A comparison between conventional scintigraphy and emission tomography with thallium-201 in the detection of myocardial infarction: concise communication.

We have compared emission tomography and conventional scintigraphy with thallium-201 in a series including 15 normal subjects and 64 patients showing transmural myocardial necrosis in various locations, fully documented by clinical, electrocardiographic, and enzymatic evidence. The reconstruction was derived from 32 projection images collected around the left side of the patient's chest by a rotating scintillation camera. The conventional views and the transverse, frontal, and sagittal sections were interpreted independently by two observers. The final calculated sensitivity was 89% with conventional scintigraphy and 98% with emission tomography, and the specificity was 93% in the two cases. Thus, emission tomography provides a better sensitivity and also a better interobserver agreement than conventional scintigraphy in the detection of transmural myocardial necrosis with thallium-201.

[Anisoylated plasminogen streptokinase complex during the acute phase of myocardial infarction. Results of a multicenter double-blind study versus heparin]. / Le complexe streptokinase plasminogène acylé à la phase aiguë de l'infarctus du myocarde. Résultats d'une étude multicentrique en double aveugle versus héparine.

Two hundred and thirty-one patients admitted to hospital within 5 hours of the onset of symptoms of a primary myocardial infarction were randomised into 2 groups: one received thrombolytic therapy [anisoylated plasminogen streptokinase activator complex (APSAC): 30 IU in 5 minutes] and the other was given conventional heparin therapy (5,000 IU). Heparin was given to both groups 4 hours later (500 IU/kg/day); the APSAC (N = 119) was identical with respect to age, location of infarct, Killip classification, delay before randomisation (188 +/- 62 minutes). Coronary angiography and ventriculography were performed after 3.4 +/- 1.2 days, and angioscintigraphy and myocardial scintigraphy after 19 +/- 2.5 days to determine the size of the infarct and the quality of left ventricular function. Coronary patency was much higher in the APSAC group (77%) than the heparin group (37%) (p less than 0.001). The angiographic ejection fraction was significantly greater in the thrombolytic group than in the heparin group (53 +/- 13% vs 47 +/- 12%, p less than 0.002), the difference being statistically significant in the anterior and inferior infarct subgroups. At the third week, the difference remained significant in the anterior infarct subgroup: a 31 per cent reduction in necrosed myocardial mass was observed in the APSAC group (33% in anterior infarcts: p less than 0.05 and 16% in inferior infarcts: NS). The limitation of infarct size explained the smaller reduction in left ventricular systolic function (r = 0.73; p less than 0.01). The hospital and one year mortality was comparable in the two groups which was not surprising given the small number of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

[Dystrophic aortic insufficiency: influence of dilatation of the ascending aorta on secondary outcome]. / Insuffisance aortique dystrophique: influence de la dilatation de l'aorte ascendante sur l'évolution secondaire.

This cooperative study recensed 89 cases of patients operated for aortic regurgitation in whom the dystrophic process was confirmed on anatomical (thin, translucent valves without symphysis, multilation or sclerosis) and histological criteria (mucinous infiltration). They included 81 men (91%) and the average age was 52 +/- 14 years. The valvular degeneration was part of a generalised dystrophy of elastic tissue in 8 patients (6 "formes frustes" of Marfan's syndrome, 2 Lobstein's syndrome). The patients were divided into 2 groups according to the diameter of the ascending aorta measured by echocardiography and/or aortography. In Group 1 (n = 40), the aorta was not dilated (diameter less than 40 mm) whereas in Group 2 (n = 49), the diameter of the ascending aorta was dilated (40-55 mm) but not aneurysmal (loss of parallelism of the aortic walls). The two groups were comparable before surgery with respect to age, sex, functional class, degree of left ventricular dilatation, left ventricular ejection fraction and presence of associated coronary disease). There were no differences in the operative parameters but aortic parietal biopsy (n = 35) revealed clear signs of cystic medianecrosis more often in Group 2 than in Group 1 (14/25 versus 1/10, p less than 0.05). No operative procedure was performed on the ascending aorta during aortic valve replacement. One operative death occurred in each group. After an average follow-up of 4 years, there was a higher mortality in Group 2: the actuarial 7 year survival rate being 74% in Group 1 and 54% in Group 2. This was explained by a higher incidence of ascending aortic complications. Only 1 patient in Group 1 developed an aneurysm of the ascending aorta requiring reoperation compared to 14 patients in Group 2, 8 of whom were reoperated (p less than 0.01). These results suggest that non-aneurysmal dilatation of the ascending aorta in patients with dystrophic aortic regurgitation is a poor prognostic factor because of the high incidence of secondary aortic parietal complications (aneurysm, dissection).

[Myocobacterium tuberculosis endomyocarditis. Apropos of a case in a patient with a mitral valve prosthesis]. / Endomyocardite à Mycobacterium tuberculosis. A propos d'un cas chez un patient porteur d'une prothèse valvulaire mitrale.

A case of lethal cardiac tuberculosis with myocardial and endocardial involvement is reported in a 46 year old man with a Starr-Edwards mitral valve prosthesis inserted two years previously for severe mitral regurgitation, secondary to ruptured chordae of the posterior mitral leaflet. Apart from tuberculous pericarditis, cardiac involvement is extremely rare; it occurs in "tuberculous septicemia" whose characteristic features--tuberculinic anergy, hematological abnormalities especially pancytopenia,--lead to delay in diagnosis, which is usually fatal. The case presented is an example.

[General physiopathology of chronic left ventricular insufficiency]. / Physiopathologie générale de l'insuffisance ventriculaire gauche chronique.

