Atresia of the right atrial ostium of the coronary sinus

A case of asymptomatic congenital occlusion of the ostium of the coronary sinus is described. The myocardial venous drainage was maintained via a persistent left superior vena cava as well via ectatic, widened atrial veins of the dorsal wall of the left atrium. The study shows that complete ostial occlusion of the coronary sinus does not reduce cardiac venous drainage. The view of the literature allows a comparison with the comprehensive classification of coronary sinus anomalies.     

Cannulation of the middle cardiac vein during MICS

Coronary sinus cannulation for retrograde cardioplegia administration during cardiac surgery is common practice. Several of the cannulas that are placed by the cardiac surgeon on open procedures are now placed by the cardiac anesthesiologist during minimally invasive cardiac surgery, including the coronary sinus catheter. The understanding of the cardiac venous anatomy is very important during coronary sinus catheter placement. We present a case where a percutaneously placed coronary sinus catheter was inadvertently placed into the middle cardiac vein but detected with the use of fluoroscopy.     

Simulation of coronary circulation with special regard to the venous bed and coronary sinus occlusion

The vascular beds of the left circumflex and the left anterior descending coronary arteries are modelled by means of coupled differential equations that consider an arterial, a capillary and a venous section. In a stepwise procedure, experimental data from normal coronary perfusion and coronary sinus occlusion are used to assess the model parameters. For venous distensibility, a non-linear form of pressure-volume relationship proved vital to reproduce the characteristics of the rise in venous pressure after the onset of coronary sinus occlusion. Numerical integration was carried out for normal perfusion and for coronary sinus occlusion, yielding time courses of flows, volumes and pressures within large coronary arteries, capillaries and coronary veins. Coronary sinus occlusion reduces total mean flow by 18% and divides intramyocardial flow between the capillaries and the veins into a forward component of 3.03 mls⁻¹ and a backward component of − 1.54 mls⁻¹. This result represents a prediction for a haemodynamic quantity which is therapeutically important but inacessible to measurement. Varying degrees of systolic myocardial squeezing are studied to display the impact of myocardial contractility and vessel collapse on the mean values and phasic components of intra-myocardial flows.     

Coronary sinus of the heart in various anomalies of the conotruncus

Thirty-one hearts with anomalous conotruncus (common arterial trunk, hypoplasia of the aorta with transposition, atresia of the pulmonary trunk) have been studied. There are some peculiarities in anatomy and topography of the coronary sinus, concerning its sources, that is veins forming the venous sinus, position and interrelations with the venous sulcus and with the interatrial septum, size and form of the ostium and valve of the coronary sinus. The most amount of the anatomical peculiarities of the sinus are observed in the preparations, where the anomalous conotruncus is combined with absence of one or both cardiac septa.     

Coronary venous pressure and flow: effects of vagal stimulation, aortic occlusion, and vasodilators

Coronary venous pressure and coronary sinus flow in the canine heart were compared with intramyocardial, intraventricular, aortic, and coronary artery pressures. Stimulation of the thoracic vagus augmented coronary venous pressure, mean venous flow per systole, and coronary venous systolic resistance, but decreased the mean venous flow. Partial occlusion of the aorta augmented coronary venous pressure and coronary venous flow, while systolic coronary venous resistance remained unchanged. Adenosine increased peripheral and central coronary venous pressure and venous flow; it reduced peripheral coronary artery pressure. Adenosine augmented flow per systole and reduced venous resistance more than the other interventions. Dipyridamole decreased left ventricular, aortic, and central coronary artery systolic pressures and systolic venous resistance. It increased the venous flow, mean flow per systole, and coronary venous pressure, even though intramyocardial pressure remained unchanged. Nitroglycerine elevated coronary venous pressure and flow, as well as venous flow per systole, even though it decreased left ventricular, aortic, and central coronary artery pressures. Nitroglycerine significantly decreased coronary venous resistance. It is concluded that coronary venous resistance may be an important resistive component to consider when the total coronary circulation is studied.     

Feedforward sympathetic coronary vasodilation in exercising dogs.

