The aim of this study was to: (1) compare the usefulness, in clinical practice, of different echocardiographic methods of left ventricular (LV) function determination in patients with a recent thrombolytic-treated acute myocardial infarction (AMI); (2) compare these measurements with the reference method radionuclide imaging; and (3) evaluate the reproducibility of visual estimation of the LV ejection fraction (EF) and the use of the biplane method of discs (Simpson's rule) in clinical practice. Echocardiography and radionuclide imaging were performed within 2 hours of each another, 5 to 8 days after hospital admission. Ninety-six patients (70 men and 26 women) age 64 +/- 9 years (range 45 to 75) were studied. The echocardiographic study was performed by 2 experienced physicians, independently of each another. LV wall motion score index and visual estimation of the EF correlated best with the radionuclide EF (r = 0.72 and r = 0.71), thereafter simply counting the number of affected LV segments (r = 0.67) or atrioventricular plane measurements (r = 0.64). Simpson's rule had low correlation to the radionuclide EF (r = 0.45 to 0.51) and could not be used in approximately half of the patients due to poor identification of endocardial borders. The interobserver coefficient of variation for independent visual echocardiographic estimation of the EF was 10%, for Simpson's rule 18%, and for the radionuclide EF 5%. We conclude that the EF estimated from quantitative echocardiographic volume calculations (Simpson's rule) may differ substantially from radionuclide methods of measuring the EF. However, with experienced sonographers, the LV wall motion score index or visual estimation of the EF had reasonable agreement with the radionuclide EF in most of the patients. Atrioventricular plane measurement is an acceptable alternative.

A total of 61 patients with first-time mild to moderate acute myocardial infarction and no reinfarction within the following 2 months were studied prospectively by Doppler echocardiography before hospital discharge and after 2 months to evaluate the prevalence of mitral regurgitation. Twenty-one age-matched healthy subjects served as controls. At baseline, the prevalence of Doppler-recorded mitral regurgitation was 74% and 29% in patients and controls, respectively. In the patients, the regurgitant flow measured by color flow Doppler was 1.04 cm2 (range 0.2-8 cm2) and occupied 7.5% (range 2-45%) of the left atrial area. Corresponding figures for controls were 0.35 cm2 (0.1-0.6) and 2.4% (0.7-4.5), respectively. On continuous wave Doppler, most patients (33/45) had Doppler signals similar to those of healthy controls. The prevalence of mitral regurgitation was about the same in anterior and inferior infarction (75 and 72% respectively). In the patients, the prevalence was similar after 2 months (79%) with minor changes in the Doppler characteristics of the regurgitation (regurgitant flow 1.12 cm2 and occupying 8.1% of left atrial area). The study demonstrates that in a group of patients with first-time mild to moderate myocardial infarction the prevalence of Doppler-recorded mitral regurgitation is high and mild in severity in the majority of the cases. The changes remain almost similar even after 2 months.

The atrioventricular (AV) plane displacement was studied by echocardiography in 79 subjects (45 healthy subjects and 34 patients with acute myocardial infarction or chronic congestive heart failure). From apical 4- and 2-chamber views the displacement of the AV plane towards the apex in systole was recorded at 4 sites in the left ventricle (LV) corresponding to the septal, anterior, lateral, and posterior walls and the mean value from the above 4 sites (AV-mean) was calculated. In addition, in healthy subjects, the AV plane displacement at right ventricular free wall was also recorded. The AV-mean correlated well with the echocardiographic ejection fraction determined by biplane area-length method (r = 0.96, P less than 0.001). The correlation was also high when the percentage of the left ventricular shortening along the long axis was used (r = 0.97, P less than 0.001). The correlation between ejection fraction and AV-mean was also good when separate analysis was made for the subjects with preserved ejection fraction (r = 0.86, P less than 0.001) and decreased ejection fraction (r = 0.82, P less than 0.001). The right ventricle had a significantly higher AV plane displacement (P less than 0.001) than the LV. The study also includes determination of the muscular excursions of the septal and posterior walls along the short axis of the left ventricle from the parasternal long axis view. The AV plane displacement of the respective walls was relatively greater (P less than 0.001) compared to concentric contractions. The septal and posterior wall excursions along the short axis correlated poorly with the AV plane displacement of the respective walls (r = 0.55, P less than 0.01 and r = 42, P less than 0.05).

