Clinical significance of magnetic resonance and echocardiographic correlations in the evaluation of hypertrophic cardiomyopathy

Relatively few clinical studies have investigated the role of MRI in the patients with hypertrophic cardiomyopathy. To assess MR capabilities in defining the presence, distribution and severity of left ventricular hypertrophy, the prevalence and clinical correlations of right ventricular hypertrophy and the prevalence and clinical implications of structural myocardial abnormalities, MRI and echocardiography were performed on 37 unselected patients with hypertrophic cardiomyopathy. The two methods were in agreement in 100% of cases in diagnosing the disease and classifying left ventricular hypertrophy as asymmetric, concentric or apical, and in 92% of cases in assessing the topographic distribution of hypertrophy of ventricular segments. A statistically significant linear correlation was found between echocardiographic and MR measurements of interventricular septum (r = 0.69, p < 0.0001, SEE = 4) and left posterior wall of the left ventricle (r = 0.67, p < 0.0001, SEE = 2.4). Right ventricular hypertrophy (right anterior wall diastolic thickness > 5 mm) was demonstrated by MRI in 23 of 33 patients (70%). In this group, left posterior wall thickness and left atrial diameter were higher (15 +/- 4 vs 11 +/- 2, p < 0.01 and 45 +/- 9 vs 38 +/- 5 mm, p < 0.05, respectively). On T2-weighted sequences, areas of reduced signal intensity, probably due to myocardial fibrosis, were detected in 16 cases (43%). This group was characterized by higher max. septal thickness (25 +/- 7 vs 21 +/- 6 mm, p < 0.05) and max. left posterior wall thickness (15 +/- 9 vs 7 +/- 8 mm, p < 0.05). All the three cases with dilated and hypokinetic left ventricle showed this kind of tissue abnormality. In conclusion, MRI provided clear, accurate and exhaustive data on the presence and distribution of left ventricular hypertrophy in hypertrophic cardiomyopathy. Right ventricular hypertrophy and structural abnormalities of ventricular myocardium can also be detected and quantified. Right ventricular involvement is associated with more severe hypertrophy of left ventricular posterior wall. Structural myocardial abnormalities, probably due to fibrosis, are related to the extent of left ventricular hypertrophy.     

Assessment of quantitative hypertrophy scores in hypertrophic cardiomyopathy: magnetic resonance imaging versus echocardiography

To compare the diagnostic value of spin-echo magnetic resonance (MR) imaging and transthoracic echocardiography in quantitative assessment of the extent of hypertrophy in patients with hypertrophic cardiomyopathy (HCM), we examined 52 consecutive patients with HCM. The Spirito-Maron and Wigle hypertrophy scores were calculated with wall thickness measurements obtained by both imaging modalities. MR imaging yielded complete assessment of anatomic features and allowed calculation of hypertrophy scores in 49 patients (94%). Adequate echocardiograms were obtained in 33 patients (63%) and correlated well with MR imaging for wall thickness measurements and for determination of the two hypertrophy scores (both r> 0.9). MR imaging provided additional information not available by echocardiography in 16 patients (31%). We conclude that the Spirito-Maron and Wigle hypertrophy scores correlated well between echocardiography and MR imaging. Because echocardiography was of insufficient quality for calculating adequate hypertrophy scores in 19 (37%) patients, MR imaging provided the most comprehensive diagnostic information in patients with HCM.     

Left ventricular geometry in presenting untreated hypertension

In order to investigate the spectrum of geometry in our patient population, 63 untreated hypertensives underwent two-dimensional echocardiography. Left ventricular (LV) mass index and relative wall thickness, a measure of wall thickness in relation to cavity size, were calculated from the M-mode strip. In addition, to assess the sphericity of the left ventricle the ratio of LV minor to major hemiaxis was calculated. The subjects comprised 41 men (17 Caucasian, 22 Afro-Caribbean and two Oriental), and 21 women (five Caucasian, 12 Afro-Caribbean and two Oriental). Concentric hypertrophy was present in 46% of subjects, concentric remodelling in 32% of subjects, eccentric hypertrophy in only 6% of subjects and a normal left ventricular shape in 16% of subjects. The degree of sphericity of the left ventricle was similar among the four groups, suggesting that it does not change in uncomplicated hypertension. In contrast to the previously published combined series from Sassari and New York we had a low proportion of patients with either eccentric hypertrophy or normal left ventricular geometry. This is probably due to the high proportion of Afro-Caribbean subjects in our clinic population who are more likely to have left ventricular hypertrophy.     

