Local Myocardial Perfusion Research Articles

Normal Coronary Artery Patient Presenting with Left Ventricular Aneurysm

Left ventricular aneurysm (LVA) is one of the most important complications of myocardial infarction LVA is strictly defined as a distinct area of abnormal left ventricular diastolic contour with systolic dyskinesia or paradoxical bulging. LVA usually results from myocardial infarction. Other rare aetiologies of LVA include hypertrophic cardiomyopathy, Chagas' disease, sarcoidosis, congenital LVA, and idiopathic However, LVA formation in patients with idiopathic dilated cardiomyopathy is rarely reported, and the incidence, clinical features, and pathogenesis of LVA formation in patients with idiopathic dilated cardiomyopathy is not well understood. Here, we present a 45 years old, idiopathic dilated cardiomyopathy patient with LVA and normal coronary arteries The pathogenesis of LVA formation in patients with idiopathic dilated cardiomyopathy is not clear. One acceptable hypothesis is that coronary artery emboli originate from mural thrombi, present in some patients with idiopathic dilated cardiomyopathy, which develop due to local wall infarction and fibrosis. The local myocardial perfusion differences could be seen in idiopathic dilated cardiomyopathy and predominantly found in the anteroposterior axis of the left ventricle. Local fibrosis occurs more frequently on the anterior wall or posterior wall, and less frequently on the lateral or septal wall. In our patient, LVA existed in the septal segments.We could not define the exact mechanism of the septal aneurysm in our patient but we decided to present this abnormal case, which is different from cases thus far reported in the literature.

Effects of Right, Left, and Biventricular Pacing on Myocardial Perfusion in Ischemic Conditions

In normal hearts, the distribution of regional myocardial perfusion is altered by ventricular pacing. Little is known about the impact of ventricular pacing on regional myocardial perfusion in ischemic conditions. In this acute echocardiographic study, we compared the respective effects of right ventricular pacing (RVP), left ventricular pacing (LVP), and biventricular pacing (BVP) on regional perfusion in a swine model of graded ischemia. Ventricular pacing leads were placed at the apex of the right ventricle and on the lateral wall of the left ventricle in nine open-chest pigs. Myocardial contrast echocardiography was successively performed during spontaneous rhythm (SR), RVP, LVP, and BVP in random order at baseline and during three stages of incremental ischemia (left anterior descending + circumflex). At baseline, RVP decreased myocardial perfusion of the septal and inferior walls compared to SR (P < 0.05), whereas LVP decreased perfusion of the lateral wall (P < 0.05). No significant differences were observed in regional perfusion during BVP compared to SR. In ischemic conditions, RVP worsened myocardial perfusion in the ischemic anterior wall as well as in the septal and inferior walls (P < 0.05), whereas both LVP and BVP did not alter perfusion in the ischemic area compared to SR. Compared to baseline, in ischemic conditions, RVP has a more pronounced detrimental impact on perfusion abnormalities. In contrast, BVP induced a significant improvement in local myocardial perfusion. Therefore, BVP could be preferred to RVP in patients with ischemic cardiomyopathy.

A computer model of fractal myocardial perfusion heterogeneity to elucidate mechanisms of changes in critical coronary stenosis and hypotension

Critical coronary stenosis (critical CS) alone does not lead to an alteration of fractal dimension ( D) under resting conditions in a pig model, indicating undisturbed local myocardial perfusion. If critical CS is combined with hypovolemic anemia the resulting hypotension leads to a significant decline of D. The mechanisms involved in this phenomenon have not yet been elucidated. A computer program was developed enabling calculation of D for normal vascular trees, for single vessel coronary stenosis (CS), and for CS in combination with reduced coronary perfusion pressure (CPP). The values of D obtained by the computer program were compared to those available from an existing animal study to confirm that changes of D can largely be explained by changes of arterial branching pattern simulated by the computer program. Using our computer model, D was 1.15±0.06 in normal vascular trees. Third branch critical CS did not alter D (1.14±0.06; n.s.) , wheras critical CS combined with a reduction of CPP to 40 mmHg reduced D (1.07±0.03; P<0.05) . These data are comparable to those obtained in the animal study, and therefore show that alterations of vessel diameter and regional blood flow can largely explain changes of fractal dimension during critical CS and hypotension while changes of functional myocardial parameters might play a minor role.

