Distribution Of Myocardial Blood Flow Research Articles

Normal values of myocardial blood flow measured with dynamic myocardial CT perfusion.

Dynamic myocardial CT perfusion (DM-CTP) can, in combination with coronary CT angiography (CCTA), provide anatomical and functional evaluation of coronary artery disease (CAD). However, normal values of myocardial blood flow (MBF) are needed to identify impaired myocardial blood supply in patients with suspected CAD.We aimed to establish normal values for MBF measured using DM-CTP, to assess the effects of age and sex, and to assess regional distribution of MBF. A total of 82 healthy individuals (46 women) aged 45-78 years with normal coronary arteries by CCTA underwent either rest and adenosine stress DM-CTP (n = 30) or adenosine induced stress DM-CTP only (n = 52). Global and segmental MBF were assessed. Global MBF at rest and during stress were 0.93 ± 0.42 mL/min/g and 3.58 ± 1.14 mL/min/g respectively. MBF was not different between the sexes (P = 0.88 at rest and P = 0.61 during stress) and no correlation was observed between MBF and age (P = 0.08 at rest and P = 0.82 during stress). Among the 16 myocardial segments, significant inter-segmental differences were found (P < 0.01), which was not related to age, sex or coronary dominance. Myocardial blood flow assessed by DM-CTP in healthy individuals with normal coronary arteries displays significant intersegmental heterogeneity which does not seem to be affected by age, sex or coronary dominance. Normal values of myocardial blood flow may be helpful in the clinical evaluation of suspected myocardial ischemia using DM-CTP.

Personalized Pressure Conditions and Calibration for a Predictive Computational Model of Coronary and Myocardial Blood Flow

Predictive modeling of hyperemic coronary and myocardial blood flow (MBF) greatly supports diagnosis and prognostic stratification of patients suffering from coronary artery disease (CAD). In this work, we propose a novel strategy, using only readily available clinical data, to build personalized inlet conditions for coronary and MBF models and to achieve an effective calibration for their predictive application to real clinical cases. Experimental data are used to build personalized pressure waveforms at the aortic root, representative of the hyperemic state and adapted to surrogate the systolic contraction, to be used in computational fluid-dynamics analyses. Model calibration to simulate hyperemic flow is performed in a “blinded” way, not requiring any additional exam. Coronary and myocardial flow simulations are performed in eight patients with different clinical conditions to predict FFR and MBF. Realistic pressure waveforms are recovered for all the patients. Consistent pressure distribution, blood velocities in the large arteries, and distribution of MBF in the healthy myocardium are obtained. FFR results show great accuracy with a per-vessel sensitivity and specificity of 100% according to clinical threshold values. Mean MBF shows good agreement with values from stress-CTP, with lower values in patients with diagnosed perfusion defects. The proposed methodology allows us to quantitatively predict FFR and MBF, by the exclusive use of standard measures easily obtainable in a clinical context. This represents a fundamental step to avoid catheter-based exams and stress tests in CAD diagnosis.

Wide dynamic range measurement of blood flow in vivo using laser speckle contrast imaging.

Laser speckle contrast imaging (LSCI) is a real-time wide-field technique that is applied to visualize blood flow in biomedical applications. However, there is currently a lack of relevant research to demonstrate that it can measure velocities over a wide dynamic range (WDR), which is critical for monitoring much higher and more pulsatile blood flow in larger size myocardial vessels, such as the coronary artery bypass graft, and visualizing the spatio-temporal evolution of myocardial blood flow perfusion in cardiac surgery. We aim to demonstrate that the LSCI technique enables measuring velocities over a WDR from phantom experiments to animal experiments. In addition, LSCI is preliminarily applied to imaging myocardial blood flow distribution in vivo on rabbits. Phantom and animal experiments are performed to verify that the LSCI method has the ability to measure blood velocities over a wide range. Our method is also validated by transit time flow measurement, which is the gold standard for blood flow measurement in cardiac surgery. Our method is demonstrated to measure the blood flow over a wide range from 0.2 to . To validate the phantom results, the varying blood flow rate from 0 to is detected in the rat carotid artery. Additionally, our technique also obtains blood flow maps of different myocardial vessels, such as superficial large/small veins, veins surrounded by fat, and myocardial deeper arteriole. Our study has the potential to visualize the spatio-temporal evolution of myocardial perfusion in coronary artery bypass grafting, which would be of great benefit for future research in the life sciences and clinical medicine.

