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Abacavir is a component of the recommended regimen of dolutegravir/ abacavir/lamivudine order januvia no prescription blood glucose 360. Reasons for considering switching therapy in such patients include the development of adverse effects buy 100mg januvia otc diabetes diet for dummies, the benefits of reducing dosages or the number of pills to be taken buy 100 mg januvia otc diabetes mellitus y odontologia, or the occurrence of drug-drug interactions purchase januvia us diabetes syndrome x diet. Some patients may benefit from switching even if they are doing well on their current treatment. For instance, switching is reasonable for patients taking regimens containing stavudine, didanosine, or zidovudine because of long-term toxic effects or regimens of older protease inhibitors that have higher pill burdens and greater metabolic toxicities than darunavir or atazanavir. Some drugs that are no longer recommended for initial use may be safely continued for patients who are tolerating them. For example, although nevirapine and efavirenz have substantial early toxic effects, they are safe and tolerable over the 56 long term. Genotypic resistance assays for reverse-transcriptase and protease should be ordered for all patients. Routine pretreatment screening for integrase resistance is not currently routinely recommended. Other laboratory assessments should be individualized, in keeping with current guidelines. Both protease inhibitors and non-nucleoside reverse-transcriptase inhibitors can affect cytochrome P450 isoforms. Both simvastatin and lovastatin blood levels increase dramatically with protease inhibitor use, and thus these statins are contraindicated with protease inhibitors because of the risk of rhabdomyolysis. Atorvastatin blood levels increase to a lesser extent, so that it may be used at lower doses. Rosuvastatin has minimal P450 metabolism, although levels appear to be increased when it is used in combination with atazanavir/ritonavir and lopinavir/ritonavir, so limiting doses to 10 mg with those drugs is advised. Statin therapy, when dose adjusted for drug-drug interactions, was associated with low rates of adverse events. Fibrates and statins have a drug-drug interaction and should be used only at low doses when combined. In a recent placebo-controlled trial, atorvastatin decreased the volume of such noncalcified plaques and also decreased their high-risk features, but no impact on vascular inflammation 64 or inflammatory markers was demonstrated. Studies comparing different models have yielded quite different results with less overlap than would be expected. None of these markers have been developed to the point where they are used clinically to aid in the diagnosis of coronary disease. In addition, if all plaques are noncalcified, the diagnosis of coronary disease would be missed. Statin therapy, smoking cessation, and aggressive control of hypertension and diabetes become mandatory in this setting. It includes intimal thickening of small pulmonary arteries with plexogenic lesions in the media, leading ultimately to obstruction of small pulmonary arteries. The drug-drug interaction between calcium channel blockers and protease inhibitors means that the dose of the calcium channel blocker should be limited. Of note, the recommended dose of bosentan for individuals taking protease inhibitors is 62. Sildenafil is metabolized by the 3A4 isoform of the cytochrome P450 system, and interactions have been described with the protease inhibitors saquinavir, ritonavir, and indinavir. Now that the disease has changed to more nuanced myocardial dysfunction, the understanding of mechanisms has become more nuanced as well. Proinflammatory cytokines such 80 as interleukin-1β and tumor necrosis factor have also been shown to depress systolic function. Symptoms of heart failure or echocardiographic evidence of cardiomyopathy 80 greatly increase the risk of death. Patients with a contractile reserve were also more likely to experience an improvement in the ejection fraction. Pathologic examination of affected vessels revealed subintimal fibrosis, disruption of the internal elastic lamina, and thinning of the media layer. Yet even treated individuals with well-controlled infection show evidence of inflammation and immune activation, and probably are at increased risk for stroke. Arterial Disease in Patients With Human Immunodeficiency Virus InfectionWhat Has Imaging Taught Us? A prospective, randomized clinical trial of antiretroviral therapies on carotid wall thickness. Safety and Long-term Outcomes After Percutaneous Coronary Intervention in Patients with Human Immunodeficiency Virus. Outcomes of patients with human immunodeficiency virus infection undergoing cardiovascular