Nicardipine augments local myocardial perfusion after coronary artery reperfusion in dogs.

Nicardipine is a potent coronary and systemic vasodilator without depression of ventricular function. We investigated the changes in local myocardial perfusion (LMP) according to the nicardipine administration after coronary reperfusion in a beating canine model. A Doppler probe was placed around the left anterior descending coronary artery (LAD) and thermal diffusion microprobe was implanted in the myocardium perfused by the exposed LAD. To define the nicardipine effects, we compared the two groups (control group, n=7 vs nicardipine group, n=7). In nicardipine group, 5 microgram/kg/min nicardipine was infused continuously. After the release of the LAD occlusion, LAD blood flow were increased compared to the baseline of both groups. However, there was no difference between groups in the LAD blood flow. The LMP after LAD reperfusion did not recover to the baseline level until 30 min after LAD reperfusion in control group (74%, 52% and 70% at 10, 20 and 30 min after LAD reperfusion, respectively). In nicardipine group, however, the LMP recovered to the baseline level at 20 min (99%), and increased more than the baseline level at 30 min (141%) after LAD reperfusion. Our findings suggest that the nicardipine augments the LMP following the release of a coronary occlusion.

Spatial heterogeneity in the heart: recent insights and open questions.

Within the left ventricular myocardium and despite its rather homogeneous structure, local myocardial perfusion varies substantially. Areas of low and high local flow differ with regard to substrate uptake, energy turnover, and demand. This spatial heterogeneity is related to distinct differences in local protein expression, forming the basis of a novel homeostatic mechanism.

Invited commentary

In this article, Dr Liu and colleagues demonstrate the vasodilating effects of vascular endothelial growth factor (VEGF, also known as vascular permeability factor) on isolated internal mammary artery vascular rings. It is further demonstrated that this relaxation is endothelium-dependent and is mediated by nitric oxide (NO). This study reports important confirmatory data of prior studies. Vasodilatory actions of VEGF have been demonstrated previously in animal and human endothelium and this has been demonstrated to be dependent upon NO release [1Van der Zee R. Murohara T. Luo Z. et al.Vascular endothelial growth factor/vascular permeability factor augments nitric oxide release from quiescent rabbit and human vascular endothelium.Circulation. 1997; 95: 1030-1037Crossref PubMed Scopus (371) Google Scholar]. The mechanism by which VEGF induces endothelial NO production involves a reasonably well characterized signaling cascade. VEGF binding to the Flk-1/KDR receptor induces phosphorylation of Akt [2Gerber H.P. McMurtrey A. Kowalski J. et al.Vascular endothelial growth factor regulates endothelial cell survival through the phosphatidylinositol 3′-kinase/Akt signal transduction pathway. Requirement for Flk-1/KDR activation.J Biol Chem. 1998; 273: 30336-30343Crossref PubMed Scopus (1734) Google Scholar] which in turn phosphorylates endothelial NO synthase (eNOS), enhancing its ability to generate NO [3Fulton D. Gratton J.P. McCabe T.J. et al.Regulation of endothelium-derived nitric oxide production by the protein kinase Akt.Nature. 1999; 399: 597-601Crossref PubMed Scopus (2214) Google Scholar]. Importantly, increased NO release is also believed to fundamentally contribute to the angiogenic effects of VEGF [4Ziche M. Morbidelli L. Choudhuri R. et al.Nitric oxide synthase lies downstream from vascular endothelial growth factor-induced but not basic fibroblast growth factor-induced angiogenesis.J Clin Invest. 1997; 99: 2625-2634Crossref PubMed Google Scholar]. Local myocardial vasodilation in the heart could help enhance blood flow to treated areas independent of new blood vessel growth, though this effect would be expected to be short lived, being confined to the time period of increased local VEGF concentration. On the other hand, this effect of VEGF has been considered to be responsible for systemic hypotension seen following VEGF injections in animals [5Horowitz J.R. Rivard A. Van der Zee R. et al.Vascular endothelial growth factor/vascular permeability factor produces nitric oxide-dependent hypotension. Evidence for a maintenance role in quiescent adult endothelium.Arterioscler Thromb Vasc Biol. 1997; 17: 2793-2800Crossref PubMed Scopus (246) Google Scholar, 6Hariawala M.D. Horowitz J.R. Esakof D. et al.VEGF improves myocardial blood flow but produces EDRF-mediated hypotension in porcine hearts.J Surg Res. 1996; 63: 77-82Abstract Full Text PDF PubMed Scopus (238) Google Scholar] and man [7Henry T.D. Annex B.H. Azrin M.A. et al.Final results of the VIVA trial of rhVEGF for human therapeutic angiogenesis [Abstract].Circulation. 1999; 100: 476Google Scholar]. Several strategies to achieve therapeutic angiogenesis using VEGF genes or proteins, as well as other growth factors, are in various stages of investigation. With the exception of small feasibility studies, larger scale multicenter studies have not yet indicated which, if any, strategy will provide a successful angiogenic therapy. For peripheral vascular disease, bFGF treatment appears promising [8Lederman R.J. Tenaglia A.N. Anderson R.D. et al.Design of the therapeutic angiogenesis with recombinant fibroblast growth factor-2 for intermittent claudication (TRAFFIC) trial.Am J Cardiol. 2001; 88: 192-195Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar]. Although still preliminary, the safety profile of these agents, including VEGF, appears to be acceptable in a variety of settings [9Isner J.M. Vale P.R. Symes J.F. Losordo D.W. Assessment of risks associated with cardiovascular gene therapy in human subjects.Circ Res. 2001; 89: 389-400Crossref PubMed Scopus (128) Google Scholar]. This includes the hypotensive side effects. Thus, the vasodilator effects of VEGF may provide an added potential benefit on local myocardial perfusion above and beyond its potential to enhance angiogenesis. It is important that the systemic effects of VEGF be investigated, though preliminary results indicate that this is not a limiting factor, especially when delivered locally to the heart as a gene product. It is only through careful studies such as those of Dr Liu and colleagues which increase our understanding of the actions and mechanisms of growth factors such as VEGF that the promise of therapeutic angiogenesis can be realized.

