Troponin measurement is used in the assessment and risk stratification of patients presenting acutely with chest pain when the main cause of elevation is coronary artery disease. However, some patients have no coronary obstruction on angiography, leading to diagnostic uncertainty. We evaluated the incremental diagnostic value of cardiovascular magnetic resonance (CMR) in these patients. Sixty consecutive patients (mean age 44 years, 72% male) with a troponin-positive episode of chest pain and unobstructed coronary arteries were recruited within 3 months of initial presentation. All patients underwent CMR with cine imaging, T2-weighted imaging for detection of inflammation, and late gadolinium enhancement imaging for detection of infarction/fibrosis. An identifiable basis for troponin elevation was established in 65% of patients. The commonest underlying cause was myocarditis (50%), followed by myocardial infarction (11.6%) and cardiomyopathy (3.4%). In the 35% of patients where no clear diagnosis was identified by CMR, significant myocardial infarction/fibrosis was excluded. CMR is a valuable adjunct to conventional investigations in a diagnostically challenging and important group of patients with troponin-positive chest pain and unobstructed coronary arteries.
Cardiac complications secondary to iron overload are the leading cause of death in beta-thalassemia major. Approximately two thirds of patients maintained on the parenteral iron chelator deferoxamine have myocardial iron loading. The oral iron chelator deferiprone has been demonstrated to remove myocardial iron, and it has been proposed that in combination with deferoxamine it may have additional effect. Myocardial iron loading was assessed with the use of myocardial T2* cardiovascular magnetic resonance in 167 patients with thalassemia major receiving standard maintenance chelation monotherapy with subcutaneous deferoxamine. Of these patients, 65 with mild to moderate myocardial iron loading (T2* 8 to 20 ms) entered the trial with continuation of subcutaneous deferoxamine and were randomized to receive additional oral placebo (deferoxamine group) or oral deferiprone 75 mg/kg per day (combined group). The primary end point was the change in myocardial T2* over 12 months. Secondary end points of endothelial function (flow-mediated dilatation of the brachial artery) and cardiac function were also measured with cardiovascular magnetic resonance. There were significant improvements in the combined treatment group compared with the deferoxamine group in myocardial T2* (ratio of change in geometric means 1.50 versus 1.24; P=0.02), absolute left ventricular ejection fraction (2.6% versus 0.6%; P=0.05), and absolute endothelial function (8.8% versus 3.3%; P=0.02). There was also a significantly greater improvement in serum ferritin in the combined group (-976 versus -233 microg/L; P<0.001). In comparison to the standard chelation monotherapy of deferoxamine, combination treatment with additional deferiprone reduced myocardial iron and improved the ejection fraction and endothelial function in thalassemia major patients with mild to moderate cardiac iron loading.
eart failure is a common disorder that is associated with significant morbidity, mortality and financial burden to healthcare services.In the UK, around 900 000 people have been diagnosed with heart failure and the prevalence of the condition increases as the population ages.w1 Population-based studies suggest that heart failure carries a worse prognosis than breast and colon cancer, with estimates suggesting a 1 year mortality of 40% from the time of diagnosis.Heart failure currently accounts for a total of one million inpatient bed days and admissions are projected to rise by 50% over the next 25 years.Heart failure treatment currently absorbs 1.8% of the total National Health Service budget, of which 70% is spent on hospitalisation.Accurate diagnosis, assessment and risk stratification of such patients by imaging modalities is important, particularly with the advent of effective but expensive implantable devices.In the last 5 years, there have been tremendous advances in the ability of cardiovascular magnetic resonance (CMR) to fulfil many of these needs and provide a comprehensive assessment. 