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Fine structure of cells and their histologic organization within internodal pathways of the heart: clinical and electrocardiographic implications.

The fine structure of the normal internodal pathways was studied in 1 human and 2 canine hearts and correlated with histologic observations on more than 100 human and 10 canine hearts. From the electron microscopic studies six different kinds of myocardial cells were classified from two locations: the Eustachian ridge (posterior internodal pathway) and the Bachmann bundle (anterior internodal pathway). Five of the six kinds of cells (working myocardial cells, Purkinje-like cells, either broad or slender transitional cells and P cells, all previously described) were present in both locations. A sixth cell, pleomorphic and dark in appearance, with a special intertwined relation to P cells, is newly designated as an ameboid cell. It was found solely in the Eustachian ridge. In the same area a rare direct contact between a nerve and a myocardial cell was observed. The importance of these different kinds of cells, their respective cell connections, and their topographic locations inside the internodal pathways are discussed relative to certain functions such as rapid conduction and subsidiary pacemaking. The possible influence of these factors on clinical electrocardiographic changes is considered.

Animals↗

Right atrial isolation associated with atrial septal closure in patients with atrial septal defect and chronic atrial fibrillation.

To restore sinus rhythm in the remaining heart chambers of six adult patients with atrial septal defect and chronic or paroxysmal atrial fibrillation, electrical, right atrial isolation associated with surgical correction of the defect was performed. All but one patient was free from atrial fibrillation without medication 2-25 months after operation. The isolated right atrial appendages showed intrinsic rhythmical activity in five patients and no electrical activity in one. Right atrial isolation is a safe and effective procedure that abolishes atrial fibrillation in patients with arrhythmia after surgical correction of atrial septal defect.

Adult↗

[Discovery of the pacemaker and heart conduction system in mammals. Fantasy and truth].

The first report about experimental investigations on the origin of the rhythms in the mammalian heart were published in 1888 by McWilliam. Similar experiments were described by Hering in several publications starting from 1900. The results led to the hypothesis of the myogenic genesis of the rhythms. However, in 1907, Hering stated that the origin of the stimulus in the mammal heart was probably a nervous function. In 1898, 1903, and 1906 Wenckebach described the function and the functional localization of the pacemaker in the heart of the intact man, and in 1906, he described the morphology of the pacemaker and its blood supply in the post mortem human heart. In the same year, Adam analyzed the localization of the "natural" pacemaker and the regions of the secondary pacemakers in the mammal heart. In 1907, Keith and Flack introduced the term "sino-auricular node". They quoted the findings of Wenckebach and Hering, and they mentioned McWilliam. A muscular connection between the right atrium and both ventricles of the mammal heart was found by Kent and by His in 1893. In 1907, Tawara called the structure of the origin of the a-v connection "atrio-ventricular node". It was, however, the scientific discovery of Tawara that the a-v pathway was connected with the muscles of the ventricles by the Purkinje fibers. He discovered that the pathway consists of muscles which are histologically divided and functionally different from the other heart muscles. It is a system of specialized muscles which conduct the stimulus for the contraction without contracting themselves.

Animals↗

Effects of ACTH and cortisol administration on blood pressure, electrolyte metabolism, atrial natriuretic peptide and renal function in normal man.

Both Adrenocorticotrophin (ACTH) and glucocorticoids raise blood pressure in man and animals, but the relationship of this and altered renal function to other cardiovascular variables, and the differences and similarities of the effects of the two agonists have not been fully explained. The present study compares the effects of ACTH (0.5 mg i.m; every 12 h) and cortisol (50 mg orally, every 6 h) in six normal men over a period of 5 days, preceded and followed by control periods of 3 and 2 days, respectively. Plasma cortisol levels were higher during ACTH treatment than during cortisol treatment. Both treatments raised blood pressure significantly and caused a marked antinatriuresis and expansion of extracellular fluid and plasma volume. ACTH also enhanced potassium excretion but this was less obvious for cortisol. Plasma concentrations of atrial natriuretic peptide rose to more than twice the basal level with both treatments. Both treatments markedly altered renal function. They raised glomerular filtration rate (GFR), i.e. inulin clearance (141% with ACTH; 113% with cortisol) although creatinine clearance was not changed, showing this to be an unreliable index during steroid administration. Filtration fraction (FF) also increased during both treatments, and renal blood flow (RBF) fell, although this achieved statistical significance only during cortisol treatment. Effective renal plasma flow [para-amino hippurate (PAH) clearance] remained unchanged while calculated renal vascular resistance increased. Fractional sodium reabsorption also rose but achieved statistical significance only during ACTH treatment. The similarity of response to treatment suggests that cortisol is largely responsible for the effects of ACTH.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

Velocity of closure of Björk-Shiley Convexo-Concave mitral valves: effect of mitral annulus orientation and rate of left ventricular pressure rise.

