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Computed tomography angiogram of the head and neck has lately become a pivotal imaging modality in the patient with acute stroke symptoms due to its high resolution, accuracy, speed, and sensitivity in the assessment of brain parenchyma and vascular patency.
OBJECTIVE: The purpose of this paper is to describe the radiographic and MR imaging appearance of heterotopic calcification in the ulnar collateral ligament. MATERIALS AND METHODS: Retrospective radiographic review of 710 patients examined for elbow pain yielded 42 individuals (age range, 16-38 years) with heterotopic calcification in the ulnar collateral ligament. Radiographic and MR imaging findings were compared with surgical findings. RESULTS: Fifty-one heterotopic calcifications were identified in 42 patients; nine patients had two sites of heterotopic calcification. Average initial calcification size in the craniocaudal dimension was 4 mm (range, 1-12 mm) and in the transverse dimension was 1 mm (range, 1-4 mm). Five of 42 patients had enlargement of the calcification on follow-up radiography. The largest heterotopic calcification that was not visualized on MR imaging measured 5 x 4 mm in craniocaudal and transverse dimensions. Of 34 patients with heterotopic calcification who underwent surgery, 26 patients (76%) had either partial or complete tears of the ulnar collateral ligament. CONCLUSION: Heterotopic calcification in the ulnar collateral ligament may be associated with partial or complete tears. The MR imaging detection of heterotopic calcification is less sensitive than that of radiography of the elbow.
BACKGROUND AND PURPOSE: Because cerebral perfusion imaging for acute stroke is unavailable in most hospitals, we investigated the feasibility of a method of perfusion scanning that can be performed rapidly during standard cranial CT. Our aim was to identify the scanning parameters best suited to indicate tissue at risk and to measure a perfusion limit to predict infarction. METHODS: Seventy patients who had suffered stroke and had undergone cranial CT 0.5 to 12 hours (median, 3.75 hr) after the onset of symptoms participated in the study. While undergoing conventional CT, each patient received a bolus of iodinated contrast medium. Maps of time to peak (TTP), cerebral blood volume (CBV), and CBF were calculated from the resulting dynamically enhanced scans. These perfusion images were compared with follow-up CT scans or MR images showing the final infarctions. RESULTS: CBF maps predicted the extent of cerebral infarction with a sensitivity of 93% and a specificity of 98%. In contrast, CBV maps were less sensitive and TTP maps were less specific and also showed areas of collateral flow. Infarction occurred in all of the patients with CBF reduction of more than 70% and in half of the patients with CBF reduction of 40% to 70%. CONCLUSION: Dynamic CT perfusion imaging safely detects tissue at risk in cases of acute stroke and is a feasible method for any clinic with a third-generation CT scanner.
Two hundred twenty upper extremity radionuclide venograms were performed using upper extremity injection of 5 mCi of Tc-99m DTPA in each arm of patients with indwelling central lines. Evidence of obstruction was found in 123 patients, collateral flow without anatomic obstruction in six patients, and a slow-flow pattern in 12 patients. Twenty-six of these also underwent upper extremity contrast venography within 48 hours of the scan. Contrast venograms and radionuclide venograms agreed in 19 patients (16 correctly identified as obstructed, three correctly identified as unobstructed). Six patients showed the slow-flow pattern without collaterals or obstruction. Subsequently, six follow-up contrast studies showed no evidence of obstruction or collaterals. The authors conclude that obstruction with collateral flow on radionuclide venograms correctly predicts obstruction. However, the slow-flow pattern does not and should not be used as the sole criterion to diagnose partial obstruction.