The hypothesis that exercise-induced coronary vasodilation is a result of sympathetic activation of coronary smooth muscle beta-adrenoceptors was tested. Ten dogs were chronically instrumented with a flow transducer on the circumflex coronary artery and catheters in the aorta and coronary sinus. During treadmill exercise, coronary venous oxygen tension decreased with increasing myocardial oxygen consumption, indicating an imperfect match between myocardial blood flow and oxygen consumption. This match was improved after alpha-adrenoceptor blockade with phentolamine but was significantly worse than control after alpha + beta-adrenoceptor blockade with phentolamine plus propranolol. The response after alpha-adrenoceptor blockade included local metabolic vasodilation plus a beta-adrenoceptor vasodilator component, whereas the response after alpha + beta-adrenoceptor blockade contained only the local metabolic vasodilator component. The large difference in coronary venous oxygen tensions during exercise between alpha-adrenoceptor blockade and alpha + beta-adrenoceptor blockade indicates that there is significant feedforward beta-adrenoceptor coronary vasodilation in exercising dogs. Coronary venous and estimated myocardial interstitial adenosine concentrations did not increase during exercise before or after alpha + beta-adrenoceptor blockade, indicating that adenosine levels did not increase to compensate for the loss of feedforward beta-adrenoceptor-mediated coronary vasodilation. These results indicate a meaningful role for feedforward beta-receptor-mediated sympathetic coronary vasodilation during exercise.     

A METHOD OF CORONARY RETROPERFUSION FOR THE TREATMENT OF ACUTE MYOCARDIAL ISCHEMIA

A method of retrograde perfusion of the myocardium has been developed in dogs. It consists of a double lumen balloon-tipped catheter inserted transvenously into the coronary sinus, with one lumen connected to a roller pump, the other to a helium counterpulsing pump. Oxygenated heparinized blood is obtained from the femoral artery and pumped continuously into the coronary sinus at a pressure of 50-75 mm Hg. The balloon is inflated during diastole, sealing the coronary sinus and promoting retrograde flow, and is deflated during systole, allowing blood drainage into the right atrium and preventing venous congestion. Thirteen anesthetized open-chest dogs were subjected to 15 minutes of proximal LAD artery occlusion and 30 minutes of diastolic coronary sinus perfusion (DCSP). The area of ischemia was mapped by means of platinum electrodes capable of simultaneously measuring myocardial tissue oxygen tension M(p)O(2)) and electrograms. Reduction of M(p)O(2) with simultaneous elevation of the ST segment on the corresponding electrogram was considered an indication of ischemia. Diastolic coronary sinus perfusion improved myocardial oxygen tension in the ischemic myocardium, reduced ST segment elevation, and tended to restore arterial blood pressure. Histologically, there was no intramyocardial hemorrhage.     

Arteriovenous difference of the blood density in the coronary circulation

The mechanical oscillator technique permits determining blood density continuously with high accuracy. Using this technique arteriovenous density gradients were recorded in the coronary vascular bed of anesthetized dogs. It was found that the coronary sinus blood has a higher density than arterial blood due to the loss of filtered fluid in the microcirculation. The amount of fluid loss corresponds to the lymph flow in the myocardium. Increase of venous pressure leads to an increase of the density gradient. Intermittent coronary sinus occlusion (ICSO) surprisingly leads to a reduction of the density gradient. Injection of osmotically hypertensive fluids influences the arteriovenous gradient by shifting extravascular fluid into the blood. The method permits the determination of filtration coefficients and to estimate the tissue volume available for fluid exchange.     

Adenosine is not responsible for local metabolic control of coronary blood flow in dogs during exercise

