMed1988

Right atrial dilatation increases inositol-(1,4,5)trisphosphate accumulation. Implications for the control of atrial natriuretic peptide release.

Stretching the right atrium of isolated perfused [3H]inositol-labelled rat hearts was shown to stimulate the phosphatidyl-inositol turnover pathway as demonstrated by the accumulation of [3H]inositol-(1,4,5)trisphosphate and its degradation products. Stimulation was detectable after 1 min with larger increases observed after 10 or 20 min. These findings demonstrate that the myocardium can respond to dilatation by an activation of the phosphatidylinositol turnover pathway. Such a mechanism has implications for the release of atrial natriuretic peptide following right atrial distention.

Animals↗
PubMed1987

Spacelab Life Sciences flight experiments: an integrated approach to the study of cardiovascular deconditioning and orthostatic hypotension.

The microgravity environment of spaceflight produces rapid cardiovascular changes which are adaptive and appropriate in that setting, but are associated with significant deconditioning and orthostatic hypotension on return to Earth's gravity. The rapidity with which these space flight induced changes appear and disappear provides an ideal model for studying the underlying pathophysiological mechanisms of deconditioning and orthostatic hypotension, regardless of etiology. Since significant deconditioning is seen after flights of very short duration, muscle atrophy due to inactivity plays, at most, a small role. These changes in circulatory control associated with cephalad fluid shifts, rather than inactivity per se, are probably more important factors. In order to test this hypothesis in a systematic way, a multidisciplinary approach which defines and integrates inputs and responses from a wide variety of circulatory sub-systems is required. The cardiovascular experiments selected for Spacelab Life Sciences flights 1 and 2 provide such an approach. Both human and animal models will be utilized. Pre- and post-flight characterization of the payload crew includes determination of maximal exercise capacity (bicycle ergometry), orthostatic tolerance (lower body negative pressure), alpha and beta adrenergic sensitivity (isoproterenol and phenylephrine infusions), baroreflex sensitivity (ECG-gated, stepwise changes in carotid artery transmural pressure with a pneumatic neck collar), and responses to a 24 h period of 5 deg head-down tilt. Measurements of cardiac output (CO2 and C2H2 rebreathing), cardiac chamber dimensions (phased-array 2-dimensional echocardiography), direct central venous pressure, leg volume (Thornton sock), limb blood flow and venous compliance (occlusion plethysmography), blood and plasma volumes, renal plasma flow and glomerular filtration rates, and various hormonal levels including catecholamines and atrial natriuretic factor will also be obtained. The central venous catheter will be inserted immediately pre-launch and monitored with heart rate and blood pressure in-flight until cardiac output, respiratory gas exchange and quantitative 2D echocardiography measurements can be performed. In-flight hemodynamic measurements will be repeated at rest and during submaximal exercise daily and also during maximal exercise midway through the flight to document the timecourse and extent of cardiovascular changes in the payload crew. Parallel studies are planned for the animals. In addition to measurements of right atrial and aortic pressures and cardiac output, a dorsal micro-circulatory chamber will allow determinations of changes in capillary and venular architecture and function in six of the rats. The techniques and findings from many of the SLS-1 and 2 supporting studies have already yielded significant information about circulatory regulation in patients with both hypo- and hypertension. The flight experiments themselves will provide new data to test the validity of both animal and human models currently used for simulating the fluid shifts of a micro-gravity environment. The development of effective countermeasures, not only for short and long duration space travellers, but also for Earth-bound medical patients can then be physiologically based on experimental data rather than anecdote.

Animals↗
PubMed2003

Marked improvement in left ventricular ejection fraction during long-term beta-blockade in patients with chronic heart failure: clinical correlates and prognostic significance.

BACKGROUND: Some patients with heart failure (HF) may have a marked improvement in left ventricular ejection fraction (LVEF) after long-term beta-blockade. We compared the clinical characteristics and the prognosis of these patients with those of other patients. METHODS: One hundred seventy-one patients with chronic HF were assessed before and after 9 to 12 months of maintenance therapy with metoprolol or carvedilol. RESULTS: Thirty-eight patients (22%) showed an increase in their LVEF >or=15 units (from 20% +/- 8% to 43% +/- 10%). Compared with the other patients (LVEF change from 21% +/- 7% to 26% +/- 9%, P <.0001 for differences between groups), these patients also had a greater decline in the left ventricular end-diastolic volume (from 175 +/- 74 mL/m(2) to 113 +/- 36 mL/m(2)) and in the right atrial, mean pulmonary artery, and pulmonary wedge pressures, with a greater increase in the cardiac index, stroke volume index, stroke work index, and maximal functional capacity. Their long-term prognosis was excellent, with a 2-year cumulative survival rate of 95%, versus 81% for the other patients, and a hospitalization-free survival rate of 73%, versus 50% for the other patients (all P <.05). By means of multivariate analysis, only the nonischemic cause of HF and the mean arterial pressure at baseline were independently associated with an increase of >or=0.15 in LVEF. CONCLUSIONS: Patients who show a marked improvement in their LVEF after long-term beta-blockade have an excellent prognosis and have a high prevalence of nonischemic HF and a higher blood pressure at baseline.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Clinical electrophysiological properties of N-allyl-clonidine (ST 567) in man.

