Hemodynamic evaluation in acute myocardial infarct. Application to the treatment of contractile insufficiency syndromes of the left ventricle

Even though the coronary care units have reduced to a minimum the mortality due to arrhythmias, the syndromes of left ventricular failure are responsible for the greatest part of hospital deaths in patients with acute myocardial infarction. The poor results depend upon the extensive destruction of left ventricular mass. The management in these cases should be directed to improve the performance of viable muscle as well as to preserve thejeopardized ischemic myocardium that is potentially viable. These goals may be adequately pursued by continuous hemodynamic characterization of left ventricular function. The experience of the Coronary Care Unit of the Instituto Nacional de Cardiología de México in the study of 30 of these patients is presented. Hemodynamic evaluations were performed by means of a Swan-Ganz catheter and cardiac output determinations by the thermodilution technique. The studies may be performed with a minimum of risk. Central venous pressure measurements do not adequately indicate the status of the left ventricle. Its function may be evaluated by the use of end diastolic pulmonary artery pressure which reflects, quite accurately, the left ventricular filling pressure in these patients. Continuous hemodynamic monitorization facilitates the proper manipulation of the determinants of ventricular performance (preload, afterload, cardiac rate and contractility) and permits an attempt to improve the balance between available oxygen and myocardial oxygen requirements. Hemodynamic studies and ventricular function curves are presented in selected patients with acute myocardial infarction. The mortality due to left ventricular failure and cardiogenic shock in patients with acute myocardial infarction remains extremely high. However, it is only through the early recognition by continuous hemodynamic monitorization and the aggressive management of the patient with incipient left ventricular failure that the number of survivors may be increased.     

Enhanced detection of proximal right coronary artery stenosis with the additional analysis of right ventricular thallium-201 uptake in stress scintigrams

The value of right ventricular thallium-201 analysis in detecting proximal right coronary artery stenosis in exercise myocardial scintigraphy was analyzed in 52 patients, 27 with and 25 without proximal right coronary artery stenosis. For the detection of proximal right coronary artery stenosis, the sensitivity and specificity of thallium scintigraphic analysis were 59 and 88% for a right ventricular abnormality, 67 and 68% for a left ventricular inferior wall abnormality, and 93 and 56% for an abnormality of either. When both right and left ventricular thallium images were abnormal, all 9 patients had proximal right coronary artery stenoses, and when both were normal, 26 of 28 patients had a normal proximal right coronary artery. The sensitivity and specificity of blood pool scintigraphic variables during exercise (right ventricular ejection fraction and left ventricular inferior wall motion) were not significantly different for detection of proximal right coronary artery stenosis. Thus, the additional analysis of the right ventricle on thallium-201 stress scintigrams can improve the detection of proximal right coronary artery stenosis. When both right ventricular and left ventricular thallium scintigrams are abnormal (or normal), the ability to predict the presence (or absence) of proximal right coronary artery stenosis is very high.     

Small genes/gene-products in Escherichia coli K-12

OBJECTIVE: We tested the hypothesis that right heart failure during endotoxin shock may result from altered ventriculovascular coupling responsible for impeding power transfer to the pulmonary circulation. METHODS: The changes in vascular pulmonary input impedance and right ventricular contractility produced by low-dose endotoxin infusion were studied in 6 intact anesthetized dogs. RESULTS: Endotoxin insult resulted in pulmonary hypertension (from 22 +/- 2 to 33 +/- 3 mmHg) associated with significant decreases in stroke volume (from 26.9 +/- 4 to 20.2 +/- 3 ml) and right ventricular ejection fraction (from 41 +/- 3 to 32 +/- 2%). The first minimum of input impedance spectrum and zero phase were shifted towards higher frequencies. Input resistance and characteristic resistance were dramatically increased. The latter change contributed to a significant increase in the pulsatile component of total right ventricular power output from 13 to 21%, indicating a reduction in the hydraulic right ventricle power output delivered into the main pulmonary artery. Overall changes in input pulmonary impedance were indicative of increased afterload facing the right ventricle leading to depressed performance. In contrast, right ventricular systolic elastance was simultaneously increased from 0.56 to 0.93 mmHg/ml indicating an increase in right heart contractility. CONCLUSION: These data suggest that pulmonary hypertension in the setting of experimental endotoxin shock is accompanied by deleterious changes in the pulmonary impedance spectrum, which are responsible for a mismatch of increased contractile state of the right ventricle to the varying hydraulic load ultimately leading to ventricular-vascular uncoupling.     

