Non-alcoholic fatty liver disease is independently associated with left ventricular hypertrophy in hypertensive Type 2 diabetic individuals.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) and left ventricular hypertrophy (LVH) are highly prevalent in Type 2 diabetes and both conditions are associated with an increased risk of incident cardiovascular disease. The aim of this study is to evaluate whether there is an association between NAFLD and echocardiographically detected LVH in Type 2 diabetes. METHODS: We studied 116 consecutive patients with hypertension and Type 2 diabetes after excluding those with pre-existing history of cardiovascular disease, advanced kidney disease, excessive alcohol consumption and other known causes of chronic liver disease (e.g., virus, medications, autoimmunity, iron overload). NAFLD was diagnosed by means of ultrasonography, whereas LVH was diagnosed by means of conventional trans-thoracic echocardiography in all patients. RESULTS: The prevalence of LVH was markedly higher among diabetic patients with NAFLD than among those without this disease (82% vs 18%; p=0.01). Multivariate logistic regression analysis revealed that NAFLD was associated with LVH independently of age, sex, body mass index, systolic blood pressure, glycated hemoglobin, duration of diabetes, and parameters of kidney function. CONCLUSIONS: Our findings suggest that hypertensive Type 2 diabetic patients with NAFLD have a remarkably higher frequency of LVH than do hypertensive diabetic patients without steatosis, and that NAFLD is associated with LVH independently of classical cardiovascular risk factors and other potential confounders.

Left atrial filling volume can be used to reliably estimate the regurgitant volume in mitral regurgitation.

OBJECTIVES: The objective was to analyze the accuracy and diagnostic value of the estimated regurgitant volume of mitral regurgitation using 1) left atrial volume variation during ventricular systole (left atrial filling volume) and 2) the percent of systolic pulmonary vein velocity integral compared with its total. BACKGROUND: Left atrial filling volume (LAfill), which represents the atrial volume variation during ventricular systole, has been used for the assessment of mitral regurgitation severity. A good correlation with invasive semiquantitative evaluation was found, but with an unacceptable overlapping among grades. The reason could be the absence of information concerning the contribution of blood entering into the left atrium from the pulmonary veins. METHODS: Doppler regurgitant volume (Dpl-RVol) (mitral stroke volume - aortic stroke volume) was measured in 30 patients with varying degrees and etiological causes of mitral regurgitation. In each patient atrial volumes were measured from the apical view, using the biplane area-length method. The systolic time-velocity integral of pulmonary vein flow was expressed as a percentage of the total (systolic-diastolic) time-velocity integral (PVs%). These parameters were used in this group of patients to obtain an equation whose reliability in estimating Dpl-RVol was tested in a second group of patients. RESULTS: In the initial study group, with linear regression analysis the following parameters correlated with Dpl-RVol: end-systolic left atrial volume (R2=0.37, p=0.0004); LAfill (R2=0.45, p < 0.0001); PVs% (R2=0.56, p < 0.0001). In multiple regression analysis the combination of LAfill and the percent of the systolic pulmonary vein velocity integral (PVs%) provided a more accurate estimate of regurgitant volume (R2=0.88; SEE 10.6; p < 0.0001; Dpl-RV=6.18 + (1.01 x LAfill) - (0.783 x PVs%). The equation was subsequently tested in 54 additional patients with mitral regurgitation with a mean Dpl-RVol 27+/-37 ml. Estimated regurgitant volume and Dpl-RVol correlated well with each other (R2=0.90; SEE 12.1; p < 0.0001). In the test population, the equation was 100% sensitive and 98% specific in detecting a regurgitant volume higher than 55 ml. CONCLUSIONS: Left atrial filling volume and pulmonary vein flow give a reliable estimate of regurgitant volume in mitral regurgitation.

Skeletal muscle mass independently predicts peak oxygen consumption and ventilatory response during exercise in noncachectic patients with chronic heart failure.

