BACKGROUND:The fact that brief repeated episodes of ischemia may induce prolonged functional depression of the left ventricle is still a matter of debate. During an angioplasty several brief (20-90 sec) coronary occlusions are performed, with the potential risk of inducing myocardial jeopardy.METHODS:We performed 4 repeated LAD occlusions in 7 open chest pigs under general anesthesia and controlled ventilation. The following parameters were evaluated: mean systemic arterial pressure (MAP), left ventricular peak systolic pressure (LVPSP), heart rate (HR), and peak negative and positive dP/dt (dP/dt- and +). Each parameter was measured in the basal state and every 4 sec, in the expiratory phase, during the coronary occlusion, the first min and after 10 min of reperfusion. The percent change from control values for each parameter was also calculated and, by means of the ANOVA test, the differences among the 4 consecutive occlusions for each parameter were tested.RESULTS:The results showed that: 1) coronary occlusions significantly depressed dP/dt + and -, MAP and LVPSP, while HR did not change; 2) each variable returned to control values within 1 min of reperfusion; 3) the response to ischemia (percent change) was the same in each of the 4 consecutive occlusions for all parameters at every recording time.CONCLUSIONS:We can conclude that: 1) each experimental coronary occlusion induces a depression of myocardial function that is reversible in 1 min of reperfusion; 2) four repeated 2 minutes coronary occlusions do not induce cumulative effects on myocardial response to ischemia.

OBJECTIVES:The present study was designed in order to evaluate the prevalence of mitral regurgitation in patients with the "incomplete mitral leaflet closure" echocardiographic pattern, to verify whether the amount of "incomplete mitral leaflet closure" is related to the severity of mitral regurgitation and, last, to verify the relation between the "incomplete mitral leaflet closure" and left ventricular morphology and function.METHODS:We studied 80 patients (14 patients with dilatative cardiomyopathy, 26 patients with coronary artery disease, and 40 patients with hypertensive heart disease or aortic valve disease) showing the "incomplete mitral leaflet closure" pattern, retrospectively selected from a population composed of 1700 consecutive patients routinely examined in our echocardiographic laboratory. In all patients we evaluated the presence and the severity of mitral regurgitation, the morphological and functional parameters of the left ventricle, the systolic diameter of the mitral annulus, the distance between the point of mitral leaflet coaptation and the annular plane, and the incomplete mitral closure area, assuming the last two parameters as indexes of the severity of incomplete closure of the mitral valve.RESULTS:We observed the presence of mitral regurgitation in 51 out of 80 patients (64%). The valvular insufficiency was considered mild in 78% of the patients. We observed no significant difference between patients with mitral regurgitation and without, as regards the diameter of the mitral annulus, the distance between the point of mitral leaflet coaptation and the annular plane, and the incomplete mitral closure area in different types of heart diseases. The incomplete mitral closure area and the diameter of the mitral annulus showed a significant, although not elevated, correlation with the severity of the mitral regurgitation (r = 0.36 and r = 0.32, respectively). The severity of mitral regurgitation showed significant correlations with all of the left ventricular morphological and functional parameters evaluated. Finally, we observed significant correlations between the incomplete mitral closure area and all of the morphological and functional parameters of the left ventricle.CONCLUSIONS:On the basis of the results obtained we can conclude that: 1) the "incomplete mitral leaflet closure" pattern does not appear to be a highly specific marker of mitral regurgitation, 2) this pattern appears to be related to the morphology and function of the left ventricle, and 3) the severity of the incomplete mitral valve closure is more easily evaluated by a parameter that takes into account the numerous factors acting on the mitral apparatus, that is the incomplete mitral closure area.