Temperature of the sclera during diathermocoagulation carried out in patients with retinal detachment

Regional coronary blood flow was measured by injecting radioactive microspheres (15 mum +/- 5 in diameter) into the left atrium of anesthetized ponies with surgically prepared open thorax before and during occlusion of the coronary arteries. The normal blood flow to the myocardium of the interventricular septum and the left ventricular wall were highest, followed in decreasing order by the right ventricular wall, the interatrial septum, the atrial walls, and the valves. Measurement of transmural blood flow in the normal left ventricle yielded a mean endocardial/epicardial flow ratio of 1.36 in the free wall. The left ventricular flow ratio was 1.33 in the septal wall. The percentage of the left ventricular myocardium made ischemic during occlusion of the right coronary artery or of the left coronary artery (cranial descending and circumflex arteries) was approximately equal. Blood flow to the ischemic areas of the left ventricle after occlusion of coronary arteries ranged from 3.8 to 20.6% of the normal flow. A disproportionate decrease in flow to the endocardial regions of the left ventricle was also observed in ischemic areas (mean inner/outer left ventricular wall flow ratio was 68.89% of the normal flow ratio).     

Influence of basal release of nitric oxide on systolic and diastolic function of both ventricles

Nitric oxide is continuously released by coronary artery endothelium under basal conditions; it maintains vascular tone and regulates coronary blood flow. The objective of this study was to investigate the influence of this basal release of nitric oxide on right and left ventricular systolic and diastolic function. Isolated pig hearts perfused at a constant pressure with enriched autologous blood were used. Systolic and diastolic pressure-volume relationships of isovolumically contracting hearts were studied in the control setting and after addition of 1 mmol/L L-N(G)-monomethyl-arginine followed by 5 mmol/L L-arginine to the perfusate. Addition of L-N(G)-monomethyl-arginine caused an acute rise in coronary vascular resistance and a reduction in right and left ventricular systolic function as evaluated by the slope values of the pressure-volume curves, but had little effect on the diastolic function of either ventricle. L-Arginine restored the systolic function to the control level. This alteration in ventricular function was not a result of ischemia because myocardial oxygen consumption was not significantly affected by the acute increase in coronary vascular resistance induced by L-N(G)-monomethyl-arginine. We conclude that basal release of nitric oxide has no direct negative inotropic effect, but in fact plays an important role in preserving right and left ventricular systolic function and maintains the basal coronary vascular tone.     

Gross anatomy of the cardiac blood vessels in the North American beaver (Castor canadensis)

The cardiac arteries and veins are described in the North American beaver (Castor canadensis) following the injection of the vessels of 15 hearts with either latex, vinyl plastic or barium sulfate. The left coronary artery gives off the typical circumflex and paraconal interventricular branches which supply the left atrium and ventricle and part of the right ventricle and interventricular septum. The right coronary artery vascularizes the right atrium and ventricule and by means of its subsinuosal interventricular branch, part of the left ventricle and interventricular septum. The paraconal interventricular branch of the left coronary artery lies within the myocardium and is not visible on the surface of the heart. There are no intercoronary anastomoses between the right and left vessels. The major cardiac veins open into the terminal end of the left cranial vena cava. Unlike the arteries, there are venous anastomoses interconnecting the great cardiac vein and the middle cardiac vein. It is concluded that the cardiac blood vessels in Castor canadensis are typically mammalian and resemble those of both land and aquatic mammals.     

Age-related variation in left ventricular myocardial contractile state expressed by the stress velocity relation