The purpose of this investigation was to quantitatively evaluate the role of adenosine in coronary exercise hyperemia. Dogs (n = 10) were chronically instrumented with catheters in the aorta and coronary sinus, and a flow probe on the circumflex coronary artery. Cardiac interstitial adenosine concentration was estimated from arterial and coronary venous plasma concentrations using a previously tested mathematical model. Coronary blood flow, myocardial oxygen consumption, heart rate, and aortic pressure were measured at rest and during graded treadmill exercise with and without adenosine receptor blockade with either 8-phenyltheophylline (8-PT) or 8-p-sulfophenyltheophylline (8-PST). In control vehicle dogs, exercise increased myocardial oxygen consumption 4.2-fold, coronary blood flow 3.8-fold, and heart rate 2.5-fold, whereas mean aortic pressure was unchanged. Coronary venous plasma adenosine concentration was little changed with exercise, and the estimated interstitial adenosine concentration remained well below the threshold for coronary vasodilation. Adenosine receptor blockade did not significantly alter myocardial oxygen consumption or coronary blood flow at rest or during exercise. Coronary venous and estimated interstitial adenosine concentration did not increase to overcome the receptor blockade with either 8-PT or 8-PST as would be predicted if adenosine were part of a high-gain, negative-feedback, local metabolic control mechanism. These results demonstrate that adenosine is not responsible for local metabolic control of coronary blood flow in dogs during exercise.     

K(ATP)(+) channels, nitric oxide, and adenosine are not required for local metabolic coronary vasodilation

The role of ATP-sensitive K(+) (K(ATP)(+)) channels, nitric oxide, and adenosine in coronary exercise hyperemia was investigated. Dogs (n = 10) were chronically instrumented with catheters in the aorta and coronary sinus and instrumented with a flow transducer on the circumflex coronary artery. Cardiac interstitial adenosine concentration was estimated from arterial and coronary venous plasma concentrations using a previously tested mathematical model. Experiments were conducted at rest and during graded treadmill exercise with and without combined inhibition of K(ATP)(+) channels (glibenclamide, 1 mg/kg iv), nitric oxide synthesis (N(omega)-nitro-L-arginine, 35 mg/kg iv), and adenosine receptors (8-phenyltheophylline, 3 mg/kg iv). During control exercise, myocardial oxygen consumption increased ~2.9-fold, coronary blood flow increased ~2.6-fold, and coronary venous oxygen tension decreased from 19.9 +/- 0.4 to 13.7 +/- 0.6 mmHg. Triple blockade did not significantly change the myocardial oxygen consumption or coronary blood flow response during exercise but lowered the resting coronary venous oxygen tension to 10.0 +/- 0.4 mmHg and during exercise to 6.2 +/- 0.5 mmHg. Cardiac adenosine levels did not increase sufficiently to overcome the adenosine receptor blockade. These results indicate that combined inhibition of K(ATP)(+) channels, nitric oxide synthesis, and adenosine receptors lowers the balance between total oxygen supply and consumption at rest but that these factors are not required for local metabolic coronary vasodilation during exercise.     

经桡动脉心导管术诊断和治疗冠状动脉疾病的临床研究

目的:观察经桡动脉介入诊治冠心病的安全性和有效性。方法:对1503例患者进行了经桡动脉途径介入诊治,其中包括心绞痛患者1218例,心梗患者268例,二尖瓣和/或动脉瓣手术前对冠状动脉进行解剖学评估17例,观察患者手术安全性、成功率以及与经桡动脉手术相关的并发症发病率。结果:介入治疗成功率为93.1%(1400/1503),手术失败的主要原因为桡动脉穿刺失败(39例),严重桡动脉痉挛(42例),右锁骨下动脉不同程度的弯曲(18例),近端严重狭窄(14例)。术后有14例患者出现严重并发症(瞬时缺血性病变),60例出现有症状的窦性心动过缓,43例出现静脉血栓,77例出现血肿,88例出现桡动脉梗阻。结论:经桡动脉途径是一种安全、有效、患者更容易接受的冠心病介入诊治方法。     

The endothelial microenvironment in the venous valvular sinus: thromboresistance trends and inter-individual variation

