Myocardial Bed Research Articles

Trans-myocardial omega-3 fatty acid gradient in coronary microvascular dysfunction

BackgroundCardiac remodeling is a process mediated, in part, by 18-hydroxyeicosapentaenoic acid (HEPE), a metabolite of the omega-3 polyunsaturated fatty acid, eicosapentaenoic acid (EPA). We hypothesized that trans-myocardial levels of 18-HEPE could inform the pathophysiologic processes involved in heart failure with preserved ejection fraction (HFpEF). MethodsWe measured the concentration of 18-HEPE and EPA in trans-myocardial plasma samples from 10 subjects enrolled in The Women's Ischemia Syndrome Evaluation [WISE] Mechanisms of Coronary Microvascular Dysfunction Leading to Pre-HFpEF project. ResultsConcentrations of 18-HEPE were significantly lower in coronary venous compared to the aortic plasma (270.5 pg/mL [212.8–480.8] vs. 430.5 pg/mL [299.5–655.8], p = 0.0039). There was a significant correlation between the concentrations of coronary venous EPA and aortic 18-HEPE (r = 0.94, p = 0.0002), and aortic EPA and aortic 18-HEPE (r = 0.82, p = 0.0058). ConclusionsResults of this small pilot study support the suggestion that 18-HEPE is synthesized outside the heart and utilized within the myocardial bed.

Setd4 controlled quiescent c-Kit+ cells contribute to cardiac neovascularization of capillaries beyond activation

Blood vessels in the adult mammal exist in a highly organized and stable state. In the ischemic heart, limited expansion capacity of the myocardial vascular bed cannot satisfy demands for oxygen supply and the myocardium eventually undergoes irreversible damage. The predominant contribution of endogenous c-Kit+ cells is understood to be in the development and homeostasis of cardiac endothelial cells, which suggests potential for their targeting in treatments for cardiac ischemic injury. Quiescent cells in other tissues are known to contribute to the long-term maintenance of a cell pool, preserve proliferation capacity and, upon activation, facilitate tissue homeostasis and regeneration in response to tissue injury. Here, we present evidence of a Setd4-expressing quiescent c-Kit+ cell population in the adult mouse heart originating from embryonic stages. Conditional knock-out of Setd4 in c-Kit-CreERT2;Setd4f/f;Rosa26TdTomato mice induced an increase in vascular endothelial cells of capillaries in both neonatal and adult mice. We show that Setd4 regulates quiescence of c-Kit+ cells by the PI3K-Akt-mTOR signaling pathway via H4K20me3 catalysis. In myocardial infarction injured mice, Setd4 knock-out resulted in attenuated cardiomyocyte apoptosis, decreased infarction size and improved cardiac function. Lineage tracing in Setd4-Cre;Rosa26mT/mG mice showed that Setd4+ cells contribute to each cardiac lineage. Overall, Setd4 epigenetically controls c-Kit+ cell quiescence in the adult heart by facilitating heterochromatin formation via H4K20me3. Beyond activation, endogenous quiescent c-Kit+ cells were able to improve cardiac function in myocardial infarction injured mice via the neovascularization of capillaries.

Beta 1 adrenoceptor blockade promotes angiogenesis in hypertrophied myocardium of transverse aortic constricted mice.

Left ventricular hypertrophy (LVH) is an adaptive structural remodelling consequent to uncontrolled blood pressure. Impaired angiogenesis plays a vital role in transiting LVH into cardiac failure. Catecholamines modulate myocardial function through beta adrenoceptors, and their blockers (β-AR) reduce cardiovascular morbidity and mortality by decelerating the LVH progression. Nonetheless, the effect of β-AR blockers on myocardial vascular bed remains largely obscure. Hence, this study is focussed on analysing the possible outcomes of β-AR blockers on myocardial vascular remodelling using a surgically induced LVH mice model. Transverse aortic constricted mice and sham-operated mice were administered with metoprolol at a dose of 30mg/kg/d for 60days and myocardial vascular endothelial growth factor (VEGF) alpha levels, GSH/GSSG ratio, myocardial protein carbonyl content, hypertrophy index and global myocardial function, trans-aortic fluid dynamics and expression pattern of angiopoietin-1 and VEGF alpha were assessed. These findings were further confirmed by histochemical analysis for myocardial capillary density, perivascular fibrosis ratio and intimal thickening. Sub- chronic β-AR blockade reduced the oxidative stress, hypertrophic index, intimal thickening and perivascular fibrosis ratio. A marked increase in myocardial VEGF, angiopoietin 1, global myocardial function and myocardial capillary density was also observed. There was a reduction in the LVH and upregulation of myocardial angiogenesis concluding that β-AR blockers prevent adverse vascular remodelling which might underlie its concealed mechanism of action.