Relation of electrocardiographic features and distribution of hypertrophy in hypertrophic non-obstructive cardiomyopathy during childhood

The relationship between the electrocardiographic features and the distribution of ventricular hypertrophy in pediatric patients with hypertrophic non-obstructive cardiomyopathy (HNCM) aged from 6 to 16 years (mean 11.6 years) was studied during a period of 6 months to 10 years (mean 3.9 years). Hypertrophy in the three segments (anterior septum, lateral free wall, posterior free wall) of the left ventricle in 17 patients with HNCM was evaluated by two-dimensional echocardiography (short-axis cross section of the left ventricle) at the end-diastolic period. The 17 patients were divided into four groups according to the echocardiographic findings as follows: Group A: hypertrophy in the ventricular anterior septum with or without posterior septum (eight patients). Group B: hypertrophy in both the ventricular septum and lateral left ventricular free wall (three patients). Group C: hypertrophy in the lateral left ventricular free wall (three patients). Group D: hypertrophy in the posterior left ventricular free wall with or without posterior septum (three patients). The incidence of electrocardiographic abnormalities in each group was analyzed using serial standard 12-lead electrocardiography. Electrocardiographic abnormalities and the distribution of the ventricular hypertrophy were related as follows: Lateral free wall: increased SV1 + RV6 (p < 0.05), ST-T change in leads V5.6 (p < 0.01). Posterior free wall: ST-T change in leads II.aVF (p < 0.05). Electrocardiographic abnormalities in HNCM patients in the hypertrophy were: Group A: abnormal Q waves in leads II.III.aVF (75%) and V5.6 (50%), high voltage R waves in leads II.III.aVF (25%) and V1 (38%), low voltage R waves in leads V2.3 (13%) and V5.6 (38%), and ST-T changes in leads I.aVL (25%), II.aVF (13%) and V2-4 (50%). Group B: abnormal Q waves in leads II.III.aVF (33%), high voltage R wave in lead V1 (33%), increased SV1 + RV6 (67%), low voltage R waves in leads V2.3 (33%) and V5.6 (33%), and ST-T changes in leads I.aVL (33%), II.aVF (33%), V2-4 (67%) and V5.6 (67%). Group C: abnormal Q waves in leads I.aVL (33%) and V5.6 (33%), high voltage R waves in leads II.III.aVF (33%), V1 (67%) and V5.6 (33%), increased SV1 + RV6 (67%), low voltage R waves in leads V5.6 (33%) and ST-T changes in leads II.aVF (33%), V2-4 (33%) and V5.6 (67%).     

Effect of 3 hypertensive++ agents on ventricular geometry and function

BACKGROUND: To assess the prevalence of left ventricular hypertrophy in hypertensive patients referred to an outpatient cardiology unit, and to assess its evolution under antihypertensive treatment. METHODS: One hundred and seven mild to moderate hypertensive patients were randomized to receive either xipamide, verapamil or atenolol. Cross-sectional echocardiography was performed in order to assess left ventricular mass and function. RESULTS: Mean age was 56 years, with a 4:1 female/male ratio. Mean follow-up was 120 days. Left ventricular hypertrophy was very common (65%) and decreased to 54% under antihypertensive treatment. Left ventricular mass decreased from 134.3 g/m2 to 118.1 g/m2 (p < 0.001). Concentric hypertrophy was the most common geometric pattern (42%), decreasing to 30% with treatment. Xipamide decreased ventricular mass by decreasing left ventricular diameters, while verapamil and atenolol decreased left ventricular thickness, mainly in septal wall. Systolic function was not modified during the treatment period. Diastolic function was not modified by xipamide and verapamil, and improved with atenolol. CONCLUSIONS: Left ventricular hypertrophy is very frequent when determined by echocardiography and all three drugs produced regression of left ventricular hypertrophy in a different way with respect to left ventricle geometry, an effect which could have potential therapeutic implications.     