surgery in the United States. Comparative safety and efficacy of statins for primary prevention in human immunodeficiency virus-positive patients: a systematic review and meta-analysis. Epicardial Fat is Associated with Duration of Antiretroviral Therapy and Coronary Atherosclerosis. Carotid intima-media thickness among human immunodeficiency virus-infected patients without coronary calcium. Arterial disease in patients with human immunodeficiency virus infection: what has imaging taught us? Prevalence and hospital discharge status of human immunodeficiency virus–associated pulmonary arterial hypertension in the United States. Heart failure in patients with human immunodeficiency virus infection: epidemiology, pathophysiology, treatment, and future research. Human Immunodeficiency Virus and Heart Failure in Low- and Middle-Income Countries. Declining Incidence of Systolic Left Ventricular Dysfunction in Human Immunodeficiency Virus–Infected Individuals Treated With Highly Active Antiretroviral Therapy. Effect of Left Ventricular Dysfunction and Viral Load on Risk of Sudden Cardiac Death in Patients With Human Immunodeficiency Virus. Anatomy and Physiology of the Pericardium The pericardium is composed of two layers, the visceral pericardium, a monolayer of mesothelial cells and collagen and elastin fibers adherent to the epicardial surface of the heart, and the fibrous parietal 1 layer, which is normally about 2 mm thick and surrounds most of the heart (Fig. The parietal pericardium is largely acellular and contains collagen and elastin fibers. The visceral pericardium reflects back near the origins of the great vessels and is continuous with and forms the inner layer of the parietal pericardium. The pericardial space or sac is contained within these two layers, and normally contains up to 50 mL of serous fluid. The reflection is a few centimeters proximal to the junctions of the caval vessels with the right atrium; thus, portions of the caval vessels lie within the pericardial sac. Posterior to the left atrium, the reflection occurs at the oblique sinus of the pericardium.

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Cases involving three or more levels are at high risk for excessive soft-tissue swelling and airway obstruction discount januvia diabetic diet juice, and continued intubation may be a strong consideration discount 100 mg januvia amex is diabetes in dogs fatal. Prior to turning the patient prone cheap januvia 100 mg without prescription diabetes signs hands, a head holder (Mayfield versus Gardner-Wells) is applied cheap 100mg januvia amex diabetes insipidus diagnostic test, and the surgeon generally controls the head while the anesthesiologist controls the airway in the process of log-rolling. As with the anterior approach, the arms are tucked in at the side, and gentle traction is applied for visualization of the entire cervical spine with fluoroscopy. The hips and knees are gently flexed in a sling while the remainder of the body is supported by bolsters allowing the abdomen to hang free on an open frame (Jackson) operating table. A reverse Trendelenburg position further aids in distribution of blood into the abdomen and legs. An extensive exposure can be created from the greater occipital protuberance to the thoracic spine. Dissection is carried down sharply through subcutaneous tissue and fat to the trapezius fascia with care taken to stay in the midline. A dry surgical dissection with electrocautery can be achieved in this manner as the ligamentum nuchae is relatively avascular. Subperiosteal dissection is then carried from the tip of the spinous processes over the laminae elevating the paraspinal muscles as a cuff. Depending on the intended surgery, procedures such as laminoforaminotomies, laminotomies, and laminectomies can be performed. Blood loss may be significant depending on the length of surgery as well as the extent of bony resection. Usual preop diagnosis: Cervical radiculopathy, cervical myelopathy, spinal cord syndromes secondary to trauma Suggested Readings 1. Audu P, Artz G, Scheid S, et al: Recurrent laryngeal nerve palsy after anterior cervical spine surgery: the impact of endotracheal tube cuff deflation, reinflation, and pressure adjustment. Hukuda S, Mochizuki T, Ogata M, Shichikawa K, Shimomura Y: Operations for cervical spondylotic myelopathy. Jung A, Schramm J, Lehnerdt K, Herberhold C: Recurrent laryngeal nerve palsy during anterior cervical spine surgery: a prospective study. Types of scoliosis include idiopathic, congenital, neuromuscular, myopathic, traumatic, tumor-related, and mesenchymal disorders. Normally, the cervical spine and lumbar spine are lordotic, whereas the thoracic spine is kyphotic. The instrumentation is intended to stabilize the spine until bony fusion