Coronary Blood Flow Pattern Research Articles

Transmural distribution of myocardial blood perfusion and phasic coronary blood flow pattern in a canine model of acute ischemia

Background Although several investigators have analyzed coronary artery blood flow under various conditions, almost all these studies have measured only some branches of the left anterior descending (LAD), left circumflex (LCX), or right coronary (RCA) artery. Methods In a canine model of acute ischemia ( n = 5), we simultaneously assessed (a) regional myocardial blood perfusion using microspheres and (b) phasic coronary blood flow patterns as measured by three epicardial flow probes placed around the LAD, LCX, and RCA. Results The results from this study indicated that the LAD supplies blood to the epicardial ( r = 0.687, p < 0.0001), midwall ( r = 0.556, p = 0.0021), and endocardial layers ( r = 0.666, p = 0.0001) of the LAD area; the LCX supplies the midwall ( r = 0.514, p = 0.0051) and endocardial layer ( r = 0.621, p = 0.0004) of the LCX area, antero-lateral papillary muscle ( r = 0.548, p = 0.0025), and postero-medial papillary muscle ( r = 0.641, p = 0.0002), especially during the diastolic phase; and the RCA supplies the right ventricular apex ( r = 0.559, p = 0.0020), left atrium ( r = 0.618, p = 0.0005), right atrium ( r = 0.471, p = 0.0114), and postero-medial papillary muscle ( r = 0.486, p = 0.0088), especially during the systolic phase. Conclusions These results are potentially relevant to understanding the physiology of myocardial blood perfusion and to improving treatment of acute myocardial ischemia and infarction.

Detection of coronary arterial microvascular disorders using (99m)Tc-tetrofosmin uptake increase during exercise and coronary blood flow velocity patterns obtained by magnetic resonance imaging.

This study reports an evaluation of coronary arterial blood flow patterns in patients with diabetes mellitus and healthy subjects using magnetic resonance coronary angiography (MRCA). Twenty patients with diabetes mellitus (DM group) and 20 healthy subjects (N group) were studied using MRCA and myocardial SPECT images using (99m)Tc-tetrofosmin (TF). The rate of change in myocardial TF uptake was measured during a 1-day protocol of exercise and rest. Initial and delayed exercise single photon emission computed tomography (SPECT) images were acquired 30 min and 3 h after injection (370 MBq of TF) (TF1 and TF2, respectively). Thereafter, 740 MBq of TF was administered intravenously, again, and resting SPECT images (TF3) were acquired 30 min later. The myocardial counts of these three points of acquisition were defined, and the rate of change of myocardial TF uptake between exercise and rest was determined. The % increase in uptake was significantly lower in the DM group than in the N group in all myocardial segments. The average coronary arterial diastolic velocity determined using MRCA was slightly lower in the DM group than in the N group, and the average systolic peak velocity (ASPV) was slightly greater in the DM group than in the N group, although these values were not statistically significant. The diastolic/systolic velocity ratio (DSVR) in the DM group was significantly lower than that in the N group ( P < 0.05). There was a significant correlation between DSVR and % uptake increase ( r = 0.605, P < 0.05). These results indicate that the measurements made using MRCA and the % uptake increase measured using TF myocardial scintigraphy represent a potentially useful noninvasive method for diagnosing microvascular dysfunction in diabetic patients.

Absence of postprandial surge in coronary blood flow distal to significant stenosis: a possible mechanism of postprandial angina

