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PubMed2004

Cardioprotective functions of atrial natriuretic peptide and B-type natriuretic peptide: a brief review.

1. If one was to design a hormone to protect the heart, it would have a number of features shown by the cardiac natriuretic peptides atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP). These hormones are made in cardiomyocytes and are released into the circulation in response to atrial and ventricular stretch, respectively. Atrial natriuretic peptide and BNP can reduce the preload and after-load in normal and failing hearts. They reduce blood volume over the short term by sequestering plasma and over the longer term by promoting renal salt and water excretion and by antagonizing the renin-angiotensin-aldosterone system at many levels. Each of these actions affords indirect benefit to a volume- or pressure-threatened heart. 2. Recent studies have identified additional modes of action of the natriuretic peptides that may also confer cardioprotective benefits, especially in heart disease. The emerging findings are: (i) that ANP and BNP antagonize the cardiac hypertrophic action of angiotensin II and continue working under conditions where endothelial nitric oxide (NO) function is compromised, such as in the presence of high glucose in diabetes; (ii) they potentiate the bradycardia caused by inhibitory ('autoprotective') cardio-cardiac reflexes; and, furthermore, (iii) BNP can suppress cardiac sympathetic nerve activity in humans, including those with heart failure. Thus, it appears that natriuretic peptides can shift sympathovagal balance in a beneficial direction (away from the sympathetic). The vagal reflex and antihypertrophic actions of the peptides are mediated by particulate guanylyl cyclase (pGC) natriuretic peptide receptors. 3. The multiple synergistic actions of the natriuretic peptides make them and their pGC receptors attractive targets for therapy in heart disease. Encouragingly, exogenous natriuretic peptides remain effective even when endogenous peptide levels are raised, as is the case in heart failure. They also remain effective in disease states where other protective mechanisms, such as the NO system, have become ineffective, offering yet further encouragement for the therapeutic use of the natriuretic peptides.

Animals↗
PubMed1978

Comparison of SA nodal and subsidiary atrial pacemaker function and location in the dog.

A 3-4 cm length of sulcus terminalis tissue including the sinoatrial node (SAN) was excised from 14 dogs. After an initial junctional rhythm with SAN excision a P wave emerged within days to weeks in 12 animals. Maximum heart rates of the SAN (preoperative) in response to exercise (276 +/- 15 beats/min), isoproterenol infusion in conscious animals (272 +/- 11 beats/min), and stellate stimulation during anesthesia (273 +/- 9 beats/min) were significantly greater than subsidiary pacemakers (postoperatively) for exercise (219 +/- 9 beats/min), isoproterenol (226 +/- 8 beats/min), and stellate stimulation (197 +/- 9 beats/min). During a final experiment, electrophysiological mapping of the area of earliest epicardial activation (pacemaker location) was carried out. By use of a suction electrode in reference to plunge electrodes located in the anterior interatrial band (AIB), eustachian ridge of the coronary sinus, and limbus of the fossa ovalis, the pacemaker was located at the inferior vena cava-inferior right atrial junction in 80% of the animals mapped. During isoproterenol infusion the foci shifted to regions of the AIB in 70% of the animals mapped. The concept of pacemaker hierarchy is discussed.

Animals↗
PubMed1988

Functional abnormalities of the conduction system in children with an atrial septal defect.

We performed an electrophysiologic study in 40 children with an atrial septal defect and analyzed their pre- and postoperative electrocardiograms and 24-hour Holter recordings. The electrophysiologic study showed a prolonged corrected sinus node recovery time in 83% and an abnormal sinuatrial conduction time in 25% of the children. An early Wenckebach response to atrial pacing was seen in 18%. Sixteen percent had a prolonged atrial conduction time. The atrial functional refractory period was abnormal in 35%. Two children developed nonsustained supraventricular tachycardia during the electrophysiologic study. The preoperative electrocardiogram showed first-degree atrioventricular block in 15% of the children; prolonged periods of accelerated atrial rhythm were found in 35% of the preoperative 24-hour Holter recordings. The incidence of first-degree atrioventricular block and accelerated atrial rhythm decreased postoperatively. We could not find a significant correlation between age or shunt size and the presence of electrophysiologic abnormalities or arrhythmias. These results indicate that the sinus node, atrioventricular node and atrial myocardium show some degree of dysfunction in patients with an atrial septal defect. An early operation may prevent further progression of electrophysiologic abnormalities and the development of symptomatic arrhythmias.

