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PubMed2006

Lymphatic vessel density in the neoplastic progression of Barrett's oesophagus to adenocarcinoma.

BACKGROUND: Oesophageal adenocarcinoma is an aggressive neoplasm with poor prognosis as a result of early lymph node metastasis. AIMS: To measure lymphatic vessel density (LVD) in the neoplastic progression from Barrett's metaplasia to adenocarcinoma and determine whether LVD can predict the risk of cancer. In addition, to correlate LVD with lymph node metastasis and assess whether LVD could be used as a prognostic indicator for outcome or survival. METHODS: LVD and microvascular density (MVD) were assessed after immunohistochemical staining of vessels in Barrett's metaplasia, dysplasia, and adenocarcinoma tissues and were correlated with clinicopathological features. RESULTS: LVD was significantly reduced in adenocarcinoma, being half that seen in normal stomach/oesophagus or metaplasia/dysplasia. LVD did not correlate with tumour grade, stage, or clinical outcome; however, patients who had either lymph node metastasis or invasion of tumour cells into peritumorous lymphatic vessels had a significantly worse overall survival. MVD was also assessed as a prognostic marker; its increase appeared to be linked more with the development of Barrett's metaplasia than adenocarcinoma. CONCLUSIONS: The reduction in lymphatic vessel numbers was not useful for determining disease outcome in the patient group studied. It is the entry of tumour cells into pre-existing peritumorous lymphatic vessels that confers a significantly worse overall survival.

Adenocarcinoma↗
PubMed2003

Blood vessel constitutive models-1995-2002.

Knowledge of blood vessel mechanical properties is fundamental to the understanding of vascular function in health and disease. Analytic results can help physicians in the clinic, both in designing and in choosing appropriate therapies. Understanding the mechanical response of blood vessels to physiologic loads is necessary before ideal therapeutic solutions can be realized. For this reason, blood vessel constitutive models are needed. This article provides a critical review of recent blood vessel constitutive models, starting with a brief overview of the structure and function of arteries and veins, followed by a discussion of experimental techniques used in the characterization of material properties. Current models are classified by type, including pseudoelastic, randomly elastic, poroelastic, and viscoelastic. Comparisons are presented between the various models and existing experimental data. Applications of blood vessel constitutive models are also briefly presented, followed by the identification of future directions in research.

Animals↗
PubMed1996

Central intraluminal saturation stripe on MR angiograms of curved vessels: simulation, phantom, and clinical analysis.

PURPOSE: To investigate the appearance of reduced signal intensity in the center of blood vessels on magnetic resonance (MR) angiograms that can mimic intraluminal thrombus. MATERIALS AND METHODS: Simulations and phantom studies were performed to analyze MR angiogram appearance distal to a pronounced curve. RESULTS: Saturation effects substantially lower the signal strength in the center of the vessel relative to that at the vessel periphery. These effects appeared even though the flow was well ordered and laminar. In curved geometries, secondary flow patterns produced counter-rotating vortices, which moved the fastest-moving particles to the outside of the curve and folded the slow-moving particles to the center of the vessel. CONCLUSION: Imaging parameter choices that reduce saturation, such as acquisition of a two-dimensional section transverse to the vessel and through the questionable region, effectively eliminate the central hypointensity effect in vivo.

Adult↗
PubMed2004

Engineering of fibrin-based functional and implantable small-diameter blood vessels.

We engineered implantable small-diameter blood vessels based on ovine smooth muscle and endothelial cells embedded in fibrin gels. Cylindrical tissue constructs remodeled the fibrin matrix and exhibited considerable reactivity in response to receptor- and nonreceptor-mediated vasoconstrictors and dilators. Aprotinin, a protease inhibitor of fibrinolysis, was added at varying concentrations and affected the development and functionality of tissue-engineered blood vessels (TEVs) in a concentration-dependent manner. Interestingly, at moderate concentrations, aprotinin increased mechanical strength but decreased vascular reactivity, indicating a possible relationship between matrix degradation/remodeling, vasoreactivity, and mechanical properties. TEVs developed considerable mechanical strength to withstand interpositional implantation in jugular veins of lambs. Implanted TEVs integrated well with the native vessel and demonstrated patency and similar blood flow rates as the native vessels. At 15 wk postimplantation, TEVs exhibited remarkable matrix remodeling with production of collagen and elastin fibers and orientation of smooth muscle cells perpendicular to the direction of blood flow. Implanted vessels gained significant mechanical strength and reactivity that were comparable to those of native veins. Our work demonstrates that fibrin-based TEVs hold significant promise for treatment of vascular disease and as a biological model for studying vascular development and pathophysiology.