ObjectivesThis study was designed to investigate a possible mechanism of postprandial angina. BackgroundPostprandial angina has been recognized for more than two centuries; however, its mechanism is still controversial. The most widely accepted mechanism involves increased myocardial oxygen demand after food intake. Recently, the redistribution in coronary blood flow (CBF) was suggested as a possible mechanism. MethodsTwenty young, healthy volunteer controls and 20 patients with significant stenosis in the left anterior descending (LAD) or left main coronary artery were enrolled in the study. Coronary blood flow was evaluated in the distal LAD by using transthoracic Doppler echocardiography before and 15, 30, 45, and 60 min after food intake. In the CBF curve, the time velocity integral of diastolic flow (Dtvi) and the product of Dtvi and heart rate (HR) were measured. In six patients, these measurements were repeated after successful coronary intervention. ResultsIn the healthy volunteer controls, Dtvi and Dtvi × HR increased after food intake with a peak value at 15 min, which indicates the presence of postprandial surge in the CBF. Fasting values and peak values at 15 min were significantly different (Dtvi: 15.1 ± 4.9 cm/s vs. 18.9 ± 5.9 cm/s, p = 0.04, Dtvi × HR: 862.2 ± 261.5 cm/min vs. 1,174.2 ± 307.5, p = 0.002). In contrast with the controls, despite postprandial increase in double product (HR × blood pressure), Dtvi and Dtvi × HR in the patient group decreased after food intake, with a nadir value at 45 min. Fasting values and nadir values at 45 min were significantly different (Dtvi: 24.0 ± 19.6 cm/s vs. 19.3 ± 17.1 cm/s, p < 0.001, Dtvi × HR: 1,449.6 ± 1,044.0 cm/min vs. 1,273.4 ± 1,000.9 cm/min, p = 0.002). In six patients, the CBF pattern resumed the normal pattern of postprandial surge in the CBF after successful coronary intervention. ConclusionsResults of our study suggest that “steal phenomenon” may play a role in the mechanism of postprandial angina.

Dynamic curvature strongly affects wall shear rates in a coronary artery bifurcation model

This study was motivated by the need for a better understanding of coronary artery blood flow patterns and their possible role in atherosclerosis formation. Of particular interest in this study was the effects of the dynamic deformation due to myocardial contraction on wall shear rate patterns in the coronary arteries. A better understanding of these effects on wall shear rate in a bifurcation geometry and an evaluation of the importance of these effects was desired. A three-dimensional computer model of a bifurcation lying on the surface of a sphere with time-varying radius of curvature was employed to simulate the motion and deformation of the arteries. The results indicated low mean shear rates along the myocardial wall and very high shear rate variations (over 100% of the static mean shear rate) along the outer wall. The results obtained using a quasi-static analysis were found to underestimate the dynamic wall shear rate variation along the myocardial and outer walls. It was concluded that dynamic geometry effects are important in determining sites of low mean and oscillating wall shear that have been associated with atherogenesis in curved, bifurcating arteries.

Relation between Perfusion Status of Dysfunctional Myocardium and Coronary Flow Reserve in Acute Myocardial Infarction

Background：Dysfunction of microvasculature was frequently observed despite of successful revascularization with alteration of coronary flow dynamics in acute myocardial infarction(AMI. Reduction of coronary vasodilatory reserve was found in poorly perfused infarcted myocardium. The objectives of this study was to evaluate the vasodilatory reserve in infarcted myocardium and determined its relationship to perfusion status of myocardium in early recovery phase of acute myocardial infarction. Method：The study subjects consisted of 14 patients with anterior AMI and 6 controls with atypical chest pain and have normal coronary artery. The coronary flow pattern was assessed using intracoronary Doppler wire and vasodilatory reserve was measured after injection of 18μ g of adenosine to infarct-related artery after successful revascularization by percutaneous angioplasty at average 11days post-AMI. After measurement of coronary blood flow pattern, myocardial perfusion status was evaluated by myocardial contrast echocardiography(MCE. Perfusion status by MCE was analysed semiquantitatively and compared to various parameters of coronary flow and vasodilatory reserve of infarct-related artery. Results：After successful revascularization, perfusion defect by MCE was observed in 50%(n＝7 of patients. The vasodilatory reserve was lower in patients with perfusion defect by MCE than those of patients without perfusion defect(p<0.05 and contol(p<0.05. There was no difference in coronary