Comparison of clinical and morphologic cardiac findings in patients having cardiac transplantation for ischemic cardiomyopathy, idiopathic dilated cardiomyopathy, and dilated hypertrophic cardiomyopathy

This article compares intergroup and intragroup clinical and morphologic findings in patients with ischemic cardiomyopathy (IC), idiopathic dilated cardiomyopathy (IDC), and dilated hypertrophic cardiomyopathy (HC) undergoing cardiac transplantation (CT). Few previous publications have described findings in native hearts explanted at the time of CT. The explanted heart in 92 patients having CT was examined in uniform manner with particular attention to the sizes of the ventricular cavities and the presence of and extent of ventricular scarring. Of the 92 hearts examined, 47 had IC, 35 had IDC, and 10 had dilated HC. Although considerable degrees of intragroup variation occurred, the mean degree of left ventricular dilatation was similar among the patients with IC, IDC, and dilated HC. All patients with IC had left ventricular free wall scarring more extensive than that involving the ventricular septum, but the intragroup variation in the amounts of scarring was considerable. Nine of the 10 patients with dilated HC also had ventricular wall scarring, but it was more extensive in the ventricular septum than in the left ventricular free wall and involvement of the right ventricular wall also was present. Eight (23%) of the 35 IDC patients also had grossly visible ventricular scars but they were small and only 1 of the 8 had coronary narrowing and that was not in the distribution of the scarring. Narrowing of 1 or more epicardial coronary arteries >75% in cross-sectional area by plaque was present in all 47 IC patients, in 8 of the 35 IDC patients (7 had no ventricular scars), and in none of the 10 dilated HC patients. Coronary angiography was the major clinical tool allowing separation of the IC, IDC, and HC patients. Coronary angiography did not detect narrowing in any of the 8 patients with IDC who were found to have coronary narrowing on anatomic study. Thus, among patients with IC, IDC, and dilated HC having CT, distinctive anatomic features allow separation of patients with IC, IDC, and dilated HC, but within each group considerable variation in left ventricular cavity size and extent of ventricular scarring occurs.     

Important metabolites to measure in pharmacodynamic studies of chlorpromazine

Left ventricular hypertrophy occurs in numerous hypertensive patients. It can be diagnosed by using echocardiography, whose sensibility (93%) and sensitivity (95%) are both excellent, provided the quality of the recordings is good enough (80%). Most often, left ventricular hypertrophy is a concentric one (relative wall thickness greater than 0.45). The determinants of hypertensive left ventricular hypertrophy are of mechanical and hormonal origin; Weber's and Brilla's recent findings suggest that the haemodynamic burden should be responsible for myocytes hypertrophy, whereas hormonal factors stimulate fibrosis proliferation. Although left ventricular hypertrophy is initially an adaptative process, it eventually results in numerous deleterious effects: arrhythmias, myocardial ischemia, left ventricular filling abnormalities. Left ventricular hypertrophy is now recognized as a powerful blood-pressure independent risk factor for cardio-vascular morbidity and mortality. Therefore, antihypertensive therapy must be aimed at reducing not only blood pressure but also left ventricular mass. Most of the published regression studies have however to be criticized from a methodologic standpoint.     

