Distribution Of Coronary Blood Flow Research Articles

Left and right coronary artery blood flow distribution method based on dominant type.

The purpose of the current study was to investigate the effects of left/right coronary artery flow distribution on calculation of fractional flow reserve derived from coronary computed tomography angiography (FFRct) in different dominant types. First, 195 patients were collected to count the distribution ratios of the three categories: right dominance (RD), balanced dominance (BD), and left dominance (LD). Ratios of diameters of the left/right coronary arteries (DLCA :DRCA ) of the three types were calculated and used to represent the ratio of flow distribution (QLCA :QRCA ) in the dominant type method. The other method was known as the fixed ratio method (QLCA :QRCA =6:4). Second, a total of 73 patients with coronary artery disease (CAD) were enrolled for numerical calculation. A 0D/3D geometric multiscale model was used for the numerical simulation of FFR and the results of the fixed ratio method and the dominant type method were recorded as F-FFRct and D-FFRct. Lastly, invasive FFR(clinic-FFR)was used as a standard to evaluate the consistency and diagnostic performance of F-FFRct and D-FFRct. Corresponding flow distributions for the dominant type method were QLCA :QRCA =5:5 for RD, QLCA :QRCA =5.5:4.5 for BD, and QLCA :QRCA =6:4 for LD. D-FFRct showed a better correlation than F-FFRct (r=0.85 vs. r=0.81, both p < .001); the AUC (95%CI) were 0.974 (0.906-0.997, p < .0001) and 0.960 (0.886-0.992, p < .0001). Accuracy, specificity, sensitivity, positive predictive value (PPV) and negative predictive values (NPV) for D-FFRct and F-FFRct were 94.52%, 93.75%, 94.74%, 83.33%, 98.18% and 90.41%, 87.50%, 91.23%, 73.68%, 96.30%, respectively. Overall, the left/right coronary artery flow distribution was affected by the dominant type and the dominant type method was superior to the fixed ratio method in detecting coronary ischemic lesions.

Personalized coronary blood flow model based on CT perfusion to non-invasively calculate fractional flow reserve

Coronary outlet resistance, influenced by quantification and distribution of total hyperemic coronary blood flow, is critical for accurately estimating the computation of fractional flow reserve from computed tomography angiography (FFRCT). However, accurate estimation of FFRCT is still a challenging task due to the impractical of non-invasively measuring coronary outlet resistance in the clinic. While traditional methods have been used to estimate outlet resistance through population-averaged physiological assumption models, individual differences between patients limit the reliability of the models. In this work, we propose a personalized coronary flow model based on dynamic stress computed tomographic perfusion (CTP), called CTPV, to achieve a noninvasive estimation of the outlet resistance and FFRCT. The CTPV model employs myocardial blood flow (MBF) obtained from CTP to quantify the total hyperemic coronary blood flow directly. Then, myocardial perfusion territories corresponding to coronary artery branches are proposed to distribute the outlet coronary blood flow. For this purpose, we use the Voronoi algorithm to segment the myocardial perfusion territory. Finally, the outlet resistance and FFRCT are estimated based on the outlet coronary blood flow. Experiment studies on a clinical dataset consisting of 138 vessels from 86 subjects show the superiority of our CTPV model against the CTPD and LVMD models, including the method of quantifying total hyperemic coronary blood flow based on left ventricular myocardial mass (LVM) and distributing the outlet coronary blood flow based on outlet diameter. The CTPV model estimates a higher AUC for FFRCT (AUC = 0.96) than the CTPD model (AUC = 0.93) and the LVMD model (AUC = 0.92). The accuracies of CTPV, CTPD, and LVMD models are 90.6%, 87.7%, and 84.1%, respectively. Additionally, we use different outlet truncation locations to evaluate the repeatability of the CTPV and CTPD models for estimating FFRCT on a random dataset of 10 vessels. The result shows that the repeatability of the CTPV model is better than the CTPD model. These compelling results evince that the proposed CTPV model can accurately estimate the coronary outlet resistance and improve the diagnostic performance and repeatability of FFRCT.

