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The authors report a case of thrombolytic therapy with streptokinase in the early postoperative period after aortic valve replacement with a Saint Jude medical prosthesis. After good initial progress, the patient had to be reoperated on the 12th postoperative day for sternal disunion. Reoperation was followed rapidly by progressive thrombosis of the aortic prosthesis demonstrated by repeated Doppler echocardiographic examination. The impossibility of eliminating mediastinitis led to medical thrombolysis. The outcome was favourable after a regressive cerebral embolic event. This case illustrates the value of Doppler echocardiographic examination in the postoperative period. Thrombolysis may constitute an alternative to reoperation when the operative risk is high. The risk of thrombolysis may not be as great as some believe.

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In a double-blind 6 month trial, the cardiac effects of captopril and minoxidil, administered as third step treatments, were compared in 34 men with essential hypertension and diastolic blood pressure greater than 95 mm Hg who were taking 200 mg/day of metoprolol and 80 mg/day of furosemide. Average daily doses of captopril and minoxidil were 269 mg (range 150 to 300) and 20 mg (range 7.5 to 30), respectively. At the end of the 6 months' treatment, blood pressure had dropped significantly in both groups, but echocardiographic criteria of hypertrophy improved only in the captopril group (intragroup comparison): blood pressure, thickness of the intraventricular septum and posterior wall, and the left ventricular mass index, respectively, decreased from 163/102 to 135/89 mm Hg (p less than 0.001), 17.4 to 15.9 mm (p less than 0.05), 14.5 to 13.4 mm (p less than 0.05) and 236 to 198 g/m2 (p less than 0.001). In the minoxidil group, blood pressure dropped from 160/99 to 137/87 mm Hg (p less than 0.001), but echocardiographic criteria were not significantly modified. Fractional shortening remained normal in both groups. These results show that in patients with severe left ventricular hypertrophy, captopril-based triple therapy reduces left ventricular mass without altering systolic performance, whereas minoxidil-based therapy does not.

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Instantaneous intracardiac flow volumes can be calculated as the product of instantaneous flow velocity and instantaneous orifice area. This was accounted for in a new method of measuring stroke volume and cardiac output in the mitral orifice by pulsed Doppler echocardiography. This method was compared with simultaneous thermodilution in 30 adult patients in sinus rhythm without substantial atrioventricular or pulmonary valve abnormalities. The mitral orifice was assimilated to a conduit with 1) an ellipse-shaped inlet and outlet, 2) the same (and constant) long axis for the inlet and outlet ellipses (that is, the mediolateral anulus diameter measured on apical four chamber views), and 3) a varying outlet short axis (that is, the mitral anteroposterior leaflet separation derived from left parasternal M-mode recordings). This method design avoided the need for a short-axis view of the whole circumference of the mitral outlet orifice, which is difficult to obtain in many adult patients. The mitral flow velocity was recorded from the apex under two-dimensional guidance, within the mitral canal, close to the outlet section. Integration of instantaneous mitral leaflet separation multiplied by instantaneous flow velocity was performed using Simpson's rule. In addition to the proposed "instantaneous orifice area" method (method A), a "mean orifice area" method (method B) was also compared with thermodilution. In this simplified method, mitral flow was the product of mean orifice area and the diastolic mitral velocity integral, both derived from the same recordings as for method A.(ABSTRACT TRUNCATED AT 250 WORDS)

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A randomised double blind study was performed in order to compare the cardiac effects of captopril and minoxidil in a subset of patients with severe primitive hypertension, uncontrolled (diastolic BP greater than 100 mmHg) by Metroprolol 200 mg/d and Furosemide 80 mg/d. 25 male pts completed the six month study, 33 pts having been excluded before randomisation (22 inadequate echoes) and 20 after randomisation (7 ambiguities on wall measurement). Average captopril dosage was 265 mg/d (150-300 mg), average minoxidil dosage was 19.6 mg/d (7.5-30 mg), dosages of Furosemide, Spironolactone and Metroprolol were similar in the two groups. Blood pressure decreased dramatically with both regimens (208/130 to 148/96 with captopril, 194/115 to 154/100 with minoxidil). Sokolow index was at the upper range of normal and decreased with both drugs. Cardiothoracic ratio decreased only with captopril. Echocardiograms were performed and read blindly at the end of the study. LV mass was measured according to Devereux, method. All patients had severe LVH. After 6 months posterior wall thickness decreased from 14.8 to 13.8 mm with captopril, remained stable from 14.1 to 14.9 mm with minoxidil, septal thickness decreased from 17.2 to 15.7 mm with captopril and remained stable (14.8 to 15.2 mm) with minoxidil. LV mass and mass index respectively decreased from 456 g and 232 g/m2 to 372 g and 190 g/m2 with captopril, and remained unchanged from 413 g and 215 g/m2 to 420 g and 218 g/m2 with minoxidil. Fractional shortening remained normal in both groups. Intra patients reproducibility was suboptimal because of difficulties in precise delineation of the endocardium in the severely hypertrophied ventricles.(ABSTRACT TRUNCATED AT 250 WORDS)