Regression of left ventricular hypertrophy after aortic valve replacement for aortic stenosis with different valve substitutes

OBJECTIVE: Stentless biologic aortic valves are less obstructive than stented biologic or mechanical valves. Their superior hemodynamic performances are expected to reflect in better regression of left ventricular hypertrophy. We compared the regression of left ventricular hypertrophy in 3 groups of patients undergoing aortic valve replacement for severe aortic stenosis. Group I (10 patients) received stentless biologic aortic valves, group II (10 patients) received stented biologic aortic valves, and group III (10 patients) received bileaflet mechanical aortic valves. METHODS: Echocardiographic evaluations were performed before the operation and after 1 year, and the results were compared with those of a control group. Left ventricular diameters and function, left ventricular wall thickness, and left ventricular mass were assessed by echocardiography. RESULTS: Group I patients had a significantly lower maximum and mean transprosthetic gradient than the other valve groups (P = .001). One year after operation there was a significant reduction in left ventricular mass for all patient groups (P < .01), but mass did not reach normal values (P = .05). Although the rate of regression in the interventricular septum and posterior wall thickness differed slightly among groups, their values at follow-up were comparable and still higher than control values (P = .002). The ratio between interventricular septum and posterior wall and the ratio between wall thickness and chamber radius did not change significantly at follow-up. CONCLUSIONS: Because the number of patients was relatively small, we could not use left ventricular mass regression after I year to distinguish among patients undergoing aortic valve replacement for aortic stenosis by means of valve prostheses with different hemodynamic performances.     

Validations of time-resolved fluoroimmunoassays for urinary estrone 3-glucuronide and pregnanediol 3-glucuronide

OBJECTIVE: In this study, we determined the effect of age, sex, and body size on left ventricular mass. DESIGN: Two-dimensional-guided M-mode echocardiography was used in an assessment of 111 healthy, normal adults. MATERIAL AND METHODS: Left ventricular mass was calculated with the cube function formula corrected by a regression equation to agree with autopsy estimates of left ventricular mass. Calculated left ventricular mass, indexed by body surface area and by height, was analyzed on the basis of sex and age of the study participants. Age was analyzed as a dichotomous, trichotomous, and continuous variable. The effects of age, sex, and obesity, as well as interactions, were tested within a multiple linear regression model framework. RESULTS: Left ventricular mass, when indexed for either body surface area or height, was greater in men than in women. For women, but not men, we found a small but significant increase in left ventricular mass with advancing age. Body mass index, an indicator of obesity, increased with aging in women but not in men and affected left ventricular mass. No significant changes were noted in left ventricular cavity size with advancing age, and the increase in left ventricular mass in women was due to increased ventricular wall thickness. CONCLUSION: The findings in this study suggest that left ventricular mass, as assessed by two-dimensional-guided M-mode echocardiography, is affected not only by sex and body size but also by age in women. This phenomenon may be related to an increase in body mass index with advancing age in women. In clinical studies that use echocardiographic left ventricular mass to diagnose left ventricular hypertrophy, these observations should be considered.     

Correlation of thallium uptake with left ventricular wall thickness by cine magnetic resonance imaging in patients with acute and healed myocardial infarcts

Myocardial infarction (MI) is characterized by cellular necrosis which undergoes fibrotic transformation over time. Cine magnetic resonance imaging (MRI) offers high-resolution 3-dimensional images of the left ventricular myocardium, allowing sampling of the myocardial wall thickness over the entire left ventricle. Tomographic (single-photon emission computed tomography [SPECT]) thallium images also provide 3-dimensional information on the location and level of thallium uptake, which has been shown to correlate with myocardial viability. The purposes of this study were: (1) to examine the relation between both end-diastolic and end-systolic wall thickness and normalized thallium-201 uptake over the left ventricle in a group of patients with MI, (2) to examine the relation between regional wall thickening and normalized thallium uptake, and (3) to examine the relation between thallium uptake and wall thickness both early and late after infarction. Twenty-four patients with MI underwent stress, redistribution, and reinjection thallium SPECT imaging and cine MRI within several days. Seventeen patients underwent imaging late after infarction and 7 underwent imaging early after infarction. Normalized thallium activity was correlated with MRI wall thicknesses at both end-diastole and end-systole for 18 segments for each ventricle. In addition, end-diastolic and end-systolic wall thicknesses were grouped by their corresponding thallium activity levels into percentiles. End-systolic wall thickness correlated significantly with normalized thallium uptake in 14 of 18 segments, end-diastolic wall thickness in only 4 of 18 segments, and wall thickening in only 3 of 18 segments. Mean values for end-diastolic and end-systolic wall thicknesses corresponding to severely reduced (<50%) normalized thallium activity were 9.9 +/- 1.1 and 8.5 +/- 0.6, respectively. Using receiver-operating curve analysis, end-systolic wall performed as a better diagnostic parameter than end-diastolic wall for identifying severely reduced thallium activity levels. For all levels of thallium activity, end-diastolic wall thicknesses were all thinner late versus early after MI, whereas end-systolic wall thickness was thinner only in the segments corresponding to severely reduced thallium activity. Based on these results, end-systolic wall thickness is the best noninvasive anatomic parameter of myocardial scar.     

