The assessment of results of medical treatment, angioplasty and coronary bypass surgery in diabetic coronary patients is difficult because of the absence of distinction in the subgroups of type 1 and 2 diabetes and of stable and unstable angina. With respect to medical therapy, betablockers are practically without deleterious effects and are effective in diabetic populations. The same is true of other antianginal drugs. Conventional coronary angioplasty is associated with poorer results than the general population in the long-term, partly because of progression of the coronary artery disease and partly because of an increased incidence of restenosis. The use of stents improves these results, which are similar to those of the general population with single vessel disease or those without proteinuria. Coronary bypass surgery, despite a certain perioperative morbidity, is associated with an identical survival rate at 5 years as non-diabetics, providing the internal mammary artery is grafted. The comparison between these methods is resumed in the ACIP study which opposes the 3 strategies, in Morris et al's study comparing medical and surgical approaches and, finally, in the recent BARI trial where patients were randomly allocated to angioplasty or surgery. It would appear that the surgical strategy gives better results in multivessel disease. However, many reserves have been voiced because of the small numbers of patients, the high number of excluded patients and the fact that recent progress in angioplasty with widespread use of stenting associated with the prescription of new antiaggregant drugs was not taken into account.

We describe the case of a fatal cerebral hemorrhage associated with a severe thrombocytopenia (4.0 x 10(9)/l), occurring only 90 min after starting treatment with abciximab, in a patient undergoing primary percutaneous transluminal coronary angioplasty (PTCA) for an acute myocardial infarction. Cathet. Cardiovasc. Intervent. 49:177-180, 2000.