Requirement of Postoperative Ventilation and analgesics during Off-Pump Coronary Artery Bypass (OPCAB) surgery – A Comparison between Combined High Thoracic Epidural Anaesthesia (HTEA) with GA and GA Alone

Beckground: This is often difficult to achieve optimal pain relief after coronary artery bypass surgery and also great challenge to choice appropriate analgesics with minimize the duration of mechanical ventilation. In the postoperative period inadequate analgesia may increase morbidity by causing adverse haemodynamic, metabolic, immunologic and haemostatic attentions and prolong mechanical ventilation with more ICU stay. High Thoracic Epidural Anaesthesia (HTEA) as an adjunct to general anaesthesia has been shown to be potentially beneficial in postoperative pain relief and the requirement of mechanical ventilationin patients with off-pump coronary artery bypass surgery (OPCAB). HTEA provides good protection from stress response, ensures hemodynamic stability, improves distribution of coronary blood flow with reducing demand of oxygen, less requirement of postoperative analgesia , mechanical ventilation and ICU stay. Objective: This study has been undertaken with a view to compare requirement of postoperative mechanical ventilation and analgesics in OPCAB surgery between HTEA with GA and GA alone. Methods: This prospective, randomized case control comparative study was carried out in sixty patients without having left main coronary artery disease, left ventricular ejection fraction &lt;30% or contraindication of regional anaesthesia scheduled for OPCAB. They were divided into two groups, thirty in each group. Group A received GA alone and group B received high thoracic epidural anaesthesia with GA. Requirement of postoperative analgesics, pain score, consciousness score, sedation score, satisfection level and duration of ventilation with length of stay in intensive care unit were recorded in the post-operative period. Results: Rescue analgesics received and found 16(53.3%) and 6(20.0%) needed analgesia in group A and group B respectively and the difference was statistically significant (p&lt;0.05). Regarding the pain score (VAS) during maintenance with ventilator with awareness at first fourth hour significant (p&lt;0.05) change between two groups. After extubation at rest in different time interval and found significant (p&lt;0.05) change between two groups in all follow-up times. Post-operative pain score (VAS) after extubation at movement in different time interval and found significant (p&lt;0.05) change between two groups. Post-operative pain score (VAS) after extubation at during coughing in different time interval and found significant (p&lt;0.05) change between two groups. Post-operative sedation score at first six hour (hourly) and found significant (p&lt;0.05) change between two groups except 1st hour, which was not significant (p&gt;0.05). The mean extubation hours were 7.4±1.09 hours in group A and 5.3±0.81 hours in group B. The mean ICU stay was 72.9±9.2 hours in group A and 57.1±12.0 hours in group B and the difference was statistically significant (p&lt;0.05) in unpaired t-test. No postoperative complication was observed in both groups. Conclusion: HTEA with GA appeared to be most reliable postoperative pain relief, shorter mechanical ventilation, ICU stay in OPCAB surgery Bangladesh Heart Journal 2021; 36(2): 74-81

Severe familial hypercholesterolemia impairs the regulation of coronary blood flow and oxygen supply during exercise.

Accelerated development of coronary atherosclerosis is a defining characteristic of familial hypercholesterolemia (FH). However, the recent data highlight a significant cardiovascular risk prior to the development of critical coronary stenosis. We, therefore, examined the hypothesis that FH produces coronary microvascular dysfunction and impairs coronary vascular control at rest and during exercise in a swine model of FH. Coronary vascular responses to drug infusions and exercise were examined in chronically instrumented control and FH swine. FH swine exhibited~tenfold elevation of plasma cholesterol and diffuse coronary atherosclerosis (20-60% plaque burden). Similar to our recent findings in the systemic vasculature in FH swine, coronary smooth muscle nitric oxide sensitivity was increased in vivo and in vitro with maintained endothelium-dependent vasodilation in vivo in FH. At rest and during exercise, FH swine exhibited increased myocardial O2 extraction resulting in reduced coronary venous SO2 and PO2 versus control. During exercise in FH swine, the transmural distribution of coronary blood flow was unchanged; however, a shift toward anaerobic cardiac metabolism was revealed by increased coronary arteriovenous H(+) concentration gradient. This shift was associated with a worsening of cardiac efficiency (relationship between cardiac work and O2 consumption) in FH during exercise owing, in part, to a generalized reduction in stroke volume which was associated with increased left atrial pressure in FH. Our data highlight a critical role for coronary microvascular dysfunction as a contributor to impaired myocardial O2 balance, cardiac ischemia, and impaired cardiac function prior to the development of critical coronary stenosis in FH.

The coronary circulation in exercise training.