Effect of iterations and time of flight on normal distributions of 82Rb PET relative perfusion and myocardial blood flow

BackgroundAs clinical use of myocardial blood flow (MBF) increases, dynamic series are becoming part of the typical workflow. The methods and parameters used to reconstruct these series require investigation to ensure accurate quantification. MethodsFifty-nine rest/stress dynamic 82Rb PET studies, acquired on a Biograph mCT, from a combination of normal volunteers and low-likelihood patients were reconstructed with and without time of flight (TOF) for varying iterations and processed to obtain relative perfusion and MBF polar maps. Regional values from mean polar maps were fit to a linear mixed-effect model to quantify convergence and select the optimal number of iterations. ResultsTOF reconstructions converged faster and yielded more uniform relative perfusion polar maps. However, the stress MBF distribution for TOF reconstructions was more heterogeneous, with a higher-intensity septal wall. This phenomenon requires further investigation, with right ventricle blood pool spillover possibly having an effect. Optimal reconstructions were defined as 5-iteration non-TOF (24-subset) reconstructions and 3-iteration TOF (21-subset) reconstructions. ConclusionOptimal cardiac reconstructions were identified for non-TOF and TOF reconstructions of dynamic series. TOF reconstruction presents as the more accurate method, given the more uniform relative perfusion distribution.

Association of Quantitative Flow Ratio with Lesion Severity and Its Ability to Discriminate Myocardial Ischemia.

Background and ObjectivesQuantitative flow ratio (QFR) is an angiography-based technique for functional assessment of coronary artery stenosis. This study investigated the response of QFR to different degree of stenosis severity and its ability to predict the positron emission tomography (PET)-defined myocardial ischemia.MethodsFrom 109 patients with 185 vessels who underwent both 13N-ammonia PET and invasive physiological measurement, we compared QFR, fractional flow reserve (FFR) and instantaneous wave-free ratio (iFR) for the responses to the different degree of anatomical (percent diameter stenosis [%DS]) and hemodynamic (relative flow reserve [RFR], coronary flow reserve, hyperemic stenosis resistance, and stress myocardial flow) stenosis severity and diagnostic performance against PET-derived parameters.ResultsQFR, FFR, and iFR showed similar responses to both anatomic and hemodynamic stenosis severity. Regarding RFR, the diagnostic accuracy of QFR was lower than FFR (76.2% vs. 83.2%, p=0.021) and iFR (76.2% vs. 84.3%, p=0.031). For coronary flow capacity (CFC), QFR showed a lower accuracy than iFR (74.1% vs. 82%, p=0.031) and lower discriminant function than FFR (area under curve: 0.74 vs. 0.79, p=0.044). Discordance between QFR and FFR or iFR was shown in 14.6% of cases and was driven by the difference in %DS and heterogeneous distribution of PET-derived RFR and stress myocardial blood flow.ConclusionsQFR demonstrated a similar response to different anatomic and hemodynamic stenosis severity as FFR or iFR. However, its diagnostic performance was inferior to FFR and iFR when PET-derived RFR and CFC were used as a reference.

Nitric oxide bioavailability affects cardiovascular regulation dependent on cardiac nerve status.

The sympathetic nervous system and nitric oxide (NO) contribute to regulation of vascular tone, blood flow regulation and cardiac function. Intrinsic cardiac neurons are tonically influenced by locally released NO and exogenous NO donors; however, the role of intact central neural connections remains controversial. We investigated the effects of S-nitroso-N-acetylpenicillamine (SNAP) administered into an intracoronary artery near the ventral interventricular ganglionated plexus (VIVGP) to evaluate distribution of myocardial blood flow (MBF) and ventricular function in normal and acute cardiac decentralized dogs. MBF was measured with microspheres during infusion of SNAP (100μM, IC) after systemic administration of 7-nitroindazole (nNOS blocker) followed by N(ω)-nitro-L-arginine methyl ester (LN; non-selective NOS blocker). Cardiac dynamics were not significantly affected by cardiac decentralization; several of these parameters (aortic systolic and diastolic pressures) were significantly increased after systemic administration of LN. Overall SNAP administered to the VIVGP increased blood flow in the anterior LV wall (vs. posterior LV wall) without affecting other cardiodynamic factors. In cardiac decentralized dogs subepicardial blood flow to the anterior LV wall during LN+SNAP was diminished resulting in a significantly higher inner:outer blood flow ratio (index of blood flow uniformity across the LV wall). LV function was not affected by acute cardiac decentralization; however, LV ejection fraction decreased markedly after LN (reduced NO bioavailability). These results validate earlier claims that reduced NO bioavailability imposes an upper limit on myocardial blood flow regulation and its transmural distribution. These effects are exacerbated after disconnection of intrinsic cardiac neurons from intact central neuron connections.