HomeCirculationVol. 101, No. 10Myocardial Infarction in Children With Hypoplastic Coronary Arteries Free AccessOtherPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessOtherPDF/EPUBMyocardial Infarction in Children With Hypoplastic Coronary Arteries A. Fraisse, J. Quilici, I. Canavy, B. Savin, F. Aubert and M. Bory A. FraisseA. Fraisse From the Service de Cardiologie A, Hôpital de la Timone, and the Service de Chirurgie thoracique et cardiovasculaire, Hôpital d'enfants de la Timone (F.A.), Marseille, France. , J. QuiliciJ. Quilici From the Service de Cardiologie A, Hôpital de la Timone, and the Service de Chirurgie thoracique et cardiovasculaire, Hôpital d'enfants de la Timone (F.A.), Marseille, France. , I. CanavyI. Canavy From the Service de Cardiologie A, Hôpital de la Timone, and the Service de Chirurgie thoracique et cardiovasculaire, Hôpital d'enfants de la Timone (F.A.), Marseille, France. , B. SavinB. Savin From the Service de Cardiologie A, Hôpital de la Timone, and the Service de Chirurgie thoracique et cardiovasculaire, Hôpital d'enfants de la Timone (F.A.), Marseille, France. , F. AubertF. Aubert From the Service de Cardiologie A, Hôpital de la Timone, and the Service de Chirurgie thoracique et cardiovasculaire, Hôpital d'enfants de la Timone (F.A.), Marseille, France. and M. BoryM. Bory From the Service de Cardiologie A, Hôpital de la Timone, and the Service de Chirurgie thoracique et cardiovasculaire, Hôpital d'enfants de la Timone (F.A.), Marseille, France. Originally published14 Mar 2000https://doi.org/10.1161/01.CIR.101.10.1219Circulation. 2000;101:1219–1222An 11-year-old boy with a past history of asthma was admitted to the pediatric intensive care unit (ICU) for a non–Q-wave myocardial infarction that occurred during sustained exercise (a handball match). He presented with chest pain, anterior ST-segment depression on the ECG (Figure 1), and elevation of creatinine kinase (peak, 2580 mU; MB, 240). Initial physical examination was normal, and his ICU course was uncomplicated. He was discharged to the ward after 2 days, and cardiac catheterization was performed 8 days after admission. Left ventriculography (Figure 2) revealed mild apical hypokinesia with an ejection fraction of 55%. Selective coronary arteriography showed no atherosclerotic lesion but hypoplasia of the distal left anterior descending (LAD) and right coronary (RCA) arteries (Figures 3 and 4). There was no supply of the inferior aspect of the interventricular septum by a posterior branch from the RCA or left circumflex coronary artery (LCx). The proximal LAD was normal, with well-developed septal branches but no diagonal branches filled by contrast on the anterolateral free wall of the left ventricle (Figure 4). Intracoronary infusion of nitroglycerin showed no significant changes in coronary artery diameter (Figure 5). Total cholesterol, HDL, sedimentation rate, serological studies for connective-tissue diseases, antithrombin III, protein C, protein S, endogenous tissue plasminogen activator, and plasminogen activator inhibitor were normal. The patient was discharged home on diltiazem after a normal maximal exercise test 16 days after admission.In 85% of patients, the coronary circulation is right-dominant, and the RCA supplies the inferior aspect of the interventricular septum by giving rise to the posterior descending artery. The LCx, which is often small, does not reach the crux of the heart. Conversely, when the LCx is the dominant coronary artery, it courses to the crux of the heart and the RCA is often small.1 In ≈7% of patients, there is a codominant or balanced system in which both RCA and LCx give rise to a posterior descending branch. Hypoplastic coronary artery disease (HCAD) occurs rarely and refers to the underdevelopment of ≥1 coronary arteries or their major branches.2 Most of the patients reported were young adults and experienced sudden cardiac death without antecedent symptoms. Diagnosis is often made at autopsy.12 Although reversible myocardial ischemia has previously been angiographically documented in an infant, it is unusual to see a patient with myocardial infarction and isolated HCAD diagnosed at coronary angiography, as in our patient.3 Hypoplasia of the RCA and LCx with no posterior descending artery supplying the inferior aspect of the interventricular septum is more commonly found.1 Hypoplasia of the LAD has also been reported.23 In addition, HCAD was found in several cases of myocardial infarction distal to atherosclerotic or thrombotic occlusions.2The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke's Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.Circulation encourages readers to submit cardiovascular images to Dr Hugh A. McAllister, Jr, St Luke's Episcopal Hospital and Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.Download figureDownload PowerPoint Figure 1. ECG on admission showing anterior ST-segment depression.Download figureDownload PowerPoint Figure 2. A 30° right anterior oblique left ventriculograph in end diastole (left) and end systole (right) showing apical hypokinesia.Download figureDownload PowerPoint Figure 3. Lateral-view angiogram showing hypoplastic RCA without posterior descending artery supplying crux of heart.Download figureDownload PowerPoint Figure 4. A 30° right anterior oblique left main coronary artery angiogram showing