227 research outputs found

    Myocardial Defect Detection Using PET-CT: Phantom Studies

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    It is expected that both noise and activity distribution can have impact on the detectability of a myocardial defect in a cardiac PET study. In this work, we performed phantom studies to investigate the detectability of a defect in the myocardium for different noise levels and activity distributions. We evaluated the performance of three reconstruction schemes: Filtered Back-Projection (FBP), Ordinary Poisson Ordered Subset Expectation Maximization (OP–OSEM), and Point Spread Function corrected OSEM (PSF–OSEM). We used the Channelized Hotelling Observer (CHO) for the task of myocardial defect detection. We found that the detectability of a myocardial defect is almost entirely dependent on the noise level and the contrast between the defect and its surroundings

    Heart failure and sudden cardiac death in heritable thoracic aortic disease caused by pathogenic variants in the SMAD3 gene

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    Background: Predominant cardiovascular manifestations in the spectrum of Heritable Thoracic Aortic Disease include by default aortic root aneurysms- and dissections, which may be associated with aortic valve disease. Mitral- and tricuspid valve prolapse are other commonly recognized features. Myocardial disease, characterized by heart failure and/or malignant arrhythmias has been reported in humans and in animal models harboring pathogenic variants in the Fibrillin1 gene. Methods: Description of clinical history of three cases from one family in Ghent (Belgium) and one family in St. Louis (US). Results: We report on three cases from two families presenting end-stage heart failure (in two) and lethal arrhythmias associated with moderate left ventricular dilatation (in one). All three cases harbor a pathogenic variant in the SMAD3 gene, known to cause aneurysm osteoarthritis syndrome, Loeys-Dietz syndrome type 3 or isolated Heritable Thoracic Aortic Disease. Conclusions: These unusual presentations warrant awareness for myocardial disease in patients harboring pathogenic variants in genes causing Heritable Thoracic Aortic Disease and indicate the need for prospective studies in larger cohorts

    Delayed cardiac tamponade in a patient with previous minor blunt chest trauma

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    Hemopericardium with cardiac tamponade after non-penetrating chest trauma is a very rare but life-threatening condition. If this complication develops after an interval of several weeks following the non-penetrating chest trauma, the causal relation with the traumatic event is less evident, which may delay proper diagnosis and adequate treatment. We describe diagnosing and therapeutic management of a patient in shock who suffered from cardiac tamponade four weeks after a minor blunt chest trauma

    Prediction of sarcomere mutations in subclinical hypertrophic cardiomyopathy.

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    BACKGROUND: Sarcomere protein mutations in hypertrophic cardiomyopathy induce subtle cardiac structural changes before the development of left ventricular hypertrophy (LVH). We have proposed that myocardial crypts are part of this phenotype and independently associated with the presence of sarcomere gene mutations. We tested this hypothesis in genetic hypertrophic cardiomyopathy pre-LVH (genotype positive, LVH negative [G+LVH-]). METHODS AND RESULTS: A multicenter case-control study investigated crypts and 22 other cardiovascular magnetic resonance parameters in subclinical hypertrophic cardiomyopathy to determine their strength of association with sarcomere gene mutation carriage. The G+LVH- sample (n=73) was 29 ± 13 years old and 51% were men. Crypts were related to the presence of sarcomere mutations (for ≥1 crypt, β=2.5; 95% confidence interval [CI], 0.5-4.4; P=0.014 and for ≥2 crypts, β=3.0; 95% CI, 0.8-7.9; P=0.004). In combination with 3 other parameters: anterior mitral valve leaflet elongation (β=2.1; 95% CI, 1.7-3.1; P<0.001), abnormal LV apical trabeculae (β=1.6; 95% CI, 0.8-2.5; P<0.001), and smaller LV end-systolic volumes (β=1.4; 95% CI, 0.5-2.3; P=0.001), multiple crypts indicated the presence of sarcomere gene mutations with 80% accuracy and an area under the curve of 0.85 (95% CI, 0.8-0.9). In this G+LVH- population, cardiac myosin-binding protein C mutation carriers had twice the prevalence of crypts when compared with the other combined mutations (47 versus 23%; odds ratio, 2.9; 95% CI, 1.1-7.9; P=0.045). CONCLUSIONS: The subclinical hypertrophic cardiomyopathy phenotype measured by cardiovascular magnetic resonance in a multicenter environment and consisting of crypts (particularly multiple), anterior mitral valve leaflet elongation, abnormal trabeculae, and smaller LV systolic cavity is indicative of the presence of sarcomere gene mutations and highlights the need for further study

    Prevalence of anginal symptoms and myocardial ischemia and their effect on clinical outcomes in outpatients with stable coronary artery disease: data from the international observational CLARIFY registry