of the spine has occurred. After the fusion is solid (6–12 mo), the instrumentation may be removed if it is broken, causes protrusions or lumps in the back, or the patient is having residual back pain. Nonscoliotic patients presenting for this surgery may have spinal instability as a result of trauma, metastatic cancer, or infection (e. The patients with metastatic cancer may need a careful workup with regard to respiratory, nutritional, and chemotherapeutic status. For operations in the prone position, use a wire-reinforced tube to prevent kinking and airway obstruction. Adamus M, Hrabalek L, Wanek T, Gabrhelik T, Zapletalova J: Intraoperative reversal of neuromuscular block with sugammadex or neostigmine during extreme lateral interbody fusion, a novel technique for spine surgery. Buvanendran A, Thillainathan V: Preoperative and postoperative anesthetic and analgesic techniques for minimally invasive surgery of the spine. Fritzell P, Hagg O, Wessberg P, et al: Chronic low back pain and fusion: a comparison of three surgical techniques: a prospective multicenter randomized study from the Swedish Lumbar Spine Study Group. Hoppenfeld S, deBoer P: Surgical Exposures in Orthopaedics: The Anatomic Approach, 2nd edition. O’Brien T, Akmakjian J, Ogin G, et al: Comparison of one-stage versus two- stage anterior/posterior spinal fusion for neuromuscular scoliosis. Schubert A, Deogaonkar A, Lotto M, Niezgoda J, Luciano M: Anesthesia for minimally invasive cranial and spinal surgery. Suggested Viewing Links are available online to the following videos: Posterior Spinal Instrumentation & Fusion for Idiopathic Scoliosis: http://www. Major trauma mechanisms produce pelvic-ring injuries, and patients with pelvic-ring disruptions frequently have associated systemic injuries, which may be life-threatening (e. Pelvic stabilization and surgical control of hemorrhage may be performed acutely in the polytrauma patient who is hemodynamically unstable. This is in conjunction with an exploratory laparotomy performed by a trauma surgeon. Pelvic fractures that do not heal are “nonunions,” whereas those that heal in an unsatisfactory position are “malunions. These procedures are often lengthy and are staged, requiring changes in patient position. The posterior approach requires a large operative field, which may prevent the use of an epidural catheter. The goal of pelvic reconstruction is to restore the anatomy and stability of the pelvis, which will decrease hemorrhage in the hemodynamically unstable patient, aid in mobilization of the multiply injured patient, and improve long-term function. Schematic view of the principal pelvis injury patterns, as determined by the vector of the provocative blow. Prevezas N: Evolution of pelvic and acetabular surgery from ancient to modern times. The pins for the external fixator are inserted into the iliac crest either percutaneously or through small incisions. In some centers, this procedure is done in the emergency department as a lifesaving procedure. Prevezas N: Evolution of pelvic and acetabular surgery from ancient to modern times. The goal of surgical treatment of acetabulum fractures is to preserve the hip joint by accurately reconstructing the supporting bony anatomy. Surgical treatments of these challenging injuries are performed by surgeons who have undergone specialized training in orthopedic pelvic surgery. Associated injuries to the pelvis are common, as are associated systemic injuries. The most difficult portion of the procedure is the reduction; it may be facilitated by neuromuscular relaxation, pelvic reduction instruments, and traction. A radiograph also is obtained at the end of the case to verify a satisfactory reduction and position of the implants. Patients are anticoagulated in the postop period to prevent thromboembolic complications. Weight-bearing restrictions are maintained until enough healing has occurred to permit functional ambulation. Ilioinguinal approach, right side: (i) Penrose drain around iliopsoas, femoral nerve, and lateral femoral cutaneous nerve; (ii) Penrose drain around femoral vessels; (iii) bladder and space of Retzius; (iv) pubis; (v) pubic tubercle; (vi) symphysis pubis; (vii) Penrose drain around spermatic cord. Extended iliofemoral approach: (i) Gluteus minimus tendon; (ii) gluteus medius tendon; (iii) gluteus maximus tendon; (iv) superior gluteal neurovascular bundle; (v) sciatic nerve; (vi) piriformis and conjoint tendons; (vii) hip joint capsule; (viii) greater trochanter; (ix) medial femoral circumflex artery overlying quadratus femoris. Prevezas N: Evolution of pelvic and acetabular surgery from ancient to modern times. This condition of the hip produces joint incongruity and instability, eventually leading to arthrosis and a dysfunctional hip joint.

