Mitral valve and tricuspid valve dysplasia in a 9‐week‐old Standardbred colt

A 9‐week‐old Standardbred colt was presented for investigation of dull demeanour, exercise intolerance and heart murmurs. Cardiac auscultation revealed a grade 5/6 holosystolic murmur and a grade 5/6 pansystolic murmur over the left and right cardiac apex respectively, and an irregularly irregular cardiac rhythm. Electrocardiographic examination findings were consistent with atrial fibrillation and tachycardia. Echocardiographic examination identified marked atrioventricular regurgitation and atrial dilation bilaterally, thickening of the mitral and tricuspid valves and dilation of the pulmonary artery consistent with pulmonary hypertension. No ventricular or atrial septal defect was present. Cardiomegaly and diffuse pulmonary oedema were evident on examination of lateral thoracic radiographs. Dysplasia of the mitral and tricuspid valves, eccentric cardiomegaly and pulmonary oedema were confirmed by post mortem examination. Dysplasia of the atrioventricular valves represents a rare cause of biventricular failure in the horse.     

Natriuretic peptides and the control of catecholamine release in two freshwater teleost and a marine elasmobranch fish

Experiments were carried out in situ and in vivo to investigate the relationship between natriuretic peptides (NPs) and humoral catecholamine secretion in the American eel (Anguilla rostrata), rainbow trout (Oncorhynchus mykiss) and spiny dogfish (Squalus acanthias). In situ perfusion of the chromaffin tissue of A. rostrata with homologous atrial NP (ANP; 10–9 mol l–1) or ventricular NP (VNP; 10–9 mol l–1), or O. mykiss with either rat ANP (10–9 mol l–1), eel VNP (10–9 mol l–1), or trout VNP (10–9 mol l–1), did not significantly affect basal or carbachol-elicited (10–5 mol kg–1) catecholamine release. Bolus injections of homologous ANP (10–9 mol kg–1) or VNP (10–9 mol kg–1) in A. rostrata in vivo elicited a rapid and prolonged reduction in arterial blood pressure and an increase in heart rate (fH); circulating plasma catecholamine levels were unaffected. In O. mykiss, bolus injections of rat ANP (10–9 mol kg–1) or trout VNP (10–9 mol kg–1) elicited a significant bi-phasic pressor- depressor response and a marked increase in fH. Neither the acute pressor or the longer-term depressor effects of NPs in O. mykiss were associated with any change in circulating plasma catecholamine levels. In S. acanthias, bolus injections of homologous C-type natriuretic peptide (CNP; 10–9 mol kg–1) elicited a bi-phasic pressor-depressor response, an increase in systemic resistance, a decrease in cardiac output and stroke volume, but no change in fH. Plasma noradrenaline levels were elevated 15- fold after CNP injection while circulating adrenaline levels remained unchanged. These results show that NPs of systemic origin do not directly or indirectly affect basal or cholinergically-mediated catecholamine release in A. rostrata and O. mykiss and that the initial pressor response to NP's in trout cannot be attributed to an elevation of circulating catecholamines. Conversely, CNP appears to be a potent secretagogue (direct or indirect) of noradrenaline release in S. acanthias and thus there is likely to be a significant humoral adrenergic component to the cardiovascular effects of NPs in this species.     

Effects of atorvastatin on atrial electrical remodeling in a rabbit model of chronic atrial fibrillation