Differential characterization of human coronary collateral blood flow velocity

The functional importance and protective nature of the coronary collateral circulation has been well established. There are few data, however, regarding the phasic nature and absolute velocities of collateral flow in patients. The aim of this study was to characterize and quantify ipsilateral coronary collateral blood flow velocity in patients during coronary angioplasty. Coronary collateral flow velocity was measured in 49 patients during coronary angioplasty. Angiographic collateral filling was categorized by the Rentrop grading scale (0 to 3) and by anatomic pathway (epicardial, intramyocardial, or unknown [acutely recruited]). Collateral blood flow velocity was measured with a Doppler-tipped guide wire placed distal to the balloon occlusion in the collateralized vessel. Collateral flow velocity was characterized as predominantly systolic or diastolic, and phasic flow patterns were defined as biphasic (both systolic and diastolic), monophasic (only systolic or diastolic), or bidirectional (antegrade and retrograde velocity). Twenty-three (47%) patients had biphasic flow; 17 (35%) patients had monophasic flow; and 9 (18%) patients had bidirectional flow. Thirty-six (73%) of 49 patients had predominantly systolic flow signals. Epicardial collateral pathways had the highest total flow velocity integral, at 15.0 ± 7.0 (vs intramyocardial [8.4 ± 5.7] and acutely recruitable [5.4 ± 2.1]; p < 0.05). There were no differences in flow velocity integrals among the Rentrop angiographic grades of collateral filling. These data establish three patterns of coronary collateral blood flow and demonstrate that the majority of collateral flow in the ipsilateral receiving vessel occurs during systole. The measurement of coronary collateral flow velocity provides a unique means to study the effects of pharmacologic or mechanical interventions on human collateral blood flow.

Coronary blood flow reserve in acute aortic regurgitation

This study sought to determine the impact of acute aortic regurgitation on coronary blood flow reserve and phasic epicardial coronary blood flow in closed-chest dogs. Hemodynamic changes in acute aortic regurgitation are known to precipitate myocardial ischemia. Coronary blood flow reserve has not been studied in closed-chest experimental preparations with acute aortic regurgitation. Graded temporary acute aortic regurgitation was produced in 11 mongrel dogs. Phasic coronary blood flow velocities were measured using a Doppler guide wire. Coronary flow reserve was defined as the ratio of the time average of spectral peak velocity after administration of papaverine to that of the baseline state. Under control conditions (mean [+/- SEM] diastolic blood pressure 82.2 +/- 4.5 mm Hg), coronary flow reserve was 3.51 +/- 0.27 with predominantly diastolic epicardial coronary blood flow. With mild acute aortic regurgitation (diastolic blood pressure 61.8 +/- 3.0 mm Hg), coronary flow reserve decreased to 2.38 +/- 0.27, with an increase in phasic systolic epicardial coronary blood flow. At the onset of moderate acute aortic regurgitation (diastolic blood pressure 42.1 +/- 0.9 mm Hg), coronary flow reserve declined further to 1.46 +/- 0.12, and the phasic systolic epicardial coronary blood flow became more prominent. With severe aortic regurgitation (diastolic blood pressure 29.2 +/- 2.2 mm Hg), coronary flow reserve reached 1.20 +/- 0.05, and the phasic epicardial coronary blood flow pattern was found to be predominantly systolic with retrograde diastolic flow. The ratio of diastolic to systolic pressure-time indexes with severe aortic regurgitation suggested subendocardial underperfusion. This study demonstrates a marked decline in coronary blood flow reserve and documents a progressive change in the phasic epicardial blood flow to a predominantly systolic pattern with increasing degrees of acute aortic regurgitation.

Effects of heart rate on phasic coronary blood flow pattern and flow reserve in patients with normal coronary arteries: A study with an intravascular Doppler catheter and spectral analysis

To assess the effects of pacing-induced tachycardia on phasic coronary blood flow pattern and flow reserve of left anterior descending artery, we examined 16 patients with chest pain and angiographically normal coronary arteries by using an intravascular Doppler catheter with spectral analysis of the velocity signal. The heart rate was increased from a mean of 68 ± 11 beats/min during sinus rhythm to 100 beats/min and again to 120 beats/min. Cross-sectional area of the epicardial artery and resting systolic and diastolic coronary blood flows increased progressively, resulting in an elevation of total coronary flow from 142 ± 54 ml/min during sinus rhythm to 190 ± 66 ml/min at 100 beats/min ( p < 0.05) and to 219 ± 69 ml/min at 120 beats/min ( p < 0.01). During maximal hyperemia with intracoronary injection of 10 to 12 mg of papaverine, there was an increase in the systolic coronary blood flow with a decrease in the diastolic flow, resulting in no significant change in the total flow. These alterations led to progressive reductions in coronary flow reserve from 3.9 ± 0.7 during sinus rhythm to 2.9 ± 0.9 at 100 beats/min ( p < 0.01) and to 2.3 ± 0.3 at 120 beats/min ( p < 0.001). Thus careful consideration should be given to the effects of heart rate when phasic coronary blood flow pattern and flow reserve are assessed.

