Showing 1 – 20 of 1242
Relevance | Newest | Oldest |
  • JAMA March 6, 2013

    Figure 5: Relationship of Scarring to Myocardial Remodeling

    A, Inverse relationship between scar burden and change in regional end-diastolic wall thickness (EDWT) after revascularization. Data were fit using linear regression (n = 42 patients). B, Patients dichotomized into those with limited scar burden (≤50%) and those with extensive scar burden (>50%). Dotted line represents an end-diastolic wall thickness (EDWT) of 5.5 mm, below which defined regional wall thinning. In patients with limited scar burden, there was reversal of thinning (ie, significant increase in EDWT) after revascularization (P < .001; P = .14 in those with extensive scarring). Error bars indicate 95% CIs. C and D, Change in EDWT was not related to change in LV mass (C) but was related to global LV end-diastolic volume (D). Data were fit using linear regression (n = 42 patients).
  • Prevalence of Regional Myocardial Thinning and Relationship With Myocardial Scarring in Patients With Coronary Artery Disease

    Abstract Full Text
    free access has multimedia
    JAMA. 2013; 309(9):909-918. doi: 10.1001/jama.2013.1381
    To determine the relationship of regional myocardial thinning to myocardial scarring and functional improvement, Shah and coauthors assessed myocardial thinning and scarring and changes in myocardial morphology and function in patients with known coronary artery disease. Gupta and coauthors provide comment in the related Editorial.
  • JAMA March 6, 2013

    Figure 6: Cardiovascular Magnetic Resonance (CMR) Imaging and Electrocardiographic Changes in an Example Patient with Wall Thinning and Limited Scar Burden

    A, Before revascularization, cine-CMR still frames in systole and diastole demonstrate akinesis and thinning of the anteroseptal, anterior, and apical walls. Delayed-enhancement images demonstrate limited scar burden (≤50%) within the thinned region. B, The electrocardiogram (ECG) demonstrates QS complexes in leads V1 through V3, with poor R-wave progression. C, After revascularization, cine-CMR still frames demonstrate improvement in myocardial contractility along with reversal of thinning in the previously thinned region. End-diastolic wall thickness changed from 4.5 to 9.5 mm after revascularization. D, The ECG, following revascularization, demonstrates presence of r waves in leads V1 through V3 that were not previously present. Full-motion cine sequences can be viewed here.
  • JAMA December 12, 2012

    Figure 4: Improvement in Early Enhancement Defect (EED) After Transendocardial Allogeneic Stem Cell Injection

    Upper panel, baseline early-phase short-axis multidetector computed tomography images in a representative patient with chronic myocardial infarction (EED total, 40.34 g). Lower panel, 13 months after transendocardial stem cell injection of allogeneic mesenchymal stem cells (100 million cells). There was a decrease of 34.68% in EED (26.35 g). The reduction of the myocardial defects was accompanied by decrease of end-diastolic volume from 433.68 mL to 365.81 mL, decrease of end-systolic volume from 371.83 mL to 277.38 mL, increase of ejection fraction from 14.26% to 24.17%, and improvement of sphericity index from 0.60 to 0.51. See Interactive of the patient’s 3D multidetector tomography scan reconstructions showing the EED before and after transendocardial stem cell injection.
  • JAMA September 5, 2012

    Figure 1: Representative Examples of Cardiac Magnetic Resonance Images Showing Recognized MI, No MI, and Unrecognized MI

    All images are short-axis view, cardiac magnetic resonance (CMR) with late gadolinium enhancement (LGE) on the left and end-diastolic cine frames on the right. A, Recognized myocardial infarction (MI) involving the typical left anterior descending artery distribution (arrowhead). On LGE images, an MI is brighter than remote or normal myocardium, which appears dark. B, Participant with no evidence of MI. The myocardium is uniformly dark (“nulled”) on the LGE image. C, Unrecognized MI in the basal inferolateral wall (arrowhead). D, Two unrecognized MIs in different coronary territories in the same participant.
  • JAMA July 25, 2012

    Figure 1: Use of 18F-FDG-PET/CT Imaging for Determination of Mean Arterial Target-to-Background Ratio (TBR)

    18F-FDG-PET indicates 18fluorine-2-deoxy-D-glucose positron emission tomography; CT, computed tomography; SUV, standardized uptake value. The FDG uptake was measured from a point distal to the origin of coronary vessels to avoid myocardial spillover. 18F-FDG-PET/CT imaging of the ascending thoracic aorta was performed according to validated, reproducible methods. A, To determine the TBR of the aorta, regions of interest are drawn around the aorta in the axial position. This is repeated along the length of the aorta (every 5 mm along the long axis of the vessel). A mean arterial SUV is derived from the average of the maximum SUV values in serial axial measurements (1.71 in this example). The venous background SUV is derived from 10 measurements obtained in the superior vena cava. B, TBR is calculated by dividing the mean arterial SUV by the mean venous SUV (TBR = 3.42 in this example). The SUV is the decay-corrected tissue concentration of FDG (in kBq/mL) divided by the injected dose per body weight (kBq/g).
  • JAMA July 20, 2011