OBJECTIVES: We sought to assess whether skeletal muscle mass might be a predictor of peak oxygen consumption (Vo2) and relation of the ventilation to carbon dioxide production (VE/VCo2) slope in patients with chronic heart failure (CHF) independent of clinical conditions, neurohormonal activation and resting hemodynamics. BACKGROUND: A variety of abnormalities characterize skeletal muscle and contribute to exercise intolerance in patients with CHF. Skeletal muscle mass is a determinant of peak Vo2 both in healthy patients and in patients with CHF, but there are no reports on the independent predictive value of this parameter, which can be measured with great accuracy by whole-body dual energy X-ray absorptiometry (DEXA). The influence of skeletal muscle mass on VE/VCo2 slope is not known either. METHODS: We prospectively evaluated 120 consecutive noncachectic patients with CHF. Every patient underwent a cardiopulmonary exercise test, an echo-Doppler examination and an evaluation of neurohormonal activation and body composition as assessed by DEXA. RESULTS: At the univariate analysis, New York Heart Association (NYHA) class (p < 0.0001), age (p < 0.0001), male gender (p < 0.0001) and plasma renin (p < 0.0001) significantly related with peak Vo2. There was a significant correlation between lean mass and absolute peak Vo2 (r = 0.70, p < 0.0001) and VE/VCo2 slope (r = -0.27; p < 0.01). At the multivariate analysis, lean mass predicted peak Vo2 and VE/VCo2 slope independently of NYHA functional class, age, gender, neurohormonal activation and resting hemodynamics. CONCLUSIONS: Skeletal muscle mass is an independent predictor of peak Vo2 and VE/VCo2 slope in stable noncachectic patients with CHF. Future studies will determine whether an increase in skeletal muscle mass in the individual patient might result in an improvement in parameters of exercise capacity.

Frequency of predischarge ventricular arrhythmias in postmyocardial infarction patients depends on residual left ventricular pump performance and is independent of the occurrence of acute reperfusion. The GISSI-2 Investigators.

OBJECTIVES: To test whether acute reperfusion of the infarct-related vessel after an acute myocardial infarction is associated with a subsequent reduction in spontaneous ventricular arrhythmias that is independent of ventricular ejection fraction, 1,944 patients from the GISSI-2 study population were studied. The patients were selected on the basis of a first myocardial infarction and the availability of two-dimensional echocardiographic ejection fraction and data on the number of premature ventricular contractions per hour on Holter monitoring. BACKGROUND: It has been suggested that postthrombolytic reperfusion of the culprit vessel may be associated with an increased electrical stability of the infarcted heart, irrespective of its residual pump performance. METHODS: The predischarge relation between ejection fraction and number of premature ventricular contractions per hour was plotted according to the occurrence (1,309 patients) or not (635 patients) of acute reperfusion, identified noninvasively according to the modifications of the ST segment in serial electrocardiograms obtained in the first 24 h after infarction. RESULTS: The frequency of premature ventricular contractions increased in a linear fashion with decreasing ejection fraction in both cohorts (p < 0.005 and p < 0.0001); however, there was no significant difference between the slopes and the intercepts of the two regression lines, so that the relation between ejection fraction and number of premature ventricular contractions per hour could be adequately described by a single equation: y (number of premature ventricular contractions) = 33.0-0.42x (ejection fraction) (r = -0.107, p < 0.0001). The results were the same even when differences between group characteristics were accounted for in a multiple regression model. CONCLUSIONS: It is concluded that 1) the number of premature ventricular contractions per hour after an acute myocardial infarction is dependent in a linear, inverse fashion on the residual ventricular ejection fraction, and 2) this relation is independent of the occurrence of reperfusion in the acute phase of infarction.

Failure of aldosterone suppression despite angiotensin-converting enzyme (ACE) inhibitor administration in chronic heart failure is associated with ACE DD genotype.

OBJECTIVES: The objective of this study was to assess whether the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism influences the adequacy of the neurohormonal response to ACE inhibitors in patients with chronic heart failure (CHF). BACKGROUND: The renin-angiotensin-aldosterone system (RAAS) plays an important role in the pathophysiology of CHF, and aldosterone levels closely relate to outcome in patients with CHF. Angiotensin-converting enzyme inhibitors suppress the RAAS, but a significant proportion of patients exhibit elevated serum levels of aldosterone despite long-term administration of apparently adequate doses of these agents. METHODS: We prospectively studied 132 patients with CHF (ejection fraction <45%) receiving long-term therapy with ACE inhibitors for over six months. Patients taking aldosterone antagonists were excluded from the study. "Aldosterone escape" was defined as being present when plasma aldosterone levels were above the normal range in our laboratory (>42 nmol/L). Patients were then divided into two subgroups according to the presence (group 1) or absence (group 2) of aldosterone escape. Genotype analysis for the ACE I/D polymorphism was performed by polymerase chain reaction. RESULTS: The prevalence of aldosterone escape in our patients was 10% (13/132). The two groups of patients did not differ regarding the dose of ACE inhibitor, diuretics and their renal function. There was a statistically significant different distribution of genotypes between the two groups, with a higher proportion of DD genotype in group 1 compared with group 2 (62% vs. 24%, p = 0.005). CONCLUSIONS: Patients with CHF with aldosterone escape have a higher prevalence of DD genotype compared with patients with aldosterone within the normal limits. Angiotensin-converting enzyme gene polymorphism contributes to the modulation and adequacy of the neurohormonal response to long-term ACE-inhibitor administration in CHF.