Coronary collateral development in Kawasaki disease

We studied on the relationship of either angiographic severity of stenotic lesion or coronary blood flow pattern to coronary collateral(CC) development in 30 patients (age range;4 months-20 years, mean;9.8 years) with Kawasaki disease with angiographic evidence of severe stenotic lesion(90%) or occlusion. CC was detected in 22(73%)(31 branches). Myocardial infarction was confirmed in 14(64%) of 22 patients with CC and in 3(37%) of the residual 8 patients without CC. CC was observed in 100% of the patients with occlusion, in 62.5 % with recanalization, and in 33% with stenosis. From the viewpoints of angiographic coronary perfusion, CC was observed in 18% of the patients with good perfusion, in 93.8% with hypoperfusion, andin 100% with severe hypoperfusion. CC development was significantly higher in the patient:s with hypoperfusion at the stenotic lesion. These results suggest that CC development depends on the severity of hypoperfusion rather than that of angiographic stenosis. SERUM CHOLESTEROL DURING AND AFTER KAWASAKI DISEASE

ATP-sensitive potassium channel is essential to maintain basal coronary vascular tone in vivo.

Glibenclamide, a known selective inhibitor of ATP-sensitive potassium channels, was infused into the coronary vasculature of anesthetized dogs and of isolated perfused rabbit hearts to assess the role of this channel in the maintenance of basal coronary resistance. Infusion of glibenclamide at a concentration of 55-80 microM in the dogs resulted in a twofold steady-state increase in coronary resistance with resultant tissue ischemia. Infusion of 1 microM glibenclamide in the isolated hearts resulted in a 67% increase in coronary resistance with resultant tissue ischemia. The ischemic changes were reversible upon removal of the drug. These findings indicate that the ATP-sensitive K+ channel plays a significant role in the maintenance of basal coronary resistance in vivo. Higher concentrations of glibenclamide (80-100 microM) in the in vivo dog heart consistently gave rise to an oscillating pattern of coronary flow. These oscillations were either eliminated or decreased in amplitude and frequency by the infusion of 8-phenyltheophylline, a specific competitive inhibitor of adenosine receptors. 31P-nuclear magnetic resonance spectroscopy performed at the peaks and troughs of these oscillations revealed oscillation of the phosphorylation potential at the same frequency. Thus adenosine release caused by tissue ischemia appears to play a major role in creating the oscillating pattern of coronary blood flow, that occurs during the inhibition of ATP-sensitive K+ channels by glibenclamide.

Right ventricular coronary blood flow patterns during aortic pressure reduction in renal hypertensive dogs

We measured right ventricular coronary blood flow with radioactive microspheres during graded aortic pressure reduction in 13 normal dogs and in 13 renal hypertensive dogs with left ventricular hypertrophy. Under anaesthesia and controlled loading conditions, mean aortic pressure was lowered from control (128 mmHg in normal and 146 mmHg in hypertensive dogs) to approximately 100, 90 and 80 mmHg. In normal dogs, right ventricular blood flow was not affected by this pressure reduction, consistent with effective right ventricular autoregulation. In hypertensive dogs, however, right ventricular blood flow was maintained between a mean aortic pressure of 146 and 90 mmHg (range 75-79 ml min(-1) 100 g(-1] but fell by 18% to 63 ml min 100 g(-1) at a mean aortic pressure of 80 mmHg (P less than 0.005). We conclude that autoregulation of right ventricular blood flow was preserved in chronic hypertension but that, compared to normal dogs, the lower limit of autoregulation was reset to a higher pressure level. Moreover, the similarity of right ventricular-to-body weight ratios in the two groups implied that this change was a consequence of hypertension-induced structural changes in the coronary vasculature.

Synthesis of lipoxygenase and epoxygenase products of arachidonic acid by normal and stenosed canine coronary arteries.