    Figure 3: Cardiovascular Magnetic Resonance Identification of Myocardial Edema in a Representative Patient With Stress Cardiomyopathy

    T2-weighted images (short-axis view) demonstrating normal signal intensity (SI) of the basal myocardium but global edema of the mid and apical myocardium. Computer-aided SI analysis (bottom row) of the T2-weighted images with color-coded display of relative SI normalized to skeletal muscle (blue indicates an SI ratio of myocardium to skeletal muscle of ≥1.9 or higher, indicating edema; green/yellow indicates a normal SI ratio of <1.9) confirm the presence of global mid and apical edema. Outlines of regions of interest are manually drawn around the myocardium (red contour = subendocardial border; green contour = subepicardial border) and within the skeletal muscle (contour not shown).
  • JAMA July 20, 2011

    Figure 4: Cardiovascular Magnetic Resonance Identification of Necrosis/Fibrosis in a Representative Patient With Stress Cardiomyopathy

    Myocardial fibrosis was quantified, B, by selecting a region of interest in nonenhancing healthy myocardium (blue contour) and setting automated computer detection to 3 SDs (left) and 5 SDs (right) above the mean of healthy myocardium to identify fibrosis. Computer-aided signal intensity analysis detected positive late gadolinium enhancement (LGE) more than 3 SDs above the mean (red overlay), but no significant LGE more than 5 SDs above the mean was present (red contour = subendocardial border; green contour = subepicardial border of the myocardium).
  • Clinical Characteristics and Cardiovascular Magnetic Resonance Findings in Stress (Takotsubo) Cardiomyopathy.

    Abstract Full Text
    free access has multimedia
    JAMA. 2011; 306(3):277-286. doi: 10.1001/jama.2011.992
  • Association of Myocardial Enzyme Elevation and Survival Following Coronary Artery Bypass Graft Surgery

    Abstract Full Text
    free access
    JAMA. 2011; 305(6):585-591. doi: 10.1001/jama.2011.99
  • Insurance and Financial Concerns Among Patients Seeking Care for Acute Myocardial Infarction—Reply

    Abstract Full Text
    JAMA. 2010; 304(5):523-524. doi: 10.1001/jama.2010.1071
  • JAMA May 20, 2009

    Figure 2: Improvements in Segments With Inducible Myocardial Ischemia as Assessed by SPECT

    Each additional spoke on the data markers denotes another patient with the same number of ischemic segments. In the bone marrow cell group, there is a larger decrease in segments with inducible ischemia than in the placebo group (P < .001). Square data markers with error bars are the mean (SD) number of ischemic myocardial segments per patient for each group.
  • JAMA March 25, 2009

    Figure 4: Left Ventricular Histopathology in LAMP2 Cardiomyopathy (Patient 2)

    From the same patient shown in Figure 1, with findings consistent with a lysosomal storage disease. A, Small focal scars (stained blue) surrounded by viable myocardium (Masson trichrome, original magnification ×40). B, Similar area of myocardium shows subepicardial distribution of scarring and vacuolated myocytes (Masson trichrome, original magnification ×40). C, Clusters of myocytes with vacuolated sarcoplasm (stained red) embedded in an area of scar (stained blue, Masson trichrome, original magnification ×100). D, High-power photomicrograph showing a large empty myocyte surrounded by smaller vesicles in an area of replacement fibrosis (Masson trichrome).
  • JAMA December 19, 2007

    Figure 2: Pattern of Myocardium on Left Atrium and Pulmonary Veins (PV) and Representative Electroanatomical Map of Left Atrium in Patient Receiving Successful Ablative Therapy

    A, Common pattern of myocardial fibers of the posterior left atrium and pulmonary vein trunks. Anatomical studies have demonstrated that myocardial fibers on the posterior aspect of the left atrium extend to surround the trunks of the pulmonary veins as myocardial sleeves. The pattern and thickness of myocardial fibers vary between individuals. The pulmonary venous myocardial sleeves extend from 6 mm to 14 mm from the left atrium and include a mixture of horizontal, vertical, and oblique fiber contributions. The relationship of these anatomical features to the genesis of arrhythmias, however, is not known. B, Representative map of the left atrium (in a similar posterior view) of a patient receiving ablative treatment for atrial fibrillation. Creation of the 3-dimensional map is based on a preacquired computed tomography or magnetic resonance image. Ablation lesions surrounding the ostia of the pulmonary veins are shown as red dots; each point represents approximately 5 to 10 seconds of radiofrequency application. The procedural end point is electrical isolation of each pulmonary venous myocardial sleeve from the body of the left atrium. Image courtesy of Hugh Calkins, MD.
  • JAMA October 18, 2006

