Mean Coronary Sinus Blood Flow Research Articles

Intracoronary albunex. Its effects on left ventricular hemodynamics, function, and coronary sinus flow in humans.

Albunex is a recently developed ultrasonic contrast agent made from sonicated human serum albumin. The effects on left ventricular hemodynamics, function, and coronary sinus flow of intracoronary Albunex in humans have not been reported. Eighteen patients with known or suspected coronary artery disease were examined at the time of coronary arteriography with simultaneous two-dimensional echocardiography and left ventricular catheter-tip manometry. Intracoronary injections of Albunex into the left main coronary artery were performed, as were injections of 5% human serum albumin and iohexol, a widely used angiographic contrast agent. Mean coronary sinus flow was determined before and after injections of iohexol and 2 mL of Albunex. Injection of 1 mL of Albunex induced no changes in any of the measured hemodynamic parameters (heart rate, peak left ventricular [LV] systolic pressure, LV end-diastolic pressure, positive or negative LV dP/dt, or time constant of relaxation) or echocardiographic determinants of LV function (regional wall motion and global ejection fraction). Injection of 2 mL or more of Albunex caused small, transient (less than 30 seconds) changes in measures of isovolumic relaxation (negative LV dP/dt; 95% confidence interval: mean, -2.41 [-4.3, -0.52] and tau 1; confidence interval mean, 3.52; [1.48, 5.58]) but not in functional measures. Intracoronary injection of 5% human serum albumin had no effect. Iohexol induced small but significant changes in both systolic and diastolic parameters, which lasted beyond 30 seconds after injection. Mean coronary sinus blood flow increased. The effects of Albunex on hemodynamics, left ventricular function, and coronary sinus blood flow compare favorably with iohexol. Albunex can be considered to be an essentially inert contrast agent if used in patients with stable coronary artery disease.

Coronary hemodynamic effects of atrial natriuretic peptide in humans

Studies of the effects of atrial natriuretic peptide on the coronary circulation have yielded conflicting results in animals and have not been fully investigated in human subjects. To further characterize the direct coronary hemodynamic actions of atrial natriuretic peptide in humans and to assess the safety of its administration in patients with coronary artery disease, incremental doses of synthetic atrial natriuretic peptide and nitroglycerin were infused into the left coronary artery in 14 patients, 11 of whom had coronary artery disease.Both agents caused dose-related increases in total coronary sinus blood flow. The largest dose of atrial natriuretic peptide given to all patients (100 μg) increased mean coronary sinus blood flow from 127 ± 7 to 149 ± 9 ml/min (p < 0.05) and decreased coronary vascular resistance from 0.93 ± 0.07 to 0.81 ± 0.05 mm Hg/ml per min (p < 0.05); mean arterial blood pressure and heart rate were not affected by this dose of atrial natriuretic peptide. The greatest changes in coronary sinus blood flow (+25%) and coronary vascular resistance (−18%) after atrial natriuretic peptide administration occurred in the patients with coronary artery disease and no other associated cardiovascular disease. The maximal effects of atrial natriuretic peptide were similar to those of nitroglycerin, and no untoward effects were observed.Thus atrial natriuretic peptide is a direct coronary vasodilator in humans. Its maximal dose effects are similar to those of nitroglycerin and were well tolerated in this small group of patients. The physiologic importance and therapeutic potential of atrial natriuretic peptide in patients with coronary artery disease merit further investigation.

Effect of arginine vasopressin on coronary and systemic hemodynamics in man

Arginine vasopressin is a potent constrictor of isolated arterial segments in vitro. However, it is disputed whether, in vivo, arginine vasopressin acts as either a systemic or coronary vasoconstrictor. The purpose of this study was to determine the effect of arginine vasopressin on coronary and systemic vascular tone in man. Six patients undergoing routine diagnostic cardiac catheterization were studied. At angiography, all patients were found to have severe coronary artery disease. Cardiac and systemic pressures and coronary blood flow as well as serum arginine vasopressin and osmolality levels were measured before and after administration of hypertonic contrast dye and then following intravenous injection of an analog inhibitor of arginine vasopressin. At baseline, serum arginine vasopressin levels were within the normal range in all patients, but, following infusion of contrast dye, rose above physiological levels in 5 patients. In these latter patients, there were no significant changes in coronary and systemic hemodynamics between baseline (condition 1), following administration of contrast dye (condition 2) and 10 minutes after injection of arginine vasopressin inhibitor (condition 3). Mean coronary sinus blood flow (ml/min) and mean coronary vascular resistance (dyne·sec·cm −5) were 184±49 and 41,235±8275 during condition 1, 204±62 and 39,442±8781 during condition 2, and 192±75 and 44,930±11455 during condition 3. Mean arterial pressure (mm Hg) and mean systemic vascular resistance (dyne·sec·cm −5) during conditions 1, 2 and 3 were 105 ± 12 and 1454 ± 174, 114 ± 21 and 1432 ± 210, and 114 ± 15 and 1436 ± 147, respectively. These data suggest that arginine vasopressin has no effect on coronary or systemic vascular tone in patients with coronary artery disease.