hypoplasia of distal LAD with well-developed septal branches but no diagonal branches filled by contrast on anterolateral free wall of left ventricle. There is no supply of inferior aspect of interventricular septum by a posterior branch from LCx (no left-dominant system).Download figureDownload PowerPoint Figure 5. Lateral-view angiogram showing hypoplasia of distal LAD with absence of diagonal branches and no significant changes in coronary artery diameter after intracoronary infusion of nitroglycerin.FootnotesCorrespondence to A. Fraisse, MD, Service de Cardiologie A, Hôpital de la Timone, Blvd Jean Moulin, 13385 Marseille Cedex 5, France. E-mail [email protected] References 1 Roberts WC, Glick BN. Congenital hypoplasia of both right and left circumflex coronary arteries. Am J Cardiol.1992; 70:121–123.CrossrefMedlineGoogle Scholar2 Zugibe FT, Zugibe FT Jr, Costello JT, Breithaupt MK. Hypoplastic coronary artery disease within the spectrum of sudden unexpected death in young and middle age adults. Am J Forensic Med Pathol.1993; 14:276–283.CrossrefMedlineGoogle Scholar3 Casta A. Hypoplasia of the left coronary artery complicated by reversible myocardial ischemia in a newborn. Am Heart J.1987; 114:1238–1241.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Morales R, Bokowski J, Aljemmali S, Murphy J, Bharati S and Abdulla R (2020) A Rare Report of Hypoplastic Coronary Arteries and Pulmonary Veins: A Case Report and Review of the Literature, Pediatric Cardiology, 10.1007/s00246-020-02334-x, 41:6, (1231-1237), Online publication date: 1-Aug-2020. Shi X, Liu J, Wu J, Hua Y, Zhou K and Li Y (2020) Hypoplastic coronary arteries in a child with a mutation in Notch1, Medicine, 10.1097/MD.0000000000021355, 99:33, (e21355) Sueda S and Kohno H (2019) Clinical characteristics in patients with rest angina and hypoplastic right coronary artery, Heart and Vessels, 10.1007/s00380-019-01507-w, 35:4, (443-450), Online publication date: 1-Apr-2020. Kastellanos S, Aznaouridis K, Vlachopoulos C, Tsiamis E, Oikonomou E and Tousoulis D (2018) Overview of coronary artery variants, aberrations and anomalies, World Journal of Cardiology, 10.4330/wjc.v10.i10.127, 10:10, (127-140), Online publication date: 26-Oct-2018. Foley T and Krantz M (2017) Resuscitated sudden cardiac death due to diminutive coronary artery syndrome, HeartRhythm Case Reports, 10.1016/j.hrcr.2016.11.003, 3:2, (141-144), Online publication date: 1-Feb-2017. Wang Y, Wu B, Lu P, Zhang D, Wu B, Varshney S, del Monte-Nieto G, Zhuang Z, Charafeddine R, Kramer A, Sibinga N, Frangogiannis N, Kitsis R, Adams R, Alitalo K, Sharp D, Harvey R, Stanley P and Zhou B (2017) Uncontrolled angiogenic precursor expansion causes coronary artery anomalies in mice lacking Pofut1, Nature Communications, 10.1038/s41467-017-00654-w, 8:1, Online publication date: 1-Dec-2017. Riede F, Bulla S, Grundmann S, Werner M, Riede U and Otto C (2013) Isolated hypoplastic circumflex coronary artery: a rare cause of haemorrhagic myocardial infarction in a young athlete, Diagnostic Pathology, 10.1186/1746-1596-8-91, 8:1, Online publication date: 1-Dec-2013. Ma S, Kim D, Hur J, Kim K, Byun S, Park K and Yoon S (2012) Right Ventricular Myocardial Infarction due to Right Coronary Artery Total Occlusion Originating From the Distal Left Circumflex Artery, Korean Circulation Journal, 10.4070/kcj.2012.42.8.565, 42:8, (565), . Dermengiu D, Dermengiu S, Curca C and Ceausu M (2011) Sudden Death Due to Coronary Tree Hypoplasia, American Journal of Forensic Medicine & Pathology, 10.1097/PAF.0b013e318219c8e6, 32:3, (227-231), Online publication date: 1-Sep-2011. McFarland C, Swamy R and Shah A (2011) Hypoplastic coronary artery disease: A rare cause of sudden cardiac death and its treatment with an implantable defibrillator, Journal of Cardiology Cases, 10.1016/j.jccase.2011.08.005, 4:3, (e148-e151), Online publication date: 1-Dec-2011. De Giorgio F, Abbate A, Stigliano E, Capelli A and Arena V (2010) Hypoplastic coronary artery disease causing sudden death. Report of two cases and review of the literature, Cardiovascular Pathology, 10.1016/j.carpath.2009.05.002, 19:4, (e107-e111), Online publication date: 1-Jul-2010. Durán A, Arqué J, Fernández B, Fernández M, Fernández-Gallego T, Rodríguez C and Sans-Coma V (2009) Rudimentary Coronary Artery in Syrian Hamsters ( Mesocricetus auratus ) , Anatomia, Histologia, Embryologia, 10.1111/j.1439-0264.2009.00935.x, 38:4, (270-274), Online publication date: 1-Aug-2009. Wick R, Otto S and Byard R (2007) Is Right Coronary Artery Hypoplasia and Sudden Death an Underdiagnosed Association?, American Journal of Forensic Medicine & Pathology, 10.1097/PAF.0b013e31805c93fd, 28:2, (128-130), Online publication date: 1-Jun-2007. Kim M, Han J, Lee S, Kim S, Park K, Koo B and Lee H (2007) Cases of Right Ventricular Myocardial Infarction in Patients with an Absent or Hypoplastic Right Coronary Artery, Korean Circulation Journal, 10.4070/kcj.2007.37.2.84, 37:2, (84), . Feger J (2021) Hypoplastic left anterior descending artery Radiopaedia.org, 10.53347/rID-86359 Jones J and Feger J (2021) Coronary hypoplasia Radiopaedia.org, 10.53347/rID-86153 March 14, 2000Vol 101, Issue 10 Advertisement Article InformationMetrics Copyright © 2000 by American Heart Associationhttps://doi.org/10.1161/01.CIR.101.10.1219 Originally publishedMarch 14, 2000 PDF download Advertisement