Exercise training (EX) induces increases in coronary transport capacity through adaptations in the coronary microcirculation including increased arteriolar diameters and/or densities and changes in the vasomotor reactivity of coronary resistance arteries. In large animals, EX increases capillary exchange capacity through angiogenesis of new capillaries at a rate matched to EX-induced cardiac hypertrophy so that capillary density remains normal. However, after EX coronary capillary exchange area is greater (i.e., capillary permeability surface area product is greater) at any given blood flow because of altered coronary vascular resistance and matching of exchange surface area and blood flow distribution. The improved coronary capillary blood flow distribution appears to be the result of structural changes in the coronary tree and alterations in vasoreactivity of coronary resistance arteries. EX also alters vasomotor reactivity of conduit coronary arteries in that after EX, α-adrenergic receptor responsiveness is blunted. Of interest, α- and β-adrenergic tone appears to be maintained in the coronary microcirculation in the presence of lower circulating catecholamine levels because of increased receptor responsiveness to adrenergic stimulation. EX also alters other vasomotor control processes of coronary resistance vessels. For example, coronary arterioles exhibit increased myogenic tone after EX, likely because of a calcium-dependent PKC signaling-mediated alteration in voltage-gated calcium channel activity in response to stretch. Conversely, EX augments endothelium-dependent vasodilation throughout the coronary arteriolar network and in the conduit arteries in coronary artery disease (CAD). The enhanced endothelium-dependent dilation appears to result from increased nitric oxide bioavailability because of changes in nitric oxide synthase expression/activity and decreased oxidant stress. EX also decreases extravascular compressive forces in the myocardium at rest and at comparable levels of exercise, mainly because of decreases in heart rate and duration of systole. EX does not stimulate growth of coronary collateral vessels in the normal heart. However, if exercise produces ischemia, which would be absent or minimal under resting conditions, there is evidence that collateral growth can be enhanced. While there is evidence that EX can decrease the progression of atherosclerotic lesions or even induce the regression of atherosclerotic lesions in humans, the evidence of this is not strong due to the fact that most prospective trials conducted to date have included other lifestyle changes and treatment strategies by necessity. The literature from large animal models of CAD also presents a cloudy picture concerning whether EX can induce the regression of or slow the progression of atherosclerotic lesions. Thus, while evidence from research using humans with CAD and animal models of CAD indicates that EX increases endothelium-dependent dilation throughout the coronary vascular tree, evidence that EX reverses or slows the progression of lesion development in CAD is not conclusive at this time. This suggests that the beneficial effects of EX in CAD may not be the result of direct effects on the coronary artery wall. If this suggestion is true, it is important to determine the mechanisms involved in these beneficial effects.

Effect of Geometrical Assumptions on Numerical Modeling of Coronary Blood Flow Under Normal and Disease Conditions

Shear stress plays a pivotal role in pathogenesis of coronary heart disease. The spatial and temporal variation in hemodynamics of blood flow, especially shear stress, is dominated by the vessel geometry. The goal of the present study was to investigate the effect of 2D and 3D geometries on the numerical modeling of coronary blood flow and shear stress distribution. We developed physiologically realistic 2D and 3D models (with similar geometries) of the human left coronary artery under normal and stenosis conditions (30%, 60%, and 80%) using PROE (WF 3). Transient blood flows in these models were solved using laminar and turbulent (k-ω) models using a computational fluid dynamics solver, FLUENT (v6.3.26). As the stenosis severity increased, both models predicted a similar pattern of increased shear stress at the stenosis throat, and in recirculation zones formed downstream of the stenosis. The 2D model estimated a peak shear stress value of 0.91, 2.58, 5.21, and 10.09 Pa at the throat location under normal, 30%, 60%, and 80% stenosis severity. The peak shear stress values at the same location estimated by the 3D model were 1.41, 2.56, 3.15, and 13.31 Pa, respectively. The 2D model underestimated the shear stress distribution inside the recirculation zone compared with that of 3D model. The shear stress estimation between the models diverged as the stenosis severity increased. Hence, the 2D model could be sufficient for analyzing coronary blood flow under normal conditions, but under disease conditions (especially 80% stenosis) the 3D model was more suitable.