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Induction of pluripotent stem cells from adult human fibroblasts by defined factors januvia 100 mg online diabetes prevention 5 tips for taking control. Differentiation of human embryonic stem cells and induced pluripotent stem cells to cardiomyocytes: a methods overview purchase generic januvia on line diabetes prevention in india. Genetic and epigenetic regulation of human cardiac reprogramming and differentiation in regenerative medicine discount januvia 100mg on-line diabetes medications and cancer risk. Robust cardiomyocyte differentiation from human pluripotent stem cells via temporal modulation of canonical Wnt signaling purchase januvia with amex blood sugar 96. Distinct metabolic flow enables large-scale purification of mouse and human pluripotent stem cell-derived cardiomyocytes. Concise review: maturation phases of human pluripotent stem cell-derived cardiomyocytes. Human induced pluripotent stem cell-derived cardiomyocytes: insights into molecular, cellular, and functional phenotypes. Sinoatrial node cardiomyocytes derived from human pluripotent cells function as a biological pacemaker. Human engineered heart muscles engraft and survive long term in a rodent myocardial infarction model. Engineered heart tissues and induced pluripotent stem cells: macro- and microstructures for disease modeling, drug screening, and translational studies. Potential strategies to address the major clinical barriers facing stem cell regenerative therapy for cardiovascular disease: a review. Human embryonic-stem-cell-derived cardiomyocytes regenerate non-human primate hearts. Human embryonic stem cell-derived cardiac progenitors for severe heart failure treatment: first clinical case report. Lineage reprogramming of fibroblasts into proliferative induced cardiac progenitor cells by defined factors. Automated, high-throughput derivation, characterization and differentiation of induced pluripotent stem cells. Genome editing of human pluripotent stem cells to generate human cellular disease models. Human induced pluripotent stem cells as a platform for personalized and precision cardiovascular medicine. Abnormal calcium handling properties underlie familial hypertrophic cardiomyopathy pathology in patient-specific induced pluripotent stem cells. Study familial hypertrophic cardiomyopathy using patient-specific induced pluripotent stem cells. Patient-specific induced pluripotent stem cells as a model for familial dilated cardiomyopathy. Modeling the mitochondrial cardiomyopathy of Barth syndrome with induced pluripotent stem cell and heart-on-chip technologies. Screening drug-induced arrhythmia using human induced pluripotent stem cell-derived cardiomyocytes and low-impedance microelectrode arrays. Assessment of beating parameters in human induced pluripotent stem cells enables quantitative in vitro screening for cardiotoxicity. Human induced pluripotent stem cell-derived cardiomyocytes recapitulate the predilection of breast cancer patients to doxorubicin-induced cardiotoxicity. High-throughput screening of tyrosine kinase inhibitor cardiotoxicity with human induced pluripotent stem cells. Human induced pluripotent stem cell–derived cardiomyocytes as an in vitro model for coxsackievirus B3–induced myocarditis and antiviral drug screening platform. Drug screening using a library of human induced pluripotent stem cell–derived cardiomyocytes reveals disease-specific patterns of cardiotoxicity. A small-molecule inhibitor of sarcomere contractility suppresses hypertrophic cardiomyopathy in mice. Allele-specific silencing of mutant Myh6 transcripts in mice suppresses hypertrophic cardiomyopathy. Successful therapies have since rerouted the course of almost every cardiovascular disease (Fig. Early coronary revascularization and secondary prevention have increased survival after acute myocardial infarction, with a parallel increase in the prevalence of heart failure (see Chapter 21). Improved surgical techniques for congenital heart disease have created a growing population of adults with unique structural heart disease (see Chapter 75). Advances in cancer chemotherapy and radiation have left many survivors with new, life-threatening cardiac disease (see Chapter 81). Widespread use of neurohormonal blockade and implantable devices in patients with reduced left ventricular ejection fraction has contributed to a decrease in sudden death associated with prolongation of life and death with pump failure (see Chapter 25). The aging of the population yields an increasing number of patients with senile aortic stenosis and vascular pathology who may now be eligible for percutaneous procedures, but they remain limited by the multimorbidity and frailty that rendered them 1 ineligible for open surgery in the first place (see Chapter 88). Patients with a history of myocardial infarction or dilated cardiomyopathy have extended survival with good quality of life, particularly because of decreases in ventricular remodeling and decreases in sudden death, as well as decreased reinfarction with coronary artery disease. Both heart failure and aortic stenosis are often diagnosed in the aging population, in whom the increased prevalence of diabetes and obesity also increase symptoms and death from noncardiac comorbidities. Once prolongation of life no longer drives treatment, the focus of disease management shifts to palliation of symptoms. Unfortunately, in practice, this