Animals↗
PubMed2005

ETa-receptor blockade, but not ACE inhibition, blunts retinal vessel response during isometric exercise.

Angiotensin II and endothelin-1 are potent vasoconstrictors that appear to play a role in retinal blood flow regulation. In the present study, we investigated the possible role of the angiotensin and the endothelin system in the regulation of retinal vessel diameters during isometric exercise in healthy humans. The study design was randomized, double-masked, placebo-controlled, and three-way cross over. Twelve healthy subjects performed squatting exercises for 6 min during infusion of either an angiotensin-converting enzyme inhibitor (enalapril), an ET(A)-receptor antagonist (BQ-123), or placebo. Retinal vessel diameters were measured continuously with the Zeiss retinal vessel analyzer. Systemic hemodynamics were assessed noninvasively, and intraocular pressure was measured with applanation tonometry. Squatting induced a significant increase in blood pressure and pulse rate, which was paralleled by a vasoconstriction in retinal arteries and veins. Intraocular pressure was only slightly increased during the squatting periods. BQ-123 significantly blunted the exercise-induced decrease in venous (P < 0.01) and arterial (P < 0.02, ANOVA) vessel diameters but had no effect on basal retinal diameters. By contrast, enalapril did neither influence vessel diameter at baseline conditions nor in response to isometric exercise. The data of the present study indicate that retinal vasoconstriction during isometric exercise is modified by ET(A)-receptor blockade, whereas it is not altered by angiotensin-converting enzyme inhibition. Hence, the present data indicate that endothelin-1, but not angiotensin II, is involved in retinal blood flow regulation during isometric exercise.

Adult↗
PubMed1995

Modeling pressure-area relations of coronary blood vessels embedded in cardiac muscle in diastole and systole.

Pressure-cross-sectional area (P-A) relations of a (thick-walled) arteriole and (thin-walled) small vein (both maximally dilated), embedded in cardiac muscle in both static systole and diastole at slack length and at 90% of maximal length (Lmax), were calculated. The elastic properties of cardiac muscle and vessel wall per se were taken into account. Muscle fibers and vessels were assumed to run in parallel. The muscle tissue (fibers + collagen) was assumed to be incompressible, homogeneous, nonlinearly elastic, and transversely isotropic. Cross-fiber stress-strain relations were assumed to be proportional to those in fiber direction. It is predicted that cardiac muscle in diastole has little effect on the P-A relation of the arteriole but strongly affects that of the small vein. In systole, the myocardium strongly affects the P-A relations of both vessels. Isometric transition from static diastole to static systole (isometric "contraction") was found to reduce arteriolar and venous area (at constant pressures of 35 and 7 mmHg, respectively) by approximately 50 and 40, respectively. Contraction with a 14% shortening was found to reduce these areas by 48 and 32%, respectively. The differences in the results for the two vessels were found to be determined mainly by their difference in the ratio of outer to inner radius. Furthermore, it was found that the area reductions are much larger for contractions (with or without shortening) than for muscle stretch per se. It is concluded that the change in elastic properties and, more specifically, development of stress in cross-fiber direction of the cardiac muscle during contraction causes the area reductions of coronary vessels.

Animals↗
PubMed1994

Angiotensin II relaxation of rainbow trout vessels in vitro.