Time dependent impairment of vagally mediated inhibition of noradrenaline release in the dog heart.

The effects of right vagal nerve stimulation on changes in heart rate, mean coronary sinus blood flow, and noradrenaline overflow rate induced by right cardiac sympathetic nerve stimulation were investigated in anaesthetised decentralised, open chest dogs, when autonomic nerve fibres were stimulated tonically at a frequency of 4 or 5 Hz for 2.5 min. Sympathetic nerve stimulation produced a mean(SEM) increase in each of the variables (50(7.0)% in heart rate, 48(6.3)% in coronary sinus blood flow, and 87.0(12.3) ng.min-1 in noradrenaline overflow rate into coronary sinus blood at 30 s), and the increments remained almost constant during continued stimulation. Vagal nerve stimulation induced a decrease of 34(3.4)% in heart rate and of 22(4.5)% in coronary sinus blood flow and a slight reduction (-9(3.2) ng.min-1) in noradrenaline overflow rate at 30 s. Only the decrease in heart rate faded slightly with time. Combined stimulation of the sympathetic and parasympathetic nerves induced a decrease of 19(5.0)% in heart rate and 4(7.5)% in coronary sinus blood flow and an increase of 34.3(12.0) ng.min-1 in noradrenaline overflow rate at 30 s. The decrease in heart rate and coronary sinus blood flow faded, and noradrenaline overflow rate increased significantly to 86.4(17.3) ng.min-1 at 120 s. The temporal changes in heart rate, coronary sinus blood flow, and noradrenaline overflow rate caused by combined nerve stimulation were readily inhibited by treatment with atropine.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of exercise on coronary sinus blood flow determinations

Consecutively measured values of coronary sinus blood flow were compared to assess the reproducibility of the coronary sinus thermodilution technique. Values measured at rest and during exercise were evaluated and the influence of the respiratory cycle on reproducibility was studied. Correlation of consecutive values revealed a coefficient of 0.94 at rest and 0.93 during exercise. Differences between mean values of consecutive measurements were nonsignificant. A comparison of the coefficients of variation at rest (8.50 ± 7.09) and exercise (8.02 ± 4.75) revealed no significant difference. Variation about mean coronary sinus blood flow due to inspiration and expiration was similar at rest and during exercise (42% and 37%, respectively). Provided that critical variables are closely monitored the coronary sinus thermodilution technique is a highly reproducible technique in a clinically feasible setting.

Effects of intubation on coronary blood flow and myocardial oxygenation.

Effects on haemodynamics and myocardial oxygenation of endotracheal intubation were examined in 17 patients after halothane induction and 12 after 1 mg X kg-1 of IV morphine. Six patients having each anaesthetic were pretreated with IV propranolol (0.1 mg X kg-1) 45 minutes earlier. Arterial and intracardiac pressures, cardiac output and total coronary sinus blood flow (CSBF), both by thermodilution, were determined plus arterial-coronary differences of oxygen, haemoglobin and lactate. Blood pressure (BP), heart rate and CSBF were recorded continuously during intubation. The subjects were candidates for coronary bypass grafts, but had good ventricular function (mean ejection fraction 0.68 +/- 0.13 SD). From their reduced levels after induction, BP, cardiac index and systemic vascular resistance increased to awake levels following intubation. Mean CSBF in nonbetablocked patients increased to awake level along with BP. More myocardial oxygen was extracted and consumed after intubation, but lactate extraction continued: these data are evidence of adequate oxygen supply. Induction with either halothane or morphine effectively prevented the hypertensive response to intubation. Acute beta blockade led to less increase in heart rate from intubation.