Coronary vascular injury promotes blood cell-vessel wall interactions that influence arachidonic acid metabolism and coronary blood flow patterns. Since lipoxygenase and cytochrome P-450 epoxygenase metabolites of arachidonic acid are synthesized by vascular and inflammatory cells and have a variety of important biological actions, we investigated the metabolism of arachidonic acid by these pathways in normal and stenosed, endothelially injured canine coronary arteries. We found and confirmed by gas chromatography/mass spectrometry that primarily 12- and 15-hydroxyeicosatetraenoic acids (HETEs) are synthesized by both coronary artery segments. Lesser amounts of 11-, 9-, 8-, and 5-HETEs are also produced. 15-Ketoeicosatetraenoic acid is also synthesized. The synthesis of 14C-HETEs is fivefold to 10-fold greater by the stenosed than the normal coronary artery. Specific radioimmunoassays indicated that the stenosed coronary artery synthesized 93 +/- 14 and 1,102 +/- 154 ng/g of tissue of 15- and 12-HETE, respectively, while the normal coronary artery produced 17 +/- 3 and 162 +/- 68 ng/g of tissue of 15- and 12-HETE, respectively. Products comigrating with 14,15-; 11,12-; 8,9-; and 5,6-epoxyeicosatrienoic acids (EETs) and the corresponding dihydroxyeicosatrienoic acids (DHETs) were detected predominantly in stenosed coronary arteries by high-pressure liquid chromatography. The structures of the EETs were confirmed by GC/MS. The EETs and prostaglandin I2 produced endothelium-independent, concentration-related relaxations of dog coronary artery rings. These data indicate that normal and stenotic coronary arteries metabolize arachidonic acid to HETEs, DHETs, and EETs along with prostaglandins; however, the synthesis of these metabolites is greater in the stenosed, endothelially injured vessel. The EETs may be synthesized during the development of cyclic flow variations and counteract the vasoconstrictor effects of thromboxane A2.

Antiplatelet antibody [7E3 F(ab')2] prevents rethrombosis after recombinant tissue-type plasminogen activator-induced coronary artery thrombolysis in a canine model.

Coronary artery rethrombosis can complicate initially effective thrombolytic therapy. Platelets interacting with injured vascular endothelium in a region along the coronary artery with reduced luminal cross-sectional area contribute to rethrombosis. The purpose of this study was to investigate the potential of the F(ab')2 fragment of the murine monoclonal antibody 7E3 [7E3 F(ab')2] to prevent rethrombosis after intracoronary clot lysis with recombinant tissue-type plasminogen activator (rt-PA) in an experimental model. The 7E3 F(ab')2 binds to the platelet glycoprotein IIb/IIIa complex (GPIIb/IIIa), thereby preventing platelet-fibrinogen interaction and intravascular thrombus formation. Experimental coronary artery thrombosis was produced in the anesthetized dog by application of direct anodal current to the intimal surface of the left circumflex coronary artery in the region of an external stenosis. Lysis of the established intracoronary thrombus was achieved with the intravenous administration of rt-PA (25 mg) after which the animals were randomized into two groups. Group 1 (n = 10) served as the control, receiving the saline diluent, and group 2 (n = 9) received 7E3 F(ab')2, given as a single intravenous injection (0.8 mg/kg). The times required for occlusive thrombus formation, rt-PA-induced thrombolysis, and rethrombosis (if it occurred) were similar in the animals treated with saline and those treated with 7E3 F(ab')2. The initial left circumflex coronary artery blood flow was similar in both groups but decreased to a negligible level in group 1. In group 2, left circumflex coronary artery blood flow declined modestly (24 +/- 2 to 10 +/- 2 ml/min). Rethrombosis occurred in all animals in group 1 but in only two of nine animals in group 2 (p less than 0.05). Oscillations in coronary blood flow preceded rethrombosis in group 1, whereas 7E3 F(ab')2 stabilized left circumflex coronary artery blood flow patterns during the course of teh experimental protocol (5.2 +/- 0.9 vs. 0.7 +/- 0.4 oscillations, respectively; p less than 0.05). Thrombus mass recovered from the left circumflex coronary artery at the conclusion of each experiment was greater in group 1 as compared with group 2 (7.0 +/- 2.3 vs. 1.5 +/- 0.7 mg, respectively; p less than 0.05). The area of left ventricle at risk for infarction was similar in both groups but infarct size, infarction/at risk assessed histochemically, was larger in group 1 than group 2 (35 +/- 9% vs. 6 +/- 4%, respectively; p less than 0.05). Platelet aggregation induced by ADP and arachidonic acid was similar at baseline for all of the animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Analysis of coronary artery blood flow pattern using Doppler catheter in patients with ischemic heart disease

Analysis of coronary artery blood flow pattern using Doppler catheter in patients with ischemic heart disease