The purpose of this study was to determine analytically the hemodynamic factors that affect the closing velocity of the disc of Björk-Shiley convexo-concave (BSCC) prosthetic mitral valves. The motion of the BSCC disk was modelled by Newton's second law written in the form of a second order differential equation which expressed the instantaneous angle of the disc with respect to the valve ring as a function of the instantaneous pressure drop across the mitral valve, delta P(t), and the angle of the pressure gradient vector acting upon the disc during closure. The disc closes in response to the negative pressure drop created by the crossover of left atrial and left ventricular (LV) pressures. The rate of closure depends on the rate of development of the pressure drop across the valve, d delta P/dt, which is largely dependent upon the rate of change of left ventricular pressure during isovolumic contraction, LV dP/dt. The closure rate is also strongly dependent on the initial angle of the pressure drop vector with respect to the disc. The disc was predicted to reach its highest velocity at the moment of impact, based on the Runge-Kutta solution. Modelling suggests that a high LV dP/dt during valve closure or distorted LV geometry, causing the angle between the fully open disc and the pressure drop vector to shift, will cause the valve to have a high velocity at the moment of impact and may produce high impact loads.

Algorithms↗

Contractile properties of the functionally divided python heart: two sides of the same matter.

The heart of Python regius is functionally divided so that systemic blood pressure is much higher than pulmonary pressure (6.6+/-1.0 and 0.7+/-0.1 kPa, respectively). The present study shows that force production of cardiac strips from the cavum arteriosum and cavum pulmonale exhibits similar force production when stimulated in vitro. The high systemic blood pressure is caused, therefore, by a thicker ventricular wall surrounding the cavum arteriosum rather than differences in the intrinsic properties of the cardiac tissues. Similarly, there were no differences between the contractile properties of right and left atria. Force production was similar in atria and ventricle but the atria contracted and relaxed much faster than the ventricle. Graded hypoxia markedly reduced twitch force of all four cardiac tissues, and this was most pronounced when PO(2) was below 40 kPa. In contrast, the four cardiac tissues were insensitive to acidosis during normoxia although acidosis increased the sensitivity to hypoxia. Adrenergic stimulation increased twitch force of all cardiac tissues, while cholinergic stimulation only affected the atria and reduced twitch force markedly. In spite of the different oxygen availability of the two sides of the heart, the biochemical and functional properties are alike and the differences may instead be overcome by the coronary blood supply.

Acetylcholine↗

Different patterns of interatrial conduction in clockwise and counterclockwise atrial flutter.

BACKGROUND: The terms counterclockwise (CC) and clockwise (C) atrial flutter (Afl) are used to describe right atrial activation around the tricuspid valve in the left anterior oblique view. The manner in which the left atrium is activated, as reflected by coronary sinus (CS) recordings, has not been systematically evaluated. METHODS AND RESULTS: Nine patients with both CC and C Afl underwent electrophysiological study with CS recordings during both rhythms with the use of a decapolar catheter with the tip placed in the distal CS. Patterns of CS activation during each type of Afl as well as during during sinus rhythm were categorized into 1 of 3 patterns: sequential proximal-to-distal, sequential distal-to-proximal, and fused, indicating activation from different directions. In 7 of 9 patients, the pattern of CS activation in CC Afl and C Afl differed, with a proximal-to-distal pattern in CC Afl and a fused pattern in C Afl. In 2 patients, pacing the high right atrial septum near the presumed site of Bachmann's bundle in sinus rhythm showed a similar fused pattern of CS activation. CONCLUSIONS: These results demonstrate different patterns of CS activation in CC Afl and C Afl in the majority of patients and are consistent with a model in which the left atrium is activated predominantly over Bachmann's bundle during C Afl and over the CS os in CC Afl. These findings may have implications for maintenance of Afl, interpretation of flutter wave morphology on surface ECG, and left atrial mechanical function in Afl.