Nineteen asymptomatic patients affected by isolated chronic aortic regurgitation received 20 mg of nifedipine sublingually: the acute hemodynamic effects of nifedipine were evaluated by combined cross-sectional and Doppler echocardiography. To assess variations in the regurgitant flow volume, the flow volume across the mitral and aortic valves was calculated as the product of velocity-time integral multiplied by the orifice valve area. Flow volume across these valves represented the total stroke volume, and forward stroke volume, respectively: the regurgitant volume was obtained by calculating the difference between total and forward stroke volume. Nifedipine induced a redistribution of the two components of the total left ventricular stroke volume: regurgitant stroke volume decreased from 57 +/- 22 ml/beat to 46 +/- 21 ml/beat (P < 0.002), while forward stroke volume increased from 83 +/- 12 to 93 +/- 15 ml/beat (P < 0.0005), as a consequence of the reduction in systemic vascular resistance from 1513 +/- 378 to 1092 +/- 307 dynes . sec . cm-5 (P < 0.0001). The reduction of regurgitant volume was due to either a 24.8% decrease of the aortic-left ventricular mean pressure gradient during diastole (P < 0.008) or a 6% decrease of the diastolic time interval (P < 0.04).The effect of these acute changes on left ventricular loading was to induce a reduction in oxygen consumption which was expressed by a decrease in the double product (from 10176 +/- 1767 to 9444 +/- 1559 mmHg . beats/min; P < 0.002), in spite of a significant increase in heart rate.This study, therefore, shows the beneficial acute hemodynamic effect induced by nifedipine in asymptomatic patients affected by chronic aortic regurgitation and shows that Doppler-echocardiography is a useful instrument for the evaluation of hemodynamic changes immediately after the administration of drugs.

The use of body surface area to assess the normalcy of cardiac dimensions has several limitations. To determine whether cardiac dimensions can be assessed by other indexes of body size and growth, this study evaluated the relations between cardiac dimensions assessed by two-dimensional echocardiography and age, height, weight and body surface area. The study group included 268 normal persons aged 6 days to 76 years of age. The dimensions examined included the aortic anulus, left atrium and left ventricular end-diastolic diameter, each measured in the parasternal long-axis plane, and left ventricular length measured from the apical two-chamber view. The analysis confirmed that the heart and great vessels grow in unison and at a predictable rate after birth, reaching 50% of their adult dimensions at birth, 75% by 5 years and 90% by 12 years. Although each cardiac dimension related linearly with height (aortic anulus, r = 0.96; left atium, r = 0.91; left ventricular diameter, r = 0.94; left ventricular length, r = 0.93), the relations among age, weight and body surface area were best expressed by quadratic equations. Multiple regression confirmed that after adjustment for height, other indexes including age, gender, weight and body surface area had no independent effect on the prediction of each dimension. Therefore, because height is a nonderived variable that relates linearly with cardiac dimensions independent of age, it offers a simple yet accurate means of assessing the normalcy of cardiac dimensions in children and adults.

The aim of this study was to evaluate the effects of preload reduction on the Doppler transmitral flow pattern in the presence of diastolic dysfunction (hypertensive patients) and normal diastolic function (normal subjects) to identify, if present, one or more indexes of abnormal diastolic ventricular filling independent of variations in preload. For this purpose Doppler echocardiography was performed in 17 patients with hypertension and in 18 normal subjects under basal conditions and after 5 minutes of blood pressure cuff inflation at the root of the four limbs. The two groups showed a similar response to preload reduction: a significant reduction in peak velocity and the time-velocity integral of the E wave and in the ratio of peak velocities of E and A waves. Therefore the differences in left ventricular filling patterns between hypertensive and normal subjects observed under basal conditions were still present after preload reduction. The comparison between normal subjects after preload reduction and hypertensive patients in the basal state showed a higher peak velocity and time-velocity integral of the A wave in the latter (61.2 ± 16.2 vs 46.2 ± 9 cm/sec [p < 0.002] and 5.4 ± 1.8 vs 3.7 ± 1 cm [p < 0.002], respectively) with no differences in the ratios of peak velocities and time-velocity integrals of the E and A waves. It was concluded that the response of the Doppler transmitral flow pattern to preload reduction appears to be similar in normal subjects and patients with hypertension, irrespective of the presence of diastolic dysfunction, and the peak velocity and time-velocity integral of the A wave may be considered indexes of diastolic dysfunction independent of preload reduction.