Adolescent↗
PubMed1994

Comparison of ventricular function in atrial rate adaptive versus dual chamber rate adaptive pacing during exercise.

The hemodynamic effects of two different pacing modes--rate adaptive atrial (AAIR) versus dual chamber (DDDR) pacing--were assessed in 12 patients with DDDR pacemakers during upright bicycle exercise first-pass radionuclide angiography using a multiwire gamma camera with tantalum-178 as a tracer. All patients had sinus node disease with intact AV conduction. Patients exercised to the same heart rate in random order in these two different pacing modes, AAIR and DDDR with AV delay (of 100 msec) selected to maintain 100% ventricular capture. Cardiac output increased significantly above baseline values during exercise in both pacing modes: 154 +/- 41% (mean +/- SEM, P = 0.002) with AAIR, versus 95 +/- 24% (P = 0.004) with DDDR (P = NS between the two modes). The peak filling rate, likewise, increased in both pacing modes (2.3 +/- 0.21 end-diastolic volumes/sec to 3.8 +/- 0.31 end-diastolic volumes/sec in AAIR [P = 0.0004] and 2.2 +/- 0.18 end-diastolic volumes/sec to 3.4 +/- 0.27 end-diastolic volumes/sec in DDDR [P = 0.0008]). LV ejection fraction was normal at rest (60 +/- 4%, SEM) and did not significantly change with submaximal exercise in either pacing mode (both 56%, P = NS). No significant changes in end-diastolic volume or stroke volume indexes occurred with exercise in either pacing mode. Our study demonstrates that in patients with normal resting LV function, AAIR and DDDR pacing are equally effective in attaining appropriate increases in cardiac output and LV filling during exercise.

Adult↗
PubMed2001

Desflurane, sevoflurane, and isoflurane affect left atrial active and passive mechanical properties and impair left atrial-left ventricular coupling in vivo: analysis using pressure-volume relations.

BACKGROUND: The effects of volatile anesthetics on left atrial function in vivo have not been described. The authors tested the hypothesis that desflurane, sevoflurane, and isoflurane alter left atrial mechanics evaluated with invasively derived pressure-volume relations. METHODS: Barbiturate-anesthetized dogs (n = 24) were instrumented for measurement of aortic, left atrial, and left ventricular pressures (micromanometers) and left atrial volume (orthogonal sonomicrometers). Left atrial contractility and chamber stiffness were assessed with end-systolic and end-reservoir pressure-volume relations, respectively, obtained from differentially loaded diagrams. Relaxation was determined from the slope of left atrial pressure decline after contraction. Stroke work and reservoir function were assessed by A and V loop areas, respectively. Left atrial-left ventricular coupling was determined by the ratio of left atrial contractility and left ventricular elastance. Dogs received 0.6, 0.9, and 1.2 minimum alveolar concentration desflurane, sevoflurane, or isoflurane in a random manner, and left atrial function was determined after 20-min equilibration at each dose. RESULTS: Desflurane, sevoflurane, and isoflurane decreased heart rate, mean arterial pressure, and maximal rate of increase of left ventricular pressure and increased left atrial end-diastolic, end-systolic, and maximum volumes. All three anesthetics caused dose-related reductions in left atrial contractility, relaxation, chamber stiffness, and stroke work. Administration of 0.6 and 0.9 minimum alveolar concentration desflurane, sevoflurane, and isoflurane increased V loop area. All three anesthetics decreased the ratio of stroke work to total left atrial pressure-volume diagram area, increased the ratio of conduit to reservoir volume, and reduced left atrial contractility-left ventricular elastance to equivalent degrees. CONCLUSIONS: The results indicate that desflurane, sevoflurane, and isoflurane depress left atrial contractility, delay relaxation, reduce chamber stiffness, preserve reservoir and conduit function, and impair left atrial-left ventricular coupling in vivo.