Aged↗

Learning on the Web. Case 7: recurrent pleural effusions, resistant atrial arrhythmias, and abnormal liver function tests: general medicine or cardiology?

A 65 year old man presented with recurrent pleural effusions. Repeated pleural fluid examination and pleural biopsy were unremarkable. Pericardial calcification was noted on admission and attributed to an uncomplicated episode of pericarditis 30 years previously. His symptoms and signs were not thought not to be associated with the heart. While awaiting an open pleural biopsy the patient was admitted with a further pleural effusion, jaundice, resistant atrial arrhythmias, and dyspnoea. Hepatic investigations including autoantibody screen and transjugular liver biopsy were normal. The significance of these signs and symptoms, the diagnosis, and the management of these problems are discussed in an interactive case presentation.

Aged↗

Intraoperative radiofrequency microbipolar coagulation to replace incisions of maze III procedure for correcting atrial fibrillation in patients with rheumatic valvular disease.

OBJECTIVE: Radiofrequency catheter ablation of atrial tachycardias and flutter is an established technique. The same modality in the microbipolar mode is effective in producing full thickness coagulation injury. Cox's maze procedure is highly successful in curing atrial fibrillation (AF) surgically. However, it consumes relatively long cross clamp time and cardiopulmonary bypass time. In this study, radiofrequency microbipolar coagulation was used as an adjunct to corrective valve surgery, as an intraoperative ablative modality to replace Cox's maze III incisions, thus remarkably shortening the procedure. The results of this procedure are compared historically with those of 26 patients who underwent corrective valve surgery alone. METHODS: Radiofrequency microbipolar coagulation was used to produce conduction blocks along the Cox's maze III incision lines as an adjunct to valve surgery in 18 patients in atrial fibrillation undergoing surgery for rheumatic valvular disease. A bayonet type bipolar forceps with an active tip length of 7 mm drawing current from a microbipolar port of Valleylab Force 4 electrosurgical unit (Valleylab, Boulder, CO) was used for microbipolar coagulation. A 3-mm retinal handheld cryoprobe working on nitrous oxide gas was used for cryoablation. RESULTS: A total of 15 survivors in the coagulation maze group were followed from 43 to 224 days (149.7 +/- 73.1 mean +/- S.D.). Twelve of the 15 survivors (80%) converted to normal sinus rhythm (70% confidence limit: 64.7-90.6%). Atrial transport function studies with pulsed wave doppler, showed presence of a wave in all the 12 (100%) patients in tricuspid valve flow and in nine (75%) patients in mitral valve flow. The procedure took 11.62 +/- 3.86 min of elective cardioplegic arrest time for the left atrial portion and 18.71 +/- 4.25 min of cardiopulmonary bypass time during reperfusion for the right atrial portion. Of the 23 survivors out of 26 patients who underwent the valve procedure alone, only one patient (4.3%) converted to normal sinus rhythm (70% confidence limit: 0.6-14%). CONCLUSION: Thus, our modification considerably shortened the time taken for creating the maze in comparison to the Cox's maze procedure and was effective in restoring normal sinus rhythm in 80% of the patients.

Adult↗

[Influence of sinus rhythm restoration and maintenance on left ventricle diameter and function in patients with persistent atrial fibrillation--one year follow-up].

UNLABELLED: Aim of our study was to determine the dynamics of selected echocardiographic parameters after sinus rhythm (SR) restoration and maintenance in pts with persistent nonvalvular atrial fibrillation (AF) during one year follow-up period. MATERIAL AND METHODS: Our study population comprised 104 pts (F/M 33/71; mean age 60.4 +/- 7.4) assigned to SR restoration and maintenance with serial antiarrhythmic drug usage, for whom transthoracic echocardiographic (TTE) variables were recorded prior to, 2 and 12 months after cardioversion (CD). Left ventricle diastolic diameter and fractional shortening were variables of interest. RESULTS: SR was presented in 66 (63.5%) pts at one year. There was no significant differences in left ventricle diastolic diameter during the follow up. A significant increase in left ventricular fractional shortening (29.9 +/- 6.9% vs 34.5 +/- 8.9%; p < 0.001) was found in pts assigned to the sinus rhythm restoration according to intention-to-treat analysis. Such trend was noted only in pts who maintained SR during the follow up (29.9 +/- 7.6% vs 35.6 +/- 9.3%; p < 0.001). CONCLUSIONS: Among all considered variables only value of left ventricular fractional shortening increased after successful CV of persistent AF in one year follow-up.