Regadenoson, a selective A2A adenosine receptor agonist, causes dose-dependent increases in coronary blood flow velocity in humans

Regadenoson is a selective A2A adenosine receptor agonist and vasodilator used to increase the heterogeneity of distribution of coronary blood flow during myocardial perfusion imaging. This study characterized the dose dependence of regadenoson-induced coronary hyperemia. An open-label, dose-escalation study of regadenoson (10-500 microg, rapid intravenous bolus) was performed in 34 subjects; in 4 additional subjects, the effect of aminophylline to reverse the response to regadenoson was determined. Intracoronary peak blood flow velocity in either the left anterior descending or left circumflex artery was measured by continuous Doppler signal recording, heart rate, central aortic blood pressure, and adverse effects were recorded. Regadenoson increased peak blood flow velocity by up to 3.4-fold in a dose-dependent manner. The mean duration of the increase in flow velocity of 2.5-fold or greater caused by 400 to 500 microg of regadenoson was 2.3 to 2.4 minutes. Regadenoson (400-500 microg) increased heart rate by up to 21 +/- 6 beats/min and decreased systolic blood pressure (-5 +/- 8 mm Hg to -24 +/- 16 mm Hg) and diastolic blood pressure (-8 +/- 4 mm Hg to -15 +/- 14 mm Hg). Aminophylline (100 mg) attenuated the increase in peak flow velocity but not tachycardia caused by 400 microg of regadenoson. The results of this study demonstrate the utility of regadenoson as a coronary vasodilator for myocardial perfusion imaging.

Perioperative Care in Cardiac Anesthesia and Surgery.

Baylor College of Medicine, Division of Cardiovascular Anesthesiology at Texas Heart Institute, Houston, Texas. ccollard@heart.thi.tmc.eduPerioperative Care in Cardiac Anesthesia and Surgery. Edited by Davy C. H. Cheng, M.D., M.Sc., F.R.C.P.C., and Tirone E. David, M.D., F.R.C.S.C. Philadelphia, Lippincott Williams &amp; Wilkins, 2006. Pages: 526. Price: $74.95.Although labeled as a first-edition text, this book is in reality an outgrowth of a small, portable “handbook” first published by Landes Bioscience in 1999 under the same title and editors. In contrast to the original handbook, which was primarily based on the contributors' clinical experience at the Peter Munk Cardiac Centre in Toronto, the current book has grown to include both contributors from outside institutions and a wider breadth of surgical and anesthetic topics relevant to the care of adult cardiac surgical patients (noticeably still absent, however, is the pediatric cardiac surgical patient). Contributors include anesthesiologists, surgeons, intensivists, and perfusionists, reflecting the book's multidisciplinary team approach to the management of the adult cardiac surgical patient.Primarily targeted for the practicing resident or physician, the book assumes a basic level of medical knowledge. For example, there are no traditional chapters on cardiovascular pharmacology and physiology. Instead, the book is composed of 50 chapters divided into six sections, progressing from preoperative assessment and prognostic risk factors to postoperative intensive care unit and ward management. Sections include Introduction, Anesthesia and Cardiopulmonary Bypass Management, Surgical Technique and Postoperative Consideration, Cardiac Surgical Recovery Unit, Surgical Ward Management, and Appendices. Coverage includes up-to-date information on cardiac and neurologic monitoring, off-pump surgery, new devices for anastomosis, robotic surgery, heparin alternatives, blood conservation, management of pulmonary hypertension, and neurologic complications and outcomes. Fifteen appendices summarize key facts, protocols, and clinical decisions. Indeed, the final section contains some of the most useful, hands-on information for the practicing clinician, because this section contains not only the clinical protocols of the Toronto General Hospital and London Health Science Centre, but also cardiovascular drug tables that list the dose, mechanism, physiologic effects, and contraindications of each drug.In general, information within each chapter is presented in bulleted fashion, making the text easily readable. However, like all bulleted texts, the information at times is presented with little or no explanation. Compounding this problem is the fact that there are no references within the chapter text. Instead, there is only a short, unnumbered bibliography at the end of each chapter (usually less than 10 references). Therefore, readers who wish to pursue a particular topic in more depth are basically left to fend for themselves.In addition, there are topics that suffer not only from brevity, but because the information is scattered throughout the book. For example, chapter 8, “Anesthesia for Patients with Ventricular Assist Devices (VAD),” is only 4 pages long and contains no figures. Moreover, it is not until chapter 36 that VAD surgical considerations are presented (which is again only 4 pages long and contains no figures). Therefore, it may be challenging for the true beginner using this book to assimilate the multitude of intraoperative VAD anesthetic and surgical considerations, because there are no figures and because of the nearly 300 pages of intervening text between chapters (as opposed to texts that have a unified chapter on VAD intraoperative considerations, including figures).The first edition of this book also contains errors. For example, in the chapter on “fast-track” cardiac anesthesia (chapter 3), there is a statement that suggests that fast-tracking increases perioperative morbidity and mortality. Similarly, the running title of chapter 14 is mislabeled as the “Essence of CBC and IABP.” Another example is figure 13-3, which is referred to in the text as being the American Society of Echocardiography and the Society of Cardiovascular Anesthesiology recommended 16-segment transesophageal echocardiographic examination of the left ventricle. In fact, it illustrates the myocardial coronary blood flow distribution. However, all of these oversights can be easily corrected in subsequent editions.With the recent decision by the Accreditation Council for Graduate Medical Education to accredit fellowships in adult cardiothoracic anesthesiology, there will likely be a growing need for up-to-date, definitive cardiothoracic anesthesiology texts (especially should the Accreditation Council for Graduate Medical Education also decide to institute a written board examination in the future). Although this book provides an excellent overview of the perioperative anesthetic and surgical management of the cardiac surgical patient, it may not be definitive enough for the full-time practitioner of cardiac anesthesia and surgery. Nonetheless, this book will be a valuable resource for individuals seeking a basic introduction and overview of the anesthetic and surgical management of the cardiac surgical patient.Baylor College of Medicine, Division of Cardiovascular Anesthesiology at Texas Heart Institute, Houston, Texas. ccollard@heart.thi.tmc.edu

