Jun 17, 2012 - segment depression in leads aVL, V2 and V3. He was discharged unevent- fully on the 15th day of his hospitali- zation with ECG evolutionary ...
European Heart Journal (1996) 17, 317-321
Letters to the Editor Myocardiai infarction with normal coronary arteries in Slfi thalassaemia patients
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Figure 1 Evolutionary changes of an inferior wall myocardiai infarction in the serial twelve-lead electrocardiogram of patient 1. Eur Heart J, Vol. 17, February 1996
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Myocardiai infarction with normal coronary arteries has been reported as a rare complication of sickle cell disease1'1, but as far as we know it has not been reported in patients with HbS//? thalassaemia. We report two cases of myocardiai infarction in S//? thalassaemia patients with normal coronary arteries and no other risk factors. The first patient was a 22-yearold white male. He had frequent, but not severe, painful crises and was rarely hospitalized or transfused. Three days before his admission, the patient had an episode of intense chest pain. He considered it a painful crisis and stayed at home taking analgesics. During the next 2 days the patient felt extremely tired and because of this he was admitted to hospital. On admission he was ambulatory but pale and mildly icteric. Physical examination disclosed palpable spleen 5 cm below the costal margin. Haemoglobin concentration, which was usually 10g.dl~', was 4-9g. dl~'. Creatinine kinase, aspartate
An echocardiogram revealed aminotransferase, anticardiolipin antibodies, protein C and protein S were inferior-lateral akinesia, fibrosis with normal. Cholesterol, HDL and triglyc- a marked decrease in total left venerides were low, and lactate dehydro- tricular function and left atrium genase was elevated. ECG showed (d=4-5cm) and ventricle (d=6-7cm) abnormal Q waves in leads D2, D 3 and dilatation. The patient was discharged aVF, ST segment elevation in leads on the 16th day of his hospitalization D2, D3, aVF, V4, V? and V6 and ST having only residual neurological segment depression in leads aVL, V2 signs. Two months later he underwent and V3. He was discharged unevent- heart catheterization. The coronary fully on the 15th day of his hospitali- arteries had increased calibre and norzation with ECG evolutionary changes mal patency. There was left ventricuas a results of a recent inferior lar dilatation with inferior scarring, wall myocardiai infarction (Fig. 1) diffuse hypokinesia, and decreased and a haemoglobin concentration of left ventricular function (estimated 11-5 g . dl" '. Forty-five days after the ejection fraction 30%). infarction he underwent heart cathS//? thalassaemia or sickle thaeterization which showed normal cor- lassaemia is an inherited disorder of onary arteries, inferoapical akinesia, haemoglobin that expresses a double and a normal estimated ejection frac- heterozygous state of HbS disease and tion (55%). P thalassaemia. It is a relatively comThe second patient was a 43- mon disorder in the Mediterranean year-old white male. He had sparse basin and its clinical manifestations and mildly painful crises each year, are similar but generally milder than but did not require transfusions. He those of sickle cell disease (SCD). was admitted in a state of acute conDespite the tendency of fusion. Neurological examination dis- patients with sideling disorders to closed conduction aphasia and space develop vascular occlusion, typical and time disorientation. A brain CT myocardiai infarction is rare1'1. scan demonstrated a recent infarct in Autopsy studies in unselected SCD the region of the right middle cerebral patients showed that the coronary artery. Haemoglobin concentration arteries were widely patent and was, as normal, 11-9 g . dl ~ '. The re- increased in calibre and that atherosults of the laboratory work-up were sclerotic changes were impressively similar to the first patient's. ECG minimal121. Therefore, the mechanism showed abnormal Q waves in leads D2, of myocardiai infarction in SCD has D3 and aVF, consistent with an old to be related mainly to the sideling inferior wall myocardiai infarction. process'31 and to hypoxia in some
318 Letters to the Editor
[4] Norris S, Johnson CS, Haywood LJ. Sickle cell anemia: Does myocardial ischemia occur during crisis? J Natl Med Assoc 1991; 83: 209-13. [5] Powars D, Weiman JA, Odom-Maryon T, Niland J, Johnson C. Sickle cell chronic lung disease: prior morbidity and the risk of pulmonary failure. Medicine 1988; 67: 66-76.