Ventricular remodeling and infarct expansion.

Infarct expansion, defined as an alteration in the ventricular topography due to thinning and lengthening of the infarcted segment, develops within the first few hours of the acute symptoms, mostly in patients with a large, transmural, anterior myocardial infarction. Shape changes, peculiar to risk region location and due to disparity in regional ventricular architecture, could be posited as the first step in the process of infarct expansion, with various cellular mechanisms contributing to subsequent continued early and late ventricular dilation. Because the increase in left ventricular volume is expected to be linearly dependent on the extent of the infarction, limiting infarct size, by thrombolysis, would proportionally reduce enlargement of the cavity. The effect of thrombolysis on left ventricular volume, however, seems not to be completely accounted for by the lessening effect of reperfusion on infarct size, because data suggest a restraining effect of reperfusion on the process of ventricular dilation in addition to the lessening effect on infarct size. If this turns out to be true, then the achievement of a patent vessel even beyond the time period when that patency may be expected to salvage myocardium would be further justified. Theoretical predictions substantiate the potential effectiveness in restraining ventricular dilation of stiffening of the necrotic region alone, independently of myocardial salvage in infarcted patients. The process of progressive ventricular dilation involves not only a primary alteration in function of the infarcted region, but also a time-dependent secondary change in the noninfarcted tissue itself, finalized to restore stroke volume despite a persistently depressed ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of left ventricular function and volumes during transesophageal atrial pacing combined with two-dimensional echocardiography in patients with syndrome X, atherosclerotic coronary artery disease, and normal subjects.

Nine patients with syndrome X were compared with 2 groups of patients known to have coronary artery disease (CAD) (8 patients who developed regional wall motion abnormalities [group ECHO+] and 6 patients who showed only ST depression at echo-pacing [group ECG+]) and with 6 healthy volunteer control subjects. Left ventricular function at rest was normal in all patients. End-diastolic and end-systolic volumes (ml/m2) and ejection fraction were calculated at baseline and at peak of echo-pacing using a Simpson's biplane method. No regional wall motion abnormalities were observed during the echo-pacing in patients with syndrome X or in the volunteers. End-diastolic volume decreased in patients with syndrome X, in the volunteers (from 47 +/- 11 to 30 +/- 12 and from 72 +/- 7 to 38 +/- 6, respectively, p <0.01 for both), and in ECG+ patients (from 48 +/- 10 to 33 +/- 6, p <0.05), whereas it did not change in ECHO+ patients. End-systolic volume decreased in patients with syndrome X and in the volunteers (from 17 +/- 5 to 11 +/- 4 and from 28 +/- 6 to 16 +/- 4, respectively, p <0.01 for both), whereas it did not change or else slightly increased in patients with CAD (from 18 +/- 10 to 16 +/- 5 for ECG+ patients and from 19 +/- 5 to 24 +/- 9 for ECHO+ patients, p = NS for both), regardless of whether regional wall motion abnormalities appeared. Ejection fraction decreased in ECG+ and ECHO+ patients (from 64 +/- 12 to 52 +/- 11 and from 62 +/- 9 to 44 +/- 13, respectively, p <0.01 for both), whereas it did not change in patients with syndrome X and in the volunteers (from 64 +/- 8 to 61 +/- 8 and from 61 +/- 7 to 58 +/- 7, respectively, p = NS for both). During echo-pacing in syndrome X patients no regional wall motion was detected. Left ventricular volumes and ejection fraction showed the same patterns of variation in these patients as they did in the healthy control subjects, in contrast with those patients with CAD, whether or not regional wall motion abnormalities appeared in the latter.

Usefulness of left atrial size in predicting postoperative symptomatic improvement in patients with aortic stenosis.

Although surgery is highly effective for symptomatic relief in patients with aortic stenosis, symptoms of congestive heart failure may be still present postoperatively. This group of patients with aortic stenosis is characterized by a wide range of left atrial size, which can predict postoperative symptomatic improvement.

Usefulness of transesophageal atrial pacing combined with two-dimensional echocardiography (echo-pacing) in predicting the presence and site of residual jeopardized myocardium after uncomplicated acute myocardial infarction.