The failing heart is unable to provide some organs, notably the brain and the myocardium, with the amount of blood flow they require. To this myocardial inadequacy and resulting "circulatory insufficient" the body reacts by setting in action compensatory mechanisms which are "intracardiac" first (Starling's heterometric regulation, ventricular hypertrophy), then neurohormonal, with the activation of vasoconstrictor systems (noradrenergic system, renin-angiotensin-aldosterone system, arginine-vasopressin system) counterbalanced by the activation of vasodilator systems (vasodilator prostaglandins, atrial natriuretic factor and kinins). However, the vasoconstrictor systems outweigh the vasodilator systems. They create an excessive arterial and venous vasoconstriction, together with water-and-salt retention, which leads to an increase of left ventricular work during both systole and diastole and to a gradual worsening of the heart failure. The present-day treatment of heart failure aims at reducing the water-and-salt retention and at restoring the balance between the vasoconstrictor and vasodilator systems.

[Severe aortic incompetence from dysplasia of the valve. A report on 19 cases of this real but often unrecognized disorder (author's transl)]. / Les insuffisances aortiques volumineuses par dysplasie valvulaire: réalité souvent méconnue. A propos de dix-neuf observations.

A total of 19 patients were found to have severe aortic incompetence from dysplasia of the valve (thin, spread-out valves having a tendency towards eversion). This type of valve abnormality is often unrecognized but is found in 13,6% of cases of severe aortic incompetence. The relationship between this condition and Marfan's syndrome or its aberrant forms are discussed, as well as its frequency when unrelated to this disease. The dysplasias can be isolated phenomena or associated with pathological conditions of the ascending aorta. The results of this review suggest that some of these dysplasias might be rheumatic in origin.

[Hemodynamic effects of intravenous isosorbide dinitrate in chronic heart failure (author's transl)]. / Effets hémodynamiques du dinitrate d'isosorbide intraveineux dans l'insuffisance cardiaque chronique.

During cardiac catheterization, isosorbite dinitrate (ISDN) was given intravenously to ten patients with confirmed left ventricular failure (10 NOMC, 1 ischemic cardiopathy, 1 valvular disease). When the left ventricular filling pressure was above 15 mmHg and the systemic systolic pressure exceeded 100 mmHg, a 500 gamma (first half of patients) or 800 gamma (second half of patients) bolus of ISDN was given intravenously, followed by an infusion of 2.5, 5 or 10 mg ISDN per hour. In all patients, the functional tolerance was excellent ; the heart rate remained unchanged and the systolic systemic pressure decreased only slightly (10 %). Left ventricular filling pressures returned to normal in four patients, decreased significantly in three, and remained unchanged in three. The cardiac output increased significantly in four patients. The poor initial hemodynamic conditions and the doses given, subsequently considered insufficient especially during the first part of the study, probably explain why ISDN was only partly effective.

[Intravenous isosorbide dinitrate in acute cardiac failure (author's transl)]. / Utilisation du dinitrate d'isosorbide par voie intraveineuse dans l'insuffisance cardiaque aiguë.

Isosorbide dinitrate (ISDN) was used by intravenous infusion in 7 patients with acute cardiac failure consecutive to acute (5) or chronic (1) myocardial infarction or to non-obstructive cardiomyopathy (1). Pulmonary artery pressure (PAP), pulmonary capillary pressure (PCP), right atrial pressure (RAP) and cardiac output were measured (PCP), right atrial pressure (RAP) and cardiac output were measured by intracardiac catheterization. The initial dosage of 2.5 mg/hour was increased until PCP was reduced to 15 mmHg or less or until troublesome side-effects developed. Control was achieved in 3 patients with doses of 2.5 to 7 mg/hour and, to a lesser extent, in one patient with up to 20 mg/hour. Three patients failed to respond even to higher doses and needed furosemide i.v. or furosemide + dobutamine. One patient died of cardiogenic shock. No changes in cardiac output, heart rate and blood pressure and no clinical side-effects were recorded. Thus, in acute cardiac failure ISDN may be effective in doses slightly superior to those of nitroglycerin, but increasing the dosage above 7 or 8 mg/hour does not bring additional benefits. The drug is remarkably well tolerated.

[Unidimensional echocardiogram of normal infants and children (author's transl)]. / L'échocardiogramme de l'enfant normal. Les paramètres de la fonction ventriculaire gauche.

One hundred and one echocardiograms were performed in children 8 days to 15 years old. The values measured were : end-diastolic and end-systolic left ventricular diameters, aortic root diameter, left atrial diameter, end-diastolic septal and posterior wall thickness, mitral valve excursion. There is a good correlation of these values with the square root surface area. The indices of left ventricular performance are : mean velocity of circumferential fiber shortening (correlated with heart rate), ejection fraction and shortening fraction. These indices are not correlated with body surface area. These data can be used in the echocardiographic investigation of infants or children with heart diseases.

Feasibility of gated single-photon emission transaxial tomography of the cardiac blood pool.

A procedure for gated single-photon emission transaxial tomography of the cardiac blood pool using a commercially available rotating camera and a computer is described. During image acquisition, the end-diastolic and end-systolic frames are retained after each of the 16 angular steps of the rotation of the camera around the anterior side of the patient's chest. Complete acquisition takes 25 minutes; 10 more minutes are required for the reconstruction and processing of the sections. One set of images is oriented transaxially; the other set includes vertical sections obtained by rotation around a vertical axis passing through the center of the left ventricular cavity. Results from the planar and tomographic examinations were in good agreement for most of the 18 patients who underwent both studies, although more inferior abnormalities were detected with tomography.