Anesthetics, Inhalation↗
PubMed2001

Remodeling of atrial dimensions and emptying function in canine models of atrial fibrillation.

OBJECTIVES: Atrial tachycardia-induced remodeling (ATR) and ventricular tachypacing-induced heart failure (HF) create experimental substrates for atrial fibrillation (AF), and both have been reported to produce atrial dilation and hypocontractility. The relative importance of changes in atrial size and contractility in the two models is unknown. This study compared changes in atrial dimensions and emptying in ATR versus HF dog models and related them to AF promotion. METHODS: In ATR dogs (n=11), the right atrium (RA) was paced at 400/min for 42 days. In HF dogs (n=10), the right ventricle was paced at 240 bpm for 2 weeks, followed by 3 weeks at 220 bpm. Transthoracic echocardiography was performed at baseline and weekly thereafter. At a terminal electrophysiological study, RA effective refractory period (ERP) was recorded and AF induced repeatedly by atrial burst pacing to measure mean AF duration (DAF). RESULTS: Left atrial (LA) systolic area increased by 10.0% in ATR versus 48.2% in HF dogs (P=0.008), with significant time-dependent changes in HF (P=0.0001), but not ATR (P=0.16). LA diastolic area increased over time in both groups (P=0.004, 0.0001 for ATR and HF respectively), but increases were much larger in CHF (80.2%) compared to ATR (24.2%, P=0.0002). Similar findings were obtained for RA. Fractional area shortening (FAS) decreased by 19.4% (ATR) versus 41.8% (HF, P=0.007) in LA and 13.7% (ATR) versus 33.7% (HF, P=0.03) in RA. RA ERP correlated with DAF in ATR dogs (r=-0.79, P<0.001), but not in HF dogs (r=0.20, P=NS). DAF and diastolic areas of RA and LA were highly correlated (r=0.71, 0.77; P<0.01 for each) in HF dogs, but not in ATR dogs (r=-0.18, 0.29; P=NS). CONCLUSIONS: Remodeling of atrial size and emptying function is much greater in HF than in ATR. Whereas in ATR, electrophysiological remodeling is of prime importance in AF promotion, structural remodeling (as reflected in changes in atrial size and contraction) appears much more important in HF-induced AF.

Animals↗
PubMed1984

Left ventricular function during atrial pacing: a radionuclide angiographic study.

Multigated radionuclide angiography was performed at rest and during atrial pacing in 10 normal subjects. Left ventricular volumes in diastole and systole were measured by total counts in the region of interest of the left ventricle. Stroke volume, cardiac output, ejection fraction, and rates of ejection for each heart rate were calculated. As heart rate increased, there was a gradual decrease in end-diastolic, end-systolic, and stroke volumes without a significant change in cardiac output and ejection fraction. Ejection fraction rate increased and the uncorrected ejection rate decreased with the increase in heart rate. The normal response to tachycardia induced by atrial pacing was a decrease in ventricular volumes without a change in ejection fraction or cardiac output.

Adult↗
PubMed1992

Modulation of rat olfactory bulb mitochondrial function by atrial natriuretic peptide.

Atrial Natriuretic Peptide (ANP) and receptors for ANP are widely distributed in many tissues and cell types in vertebrates. ANP has been shown to be internalized into the cytoplasm in several cell types and thus it raises the possibility that it may act on intracellular receptors. Displacement experiments of [125I]-ANP binding to rat olfactory bulb mitochondrial fraction demonstrated the presence of high affinity (Kd < 10(-9)M) binding sites (Bmax, 112 fmol/mg protein) in this preparation. The addition of ANP (10(-8) M) to this mitochondrial preparation resulted in a 25% increase in TPP+ accumulation, signifying a striking hyperpolarization of the mitochondrial membrane. In contrast ANP did not increase TPP+ uptake to liver mitochondrial preparations. This direct effect of ANP on Olfactory bulb mitochondrial membrane potential may underly the known effects of this hormone on steroidogenesis.

