Usefulness of technetium-99m pyrophosphate myocardial scintigraphy in amyloid polyneuropathy and correlation with echocardiography.
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Publications and source records attributed to B Boujon.
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Technetium 99m cardiac scintigraphy as practiced at present for diagnosing amyloisodid only provides a visual semi-quantitative assessment of uptake of the isotope. To improve the diagnostic accuracy of the method, the authors evaluated prospectively a personal technique of scintigraphy quantification based on early images obtained at the 20th minute in 15 patients with neuropathic amyloidosis. Doppler echocardiographic studies indicated that 9 patients had cardiac involvement whilst 6 were free of cardiac amyloidosis. The index of isotopic uptake (ratio of cardiac/abdominal uptake) was 0.44 to 1.58 in the first group and 0.09 to 0.31 in the second group. The correlation between the scintigraphic index and interventricular septal or posterior wall thickness measured by echocardiography was poor. These results obtained in 15 patients with neuropathic amyloidosis suggest that the scintigraphic index measured at the 20th minute is discriminatory and allows identification of those patients with cardiac involvement. On the other hand, the correlations with echocardiographic wall thickness are poor. Technetium 99m cardiac scintigraphy with this technique of quantification is a useful tool for diagnosing cardiac amyloidosis, especially when echocardiography is difficult to interpret.
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A 52 year old patient presenting with spontaneous anginal chest pain for 4 days was admitted to hospital for a more intense and prolonged chest pain associated with signs of left ventricular failure (gallop, pulmonary crepitations, hypoxemia). Coronary angiography showed marked septal hypokinesia and spontaneous localised spasm of the left anterior descending and marginal arteries with a variable degree of luminal narrowing of the other segments of these two arteries and of the right coronary artery. These changes regressed after intracoronary injection of molsidomine. The signs of left ventricular failure disappeared in 48 hours. The wall motion abnormality, monitored by 2D echocardiography, regressed slowly over 3 days. On the other hand, the electrocardiogram, which showed anterior wall subendocardial ischaemia with prolongation of the QTc interval during the spasm, remained abnormal for a long time. Therefore, in the absence of organic heart disease, coronary spasms associated with vasoconstriction can induce a sufficiently severe and durable alteration of left ventricular function to create clinical signs of cardiac failure and profound and prolonged ST-T wave changes on the electrocardiogram.
The purpose of this prospective randomized trial was to compare the efficacy of propranolol and amiodarone in suppressing ventricular arrhythmias during the first 6 months following myocardial infarction (MI). 97 patients were treated with either amiodarone (n = 48) or propranolol (n = 49) starting on the 9th day following MI. Holter monitoring was carried out on four occasions: on D7, D21, D90 and D180. There was no statistical difference in the incidence of 'major' arrhythmias (an average of at least 10 ventricular premature complexes (VPCs) h-1, multiform or paired VPCs or runs) between the two groups on D7. A significant difference in favour of amiodarone became apparent at D180 (P = 0.04). Patients were also classified according to whether treatment failed or was successful. 'Success' was recorded when arrhythmias remained minor or became minor (less than 10 uniform VPCs h-1) and 'failure' when arrhythmias remained major or became major, or when patients were withdrawn because of side-effects, or lost to follow-up. The difference remained in favour of amiodarone (P = 0.03 at D21; P = 0.05 at D90; P = 0.06 at D180). Evaluation of the percentage reduction in the number of VPCs at D21, D90 or D180 compared with D7 showed superiority of amiodarone at D90 (P less than 0.01) and D180 (P less than 0.04). In this study, the overall effect of amiodarone on ventricular arrhythmias following MI was shown to be superior to that of propranolol.
Cardiotoxicity is the main obstacle to the use of high-dosage adriamycin in chemotherapy. It is difficult to decide whether or not treatment should be continued when the cardiac function -- irrespective of the method by which it is evaluated -- is at the lower limit of normality. Some authors consider that chemotherapy can be pursued as long as the shortening fraction of the echocardiographic diameter remains within normal limits in relation to the end-systolic constraint. We have established the limits of normality of this relationship before chemotherapy in 53 patients with normal cardiovascular system. We conclude that the end-systolic constraint essentially depends on the end-systolic diameter, so that the results provided by the study of the shortening fraction end-systolic constraint relationship are qualitatively the same as those of the shortening fraction-end-systolic diameter relationship, which is much easier to obtain. It seems to us that the criteria of cardiotoxicity after administration of adriamycin 300 mg/m2 are: (1) shortening fraction lower than 25 p. 100; (2) ventricular dilatation (end-systolic diameter greater than 40 mm) without associated valve disease; (3) reduction of the shortening fraction (whatever its value) in relation to the end-systolic diameter by more than 2 standard deviations on the regression slope of the correlation; (4) more than 25 p. 100 reduction of the shortening fraction after administration of adriamycin 300 mg/m2, betraying a high sensitivity to the cardiotoxic effects of the drug. Such individual sensitivity, studied in 25 patients, seemed to vary widely from one subject to another and to be independent of the initial status.(ABSTRACT TRUNCATED AT 250 WORDS)
It has long been known that the morphology of ventricular repolarization is extremely sensitive to acute or chronic myocardial anoxia. In patients with coronary disease, we are used to observe a wide variety of ST segment, T wave and sometimes U wave abnormalities. The classical description of "lesions" or "ischaemia", as well as their anatomical locations called, perhaps rather arbitrarily, "subendocardial" or "subepicardial" account for ST segment displacements and T wave inversions the patterns of which are well known to all of us. It may happen, however, that repolarization takes a frankly unusual appearance very different from the conventional images. On several occasions we were surprised to find, in a situation of acute or subacute coronary obstruction, a highly atypical and characteristically very transient repolarization pattern with considerable lengthening of QT and broad and deep inversion of T wave which, to our knowledge, have never been described in the literature. A systematic search for such unusual ECG patterns, conducted over the last 4 years in the Cardiology department of the Bicêtre Hospital on patients with ischaemic heart disease, has yielded 16 cases which are reported in the present study.
Fifty-one consecutive patients with atrial tachycardia [atrial fibrillation (FA) 37, atrial flutter (Fl) 10, tachycardia (TSA) 4] received a single 2 mg/kg dose of flecainide injected intravenously over 5 to 10 minutes. Patients over 75 years of age or presenting with heart failure or disorders of conduction were excluded from the study. Sinus rhythm was restored during the injection or within the following 5 minutes in 15 patients (FA 12, Fl 1, TSA 2). The most frequent side-effects were visual disorders (5 cases) and moderate prolongation of QRS (all cases). Five patients had more pronounced disorders of conduction, but none developed heart failure. Reduction was obtained in 12 of the 18 patients whose arrhythmia had lasted for less than 8 days, against only 3 of the patients whose arrhythmia was more than 8 days old. Drug-induced reduction always failed in patients with left atrial dilatation (greater than 45 mm at echocardiography). An increase in the ventricular rate of unreduced flutter was observed in only one patient. Plasma flecainide levels were high (1.5 and 5.5 mg/l) at the end of the injection, but they fell to the therapeutic range within less than 10 minutes. Flecainide therefore appears to be effective in reducing recent atrial fibrillation on a non-dilated atrium. In cases with disorders of conduction, altered ventricular function or flutter, the therapeutic risk is such that another method of conversion should be used.