The valve sinuses of the deep venous system are frequent sites of venous thrombus initiation. We previously reported that, in comparison with the non-valvular lumenal endothelium, the valve sinus endothelium had decreased expression of von Willebrand factor (vWF) and increased expression of endothelial protein C receptor (EPCR) and thrombomodulin (TM), suggesting alteration in the procoagulant/anticoagulant balance. We hypothesized that increased stasis in the deeper recesses of the venous valves would be associated with a gradient of increased thromboresistance. Expression of EPCR, TM, and vWF was analyzed via quantitative confocal immunofluorescence in residual saphenous veins collected following coronary artery bypass procedures. In agreement with our hypothesis, endothelial expression of vWF in the valve sinus decreased from the uppermost to the deepest region of the valve sinus. In contrast to our hypothesis, EPCR expression decreased from the uppermost to the deepest region of the valve sinus (p < 0.001) and TM expression remained unchanged throughout the valve sinus. Comparison of the non-valvular lumenal endothelium with the valve sinus endothelium demonstrated significantly decreased vWF expression (p < 0.001) in the valvular sinus consistent with our previous report; however, we did not observe statistically significant differences in EPCR or TM expression in this comparison. In addition, remarkable inter-individual variation in expression of these three proteins was also observed. These findings suggest that the genesis of these observations is more complex than predicted by our initial hypothesis, likely due, at least in part, to the complex rheology of the valvular sinus microenvironment.     

Alteration in myocardial oxygen balance during exercise after beta-adrenergic blockade in dogs

The effects of beta-adrenergic blockade upon myocardial blood flow and oxygen balance during exercise were evaluated in eight conscious dogs, instrumented for chronic measurements of coronary blood flow, left ventricular pressure, aortic blood pressure, heart rate, and sampling of arterial and coronary sinus venous blood. The administration of propranolol (1.5 mg/kg iv) produced a decrease in heart rate, peak left ventricular (LV) dP/dt, LV (dP/dt/P, and an increase in LV end-diastolic pressure during exercise. Mean coronary blood flow and myocardial oxygen consumption were lower after propranolol than at the same exercise intensity in control conditions. The oxygen delivery-to-oxygen consumption ratio and the coronary sinus oxygen content were also significantly lower. It is concluded that the relationship between myocardial oxygen supply and demand is modified during exercise after propranolol, so that a given level of myocardial oxygen consumption is achieved with a proportionally lower myocardial blood flow and a higher oxygen extraction.     

Histological and immunocytochemical investigation of human coronary vessel development with anti-CD34 antibodies

Information about embryonic development of coronary endothelium is the main clue for the creation of new methods in tissue engineering for treatment of ischemic heart diseases. The purpose of the research was to describe human coronary vessels development on early stages of the prenatal ontogenesis. The first step in human coronary vessels development is the formation of endothelium de novo by transformation of some epicardial and, possibly, endocardial cells. The next step is the ingrowth of sinus venosus endothelium in subepicardium over ventricles and atria, which gives rise to the coronary vessels. Only after 7 days does the primitive coronary plexus of the heart communicate with aorta (third step). During this period, some subepicardial vessels invade myocardium and some intramyocardial vessels contact with the heart cavity. Such intercommunications could help in regulation of blood circulation in primitive coronary plexus before establishment of effective contacts between arterial and venous vessels—excess of blood could be discharged directly into the heart cavity. Additional population of CD34+ cells were revealed inside condensed mesenchyme of the conotruncus; it participates in the formation of vasa vasorum in the aorta. Epicardium and sinus venosus generate endothelium of coronary vessels by neovasculo- and angiogenesis, respectively. During a week after ingrowth of vessels from SV and before their ingrowth to the aorta, ventriculo-coronary communications could be found in the heart.     

Persistent left superior caval vein draining into right atrium,but not through the coronary sinus

Persistence of the left superior caval vein is the most commonly reported thoracic venous anomaly. The vein usually drains into the right atrium through the coronary sinus, reflecting its developmental origin. We describe an unusual variant, in which the vein drained directly into the right atrium.     

Obtaining a representative blood sample in lactate tracer studies

Reasons why venous tracer infusion with arterial sampling [(v-a) mode] has advantages compared to arterial infusion and venous sampling [(a-v) mode] for studies of blood lactate kinetics are presented. Arterial tracer infusion can result in biased tracer input due to streaming and unequal blood flow distribution. The procedure is impractical for human studies. Venous sampling from the jugular, or any other peripheral or great vein, provides a sample which may, or may not represent mixed venous systemic blood, which exists only in the pulmonary artery. Venous sampling will not represent cardiac lactate metabolism because the coronary arteries drain into the coronary sinus. Venous sampling, as well as pulmonary artery sampling, will also ignore lactate metabolism in the lungs which drain into the left atrium from bronchial and pulmonary circulations. Turnover rates calculated from either venous or arterial specific activities underestimate true tissue turnover. Correction for either measurement depends on good estimates of blood flows to lactate exchanging and non-exchanging tissue. Equilibration between lactate and pyruvate pools does not invalidate the use of tracers to measure lactate turnover. The (v-a) mode with venous infusion and arterial sampling has advantages for lactate tracer studies.     