The assessment of results of medical treatment, angioplasty and coronary bypass surgery in diabetic coronary patients is difficult because of the absence of distinction in the subgroups of type 1 and 2 diabetes and of stable and unstable angina.With respect to medical therapy, betablockers are practically without deleterious effects and are effective in diabetic populations. The same is true of other antianginal drugs.Conventional coronary angioplasty is associated with poorer results than the general population in the long-term, partly because of progression of the coronary artery disease and partly because of an increased incidence of restenosis. The use of stents improves these results, which are similar to those of the general population with single Vessel disease or those without proteinuria.Coronary bypass surgery, despite a certain perioperative morbidity, is associated with an identical survival rate at 5 years as non-diabetics, providing the internal mammary artery is grafted.The comparison between these methods is resumed in the ACIP study which opposes the 3 strategies, in Morris et al's study comparing medical and surgical approaches and, finally, in the recent BARI trial where patients were randomly allocated to angioplasty or surgery. It would appear that the surgical strategy gives better results in multivessel disease. However, many reserves have been voiced because of the small numbers of patients, the high number of excluded patients and the fact that recent progress in angioplasty with widespread use of stenting associated with the prescription of new antiaggregant drugs was not taken into account.

Vascular disease is a multifactorial disease that involves atherosclerotic and thrombotic factors. Genetic polymorphisms have been associated with myocardial infarction and angina pectoris. The aim of the present study was to assess the relationship between some genetic polymorphisms and myocardial infarction (MI) or vasospastic angina pectoris in a population from southern France. Genetic polymorphisms of the renin angiotensin system (the D/I polymorphism of the ACE gene and the A1166C polymorphism of the angiotensin II type 1 receptor [AT1R]) and of haemostatic factors (the -675 4G/5G polymorphism of the plasminogen-activator inhibitor 1[PAI-1] gene, and the G to T common point mutation in exon 2, codon 34 of the Factor XIII A-subunit gene) were examined. We assessed the genotype distribution in consecutive coronary artery disease (CAD) patients with MI (n = 201) and vasospastic angina pectoris (n = 43) and in 244 healthy controls comparable in age, sex, body mass index and total cholesterol level. The genotype distribution of AT1R polymorphism was significantly different between controls and patients, the prevalence of the C allele carriers being higher in patients with MI after the age of 45 than in control individuals (61 vs 45%, p <0.01), leading to an odds ratio (OR) of 2 (CI: 1.2-3.4). When looking at the group of patients with vasospastic angina the difference was even higher (76 vs 45%, p <0.01) yielding an OR of 4.3 (CI: 1.4-17.4). Genotype distributions of ACE, PAI-1 and Factor XIII polymorphisms were similar in patients and in controls. This study is in favor of a role of ATIR gene polymorphism in myocardial infarction and vasospastic angina.

Out of 1 141 successive transoesophageal echocardiographic studies performed prospectively between 01/05/1993 and 31/12/1995, 26 cases of left atrial thrombosis were observed (2.2%); 5 were in the left atrium (20%), 19 in the left atrial appendage (73%) and the thrombi were in both atrium and left atrial appendage in 2 cases (7%). The 26 patients included 15 women and 11 men, with an average age of 69 +/- 16 years (range 25-89 years); 22 patients (84%) had permanent atrial fibrillation and 4 were in sinus rhythm. Only 5 of the patients were on oral anticoagulant therapy.All had underlying cardiac disease : 11 mitral valve diseases; 10 dilated cardiomyopathies; 2 hypertrophic cardiomyopathies; 3 other cardiac diseases. The indication for transoesophageal echocardiography was systemic embolism in 13 cases (50%); before D.C. cardioversion in 19 cases (38%) and before percutaneous mitral valvuloplasty in 3 cases.The thrombus was adherent in 18 cases (69%) and mobile in 8 cases (31%). Spontaneous contrast was observed in 23 cases (88%). Intravenous heparin was given as soon as the diagnosis was made. In 4 patients, thrombectomy was indicated in View of the threatening nature of the thrombus and/or the necessity for associated valve replacement.In 22 patients, heparin was relayed by oral anticoagulants on the 10th day of treatment. Control transoesophageal echocardiography was not performed because of the patient's refusal or poor general condition. The other 15 patients were reexamined 1 to 5 times between the 4th day and 12th month : a regression was observed in 13 cases (86%) which was complete in 11 and partial in 2 cases. No cases of embolism occurred during follow-up but six patients died : 1 of the operated cases and 5 of the patients treated medically (3 cardiac failures and 2 cerebral haemorrhages).The authors conclude that left atrial thrombosis is rare in the absence of classical embolic cardiac disease. With the exception of the surgical indication of a life-threatening thrombus and/or associated surgical mitral valve disease, anticoagulant therapy results in complete or partial regression of the thrombus visualised by transoesophageal echocardiography which is essential for follow-up. The prognosis depends on the severity of the underlying heart disease.