Aged↗

Acute volume loading, atrial natriuretic peptide release and cardiac function in healthy men. Effects of beta-blockade.

Release of ANP is dependent on right atrial distension and pressure, which in turn are dependent on both venous return and left ventricular function. These two latter parameters are both modulated by beta-receptors. In the present study, the effects of selective beta-blockade vs non-selective beta-blockade on hypertonic volume expansion induced changes in ANP release and systemic hemodynamics were assessed in 8 healthy normotensive male volunteers. On placebo, infusion of hypertonic saline (1200 ml of 2.5% NaCl) caused an intravascular volume expansion of 10-11%, and small non-significant increases in cardiac performance (LVEDV, SV, or CI), but it provoked a 2-fold increase in plasma ANP. Beta-blockade by either atenolol or propranolol blunted the increase in cardiac volume load (reflected by LVEDV) as compared to placebo, but did not affect the ANP response to volume expansion. The increase in ANP correlated closely with the intravascular volume expansion on placebo and to a lesser extent on beta-blockade. In healthy men, therefore, intravascular volume expansion that caused only small changes in cardiac activity, resulted in clear increases in release of ANP. Inhibition of the increase in cardiac volume load by beta-blockade did not interfere with ANP increase, suggesting a role for extra-cardiac receptors in the release of ANP or a change in the pressure/volume relationship.

Adrenergic beta-Antagonists↗

The mechanical atrioventricular time of isolated hearts as a correlate of the atrioventricular conduction time.

The time difference between onset of contraction in right atrium and left ventricle of isolated guinea pig hearts (mechanical AV time) was measured continuously by an impulse-triggered interval counter and taken as an equivalent of the electrophysiological AV conduction time derived from the epicardial ECG. Excellent correlation between these two parameters was established over a broad range of experimentally modified conduction times. The method was used to analyze the influence of electrical pacing, epinephrine, Ca2+ ions, and adenosine both on the AV conduction and on functional parameters of the hearts and revealed advantages in comparison to separate tests of single parameters in different experimental arrangements.

Adenosine↗

Early cardiovascular changes in 10- to 15-year-old stunted children: the Transition and Health during Urbanization in South Africa in Children study.

OBJECTIVE: Early changes in vascular function could be associated with stunting, which may contribute to the development of cardiovascular diseases in later life. In this study we tested the hypothesis that stunting may be related to changes in cardiovascular function in African children ages 10 to 15 y. METHODS: In the Transition and Health during Urbanization in South Africa in Children study, the health status of children in the North-West Province of South Africa was studied. It was an epidemiologic, cross-sectional study in which 583 black non-stunted and 192 stunted children (stature below the fifth percentile for age) of both sexes ages 10 to 15 y were recruited from 44 schools. Blood pressure was monitored with the Finapres (finger-arterial pressure) apparatus and by means of the Fast Modelflo software program; measurements for systolic and diastolic blood pressure, mean arterial pressure, pulse pressure, heart rate, cardiac output, stroke volume, total peripheral resistance, and arterial compliance were obtained. Dietary intake data were collected with a 24-h dietary recall questionnaire. Nutrient coding was the same for all recalls and macro- and micronutrients were calculated. Anthropometric measurements were done according to standard methods. RESULTS: There were no significant differences in systolic blood pressure and diastolic blood pressure between stunted and non-stunted children after correction for body mass index and heart rate. Stroke volume, arterial compliance, and cardiac output were significantly lower and total peripheral resistance was significantly higher in stunted children than in non-stunted children. No significant differences in dietary intake could be detected, although dietary intakes were slightly lower in the stunted children. CONCLUSIONS: We found that compliance, a marker of vascular function, is significantly lower in stunted children. Stunting was related to early changes in cardiovascular function in African children ages 10 to 15 y.

Adolescent↗

Coordination of membrane excitability through a GIRK1 signaling complex in the atria.