Influence of Acute Renal Failure on Coronary Vasoregulation in Dogs

Impaired renal function is associated with an increased risk for cardiovascular events and death, but the pathophysiology is poorly defined. The hypothesis that coronary blood flow regulation and distribution of ventricular blood flow could be compromised during acute renal failure (ARF) was tested. In two separate groups (n = 14 each) of dogs with ARF, (1) coronary autoregulation (pressure-flow relations), vascular reserve (reactive hyperemia), and myocardial blood flow distribution (microspheres) and (2) coronary vessel responses to intracoronary infusion of select endothelium-dependent and -independent vasodilators were evaluated. In addition, coronary pressure-flow relations and vascular reserve after inhibition of nitric oxide and prostaglandin release were evaluated. Under resting conditions, myocardial oxygen consumption increased in dogs with ARF compared with no renal failure (NRF; 11.8 +/- 9.2 versus 5.0 +/- 1.5 ml O(2)/min per 100 g; P = 0.01), and the autoregulatory break point of the coronary pressure-flow relation was shifted to higher diastolic coronary pressures (60 +/- 17 versus 52 +/- 8 mmHg in NRF; P = 0.003); the latter was shifted further rightward after inhibition of both nitric oxide and prostaglandin release. The endocardial/epicardial blood flow ratio was comparable for both groups, suggesting preserved ventricular distribution of blood flow. In dogs with ARF, coronary vascular conductance also was reduced (P = 0.001 versus NRF), but coronary zero-flow pressure was unchanged. Vessel reactivity to each endothelium-dependent/independent compound also was blunted significantly. In conclusion, under resting conditions, coronary vascular tone, reserve, and vessel reactivity are markedly diminished with ARF, suggesting impaired vascular function. Consequently, during ARF, small increases in myocardial oxygen demand would induce subendocardial ischemia as a result of a limited capacity to increase oxygen supply and thereby contribute to higher risk for adverse coronary events and mortality.

Large-Scale 3-D Geometric Reconstruction of the Porcine Coronary Arterial Vasculature Based on Detailed Anatomical Data