Valvular apparatus of the cardiac veins in the pig]

The valvular apparatus of the subepicardial venous network has been studied in reflected light of the diaphragmated source. Structure, form and variations of the valvular apparatus have been determined in different parts of the coronary sinus, in the large cardiac vein, in the median cardiac and in the posterior veins of the left ventricle and their main branches.     

Coronary venous flow and O2 saturation during transitional phases between various cardiac rates.

The instantaneous and continuous interrelationship between coronary blood flow and coronary venous O2 saturation was determined during transient periods following abrupt rate change in the electrically paced canine heart. Through a catheter in the coronary sinus, O2 saturation was continuously monitored using a fibreoptics technique, and venous flow was measured with an electromagnetic flowmeter. Various patterns of change in flow and O2 saturation were observed depending both on the absolute values of the cardiac rates as well as on the relative difference between them during changes from one rate to another. Whereas elevation of coronary flow was monophasic when the magnitude of heart rate change was below 75 beats per minute, a drop in flow was observed preceeding its elevation when the difference was greater. At high rates further increase in rate caused either no alteration or led to a monophasic drop in flow during the transitional period. Changes in O2 saturation were observed only when heart rate difference exceeded 60 beats per minute. Between 60-90 beats per minute O2 saturation remained steady except during the transient rate elevation, ending in a lower steady state O2 saturation. The results indicate that both O2 saturation and coronary flow change with heart rate initially because of mechanical consequence of the increased rate on the myocardium, and later according to its new metabolic needs also manifested by changed O2 extraction.     

Outflow pathways of venous blood from the myocardium in the dog and structures participating in their regulation

The intramural pathways of the venous blood outflow from the cardiac wall have been studied histologically, histochemically and micrometrically in 20 control and 84 experimental dogs with an artificially produced circulatory disturbances, peculiar for congenital heart disease (open arterial canal, coarctation of the aorta and stenosis of the pulmonary trunk). The experimental animals have been observed for 6-12 months. In the venous line of the coronary basin several morphologically differed parts, anatomically and functionally connected between themselves and ensuring blood outflow from the myocardium, are distinguished: coronary sinus, subepicardial veins, paired sinusoid veins, myocardial sinusoids and endocardial cushions. In each of them there are their own adaptive structures, participating in regulation of the venous blood stream. In the cardial sinus, in the subepicardial and paired sinusoid veins--these are valves of various complexity. In the myocardial sinusoids, the regulatory function, together with the valves, are performed by the intimal and muscle cushions, connective tissue and muscle bridges. In the endocardial cushions they are realized by the valves, muscle sphincters, bundles of obliquely and longitudinally oriented leiomyocytes. All the adaptive structures mentioned are also found in the hearts of the control animals. Under modelling various hemodynamic disturbances, the degree of their development increases sharply. The latter ensures the maintenance of an optimal regimen of blood circulation in the myocardium of a functionally loaded heart and prevents development of decompensation in the organ.     

Comparative histochemical and electron microscopic studies of the sinus and venous walls of the human spleen with special reference to the sinus-venous connections

Sinus and venous walls of normal human spleens were studied with enzyme histochemical and electron microscopic methods. Particular attention was paid to the connections between sinuses and veins. Histochemically the sinus lining cells revealed a distinct naphthol-AS-acetate-esterase activity but no reaction for alkaline phosphatase. Venous endothelial cells were positive for the latter but negative for the former enzyme. In the sinus-venous junctional area there were no endothelial cells with reactivity for both enzymes. Electron microscopically both the sinus lining cells and the venous endothelial cells could be clearly characterized and therefore easily distinguished from one another on morphological grounds. There were no clear ultrastrural indications of transitional forms between sinus lining cells and venous endothelial cells in the sinus-venous area. According to these findings, sinus lining cells represent a specialized endothelium, but one with practically no morphological similarities to the venous endothelium.