A trial fibrillation (AF) is a clinically important arrhythmia with important therapeutic and prognostic implications. The disorganized electrical and mechanical activity causes loss of active atrial contraction. This in turn results in insufficient atrial emptying and impaired ventricular filling.1 AF may be converted to sinus rhythm by means of direct-current countershock. Hemodynamic studies before and after cardioversion of AF to normal sinus rhythm report conflicting results regarding improvement in hemodynamic function.2–4 Some studies suggested that normal atrial contraction may not occur immediately after successful cardioversion of AF to sinus rhythm.1,3 The purpose of this study was to evaluate, using echocardiography and Doppler, the mechanical activity of the left atrium and its effect on left ventricular (LV) function after electrocardioversion of AF to sinus rhythm.

Echocardiographic quantitative assessment of the atrioventricular plane displacement (AVPD) in systole towards the apex has been used to estimate global left ventricular (LV) function. The study population consisted of 106 patients with coronary artery disease (CAD) with or without previous myocardial infarction and 40 age-matched healthy subjects. The AVPD was recorded from the apical four- and two-chamber views at four sites corresponding to the septal, lateral, anterior and posterior walls of the left ventricle. A mean displacement (AVmean) was calculated from the above sites. AVmean was significantly decreased in patients with CAD compared to healthy subjects (P less than 0.001). In patients in whom the left ventricular ejection fraction (LVEF) was calculated from cineangiograms a good correlation between AVmean and LVEF was found (r = 0.89, P less than 0.001, SEE = 6.4). Selecting an AVmean of 10 mm or more to define a normal LVEF (greater than or equal to 55%) resulted in a sensitivity of 92% and a specificity of 87% in predicting a normal versus abnormal left ventricular systolic function. It is concluded that the ease of recording the AVPD by echocardiography provides a simple and valuable noninvasive method to assess global left ventricular function in patients with CAD.

The effect of exercise on the displacement of the atrioventricular (AV) plane was studied by echocardiography (echo) in 48 patients with stable angina pectoris without prior myocardial infarction and 20 age-matched healthy subjects. Echo was performed at rest, immediately after and 10 and 30 min after the test. The patients also underwent thallium stress scintigraphy and coronary angiography. From the apical four- and two-chamber views, the atrioventricular plane displacement (AVPD) during the cardiac cycle was recorded at four sites corresponding to the septal, anterior, lateral and posterior walls of the left ventricle and a mean value was calculated (AV-mean). The healthy subjects and patients had almost the same AVPD at all the sites at rest (AV-mean of 14.5 and 14.2 mm respectively). Immediately post-exercise the healthy subjects showed a significant (P less than 0.001) and equally distributed increase in the AVPD at all the sites with an AV-mean value of 19.2 mm. In most of the patients with angiographically confirmed coronary artery disease (CAD), there was a reversible decrease of AVPD (greater than or equal to 3 mm) at one or more of the AV plane sites. The overall sensitivity and specificity were 80% and 100% respectively in identifying CAD patients. The changes correlated well with the reversible ischaemic changes on the thallium scan (sensitivity, 88%, and specificity, 83%). A generalized exercise-induced decrease in AVPD at all the recorded sites had a high specificity (91%) in detecting patients with three-vessel disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract. Echocardiographic recording of the atrioventricular (AV) plane displacement during the cardiac cycle was used to assess left ventricular (LV) global function in patients with congestive heart failure (CHF). The study population consisted of 70 patients with chronic CHF (NYHA functional groups III and IV) following dilated cardiomyopathy (DCM) or myocardial infarction (MI), and 35 age‐matched healthy subjects. The AV plane displacement was recorded from the apical 4‐ and 2‐chamber views at four LV sites located about 90 degrees apart and representing the septal, anterior, lateral and posterior parts of the LV wall. A mean value was calculated from the above sites (AV‐mean). Patients with CHF showed a significant generalized reduction of AV plane displacement compared to healthy subjects (5.6 mm vs. 14.5 mm, P < 0.001). Thirty CHF patients also underwent radionuclide angiography in order to determine the ejection fraction (EF). The correlation between AV‐mean and EF was good (r=0.82, P < 0.001). The selection of an AV‐mean of < 7 mm to define a severely depressed LV function (EF < 30%) gave a sensitivity of 92% and a specificity of 67%. It is concluded that the AV plane displacement can be used to estimate LV systolic function in patients with CHF.