Abstract 644: Some Perspectives of Preventive Cardiology Development

Background: The role of preventive cardiology becomes more significant in solving heart problems. The analysis of our research results allows making assumptions, promising for prevention of coronary atherosclerosis (CA). Material and Methods: The studies were carried out on: hearts of humans died from accidents, from acute myocardial infarction; myocardial biopsies, heart surgical material of patients; hearts of animals; insects flying muscles; placentas of human and animals. The methods were used: autopsy, planimetry of atherosclerotic lesions of aorta and main coronary arteries, heart biopsy, microangio-x-ray, histology, stereology, experimental modeling, measuring of hemodynamic parameters, micromechanography, electron microscopy, cytochemistry, mathematical modeling, statistics. Aim: To show that existing data may serve as a basis for further development of new ways to prevent CA. Results: Huge differences of myocardial arterial bed (MAB) density exist. The richness of MAB correlates directly with life expectancy of people. In hearts with scant MAB CA develops earlier and atherosclerotic lesions are more severe. Therefore scant MAB is considered as an intracardial risk factor (IRF) for IHD. Large individual differences exist in human hearts also for values for the duration of myocardial fibers oxygen supply. The long time is another IRF for IHD. The density of intraorganic arterial bed in human placentas varies widely. There is a positive correlation between placental arterialization density and newborn weigh. The following morphological multifactorial systemic measurement methods are developed: a) for heart muscle oxygen supply; b) for contractility of cardiomyocyte using small heart muscle biopsies (patented); c) for gas exchangeability of placenta. The efficiency and exactness of each method were examined. Conclusion: The received data allow assuming that atherosclerotic profile of human heart CA will be possible to foretell on the next day of born. In cases of bad prognosis a plan of enrichment of MAB, a plan for spatial improvement of the “capillary - myocardial fiber” system may be composed and undertaken. The received data allow in advanced future to draw up a project of new heart with necessary preset structural parameters.

An Outflow Boundary Condition Model for Noninvasive Prediction of Fractional Flow Reserve in Diseased Coronary Arteries.

This paper reports on a new boundary condition formulation to model the total coronary myocardial flow and resistance characteristics of the myocardial vascular bed for any specific patient when considered for noninvasive diagnosis of ischemia. The developed boundary condition model gives an implicit representation of the downstream truncated coronary bed. Further, it is based on incorporating patient-specific physiological parameters that can be noninvasively extracted to account for blood flow demand to the myocardium at rest and hyperemic conditions. The model is coupled to a steady three-dimensional (3D) collocated pressure-based finite volume flow solver and used to characterize the "functional significance" of a patient diseased coronary artery segment without the need for predicting the hemodynamics of the entire arterial system. Predictions generated with this boundary condition provide a deep understanding of the inherent challenges behind noninvasive image-based diagnostic techniques when applied to human diseased coronary arteries. The overall numerical method and formulated boundary condition model are validated via two computational-based procedures and benchmarked with available measured data. The newly developed boundary condition is used via a designed computational methodology to (a) confirm the need for incorporating patient-specific physiological parameters when modeling the downstream coronary resistance, (b) explain the discrepancies presented in the literature between measured and computed fractional flow reserve (FFRCT), and

Evaluation of white blood cell and neutrophil/lymphocyte ratio in acute coronary syndrome patients admitted to emergency department