The effects of salmonid angiotensin II ([Asn1,Val5]ANG II) were examined in isolated trout arteries [celiacomesenteric (CMA), coronary (COA), 3rd or 4th gill arch epibranchial (EBA), ventral aorta (VA)] and veins [anterior cardinal (ACV) and ductus Cuvier strips (DOC)]. ANG II (10(-10)-10(-6) M) produced modest (< 50% other agonists) transient contractions in otherwise unstimulated COA but was a poor agonist in other vessels. In precontracted vessels, ANG II responses were triphasic; transient contraction (P1), relaxation (P2), and partial recovery (P3) and vessel specific. P1 was similar to uncontracted vessels. With 10(-6) MANG II, %P2 was: EBA, 60.3 +/- 8.3% (n = 22); CMA, 48.8 +/- 8.8% (n = 4); ACV, 38.8 +/- 5.3% (n = 29); VA, 29.4 +/- 4.9% (n = 8); DOC, 25.5 +/- 2.4% (n = 14); COA, 13.2 +/- 6.7% (n = 4). P2 in EBA and ACV was dose dependent [EBA vs. ACV: mean effective concentration (EC50) = 3.6 x 10(-9) +/- 8.1 x 10(-10) M, n = 7 vs. 6.2 x 10(-8) +/- 2.3 x 10(-8) M, n = 8, respectively; P < or = 0.05] and inhibited by indomethacin but unaffected by propranolol, NG-monomethyl-L-arginine, saralasin, PD-123177, or DuP-753. Removal of EBA endothelium also inhibited relaxation. By comparison, ANG II did not relax bullfrog arteries (dorsal aorta, systemic arch, CMA) or femoral veins. These results show that, in large vessels of trout, the predominant effect of ANG II is an endothelium-dependent, prostanoid-mediated relaxation that is unaffected by classical ANG II-receptor antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1995

Chronic L-NAME hypertension in rats and autoregulation of juxtamedullary preglomerular vessels.

The impact of chronic NG-nitro-L-arginine methyl ester (L-NAME)-induced hypertension (20 mg.kg-1.day-1 po, for 25 days) on pressure responsiveness was assessed in vessels ranging from arcuate arteries (ArcA) to juxtaglomerular afferent arterioles (JAA), using videomicroscopy and blood-perfused juxtamedullary nephron (JMN) preparations. Respective tail-cuff pressures of control and L-NAME rats were 127 +/- 2 (n = 8) and 173 +/- 4 mmHg (n = 5). Corresponding vessels of both groups had similar calibers at 60 mmHg. Increasing blood perfusion pressure to 200 mmHg constricted control ArcA and JAA by 26 +/- 4% (n = 20) and 43 +/- 5% (n = 15), respectively. Instead, a respective 3 +/- 4% (n = 15) and 21 +/- 9% (n = 6) pressure-induced dilation occurred in L-NAME vessels, and 86 +/- 2% of glomeruli expressed alpha-smooth muscle actin. Responses to acetylcholine (1 microM) but not to nitroprusside (1 mM) were impaired by L-NAME. Maximal relaxation induced by Mn2+ (10 mM) revealed equal basal tone and similar passive viscoelastic properties in control and L-NAME vessels. No vascular hypertrophy was found in L-NAME vessels. Chronic L-NAME hypertension is therefore associated with a selective loss of vascular autoregulation in JMNs, which may contribute to glomerular injury.

Actins↗
PubMed1987

Alveolar vessel behavior in the zone 2 lung inferred from indicator-dilution data.

To gain insight into the changes occurring in alveolar vessels when alveolar pressure exceeds venous pressure at the downstream end of the alveolar vessels (zone 2), we compared the uptake of serotonin and the extravascular volume accessible to 3HOH (Qev) under zone 2 and 3 conditions in isolated dog lung lobes. We also examined the influence of occluding some of the small pulmonary arteries with 58- to 548-micron-diam beads on the serotonin uptake and Qev. We found that, with the bead embolization, both the serotonin uptake and the Qev were reduced, whereas the change from zone 3 to 2 reduced serotonin uptake but did not change Qev. A plausible explanation for these observations is that the beads occluded vessels that were relatively large compared with those in which significant transvascular 3HOH exchange and serotonin uptake take place. Perfusion ceased in the collection of capillaries normally served by the obstructed arteries. Thus the extravascular water and the serotonin uptake sites downstream from the obstructions were not accessible to the indicators during the short time interval of the indicator passage through the lung. On the other hand, the change from zone 3 to zone 2 resulted in the collapse of small individual capillary segments within the alveolar vessel bed. Since the serotonin does not readily diffuse from the vessels through the tissue, it could not reach the endothelial cells of the collapsed capillaries. However, since the distances for diffusion between collapsed capillaries and neighboring perfused capillaries were small, the more highly diffusible 3HOH had access to the same Qev under both zone 2 and 3 conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1990

Relationships between permeable vessels, nerves, and mast cells in rat cutaneous neurogenic inflammation.