shift too often jolts patients and families as a sudden reversal of strategy from “do everything” to “do nothing,” rather than a gradual transition away from procedural intervention through a phase of care increasingly but not exclusively focused on quality of life. Guiding patients and families to understand prognosis and express goals of care is crucial for them to share in decisions about the intensity and timing of care. When a cardiac condition is likely to cause or accelerate death within the coming year, cardiac specialists may often have a good vantage point from 2 which to survey the disease trajectory and steer the direction of care. Ideally, patients continue to the end guided by health care providers who maintain longitudinal relationships with them and apply palliative care principles to smooth this journey. This chapter clarifies main concepts and provides practical approaches to the management of patients with cardiovascular disease nearing the end of life (Table 31. Worsening disease should trigger preparation with patients and families, but without specifically answering the question of how much time remains, which is usually bounded by wide uncertainty. Shared decisions include a broad spectrum of potential interventions beyond those relating to resuscitation preferences. Deactivation of the defibrillation function of implantable cardioverter-defibrillators should be explained and offered regularly to patients with poor prognosis and must be done before transition to hospice. Palliative care specialist consultation may be particularly helpful to facilitate decision making within challenging family dynamics and to improve relief of refractory symptoms. Clinicians with existing relationships should shoulder the primary responsibility for presenting an end-of-life plan consistent with values and goals expressed by patient and family. The transition separating “do everything” from hospice may be bridged through a phase of “quality survival” during which patients increasingly weigh the benefits, risks, and burdens of initiating or continuing life-sustaining treatments. Revision of the medical regimen for symptom relief and quality of life may involve discontinuation of some recommended therapies and addition of therapies not usually recommended. The end-of-life plan should honor patient preference for the site of death as feasible, with agreement on a “plan B” if that becomes unsupportable.

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B discount januvia 100 mg fast delivery diabetes mellitus headaches, The polar map quantitation documents defects crossing into all vascular territories purchase januvia overnight blood sugar tester, with extensive reversibility (white cross-hatched area discount 100mg januvia fast delivery diabetes prevention with exercise, white arrow) generic januvia 100 mg with visa blood sugar emergency, and a small irreversible area in the basal inferior wall (blacked-out area, yellow arrow). Reporting guidelines also outline the elements of a comprehensive reporting structure when 7 semiquantitative and/or quantitative analysis are used. Bayes theorem posits that the post-test probability of disease (or risk of an event after a test) is influenced not only by the sensitivity and specificity of the test, but also by the pretest probability of disease (see Chapter 13). For a given positive test result, the post-test probability of disease may be distinctly lower in a patient with a very low pretest probability of disease compared with a different patient with a much higher pretest probability (eFig. A, For patient with low pretest probability of disease (point A at 15% on x axis) with a positive test result, post-test probability of disease (point A at 50% on y axis) is lower than for a different patient with a higher pretest probability with the same positive test result (point B at 50% pretest probability on x axis, 90% post-test probability on y axis). In B, the “test positive” curve can be thought of as a family of curves influenced by how strongly positive the images can be. For a given pretest probability, the post-test probability becomes progressively higher as the image becomes more strongly abnormal. For a borderline abnormal study (+ curve), the post-test probability may be only slightly higher than the pretest value. For a strongly positive study (+++ curve), the post-test probability is very high no matter what the pretest probability. If reported as positive, there is actually a greater chance that such a result represents a false-positive result (70%) as opposed to a true-positive result (30%). Although this defect may represent a small area of inferior inducible ischemia, the image also may reflect diaphragm attenuation of the inferobasal wall predominantly affecting the stress image. A result reported as positive is more likely to represent a false-positive than a true-positive finding. Lung Uptake In some patients, substantial tracer uptake is apparent throughout the lung fields after stress that is not present at rest (Fig. It is likely that ischemia-induced elevation in left atrial and pulmonary pressures slows pulmonary transit of the tracer, allowing more time for extraction or transudation into the interstitial spaces of the lung, accounting for this imaging sign. Splanchnic or background activity is minimal after thallium stress injection, allowing image acquisition earlier after stress. In addition, the redistribution