The aim of this study was to evaluate prospectively the respective roles of the atheromatous plaque, coronary spasm and abnormalities of haemostasis in patients with myocardial infarction with normal coronary arteries. The study population included 25 patients (19 men and 6 women) with a mean age of 52.1 +/- 11.1 years (34-76 years). The diagnosis of myocardial infarction was made as the finding of 2 out of 3 WHO criteria. It occurred spontaneously and was transmural in 80% of cases, inferior wall infarction in 9 patients (36%), anterior in 12 (48%) and lateral in 4 patients (16%). All patients underwent investigation on average 10 days after infarction (1-42 days) by coronary angiography with quantitative angiography, endocoronary ultrasonography, an ergometrine provocation test for coronary spasm and a blood coagulation study. Coronary angiography was normal in 4 patients but showed wall changes without stenosis > 50% in 20 patients and one case of aneurysmal arterial disease. Intracoronary thrombosis was detected in 6 cases. Endocoronary ultrasonography confirmed the normality of the coronary arteries in 2 cases and showed atheroma in 23 cases (soft atheroma: n = 17 and hard: n = 6). It detected 66% of the coronary thrombi observed at angiography and found 3 other cases. Coronary spasm was verified in 10 patients (40%). The coagulation study was normal in 19 patients and showed increase in Pai-1 in 5 patients and primary thrombocythemia in one case. The authors conclude that coronary angiographic data is less accurate than endo-coronary ultrasonography which best shows the extent and, above all, the nature of the plaques present in 23 of the cases (92%). Coronary spasm may be a contributing factor in 40% of cases, in situ thrombosis in 36% of cases despite usually normal blood clotting studies. None of these abnormalities was observed in one case. The embolic cause of infarction was certain in 2 cases.

The immediate results of transluminal coronary angioplasty (TCA) have improved considerably during recent years. Balloon dilatation of the arterial stenosis is the basis of this technique of revascularisation but new tools may be used to treat specific lesions. Coronary occlusion is the most feared complication of TCA. It may cause myocardial infarction or death of the patient. It is usually secondary to dissection and/or thrombus of the artery. The implantation of a stent successfully treats most cases of dissection. New anti-platelet (GP IIb/IIIa) drugs seem to be very effective in the prevention and treatment of the thrombosis. The systematic use of ticlopidine limits the risk of stent occlusion. Improved features enable satisfactory implantation of stents in the majority of cases. In some patients, the clinical consequences of occlusion may be limited by vascular bypass techniques, especially intra-aortic balloon pumping. In other cases, emergency coronary bypass surgery may be necessary. When TCA is considered to be a very high risk procedure, effective surgical cover is essential.