An electrogram was recorded from the angioplasty catheter guide wire when coronary blood flow was interrupted in 20 patients undergoing percutaneous transluminal coronary angioplasty. Monophasic action potentials were recorded from the right ventricular septum together with the routine electrocardiogram. The patients were studied during angioplasty for lesions in the left anterior descending (12), circumflex (3), and right coronary arteries (6). ST elevation in the electrogram recorded in the left anterior descending and circumflex systems was usually more obvious than that in the electrocardiogram. Signals obtained from the right coronary artery were of very low amplitude and registered only minimal ST changes. The ST elevation developed in the electrogram during insertion of the catheter before inflation of the balloon in 11 of the 15 patients undergoing angioplasty of the left system. In eight of the patients showing pre-inflation ST elevation the ST shift lessened after successive inflations. Monophasic action potential recordings were obtained during 45 balloon inflations in 19 patients. In those patients undergoing angioplasty for lesions of the circumflex coronary artery the monophasic action potential showed no change during balloon inflation. In patients undergoing angioplasty for the right coronary artery the mean normalised duration at 60 seconds' occlusion was 99.6 (1.5)% of control. Of a total of 25 occlusions in the patients undergoing angioplasty for the left anterior descending coronary artery 19 showed shortening of less than 5%, five showed shortening between 5 and 10%, and one showed a shortening of 16.4% in the monophasic action potential. The QT interval was satisfactorily measured in the electrogram during 36 balloon inflations, and in 24 of these it was also measured in the electrocardiogram. QT changes in the electrogram tended to be the opposite of those in the electrocardiogram. When changes in RR interval were minimal (less than 20 ms) during the balloon inflation 14 of 17 electrograms showed QT prolongation but only one of 12 electrocardiograms showed prolongation. Conversely one of 17 electrograms showed shortening compared with eight of 12 electrocardiograms. There was angiographic evidence of the development of collaterals in six of 15 patients undergoing angioplasty of the left system. ST segment elevation in both the electrogram and electrocardiogram was less pronounced in these patients than in those without evidence of the development of collaterals. ST segment changes recorded from the angioplasty guide wire provide a more sensitive index of ischaemia than the surface 12 lead electrocardiogram, and fall in ST segments on balloon deflation is a prognostic index of a good angiographic result in the left anterior descending and circumflex arteries, but not in the right coronary artery.
Endogenous matrix metalloproteinases (MMPs) and their inhibitors, tissue inhibitor of metalloproteinases (TIMPs), are important mediators of extracellular matrix remodeling, which is integral to plaque progression in coronary artery disease. In addition, high levels of the soluble fragment of CD40 ligand (sCD40L) have previously been associated with adverse cardiovascular outcomes. We hypothesized that circulating levels of MMP-9, TIMP-1, TIMP-2, and sCD40L were abnormal in patients who had stable coronary artery disease, and these levels were compared with those in matched controls. We also hypothesized correlations of MMPs, TIMPs, and sCD40L to each other and to high-sensitivity C-reactive protein (a proinflammatory marker), white blood cell count, severity of coronary artery disease (based on angiographic measurements of atherosclerotic burden), and coronary collateralization. We studied 204 adult patients who attended our unit for outpatient diagnostic cardiac catheterization for the investigation of suspected coronary artery disease. Coronary angiograms were scored for atheroma burden and stenosis by 2 independent observers. Circulating levels of MMP-9, TIMP-1, TIMP-2, and sCD40L were measured by enzyme-linked immunosorbent assay. Plasma levels of MMP-9 (p = 0.0099), TIMP-2 (p = 0.0019), and sCD40L (p <0.001), but not TIMP-1 (p = 0.463) were high in patients compared with healthy controls. In patients who had coronary artery disease, MMP-9 and high-sensitivity C-reactive protein levels were significantly higher in women than in men. Only MMP-9 correlated modestly with total white blood cell count (Spearman's correlation, r = 0.274, p = 0.002). Logistic regression of cardiovascular risk factors showed that only white blood cell count was independently associated with MMP-9 (p = 0.02). After standardizing for atheroma and stenosis scores, there were no statistically significant differences in our research indexes in patients who had angiographic collaterals compared with those who did not. In conclusion, stable coronary artery disease is associated with abnormal circulating levels of MMP-9, TIMP-2, and sCD40L, which do not appear to related to each other or to severity of coronary artery disease or collateralization. The gender difference in high-sensitivity C-reactive protein and MMP-9 levels may provide insight into the pathophysiology of coronary artery disease in men and women, and further studies are warranted to explore this potential link.