The assessment of ventricular function plays an important role in the pre- and postoperative management of many congenital heart abnormalities. Normal ranges in left ventricular systolic function indices have been defined during childhood and age-related alterations in left ventricular myocardial contractile state have recently been reported. This study was carried out to investigate the developmental changes in left ventricular contractile state expressed by the endsystolic meridional stress (ESS)/rate-corrected velocity of circumferential fiber shortening (VCFc) relation, calculated by echo in normal children and young adults. We examined 146 healthy subjects (80 males and 66 females), mean age 70.85 +/- 63.89 months (range 0.5-228) and body surface area (BSA) 0.807 +/- 0. 47 (range 0.18-2.01) with no clinical and echocardiographic evidence of cardiac disease and with normal blood pressure. The subjects were divided into three groups according to age: <6 months (group 1, n = 32), 6-36 months (group 2, n = 34), and >36 months (group 3, n = 80). Enddiastolic volume and mass (M) of the left ventricle were measured by M-mode Echo. ESS was considered as an index of afterload and the VCFc as an index of systolic ventricular function. The left ventricular ejection time used for the calculation of VCFc was measured from aortic flow obtained by PW-Doppler. The ESS/VCFc relation was used to assess left ventricular contractility. Systolic blood pressure, volume, and mass of the left ventricle increase with age. The gradual increase in pressure despite a stable mass/volume ratio [M/V = 0.900 + (0.0007 x age); r = 0.27, p < 0.005] resulted in a substantial increase of afterload [ESS = 29.78 + (0.116 x age); r = 0.58, p < 0.0001]. VCFc showed an inverse hyperbolic regression with afterload [VCFc = 1.01 + (7.598/ESS); r = 0.59, p < 0.0001]. The regression lines (best linear fit) between VCFc and ESS are significantly different in the three groups. The Y intercept was higher and the slope steeper in group 1 [VCFc = 1.74 - (0.017 x ESS); r = 0.65, p < 0.0005] vs group 2 [VCFc = 1.54 - (0.008 x ESS); r = 0.58, p < 0.001] and group 3 [VCFc = 1.52 - (0.007 x ESS); r = 0.57, p < 0.0001]. These data indicate that, in children, the volume and mass of the left ventricle increase, whereas the M/V ratio remains relatively constant; the progressive increase in arterial blood pressure explains the increase of afterload. The VCFc is higher in the first few years of life compared to that seen in older children due to reduced afterload and increased contractile state. Left ventricular contractility, expressed as ESS/VCFc relation, is thus inversely proportional to age. In the first months of life the left ventricular myocardium exhibits a higher basal contractile state and a greater sensitivity to changes in afterload. For obtaining an accurate assessment of left ventricular function, the ESS/VCFc relation in different age groups should be measured.     

Pharmacological profile of valsartan, a non-peptide angiotensin II type 1 receptor antagonist. 5th communication: hemodynamic effects of valsartan in dog heart failure models

Hemodynamic effects of valsartan ((S)-N-valeryl-N-?[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]meth yl?valine, CAS 137862-53-4, CGP 48933), a non-peptide angiotensin II type 1 receptor antagonist were examined in dogs with heart failure induced acutely by coronary artery ligation and chronically by rapid-ventricular pacing. Coronary artery ligation induced decrease in cardiac output and increase in left ventricular end-diastolic pressure. Valsartan at 10 mg/kg i.v. reduced blood pressure, heart rate, left ventricular pressure, left ventricular end-diastolic pressure and total systemic resistance. Similar changes were observed with enalaprilat at 0.1 mg/kg i.v. Rapid left ventricular pacing for 2 weeks reduced cardiac contractility. Valsartan, administered at a dose of 100 mg/kg/d p.o. for 2 weeks, lowered left ventricular end-diastolic pressure. Valsartan reduced preload and afterload in these two dog heart failure models.     

Right ventricular radiofrequency ablation of ventricular tachycardia after myocardial infarction

Radiofrequency transcatheter ablation of ventricular tachycardia in the setting of a prior myocardial infarction is typically performed with application of energy to the left ventricular endocardium. In this article, two cases are described in which successful radiofrequency transcatheter ablation of ventricular tachycardia occurred with energy delivery to the right ventricular septum after failed ablation attempts from the left ventricle. Both patients had tachycardias with a left bundle branch block morphology and markedly presystolic activity recorded from the right ventricular septum. Right ventricular septal activation mapping during ventricular tachycardia should be performed in patients with left bundle branch block tachycardia morphology and coronary artery disease to maximize efficacy of the catheter ablation procedure.     