The effects of acute myocardial infarction (MI) on the displacement of the left ventricular (LV) atrioventricular (AV) plane is presented. The material consisted of 40 patients with first-time Q-wave MI (26 pts with ant. MI and 14 with post. MI). Nineteen age-matched healthy subjects were used as controls. The displacement of the AV plane was determined at four sites corresponding to anterior (AV-A), septal (AV-S), posterior (AV-P) and lateral (AV-L) parts of the LV wall. In anterior and posterior MI all the sites showed significantly reduced AV-plane displacement compared to healthy subjects (P less than 0.001). Moreover, within the anterior MI group the AV-A and AV-S displacements were significantly reduced compared to the points AV-L and AV-P (P less than 0.001) and the AV-L displacement was reduced compared to AV-P (P less than 0.001). In posterior MI the displacement at AV-P was reduced compared to other points (P less than 0.001) and, to a certain extent, AV-S was reduced compared to the points AV-A and AV-L (P less than 0.001). The reduced magnitude of the AV plane displacement seems to be an expression of regionally reduced systolic function. The method described may provide a simple means of defining regional wall motion abnormalities of the LV following MI.

A method of measuring the displacement of the atrioventricular (AV) of the left ventricle plane during the cardiac cycle in 71 healthy persons is described. An echocardiographic equipment with two cursors was used. Measurements were performed from four sites in the AV plane situated about 90 degrees apart and corresponding to the septal, anterior, lateral and posterior myocardial walls. The mean displacement during systole was 16 mm towards the apex. There was no significant difference in the recordings from the four sites. The study population was divided into three groups with mean ages 28, 42 and 60 years (group I, II and III). The displacement was significantly smaller in group III compared with groups I and II. Fractional shortening, however, could not demonstrate such a difference. The determination of displacement of the AV plane may imply the introduction of a new and simple method in assessment of left ventricular function.

The effect of intravenous amitriptyline (0.5-2 mg/kg) on heart rate, blood pressure, ECG, and electrolytes in plasma and heart muscle was studied in rats. In addition, the effect on monophasic action potentials was studied in rats with open chest. Amitriptyline caused a significant decrease in blood pressure and heart rate and a significant prolongation of QRS and PQ duration. At the time of maximal QRS prolongation (mean +94%) the duration of monophasic action potentials was virtually unchanged. Beta-adrenergic blockade by means of pretreatment with 0.1 mg propranolol did not influence the amitriptyline-induced prolongation of QRS duration. Amitriptyline administration causing obvious QRS prolongation induced no detectable changes in plasma and heart muscle electrolytes. The results contradict adrenergic dominance or marked imbalance between intra- and extra-cellular electrolytes as a cause of the ECG changes. The present data indicate that the amitriptyline effect is compatible with a direct quinidine-like action on the heart, resulting mainly in a slowing of impulse propagation in the intracardiac conduction system.

The local effect of intra-arterial infusion of amitriptyline (AT) on forearm blood flow was studied in seven healthy subjects. AT was infused at rates of 0.05, 0.10, 0.15, and 0.20 mg-min--1 for periods of 5 min. Forearm blood flow showed a dose-dependent increase when the dose exeeded 0.10 mg-min--1. On the highest dose level the blood flow increased on an average by 73%. No systemic effects, as reflected by changes in heart rate, blood pressure, and blood flow in the contralateral forearm, were observed during the infusion. The present data indicate a dilatating effect of AT on resistance vessels possibly mediated by an alpha-adrenergic blockade.