The temporal and spatial distribution of coronary blood flow, pressure, and volume are determined by the branching pattern and three-dimensional (3-D) geometry of the coronary vasculature, and by the mechanics of heart wall and vascular tone. Consequently, a realistic simulation of coronary blood flow requires, as a first step, an accurate representation of the coronary vasculature in a 3-D model of the beating heart. In the present study, a large-scale stochastic reconstruction of the asymmetric coronary arterial trees (right coronary artery, RCA; left anterior descending, LAD; and left circumflex, LCx) of the porcine heart has been carried out to set the stage for future hemodynamic analysis. The model spans the entire coronary arterial tree down to the capillary vessels. The 3-D tree structure was reconstructed initially in rectangular slab geometry by means of global geometrical optimization using parallel simulated annealing (SA) algorithm. The SA optimization was subject to constraints prescribed by previously measured morphometric features of the coronary arterial trees. Subsequently, the reconstructed trees were mapped onto a prolate spheroid geometry of the heart. The transformed geometry was determined through least squares minimization of the related changes in both segments lengths and their angular characteristics. Vessel diameters were assigned based on a novel representation of diameter asymmetry along bifurcations. The reconstructed RCA, LAD and LCx arterial trees show qualitative resemblance to native coronary networks, and their morphological statistics are consistent with the measured data. The present model constitutes the first most extensive reconstruction of the entire coronary arterial system which will serve as a geometric foundation for future studies of flow in an anatomically accurate 3-D coronary vascular model.

Inferior wall restoration: anatomic and surgical considerations.

Congestive heart failure that results from inferior infarction is caused by a triangular change in ventricular geometry, which involves the septum, lateral wall, and base supplied by the right coronary artery. The extent of damage is determined by the anatomic distribution of coronary blood flow. Mitral insufficiency is accentuated from damage to the basal region, especially when the occluded right coronary vessel has multiple inferior branches and wraps around the apex. Three methods of repair are described, and include direct restoration without a patch, patch repair of the triangular scar, or use of a retriangulation suture in ventricles with trabecular scar to imbricate the noncontractile region to restrict patch size. This triangular reduction in size mirrors the design concept for suture described by Fontan in anterior infarction, which produces an oval apex. Early results in relation to left ventricular end systolic volume index and ejection fraction are defined.

Arterial wave reflections and survival in end-stage renal failure.

The increased effect of arterial wave reflections on central arteries like the common carotid artery seen in end-stage renal failure (ESRF) patients favors myocardial hypertrophy and oxygen consumption and alters coronary blood flow distribution. Nevertheless, the impact of wave reflection on the outcome and end points such as mortality remains to be demonstrated. One hundred eighty ESRF patients (age, 54+/-16 years) were monitored for 52+/-36 months (mean+/-SD). Seventy deaths, including 40 cardiovascular (CV) and 30 non-CV events, occurred. At entry, patients, in addition to standard clinical and biochemical analyses, underwent aortic pulse wave velocity measurement and determination of arterial wave reflexion by applanation tonometry on the common carotid artery that was expressed as augmentation index. Cox analyses demonstrated that predictors of all-cause and CV mortality were age, aortic pulse wave velocity, low diastolic blood pressure, preexisting CV disease, and increased augmentation index, whereas the prescription of an ACE inhibitor had a favorable effect on survival. After adjustment for all confounding factors, the risk ratio for each 10% increase in augmentation index was 1.51 (95% confidence interval, 1.23 to 1.86; P<0.0001) for all-cause mortality and 1.48 (95% confidence interval, 1.16 to 1.90; P<0.0001) for CV mortality. These results provide the first direct evidence that in ESRF patients increased effect of arterial wave reflections is an independent predictor of all-cause and CV mortality.

Coronary angiogenesis: detection in vivo with MR imaging sensitive to collateral neocirculation--preliminary study in pigs.

To assess the ability to track neovascularization over time with a magnetic resonance (MR) imaging technique sensitized to new intramyocardial collateral development as a means of evaluating therapeutic angiogenesis. Magnetization preparation plus spatial frequency reordering was applied to distinguish new intramyocardial collateral vessels from normal circulation on the basis of geometric differences. A vascular occluder was inserted in 34 pigs, and they were assigned randomly to treatment groups with either placebo or angiogenic growth factor. Collateral extent determined with collateral-sensitive MR imaging was correlated with direct measurements by means of three-dimensional (3D) computed tomography (CT), coronary blood flow distribution determined with microspheres, and findings at histologic examination. Changes in the signal at collateral-sensitive MR imaging before and after treatment were assessed by two observers blinded to treatment. The collateral extent determined with collateral-sensitive MR imaging correlated well with findings at 3D CT (r = 0.95) and with microspheres (r = 0.86). Furthermore, the collateral extent determined with collateral-sensitive MR imaging increased significantly (P < .001) in response to the administration of an angiogenic growth factor but not to placebo. The correspondence of findings at collateral-sensitive MR imaging to collateral neovascularization was confirmed at histologic examination. The presence of intramyocardial collateral microvessels was accurately determined with collateral-sensitive MR imaging. The technique may be useful in clinical studies of therapeutic angiogenesis.