The concept of afterload mismatch and its implications in the clinical assessment of cardiac contractility

The characteristics of left ventricular ejection (velocity and extent of wall shortening) can be analysed in relation to the appropriateness of the matching between afterload and the level of inotropic state (contractility), as modified by the preload (Frank-Starling) reserve. In the normal left ventricle if the preload is not allowed to compensate for an acute increase in afterload, or if the limit of preload reserve is reached, velocity (V CF) and stroke volume will diminish; that is an afterload mismatch occurs. This acute mismatch can be corrected by administration of a positive inotropic agent. In normal conscious animals and in man the ejection phase measures in the basal state (such as ejection fraction, and VCF corrected for heart size) encompass a relatively narrow range, and when the normal heart adapts successfully to a chronic pressure or volume overload such measures remain normal per unit of muscle. These findings provide the basis for their use in detecting a depressed basal level of inotropic state, even in the presence of certain valvular lesions. When there is mild depression of the basal inotropic state, enhanced preload and dilatation can allow full compensation of VCF, but acute pressure loading can allow detection of the the reduced preload reserve by inducing a substantial fall in stroke volume and VCF. When the basal inotropic state is greatly reduced, a mismatch between afterload and contractility, expressed as reduced VCF or ejection function, will become evident in the basal state even if the afterload is normal. Any increase in aortic pressure will then cause a sharp reduction in stroke volume or VCF. Also, under these circumstances therapeutic afterload reduction with agents such as nitroprusside can increase velocity and extent of wall shortening, and the cardiac output, providing the preload is maintained. The concept of afterload mismatch with limited preload reserve provides a framework for understanding the behavior of the normal or depressed ventrile and how it can operate on a "descending limb" of function. It helps to explain why measures of the ejecting phase (which are sensitive to afterload) appear to be more reliable than isovolumic phase indices (which are relatively insensitive to afterload) for detecting depressed basal inotropic state. Finally, the concept allows for interpretation of the responses observed in the clinical setting to acute and chronic increases and decreases in loading conditions on the left ventricle.     

Isolated congenital diverticulum of the left ventricle disclosed by ventricular tachycardia in a 72-year-old woman

A 72-year-old woman presented with poorly tolerated ventricular tachycardia reduced by intravenous amiodarone. The possibility of an ischaemic aetiology led us to perform coronary angiography. The coronary arteries were pathological. Left ventricular angiography revealed limited anterior hypokinesia and a large contractile apical pouch appended to the left ventricle by a long narrow neck. Despite the appearance suggestive of congenital left ventricular diverticulum (contractility, narrow neck) and because of the coexistence of ischaemic heart disease, we preferred to confirm the muscular nature of the diverticulum by myocardial thallium scintigraphy, which showed reversible decreased uptake in the anterior zone related to coronary artery disease, and confirmed the muscular nature of the diverticulum which showed normal thallium uptake. MRI clearly visualized the ventricular ectasia attached by a narrow neck to the rest the left ventricle. This long narrow neck indicated that this muscular diverticulum constituted a congenital diverticulum. The contribution of ultrasonography was limited by a poorly defined point during the examination. This congenital diverticulum, discover during adulthood, and previously asymptomatic, is a rare lesion, in the light of a review of the literature.     

Development of a numerical simulation model of the cardiovascular system

A numerical simulation model of the cardiovascular system has been developed. It consists of a model of the left atrium, the left ventricle, the coronary vascular system, the aorta, the arterial system, and the venous system. The input of the complete model is the elastance (pressure/volume ratio) developed by the left ventricle. The shape of this elastance is constant in different circumstances. Left ventricular (LV) myocardial oxygen consumption and the amount of oxygen offered to the left ventricle can be calculated with the model. The model has been validated using data from a patient suffering from coronary artery disease. The measured clinical hemodynamical waveforms could be fitted to those generated by the model. With the numerical simulation model, it is possible to predict the functioning of the left ventricle under different circumstances. This makes it possible to study in vitro various pathological clinical situations.     

A common mutation in the FACC gene causes Fanconi anaemia in Ashkenazi Jews

The biaxial mechanical properties of right ventricular free wall (RVFW) myocardium were studied. Tissue specimens were obtained from the sub-epicardium of potassium-arrested hearts and different stretch protocols were used to characterize the myocardium's mechanical response. To assess regional differences, we excised tissue specimens from the conus and sinus regions. The RVFW myocardium was found to be consistently anisotropic, with a greater stiffness along the preferred (or averaged) fiber direction. The anisotropy in the conus region was more pronounced than in the sinus region. A comparison with studies of left ventricle (LV) midwall myocardium revealed that, 1) the fiber direction stiffnesses are greater in the RVFW than in the LV, 2) the degree of anisotropy is greater in the RVFW than in the LV.     