OBJECTIVE: Silent myocardial ischemia (SMI) is more common in diabetic patients than in the general population. However, the exact prevalence of SMI is not known, and routine screening is costly. The purpose of this 1-year study was to estimate the prevalence of SMI and define a high-risk diabetic population by systematically testing patients with no symptoms of coronary artery disease (CAD). RESEARCH DESIGN AND METHODS: The criteria for inclusion in this study were age (between 25 and 75 years), duration of diabetes (>15 years for type 1 diabetes, 10 years for type 2 diabetes with no cardiovascular risk factors, and 5 years for type 2 diabetes with at least one cardiovascular risk factor), and absence of clinical or electrocardiogram (ECG) symptoms of CAD. For 1 year, 203 patients were screened, including 28 women and 45 men with type 1 diabetes (aged 41.5+/-10.9 years, mean duration of diabetes 20.9+/-7.7 years [mean +/- SD]) and 61 women and 69 men with type 2 diabetes (aged 60.7+/-8.7 years, duration of diabetes 16.5+/-7.1 years). Exercise ECG was the first choice for screening method. If exercise ECG was not possible or inconclusive, thallium myocardial scintigraphy (TMS) with exercise testing and/or dipyridamole injection was performed. If any one of these tests was positive, coronary angiography was carried out and was considered to be positive with a stenosis of > or =50%. RESULTS: Positive screening results were obtained in 32 patients (15.7%). Coronary angiography demonstrated significant lesions in 19 patients (9.3%) and nonsignificant lesions in 7 patients (1 false-positive result for exercise ECG and 6 false-positive results for TMS). Coronary angiography was not performed in six patients. All but 3 of the 19 patients (15 men and 4 women) in whom silent coronary lesions were detected presented with type 2 diabetes. The main differences between the 16 type 2 diabetic patients presenting with coronary lesions and the type 2 diabetic patients without SMI were a higher prevalence of peripheral macroangiopathy (56.2 vs. 15.1%, respectively, P < 0.01) and a higher prevalence of retinopathy (P < 0.05). No correlation was found between SMI and duration of diabetes, HbA1c level, renal status, or cardiovascular risk factors except for family history of CAD. CONCLUSIONS: The results of this study allowed us to determine a high-risk group for SMI in the diabetic population. SMI with significant lesions occurs in 20.9% of type 2 diabetic male patients who are totally asymptomatic for CAD. Based on these findings, we recommend routine screening for male patients in whom the duration of type 2 diabetes is >10 years or even less when more than one cardiovascular risk factor is present.

Out of 1,141 successive transoesophageal echocardiographic studies performed prospectively between 01/05/1993 and 31/12/1995, 26 cases of left atrial thrombosis were observed (2.2%); 5 were in the left atrium (20%), 19 in the left atrial appendage (73%) and the thrombi were in both atrium and left atrial appendage in 2 cases (7%). The 26 patients included 15 women and 11 men, with an average age of 69 +/- 16 years (range 25-89 years); 22 patients (84%) had permanent atrial fibrillation and 4 were in sinus rhythm. Only 5 of the patients were on oral anticoagulant therapy. All had underlying cardiac disease: 11 mitral valve diseases; 10 dilated cardiomyopathies; 2 hypertrophic cardiomyopathies; 3 other cardiac diseases. The indication for transoesophageal echocardiography was systemic embolism in 13 cases (50%); before D.C. cardioversion in 10 cases (38%) and before percutaneous mitral valvuloplasty in 3 cases. The thrombus was adherent in 18 cases (69%) and mobile in 8 cases (31%). Spontaneous contrast was observed in 23 cases (88%). Intravenous heparin was given as soon as the diagnosis was made. In 4 patients, thrombectomy was indicated in view of the threatening nature of the thrombus and/or the necessity for associated valve replacement. In 22 patients, heparin was relayed by oral anticoagulants on the 10th day of treatment. Control transoesophageal echocardiography was not performed because of the patient's refusal or poor general condition. The other 15 patients were reexamined 1 to 5 times between the 4th day and 12th month: a regression was observed in 13 cases (86%) which was complete in 11 and partial in 2 cases. No cases of embolism occurred during follow-up but six patients died: 1 of the operated cases and 5 of the patients treated medically (3 cardiac failures and 2 cerebral haemorrhages). The authors conclude that left atrial thrombosis is rare in the absence of classical embolic cardiac disease. With the exception of the surgical indication of a life-threatening thrombus and/or associated surgical mitral valve disease, anticoagulant therapy results in complete or partial regression of the thrombus visualised by transoesophageal echocardiography which is essential for follow-up. The prognosis depends on the severity of the underlying heart disease.