Impact of Chronic Kidney Disease on Myocardial Blood Flow Regulation in Dogs

Background/Aims: Chronic kidney disease (CKD) increases cardiovascular risk possibly due to coronary microvessel dysfunction and impaired myocardial flow reserve. This study investigated the effects of CKD on the regulation and transmural distribution of myocardial blood flow along with oxygen demand during intravenous dobutamine-induced increases in cardiac work. Methods: CKD was produced in dogs by a two-stage subtotal nephrectomy (kidney ablation-infarction model). Serum creatinine and blood urea nitrogen were evaluated during the development of CKD along with systemic blood pressure (tail-cuff plethysmography). After 5 weeks, the CKD dogs were staged according to the International Renal Interest Society staging system; all dogs were anesthetized and surgically prepared for blood flow studies. Data analyses were performed between sham control (CTR) and stage 1 and 2 CKD dogs. Results: At baseline, myocardial blood flow and diastolic aortic pressure were similar for all groups. During intravenous dobutamine, myocardial blood flow was markedly higher than CTR even though hematocrit levels declined with the severity of CKD. In the CTR dogs, myocardial blood flow increased in direct relation to cardiac work. However, in the CKD dogs (stage 1 and 2), maximum blood flow was achieved with low-dose dobutamine, indicating that coronary autoregulation is more readily exhausted with minimal increases in cardiac work during CKD. Conclusion: We report that CKD markedly impairs coronary vascular reserve and myocardial blood flow regulation which could contribute to greater cardiovascular risk and poor clinical outcomes in CKD patients.

Impact of anatomical and functional severity of coronary atherosclerotic plaques on the transmural perfusion gradient: a [15O]H2O PET study

Myocardial ischaemia occurs principally in the subendocardial layer, whereas conventional myocardial perfusion imaging provides no information on the transmural myocardial blood flow (MBF) distribution. Subendocardial perfusion measurements and quantification of the transmural perfusion gradient (TPG) could be more sensitive and specific for the detection of coronary artery disease (CAD). The current study aimed to determine the impact of lesion severity as assessed by the fractional flow reserve (FFR) on subendocardial perfusion and the TPG using [(15)O]H2O positron emission tomography (PET) imaging in patients evaluated for CAD. Sixty-six patients with anginal chest pain were prospectively enrolled and underwent [(15)O]H2O myocardial perfusion PET imaging. Subsequently, invasive coronary angiography was performed and FFR obtained in all coronary arteries irrespective of the PET imaging results. Thirty (45%) patients were diagnosed with significant CAD (i.e. FFR ≤0.80), whereas on a per vessel analysis (n = 198), 53 (27%) displayed a positive FFR. Transmural hyperaemic MBF decreased significantly from 3.09 ± 1.16 to 1.67 ± 0.57 mL min(-1) g(-1) (P < 0.001) in non-ischaemic and ischaemic myocardium, respectively. The TPG decreased during hyperaemia when compared with baseline (1.20 ± 0.14 vs. 0.94 ± 0.17, P < 0.001), and was lower in arteries with a positive FFR (0.97 ± 0.16 vs. 0.88 ± 0.18, P < 0.01). A TPG threshold of 0.94 yielded an accuracy to detect CAD of 59%, which was inferior to transmural MBF with an optimal cutoff of 2.20 mL min(-1) g(-1) and an accuracy of 85% (P < 0.001). Diagnostic accuracy of subendocardial perfusion measurements was comparable with transmural MBF (83 vs. 85%, respectively, P = NS). Cardiac [(15)O]H2O PET imaging is able to distinguish subendocardial from subepicardial perfusion in the myocardium of normal dimensions. Hyperaemic TPG is significantly lower in ischaemic myocardium. This technique can potentially be employed to study subendocardial perfusion impairment in more detail. However, the diagnostic accuracy of subendocardial hyperaemic perfusion and TPG appears to be limited compared with quantitative transmural MBF, warranting further study.