properties of thallium mandate that imaging begin relatively early after stress, so lung uptake may be more apparent. For patients in whom the entire left ventricle appears larger during stress, the pathophysiology probably is related to extensive ischemia and prolonged postischemic systolic dysfunction, resulting in a dilated, dysfunctional left ventricle during the stress acquisition relative to the rest acquisition. Contemporary processing systems can automatically quantify transient ischemic dilation. These perturbations from a completely homogeneous tracer pattern throughout the myocardium are related to structural variations of the myocardium as well as to technical factors associated with image acquisition. One example is the “dropout” of the upper septum secondary to merging of the muscular septum with the membranous septum (Fig. Apical thinning is another variation of normal that can be mistaken for a perfusion defect (Fig. The apex is anatomically thinner than other myocardial regions, creating this appearance. This difference is not caused by a disparity in lateral versus septal wall myocardial blood flow. A, Normal “dropout” of the basal septum (arrows), which would be seen in the most basal short-axis tomograms. C, The lateral wall often is slightly “hotter” than the septum, another normal variation. This refers to undetected events in the heart caused by interaction of photons with the intervening soft tissue, breast, or diaphragm. In patients with large or dense breasts, significant attenuation may create artifacts varying considerably in their appearance and location (Fig. A review of the cine display of the raw projection images 5 may reveal the presence of potential breast attenuation. The availability of gender-matched quantitative databases has had a favorable although modest impact on this issue, because such databases generally consist of individuals of average body and breast size. There was a suggestion of breast shadowing on review of the raw cine images (not shown). Thus this defect may represent either a nontransmural anterior infarct or an artifact consistent with breast attenuation. In both views, wall thickening from end diastole to end systole (arrows) appears normal. This appearance is most consistent with an attenuation artifact, because an infarct would be expected to result in abnormal wall thickening. Several approaches to minimizing the impact of breast tissue have been taken to improve specificity (lowering the false-positive rate) in women. The presence of preserved wall motion in the setting of a mildly to moderately severe fixed defect of the anterior or anterolateral wall suggests the absence of infarction and supports the interpretation of attenuation artifact (Fig. This artifact may be caused by extracardiac structures, such as the diaphragm overlapping the inferior wall (Fig. Top row, Standard supine images show an apparent inferior perfusion defect (white arrow). There was substantial diaphragm overlap of the inferior wall on the raw projection images (not shown), and the exercise stress test was very low risk, both suggesting that the defect was a false positive. Bottom row, The patient was reimaged in the prone position, which helps to create more separation between the diaphragm and the inferior wall. The prone images show normal perfusion of the inferior wall (yellow arrows), suggesting that the defect seen on the supine imaging was indeed a false positive. By imaging the patient in the prone position, the inferior wall is shifted away from the diaphragm and is therefore less subject to attenuation (Fig. When such a structure is near the heart, increased counts may reach the detector, falsely elevating the number of counts the system assigns to the nearby cardiac wall, so the cardiac region is displayed as falsely “hotter. Having the patient drink cold water may enhance clearance of tracer from visceral organs, particularly the bowel. To measure the attenuation correction factor, a rod that rotates about the patient is filled with a relatively long-lived positron emitter, germanium-68, or a single-photon emitter, cesium-137. The rod is first made to rotate at a fixed speed in the gantry, and total coincident counts are measured without the patient (the blank scan) and repeated with the patient (the transmission scan). The ratio of coincident counts of blank scan and those of transmission scan yields the array of attenuation correction factors needed to correct each projection line. Once each projection line has been corrected for attenuation (and scatter), the emission data may be reconstructed into an attenuation-corrected emission image for clinical interpretation. This recommendation presumes that, when it is performed, the attenuation correction methodology is applied by personnel highly knowledgeable about the technique and its stringent quality control. A, The scintigraphic acquisition data are collected in conjunction with the electrocardiogram. The R-R interval is divided into a prespecified number of “frames” (in this example, eight frames). At a heart rate of 60 beats/min (1000 msec/beat), each of the eight frames would comprise 125 milliseconds. For the first 125 milliseconds after the peak of the initial R wave, all imaging data are recorded in frame 1; the second 125 milliseconds are recorded in frame 2, and so on, until the peak of the next R wave is detected, and this is repeated for each beat in the acquisition.