The usefulness of transesophageal atrial pacing combined with 2-dimensional echocardiography (echo-pacing) in predicting the presence and site of jeopardized myocardium, defined as areas of myocardium perfused by a vessel with a stenosis > or = 75% or by a collateral circulation if the supplying vessel was occluded, was evaluated in 31 patients with uncomplicated acute myocardial infarction who underwent coronary angiography. All 5 patients without jeopardized myocardium had a negative test, whereas 24 of 26 with jeopardized muscle had a positive test (sensitivity 92%; specificity 100%). To identify the site of jeopardized myocardium, tests that were positive for development of new asynergies were analyzed further, distinguishing those positive in the infarct or remote zone. Seven of 8 patients with new asynergies in the remote zone had areas of jeopardized myocardium outside the territory of distribution of the infarct-related vessel, whereas only 2 of 12 with new asynergies in the infarct zone had areas of jeopardized myocardium outside that territory (p < 0.01), correctly predicting the site of jeopardized myocardium in 17 of 20 cases. In conclusion, echo-pacing is useful for detecting the presence and site of jeopardized myocardium after an acute myocardial infarction.

Prognostic value of detection of myocardial viability using low-dose dobutamine echocardiography in infarcted patients.

Revascularization can improve ventricular function in patients with viable myocardium, but whether and how the presence of viable myocardium affects prognosis of infarcted patients is still far from clear. Thus, 202 patients (173 men, 59 +/- 9 years old) with a previous or recent myocardial infarction (MI) and regional asynergies underwent low-dose dobutamine echocardiography (5-15 microg/kg per min) to assess myocardial viability and were followed for a period of 16 +/- 11 months after revascularization (89 patients) or medical therapy (113 patients). Four groups of patients were defined: (1) patients with viability, revascularized (n = 64); (2) patients with viability, treated medically (n = 52); (3) patients without viability, revascularized (n = 25); and (4) patients without viability, treated medically (n = 61). Of these patients, 45 (23%) patients suffered 57 cardiac events: 18 cardiac deaths (9%), 7 MIs, 12 unstable angina, 9 heart failures, and 11 new revascularization procedures. Patients with viability, revascularized, experienced a slightly lower event rate (22%) compared with patients with viability, treated medically, patients without viability, treated medically and patients without viability, revascularized (29%, 31%, and 36%, respectively; p = not significant [NS]). The frequency of events was then evaluated in those 108 patients with an ejection fraction < or =33%, in whom 14 cardiac deaths occurred: the incidence of cardiac death was slightly lower in patients with viability, revascularized (3/37, 8%) than in the patients with viability, treated medically (4/26, 15%), patients without viability, revascularized (2/11, 18%), or patients without viability, treated medically (5/34, 15%) (p = NS). Nonfatal cardiac events were significantly fewer (p <0.05) in patients with viability, revascularized (8%) and in patients without viability, treated medically (6%) than in patients with viability, treated medically and patients without viability, revascularized (27%). In infarcted patients with severe left ventricular dysfunction, the presence of viable myocardium, if left unrevascularized, leads to further events. On the contrary, in the absence of myocardial viability, revascularization could lead to a worse prognosis than medical therapy.

Frequency, prognosis and predictors of improvement of systolic left ventricular function in patients with 'classical' clinical diagnosis of idiopathic dilated cardiomyopathy.

In patients with dilated cardiomyopathy (DCM) of different aetiologies, a variable frequency of improvement in the left ventricular (LV) systolic function has been reported, while in patients with a 'classic' idiopathic DCM, the frequency of improvement is still under debate, and clinical and haemodynamic predictors of recovery of the LV function are needed. The aim of the present study was to determine the frequency of improvement in the LV systolic function in idiopathic DCM and to identify predictors of reversibility of the impaired LV contractility. A sample of 98 consecutive patients with idiopathic DCM was retrospectively evaluated. Echocardiographic and Doppler measurements were directly taken from the routine echo-report. LV systolic function was assessed semiquantitatively using a score index (SFSI). According to the improvement in the LV systolic function, the patients were divided into group 1 patients with improvement, and group 2 patients without improvement. During a follow-up of at least 12 months, 19 patients (19%) showed an improvement, with a significant increase in the mean SFSI; all these group 1 patients survived without heart transplant; in group 2, 18 patients (23%) died and 3 (4%) received a heart transplant. Patients in group 1 had a significantly shorter duration of symptoms (P=0.0045), a younger age (P=0.006), a shorter DtE (P=0.04), a lower SFSI (P<0.01), a worse NYHA class (P<0.001) and more frequently had a history of hypertension (P<0.0001). The same variables were significant predictors of improvement at the univariate analysis. At the multivariate logistic regression analysis, a shorter duration of symptoms (P=0.02), a history of hypertension (P=0.003), and a worse NYHA class (P=0.01) were independent predictors of improvement. A relatively large percentage of patients with an idiopathic DCM will have a marked improvement in the LV systolic function. This is more likely to happen in the presence of a short duration of symptoms and a history of hypertension. After an improvement, the prognosis is excellent.

Mitral regurgitation and left ventricular diastolic dysfunction similarly affect mitral and pulmonary vein flow Doppler parameters: the advantage of end-diastolic markers.