Calcium entry blockers are commonly believed to have a direct negative inotropic effect, but systolic function of the left ventricle (LV) can be improved when the peripheral vasodilator activity of the drug is present. The aim of our study was to evaluate the effect of diltiazem (D) on isovolumic contraction (IC) and relaxation (IR) at a dosage which is not effective on the peripheral vascular bed. We infused 10 micrograms/Kg/min i.v. of D for a 30 min period in to 12 pigs, anesthetized with ethyl urethane (1250 mg/Kg) and under artificial ventilation. The following variables were evaluated: left ventricular systolic (LVSP) and end-diastolic (LVEDP) pressure, peak - and + dP/dt, mean arterial pressure (MAP), heart rate (HR) and double product. The recordings were obtained in the control condition and 5, 10, 15, 20, 25 and 30 minutes after beginning the infusion. The statistical analysis was performed using the one-way ANOVA test. Our results show: 1) a maximal increase in the peak + dP/dt from 2228 +/- 501 to 2448 +/- 576 mmHg/sec (p less than or equal to 0.01) and of the peak . dP/dt from 1262 +/- 260 to 1348 +/- 272 mmHg/sec (p less than or equal to 0.05); 2) and increase in LVSP from 86 +/- 13 to 90 +/- 10 mmHg (p less than or equal to 0.01) and 3) no changes in HR, PAM, LVEDP and double product. As the indices representing afterload and preload (PAM and LVEDP) remained unchanged during the infusion, we suggest that the increase in dP/dt + and - are due to a direct effect of diltiazem on myocardial function.(ABSTRACT TRUNCATED AT 250 WORDS)

In the last few years, alterations in transmitral diastolic flow pattern have been used to assess changes in left ventricular diastolic properties. However, since diastolic flow primarily reflects the atrioventricular pressure gradient, loading conditions, as well as intrinsic left ventricular properties, should be able to affect this pattern. This study was selectively designed to decrease preload (a major determinant of the atrioventricular pressure gradient) in normal subjects to observe the effects on the Doppler transmitral flow pattern without pharmacologic interventions that may also affect left ventricular diastolic properties. In 12 normal subjects, preload was reduced by inflation of blood pressure cuffs placed at the level of the root of the 4 limbs. The peak velocity of early mitral flow (E wave) decreased from 62 ± 8 to 51 ±7 cm/s (p < 0.001), while no changes were found in the maximal velocity after atrial contraction; this caused a significant decrease in the ratio of these 2 velocities (the E to A ratio) from 1.5 ± 0.3 to 1.1 ± 0.1 (p < 0.001). The time-velocity integral of early diastolic inflow decreased from 7.8 ± 1.3 to 6.1 ± 1.3 cm (p < 0.001) with no significant changes of the time-velocity integral of inflow after atrial contraction. Therefore, preload reduction in normal subjects significantly reduces transmitral flow in early diastole with preserved late ventricular filling, producing a pattern that can mimic the changes previously described in left ventricular diastolic dysfunction.

Reference values for normal left atrial dimensions have been based primarily on blind M-mode measurements, with no reports based on two-dimensional echocardiography to provide a comprehensive analysis of the two-dimensional measurements from infancy to old age. This report analyzes the left atrial dimensions from two-dimensional echocardiographic studies in 268 normal healthy subjects to determine normal limits and relations among linear, area and volume measurements of the left atrium. The group mean values change with body size, fitting well to the exponential growth model (r = 0.78 to 0.92). The variance about the mean (which determines normal limits) is represented effectively by a quadratic function of body surface area (r = 0.84 to 0.99). The variables determined by this modeling simplify evaluation of normal limits for any body size at any desired level of confidence, and the data are useful reference standards for interpretation of two-dimensional echocardiograms.

Doppler echocardiography is a potentially useful tool for the non invasive evaluation of cardiac output and, therefore, for the quantitative assessment of valvular regurgitation. The aim of our study was to establish the presence of possible pitfalls in the evaluation of mitral and aortic regurgitant fraction obtained by Doppler echocardiography comparing the cardiac output measured at the level of the mitral and aortic valve. For this purpose 19 healthy volunteers, aged between 14-68 years, were studied. Stroke volume and cardiac output were calculated at the level of the mitral and aortic valve. The methods we used for the measurement of both the mitral and aortic cardiac output had already been validated and presumes that the shape of the valve annulus, is circular. No statistically significant differences were found between the parameters obtained at the two different valvular levels. Furthermore, cardiac output values correlated fairly well (r = 0.83, ESS = 0.78 l/min). In 9 subjects the aortic cardiac output was greater than the mitral one, while in the others mitral cardiac output was greater. The average of the differences between the two cardiac outputs was 0.58 +/- 0.48 l/min with a regurgitation fraction of 9.5 +/- 7.9%. Our results show that the mitral and aortic stroke volume and cardiac output, as measured by Doppler echocardiography (considering a circular shaped valve annulus, are not statistically different and correlate fairly well in our normal subjects. Nevertheless, we observed a certain degree of variability between the mitral and the aortic cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)