Changes in Hemodynamics and Local Myocardial Perfusion in the Acute Phase of Coronary Reperfusion by Using Nicardipine in Korean Mongrel Dogs

Background: The measurement of perfusion is very important to understanding the physiology in the ischemic and reperfused tissue. However, no studies have been reported using a beating heart with a real time-continuous perfusion measurement system () to check local tissue perfusion so far. In this study, the changes in hemodynamics and local myocardial perfusion (LMP) after coronary reperfusion with nicardipine (a calcium channel blocker) administration were evaluated. Methods: A total of 10 mongrel dogs were divided into two groups; group I (control group, n = 5), group II (nicardipine group, n = 5). After femoral arterial, pulmonary arterial and left ventricular catheterization, a left thoracotomy was performed. Next, the left anterior descending coronary artery (LAD) was exposed, and a thermal diffusion microprobe was inserted in the myocardium to measure LMP. Results: In group II, blood pressure and systemic vascular resistance after LAD reperfusion were significantly decreased compared to group I. Cardiac output and stroke volume were more rapidly increased in group II, while left ventricular stroke work was decreased in group II. In group I, the LMP after LAD reperfusion did not recover to the baseline level, but the LMP did recover 20 minutes after LAD reperfusion and was increased more compared to the baseline level at 30 minutes after LAD reperfusion in group II. There were no significant differences in dP/dt between the two groups. Conclusions: We found that the LMP did not recover to the baseline level in the early state of LAD reperfusion; however, nicardipine administration increased the LMP after the early reperfusion period. Cardiac output and stroke volume were also more rapidly increased when nicardipine was administrated.

Measurement of Local Myocardial Perfusion by Thermal Diffusion Microprobe during Coronary Artery Occlusion and Reperfusion in a Beating Canine Heart