Control of heart rate is a complex process that integrates the function of multiple G protein-coupled receptors and ion channels. Among them, the G protein-regulated inwardly rectifying K+ (GIRK or KACh) channels of sinoatrial node and atria play a major role in beat-to-beat regulation of the heart rate. The atrial KACh channels are heterotetrameric proteins that consist of two pore-forming subunits, GIRK1 and GIRK4. Following m2-muscarinic acetylcholine receptor (M2R) stimulation, KACh channel activation is conferred by the direct binding of G protein betagamma subunits (Gbetagamma) to the channel. Here we show that atrial KACh channels are assembled in a signaling complex with Gbetagamma, G protein-coupled receptor kinase, cyclic adenosine monophosphate-dependent protein kinase, two protein phosphatases, PP1 and PP2A, receptor for activated C kinase 1, and actin. This complex would enable the KACh channels to rapidly integrate beta-adrenergic and M2R signaling in the membrane, and it provides insight into general principles governing spatial integration of different transduction pathways. Furthermore, the same complex might recruit protein kinase C (PKC) to the KACh channel following alpha-adrenergic receptor stimulation. Our electro-physiological recordings from single atrial KACh channels revealed a potent inhibition of Gbetagamma-induced channel activity by PKC, thus validating the physiological significance of the observed complex as interconnecting site where signaling molecules congregate to execute a coordinated control of membrane excitability.

Animals↗

"Ischemic" heart disease in fire fighters with normal coronary arteries.

Near maximal stress testing conducted on a group (N = 90) of randomly selected Los Angeles City fire fighters (age 40-59 yrs.) revealed that 10% had ischemic ECG changes. These ischemic ECG responses were confirmed during a second test conducted two to four weeks after the initial test. Coronary heart disease (CHD) risk factor analysis revealed that in general the men were not at high risk for CHD. Six of the nine men elected to undergo cardiac catheterization and angiography. One patient had severe triple vessel disease and subsequently underwent aorto-coronary bypass surgery. Another had 50% obstruction in the circumflex branch of the left coronary while the other four men had no visable signs of coronary obstruction. The men with "normal" coronaries, however, did show signs of abnormal cardiac function during atrial pacing. One man had cardiac enlargement, hypokinesis, ischemic ECG and abnormal lactate metabolism. Another had abnormal lactate metabolism and ischemic ECG. A third man had moderate cardiac enlargement with anterior wall hypokinesis. The fourth had ischemic ECG changes with angina but otherwise normal cardiac function. All four of these men had pressures which were within normal limits. These data show that some fire fighters have "ischemic" heart disease with patent coronary arteries. This disease may be due to job related factors (i.e. carbon monoxide and other noxious fumes, catecholamines, etc.) which reduce myocardial oxygen supply or greatly increase myocardial oxygen demands.

California↗

Prejunctional alpha 2-adrenoceptors in mouse atria function through G-proteins which are sensitive to N-ethylmaleimide, but not pertussis toxin.

1. The identity of the G-proteins involved in prejunctional alpha 2-adrenoceptor signal transduction in mouse atria was examined by use of the G-protein inactivators N-ethylmaleimide and pertussis toxin. 2. The alpha 2-adrenoceptor partial agonist clonidine (0.03 microM) inhibited the electrical stimulation-induced (S-I) outflow of radioactivity from mouse atria which were incubated with [3H]-noradrenaline and stimulated at 5 Hz. The partial alpha 2-adrenoceptor agonist St 363 (10 microM) inhibited the S-I outflow of radioactivity at the lower stimulation frequency of 2.5 Hz. The inhibitory effects of these compounds were not altered in mice pretreated with pertussis toxin (1.5 micrograms, i.v.). 3. The alpha 2-adrenoceptor antagonist, idazoxan (0.1 microM), increased the S-I outflow of radioactivity from mouse atria stimulated at 5 Hz, and this effect was not altered in atria from mice pretreated with pertussis toxin. 4. The inhibitory effects of clonidine and St 363 and the facilitatory effect of idazoxan on the S-I outflow of radioactivity from mouse atria were significantly less in atria incubated with N-ethylmaleimide (NEM, 3 microM) for 60 min before the [3H]-noradrenaline incubation. 5. The results suggest that prejunctional alpha 2-adrenoceptors in mouse atria function through G-proteins which are NEM-sensitive, but pertussis toxin insensitive.

Adrenergic alpha-Agonists↗