Abstract 19211: The Relationship Between Anatomical and Functional Coronary Artery Disease Severity and Transmural Myocardial Blood Flow Distribution

Objectives: To determine the impact of lesion severity as assessed by the fractional flow reserve (FFR) on the transmural perfusion gradient (TPG) using H215O positron emission tomography (PET) imaging in patients evaluated for coronary artery disease (CAD). Background: Myocardial ischemia occurs principally in the subendocardial layer, whereas conventional myocardial perfusion imaging provides no information on the transmural myocardial blood flow (MBF) distribution. Methods: Sixty-six patients evaluated for CAD were prospectively enrolled and underwent H215O PET imaging for quantification of TPG. Subsequently, invasive coronary angiography was performed and FFR obtained in all coronary arteries irrespective of the PET imaging results. Results: Thirty (45%) patients were diagnosed with significant CAD (i.e. FFR ≤ 0.80), whereas on a per vessel analysis (n=198), 53 (27%) displayed a positive FFR. Hyperemic MBF decreased significantly from 3.09 ± 1.16 to 1.67 ± 0.57 mL·min-1·g-1 (p &lt; 0.001) in nonischemic and ischemic myocardium, respectively. The TPG decreased during hyperemia as compared with baseline (1.20 ± 0.14 vs. 0.94 ± 0.17, p&lt;0.001), and was lower in arteries with a positive FFR (0.97 ± 0.16 vs. 0.88 ± 0.18, p&lt;0.01). A TPG threshold of 0.94 yielded anc accuracy to detect CAD of 59%, which was inferior to transmural MBF with an optimal cutoff of 2.20 mL·min-1·g-1 and an accuracy of 85% (p &lt; 0.001). Conclusions: Cardiac H215O PET imaging is able to detect TPGs and demonstrates a significantly lower hyperemic TPG in ischemic myocardium. However, the diagnostic accuracy of TPG seems to be limited compared to quantitative transmural MBF.

High rate right ventricular pacing causes global impairment of myocardial blood flow in an experimental model of heart failure

Purpose: Prolonged right ventricular (RV) pacing at high heart rate (HR) induces progressive left ventricle (LV) dysfunction in the experimental animal. It is unclear whether RV stimulation, either acute or prolonged, may also alter regional and global myocardial blood flow (MBF). The aim of this study is to assess regional and global MBF at spontaneous sinus rhythm and during RV apical pacing at baseline and after 4 weeks of prolonged high rate RV stimulation in a group of minipigs. Methods: Six adult minipigs underwent RV pacing (220 beats/min) for 4 weeks. Positron emission tomography (ECAT HR Plus, Siemens, CTI Inc.) and 2D-echocardiography (ECHO) were performed at baseline (PRE) and soon after interruption of 4 weeks high rate pacing (POST). Global and regional myocardial blood flow (MBF) ([13N]ammonia as a flow tracer) were quantified from PET data at spontaneous HR (PM-off) and during pacing at 20 beats over spontaneous HR (PM-on). LV fractional shortening (FS) was measured from ECHO. Results: From PRE to POST, FS significantly decreased from 37±0.8% to 20±0.5% (p<0.01). Prolonged high rate pacing caused also a significant decrease of global MBF from 1.09±0.24 ml/min/g (mean HR 71 bpm) to 0.78±0.26 ml/min/g (mean HR 83 bpm) (P<0.001) at PM-off and from 1.33±0.40 ml/min/g (mean HR 94 bpm) to 1.12±0.39 ml/min/g (mean HR 103 bpm) (p<0.001) at PM-on. Acute RV pacing induced LV dyssynchrony at ECHO and inhomogeneity of regional MBF distribution (higher flow in the septum than in the lateral wall) at baseline. After 4 weeks pacing acute RV stimulation still caused LV dyssynchrony which was no more able to induce regional MBF inhomogeneity (Table I). Table I MBF values are in ml/min/g. *p<0.001 vs PRE. Conclusions: Prolonged high rate RV pacing in minipigs causes global reduction in LV function and a global decrease of MBF as observed in clinical dilated cardiomyopathy. LV dyssynchrony, caused by acute RV stimulation, is associated with regional differences in MBF only at baseline. These results suggest that prolonged tachycardia more than dyssynchrony causes MBF impairment in RV pacing induced heart failure.