The electrophysiological properties of N-allyl-clonidine (ST 567) were studied in 18 patients. Four of these patients were pretreated with intravenous propranolol, 0.2 mg/kg, and atropine, 0.04 mg/kg, to induce autonomic blockade. ST 567 produces a sustained bradycardiac effect at a dose of 40 mg, i.v., in patients without (group I) and with (group II) autonomic blockade. The mean increase in Group I was 23% and in group II, 42%. The sinus node recovery time increased in both groups, from 1,151 +/- 73 to 1,310 +/- 81 msec in group I, and from 995 +/- 145 to 1,599 +/- 248 msec (means +/- SEM) in group II. The corrected sinus node recovery time was unaffected by ST 567 in Group I and increased from 165 +/- 50 to 427 +/- 117 msec in group II. The sinoatrial conduction time was unaffected by ST 567 in group I. The effective refractory period of the right atrium, the atrioventricular node and the right ventricle, as well as the functional refractory period of the atrioventricular node, were unaffected by ST 567 in patients without autonomic blockade. Intra-atrial, atrioventricular, and intraventricular conduction were also not altered by this drug. Thus, the electrophysiological profile of ST 567 differs from other bradycardia-inducing agents such as beta-blockers or calcium antagonists.

Adult↗
PubMed1993

Cytoskeletal role in the contractile dysfunction of hypertrophied myocardium.

Cardiac hypertrophy in response to systolic pressure loading frequently results in contractile dysfunction of unknown cause. In the present study, pressure loading increased the microtubule component of the cardiac muscle cell cytoskeleton, which was responsible for the cellular contractile dysfunction observed. The linked microtubule and contractile abnormalities were persistent and thus may have significance for the deterioration of initially compensatory cardiac hypertrophy into congestive heart failure.

Actin Cytoskeleton↗
PubMed2004

Parasympathetic control of the heart. II. A novel interganglionic intrinsic cardiac circuit mediates neural control of heart rate.

Intracardiac pathways mediating the parasympathetic control of various cardiac functions are incompletely understood. Several intracardiac ganglia have been demonstrated to potently influence cardiac rate [the sinoatrial (SA) ganglion], atrioventricular (AV) conduction (the AV ganglion), or left ventricular contractility (the cranioventricular ganglion). However, there are numerous ganglia found throughout the heart whose functions are poorly characterized. One such ganglion, the posterior atrial (PA) ganglion, is found in a fat pad on the rostral dorsal surface of the right atrium. We have investigated the potential impact of this ganglion on cardiac rate and AV conduction. We report that microinjections of a ganglionic blocker into the PA ganglion significantly attenuates the negative chronotropic effects of vagal stimulation without significantly influencing negative dromotropic effects. Because prior evidence indicates that the PA ganglion does not project to the SA node, we neuroanatomically tested the hypothesis that the PA ganglion mediates its effect on cardiac rate through an interganglionic projection to the SA ganglion. Subsequent to microinjections of the retrograde tracer fast blue into the SA ganglion, >70% of the retrogradely labeled neurons found within five intracardiac ganglia throughout the heart were observed in the PA ganglion. The neuroanatomic data further indicate that intraganglionic neuronal circuits are found within the SA ganglion. The present data support the hypothesis that two interacting cardiac centers, i.e., the SA and PA ganglia, mediate the peripheral parasympathetic control of cardiac rate. These data further support the emerging concept of an intrinsic cardiac nervous system.

Animals↗
PubMed1992

Elevated concentrations of endogenous ouabain in patients with congestive heart failure.

BACKGROUND: An endogenous digitalis-like compound in mammals has long been postulated, but only recently has a substance indistinguishable from ouabain been identified in human plasma. Because of the potential significance of such a substance in patients with congestive heart failure, we sought to evaluate the pathophysiology of endogenous ouabain in these individuals. METHODS AND RESULTS: Using an immunoassay, we determined plasma ouabain concentrations in 51 patients with heart failure and in 19 control subjects. Plasma ouabain concentrations in control subjects ranged from 0.16 to 0.77 nM (mean, 0.44 +/- 0.20 nM). In 19 matched heart failure patients receiving digoxin, the mean ouabain was significantly elevated at 1.59 +/- 2.2 nM (range, 0.17-8.76 nM, p less than 0.05 versus control subjects). The ouabain concentration correlated inversely with both cardiac index (r = -0.62, p less than 0.005) and mean arterial pressure (r = -0.51, p less than 0.05). However, there was no correlation between ouabain and left ventricular filling (r = 0.19, NS) or right atrial pressures (r = 0.20, NS). In 16 heart failure patients not receiving digoxin, the mean ouabain was 1.52 +/- 2.58 nM. No relation between renal function and ouabain was detected. CONCLUSIONS: The unanticipated lack of correlation of ouabain with atrial pressures indicates that volume is not the chief determinant of ouabain concentration in patients with congestive heart failure. However, the significant relations of plasma ouabain concentration with cardiac index and mean arterial pressure imply that endogenous ouabain may be an important homeostatic factor in humans.

Digoxin↗