Objective: Inflammatory reaction, which causes tissue damage in Acute Coronary Syndrome (ACS), leads to deterioration. White Blood Cell (WBC), Neutrophil (N), Lymphocyte (L) and Neutrophil/ Lymphocyte (N/L) ratios were used to refer to the inflammation. High neutrophil levels show us acute inflammatory situation and low lymphocyte levels show us physiological stress. That is why N/L ratio is a valuable parameter which enables us to guess patient prognosis in Emergency Department (ED). In this study, white cell and NLR relations with ACS in patients with chest pain is evaluated. Material and Method: Patients referring to ED with chest pain within 3 months were investigated retrospectively. 100 patients were included in the study. Patients' WBC count, NLR and WBC values, gender, Troponin-I and CK-MB positivity, history of Coronary Heart Disease (CHD) and additional diseases were examined according to the final diagnoses. All the patients were divided into three groups according to ACS: Unstable Angina Pectoris (USAP), Non-ST Elevated Myocardial Infarction (NSTEMI), and ST-Elevated Myocardial Infarction (STEMI). Mortality and morbidity levels in hospital and after discharge were also examined in the study. Findings: WBC values in patients with positive Troponin-I were found statistically higher than patients with negative Troponin-I (p<0.05). In STEMI group, WBC values were statistically higher than USAP group (p<0.0083). When patients' N/L ratio average distribution was examined; Troponin-I and CK-MB positive patients' NLR was found to be statistically higher than Troponin-I and CK-MB negative ones (p<0.05). Conclusion: N/L ratio, which is a marker of inflammatory process in the myocardial vascular bed, may be considered as a risk marker. For this reason, N/L ratio at admission can be used as an auxiliary parameter for predicting the diagnosis of ACS.

The Importance of Perfusion Assessment for Determination of Functional Sufficiency of Myocardium

Myocardial vascular bed is represented by a network of arterial and venous vessels as well as microcirculatory vessels including arterioles, precapillaries, capillaries, postcapillaries, venules, and arteriolo-venular anastomoses. Myocardial capillaries are an exchange link providing perfusion of the myocardium with nutrients therefore sufficiency of the capillary circulation ensures the adequacy of metabolic processes in the cells of the heart muscle. There is no consensus among physicians of various specialties on the methodology of assessing coronary blood flow and blood supply to the myocardial tissue. The lack of universality and unity on measuring units, methods, and classification results in contradictions, both in defining approach to treatment strategy and to assessment of treatment effects. Currently, it is necessary to develop a common approach to assessment of coronary perfusion, which would allow to unify the criteria of sufficiency of blood supply to the heart and activity of metabolic processes in the myocardium. It is necessary to determine parameters of studying changes of myocardial vascular bed, closely related to metabolic processes in muscle tissue of the heart.

Dangerous Complication of Percutaneous Coronary Intervension (PCI) of Coronary Complete Total Occlusion (CTO) Managed by Complete Total Occlusion (CTO)

Patients having chronic total occlusion (CTO) of coronary artery who have inadequate collaterals to provide sufficient blood flow to the myocardial bed may present with anginal symptoms. Revascularisation of myocardium can be considered in those patients who remain symptomatic despite optimal medical therapy. Angioplasty in CTO may lead to complication like coronary perforation which if not managed on time can be catastrophic. However with proper back up, team work and skill such dreaded complication can be taken care of with good outcome.

CHANGES IN THE CONTRACTILE CARDIOMYOCYTES AND HEMOMICROCIRCULATORY BED IN PREGNANT RATS AND THEIR PUPS EXPOSED TO HEMIC HYPOXIA

The performed analysis of the morphology of cardiomyocytes and myocardial vascular bed in 12 pregnant rats and 16 newborn pups exposed to the hemic hypoxia induced by NaNO 2 revealed some similar degenerative and destructive changes which were more pronounced in pups. The main morphological characteristics of hypoxic myocardial damage in pregnant and newborn rats were presented in the form of phenomena of mixed dystrophy, swelling and destruction of endothelial cells and contractile cardiomyocytes along with the lysis of myofibrils, perivascular edema, capillary hyperemia, emptiness and spasm of the arterioles and contracture changes. Revealed pathological changes in the myocardium reflect the development of the myocardiodystrophy processes in pregnant rats and newborn pups.