1 A combination of hardware and software developments means that a modern CMR scanner is able to yield information on myocardial anatomy, function, tissue characterisation, viability, perfusion and flow within a single 45-60 min study. HOW DOES CMR WORK AND WHAT INFORMATION CAN IT PROVIDE? cBasic principles Understanding the way in which CMR works provides a basis for appreciating its role in evaluating patients with heart failure.CMR yields high contrast and high resolution images of the heart by mapping radio wave signals absorbed and emitted by hydrogen nuclei (protons) in a powerful magnetic field.Most cardiovascular pathologies manifest with an increase in water content which is rich in protons so that CMR is a sensitive guide to early disease states.CMR is currently mainly performed at a magnetic field strength of 1.5 Tesla (T).The two main types of sequences used are gradient echo and spin echo imaging techniques.Gradient echo techniques lead to blood and fat both appearing white.They enable the acquisition of cine images with a high temporal and spatial resolution that can be used to identify myocardial function and abnormal flow patterns.Velocity mapping is based on gradient echo and can be used in a similar way to two-dimensional Doppler or provide multidimensional flow imaging for complex flow dynamics problems.Based on the different relaxation properties of tissues such as fat, muscle, and areas of inflammation, a range of sequences can be used to enable tissue characterisation.T1-weighted spin echo techniques lead to blood appearing black, while fat appears white.They are useful for high resolution anatomical as opposed to functional imaging.T2-weighted spin echo sequences contain a water excitation pulse that can be used to highlight myocardial inflammation or oedema.Valvular function can be assessed both qualitatively from cine imaging as well as quantitatively from phase contrast velocity mapping with accurate measurements of peak velocity and regurgitant volumes.While most image acquisition is performed without the routine need for contrast agents, an important development has been the use of gadolinium-chelated contrast agents (Gd-CA), such as Gd-DTPA (gadolinium diethylenetriamine penta-acetic acid), to document perfusion defects, microvascular ischaemia and areas of scar tissue/fibrosis.Gd-CA has paramagnetic properties and thus gives a bright signal on scanning.It is metabolically inert and safe to administer via a peripheral line as a single bolus with a negligible risk of nephrotoxicity, although it is best avoided in patients with severe renal impairment.Due to its chemical properties and large molecular size, Gd-CA is unable to penetrate the intact myocyte membrane.However, it can passively diffuse and accumulate into the extracellular space around muscle cells or into myocytes where the cell membrane has been ruptured.The typical dose given is 0.1-0.2mmol/kg (usually between 12-40 ml).
A 61-year-old gentleman was admitted to his local hospital with a 5-h history of central chest pain. He was an ex-smoker with no other cardiac risk factors or history of ischaemic heart disease. ECG on presentation demonstrated ST elevation in leads 1 and aVL consistent with acute myocardial infarction (MI) and he was therefore thrombolysed with tenecteplase. Following thrombolysis, his ST segment elevation resolved and his chest pain subsided completely. Peak CK was 1015 U/l (24–173 U/l) and troponin T 3.65 ug/l (0–0.10 ug/l). A routine PA chest radiograph revealed a widened superior mediastinum, raising the possibility of aortic dissection (Figure 1). An urgent contrast enhanced CT scan was therefore requested which demonstrated a type A aortic dissection with an aneurysmal ascending aorta (Figure 2).
Figure 1.
PA chest radiograph shows widening of the mediastinum and ectasia of the descending thoracic aorta. The lung fields are clear.
Figure 2.
CT aorta demonstrates type A aortic dissection. In the dilated ascending aorta there is thrombus within the false lumen (asterisk). The dissection can be seen to extend into the descending thoracic aorta (arrow). T = true lumen.
Despite the CT findings, the patient remained well following thrombolysis with no subsequent clinical sequelae of acute aortic dissection. Further investigation with transthoracic echocardiography revealed good left ventricular function with no pericardial effusion. There was mild central aortic regurgitation but …
Results: A total of 16 (1 male 15 female) subjects were identified with a first diagnosis of TAK during 2000-2005.The median age at first onset was 43.5 years (Interquartile Range (IQR):30-65).The overall annual incidence of TAK was 0.9/million (95%CI, [0.5-1.5]).The incidence was stable throughout the study period.The point prevalence of TAK in this period was 5.2/million.Diagnosis before the age of 40 is one of the American College of Rheumatology (1990) classification criteria for TAK.There were 8 patients (one male) aged < 40 years diagnosed in 2000-2005 with TAK.The annual incidence in those aged < 40 years was 0.45/million.Conclusions: This is the first study of the incidence of TAK from a primary care population and also the first data from the UK.Previous studies have been reported from secondary or tertiary care.Our data is consistent with the previous studies and suggests that the incidence of TA is similar in the UK to that observed in other populations.1.
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