Enhanced early mitral flow and reduced systolic pulmonary vein flow may be caused both by increased left ventricular pressure as the result of diastolic dysfunction and by increased transmitral flow as the result of mitral regurgitation. Nevertheless, Doppler parameters are widely used to predict left ventricular filling pressure. We aimed to analyze the interference of mitral regurgitation with Doppler parameters usually used to estimate left ventricular filling pressure and to identify markers independent of mitral regurgitation, which could reliably estimate increased left ventricular filling pressure. Eighty-four patients (age, 62 +/- 9 years; 82% men) had a complete echocardiographic Doppler examination. Transmitral E- and A-wave velocity, E deceleration time and A duration, pulmonary vein systolic and diastolic velocities, and reversal flow duration and maximal and minimal left atrial volumes were measured. The difference between the duration of pulmonary vein and mitral A waves was calculated (A'-A). Mitral regurgitant volume was quantitatively assessed by echocardiography. Left ventricular end-diastolic pressure was measured invasively. Patients had a wide range of left ventricular ejection fraction (14% to 70%), mitral regurgitant volume (0 to 94 mL), and left ventricular end-diastolic pressure (3 to 37 mm Hg). E velocity, E/A, pulmonary vein systolic and diastolic, and systo-diastolic ratios were significantly and independently correlated with both left ventricular end-diastolic pressure and mitral regurgitant volume. A'-A showed a strong correlation with left ventricular end-diastolic pressure (r = 0.70; P <.0001), but the relation with mitral regurgitant volume was not significant (r = 0.19; P =.08). Mitral regurgitation affects the majority of Doppler parameters widely used to predict filling pressure but does not influence Ad'-Ad, which proved to be the strongest predictor of left ventricular end-diastolic pressure.

Opposite effects of the remodeling of infarcted and non-infarcted myocardium on left ventricular function early after infarction in humans. An echocardiographic study in patients examined before and after myocardial infarction.

OBJECTIVE: The purpose of this study was to evaluate infarction-related changes in the infarcted and the non-infarcted myocardium using a baseline assessment of ventricular function obtained prior to the infarction. BACKGROUND: Experimental studies have shown that both infarcted and non-infarcted myocardium contribute to the process of left ventricular dilatation soon after the infarction, but no data exist on the effect that the infarct has on the pre-infarct ventricular morphology in humans. METHODS AND RESULTS: 10 patients, out of 721 admitted to our coronary care unit with a first acute myocardial infarction over a 3-year period, had had an echocardiographic examination performed before (354 +/- 407 days) and after (10 +/- 9 days) the infarction which were adequate for quantitative evaluation. Ventricular volume (Simpson) and regional wall motion (Centerline method) were evaluated by biplane apical sections and the endocardial length of the infarct and the non-infarct segments, imaged in a cross-sectional view at the papillary muscle level, were measured. After the infarction end-diastolic and end-systolic ventricular volume increased (P = 0.0003 and P < 0.0001, respectively); diastolic and systolic infarct segment length increased (P = 0.011 and P = 0.0008, respectively), while non-infarct segment had only diastolic lengthening (P = 0.019), without systolic changes. The ejection fraction decreased after the infarction (P < 0.0001), in inverse relation to infarct size and in direct relation to diastolic non-infarct segment lengthening. In the five patients in whom there was a significant diastolic lengthening of non-infarct segment (larger than mean +/- 2 S.D. of the interobserver variability) the decrease in ejection fraction was less than in the patients without significant lengthening of this segment (P = 0.017), despite a similar echocardiographic infarct size index. CONCLUSION: Ventricular enlargement early after myocardial infarction is due to both infarct expansion and lengthening of non-infarct segment. However, while systolic stretching of the infarct segment is a deleterious process that accounts for the increase in end-systolic volume, diastolic non-infarct segment lengthening is the expression of a functional compensatory mechanism that counteracts the reduction of the ventricular pump function secondary to the infarction.

Prognostic implications of evaluation of contractile reserve in akinetic and hypokinetic segments during low dose dobutamine echocardiography in patients with acute myocardial infarction.