Endocardial tip cells in the human embryo - facts and hypotheses.

Experimental studies regarding coronary embryogenesis suggest that the endocardium is a source of endothelial cells for the myocardial networks. As this was not previously documented in human embryos, we aimed to study whether or not endothelial tip cells could be correlated with endocardial-dependent mechanisms of sprouting angiogenesis. Six human embryos (43–56 days) were obtained and processed in accordance with ethical regulations; immunohistochemistry was performed for CD105 (endoglin), CD31, CD34, α-smooth muscle actin, desmin and vimentin antibodies. Primitive main vessels were found deriving from both the sinus venosus and aorta, and were sought to be the primordia of the venous and arterial ends of cardiac microcirculation. Subepicardial vessels were found branching into the outer ventricular myocardium, with a pattern of recruiting α-SMA+/desmin+ vascular smooth muscle cells and pericytes. Endothelial sprouts were guided by CD31+/CD34+/CD105+/vimentin+ endothelial tip cells. Within the inner myocardium, we found endothelial networks rooted from endocardium, guided by filopodia-projecting CD31+/CD34+/CD105+/ vimentin+ endocardial tip cells. The myocardial microcirculatory bed in the atria was mostly originated from endocardium, as well. Nevertheless, endocardial tip cells were also found in cardiac cushions, but they were not related to cushion endothelial networks. A general anatomical pattern of cardiac microvascular embryogenesis was thus hypothesized; the arterial and venous ends being linked, respectively, to the aorta and sinus venosus. Further elongation of the vessels may be related to the epicardium and subepicardial stroma and the intramyocardial network, depending on either endothelial and endocardial filopodia-guided tip cells in ventricles, or mostly on endocardium, in atria.

Infarct size reduction in acute myocardial infarction

### Learning objectives Coronary artery disease is the leading cause of death worldwide, with ST segment elevation myocardial infarction (STEMI) an important contributor. Infarct size following STEMI is a determinant...

Abstract 9852: T Lymphocyte Depletion Following Primary Percutaneous Coronary Intervention Predicts Infarct Size and Ischemia Reperfusion Injury

Background: We have previously demonstrated acute changes in lymphocyte numbers in peripheral blood following reperfusion with primary percutaneous coronary intervention (PPCI) for STEMI. The goal of this study was to investigate a potential role for T cells in ischemia reperfusion (I/R) injury. Methods: We analyzed blood from 22 STEMI patients undergoing PPCI. Blood was taken at the start of the procedure, and at 15, 30, 90 minutes, and 24 hours post reperfusion. In 5 patients with infarcts due to LAD occlusion, coronary sinus (CS) blood was also obtained 30-60min after reperfusion along with simultaneous aortic blood. 8-colour flow cytometric analysis was performed on the fresh blood to quantify lymphocyte populations. Cardiac MRI was performed at 1-7 days, and left ventricular ejection fraction, infarct size (measured by late gadolinium enhancement), microvascular obstruction (MVO), area at risk and salvage index quantified. Results: T-lymphocytes dropped between 0 and 90 minutes by a mean of 42% (0min mean 1767/μl, 90min 931/μl), CD4 T-helper cells by 31%, and CD8 cytotoxic T-cells by 55%. The change in total T-cells correlated with infarct size (r=-0.78, p&lt;0.001), as did that of CD4 (r=-0.66, p&lt;0.01) and CD8 T cells (r=-0.76, p&lt;0.001). The T cell drop between 0 and 90 minutes also correlated strongly with MVO (r=-0.72, p&lt;0.01), as did the CD4 (r=-0.66, p&lt;0.01) and CD8 T cell drop (r=-0.77, p&lt;0.001). Myocardial salvage index correlated strongly with the change in T cells (r=0.85, p&lt;0.001), CD4 T cells (r=0.76, p&lt;0.01) and CD8 T cells (r=0.76, p&lt;0.01) between 30 and 90 minutes. Prior to reperfusion 6.4% of CD8 T cells were activated (CD69+), with progressive loss of CD69+ cells after 90 minutes (4.3%) and 24 hours (2.6%, 0min vs 24hr p&lt;0.01). However, CS sampling showed an increase in CD69 expression between aortic and CS blood, suggesting activation of T cells as they pass through the myocardial vascular bed. Conclusion: Acute changes in T lymphocyte numbers following reperfusion after PPCI predict infarct size, MVO, and salvage index. The drop in these cells following reperfusion, and the dynamics of CD69 expression, suggest a potential role for CD69+ activated T cells in I/R injury. This requires further investigation and may represent a novel therapeutic target.