Clinical variables, and especially their relation to the ECG, have been studied in 153 cases of poisonings by tricyclic antidepressants (TCA). The mean age of the patients was 34 years. Amitriptyline poisoning accounted for 112 (73%) of the cases and the mean dose ingested was about 1 000 mg. Coma was present in 87 patients (57%) and on admission 40 (26%) had a systolic blood pressure (BP) below 100 mmHg. The systolic BP on admission was significantly lower (p less than 0.001) and the heart rate (HR) higher (p less than 0.001) than when the patients left the ward. Apart from an increased HR (greater than or equal to 90 beats/min), which was present in 73% of the cases, the most characteristic ECG change was a QRS prolongation (greater than or equal to 0.11 sec), this being found in 42% of the cases. About the same proportion displayed a QT prolongation and 28% had a prolonged PQ time. The mean of the QRS times was 0.11 sec. Unlike the QT time, the QRS time was not correlated to HR. Statistical analysis of the material with regard to clinical variables (dose of TCA, BP, coma duration, etc.) showed that the QRS time was closely related to the severity of poisoning. Five patients (3) died, all of whom already on admission demonstrated advanced ECG changes with arrhythmias and a mean QRS time of 0.19 sec. Excluding dibenzepine poisonings (4 cases, all fatal), the mortality rate was 0.7%. The importance of high initial preparedness for cardiac complications is pointed out, as is the value of the QRS time as a guide to the severity of poisoning.

. Cardiovascular dynamics have been studied in 10 patients admitted because of poisoning by tricyclic antidepressants (TCA) and in 7 with hypnotic drug (HD) poisoning. Right heart catheterization (floating catheter technique) and determination of cardiac output (dye dilution technique) have been performed during and after an initial comatous phase. In the TCA group there were marked ECG changes with a mean increase of QRS duration to 0.14 sec during the comatous phase. The cardiac output was then increased in relation to the calculated oxygen uptake compared with the findings in awake state, when the ECG changes had diminished or disappeared. After i.v. administration of 5 mg propranolol the fall in cardiac output was most pronounced during the comatous phase but the broadening of QRS complexes was not affected. The central venous and systemic arterial BP were normal. As judged by the normal diastolic pressure in the pulmonary artery and the normal central venous pressure there were no signs of myocardial insufficiency. The cardiac output in the TCA group was twice as high, i.e. significantly higher, as in the HD patients. The arteriovenous oxygen difference was significantly lower (on an average 40%). The hyperkinetic circulation during TCA poisoning may be explained by a dominant adrenergic stimulatory effect on the circulation.

Abstract The hemodynamic response to infusion of norepinephrine (NE) has been measured in 12 patients with severe hypnotic drug poisoning. All patients had a mean arterial blood pressure (B.P.) of 70 mmHg or less initially. As evaluated from central venous pressure no marked hypovolemia was present. Cardiac output (C.O.) was determined by the dye dilution method and right heart catheterization by a “floating” catheter technique. Following infusion of NE the arterial B.P. and C.O. increased. The increase in C.O. resulted from increases in stroke volume and to a less extent also in heart rate (HR). There was no significant change of peripheral vascular resistance index (PVRI), in contrast to the NE effect in cardiogenic, hemorrhagic and septic shock states. The increase in arterial B.P. was accompanied by an increase in HR, which implies a disturbed function of the high pressure baroreceptor system. The rise in B.P. is primarily due to the increase in C.O. No adverse effects were noted during the NE infusion. It is concluded that NE is beneficial in the treatment of severe hypnotic drug poisoning complicated by hypotension.

Hemodynamic data have been recorded in nine patients during initial and late phases of severe poisoning by hypnotic drugs. Cardiac output (C.O.) was determined by the dye dilution method and right heart catheterization using “floating” catheter technique. Oxygen uptake was calculated from C.O. and arterio‐venous oxygen difference. During deep coma, characterized by hypothermia, the C.O., stroke volume and oxygen uptake were significantly decreased and the peripheral vascular resistance markedly increased. The arterio‐venous oxygen difference was generally normal, which implies that C.O. varied with oxygen uptake. Central venous pressures were normal or somewhat low, as also were the pressures in the pulmonary artery. During recovery the heart rate, stroke volume and C.O. increased in proportion to the increase in tissue metabolism as evaluated from the calculated oxygen uptake. The reduced tissue metabolism, reflected in reduced body temperature and low oxygen uptake, seems to be the main explanation of the hypo‐kinetic circulation in patients with deep coma because of poisoning by hypnotic drugs. The rather frequent roentgenological signs of pulmonary congestion or edema during the course of intoxication with hypnotic drugs do not seem to be explained by increased left ventricular filling pressures as reflected in elevated pulmonary artery diastolic pressures. A toxic effect on the vascular bed with increased permeability may be the most important underlying explanation.