Electrical stimulation of rat sensory nerves produces cutaneous vasodilation and plasma protein extravasation, a phenomenon termed "neurogenic inflammation". Rat skin on the dorsum of the paw developed neurogenic inflammation after electrical stimulation of the saphenous nerve. In tissue sections, the extravasation of the supravital dye monastral blue B identified permeable vessels. Mast cells were identified by toluidine blue stain. Permeable vessels were significantly more dense in the superficial 120 microns of the dermis than in the deeper dermis, whereas mast cells were significantly more frequent in the deeper dermis. The relationships between nociceptive sensory nerve fibers, permeable vessels, and mast cells were examined by indirect immunohistochemistry for calcitonin gene-related peptide (CGRP), neurokinin A (NKA), and substance P (SP). CGRP-, NKA-, and SP-containing nerves densely innervated the superficial dermis and appeared to innervate the vessels that became permeable during neurogenic inflammation. In contrast, mast cells were not associated with either permeable vessels or nerve fibers. These data suggest that electrical stimulation of rat sensory nerves produces vascular permeability by inducing the release of neuropeptides that may directly stimulate the superficial vascular bed. Mast cells may not be involved in this stage of cutaneous neurogenic inflammation in rat skin.

Animals↗
PubMed1991

An algorithm for angiographic estimation of blood vessel diameter.

This study was carried out in an attempt to develop an objective and robust method for measuring changes in the diameters of small blood vessels from X-ray angiographic images. Recognizing potential problems with edge detection methods applied to cylindrical vessels in which the contrast diminishes as the boundary is approached, we have attempted to utilize the X-ray absorbance data across the entire cross section of the vessel. Then, assuming a cylindrical geometry, the absorbance data are fit to the cylindrical absorbance function by use of nonlinear regression analysis. The method was tested and calibrated using glass tubes filled with various concentrations of contrast medium. The diameters of small pulmonary arteries were estimated by applying the method of angiograms obtained from an isolated dog lung lobe. The structure of the residuals obtained after the fitting procedure was analyzed to test the appropriateness of the model for use with images of vessels. The results suggest that this approach will have utility for systematically quantifying vessel dimensions.

Algorithms↗
PubMed2006

What determines blood vessel structure? Genetic prespecification vs. hemodynamics.

Vascular network remodeling, angiogenesis, and arteriogenesis play an important role in the pathophysiology of ischemic cardiovascular diseases and cancer. Based on recent studies of vascular network development in the embryo, several novel aspects to angiogenesis have been identified as crucial to generate a functional vascular network. These aspects include specification of arterial and venous identity in vessels and network patterning. In early embryogenesis, vessel identity and positioning are genetically hardwired and involve neural guidance genes expressed in the vascular system. We demonstrated that, during later stages of embryogenesis, blood flow plays a crucial role in regulating vessel identity and network remodeling. The flow-evoked remodeling process is dynamic and involves a high degree of vessel plasticity. The open question in the field is how genetically predetermined processes in vessel identity and patterning balance with the contribution of blood flow in shaping a functional vascular architecture. Although blood flow is essential, it remains unclear to what extent flow is able to act on the developing cardiovascular system. There is significant evidence that mechanical forces created by flowing blood are biologically active within the embryo and that the level of mechanical forces and the type of flow patterns present in the embryo are able to affect gene expression. Here, we highlight the pivotal role for blood flow and physical forces in shaping the cardiovascular system.

Animals↗
PubMedDate not supplied

Flow in elliptical vessels calculated for a physiological waveform.

Understanding the nature of pulsatile flow is an important issue in haemodynamics, especially the initiation and progression of vascular disease. The geometry of a non-circular vessel was idealised to an elliptical cross-section, and the dynamic properties of the flow were calculated for a physiological waveform. The Fourier harmonics for a common carotid waveform were determined, and the velocity profile and wall shear stress were calculated from the superposition of the individual contributions from each harmonic. The effects of ellipticity on the flow pattern were found to be significant. The velocity profile along the major axis of the elliptical cross-section developed a flattened peak, which widened as the vessel became more elliptical. Wall shear stress demonstrated an angular dependence in elliptical vessels, where the point of minimum shear stress was located at the end of the major axis. Comparison with a cylindrical vessel demonstrated a 3% decrease in peak wall shear stress (tau = 2.96, N.m(-2)) at the end of the major axis, and 10% in the mean wall shear stress (tau = 0.44 N. m(-2)), for an elliptical vessel (epsilon = 0.8). The temporal average wall shear stress, which has been associated with atherogenic sites, also displayed a minimum at the end of the major axis that decreased with more elliptical cross-sections.