When Does a Left Anterior Descending Stenosis Alter Flow Across a Left Main Segment?

Attributed to Albert Einstein, the saying, “Everything should be made as simple as possible, but not simpler,” embodies a concept that certainly applies to our understanding and interpretation of fractional flow reserve (FFR) across the most clinically important stenosis interventionalists encounter, the left main (LM) stenosis. Remarkable technical advances supported by multicenter, long-term outcome studies have validated FFR for daily use in the cardiac catheterization laboratory. FFR, the ratio of coronary pressure beyond a stenosis to the aortic pressure (representing the normal coronary pressure in the absence of a stenosis), measured during maximal hyperemia (ie, minimal myocardial bed resistance) identifies the ischemic potential of the lesion. In practice, FFR guidance for multivessel percutaneous coronary intervention compared with angiographic guidance alone produces better clinical and economic outcomes.1,2 Article see p 161 Such as occurs with all diagnostic testing in medicine, the correct interpretation of results depends not only on the quality of the testing method, but also on the clinical circumstances under which the test is conducted. The same principle applies to FFR. Measuring FFR across an LM stenosis without disease in its branches is relatively simple. The pressure wire is advanced beyond the narrowing into the unobstructed branches, either the left anterior descending (LAD) or the circumflex (CFX) artery, and hyperemic coronary and aortic pressure ratios are computed as FFR. A few caveats for obtaining an accurate FFR include correct zeroing and equilibration of pressures, ensuring the guide catheter is not obstructing LM flow, and administering an adequate dose of adenosine (Table). For the slightly more complicated scenario of a distal LM bifurcation lesion, one should measure FFR in both branches. In either case, LM lesions treated medically for FFR >0.80 are associated with excellent 5-year major adverse cardiac event rates.3 Now for the not-so simple …

Impaired left ventricular systolic function in patients with left ventricular hypertrophy

Impaired left ventricular systolic function in patients with left ventricular hypertrophy

SUBMICROSCOPIC CHANGES OF THE MYOCARDIALMICROCIRCULATORYBED IN CASE OF EXPERIMENTAL THERMAL TRAUMA

An electron microscopic research of the heart following a severe heat injury has been carried out in an experiment on albino male rats. It has been found out that fullthickness burns cause considerable changes in the components of the myocardial microcirculatory bed whose degree of affection depends on the term of the experiment. Adaptable-compensatory processes in the blood vessels are observed during the first and the 7th circadian period upon inflicting a thermal injury, whereas deep destructive changes occur over the 14th and, particularly, over the 21st circadian period.