A hemodynamic analysis of coronary capillary blood flow based on anatomic and distensibility data.

An understanding of cardiac health and disease requires knowledge of the various factors that control coronary capillary blood flow. An analysis of coronary capillary blood flow based on a complete set of actual data on the capillary anatomy and elasticity does not exist. Previously, a complete set of data on the branching pattern and the vascular geometry of the pig coronary capillary network were obtained in our laboratory. In the present study, we obtained distensibility data on the coronary capillary blood vessels on the epicardial surface in the form of a pressure-diameter relationship using intravital microscopy. A mathematical model of the coronary capillary blood flow was then constructed on the basis of measured anatomic and elasticity data of the coronary capillary network, rheology of blood, physical laws governing blood flow, and appropriate boundary conditions. The constructed model was used to examine the heterogeneity of the spatial distribution of coronary blood flow, which is an important issue in coronary physiology. One interesting result of the model is that the dispersions of pressure and flow are significantly reduced in the presence of capillary cross-connections, and the resistance to flow is reduced as well. Finally, we found that the compliance of the epicardial surface capillary vessels is so small that its effect on the blood pressure drop is negligible in the diastolic state. However, the compliance of the intramyocardial capillaries remains unknown, and the interaction of the muscle contraction and blood vessel elasticity in systole remains to be studied.

This Month in ANESTHESIOLOGY

This Month in ANESTHESIOLOGY

MYOGENIC CONSTRICTION (MC) OF RAT CORONARY ARTERIOLES IS PRESERVED BY SEVOFLURANE AND DESFLURANE

Introduction: Myogenic constriction (MC) is one of the determinants of coronary blood flow distribution, along with metabolic, endothelial, and neurohumoral influences, that help match coronary blood flow to myocardial tissue needs. [1] MC has been shown to be abolished by halothane, but preserved by isoflurane. [2] In this study, we examined the effect of the newer inhalational anesthetics, sevoflurane (SV) and desflurane (DS), on MC. Methods: Rat coronary arterioles, [similar] 100 [micro sign]m in diameter, were isolated. As the luminal pressure (LP) was varied from 0 - 120 mmHg, vessel diameter changes were monitored in vitro by videomicroscopy [2,3] with or without papaverine 10-4 M in the presence of SV 1 or 2 MAC or DS 1 or 2 MAC or no anesthetic (control). The passive response obtained with papaverine was compared to the active response without papaverine under each anesthetic condition. Data are mean +/- SD of 6-8 vessels. P < 0.05 by 2-way ANOVA was considered significant. Results: Compared to the passive response, control coronary arterioles demonstrated MC above 80 mmHg. MC was preserved in the presence of SV 1 MAC, but mildly enhanced with SV 2 MAC or DS 1 or 2 MAC. (Table 1)Table 1: Diameter Delta (% passive response at 40 mmHg) in response to Delta in LP (*: P < 0.05 vs. passive response. #: P < 0.05 vs. control response)Discussion: Unlike halothane, neither SV nor DS impairs myogenic mechanism of coronary flow distribution in rat coronary arterioles. Our findings may have implications on the variable effect of the inhalational agents on coronary blood flow.

Large artery structure and function in hypertension and end-stage renal disease.

The cardiovascular complications in hypertension are ascribed to two different but associated alterations, namely atherosclerosis and arteriosclerosis. Whereas the former disturbs principally the conduit function and the delivery of an adequate blood flow to peripheral organs and tissues, the latter disturbs the cushioning function of large arteries, inducing an inadequate increase in systolic and pulse pressure. Arteriosclerosis represents a clinical form of accelerated ageing process and is characterized by a diffuse dilation and hypertrophy of large conduit arteries and stiffening of arterial walls. Independently from the ageing, structural changes are associated with several haemodynamic alterations such as increased in blood flow and flow velocity, and increased parietal stress due to increased arterial diameters and/or intraarterial pressure. The principal consequences of arterial stiffening are: (1) an increased left ventricular afterload with development of left ventricular hypertrophy and increased myocardial oxygen demand; (2) altered coronary perfusion and blood flow distribution; and (3) decreased perfusion reserve during haemodynamic stress. In the absence of controlled studies, it is difficult to propose therapeutic interventions aimed to prevent or treat arterial abnormalities in hypertensive patients. It has been shown that long-term administration of either calcium channel blockers and angiotensin converting enzyme inhibitors led to an improvement of vessel wall elasticity. Nevertheless, these studies did not conclude whether the improvement of elastic properties were due only to decrease in blood pressure or to alterations in intrinsic properties of arterial walls. More investigations should be necessary to investigate this important problem.