Blood Flow Velocity↗
PubMedDate not supplied

Effects of atropine and propranolol on retinal vessel diameters during isometric exercise.

PURPOSE: There is controversy regarding the nervous control of retinal blood vessels in humans. Most in vitro studies indicate that the intraocular part of the central retinal artery lacks autonomic innervation. We investigated the response of retinal vessels to isometric exercise during blockade of beta-receptors (propranolol) or muscarinic receptors (atropine). METHODS: Twelve healthy subjects performed squatting for 6 min during infusion of either propranolol atropine or placebo. Blood pressure and pulse rate were measured non-invasively. Retinal vessel diameters were measured continuously using the Zeiss Retinal Vessel Analyser. RESULTS: Squatting induced a significant increase in blood pressure and pulse rate, which was paralleled by a decrease in retinal vein and artery diameters. Atropine did not change the retinal vessel response to isometric exercise. Propranolol significantly blunted the exercise-induced vasoconstriction in retinal arteries. CONCLUSION: This result likely indicates propranolol-evoked vasoconstriction in the extraocular parts of the central retinal artery during isometric exercise.

Adrenergic beta-Antagonists↗
PubMed2005

Expression of the CD44 receptor in the blood vessel system: an experimental study in rat.

The CD44 receptor is a transmembrane glycoprotein expressed on a variety of cells like endothelial, epithelial and smooth muscle cells. This molecule has many important functions, e.g. in cell-cell and cell-matrix interactions and signal transduction. The main ligand for CD44 is hyaluronan (HYA). HYA is a glycosaminoglycan with structural and cell biological properties. The localization of HYA in the vessel wall of arteries and veins in the healthy adult and newborn rat has been described earlier. In this study the occurrence of the CD44 receptor was investigated in the same vessels and compared to the localization of HYA. Both CD44 and its ligand showed an increased expression in the vessel wall of newborn rats compared to that of adult rats. Although HYA is abundant in the adventitia of adult rats, virtually no expression of CD44 was observed. Our results indicate that the CD44 receptor expression is increased during the stage of maturation of the vessel tree whereas the CD44 receptor is less needed by HYA in the healthy vessel wall.

Aging↗
PubMed2002

Quantification of mRNA for endothelial NO synthase in mouse blood vessels by real-time polymerase chain reaction.

The mouse is useful in studies of vascular biology because of its well-defined genetics and because the mouse genome can be manipulated. However, because only small amounts of mRNA can be extracted from blood vessels, the quantification of gene expression in individual mice is difficult. Endothelial NO synthase (eNOS) plays a major role in the regulation of vascular tone and growth. In addition, there appear to be sex differences in the production of NO under basal conditions in mouse aortas. The goals of this study were to develop a real-time polymerase chain reaction (PCR) method to quantify eNOS mRNA in blood vessels from mice and to examine eNOS mRNA levels in vessels from male and female mice. Blood vessels were isolated from C57BL/6 mice. Total RNA from individual mice was isolated and reverse-transcribed. The number of molecules of eNOS mRNA (after reverse transcription) was determined against cDNA standards, with 18S rRNA used as a control for RNA input and reverse-transcription efficiency. When expressed as copy numbers per nanogram of total RNA or as the ratio of eNOS to 18S rRNA, eNOS mRNA was lower in the aortas of female mice than in those of male mice at 7 to 9 months of age. In contrast, no difference in eNOS mRNA was found in the aortas of 2-month-old mice. In addition, eNOS mRNA levels were similar in the carotid, cerebral, and coronary arteries. These findings provide the first quantitative measurements of eNOS mRNA by using real-time PCR in the vessels of mice and suggest age- and sex-related differences in the basal levels of eNOS mRNA in mice. In addition, the eNOS region that was used for real-time PCR was amplified and sequenced for monkeys and other species. With modifications, this region may be used to design real-time PCR for eNOS in other species.

Animals↗
PubMed2003

Coronary vessel development: a unique form of vasculogenesis.