Oxygen consumption for constant work is minimal at lowest working contractility in normal dog hearts

We tested whether minimal myocardial oxygen consumption (MVO2) for a given external work would exist in the middle of a normal contractility range as previously predicted theoretically. The left ventricle of the excised cross-circulated dog heart preparation was connected to a volume servo pump. Myocardial contractility in terms of ventricular end-systolic elastance (Emax) was gradually increased from control 8.9 +/- 3.4 (mean +/- SD) to 30.0 mmHg/(ml/100 g) by epinephrine and decreased to 1.8 mmHg/(ml/100 g) by propranolol while heart rate, end-systolic pressure and stroke work were kept constant. MVO2 was determined as the product of total coronary flow and coronary arteriovenous oxygen content difference in each contractile state. We plotted MVO2 values against E(max) values in each heart. The MVO2-E(max) relation for a constant cardiac work showed that MVO2 was minimal at the low end of the covered E(max) range. We conclude that minimal MVO2 for a given cardiac work is generally obtained at the lowest working contractility in normal dog hearts. This conclusion might pose some problems in the previous theoretical prediction as to the contractility that achieves the minimal MVO2 in a given external work.     

Acute vascular perforation with shunt formation in the right ventricle after percutaneous transluminal coronary angioplasty. Magnetic resonance tomography and Doppler ultrasound detection of shunt flow

A coronary artery perforation is a rare complication after percutaneous transluminal coronary angioplasty. The therapy will be determined by the hemodynamic failure of the left or right ventricle. A case of a coronary artery perforation with a shunt from the right coronary artery to the right ventricle after coronary angioplasty is reported. The shunt was detected by coronary angiography and confirmed by magnetic resonance imaging and doppler echocardiography.     

Incidence of right ventricular asynergy in patients with coronary artery disease

The effects of coronary artery disease on patterns of left ventricular contractility have been thoroughly investigated. In contrast, little is known about the incidence of right ventricular dysfunction induced by this disease. To evaluate the frequency of right ventricular asynergy, biplane right ventricular cineangiograms were obtained in 26 patients. Seven segmental axes of shortening were analyzed in each end-systolic and end-diastolic frame and normalized as percent decrease (or increase) in axis from end-diastolic length. Of 26 patients, 8 (Group I) served as normal (control) subjects. The remaining 18 patients had significant coronary artery disease; 6 of these (Group II) had no significant disease of the right coronary artery, whereas 12 (Group III) had significant obstruction of this artery. Four patients in Group II had a previous anteroseptal myocardial infarction, and six in Group III had a previous inferior myocardial infarction. There was a progressive decrease in segmental axes of shortening from Group I to II and from Group II to II, but the decrease was not significant at the level P less than 0.01. Only one patient in Group II had frank dyskinetic segmental motion of the interventricular septum (this patient had had a previous anteroseptal myocardial infarction), whereas two patients in Group III had dyskinetic segmental motion of the free right ventricular wall (both had previous inferior myocardial infarction). Therefore, coronary artery disease seldom produces significant right ventricular asynergy. Abnormal septal motion is associated with previous anteroseptal myocardial infarction; however, dyskinetic motion of the free right ventricular wall occurs only in patients with a right coronary arterial lesion and previous inferior myocardial infarction.     

Lupus cardiomyopathy: cardiac mechanics, hemodynamics, and coronary blood flow in uncomplicated systemic lupus erythematosus

Right and left heart pressures, left ventricular volumes, indices of contractility, myocardial wall stiffness, and coronary blood flow were determined in five young women with systemic lupus erythematosus (SLE) during diagnostic right and left heart catheterization. Examinations revealed (1) increases of right and left ventricular enddiastolic pressures; (2) decreases of cardiac output, stroke volume, ejection fraction, contractility indices, diastolic left ventricular volume inflow; (3) decreases of pharmacologically induced coronary vasodilation in SLE. The results demonstrate impaired pump function, reduced contractility, increased myocardial wall stiffness, and decreased coronary vascular reserve in SLE. It is concluded that lupus cardiomyopathy associated with an impairment of left ventricular function may be apparent in young women with SLE who have no clinical signs of cardiac dysfunction.     