Hybrid image visualization tool for 3D integration of CT coronary anatomy and quantitative myocardial perfusion PET

Multimodal cardiac imaging by CTA and quantitative PET enables acquisition of patient-specific coronary anatomy and absolute myocardial perfusion at rest and during stress. In the clinical setting, integration of this information is performed visually or using coronary arteries distribution models. We developed a new tool for CTA and quantitative PET integrated 3D visualization, exploiting XML and DICOM clinical standards. The hybrid image tool (HIT) developed in the present study included four main modules: (1) volumetric registration for spatial matching of CTA and PET data sets, (2) an interface to PET quantitative analysis software, (3) a derived DICOM generator able to build DICOM data set from quantitative polar maps, and (4) a 3D visualization tool of integrated anatomical and quantitative flow information. The four modules incorporated in the HIT tool communicate by defined standard XML files: XML-transformation and XML MIST standards. The HIT tool implements a 3D representation of CTA showing real coronary anatomy fused to PET-derived quantitative myocardial blood flow distribution. The technique was validated on 16 data sets from EVINCI study population. The validation of the method confirmed the high matching between "original" and derived data sets as well as the accuracy of the registration procedure. Three-dimensional integration of patient- specific coronary artery anatomy provided by CTA and quantitative myocardial blood flow obtained from PET imaging can improve cardiac disease assessment. The HIT tool introduced in this paper may represent a significant advancement in the clinical use of this multimodal approach.

Mechano-energetics of the asynchronous and resynchronized heart

Abnormal electrical activation of the ventricles creates major abnormalities in cardiac mechanics. Local contraction patterns, as reflected by measurements of local strain, are not only out of phase, but often also show opposing length changes in early and late activated regions. As a consequence, the efficiency of cardiac pump function (the amount of stroke work generated by a unit of oxygen consumed) is approximately 30% lower in asynchronous than in synchronous hearts. Moreover, the amount of work performed in myocardial segments becomes considerably larger in late than in early activated regions. Cardiac Resynchronization Therapy (CRT) improves mechano-energetics of the previously asynchronous heart in various ways: it alleviates impediment of the abnormal contraction on blood flow, it increases myocardial efficiency, it recruits contraction in the previously early activated septum and it creates a more uniform distribution of myocardial blood flow. These factors act together to increase the range of cardiac work that can be delivered by the patients’ heart, an effect that can explain the increased exercise tolerance and quality of life reported in several CRT trials.

Estimates of systolic and diastolic myocardial blood flow by dynamic contrast‐enhanced MRI

Myocardial blood flow varies during the cardiac cycle in response to pulsatile changes in epicardial circulation and cyclical variation in myocardial tension. First-pass assessment of myocardial perfusion by dynamic contrast-enhanced MRI is one of the most challenging applications of MRI because of the spatial and temporal constraints imposed by the cardiac physiology and the nature of dynamic contrast-enhanced MRI signal collection. Here, we describe a dynamic contrast-enhanced MRI method for simultaneous assessment of systolic and diastolic myocardial blood flow. The feasibility of this method was demonstrated in a study of 17 healthy volunteers at rest and under adenosine-induced vasodilatory stress. We found that myocardial blood flow was independent of the cardiac phase at rest. However, under adenosine-induced hyperemia, myocardial blood flow and myocardial perfusion reserve were significantly higher in diastole than in systole. Furthermore, the transmural distribution of myocardial blood flow and myocardial perfusion reserve was cardiac phase dependent, with a reversal of the typical subendocardial to subepicardial myocardial blood flow gradient in systole, but not diastole, under stress. The observed difference between systolic and diastolic myocardial blood flow must be taken into account when assessing myocardial blood flow using dynamic contrast-enhanced MRI. Furthermore, targeted assessment of systolic or diastolic perfusion using dynamic contrast-enhanced MRI may provide novel insights into the pathophysiology of ischemic and microvascular heart disease.