OBJECTIVE: Induction of angiogenesis has been reported subsequent to eNOS overexpression or activation, the latter involving Hsp90 as a chaperone protein. Here, we investigated the potential of regional Hsp90 overexpression to induce therapeutic neovascularization in vivo in a chronic rabbit hindlimb ischemia model. METHODS: In rabbits (n=7 per group), the external femoral artery was excised at day 0 (d0). At d7, liposomes containing eGFP (control group) or Hsp90 were retroinfused into the anterior tibial vein. At day 7 and day 35, angiographies were obtained and analyzed for collateral formation and perfusion velocity (frame count score) (% of d7 values). Capillary/muscle fiber (C/MF) ratio was calculated from five muscle areas of the ischemic limb. L-NAME and Geldanamycin were co-applied, where indicated. RESULTS: Compared to mock-treated controls, Hsp90 transfected increased C/MF ratio at day 35 (1.78+/-0.15 vs. 1.19+/-0.13, p<0.05), an effect blunted by L-NAME (1.39+/-0.11). Hsp90 transfection increased collateral formation (157+/-11% vs. 110+/-13%) and frame count score (174+/-18% vs. 117+/-10%), both sensitive to inhibition by L-NAME coapplication (135+/-17% and 134+/-14%, respectively). Of note, C/MF ratio was found elevated 3 days after Hsp90 transfection (1.61+/-0.16 at d10), at a time point when collateral formation was unchanged (106+/-6%), and tended to remain elevated in the presence of L-NAME applied thereafter (1.64+/-0.35 at d35), though L-NAME blocked subsequent changes in collateral growth or increase in perfusion at d35. CONCLUSIONS: We conclude that Hsp90 is capable of inducing angiogenesis and arteriogenesis via nitric oxide (NO) in a rabbit model of chronic ischemia. Our findings describe the capillary level as an initial site of Hsp90-cDNA-induced neovascularization, followed by growth of larger conductance vessels, resulting in an improved hindlimb perfusion.
BACKGROUND AND PURPOSE: High-resolution turbo MR angiography with zero-filling interpolation (ZFI) technique is a new vascular imaging method with reduced scan time. The purpose of the present study was to evaluate high-resolution turbo MR angiography for the diagnosis and assessment of moyamoya disease. METHODS: Forty-six patients suspected of having moyamoya disease were examined with high-resolution turbo MR angiography with the ZFI technique, MRI, and conventional angiography. Moyamoya disease was diagnosed in 42 of these patients. Blind, separate interpretation of the images was performed. RESULTS: High-resolution turbo MR angiography and MRI accurately evaluated 349 (95%) and 325 (88%) of 368 arteries, respectively, but the degree of stenosis was overestimated in the other arteries. MR angiography and MRI depicted basal cerebral moyamoya vessels in 82 (98%) and 82 (98%) of 84 hemispheres, respectively. MR angiography also depicted leptomeningeal and transdural collateral vessels in 51 (100%) of 51 hemispheres and in 38 (88%) of 43 hemispheres, respectively. The sensitivity and specificity of high-resolution turbo MR angiography for the diagnosis of moyamoya disease were 98% and 100%, respectively. CONCLUSIONS: High-resolution turbo MR angiography in reduced scan time is highly accurate in the assessment of both steno-occlusive lesions and collateral vessels in moyamoya disease, thus providing a highly accurate (98%) diagnosis and assessment of moyamoya disease.