AIM: To evaluate the effects of atorvastatin (ATO) on atrial electrical remodeling in a rabbit mo-del of chronic atrial fibrillation (AF) produced by 3 weeks of rapid atrial pacing (RAP). METHODS: The sternotomy was performed and the pacing and testing electrodes were fixed to the left atria of 24 New Zealand white rabbits. The animals were randomly divided into 3 groups. The rabbits in model group and ATO group were subjected to RAP for 3 weeks, and then were treated with placebo and ATO (2.5 mg·kg^-1·d^-1), respectively. The rabbits in sham group did not receive RAP and drugs. Electrophysiological examination was performed to test heart rate, P-wave duration, atrial effective refractory period (AERP) and AF inducibility. The protein expression levels of Cav1.2, Kv4.3 and myeloperoxidase (MPO) were detected by Western blot. RESULTS: Sustained AF was induced in 5 and 4 rabbilts in model group and atorvastatin group and no rabbits in sham group was found. After 3 weeks of RAP, compared with sham group, heart rate and P-wave duration were increased and AERP was shortened in model group and ATO group (P<0.05). Compared with model group, AERP was increased in ATO group (P<0.05), while heart rate and P-wave duration had no difference between these 2 groups. Compared with sham group, the protein levels of Cav1.2 and Kv4.3 were decreased, and protein level of MPO was increased in model group and ATO group (P<0.05). Compared with model group, Cav1.2 was increased and MPO was decreased in ATO group (P<0.05), while Kv4.3 had no difference between these 2 groups. CONCLUSION: Atorvastatin suppresses the down-regulation of atrial Cav1.2 protein level and the shortening of AERP, thus preventing atrial electrical remodeling in a rabbit model of chronic AF. The effect of atrovastatin on reducing atrial MPO level may be the potential mechanism.     

Non-contact mapping and frequency analysis of vagal-mediated atrial fibrillation

AIM: To explore the mechanism of the initiation and maintenance of vagal-mediated atrial fibrillation (AF) by non-contact mapping and frequency analysis of vagal-mediated atrial fibrillation in canine.METHODS: Atrial effective refractory period (AERP) and dispersion of AERP were measured in 8 canine during baseline and bilateral cervical vagal nerve stimulation (CVNS). Left atrium (LA) and right atrium (RA) electrical activity of AF was assessed by non-contact mapping and frequency analysis.RESULTS: Compared with baseline, CVNS attenuated left and right AERP, but only increased the dispersion of left AERP. During CVNS, AF was easily induced and maintained, repetitive organized activations rotated around a preferential route were only found in the LA, and dominant frequencies (DFs) from LA were higher than those of the RA ［(12.5±1.5)Hz vs (9.3±1.2)Hz, P<0.01］. After the cessation of CVNS, DFs of AF decreased in the LA and RA ［(9.2±0.5)Hz vs (8.5±0.6)Hz, P>0.05］, and AF was spontaneously terminated.CONCLUSION: The change of electrophysiological character, difference of activation pattern, and frequency gradient between the LA and RA suggest that the initiation and maintenance of vagal-mediated AF dependent on the LA.     

瓣膜置换术围术期心房纤颤的电击转律及窦性心律维持

用术中电击除颤、控制左房压及应用乙胺碘呋酮的方法，对５４例瓣膜置换术围术期心房纤颤进行转律处理，有４６例转为窦性心律并维持一段时间，有利于术后血流动力学稳定及心功能恢复。认为：围术期采取积极措施使房颤转为窦律很有必要，术中电击除房颤是安全有效的转律方法；良好的心肌保护是提高转律率的重要措施；控制左房压及预防性应用乙胺碘呋酮是维持窦性心律的主要手段。     

Effects of diltiazem on hemodynamic variables and ventricular function in healthy horses

Quinidine is effective for treatment of atrial fibrillation (AF) in horses, but often accelerates ventricular response rate. Diltiazem effectively controls heart rate response to AF in other species. This investigation determined the effects of diltiazem on cardiac rate and rhythm, left ventricular (LV) function, central hemodynamics, and peripheral blood flow in normal, standing, nonsedated horses. A dose-finding study was performed. Afterward, 8 healthy horses were treated with diltiazem IV every 30 minutes to achieve cumulative dosages of 0 (saline control), 1, 1.5, and 2 mg/kg. Plasma diltiazem concentration, heart rate and rhythm (by electrocardiography), LV function and central hemodynamics (by cardiac catheterization), LV dimensions (by echocardiography), and forelimb blood flow (by Doppler sonography) were determined during each treatment period. Diltiazem plasma concentrations between 390 and 910 ng/mL were achieved, with considerable variation among horses. Cardiac effects of diltiazem included intermittent depression of the sinus and atrioventricular (AV) nodes and mild impairment of systolic and diastolic LV function. Vascular effects of diltiazem included arterial vasodilatation, increased limb blood flow, and decreased systemic vascular resistance. Baroreceptor reflex-mediated sympathetic activation increased sinus node rate and presumably blunted the depressive effects of diltiazem on myocardial and nodal tissues. Two horses developed transient high-grade sinus arrest with severe systemic hypotension. Diltiazem appears relatively safe in healthy horses, but dosage may be limited by hypotension from vasodilatation and direct suppression of sinus node discharge. Because of its inhibitory effects on AV nodal conduction, diltiazem may prove useful for heart rate control in horses with AF.     