A Novel 18 F-Labeled Tracer for the Quantification of Myocardial Blood Flow and Infarct Size With Positron-Emission Tomography

Currently, nuclear imaging techniques can be used to diagnose coronary macrovascular and microvascular disease and to measure infarct size and left ventricular ejection fraction. Semiquantitative assessment of regional myocardial perfusion with single-photon emission computed tomography is a noninvasive, robust, and widely available method of assessing myocardial ischemia and has an established role in the clinical setting.1 A great number of studies have assessed the sensitivity and specificity of this technique for the detection of coronary artery disease (CAD), with coronary arteriography usually being used as the standard by which the accuracy of scintigraphy is judged.1 The main limitation of single-photon emission computed tomography perfusion imaging is that it provides only semiquantitative information on the regional distribution of myocardial blood flow (MBF). This is particularly relevant in conditions in which MBF and coronary flow reserve (CFR) are diffusely abnormal, (eg, in patients with hypertrophic and dilated cardiomyopathies).2 Article p 77 The ability to make quantitative measurements of MBF with positron-emission tomography (PET) allows determination of the functional significance of epicardial coronary lesions. In patients with single-vessel CAD, chronic stable angina, and no previous history of myocardial infarction (MI), CFR in response to a standard dose of dipyridamole was found to be markedly reduced in the myocardial regions subtended by the stenosed coronary artery compared with regions subtended by angiographically normal vessels.3 Using H215O or 13NH3 with PET, the relationship between stenosis severity, measured by quantitative coronary angiography, and its consequences on regional MBF and CFR has been …

Transmural Peak Systolic Strain and Strain Rate Predict Transmural Myocardial Blood Flow in a Pig Myocardial Infarction Model

Objective: To test the hypothesis that the transmural variation of the longitudinal myocardial peak systolic strain (Sp) and strain rate (SRp) can predict the transmural distribution of myocardial blood flow (MBF) in a pig model of acute myocardial infarction. Methods: The longitudinal Sp and SRp were measured by echocardiography in both subendocardium (Sp-endo, SRp-endo) and subepicardium (Sp-epi, SRp-epi) in the normal, ischemic and infarct segments, respectively. The MBF in corresponding sites was measured by colored microspheres technique. The subendocardial to subepicardial ratio of Sp (Sp-EER), SRp (SRp-EER) and MBF (MBF-EER) were calculated. Results: In the normal segments, Sp-endo and SRp-endo were significantly higher than Sp-epi and SRp-ep, respectively. In the ischemic segments, Sp-endo and SRp-endo decreased to a greater extent than Sp-epi and SRp-epi, respectively. In the infarct segments, Sp-endo, SRp-endo Sp-epi and SRp-epi were all remarkably reduced. High correlations were found between Sp and SRp measurements and MBF in both subendocardium and subepicardium (r = –0.75 to –0.84, p < 0.001). Conclusion: Strain and strain rate imaging provides a reliable approach to the noninvasive estimation of the transmural blood distribution across the normal, ischemic and infarct segments.

Direct His bundle pacing preserves coronary perfusion compared with right ventricular apical pacing: a prospective, cross-over mid-term study

The His bundle is regarded as the most physiological site for ventricular pacing, in that it avoids the adverse effects of right ventricular apical pacing (RVAP). However, very few studies have compared the effects of direct His bundle pacing (DHBP) and RVAP. The aim of our study was the intra-patient comparison of myocardial perfusion corresponding to these two different pacing techniques, as perfusion expresses local workload and is related to long-term outcome. Twelve consecutive patients with standard pacemaker indication (9 male, 74 +/- 9 years) entered the study. Pacing leads were implanted in the right ventricular apex and directly in the His bundle, and were connected to different ports of the pacemaker. All patients first underwent 3 months of DHBP, followed by 3 months of RVAP. At the end of each 3-month period, myocardial perfusion was measured at rest using scintigraphy with Tc99m-SestaMIBI. The average values of perfusion were evaluated on a 20-segment basis. All patients also underwent clinical evaluation, echocardiography, and tissue Doppler imaging (TDI), to measure dyssynchrony, and a blood sample was taken for brain natriuretic peptide (BNP) assay. The perfusion score during DHBP pacing was significantly better than during RVAP (0.44 +/- 0.5 vs. 0.71 +/- 0.53, respectively; P = 0.011). None of the patients showed lower perfusion during DHBP than during RVAP. We found no significant difference in NYHA class, ventricular volumes, ejection fraction, or plasmatic BNP between DHBP and RVAP. However, mitral regurgitation (0.26 +/- 0.21 vs. 0.37 +/- 0.25; P < 0.001) and dyssynchrony (13.75 +/- 4.28 vs. 22.02 +/- 8.44; P = 0.008) were significantly less during DHBP than during RVAP. Direct His bundle pacing is superior to RVAP in preserving the physiologic distribution of myocardial blood flow and reducing mitral regurgitation and left ventricular dyssynchrony.