Background: The measurement of perfusion is very important to understand the physiology of the tissue level. The QFlow400 perfusion measurement system is able to measure local tissue perfusion. The aim of this study was to validate thermal diffusion microprobe (TDM) in estimating myocardial blood flow during coronary artery occlusion and reperfusion in an animal beating heart model. Methods: A total of 5 mongrel dogs were entered into the study. A left thoracotomy was performed under general anesthesia. After the left anterior descending coronary artery (LAD) was exposed, a TDM was inserted in the myocardium at the exposed LAD distributed area. The local myocardial perfusion was measured before, during and after LAD occlusion. To find the usefulness of TDM in a beating heart, k values were checked during the study. The k value or tissue conductivity should not exceed 6.23 mW/cmC in this system. Results: All the k values were below 6.23 mW/cmC in this study. Baseline local myocardial perfusion was 52.0 ± 18.3 ml/min/100 g. During LAD occlusion, the local myocardial perfusion was decreased to 18.4 ± 12.0 ml/min/100 g. At 10, 20 and 30 minutes after LAD reperfusion, the perfusion was recovered to 38.5 ± 23.2, 27.2 ± 17.4 and 36.2 ± 17.2 ml/min/100 g, respectively, but the values at 20 and 30 minutes of reperfusion were significantly lower compared to baseline value. Conclusions: We could use the QFlow400 perfusion measurement system to measure myocardial injury produced by ischemia and subsequent reperfusion in a beating heart. With this system, we found that the local myocardial perfusion was not recovered to the baseline level in early state of the coronary reperfusion. (Korean J Anesthesiol 2002; 42: S 1∼S 4) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ

Quantitative Coronary Angiography and Digital Densitometric Perfusion Measurements—How to Assess the Success of Intracoronary Balloon Dilatation

Densitometric evaluation of digital subtraction angiocardiograms allows the assessment of local myocardial perfusion before and after pharmacological stimulation of coronary flow reserve during the catheterization procedure. This report deals with a case of a severe stenosis of the left coronary artery in which PTCA was regarded successful based on an appropriate increase in luminal diameter while an intima and media dissection at the dilatation site was documented. The perfusion measurements, however, pointed out a clear impairment of poststenotic myocardial perfusion after PTCA.

Local myocardial perfusion and epicardial NADH-fluorescence after coronary artery ligation in the isolated guinea pig heart.

In Langendorff-perfused guinea pig hearts, local myocardial perfusion was evaluated by analysis of FITC-dextran-150 elution kinetics after bolus injection. Locally estimated half-times of the monoexponential elution curves showed good correlation with global undisturbed coronary flow. After ligation of the left anterior descending coronary artery indicator transit kinetics in the ischemic area were only slightly affected (increase of t/2 by 30 +/- 19%), indicating a residual flow of 80% to the ligated area. The moderate increase (40 +/- 20%) of NADH-surface fluorescence in the same area confirms a high degree of residual flow. Indicator partition volume (signal peak height after bolus injections) was additionally enhanced. Moreover, indicator transit kinetics changed from monoexponential to composed kinetics. On reperfusion these effects were partially reversible. Ligation of the left coronary artery at its aortic root produced only moderate ischemia, indicating very effective mechanisms in the isolated guinea pig heart from the right coronary artery to support the left ventricle. Severe ischemia as evidenced from NADH-surface fluorescence could be observed only after "stopped flow" ischemia.

Structure of the coronary artery adenosine receptor

Acting through specific surface receptors on coronary myocytes, adenosine may regulate local myocardial perfusion in response to changes in cardiac effort. The structure-activity relationships of adenosine analogs suggest that the purine and ribose domains of the coronary artery adenosine receptor each contain several specialized sites which effect ligand binding and or receptor activation. Such correlations identify the steric factors which influence binding and hint at the chemical forces which govern affinity.

Measurement of regional myocardial perfusion using collimated miniature radiation detectors and the method of 133-xenon washout.

A new approach to the measurement of local myocardial perfusion based on the application of highly-collimated miniature cadmium telluride radiation detectors to measure washout of 133-Xenon from well-defined tissue volumes is presented. Single-hole collimators with length/diameter ratios of 1 (L = 4 mm, D = 4 mm) and 4 (L = 12 mm, D = 3 mm) were employed as prototype designs. The probe field of view was characterized theoretically using a spherical model of the myocardium in conjunction with experimental point source response measurements for each collimator. Method evaluation using two medium resolution collimators (L/D = 1) was effected by performing left main and circumflex coronary artery perfusion studies at controlled but variable flows in the dog heart. An excellent correlation (r greater than 0.99) between actual and estimated perfusion determined from 65 washout curves over the flow range 0.38 to 3.18 ml/min/gm was demonstrated. The ability to resolve regional flow differences was verified by measuring tracer washout from circumflex and left anterior descending regions of the myocardium, using two high resolution collimators (L/D = 4), in a preparation where the left main coronary artery was cannulated and a snare was placed around the circumflex coronary artery to selectively reduce flow to that region.

A new thermal sensor for surface-based measurement of local myocardial perfusion.