UNLABELLED: Although contrast-enhanced first pass magnetic resonance imaging (MRI) has potential to quantify blood flow through extensive image post-processing, clinical utility is likely to depend on rapid qualitative analysis. AIMS: To investigate use of an on-line analytical approach for detection of coronary artery disease (CAD). METHODS AND RESULTS: Thirty subjects with CAD underwent contrast-enhanced rest/adenosine stress MRI with basal, mid-papillary and apical short-axis image acquisition. Each short axis was divided into eight regions of interest (ROI). Regional perfusion was visually classified as normal or impaired according to transmural distribution and defect reversibility. MRI and angiographic data were compared. Qualitative MRI reporting was possible for 98% ROI. Eighty-six coronary artery (CA) territories were assessed of which 71 (83%) had stenoses. Sensitivity and specificity for detection of stenoses were 93 and 60%, respectively. The proportion of hypoperfused ROI rose from 31% with < 50% stenosis to 65% with occlusion. More transmural defects were seen in infarction-related territories (75 vs. 54%, p < 0.05). More ROI demonstrated defect reversibility in occluded rather than in stenosed infarction-related vessels (89 vs. 58%, p < 0.05). Occluded vessels with grade 2-3 collaterals contained a higher proportion of normal ROI (44 vs. 25%, p < 0.05). CONCLUSIONS: Qualitative MRI analysis had high sensitivity and moderate specificity for detecting CA stenoses. Additional information was obtained relating to lesion severity, previous infarction, myocardial viability and impact of collateral circulation. The technique has potential for de novo diagnosis of CAD and as a complementary modality to angiography to assess the significance of given angiographic lesions.
Extra- and intracellular recording, electrical stimulation, receptive field mapping, and horseradish peroxidase injection techniques were used to study the structure of functionally identified neurons in trigeminal (V) brainstem subnucleus oralis of the rat. Of 15 heavily labeled cells located within oralis, 4 were local-circuit neurons with receptive fields restricted to either an incisor, guard hairs, one vibrissa, or deep facial tissue (nociceptors). Their morphologies were highly varied, with expansive and spiny dendritic trees and recurrent and intersubnuclear axon collaterals. Oralis local-circuit neurons therefore most closely resembled non-vibrissa-sensitive local-circuit cells in adjacent subnucleus interpolaris. Six other stained cells projected to contralateral thalamus, and two others projected to ipsilateral cerebellum. They typically had intramodality convergent receptive fields (i.e., spanning more than one receptor organ, such as multiple vibrissae or teeth) with widespread dendritic trees, and were therefore indistinguishable from similarly projecting cells in interpolaris. Two other cells projected to the ipsilateral spinal cord, as well as other V brainstem subnuclei. One of these responded to high-threshold mechanical stimulation of teeth; the other was discharged by deflection of one mystacial vibrissa. Their dendrites were very widespread and ended in spiny and bulbous appendages. Local axon collaterals were also extensive. The remaining oralis cell had two axons, one projecting to the thalamus, the other to the spinal cord. Its receptive field expressed convergence from multiple receptor organs, including vibrissae, guard hairs, and skin. Its somadendritic morphology was similar to that of oralis cells projecting only to thalamus. We conclude that, with some exceptions, the extensive dendritic trees, axon branching, convergence, and functional diversity of oralis cells approximate those described previously for functionally equivalent neurons in interpolaris (Jacquin et al., 1989a,b). Such anatomical and physiological properties are rarely seen, however, in nucleus principalis (Jacquin et al., 1988a). The structure and function of three atypical principalis cells with structural and functional characteristics typical of oralis cells are also described. It is argued that such cells are rostrally displaced oralis cells.