BACKGROUND: Previous studies have reported the prognostic value of myocardial viability (MV) detected using low-dose dobutamine echocardiography (DbE). However, viability was frequently evaluated as improvement in regional wall motion score index, which includes increased function in hypokinetic segments, in which viable myocardium is necessarily present. It is not known whether an evaluation focusing on akinetic segments, in which the possible presence of viable myocardium is unknown, might have more prognostic value. The aim of this study was to compare the prognostic value of the improvement of myocardial function during dobutamine infusion in akinetic and hypokinetic regions in patients with acute myocardial infarction (AMI). METHODS: 191 patients with uncomplicated AMI and at least one akinetic segment were retrospectively selected from those consecutively examined at our echo-laboratory to evaluate MV using DbE. Myocardial viability was evaluated both as an increment in RWMSI (Delta RWMSI), which takes into consideration improvement in both akinetic and hypokinetic regions, and as an improvement of function in akinetic (Delta akinetic) and hypokinetic (Delta hypokinetic), segments considered separately. Follow-up evaluation was performed at 30+/-13 months. RESULTS: On the basis of the Delta RWMSI, 94/191 patients were judged to have myocardial viability, whereas considering myocardial viability in akinetic segments only, 72/191 patients showed viability. At follow-up 18 patients had died (six viable considering Delta RWMSI; three viable considering Delta akinetic). The presence of a previous AMI, the site of AMI, RWMSI and the number of akinetic segments, and Delta RWMSI and Delta akinetic were related to mortality at univariate Cox analysis. At multivariate stepwise Cox regression analysis Delta akinetic, but not Delta hypokinetic proved to be significantly related to mortality. The Kaplan-Meier survival curves were no different in patients with or without viable myocardium evaluated as Delta RWMSI, while they were significantly different considering patients with or without viability in akinetic segments (P=0.04). CONCLUSION: In conclusion our study confirms the prognostic importance of the evaluation of myocardial viability in infarcted patients. However, it points out that it is the presence of viability in akinetic segments that affects long-term survival in these patients. This supports the hypothesis that other mechanisms, above and beyond the effect on regional wall motion, are involved in the beneficial effects of myocardial viability.

Relationship between mitral regurgitation and myocardial viability after acute myocardial infarction: their impact on prognosis.

Mitral regurgitation (MR) after acute myocardial infarction (AMI) is an important prognostic factor. Although its mechanisms are still debated, ventricular remodeling probably plays an important role. Because myocardial viability (MV) in the infarct zone reduces infarct expansion and ventricular remodeling, it is also possible that its presence counteracts the development of mitral regurgitation in infarcted patients. To evaluate this issue 191 patients with uncomplicated AMI, wall motion abnormalities (akinesis) and semiquantitative evaluation of MR were retrospectively selected from those consecutively examined at our echo-laboratory to evaluate MV using low-dose dobutamine echocardiography (DbE). Follow-up evaluation was performed at 30+/-13 months. Seventy-nine patients had no MR; 86 patients had grade 1 MR, 11 patients had grade 2 MR, nine patients had grade 3 MR, and six patients had grade 4 MR. Patients with significant MR (>grade 1) were older (63+/-7 vs. 59+/-10 years, P=0.03), had lower reduction of RWMSI (DeltaRWMSI) during DbE (0.08+/-0.11 vs. 0.22+/-0.28, P=0.01), more stenotic vessels at coronary angiography (2.35+/-0.93 vs. 1.67+/-1.12, P=0.01), and more frequently had anterior-inferior AMI (P<0.0001); they also had a non-significant tendency to higher RWMSI (2.04+/-0.38 vs. 1.92+/-0.28, P=0.06). In a multivariate regression analysis, DeltaRWMSI proved to be significantly related to the grade of MR (P=0.02). Eighteen patients died during follow-up. Death was more frequent in patients with MR (10/165 vs. 8/26, P=0.0003). At multivariate stepwise Cox regression analysis both the extent of ventricular dysfunction and the presence of MR were significantly related to mortality (P<0.0001 and P=0.01, respectively); DeltaRWMSI showed a non-significant tendency to influence mortality (P=0.09). When MR was excluded from the multivariate analysis, DeltaRWMSI remained significantly related to mortality (P=0.05). In conclusion our study suggests that the presence of MV in infarcted patients influences the development of MR. This reduction of MR may be one of the mechanisms by which MV affects mortality after AMI and should be considered in all studies that evaluate MV after myocardial infarction.

Comparison between low-dose dobutamine echocardiography and thallium-201 scintigraphy in the detection of myocardial viability in patients with recent myocardial infarction.