Management of Coronary Chronic Total Occlusion

A 67-year-old man with chronic stable angina presented with worsening angina to class III despite maximal medical therapy. He was referred for myocardial perfusion imaging, which showed a large area of inferior ischemia. Subsequent coronary angiography revealed a chronic total occlusion (CTO) of the right coronary artery with brisk collateral flow from the left anterior descending artery (Figure 1). There was minimal obstructive disease in the remainder of the coronary tree. An attempt at percutaneous coronary intervention (PCI) was unsuccessful. He was treated with continuation of his medical therapy, although he remained with lifestyle-limiting class II to III angina. Figure 1. Left, The totally occluded right coronary artery with the expected course of the distal vessel outlined in red and the total occlusion shown by the arrow. Right, Collateralization of the right coronary artery from the left anterior descending (LAD) artery with arrows pointing to the posterior descending artery (PDA) and posterolateral ventricular (PLV) branches of the right coronary artery. The septal collaterals from the LAD to RCA are highlighted. Coronary CTO is characterized by heavy atherosclerotic plaque burden within the artery, resulting in complete (or nearly complete) occlusion of the vessel. Although the duration of the occlusion is difficult to determine on clinical grounds, a total occlusion must be present for at least 3 months to be considered a true CTO.1 Patients with CTO typically have collateralization of the distal vessel on coronary angiography, but these collaterals may not provide sufficient blood flow to the myocardial bed, resulting in ischemia and anginal symptoms. CTO is clinically distinct from acute coronary occlusion, which occurs in the setting of ST-segment–elevation myocardial infarction, or subacute coronary occlusion, discovered with delayed presentation after ST-segment–elevation myocardial infarction. Clinical features and treatment considerations of these entities differ considerably from CTO. Among patients who have a clinical …

Myocardial perfusion reserve compared with peripheral perfusion reserve: A [13N]ammonia PET study

Introduction[13N]ammonia PET allows quantification of myocardial perfusion. The similarity between peripheral flow and myocardial perfusion is unclear. We compared perfusion flow in the myocardium with the upper limb during rest and adenosine stress [13N]ammonia PET to establish whether peripheral perfusion reserve (PPR) correlates with MPR. Methods[13N]ammonia myocardial perfusion PET-scans of 58 patients were evaluated (27 men, 31 women, age 64 ± 13 years) and were divided in four subgroups: patients with coronary artery disease (CAD, n = 15), cardiac syndrome X (SX, n = 14), idiopathic dilating cardiomyopathy (DCM, n = 16), and normal controls (NC, n = 13). Peripheral limb perfusion was measured in the muscular tissue of the proximal upper limb and quantified through a 2-tissue-compartment model and the PPR was calculated (stress/rest ratio). MPR was also calculated by a 2-tissue-compartment model. The PPR results were compared with the MPR findings. ResultsMean myocardial perfusion increased significantly in all groups as evidenced by the MPR (CAD 1.99 ± 0.47; SX 1.39 ± 0.31; DCM 1.72 ± 0.69; NC 2.91 ± 0.78). Mean peripheral perfusion also increased but not significantly and accompanied with great variations within and between groups (mean PPR: CAD 1.30 ± 0.79; SX 1.36 ± 0.71; DCM 1.60 ± 1.22; NC 1.27 ± 0.63). The mean difference between PPR and MPR for all subpopulations varied widely. No significant correlations in flow reserve were found between peripheral and myocardial microcirculatory beds in any of the groups (Total group: r = −0.07, SEE = 0.70, CAD: r = 0.14, SEE = 0.48, SX: r = 0.17, SEE = 0.30, DCM: r = −0.11, SEE = 0.71, NC: r = −0.19, SEE = 0.80). ConclusionNo correlations between myocardial and peripheral perfusion (reserve) were found in different patient populations in the same PET session. This suggests a functional difference between peripheral and myocardial flow in the response to intravenously administered adenosine stress.