The metabotropic glutamate receptors (mGluRs) have many important roles in regulation of neuronal excitability and synaptic transmission. In hippocampal area CA1, activation of mGluRs can reduce both excitatory and inhibitory synaptic transmission. The conventional view is that the presynaptic effects are mediated by L-2-amino-4-phosphonobutyric acid (L-AP4)-sensitive, or group III mGluRs (mGluR4, mGluR6, mGluR7, mGluR8). However, some studies suggest that other mGluR subtypes may also be involved in regulation of excitatory and inhibitory synaptic transmission in area CA1. We have found that two pharmacologically distinct presynaptic receptors are involved in the depression of excitatory transmission at the Schaffer collateral--CA1 synapse. Consistent with previous studies, one receptor subtype is an L-AP4-sensitive receptor that is pharmacologically similar to mGluR4 or mGluR7. However, we have found that a second mGluR subtype, which is pharmacologically similar to mGluR1 and mGluR5 (group I mGluRs), can also reduce excitatory synaptic transmission in area CA1. Analysis of effects of agonists of these two receptors on miniature EPSCs and paired-pulse facilitation suggest that both receptors are localized presynaptically. It is also shown that the mGluR that reduces transmission at inhibitory synapses in area CA1 is presynaptically localized, is insensitive to L-AP4, and is sensitive to agonists selective for mGluR1 and mGluR5.
A buffered solution was perfused at a constant flow rate (2 ml/min) through both iliac arteries in rat hindquarters. Perfusion pressures were measured in normal and collateralized vascular beds of the left and right hind-leg, respectively. Bolus injections of various agonists produced concentration-dependent increases in perfusion pressure in both collateralized and normal circulatory beds. Serotonin, in particular, and noradrenaline, to a lesser extent, produced more pronounced vasoconstriction on the collateral side than on the normal side. The difference in vasoreactivity to serotonin was related to a difference in both vascular structure and sensitivity of both types of vascular bed. Vasoconstriction induced by serotonin was inhibited by 5-HT2 antagonists. Selective blockade of alpha 1,alpha 2,beta 1-beta 2 adrenoceptors and amine uptake blockade were ineffective. This study indicates that, in rat hind-legs, the collateralized vascular bed is superreactive to serotonin in comparison with the normal bed. This resetting of reactivity to serotonin is due to the specific vascular structure as well as to an increased 5-HT2 receptor-mediated sensitivity.
We studied the values of oral dipyridamole needed to detect coronary arterial disease using 12-lead electrocardiography. The relationship between dipyridamole-induced ST segment depression and coronary arterial lesions, coronary collaterals and myocardial infarction was investigated. 375 mg oral dipyridamole was given to 31 patients (22 with coronary arterial disease, 9 controls). 12-lead electrocardiogram was recorded before and 45 minutes after the test. The control group and the patients, who had no ST segment depression after dipyridamole, performed isometric contraction (handgrip) for 5 minutes and then the 12-lead electrocardiogram was recorded. All patients had coronary angiography. We also performed treadmill stress testing in 28 patients. Dipyridamole testing was positive (greater than or equal to 1 mm ST depression on electrocardiogram) in 7 of 22 patients with coronary arterial disease, of whom 6 had positive treadmill stress testing. Only 2 patients had previous myocardial infarction in the group with positive dipyridamole tests. Of the 15 in whom dipyridamole testing was negative, 5 had positive treadmill stress testing, while 13 of them had had previous myocardial infarction. All patients in the control group had negative dipyridamole stress testing and normal coronary angiograms. No additional ST segment changes were observed in the group who had performed isometric contraction test (both dipyridamole test negative and control groups). Sensitivity and specificity of the test were 32 and 100%, respectively. Comparison of collateral vessels between the groups positive and negative for dipyridamole revealed no difference. But the number of patients with old myocardial infarction was higher in those testing negative than in those who proved positive.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: The clinical role of collateral vessels, which are transiently augmented during coronary artery spasm, remains controversial. OBJECTIVE: To examine the correlation between coronary arteriographic and electrocardiographic features during spasm in the left anterior descending artery (LAD). METHODS: We studied 45 patients in whom LAD spasms were induced by administration of acetylcholine or ergonovine maleate into the left coronary artery, or in whom spontaneous LAD spasms were documented during diagnostic cardiac catheterization. RESULTS: During spasm, only three patients had transient appearance or augmentation of collateral flow opacifying the LAD. In these three patients, electrocardiograms obtained from anterior precordial chest leads during LAD spasm showed ST-segment depression, ST-segment elevation followed by ST-segment depression, and only T-wave change, respectively. Except for these three patients, ST-segment elevations were observed in all other patients (31 of 34) with main-branch spasm of the LAD. However, ST-segment elevation was observed in only two of 11 patients in whom spasm of the diagonal branch alone was induced. CONCLUSIONS: Our observations suggest that the electrocardiographic changes during spasm are not always a sensitive indicator of LAD side branch spasm or LAD main-branch spasm associated with collateral circulation. From consideration of the angiographic features of the collaterals in the three patients with LAD main-branch spasm, we speculate that the balance of tonus of both the recipient and donor arteries, and the degree of organic stenosis of the recipient artery, may have important roles in the mechanism responsible for the change in the appearance of collaterals in patients with coronary spasm.