Influence of the autonomic nervous system on coronary blood flow during partial stenosis

Partial coronary stenosis produces cyclical changes in coronary blood flow (CBF) which are the result of spontaneous aggregation and disaggregation of platelet plugs at the site of occlusion. The possible influence of the autonomic nervous system on this phenomenon has not been hitherto determined. The present study was performed in 20 chloralose-anesthetized dogs in which the effects of bilateral vagotomy and stellectomy were examined during partial stenosis of the left circumflex coronary artery. Vagotomy reduced the frequency of CBF oscillations from 11.5 ± 2.1 to 5.0 ± 2.1 cycles/hr ( p < 0.05). The magnitude of the flow changes was reduced from 13.8 ± 4.0 to 9.7 ± 3.0 ml/min (NS). Bilateral cervical stellectomy reduced the frequency of CBF changes from 7.8 ± 2.7 to 3.7 ± 1.3 cycles/hr ( p < 0.025) and their magnitude from 10.6 ± 2.5 to 5.6 ± 1.8 ml/min ( p < 0.05). In five dogs in which cyclical CBF changes were reduced or abolished by decentralizing the stellate ganglia, electrical stimulation of the main body of the left ganglion evoked or enhanced the oscillations in two dogs, had no distinct effect in two dogs, and elicited no response in one dog. A 5-minute infusion of 0.5 μg/kg/min and 0.75 μg/kg/min epinephrine (four dogs) provoked the CBF changes in all animals for a period of 5 to 10 minutes. Blockade of muscarinic receptors by 0.2 mg/kg atropine resulted in a significant attenuation of flow changes, which may at least in part have been due to a direct effect of atropine on platelets. We conclude that cardiac sympathetic tone significantly influences the CBF pattern during critical coronary stenosis. While the afferent limb of the vagus may in part mediate this effect via a reflex increase of adrenal medullary catecholamines, the role of the efferent vagus awaits further clarification.

Myocardial blood flow responses to acute hypoxia and volume loading in physically trained rats.

Rats trained by a swimming programme were studied to see whether physical training can promote changes in coronary blood flow patterns that are physiologically important. Radioactive microspheres were employed in an open-chest preparation to measure coronary blood flow and cardiac output during the control state, during hypoxia, and during dextran infusion to increase the preload. Hearts from the trained groups of rats had elevated actomyosin ATPase activities, indicating that the swimming caused a cardiac training effect. In each group hypoxia produced a fall in cardiac output and myocardial blood flow, and these functions more than doubled during volume loading. However, cardiac output, stroke volume, coronary blood flow, and myocardial distribution of blood flow were not significantly different between either group during the control state, hypoxia, or volume loading. Energy supply-demand factors (ejection pressure time and diastolic pressure time) were also similar in the two groups. Therefore, despite evidence from our previous studies of increased coronary vascular responses when hearts from trained animals were perfused with aqueous solutions, the present experiments failed to demonstrate increased coronary flow responses when the hearts were perfused with blood. This study casts doubts on the physiological importance of increased vascularity in hearts of rats subjected to exercise training when only mild to moderate stress is imposed.

Effects of extracorporeal circulation on cardiac performance and coronary blood flow (total and regional). A study of differences arising from pre-existent left ventricular load and anoxic arrest.

It was researched how the ECC affects on cardiac performance and the total and regional coronary blood flow, using two groups of dogs with a hypertrophied heart and a non-hypertrophied heart, each group of which was further divided into two subgroups depending on whether the intermittent 40 mins. anoxic arrest was applied or not. Cardiac performance before and 60 mins. after cessation of ECC were compared each other. Coronary hemodynamics was studied before, during (immediately before and after anoxic arrest), and 60 mins. after cessation of ECC, using 15 +/- 5 diameter radioactive microspheres. 1) In the group of a non-hypertrophied heart, no obvious changes of cardiac performance were seen before and after ECC. The total coronary blood flow increased after ECC than before. Though the regional coronary blood flow pattern showed no differences in this group except only immediately after anoxic arrest, when the regional blood flow into the right ventricle, inner and middle layers of the left ventricle increased. 2) In the group of a hypertrophied heart, cardiac performance decreased after ECC, and further significant decrease was observed in the subgroup of anoxic arrest. No significant changes of the total coronary blood flow were observed before and after ECC in this group, even when compared with that in the group of a non-hypertrophied group. However, the increase of blood flow to the right ventricle, inner and middle layers of the left ventricle immediately after anoxic arrest was not observed, that was seen in the group of a nonhypertrophied heart. 3) It follows that the decrease of cardiac performance after ECC in the group of a hypertrophied heart is not due to the changes of the total and regional coronary blood flow. It is considered that the difference of the regional coronary blood flow pattern changes immediately after anoxic arrest between the non-hypertrophied heart group and hypertrophied group may cause the different changes of cardiac performance before and after ECC between the two groups. This consideration should be more justified by evaluating not only coronary hemodynamics but also the relationship between cardiac metabolic needs and the regional coronary blood flow.