Comprehensive analysis of aortic valve vegetation with anyplane, paraplane, and three-dimensional echoes rdiography
Echocardiographic visualization of a vegetation is now recognized as a major criterion for the diagnosis of infective endocarditis. Transoesophageal echocardiography, providing improved resolution and superior image quality, is an important modality in the evaluation of patients suspected of having infective endocarditis. Computer-controlled image acquisition with spatial and temporal information enables the integration of cross-sectional images into threedimensional dataset and dynamic three-dimensional display of cardiac structures1'1. The anatomical information can also be displayed as a reconstructed cross-section in any desired plane (anyplane mode). The acquisition of the basic images with a multiplane transoesophageal transducer minimizes both motion artifacts and patient discomfort'21. The techA. AESSOPOS nique allows a clear and convincing M. SAMARCOS picture of the pathological anatomy P. HADJINIKOLAOU and improves quantitative analysis. To G. VAIOPOULOS date, the experience with threedimensional echocardiography for the V. SKOUMAS evaluation of endocarditis remains I. KOLAINIS limited'341. D. LOUKOPOULOS We present a patient with University of Athens School of Medicine, aortic valve endocarditis in whom First Department of Internal Medicine, the dynamic three-dimensional reconLaikon General Hospital, 17, Agiou Thoma,struction of transoesphageal echo115 27 Athens. Greece cardiographic images permitted comprehensive visualization of the mass lesion as well as detailed measurements of its size. References A 71-year-old man with no [1] Barret O Jr, Saunders DE Jr, history of cardiac disease presented McFarland DE, Humphries JO. Myo- with complaints of increasing general cardial infarction in sickle cell anemia. malaise and dyspnoea over the last 5 Am J Hematol 1984; 16: 139-47. months. A transthoracic echocardio[2] Gerry JL, Buckley BH, Hutchins GM. gram made at the beginning of his Clinical pathologic analysis of cardiac symptoms demonstrated thickened dysfunction in 52 patient with sickle cell anemia. Am J Cardiol 1978; 42: 211-16. aortic valve cusps with a peak blood and grade [3] Anonymous. Easing the suffering flow velocity of 1-6 m . s II aortic regurgitation with a good caused by Sickle Cell Disease [Editorial], N Engl J Med 1994; 330- functioning but slightly enlarged left ventricle. 783-4. Eur Heart J, Vol. 17, February 1996
On admission the patient was afebrile, with heart rate of 90 beats . min~', and cuff blood pressure was 120/55 mmHg. The apex impulse was displaced leftwards and downwards. Cardiac auscultation revealed a holodiastolic aortic regurgitation grade IV/VI murmur, as well as a systolic ejection type grade IV/VI murmur at the right sternal border and a holosystolic grade III/VI murmur over the apex. Breath sounds were normal but crepitations at the base of the lungs were heard. No peripheral signs of heart failure were present, ECG tracings revealed ventricular trigeminy, incomplete right bundle branch block pattern and anterior hemiblock. The laboratory tests revealed haemoglobin 61 g . dl ~ ' and a white blood cell count of 5800 mm" 3 without leftward shift. Blood cultures were positive for Streptococcus bovis and antibiotic therapy with penicillin i.v. was started. A transoesophageal echocardiogram was performed with a 5 MHz, 64-element multiplane transducer connected to a Hewlett-Packard Sonos 500 system. Transoesophageal echocardiography thoroughly visualized the aortic valve, with its thickened cusps and severe regurgitation on colour Doppler, revealing a large mobile vegetation attached to the right aortic cusp. The size of the vegetation, measured in an optimized cutplane, was 20 x 10 mm. The left ventricle was enlarged (end-diastolic diameter 62 mm) with moderately depressed function and there was moderate mitral regurgitation due to annulus dilatation. Atherosclerotic lesions were detected in descending aorta. During the transoesophageal examination, the images for three-dimensional reconstruction were acquired with rotational scanning (2-degree interval) under ECG and respiratory gating. This method has been described in detail elsewhere12'. Reconstruction was performed off-line with a TomTec Echo-Scan system (Munich, Germany). The time required for data postprocessing was 15min and the time for reconstruction and analysis of the optimal images was about 90 min. Three-dimensional echocardiography allowed the cross-section of the vegetation to be displayed in any desired cutplane (anyplane mode), and gradient shading algorithm provided the views with the best depth perception (volume-rendered threedimensional echocardiography) (Fig. 1(A,B)). Computer-reconstructed cut-
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areas of the myocardium over a prolonged period. In contrast to the low incidence of myocardial infarction, ECG changes consistent with myocardial ischaemia and arrhythmias have been frequently found (50 and 80% of patients respectively) during painful crises of SCO14'. In addition, a large proportion of young patients with SCD had evidence of myocardial ischaemia during exercise151. On the basis of these findings it seems that myocardial ischaemia is frequent in patients with SCD, but there is no analogous data in the literature regarding cardiovascular involvement in Sip thalassaemia patients. In the two cases reported here, we found sound evidence of myocardial infarction in patients whose coronary arteries were normal. In the first case, the incident was combined with a painful crisis as well as with severe anaemia. In the second case, there was no history of chest pain, but the ECG was consistent with an old myocardial infarction. Furthermore, there was evidence of more diffuse damage of the left ventricle, which was manifested as diffuse hypokinesia in the angiogram of the left ventricle. These preliminaryfindingsand the fact that ischaemic heart episodes can be mistaken for sickle cell crises and be overlooked, point to the need for a more systematic study of cardiovascular involvement in a large sample of Sip thalassaemia patients.