The transient response of a new thermal sensor for continuous surface-based measurement of local tissue blood flow was evaluated in the beating dog heart. The sensor is 2.5 mm square, tests on the heart, and responds to flow changes only within a region of tissue 3-4 mm below its location on the epicardial surface. Initial studies demonstrate excellent sensitivity, good frequency response with a time constant of the order of 10-11 s, and an ability to continuously monitor changes in local myocardial blood flow during a variety of well-understood interventions, including coronary artery occlusion, reactive hyperemia, and intravenous administration of nitroglycerin and dipyridamole.

Modulating effect of regional myocardial performance on local myocardial perfusion in the dog.

We studied the effect of regional contractile performance on regional coronary blood flow and flow distribution in 10 dogs. The left anterior descending (LAD) coronary artery was cannulated and perfused. Maximal vasodilation was obtained with adenosine. Consequently, variations of LAD flow reflected changes of extravascular resistance. Lidocaine injected in the LAD caused a localized reduction of contractile performance as shown by the absence of systolic wall thickening. Global left ventricular performance and pressure were unchanged. Coronary extravascular resistance diminished and LAD flow increased from 4.8 +/- 0.5 to 6.2 +/- 0.6 ml/min per g (P less than 0.02). The endocardial: epicardial ratio increased from 1.02 +/- 0.07 to 1.28 +/- 0.07 (P less than 0.001). Isoproterenol in the LAD augmented systolic wall thickening. Regional coronary flow diminished from 5.1 +/- 0.5 to 3.3 +/- 0.4 ml/min per g (P less than 0.001), and the endocardial:epicardial ratio diminished from 1.08 +/- 0.07 to 0.75 +/- 0.07 (P less than 0.01). These data indicate that myocardial contractility is a major component of extravascular coronary resistance and is a mechanical determinant of coronary blood flow and its transmural distribution.

Effect of nifedipine on myocardial ischemia: Analysis of collateral flow, pulsatile heat and regional muscle shortening

Effects of intravenous nifedipine on the ischemic myocardium of dogs subjected to coronary ligation were evaluated with a newly developed myothermal technique. Sensitive, fast-reacting miniature thermistors implanted within the ventricular wall were used in conjunction with low noise thermistor bridges to monitor beat-to-beat intramyocardial heat pulses and to detect intramyocardial cold transients after mechanized injections of cold saline into the left atrium. Myocardial ischemia reduced the amplitude of the pulse signals and decreased mean intramyocardial temperature. Ischemia also reduced the amplitude of the intramyocardial cold transients detected after injection of cold saline solution. All thermal changes due to ischemia were partly reversed by nifedipine. The amplitude of the cold signals correlated positively ( r = 0.85) with local myocardial perfusion estimated by the radioactive microsphere technique. Thus, estimates of local perfusion by two independent techniques confirmed that nifedipine increased collateral perfusion. In addition, simultaneous measurements of peripheral coronary pressure indicated that the drug decreased resistance in the coronary bed distal to the occlusion. Ultrasonic measurements of myocardial segment length revealed that nifedipine improved myocardial shortening in ischemic zones, a response that accounts for the nifedipine-induced increases in local heat. Thus, the results show that nifedipine increases collateral flow to the acutely ischemic myocardium and that improved perfusion is accompanied by enhanced contractile performance. These findings also indicate that the protective action of nifedipine on ischemic myocardium is not predominantly mediated by a cardioplegic effect limiting the metabolic needs of the myocardium at risk.

Effects of nifedipine on myocardial perfusion and ischemic injury in dogs.

To determine whether nifedipine, a calcium antagonist, protects ischemic myocardium, conscious dogs were subjected to coronary occlusion and given nifedipine by intravenous infusion beginning 30 minutes after the onset of ischemia and lasting for 24 hours while systemic arterial pressure, left atrial pressure, and cardiac output were monitored. Local myocardial perfusion at selected intervals after coronary occlusion was assessed with radioactive microspheres injected into the left atrium. In regions of myocardium exhibiting moderately depressed flow 29 minutes after occlusion in control dogs (n = 8), flow was significantly greater 3 and 23.5 hours later, reflecting increases in collateral perfusion. Corresponding zones of myocardium in treated dogs (n = 9) exhibited significantly greater increases in flow at each interval after occlusion (P less than 0.05). Furthermore, myocardial creatine kinase depletion (which correlated well with morphometric estimates of necrosis) in myocardium matched for ischemia prior to treatment was 1.5 to 3 times less in treated than in control dogs (P less than 0.05). Thus, nifedipine produced sustained increases in collateral flow and reduced myocardial ischemic injury.