Effects of respiratory alkalosis and acidosis on myocardial blood flow and metabolism in patients with coronary artery disease

BACKGROUND: Variation of the arterial carbon dioxide partial pressure (PaCO2) is not uncommon in anesthetic practice. However, little is known about the myocardial consequences of respiratory alkalosis and acidosis, particularly in patients with coronary artery disease. The aim of the current study was to investigate the effects of variation in PaCO2 on myocardial blood flow (MBF), metabolism, and systemic hemodynamics in patients before elective coronary artery bypass graft surgery. METHODS: In 10 male anesthetized patients, measurements of MBF, myocardial contractility, metabolism, and systemic hemodynamics were made in a randomized sequence at PaCO2 levels of 30, 40, and 50 mmHg, respectively. The MBF was measured using the Kety-Schmidt technique with argon as a tracer. End-diastolic left ventricular pressure and the maximal increase of left ventricular pressure were assessed using a manometer-tipped catheter. RESULTS: The cardiac index significantly changed with varying PaCO2 levels (hypocapnia, - 9%; hypercapnia, 13%). This reaction was associated with inverse changes in systemic vascular resistance index levels. The MBF significantly increased by 15% during hypercapnia, whereas no change was found during hypocapnia. Myocardial oxygen and glucose uptake and the maximal increase of left ventricular pressure were not affected by varying PaCO2 levels. CONCLUSIONS: In anesthetized patients with coronary artery disease, short-term variations in PaCO2 have significant effects on MBF but do not influence global myocardial oxygen and glucose uptake. Changes in systemic hemodynamics associated with respiratory alkalosis and acidosis are caused by changes in systemic vascular resistance rather than by alterations in myocardial contractility.     

Study of changes in myocardial contraction and left ventricular diastolic regidity after aortocoronary bypass

Eighteen patients with coronary insufficiency underwent a left ventricular cineangiography before and an average of four months after aorta-to-coronary bi-pass in order to assess the post-operative changes of myocardial contractility and diastolic rigidity. The contractility indices (VCF: mean speed, and VCF max: maximum shortening speed of the equatorial diameter of the left ventricle (% delta theta) were unmodified in the group (I) of fourteen patients with at least one pervious by-pass. On the contrary, a decreased % delta theta was observed in the group (II) of four patients in whom all the by-passes were occluded. The left ventricular end-diastolic pressure (LVEDP), the end-diastolic volume (LVEDV) and the "normalized" rigidity index (K) were unmodified in both groups after operation. The cardiac rate increased in the post-operative period in the group I (p less than 0.01) and the whole of the 18 patients (p less than 0.001); there was a positive correlation (p less than 0.02) between this variation and that of VCF, VCF max. and % delta theta, the significance of which is discussed. Besides there was a negative correlation between the variations of LVEDV and the VCF, and between the equatorial end diastolic diameter of the left ventricle and VCF, VCF max. and % delta theta, both in the pre-operative and the post-operative periods.     

Retrograde perfusion as a method for myocardial revascularization

Retroperfusion of the superficial coronary venous system was studied in 44 canine fibrillating in vivo, normothermic preparations, with exclusion of the systemic circulation using cardiopulmonary bypass techniques in order to assess its value as a method of myocardial revascularization. Perfusion of either the isolated aortic arch via a brachiocephalic cannula or of the coronary sinus through the free end of a vein anastomosed to the atrial rim of the sinus was performed for 1 h at 100 cm3/min in groups II-IV following 30 min of anoxia. Oxygen uptake, vascular resistance, venous outflow and venous enzyme levels (CPK, GDH) were studied. Group I controls (antegrade perfusion, no anoxia) showed continued aerobic metabolism in contrast to group II (antegrade perfusion) and III (retrograde perfusion) which displayed negative lactate balance. Oxygen consumption was greater in group III than II (p less than 0.01) with a higher oxygen extraction in III (p less than 0.005). Group IV, which was given intravenously 30 mg/kg methylprednisolone prior to anoxia and then retroperfused, showed continued aerobic metabolism with low GDH venous levels and adequate oxygen consumption. Three dogs were then subjected to aortoatrial rim coronary sinus vein grafts with ligation of the left common coronary artery at its bifurcation with distal left circumflex and anterior descending artery-internal mammary vein anastomoses for venous drainage. The right coronary artery was left intact. Arterial inflow into the coronary sinus was associated with a left ventricular pressure of 70-80 mm Hg for up to 1.5 h while regular sinus rhythm was maintained. We conclude that retroperfusion of the coronary sinus represents a surgically feasible technique for providing oxygen delivery to the ischemic myocardium.