OBJECTIVES: Quantitative assessment of coronary collateral blood flow can be archived by measuring coronary pressure. We studied the relationships between recruitable coronary collateral blood flow and electrocardiographic changes during percutaneous coronary intervention (PCI). METHODS: We measured coronary pressure during coronary occlusion with PCI in 119 patients with left anterior descending coronary artery stenosis. During balloon inflation, the electrocardiogram was continuously recorded. The ST-segment elevation in the most elevated lead was defined as MaxST and the sum of the maximal ST elevation in leads V2-V4 was defined as sumST. Fractional collateral flow (Qc/Q(N)) was calculated as the coronary wedge pressure divided by the mean aortic pressure. Myocardial ischemia was defined as an ST-segment shift >0.1 mV in any of the V2, V3 or V4 leads. RESULTS: A significant relationship between Qc/Q(N) and MaxST was observed (r=-0.455, P<0.0001). Similarly, Qc/Q(N) was significantly correlated with sumST (r=-0.477, P<0.0001). The receiver operating characteristic curve showed that a cut-off value of 0.27 for Qc/Q(N), with sensitivity of 71.4% and specificity of 76.2%, was an indicator of electrophysiologically sufficient recruitable coronary collateral blood flow for prevention of ischemia during coronary obstruction. Qc/Q(N) values during the first, second, third and fourth inflation were not significantly different. CONCLUSIONS: Qc/Q(N) could be clinically useful for determining whether there is electrophysiologically sufficient recruitable coronary collateral blood flow for prevention of ischemia during coronary obstruction. Repeat transient coronary occlusion during PCI did not lead to increased collateral blood flow.
Bilateral occlusion of the carotid arteries (BCAO) killed 52% of the male ddY mice (N = 86) and 77% of the ICR mice (N = 96) within 10 min, and the mean survival time of the ddY strain recorded for the 10 min was significantly longer than the time of the ICR strain. Among animals that survived longer than 1 hr after BCAO, some (5 of ddY and 3 of ICR) were able to survive for more than 24 hr. All of the neurobehavioral and histopathological signs developed by BCAO and in most cases followed by death were found to be also inducible by unilateral occlusion alone, although this was in a small fraction of mice. The brain levels of ATP, glucose and acetylcholine significantly decreased in mice that died within 10 min after BCAO, while none of these changes were detectable in mice surviving BCAO for 1 hr, just as in mice that died by carbon monoxide or ether inhalation. The results obtained herein indicate that mice may not be homogeneous in the functional level of the collateral route of blood supply to the brain tissue and/or in the sensitivity toward the ischemia-inducible lethality.