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

Effects of single-ventricle physiology with aortopulmonary shunt on regional myocardial blood flow in a piglet model

In single-ventricle physiology with aortopulmonary connection, diastolic hypotension could alter regional myocardial blood flow. Also, afterload increases could impair myocardial blood flow by increased wall tension and relative subendocardial malperfusion. This study explores the effects of acute single-ventricle physiology on regional myocardial blood flow distribution and investigates the consequences of moderate afterload augmentation on myocardial blood flow. Single-ventricle physiology was created in 8 piglets without using bypass, and 8 animals served as a sham control group. Aortopulmonary shunt, echo-guided atrial septostomy, tricuspid valve avulsion, and pulmonary artery occlusion allowed the left ventricle to support systemic and pulmonary circulations. Afterload augmentation was produced by aortic balloon inflation. Physiologic recordings and stable-isotope microsphere determination of myocardial blood flow to the subepicardium and subendocardium were obtained at baseline and during single-ventricle physiology (at 30 minutes, 120 minutes, and afterload increase). Arterial oxygen content, diastolic pressure, and coronary perfusion pressure declined after creation of single-ventricle physiology (P < .05). Acute single-ventricle physiology resulted in higher myocardial blood flow (P < .05), unchanged subendocardial/subepicardial flow ratio and oxygen delivery, and lower coronary resistance (P < .01) as compared with biventricular physiology. Afterload augmentation increased coronary perfusion pressure, causing a trend for higher myocardial blood flow and oxygen delivery (P = NS), without affecting subendocardial/subepicardial flow distribution. Myocardial oxygen supply/demand balance fell in single-ventricle physiology, remaining unchanged during afterload augmentation. Our study demonstrates that, in acute single-ventricle physiology with aortopulmonary shunt, myocardial blood flow is maintained by lower coronary perfusion pressure. Further, single-ventricle physiology results in less favorable myocardial oxygen supply/demand balance, although normal transmural myocardial blood flow distribution is maintained. Avoidance of diastolic runoff (ventricle-pulmonary conduit) could improve coronary reserve. In our study, moderate afterload augmentation did not induce relative subendocardial malperfusion, nor did it worsen oxygen supply/demand balance.

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.

Rapid ventricular pacing induces delayed cardioprotection against myocardial stunning

Tachycardia with rapid ventricular pacing induces delayed preconditioning against arrhythmias secondary to coronary artery occlusion (CAO) and reperfusion (CAR) but its effects on myocardial stunning remains unknown. Accordingly, we investigated whether delayed preconditioning with ventricular pacing develops against myocardial stunning and whether this phenomenon is triggered by reactive oxygen species. Eight chronically instrumented conscious dogs underwent three experimental sequences in a random order a week apart: (a) 10-min CAO (coronary occluder) followed by CAR, i.e. “Control” sequence; (b) pacing (right ventricular electrodes, 240 beats/min during 40 min) performed 24 h before the 10-min CAO, i.e. “PC” sequence; and (c) N-(2-mercaptopropionyl)-glycine (MPG, 100 mg/kg per h) administered concomitantly to pacing and 10-min CAO performed 24 h later, i.e. “PC + MPG” sequence. During “Control”, left ventricular (LV) wall thickening (%, sonomicrometry) was dramatically reduced during CAO (–96 ± 5% from 2.9 ± 0.4 mm) and remained depressed during CAR demonstrating myocardial stunning. During “PC”, LV wall thickening was not altered by pacing per se and was similarly decreased during CAO vs. “Control”. However, during CAR, LV wall thickening was improved vs. “Control” (e.g. –24 ± 5% and –8 ± 4% from corresponding baseline for “PC” and “Control”, respectively at 2 h-CAR; P < 0.05), demonstrating delayed preconditioning. Administration of MPG during pacing ( n = 5) abolished the beneficial effects of pacing. Myocardial lactate extraction and transmural distribution of regional myocardial blood flow (fluorescent microspheres) were not modified, by pacing. In conclusion, tachycardia with rapid ventricular pacing induces delayed cardioprotection against myocardial stunning. The production of reactive oxygen species independently from ischemia appears to be a major trigger for this phenomenon.