Clinical Application of Remote Ischemic Preconditioning

Ischemic preconditioning1 has been shown to reliably reduce ischemic myocardial cell necrosis in a host of animal models.2 Although preconditioning is one of the most powerful and reproducible phenomena in cardioprotection, it has not readily translated to routine clinical use. One issue is that the timing of the long duration of ischemia must be known in advance and the treatment must be applied before the long duration of ischemia. Thus, although evidence suggests that preinfarction ischemia (angina) before an ST-segment elevation myocardial infarction is associated with smaller infarct size and better clinical outcome,3 there is no reliable way to predict when a myocardial infarction will occur and hence no way to either induce ischemic preconditioning or apply a preconditioning mimetic agent just before the infarction. There are, of course, situations in which myocardial ischemia is planned, eg, during coronary artery balloon angioplasty, during coronary artery bypass surgery, during excision and transportation of a donor heart, and before exercise in a patient with known demand-induced ischemia. Preconditioning has been applied to some of these situations. For example, multiple brief balloon inflations and deflations in the coronary artery reduce the severity of chest pain, ST-segment elevation, and lactate production on subsequent balloon inflations compared with an initial balloon inflation without necessarily recruiting blood flow.4 Intermittent aortic cross clamping before coronary artery bypass surgery has been observed to preserve cardiac high-energy phosphate levels.2 These examples of ischemic preconditioning require an invasive procedure to induce ischemia within the heart and the possibility of showering atherosclerotic emboli either down the coronaries or into the aorta as a coronary angioplasty balloon is repeatedly inflated or deflated or the aortic cross clamp is repeatedly clamped and unclamped. Article p 820 Another approach exists that has the potential to be entirely noninvasive: remote …

Clot removal in AMI—worth the hassle?

Primary percutaneous coronary intervention (PPCI) is increasingly seen as the treatment of choice in acute myocardial infarction (AMI). Compared with thrombolysis, with PPCI recanalisation of the vessel is almost guaranteed,...

Holistic polar map for integrated evaluation of cardiac imaging results

Polar map display (PM) is a comprehensive interpretation of the left ventricle. This is a non-rigid registration of the left ventricle originally for the visual and quantitative analysis of tomographic myocardial perfusion scintigrams. In this scheme the maximal-count circumferential profiles of well-defined short- and long-axis planes are plotted to a map showing the distribution of the perfusion tracer onto a two-dimensional polar representation. The usual coronary artery distribution is often indicated on the PMs of SPECT studies by referring to the regions of the three main coronary branches, nevertheless, the individual variations may differ extensively. We set out to develop an Access (Microsoft)-based computer program that permits an integrated evaluation of the imaging results (coronary angiography, echocardiography and SPECT) on patients with coronary artery disease. This semi-quantitative registration of the coronary tree to a PM focused on the relation between the supplying coronary branches and the myocardial regions of the 16-segment left ventricular evaluating model. All the recorded anatomical and functional data were related to these 16 left ventricular segments, which allowed the direct comparison and holistic synthesis of the results. Two projections were taken into consideration for generation of the coronary PM: from the right anterior oblique projections, the left anterior descendent (LAD)/right coronary artery (RCA) border was assessed through the comparison of the left and right coronary angiograms. The terminations of the visually detected end-arteries showed the separation of the myocardial beds supplied by the two branches. The border of the myocardial beds on the polar map was determined on the “vertical axis” of the local coordinate system. The RCA/ left circumflex (LCx) separation can be determined from the left anterior oblique view. In this projection, the left ventricular septal edge was delineated by the LAD, while the LCx indicated the lateral epicardial surface. The individual coronary artery circulation was typified from among 12 variations in the Holistic Coronary Care program. With this determination of the individual coronary circulation, the lesion-associated segments are generated automatically by the software. The lesion-associated regions are defined as the myocardial bed of a diseased artery distal to the lesion. The PMs generated from the coronary angiographic results were compared with those of 99Tc-labelled MIBI single photon emission computed tomography (SPECT) in order to test the accuracy of the localizing method. The overlap between the segments associated with the coronary lesion and the stress perfusion defects (<80% relative MIBI activity during stress tests) was analyzed in 10 patients with (sub)total coronary occlusion after myocardial infarction. The distributions of the segments with stress perfusion defects on MIBI SPECT gave positive and negative predictive values of coronary occlusion of 0.94 and 0.8, respectively. According to the 16-segment wall motion analysis by echocardiography, the positive and negative predictive values of coronary occlusion for wall motion abnormality were 0.82 and 0.76, respectively. While the distal part of the subtended region usually demonstrated a higher degree perfusion abnormality than the proximal part, the high positive predictive value proved that, during the stress condition, the perfusion defect could be detected in practically all the subtended regions. The low negative predictive value of the coronary lesion for the wall motion abnormality was associated with the remodeling of the entire left ventricle.