Although several Doppler echocardiographic methods for measuring transmitral flow have been described, the optimal method for calculation of flow remains unclear. Seven time/shape combinations were tested in an experimental preparation in which mitral flow could be precisely controlled and measured. Annular shape was considered to be either circular or elliptical, and the mitral orifice area was calculated from the anteroposterior and/or the mediolateral dimension(s) recorded at early and middiastole. In addition the orifice area was calculated from the maximal mitral leaflet area corrected for diastolic variation. Transmitral flow ranged between 0.4 and 4.6 L/min. Good correlations with measured transmitral flow (r = 0.83 to 0.92) were observed for all methods of calculating the mitral orifice area. Methods that assumed a circular geometry and used the mediolateral annular diameter overestimated flow. Conversely, flows calculated by means of the anteroposterior diameter with the assumption of a circular anulus underestimated flow. The best approximations of transmitral flow were obtained with the assumption of an elliptical configuration that used measurements made in early diastole (Y = 1.04x + 0.2) and with the Fisher method (y = 0.94x + 0.08). Thus in the canine model approximation of the mitral orifice as an ellipse provides the most accurate measurement of transmitral flow.

The majority of studies generating normal echocardiographic reference values for left ventricular dimensions have been based on blindly performed M-mode measurements, and there are no previous reports based on two-dimensional echocardiography that provide a comprehensive analysis of the two-dimensional measurements from infancy to old age. This report presents the results of analyzing the left ventricular internal dimensions from cross-sectional echocardiographic studies on 268 normal healthy subjects (none were hospitalized for any reason) whose ages ranged from 6 days to 76 years. The mean data are reported as functions of body surface area and, in addition, the variance is modeled as a function of body surface area to provide an accurate and clinically useful determination of normal limits and to model changes in the cardiac dimensions and in their variance representing normal growth and development. The data fit well to the exponential growth model (r values 0.85 to 0.95). Variance about the central values also depended significantly on body size; that relation is represented effectively by a quadratic function of body surface area (r values 0.82 to 0.98). The model parameters allow calculation of normal limits at any desired level of confidence. Areas determined by hand planimetry have significantly greater variance compared with variance of linear dimensions, and also compared with variance of cross-sectional area using ellipses generated from the anteroposterior and mediolateral dimensions. This implies that either biologic variations in the amount of infolding or errors in freehand planimetry constitute a significant source of variance; this may be remedied by filtering out high frequency oscillations of contour. There is no significant difference in midnormal values and confidence limits for corresponding dimensions measured from orthogonal views. Furthermore, the anteroposterior and mediolateral dimensions of the left ventricle superimpose at each body size, consistent with circular cross section for normal subjects throughout growth and development. The data presented should comprise a useful set of reference standards for interpretation of cross-sectional echocardiograms.

The purpose of this study was to answer the following questions: 1) are isovolumic contraction and relaxation affected in a different way by LAD occlusion? 2) Does proximal and distal LAD coronary occlusion induce different changes in isovolumic contraction and relaxation? In 22 pigs, LAD coronary artery was dissected free right after the first or third diagonal branch and occluded by ligation. The following variables were evaluated: left ventricular systolic and end-diastolic pressure; peak - and + dP/dt, mean arterial and pulmonary pressure. All our data were obtained in the first minute following the occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