The tilt table is a diagnostic device used to induce vagal syncope and determine etiology. Sensitivity enhancing techniques, such as the administration of isoproterenol, can be applied to children and young adults to compensate for the otherwise low sensitivity (20%‐30%) observed in that population. This study describes an improved test that offers a simplified approach while decreasing the amount of time involved by up to 50%, without compromising sensitivity. This 45‐minute procedure relies on sensitization with isoproterenol administered as a 2‐ to 8‐μg bolus instead of a continuous infusion. The isoproterenol is injected at the 30th minute of a 45‐minute 60° tilt test without returning the patient to the supine position. In this study, the isoproterenol bolus tilt test was found to be “positive” in 24 of 30 patients reporting unexplained syncope: 10 cases before the 30th minute (11.2 ± 8.4 min) and 14 cases after administration of 5.1 ± 1,9 μg of isoproterenol.

Heart rate variability is a sign of sympathetic activity. The authors compared two study populations of young males aged 19 to 30 years: population T comprised 15 healthy volunteers who had two negative tilt tests, one under basal conditions and the other after a bolus of isoproterenol; population S comprised 12 patients without cardiac or other disease, who were followed up for malaise and in whom the basal tilt test was positive, confirming the vagal origin of syncope. Temporal and spectral (total power, low frequency 0.04-0.15 Hz, hight frequency 0.16-0.40 Hz) data was obtained concerning heart rate variability from 24 hour Holter monitoring. The main difference between the two study populations was in the temporal data over 24 hours especially with respect to the heart rate (T = 73.5 +/- 6.9; S = 65.4 +/- 6.2/min; p = 0.004) and the percentage of successive R-R intervals varying by more than 50 ms (PNN 50) (T = 20.2 +/- 8.3%; S = 30.7 +/- 10.2%; p = 0.024). At night, the lowest SDANN/5 (standard deviation of RR intervals over periods of 5 minutes) were observed in group S (67.2 +/- 16.7 ms vs 87.3 +/- 24.4 ms; p = 0.026). No statistically significant differences between the two groups was observed in the spectral data. The temporal data of heart rate variability on Holter ECG monitoring over 24 hours could therefore have a good predictive value of the vagal origin of syncope in young adults.

Anatomical studies suggest that sites of coronary spasm are subject to early atherosclerosis. Coronary angiography is unable to confirm the lesions or provide information about their nature. On the other hand, endocoronary ultrasound is able to identify and, it is hoped, to determine the frequency and composition of the lesions. Nineteen patients with chest pain and angiographically normal or subnormal coronary arteries were included in a prospective study (16 men and 3 women: average age 53 +/- 10 years). Four patients had spontaneous spasm and in the other 15, spasm was induced by intravenous injection of ergometrine (6 micrograms/kg). After countering the spasm with isosorbide dinitrate, the site of spasm and adjacent segments were examined by endocoronary ultrasound. Localised vasospasm which was stenotic in 14 cases and obstructive in 5 cases, was observed. The ECG was unchanged in 4 cases and showed ST-T segment changes in 15 cases. The artery affected was the left anterior descending in 10 cases, the left circumflex in 2 cases and the right coronary in 7 cases. A plaque of atheroma, defined as significant intimal thickening, was detected in 18 out of the 19 cases. This atheroma was classified as soft in 17 cases and hard in one case. The authors conclude that vasospasm is not only associated with a plaque of atheroma, nearly always suspected at coronary angiography, but also its composition is nearly always soft (lipidic) from ultrasonographic data.

Summary— Several recent reports have described the antiarrhythmic effects of a single high oral dose of amiodarone but clinical electrophysiologic effects have not been reported. The present study was performed to assess electrophysiologic effects in 12 patients. After baseline electrophysiologic studies (EPS) patients were administered a single oral dose of 30 mg/kg of amiodarone. EPS was repeated 7.5 ± 0.5 hours later. Plasma levels of amiodarone and its metabolite desethylamiodarone were determined at the time of the second EPS. Holter monitoring was performed for 24 hours after amiodarone administration. Amiodarone significantly increased the following parameters: corrected QT interval (+4.5%), functional refractory period of the right atrium (+7%); AH interval (+12.3%), effective refractory period of the atrioventricular node (+18.5%), and cycle length of Wenckebach block (+8.4%). These effects were not correlated with plasma levels of amiodarone and desethylamiodarone. Holter monitoring detected no significant bradycardia or arrhythmia. These findings indicate that the effects of a single high oral dose of amiodarone are the same as those known to be induced by acute intravenous administration.