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    Importance: In the era of widespread revascularization and effective antianginals, the prevalence and prognostic effect of anginal symptoms and myocardial ischemia among patients with stable coronary artery disease (CAD) are unknown.&lt;p&gt;&lt;/p&gt; Objective: To describe the current clinical patterns among patients with stable CAD and the association of anginal symptoms or myocardial ischemia with clinical outcomes.&lt;p&gt;&lt;/p&gt; Design, Setting, and Participants: The Prospective Observational Longitudinal Registry of Patients With Stable Coronary Artery Disease (CLARIFY) registry enrolled outpatients in 45 countries with stable CAD in 2009 to 2010 with 2-year follow-up (median, 24.1 months; range, 1 day to 3 years). Enrollees included 32 105 outpatients with prior myocardial infarction, chest pain, and evidence of myocardial ischemia, evidence of CAD on angiography, or prior revascularization. Of these, 20 291 (63.2%) had undergone a noninvasive test for myocardial ischemia within 12 months of enrollment and were categorized into one of the following 4 groups: no angina or ischemia (n = 13 207 [65.1%]); evidence of myocardial ischemia without angina (silent ischemia) (n = 3028 [14.9%]); anginal symptoms alone (n = 1842 [9.1%]); and angina and ischemia (n = 2214 [10.9%]).&lt;p&gt;&lt;/p&gt; Exposures: Stable CAD.&lt;p&gt;&lt;/p&gt; Main Outcome and Measure: The composite of cardiovascular (CV)–related death or nonfatal myocardial infarction.&lt;p&gt;&lt;/p&gt; Results: Overall, 4056 patients (20.0%) had anginal symptoms and 5242 (25.8%) had evidence of myocardial ischemia on results of noninvasive testing. Of 469 CV-related deaths or myocardial infarctions, 58.2% occurred in patients without angina or ischemia, 12.4% in patients with ischemia alone, 12.2% in patients with angina alone, and 17.3% in patients with both. The hazard ratios for the primary outcome relative to patients without angina or ischemia and adjusted for age, sex, geographic region, smoking status, hypertension, diabetes mellitus, and dyslipidemia were 0.90 (95% CI, 0.68-1.20; P = .47) for ischemia alone, 1.45 (95% CI, 1.08-1.95; P = .01) for angina alone, and 1.75 (95% CI, 1.34-2.29; P &#60;.001) for both. Similar findings were observed for CV-related death and for fatal or nonfatal myocardial infarction.&lt;p&gt;&lt;/p&gt; Conclusions and Relevance: In outpatients with stable CAD, anginal symptoms (with or without ischemia on noninvasive testing) but not silent ischemia appear to be associated with an increased risk for adverse CV outcomes. Most CV events occurred in patients without angina or ischemia

    The Alcyone CZT SPECT camera. Evaluation of performance using phantom measurement and Monte Carlo simulations

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    Background Coronary artery disease is one of the most common causes of death. A common cardiac examination is to give a visualization of the myocardial blood flow by injecting a radio pharmaceutical and detect the radiation with a camera. The camera has for decades been using thallium doped sodium iodide (NaI(Tl)) as the detector material. New detector materials have been developed because of the physical limits of the NaI(Tl). The new clinically available material is cadmium-zinc-telluride. One manufacturer has placed 19 detector panels with pinhole collimators sharing a common focal point. This camera is relatively new on the market and not thoroughly investigated. Purpose It has been investigated if the image quality could be improved with a narrower energy window, the sensitivity and spatial resolution within the field of view (FOV), whether the image was affected by different source locations was investigated. Finally the detection limit for heart defects in a physical phantom and in XCAT phantom was found. Material & method A list mode acquisition was performed with a Data Spectrum phantom with a cardiac insert containing a basal defect, which simulated a myocardial infarction. The energy window was changed from ±10% to ±5% and the acquisition time was changed acquire the same statistics. The resolution was determined by fitting a Gaussian curve to a line source measurement. The detector specific sensitivity and the sensitivity in the reconstructed images were measured by using a spot marker at different positions. The positioning effect were investigated by placing the Data Spectrum phantom with a cardiac insert without any defects at different positions, the measurements were also performed on a patient. The defect limit was investigated by simulating defects with different positions and wall thickness in a voxel based, CT-scanned, anthropomorphic phantom and a XCAT phantom using a verified Monte Carlo software. Results It was found that a reduction in energy window did not improve image quality and the acquisition time or activity had to be increased 25% in order to compensate of the loss of counts. The spatial resolution was unchanged over the investigated area. The detector specific sensitivity varied up to a factor 2 with the source position, but the sensitivity in the reconstructed images varied only 4%. A translation of 2 cm of the patient gives rise to positioning effect which are great enough to possibly change the diagnosis. The detection limit for defects in the anthropomorphic phantom was determined to be between 15% and 30% of the wall thickness. For the NaI(Tl) camera the detection limit have been found to be 50%. The detection limit for the XCAT phantom was not found

    Burn-associated delayed dilated cardiomyopathy evaluated by cardiac PET and SPECT: Report of a case

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    AbstractDilated cardiomyopathy is a delayed-onset and rarely reported cardiac complication of burn injury although the mechanism remains unclear. We thus report a case of dilated cardiomyopathy following severe burn injury, in which technetium 99m sestamibi single-photon emission computed tomography (SPECT), iodine-123 beta-methyl-iodophenylpentadecanoic acid SPECT and 18F-fluorodeoxyglucose positron emission tomography (PET) were performed to evaluate the pathophysiologic condition in combination with cardiac catheterization and myocardial biopsy. The cardiac PET and SPECT images showed reduced myocardial blood flow, decreased fatty acid metabolism, and increased glucose utilization in the left ventricular lateral wall in spite of normal coronary angiography, no significant cardiac fibrosis, and inflammatory cell infiltration, which suggests that myocardial ischemia due to microcirculatory disturbance in hypermetabolic state associated with burn injury might be a causative mechanism of dilated cardiomyopathy in this case. A beta blocker, bisoprolol, was successfully introduced in this patient in combination with oral inotropic agents, pimobendan and digitalis after the prolonged use of intravenous dobutamine infusion, which might have been beneficial for this patient with burn-associated dilated cardiomyopathy not only to reduce regional myocardial ischemia but also to attenuate hypermetabolic state after severe burn injury.<Learning objective: Dilated cardiomyopathy complicated with burn injury has been reported to cause a sudden attack of dyspnea and death. This case report suggests that burn-associated dilated cardiomyopathy may be caused by relative myocardial ischemia due to microvascular disturbance in hypermetabolic state associated with burn injuries and can be treated effectively with beta blockers with or without oral inotropic agents.
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