Phasic coronary blood flow patterns as related to the balance between oxygen demand and supply in the myocardium.

To explore possible relationship between changing coronary arterial flow patterns and states of coronary circulation, the left circumflex arterial flow (mean and phasic) was measured simultaneously with the oxygen saturation of the great cardiac vein blood (SGCVO2) in anesthetized open-chest dogs. Coronary vasomotion was altered either with administration of drugs or with mechanical interventions. The "intermittent" flow pattern observed in the resting state persisted as far as SGCVO2 remained unchanged or lowered regardless of changes in coronary flow, aortic pressure or heart rate. On the other hand, when increase in circumflex flow occurred simultaneously with elevation of SGCVO2, a "continuous" flow pattern of the circumflwx flow was noticed. We suggest that (1) the "intermittent" flow pattern would indicate that efficient O2 uptake from the supplied arterial blood is taking place in the myocardium and (2) the "continuous" flow pattern would indicate presence of arterial flow excess to the myocardial requirement, rendering the increased coronary blood flow less effective for its amount in terms of O2 supply to the myocardium.

Effects of Myocardial Strains on Coronary Blood Flow

Systole causes a redistribution of coronary blood flow away from the subendocardium. In the present study the relative contribution of shortening of the myocardial fibers (wall strains) and of pressure development in the ventricular lumen to redistribution were determined. The distribution of coronary blood flow during systole in hearts ejecting into a severed aorta (large wall strains and near-zero afterload) was compared with that in isovolumetrically contracting hearts (reduced wall strains and significant afterload). A quantitative index of the distribution of coronary blood flow during systole was provided by the myocardial uptake of a bolus of 86 Rb or 42 K injected when constant-pressure perfusion of the left coronary artery was restricted with a solenoid-controlled pump to the period of systole. The coronary blood flow during systole in the subendocardium of the ejecting heart was 62% of that in the subepicardium. A similar gradient in the systolic flow with the endocardium receiving 37% of the blood flow to the epicardium was observed in the hearts contracting isovolumetrically. Removing the afterload by severing the aorta abolished the transmural differences in coronary blood flow. In the present experiment cardiac strains per se did not redistribute coronary blood flow through shear or traction forces on the coronary vasculature, but rather, coronary blood flow was affected only by compressive stresses in the myocardium. Contraction in the absence of afterload influenced overall coronary resistance, however; 18% of the resting coronary resistance was associated with shortening alone. An additional 11% of the resting coronary resistance appeared when pressure development accompanied shortening. Coronary blood flow patterns indicated two separate compressive stresses in the left ventricle. The first stress was associated with pressure development and increased with myocardial depth. The second stress was smaller; it was associated with shortening and uniformly distributed.

Army heart pump for postsystolic augmentation.

Postsystolic myocardial augmentation has been shown to decrease left ventricular work and improve coronary blood flow experimentally. 1,2 Increase in coronary blood flow has more frequently been demonstrated during postsystolic augmentation in animals with myocardial ischemia. 3-5 Other investigations have failed to demonstrate measurable or appreciable increases in coronary flow in normal animals despite changes in phasic coronary blood flow pattern. 6 Postsystolic myocardial augmentation with the army artificial heart pump consistently decreased aortic systolic pressure, aortic end diastolic pressure, left ventricular pressure, and left ventricular work in dogs. 7 Aortic diastolic pressure was consistently augmented and coronary blood flow usually increased. Postsystolic augmentation has not been previously studied in subhuman primates, whose physiological response should be more consistent with the expected results in man. This study was done to evaluate the response of the baboon to postsystolic augmentation with the army artificial heart pump. Materials and Methods The principles