Regional myocardial perfusion rates in patient with coronary artery disease.

Regional myocardial perfusion rates were estimated from the myocardial washout of (133)Xenon in 24 patients with heart disease whose coronary arteriograms were abnormal and 17 similar subjects whose coronary arteriograms were judged to be normal. Disappearance rates of (133)Xe from multiple areas of the heart were monitored externally with a multiple-crystal scintillation camera after the isotope had been injected into a coronary artery and local myocardial perfusion rates were calculated by the Kety formula. The mean myocardial perfusion rates in the left ventricle exceeded those in the right ventricle or atrial regions in subjects without demonstrable coronary artery disease. In this group there was a significant lack of homogeneity of local perfusion rates in left ventricular myocardium; the mean coefficient of variation of left ventricular local perfusion rates was 15.8%. In the patients with radiographically demonstrable coronary artery disease, a variety of myocardial perfusion patterns were observed. Local capillary blood flow rates were depressed throughout the myocardium of patients with diffuse coronary disease but were subnormal only in discrete myocardial regions of others with localized occlusive disease. Local myocardial perfusion rates were similar to those found in the group with normal coronary arteriograms in patients with slight degrees of coronary disease and in those areas of myocardium distal to marked coronary constrictions or occlusions which were well supplied by collateral vessels. In subjects with right coronary disease, the mean right ventricular perfusion rates were significantly subnormal; in seven subjects of this group perfusion of the inferior left ventricle by a dominant right coronary artery was absent or depressed. The average mean left ventricular perfusion rate of 12 subjects with significant disease of two or more branches of the left coronary artery was significantly lower than that of the group with normal left coronary arteriograms. In the patients with abnormal left coronary arteriograms, the average coefficient of variation of local left ventricular perfusion rates was significantly increased (24.8%). The studies provide evidence that coronary artery disease is associated with increased heterogeneity of local myocardial perfusion rates. They indicate that radiographically significant vascular pathology of the right or left coronary artery may be associated with significant reductions of myocardial capillary perfusion in the region supplied by the diseased vessel.

Measurement of regional myocardial perfusion in man with 133 xenon and a scintillation camera.

A method was devised to quantitate regional capillary perfusion in the human heart by measuring the clearance constants (k) of Xenon-133 washout from multiple areas of the myocardium with a multiple-crystal scintillation camera. In 17 subjects, (133)Xe was injected into the right or left coronary artery or both and counts per second (cps) were recorded simultaneously on magnetic tape from each of 294 scintillation crystals viewing the precordium through a multichannel collimator. Data were processed by a digital computer. Crystals detecting the myocardial washout of (133)Xe were distinguished from those monitoring pulmonary excretion by positioning radioactive markers at the cardiac margins, and by a computer printout of the peak cps recorded by each crystal and its time after isotope injection into the coronary artery. The slopes of the initial segment of the multiple (133)Xe curves obtained in each study were calculated by the method of least squares using a monoexponential model. Myocardial blood flow rates in the cardiac regions viewed by the individual crystals were calculated (assuming a blood to myocardium partition coefficient of 0.72) along with the SD of every flow measurement. The pattern of myocardial perfusion rates so obtained was superimposed over a tracing of the subject's coronary arteriogram. Scintiphotographs showing the arrival and washout of isotope from various regions of myocardium and the area of tissue perfused by each coronary artery were obtained by replaying the data tape on an oscilloscope. Significant regional variations in local myocardial perfusion rates were observed in hearts with normal coronary arteries. When capillary flow measurements from crystals overlying the various cardiac chambers were averaged in each subject, the mean myocardial blood flow rate of the left ventricle in 17 patients, 64.1 +/-13.9 (SD) ml/100 g.min, significantly exceeded that of the right ventricle, 47.8 +/-10.9 ml/100 g.min, and of the right atrial region, 33.6 +/-10.3 ml/100 g.min. The approach may facilitate more objective assessment of: myocardial capillary perfusion in patients with angina pactoris, the pharmacology of antianginal drugs, and the efficacy of surgical procedures to revascularize ischemic myocardium.