Extent of myocardial collateralization: determination with three-dimensional elastic-subtraction spiral CT.

This study was undertaken to develop a standard that can be used to assess new high-resolution collateral zone imaging methods. The authors performed ex vivo helical CT in seven pig hearts after microsphere studies of blood flow and coronary angiography. They compared the zones of collateralization depicted at CT and at microsphere studies. The extent of the collateral zone at CT, computed by using elastic subtraction, correlated well with the coronary blood flow distribution determined with microsphere analysis (r = .95). The root-mean-square error was 6.5%, which indicates good agreement. Accurate assessment of collateralization extent has become an important goal because of the discovery of agents that stimulate the growth of coronary collateral vessels. The precision of elastic-subtraction CT and its validation with respect to the blood flow distribution at microsphere analysis indicate that elastic-subtraction CT can serve as a standard for the measurement of collateralization extent.

Fluxo coronário desregulado durante reperfusão pós cardioplegia

Metabolic coronary blood flow recruitment and distribution were studied in the setting of ventricular fibrillation (VF) during post-cardioplegia reperfusion. Fifteen pigs were placed on cardiopulmonary bypass and subjected to one hour of intermittent cold blood antegrade cardioplegia, followed by controlled myocardial reperfusion. According to the electromechanical status during the first ten minutes of reperfusion, the animals were allocated into 3 groups (n=5). Whereas Group 1 remained asystolic, the other two groups developed short (Group 2) or long duration VF (Group 3). Myocardial oxygen consumption (MVO2), in m/O2 /min/g (mean ± standard error) during reperfusion was 1.325 ± 0.144 (Group 1); 2.472 ± 0.208 (Group 2) and, 2.469 ± 0.228 (Group 3). MVO2 difference between asystolic and both short and long duration VF hearts was significant (p<0.001). Groups 1.2 and 3 endo-epi ratio and global coronary blood flow rate (169.3 ± 11.7; 185.0 ± 15.7 and 179.9 ± 13.2 ml/min/100g; respectively) were similar. These results demonstrate that coronary blood flow autoregulation was impaired because there was no increase in myocardial perfusion in response to the increase oxygen consumption imposed by VF during the first ten minutes of post cryocardioplegia reperfusion. This finding is of great clinical importance because it suggests that VF can potentially aggravate reperfusion lesions in formerly compromised hearts, i.e., those with coronary artery obstruction, ventricular distension or ventricular hypertrophy.

Steady-State Myogenic Response of Rat Coronary Microvessels Is Preserved by Isoflurane but Not by Halothane

The myogenic response of vascular smooth muscle produces vasomotion in response to changes in vessel transmural pressure.While this is an important determinant of coronary blood distribution, the effect of volatile anesthetics on the response has not been previously investigated. In this study, we examined the effect of isoflurane and halothane on this myogenic response. Coronary resistance arteries were isolated from Wistar rats. As the intraluminal pressure was increased from 10 to 120 mm Hg in the presence of either isoflurane (1%, 2%, and 3%), halothane (1% and 2%), or no volatile agent (control), the vessel intraluminal diameter was monitored using a video detection system. Passive changes in vessel diameter were measured after exposure to papaverine 100 micro Meter. Additionally, the myogenic responses of endothelium-intact and endothelium-denuded vessels were compared. Endothelium-intact control vessels demonstrated myogenic constriction above 80 mm Hg of intraluminal pressure. This response was not affected by endothelial denudation. The response was preserved by isoflurane 1%, 2%, or 3% but abolished by halothane 1% or 2%. We conclude that, in rat coronary resistance arteries, myogenic constriction can be demonstrated above 80 mm Hg of intraluminal pressure and is endothelium independent. This response is preserved by isoflurane but abolished by halothane. These findings may have implications for the effect of the anesthetics on coronary blood flow distribution. (Anesth Analg 1996;82:969-74)