Development of the coronary vascular system is an interesting model in developmental biology with major implications for the clinical setting. Although coronary vessel development is a form of vasculogenesis followed by angiogenesis, this system uses several unique developmental processes not observed in the formation of other blood vessels. This review summarizes the literature that describes the development of the coronary system, highlighting the unique aspects of coronary vessel development. It should be noted that many of the basic mechanisms that govern vasculogenesis in other systems have not been analyzed in coronary vessel development. In addition, we present recent advances in the field that uncover the basic mechanisms regulating the generation of these blood vessels and identify areas in need of additional studies.

Animals↗
PubMed1994

Independent impact of thrombolytic therapy and vessel patency on left ventricular dilation after myocardial infarction. Serial echocardiographic follow-up.

BACKGROUND: It has been shown that successful reperfusion of the infarct-related artery by thrombolysis can prevent left ventricular dilation after acute myocardial infarction; these beneficial effects were detected from several days to several months after infarction. To date, however, no study has shown that these effects can be demonstrated within hours after the onset of infarction. Furthermore, data are scarce on the independent impact of thrombolytic therapy and late vessel patency on ventricular volume and function. The aim of this study was to assess separate effects of thrombolysis and patency of the infarct-related artery on left ventricular size and function by serial two-dimensional echocardiographic examinations. METHODS AND RESULTS: We evaluated 131 consecutive patients with first acute myocardial infarction by two-dimensional echocardiography in the following sequence: days 1, 2, 3, 7, and after 3 and 6 weeks. Intravenous streptokinase was administered in 81 patients, and 50 patients were treated without thrombolysis. Left ventricular end-diastolic volume, end-systolic volume, and ejection fraction were determined from apical two- and four-chamber views using the Simpson biplane formula and normalized to body surface area. Coronary angiography was performed in 107 patients after a mean of 26.0 +/- 20.2 (mean +/- SD) days after infarction. Patency of the infarct-related artery was assessed using TIMI criteria, with 54 considered patent (TIMI 3) and 53 with TIMI grade < 3. On day 1, end-systolic volume was significantly higher in patients not receiving thrombolysis (37.7 +/- 15.3 versus 33.0 +/- 10.6 mL/m2, P = .045). End-systolic volume (ESVi) was significantly higher in patients treated without thrombolysis throughout the study, whereas significant differences in end-diastolic volume (EDVi) were detected from day 3 (P = .041) onward and in ejection fraction (EF) from day 2 (P = .025) onward, all differences becoming progressively more significant with time (6-week values: EDVi, 78.8 +/- 25.4 versus 65.9 +/- 15.7 mL/m2, P = .001; ESVi, 45.4 +/- 22.6 versus 33.9 +/- 15.1 mL/m2, P = .002; EF, 45.1 +/- 11.6% versus 50.2 +/- 10.1%, P = .018). Patients with an occluded infarct-related artery (TIMI < 3) demonstrated highly significant differences at 6 weeks compared with patients with patent vessels (EDVi, 76.8 +/- 24.7 versus 65.2 +/- 15.6 mL/m2, P = .006; ESVi, 44.6 +/- 23.3 versus 31.9 +/- 12.2 mL/m2, P = .001; EF, 45.0 +/- 11.6% versus 52.1 +/- 9.0%, P < .001), but these differences developed more slowly than that seen among the thrombolytic subgroups. Indeed, multivariate analysis demonstrated that thrombolysis was the major determinant of initial volumes (P = .08, .02, and .08 for EDVi, ESVi, and EF, respectively), while vessel patency was the overwhelming determinant of subsequent changes (P = .0033, .0002, and .0024 for EDVi, ESVi, and EF, respectively). Additionally, ventricular volumes were significantly higher and ejection fractions lower in patients with anterior versus inferior infarction, but even adjusting for these differences as well as those associated with age, sex, and initial ventricular volume, the additive and independent impact of thrombolysis and infarct vessel patency persisted. CONCLUSIONS: These data indicate that the beneficial effect of thrombolysis on left ventricular size and function can be demonstrated in the earliest phases of acute myocardial infarction and that subsequent changes are mediated primarily through patency of the infarct-related artery. Thrombolytic therapy and late vessel patency thus have an additive and complementary impact in reducing ventricular dilation after myocardial infarction.

Coronary Vessels↗