The geometric or anatomic diagnosis of mitral valve prolapse, as opposed to the pathologic diagnosis of myxomatous valve disease, is based on the relationship of the mitral leaflets to the surrounding anulus. Current echocardiographic criteria for this diagnosis include leaflet displacement above the annular hinge points in any two-dimensional view; implicit in this equivalent use of intersecting views is the assumption that the mitral anulus is a euclidean plane. Prolapse by these criteria is found in a surprisingly large proportion of the general population. In most of these individuals, however, prolapse is present in the apical four-chamber view and absent in roughly orthogonal long-axis views of the left ventricle. This frequently observed discrepancy between leaflet-annular relationships in intersecting views suggests an underlying geometric property of the mitral apparatus that would produce the appearance of prolapse in one view without actual leaflet distortion. To address this possibility, a model of the mitral valve and anulus was constructed. When the model anulus was given a nonplanar, saddle-shaped configuration, the clinical observations were reproduced: the leaflets appeared to lie above the low points of the anulus in one plane, and below its high points in a perpendicular plane. Therefore, the appearance of mitral valve prolapse can occur without actual leaflet displacement above the most superior points of the mitral anulus if the anulus is nonplanar. To determine whether this pattern is reflected in the human mitral anulus, two-dimensional echocardiographic views of the mitral apparatus were obtained by rotation about the cardiac apex in 20 patients without evident annular or rheumatic valvular disease. In all cases the mitral anulus, as reconstructed from these views, had a nonplanar systolic configuration, with high points located anteriorly and posteriorly. This is consistent with the findings of other groups in animals, and would favor the appearance of prolapse in the four-chamber view and its absence in long-axis views that are oriented anteroposteriorly. This model can therefore explain the frequently observed discrepancy between leaflet-annular relationships in roughly orthogonal views. It challenges the assumption that the mitral anulus is planar as well as the diagnosis of prolapse in many otherwise normal individuals based on that assumption.

We examined fifty patients aged from 15 to 35 years, mean 23 +/- 5, with mitral valve prolapse (MVP) documented by two-dimensional echocardiography in the apical 4-chamber view as well as in the parasternal-long axis. The patients have been submitted to 4 tests: Valsalva maneuver, standing and exercise test and 24 hours ambulatory ECG monitoring. Fourty-five healthy subjects of similar age and sex served as controls. During the standing test the patients with MVP showed a significantly faster heart rate than the control subjects both in resting and in the standing position; during the exercise test they exhibited higher prevalence of ST segment and T wave abnormalities disappearing at the peak of the exercise. These observations support the hypothesis of a hyperadrenergic state. The greater bradycardia showed during the Valsalva maneuver, the lower heart rate and the higher incidence of bradyarrhythmias and A-V blocks during the sleeping period suggest an increased vagal tone. Our results suggest therefore that in subjects with MVP a dysfunction of both, sympathetic and parasympathetic nervous system is present.

The purpose of this study is to evaluate normal left ventricular regional wall motion pattern in order to answer the two following questions: does wall motion change at different levels of the left ventricle from the base to the apex? does wall motion change among different segments at the same level? Seventy-two normal subjects were submitted to a cross sectional echocardiographic examination and the tape recordings were analyzed by a computerized system. Parasternal short axis views at mitral valve and papillary muscles level were chosen and divided by the computer in 16 areas which were fitted to a more anatomical division, i.e. interventricular septum, anterior, lateral, posterior-lateral, inferior-posterior and inferior walls. From each segment, fractional area changes were obtained. Statistical analyses were carried out by the two way analysis of variance and two paired t test. Wall motion pattern of the normal left ventricle is not uniform either at different levels or among segments at the same level: we conclude that regional wall motion differences of the left ventricle are not necessarily due to abnormal conditions, but might be a normal left ventricular pattern.

The purpose of this study was to assess the hemodynamic response after prostacyclin infusion into the venous system and into the carotid artery in the pig. During the study the following circulatory variables were studied: mean systemic arterial pressure, mean pulmonary arterial pressure, wedge pressure, heart rate, cardiac output, systolic and diastolic left ventricular pressure, stroke volume, total systemic resistance, total pulmonary resistance, left ventricular stroke work. Our results confirm that prostacyclin is a powerful hypotensive agent. The hypotensive effect seems to be due to a peripheral vasodilatation of arterial and venous vessels. Venous infusion caused only 19% tachycardia, as opposed to 36% caused by arterial infusion for the same percentage of blood pressure reduction. This suggests that prostacyclin probably stimulates cardiopulmonary vagal receptors. The effect of prostacyclin on heart rate, therefore, may be twofold and in opposite directions: one action causing tachycardia secondary to hypotension, and the other inviting bradycardia through direct vagal stimulation.