After a brief tetanic stimulation of an excitatory pathway in the hippocampus, synaptic transmission through the tetanized pathway is facilitated for a long period. This phenomenon is called long-term potentiation (LTP), and has been regarded as a neuronal correlate with learning and memory. Features of LPT in Schaffer collateral-CA1 neuron are calcium-dependency, input-specificity, cooperativity and sensitivity to blockers of N-methyl-D-aspartate (NMDA) receptors. These features can be explained by properties of NMDA receptors. LTP in mossy fiber-CA3 neuron has features different from those in field CA1: It is insensitive to blockers of NMDA receptors and does not show cooperativity. Quantal analysis of transmission through mossy fiber synapses before and after generation of LTP reveals that LTP resulted from facilitated release of transmitter. Participation of the metabotropic glutamate receptor is suggested.
INTRODUCTION: According to definition, collateral circulation is an alternative to major vascular flow which has become dysfunctional. Collateral channels, initially unused, are being formed due to impossibility of the main blood vessel to provide normal coronary flow. Recent controversies about collateral circulation are mainly based on their functional significance. The aim of this work was to evaluate the function of collateral circulation in patients after the first postero-inferior myocardial infarction i.e. whether adequate collateral circulation may reduce the size of myocardial infarction and prevent development of ischemic mitral regurgitation. MATERIAL AND METHODS: The investigation included 128 patients (pts) treated at the Institute of Cardiovascular Diseases in Sremska Kamenica during 1997 and 1998. The investigation group (I) included 64 pts, 58 males and 6 females, mean age 54.42 years. The control group (C) included 64 pts, 56 males and 8 females mean age 51.71 years. In all patients the first posterior, inferior and postero-inferior myocardial infarction were proven during 1-year period. Cineventriculography confirmed kinetic disturbance of the area with or without mitral insufficiency. Degree of mitral regurgitation was evaluated according to Seller's criterion. Alterations on the right coronary or circumflex branch of the left coronary artery were confirmed, but significant stenotic alterations were not verified on the anterior descendent branch of the left coronary artery. Alterations on epicardiac coronary vessels were presented as total coronary score--modification according to Benc (18 segments) while numerical values for stenosis according to Kaltenbach. This value represents the total coronary score (SCORE-A) including alterations before and after occlusion. Gensiny's principle modified for multiplication factor according to Benc and numerical value according to Kaltenbach were used for evaluation of collateral circulation. Levin's classification was used for evaluation of collateral circulation quality. We used quantitative classification according to Cohen. RESULTS: Distribution of mitral regurgitation was not statistically and significantly frequent in the subgroup of patients with lesions on the right coronary artery in relation to subgroup of patients with combined lesions on the right coronary artery and circumflex branch of the left coronary artery (p > 0.05). None of the investigated patients with extensive lesions (lesions on ACD and RCX) had mitral regurgitation of IV degree, so the number of investigated patients was not adequate for statistical evaluation. We did not find a statistically significant difference in the percentage of collateral circulation between the investigation (59.4%) and control group (62.5%) (p > 0.05). Poorly developed collaterals were statistically and significantly more frequent in the investigation group (60.5%) in relation to control group (10%) (p < 0.01). The percentage of moderately developed collateral circulation was similar in both groups. Well developed collateral circulation was statistically and significantly more frequent in control group (52.5%) in relation to investigation group (7.9%) (p < 0.01). The extension of stenotic alterations expressed as total coronary score A was statistically and significantly higher in subgroups of investigated patients with combined alterations on ACD and RCx, proving the sensitivity of our score system in smaller extensity of stenotic lesions on epicardial coronary blood vessels. Collateral circulation was significantly better in patients with ACD occlusion (100%) in relation to patients with significant stenosis or ACD subocclusion (33.3%) (p < 0.01). DISCUSSION: The functional role of collaterals has not been explained yet. The efficacy of coronary collateral vessels and mechanism of adequate compensation of regional perfusion in a position distal from the occluded vessel is highly controversial. (ABSTRACT TRUNCATED)