    Figure 3: Schema of Potential Dose Responses and Time Courses for Altering Clinical Events of Physiologic Effects of Fish or Fish Oil Intake

    The relative strength of effect is estimated from effects of eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) on each risk factor and on the corresponding impact on cardiovascular risk. For example, dose response for antiarrhythmic effects is initially steep with a subsequent plateau, and clinical benefits may occur within weeks, while dose response for triglyceride effects is more gradual and monotonic, and clinical benefits may require years of intake. At typical Western levels of intake (eg, <750 mg/d EPA + DHA), the physiologic effects most likely to account for clinical cardiovascular benefits include (1) modulation of myocardial sodium and calcium ion channels, reducing susceptibility to ischemia-induced arrhythmia; and (2) reduced left ventricular workload and improved myocardial efficiency as a result of reduced heart rate, lower systemic vascular resistance, and improved diastolic filling. At higher levels of intake seen with fish oil supplementation or in Japanese populations (>750 mg/d EPA + DHA), maximum antiarrythmic effects have been achieved and clinically relevant effects occur on levels of serum triglycerides and possibly, at very high doses, thrombosis. Potentially important effects on endothelial, autonomic, and inflammatory responses are not shown because dose responses and time courses of such effects on clinical risk are not well established. Effects are not necessarily exclusive: eg, antiarrythmic effects may be partly mediated by effects on blood pressure (BP) or heart rate.
  • JAMA March 1, 2006

    Figure: Flow of REVIVAL-2 Study Participants

    CT indicates computed tomography; MRI, magnetic resonance imaging; REVIVAL-2, Regenerate Vital Myocardium by Vigorous Activation of Bone Marrow Stem Cells.
  • JAMA February 23, 2005

    Figure: Hypothetical Construct of the Relationship Among the Duration of Symptoms of Acute MI Before Reperfusion Therapy, Mortality Reduction, and Extent of Myocardial Salvage

    Mortality reduction as a benefit of reperfusion therapy is greatest in the first 2 to 3 hours after the onset of symptoms of acute myocardial infarction (MI), most likely a consequence of myocardial salvage. The exact duration of this critical early period may be modified by several factors, including the presence of functioning collateral coronary arteries, ischemic preconditioning, myocardial oxygen demands, and duration of sustained ischemia. After this early period, the magnitude of the mortality benefit is much reduced, and as the mortality reduction curve flattens, time to reperfusion therapy is less critical. If a treatment strategy, such as facilitated percutaneous coronary intervention (PCI), is able to move patients back up the curve, a benefit would be expected. The magnitude of the benefit will depend on how far up the curve the patient can be shifted. The benefit of a shift from points A or B to point C would be substantial, but the benefit of a shift from point A to point B would be small. A treatment strategy that delays therapy during the early critical period, such as patient transfer for PCI, would be harmful (shift from point D to point C or point B). Between 6 and 12 hours after the onset of symptoms, opening the infarct-related artery is the primary goal of reperfusion therapy, and primary PCI is preferred over fibrinolytic therapy. The possible contribution to mortality reduction of opening the infarct-related artery, independed of myocardial salvage, is not shown. Modified from Gersh and Anderson.
  • JAMA September 19, 2001

    Figure: Prediction of In-Hospital Mortality With TIMI Risk Score for STEMI

    STEMI indicates ST-elevation myocardial infarction; NRMI 3, the National Registry of Myocardial Infarction 3. Data for the Intravenous nPA for Treatment of Infarcting Myocardium Early (InTIME II) trial are from Morrow.
  • JAMA September 12, 2001

    Figure: Suddenly, 64 Stem Cell Lines

    Six types of cells derived from undifferentiated embryonic stem cells—liver, heart muscle, nerve, pancreatic islet, bone, and blood cells—are included in the agreement between the Wisconsin Alumni Research Foundation and Geron Corporation.
  • JAMA July 26, 2000

    Figure 5: Relationship Between Persistent Elevation of Cardiac Troponin I Levels and Increased Deposits of Myocardial Fibrin

    Relationship between semiquantitative evaluation of the deposition of myocardial fibrin in serial endomyocardial biopsies during the first year following transplantation and the presence of persistently elevated serum cardiac troponin I levels. Error bars represent SE.