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The purpose of this study was to determine the value and limitations of an updated Doppler echocardiographic measurement of the aortic regurgitant fraction derived from the comparison of forward and reverse flows in the aortic arch. The method was based on the improvements in sampling and displaying Doppler frequencies and blood velocities provided by pulsed-emission, two-dimensional location, and spectral analysis and on an account for variations of aortic diameter through an M mode record of the aortic arch. Relevant statistical comparisons were performed between simultaneous noninvasive and invasive determinations of the regurgitant fraction in a group of 30 patients with aortic regurgitation (group I) and between simultaneous noninvasive and invasive measurements of variations of the regurgitant fraction induced by atrial pacing or vasodilator administration in 12 patients of this group. The two basal determinations were closely correlated (r = .90). The invasive regurgitant fraction ranged from 0% to 80%. The standard error of the Doppler estimate was 8.8% in group I as a whole and was only 6% in a subgroup of 20 patients with a high systolic aortic flow pattern, defined as both peak velocity above 0.8 m/sec and duration of systolic flow above 0.24 sec. This pattern was present in almost all (19/22) patients in whom the aortic regurgitation was more than moderate by invasive criterion (regurgitant fraction above 40%). The standard error of the Doppler estimate of variations of the regurgitant fraction was only 6.6%. Among 100 additional patients with aortic regurgitation (group II), only 12 had no pandiastolic reverse flow in the arch, and their regurgitation was always mild at aortographic examination.(ABSTRACT TRUNCATED AT 250 WORDS)

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In this review paper the theoretical and technical bases of cardiac output measurement in the thoracic extracted from the literature and obtained by the authors themselves are summarized. The main physiological assumptions required for calculations (flat velocity profile in the aorta) and the main technical options (pulsed or continuous emission of ultrasounds, spectral or simplified Doppler signal analysis, evaluation or non-evaluation of the angle of incidence by two-dimensional imaging, echographic mode of measurement of the aortic diameter) are discussed. The need for controlled studies of each equipment and method on large populations of patients is emphasized.

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The aim of this study was to improve the reproducibility and the standardization of the topographical assessment of myocardial infarctions in routine two-dimensional echocardiography. A myocardial map of the left ventricle was derived from a necropsy study of normal human hearts; interventricular grooves and papillary muscles were used as anatomical landmarks defining 16 segments with similar planimetered surfaces. A reporting sheet was prepared, with diagrams of standardized echo sections and with a map showing the position of the corresponding outlines. The echocardiographic method consisted in identifying on each section the regions without systolic thickening, and displaying the results on the map, until a coherent picture of the abnormal areas was obtained. Interobserver reproducibility was studied in 50 consecutive patients with prior myocardial infarction; segments were classified as fully abnormal, partly abnormal, non-visualized, and normal. Among the 800 segments there were 1% severe and 12% moderate discrepancies; discrepancies were significantly lower for segments with confrontation in two different sections intersecting on the map. A classification of infarction topographies was obtained in 100 consecutive patients; it was compared with the data of two reanalysable pathologic series from the literature; a similar presentation of the results showed similar typical patterns of myocardial involvement, for which a nomenclature was proposed. A myocardial map may be used to provide a simple and reproducible description of infarction topographies; the results obtained lead us to recommend an echocardiographic standardization of ventricular segmentation and of nomenclature of infarction topographies, similar to that of pathological studies.

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The passive left ventricular pressure-volume relationship characterises left ventricular distensibility. However, it has recently been shown that acute pharmacological intervention can significantly change the position of the diastolic pressure-volume curve. We studied the effects of acute volumic expansion on the passive left ventricular pressure-volume relationship. In fact, the interpretation of left ventricular function curves during acute volumic expansion assumes that the left ventricular pressure-volume relationship remains unchanged. We measured the heart rate, cardiac output, left and right ventricular pressures with micromanometers, ventricular volumes by cineangiography 50 frames/sec (n = 6) or ventricular diameters by M mode echocardiography (n = 6) in 12 patients without valvular or coronary heart disease during rapid volumic expansion, and calculated stroke volumes and indices of left ventricular performance; the passive left ventricular pressure-volume or pressure-diameter relationship was adjusted to an exponential function P = a.ekp.V or P = a'.ek'p.De. After volumic expansion the cardiac output rose due to an increase in heart rate and stroke volume. The increase in stroke volume was related to that of end diastolic volume, the end systolic volume remaining unchanged: there was little difference in the indices of left ventricular performance. The pressure-volume and pressure-diameter curves were considerably shifted upwards and to the left during acute volumic expansion: this seemed to be due mainly to an increased intrapericardial pressure secondary to the increase in intrapericardial content. The relationship obtained by subtracting the simultaneous right ventricular from the instantaneous left ventricular pressure after volumic expansion was identical to the basal left ventricular pressure-volume curve. These observations demonstrate the importance of external factors of left ventricular compression in the changes in the passive left ventricular diastolic relationship during acute volumic expansion and invalidate the use of function curves obtained under these conditions for the assessment of left ventricular systolic function. The end diastolic pressure cannot be considered to reflect end diastolic volume and the function curves, in fact, illustrate changes in diastolic distensibility.

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Studies were made on 21 patients, 8 without any symptoms of left ventricular failure, group 1, and 13 with clinical symptoms of heart failure, group 2. Cardiac output, mean aortic and left ventricular pressures (using catheter tip micromanometer), and ventricular volume (obtained from left ventricular cineangiograms) were measured before and during nitroprusside infusion. The heart rate did not change in either of the groups. Only in group 2 did cardiac index and stroke volume increase significantly. Mean aortic pressure and total systemic vascular resistance decreased significantly in both the groups. Left ventricular end-diastolic pressure decreased significantly in both the groups, but this decrease was greater in group 2 (9 mmHg compared with 3 mmHg for group 1). The decrease in the left ventricular end-diastolic volume was similar in both the groups. The decrease in left ventricular end-systolic pressure was greater in group 1, but the decrease in the left ventricular end-systolic volume was greater in group 2. These facts are explained by the differences in the active and passive left ventricular pressure-volume relations in the two groups.

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