Influence of valvular insufficiency and recurrent airway obstruction on haemodynamics and therapy in warmblood horses with atrial fibrillation

The aim of this study was to investigate the potential haemodynamic effects of valvular insufficiency and recurrent airway obstruction (RAO) in horses with atrial fibrillation (AF). Therefore in ten healthy horses (group 1) and 40 horses with AF a clinical examination, a lung examination, echocardiography and right heart catheterization for measurement of intracardic and pulmonary pressures were performed. According to the clinical findings the horses with AF were subdivided into 4 groups (group 2: AF; group 3: AF/valvular insufficiency; group 4: AF/RAO; group 5: AF/valvular insufficiency/RAO). Most of the horses of group 3 and 5 suffered from two valvular insufficiencies (mitral and tricuspid valve insufficiency: n=11, mitral and aortic valve insufficiency: n=2). The remaining horses showed a single mitral (n=6), tricuspid (n=2) or aortic valve insufficiency (n=1) or more than two valvular insufficiencies (n=4). In group 2 right ventricular mean pressure (RVPm) was higher than in group 1 and 4 (P<0.025); diastolic right ventricular pressure was higher than in group 1; PWP was higher than in group 1 and group 4; PDP was lower compared to group1. Compared to group1 in group 3 left atrial diameter (LA) was greater; the PAPs was higher and the PDP lower (P<0.05). In group 4 RVPm and PWP was lower compared to group 2. In group 5 LA, fractional shortening and diastolic left ventricular diameter were greater, PWP and PAPs were higher and PDP lower compared to group1. Twenty six of the 40 horses with AF (65%) were treated. Successful cardioversion to sinus rhythm occurred in 15 horses (58%). Therapy was successful in 50% of the treated horses of group 2 and 3, in 67% of the treated horses of group 4 and in 63% of the treated horses in group 5. In conclusion the presence of valvular insufficiency or RAO influences the haemodynamics of horses with AF.     

Relationship between fibrosis and remodeling of gap junction in atrium of patients with atrial fibrillation

AIM: To examine fibrosis and remodeling of gap junction in atrial myocardium of patients with or without atrial fibrillation and to investigate the relationship between them. METHODS: Right atrial appendage (RAA) samples were collected from 44 patients with rheumatic heart disease during heart operation, 28 of which were clinically diagnosed as atrial fibrillation (AF), the left remained sinus rhythm (SR). Fibrosis and remodeling of connexin 43 were examined by polarization microscope and microscopy respectively, and analyzed with an image analyzer. Meanwhile, intercalated disc was counted under transmission electron microscope. The collagen volume fraction of type I (CVF-I) and the volume fraction of Cx43 (Cx43VF) were studied between groups of atrial fibrillation and sinus rhythm. The relationship between CVF-I and fraction of remodeled intercalated disc was studied as well. RESULTS: (1) Polarization microscope demonstrated that CVF-I collagen increased (P<0.01) in atrial fibrillation group. (2) The ratio of remodeled of intercalated disc in patients with AF was higher (P<0.01) than that in SR group whereas the number of intercalated disc was not different (P>0.05) between the two groups. (3) Cx43VF decreased (P<0.01) in the AF patients compared to those with SR. (4) A positive correlation between fibrosis and the remodeling of intercalated disc (r=0.96, P<0.01) was observed. The CVF-I was negatively correlated with the Cx43VF (r=-0.98, P<0.01). CONCLUSION: These results suggest that both fibrosis of atrial muscle and remodeling of intercalated disc are involved in the pathogenesis of human atrial fibrillation. Fibrosis of atrial muscle may play an important role in the process of atrial fibrillation by interfering with remodeling of intercalated disc and thereby involves in the remodeling of connexins.