Hemodynamic effects of intravenous prostacyclin in stable angina pectoris

Prostacyclin (PGI 2) is a naturally occurring vasodilator and inhibitor of platelet aggregation that produces vasodilatation of the systemic, pulmonary and coronary vascular beds in animal models. Because the endogenous production of PGI 2 is reduced in those with coronary arterial disease (CAD), it may have a therapeutic role in patients with ischemic heart disease. To assess its safety and efficacy in this clinical setting, 17 patients with stable angina and CAD received an incremental intravenous infusion of either PGI 2 (n = 10) to a maximum dose of 10 ng/kg/min (average 9.8 ± 0.8 [mean ± standard deviation]), or diluent buffer solution (placebo) (n = 7). All patients who received PGI 2 became flushed, but experienced no other adverse effects. PGI 2 caused an increase in heart rate (66 ± 11 to 80 ± 11 beats/min, p <0.001) and cardiac index (2.88 ± 0.65 to 3.97 ± 1.17 liters/min/m 2, p <0.001) and a decrease in mean femoral arterial pressure (96 ± 18 to 86 ± 11 mm Hg, p <0.001), but no change in mean pulmonary arterial or capillary wedge pressure. Total systemic and pulmonary vascular resistance decreased significantly (p <0.001). In response to PGI 2, mean coronary sinus blood flow did not change significantly (100 ± 40 to 121 ± 52 ml/min), but coronary vascular resistance decreased (1.07 ± 0.40 to 0.83 ± 0.36 U, p <0.001). No variable was altered by placebo infusion. PGI 2 caused a marked increase in 6-keto PGF 1α (the stable metabolite of PGI 2) concentrations in both arterial (42 ± 29 to 567 ± 216 pg/ml, p <0.001) and venous (46 ± 31 to 604 ± 229 pg/ml, p <0.001) blood but no demonstrable change in plasma renin activity. Thus, intravenous PGI 2 to a dosage of 10 ng/kg/min is a safe and effective systemic, pulmonary and coronary arterial vasodilator in patients with CAD and stable angina pectoris.

Alterations of myocardial amino acid metabolism in chronic ischemic heart disease.

Arteriovenous differences (A-V) of all naturally occurring amino acids, lactate, and oxygen were measured simultaneously with coronary sinus blood flow (CSBF) in 8 normal subjects and 11 patients with coronary artery disease at rest and during pacing stress. Mean values for CSBF and myocardial oxygen consumptions (MVO2) for the two groups were similar at rest and during pacing, although mean CSBF and MVO2 increased significantly in both groups in the paced as compared to the rest state. Alanine (ala) was the only amino acid released by the myocardium, while only glutamic acid(glu) demonstrated uptake. Mean A-V ala was negative at rest in the control and coronary disease groups (-4.8+/-3.8 vs. -22.0+/-3.0 nmol/ml, respectively), but was significantly more negative in the coronary group (P less than 0.001) and not statistically different than zero in the normals. A-V ala became significantly negative with pacing in the normals (-10.0+/-4.3 nmol/ml), remained unchanged in the coronary group (-23.0+/-2.9 nmol/ml), and was significantly more negative in the coronary group (P less than 0.05). Calculation of data on the basis of net ala flux ([A-V] X [CSBF X hematocrit]) yielded similar results as that obtained with A-V differences. A-V glu was significantly positive in normals (27.7 +/- 8.9 nmol/ml, P less than 0.01) and coronary patients (59.9 +/- 8.9 nmol/ml, P less than 0.01) at rest but significantly greater in the latter group (P less than 0.001). With pacing, A-V glu remained significantly greater than zero in coronary patients (35.3 +/- 6.3 nmol/ml) and decreased to zero in the normals (4.3 +/- 11.8 nmol/ml). Calculation of net glu flux (nmol/min) at rest yielded data similar to that based on A-V difference. With pacing, net glu flux in the coronary patients did not decrease due to the augmentation of CSBF. No relation between A-V glu or ala and CSBF, MVO2 or A-V lactate was noted. The data demonstrate that specific alterations of myocardial amino acid metabolism characterize patients with chronic ischemic heart disease.

Measurement of coronary sinus blood flow by continuous thermodilution in man.

A technique was developed for measurement of blood flow in the coronary sinus in man by continuous thermodilution. For single determinations, 5% dextrose at room temperature is injected at a constant rate of 35 ml/min for a period of about 20 sec. In 14 subjects with normal coronary arteries the mean coronary sinus blood flow was 122 ± 25 ml/min (range, 83 to 159 ml/min). The blood flow computed per 100 g of left ventricle was 82 ± 16 ml/min, which is in the range of values obtained by nitrous oxide and coincidence counting methods. In 35 patients with arteriographically confirmed coronary artery disease the mean flow was similar (128 ± 20 ml/min; range, 92 to 167 ml/min). A special catheter was used for simultaneous measurement of blood flow in the coronary sinus and great cardiac vein. In eight normal subjects the mean great cardiac vein flow was 68 ± 11 ml/min (range, 51 to 78 ml/min) or 65 ± 10% of the coronary sinus blood flow. The method allowed continuous measurement of flow over a period of several minutes and, for the first time, measurement of rapid changes in myocardial perfusion.