Animals↗
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↗
PubMed2005

Effects of antiarrhythmic drug therapy on atrioventricular nodal function during atrial fibrillation in humans.

AIMS: To assess the effects of metoprolol and amiodarone on atrial and ventricular activity during atrial fibrillation (AF) in post-surgical patients, and to develop and use a mathematical model of the atrioventricular (AV) node during AF that incorporates parameters describing the properties of the AV node to evaluate the physiological basis of the drug effects. METHODS AND RESULTS: Ten post-surgical patients were evaluated where three received no medical therapy, three received metoprolol, three received amiodarone, and one received both metoprolol and amiodarone. The medications led to increases of 37-310 ms in the mean VV interval in treated patients, but much smaller changes in the mean AA intervals in the right and left atria. The mathematical model incorporating a random influence of the concealed conduction parameter was capable of reproducing the histograms of the VV intervals based on the input from the right atrium by systematically searching parameter space. CONCLUSIONS: Changes in the ventricular rate are mainly due to the alteration in the AV nodal properties rather than changes in the atrial rhythm. The medications can display differential effects on the physiological properties of the AV node, and therefore the mathematical model may help to identify novel pharmacological targets.

Aged↗
PubMed1999

Usefulness of low-dose dobutamine stress echocardiography in predicting recovery of poor left ventricular function in atrial fibrillation dilated cardiomyopathy.

Assessment of contractile reserve was performed in 16 patients with dilated cardiomyopathy and chronic atrial fibrillation. In this prospective study, low-dose dobutamine echocardiography could predict recovery of left ventricular dysfunction and could identify tachycardiomyopathy before restoration of sinus rhythm.

Acute Disease↗
PubMed2003

AV nodal ablation and pacemaker implantation improves hemodynamic function in atrial fibrillation.

In drug refractory and highly symptomatic atrial fibrillation (AF) patients, hemodynamic effects of AV node ablation and pacing therapy (APT) were evaluated. Thirty-eight patients with drug refractory and symptomatic AF, underwent APT in eight centers in Japan. The outcome of this therapy was assessed in terms of quality-of-life, cardiac performance measured by echocardiogram, and plasma ANP and BNP levels before and after APT. Quality-of-life assessed by self-administered semi-quantitative questionnaires: WHO QOL 26 (3.0 +/- 0.5 vs 3.4 +/- 0.6, P < 0.01) and the Symptom Checklist: Frequency Scale (1.6 +/- 0.6 vs 0.7 +/- 0.7, P < 0.01) and Severity Scale (1.3 +/- 0.4 vs 0.6 +/- 0.6, P < 0.01), improved significantly 6 months after APT. Ejection fraction (EF) by echocardiogram improved 1 week after APT (59.0% +/- 13.3% vs 63.3% +/- 11.6%, P = 0.02). Plasma ANP levels in the group of ANP > 40 pg/mL at enrollment significantly decreased 1 month later (P = 0.03), and plasma BNP levels in the group of BNP > 20 pg/mL at enrollment significantly decreased 1 month later (P < 0.01). In conclusion, APT has beneficial hemodynamic effects, and plasma BNP levels can predict the most optimal candidates for ablation and pacing therapy.

Aged↗
PubMed1976

Effects of angiographic contrast media on sino-atrial nodal function.

Injection of meglumine diatrizoate (Renografin-76) into the selectively perfused sinus node artery of the dog produces bradycardia which is unaltered by autonomic blockade or by changes in sinus node artery pressure. Contrast agents and other hyperosmolar substances prolong the R-R interval in proportion to their osmolarity. Selective injection of contrast media into other cannulated segments of the coronary tree produces no change in heart rate. Transfemoral arteriography, however, produces bradycardia with both right and left coronary injections. Both direct and reflex sinus node depression occur with coronary arteriography in the dog. Direct effects are mediated by hyperosmolarity.

Adrenergic beta-Antagonists↗