AIM: To compare the predictive value of thallium-201 single photon emission computed tomography (SPECT) scintigraphy (Sci) and low-dose dobutamine echocardiography (Dob) in predicting late recovery of dysfunctioning myocardium in patients with recent, uncomplicated myocardial infarction (MI). METHODS AND RESULTS: 19 patients (18 male, aged 58+/-8 years) with recent MI and ejection fraction <50% (35.5+/-8.3%) underwent 5-15 microg/kg per min Dob, rest-redistribution Sci and coronary angiography, respectively, 14+/-6, 16+/-7 and 17+/-5 days after MI. On an eleven-segment ventricular model devised to compare Dob and Sci segment by segment, each dysfunctioning ventricular segment was considered viable if it showed recovery of mechanical function at the echocardiographic follow-up, performed 6.3+/-1.5 months after revascularization (five PTCA, five GABG) or medical therapy. Among the 104 dysfunctioning segments, of which 26 (25%) showed recovery at follow-up, Dob and Sci gave a concordant response in 50 (48%, k = 0.13), correctly predicting the recovery (or not) of function in 42. Forty-two of 54 discordant responses were due to segments judged viable only by Sci and which had no recovery at follow-up (of these 37 were akinetic or severely hypokinetic at baseline). At the segment-by-segment analysis, the sensitivity, specificity, and accuracy in predicting recovery of function at follow-up were, respectively, 69, 88 and 84% for Dob as against 88, 36 and 49% for Sci (P<0.001 for both specificity and accuracy, P=NS for sensitivity). CONCLUSION: In patients with recent MI, the specificity of Dob in the detection of myocardium capable of late mechanical recovery is significantly higher with respect to Sci, whereas sensitivity is slightly, not significantly higher for the latter. It is conceivable that Sci detects viable myocardium even if it is transmurally limited to epicardial layers in segments with severely impaired mechanical function in which viability will not affect late recovery of function.

The left atrial volume curve can be assessed from pulmonary vein and mitral valve velocity tracings.

After instantaneous left atrial volume was defined as the net difference between the forward-flowing blood from the lungs and the blood flowing through the mitral valve, we constructed the left atrial volume curve by sampling the Doppler mitral valve and the right upper pulmonary vein velocity from an apical four-chamber view in eight normal subjects and 11 patients with heart disease. The instantaneous mitral valve flow was estimated as mitral valve velocity x annular area (derived from the same view), whereas the pulmonary venous flow was obtained as right upper pulmonary vein velocity x pulmonary vein area, where pulmonary vein area = mitral valve velocity integral x mitral valve area) divided by pulmonary vein velocity integral. The left atrial volume curve can then be derived as: [(instantaneous pulmonary venous flow - mitral valve flow) + left atrial volume assessed at end diastole by two-dimensional echocardiography]. Biplane angiographic left atrial volume curves, available in four of 11 patients, compared morphologically very closely with the noninvasive curves, whereas the correlation coefficient for maximum (end-systolic) and filling (maximum minus minimum) left atrial volumes obtained from the Doppler-derived curve and the corresponding two-dimensional echocardiographic estimates was 0.95 (p < 0.001, standard error of the estimate = 11.9 ml), the dispersion of the data increased with decreasing volumes. These data demonstrate that combined Doppler mitral valve and pulmonary vein velocities can be used to construct the left atrial volume curve in human beings. The approach described, besides providing a tool for further noninvasive evaluation of the left atrial function, offers the opportunity for relating the continuous pulmonary venous flow to the intermittent filling of the ventricle through the mitral orifice in diastole, underlining the complex role that the left atrial cavity plays in this process.

The extent of regional wall motion abnormalities identifies patients at risk of extensive left ventricular remodeling: implications for the design of post myocardial infarction trials.

BACKGROUND: The FAMIS (Fosinopril in Acute Myocardial Infarction Study) was a multicenter, placebo-controlled, double-blind trial designed to evaluate the safety and the efficacy of fosinopril in reducing left ventricular enlargement after acute anterior myocardial infarction. We evaluated the echocardiographic examinations performed during the trial in order to assess the trend of the remodeling process over time and to evaluate the role of infarct size in identifying patients at risk of progressive left ventricular dilation. METHODS: A complete echocardiographic examination was performed on admission, before discharge and three months later. Patients undergoing coronary bypass surgery or PTCA had a further examination prior to the procedure. The echocardiograms were analyzed at a central laboratory, and the end-diastolic and end-systolic left ventricular volumes were computed by using a modified Simpson's rule technique. Regional wall motion was evaluated using the centerline method, analyzing the left ventricular boundary along 100 chords perpendicular to the centerline constructed midway between the end-diastolic and the end-systolic contours. A quantitative infarct-size index was then computed according to the number of chords with a fractional shortening equal to or less than 5%. RESULTS: Left ventricular end-diastolic and end-systolic volume index significantly increased over time (p < 0.0001); as a result, the stroke volume increased (p < 0.0001) but the ejection fraction did not change. Patients were then divided according to the three-month infarct-size index. For both end-diastolic and end-systolic volume, not only did larger infarcts had higher volumes, but there was also a greater increase from baseline to 3 months. Moreover, larger infarcts had a lower ejection fraction, with a further reduction over the three months, while smaller infarcts had higher values and an increase over time. An infarct-size index of 25 or larger allowed prospective identification at the baseline examination of patients at risk of subsequent left ventricular dilation. CONCLUSIONS: In conclusion, patients at greatest risk of left ventricular dilation, namely those with larger infarct size, constitute a group that is worth considering for any therapeutic effort for reducing the remodeling process. These patients could in fact benefit from therapeutic strategies aimed at the reduction of left ventricular remodeling and should be studied in clinical trials.

Left atrial overload can be used to estimate mitral regurgitant volume.

This study was conducted to assess the accuracy of the estimated mitral regurgitant volume using both the left atrial filling volume and the systolic component of pulmonary vein flow expressed as the percent of its total. Since mitral regurgitation fills the left atrial chamber, the variation in atrial volume during ventricular systole has been proposed as a means to evaluate the severity of regurgitation. Although the correlation with invasive grading of mitral regurgitation is good, there is an unacceptable overlap among grades caused by the absence of information concerning pulmonary vein flow, which enters the left atrium while regurgitation occurs. The Doppler regurgitant volume, or Dp-RVol (mitral stroke volume minus aortic stroke volume) was quantified in 74 patients with any degree and etiology of mitral regurgitation. Atrial volumes were measured from the four-chamber apical view (biplane area-length method). The systolic time-velocity integral of pulmonary vein flow was expressed as the percent of the total (PVs%) (systolic-diastolic) time-velocity integral. These parameters were subjected to multivariate analysis and a regression equation was obtained. The equation was subsequently applied to a group of 31 patients without mitral regurgitation, as evaluated by color Doppler or continuous-wave Doppler and to the overall population (105 patients) in order to estimate the mitral regurgitant volume. In 74 patients with mitral regurgitation, the Doppler regurgitant volume was univariately correlated with the left atrial filling volume (r= 0.74; p<0.0001) and the systolic pulmonary vein velocity integral expressed as the percent of the total (r=0.67; p<0.0001). In multiple regression analysis, the combination of atrial filling and the pulmonary vein velocity integral provided the more accurate estimation of the regurgitant volume (R2=0.84; standard error of the estimate [SEE], 13.9 mL; p<0.0001; Dp-RVol equals 7.84+[1.08*left atrial filling volume] 2 [0.839*PVs%]). In 31 patients with no mitral regurgitation detected by color Doppler or continuous wave Doppler the estimated regurgitant volume was 4.3±6.6 mL. In the overall population the estimated regurgitant volume and the Doppler regurgitant volume correlated well with each other (R2=0.85; SEE, 11.5 mL; p<0.0001). The equation was 100% sensitive and 98% specific in detecting a regurgitant volume higher than 55 mL. The combination of the atrial filling volume and the systolic pulmonary vein time-velocity integral expressed as the percent of the total allows reliable estimation of the regurgitant volume in patients with mitral regurgitation. (c)2001 CHF, Inc.

[Variations in left ventricular function during chronic therapy with verapamil in angina patients. Influence of the plasma concentration of the drug. Quantitative M-mode echocardiographic analysis]. / Variazioni della funzione ventricolare sinistra durante terapia cronica con verapamil in pazienti anginosi. Influenza delle concentrazioni plasmatiche del farmaco. Analisi quantitativa ecocardiografica M-mode.

In order to assess the influence of orally administered verapamil on left ventricular function, 12 anginal patients were studied using M-mode echocardiography prior to and following two weeks of treatment with verapamil, 120 mg t.i.d. Baseline measurements were obtained by averaging the three measurements from the three different echocardiographic recordings; measurements during treatment were obtained by averaging three measurements on a single recording. The following parameters were considered: end-diastolic (dD) and end-systolic diameters of the left ventricle, fractional shortening, peak ejection rate and peak filling rate. On baseline examination, the end-diastolic diameter was 52.3 +/- 7.9 mm, the end-systolic diameter was 32.4 +/- 7.2 mm, the fractional shortening was 38.5 +/- 5.2%, peak ejection rate was 2.46 +/- 0.41 and peak filling rate was 4.87 +/- 1.44 1/sec. After verapamil treatment the end-diastolic diameter was 54.5 +/- 8.1 mm and the end-systolic diameter was 34.0 +/- 6.6 mm: both parameters showed a significant increase (p less than 0.05 for both). Fractional shortening (37.9 +/- 4.8%), peak ejection rate (2.29 +/- 0.39 1/sec) and peak filling rate (4.94 +/- 1.64 1/sec) remained unchanged. Verapamil plasma level was 149 +/- 1076 ng/ml; there was no significant correlation with the percentage variations of the echocardiographic parameters. In conclusion, in patients with normal cardiac function, chronic treatment with verapamil does not affect ventricular performance. In fact, a slight but significant cardiac dilatation appears to be the mechanism adopted to maintain adequate cardiac performance.