Contrast magnetic resonance imaging in the assessment of myocardial viability in patients with stable coronary artery disease and left ventricular dysfunction

BACKGROUND: The utility of contrast MRI for assessing myocardial viability in stable coronary artery disease (CAD) with left ventricular dysfunction is uncertain. We therefore performed cine and contrast MRI in 24 stable patients with CAD and regional contractile abnormalities and compared MRI findings with rest-redistribution 201Tl imaging and dobutamine echocardiography. METHODS AND RESULTS: Delayed MRI contrast enhancement patterns were examined from 3 to 15 minutes after injection of 0.1 mmol/kg IV gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA). Comparable MRI and 201Tl basal and midventricular short-axis images were subdivided into 6 segments. Segments judged nonviable by quantitative and qualitative assessment of 201Tl scans showed persistent, systematically greater MRI contrast signal intensity than segments judged viable (P相似文献   

Electrocardiographic patterns in hypertensive patients without atherosclerotic coronary disease. Influence of the left ventricular mass

BACKGROUND: ECG ST-T segment abnormalities in hypertensive patients are traditionally associated with hypertrophy or ischaemia. Hypertensive patients with abnormalities in ST-T segment in DI, aVL and/or V5-V6 underwent an echocardiographic study in order to assess left ventricular structure. All of them, in addition to the electric changes, showed typical or non-typical thoracic discomfort, showing a normal coronariographic study. METHODS: Hypertensive patients with ST-T segment changes were classified as follows: group A, 12 patients (8 women, 4 men, mean age 63.6 +/- 7.2 years) with ECG image of left ventricular overload pattern; group B, 9 patients (3 men, 6 women, mean age 62.3 +/- 6.3 years) with flat ST segment depression; and group C, 10 patients (3 men, 7 women, mean age 62.4 +/- 9.7 years) without changes on the ST-T segment with flat or negative T wave. Control group is made up 12 hypertensive patients (7 women, 5 men, mean age 61.6 +/- 7.6 years) with normal ECG. We assess by echocardiography interventricular septal thickness (IVST) and left ventricular posterior wall thickness (PWT) in mm, left ventricular end-diastolic diameter (DTD) in mm, left ventricular mass (LVM) in grs, and the mass index (MI) in g/m2. RESULTS: IVST, PWT, LVM and MI were significantly (p < 0.05) higher in the groups A, B and C than in the control group. No statistically significant differences were observed between the A, B and C groups. Stepwise discriminant analysis showed that the only parameter with independent value for discriminating between control, group and group ABC (the union of groups A, B and C) was IVST. CONCLUSION: In hypertensive patients without coronariopathy, ST-T changes identify a group with greater left ventricular mass. The different electrocardiographic patterns considered were not associated with a significantly different left ventricular mass.     

Using the World Wide Web--a new approach to risk identification of diabetes mellitus

We evaluated 30 consecutive patients and 48 age- and sex-matched controls to explore the possibility of a pathogenic contribution by plasma endothelin-1 in the cardiac expression of systemic sclerosis. Venous plasma endothelin-1 was measured by radio-immunoassay and left ventricular function by echocardiography. The patient group had elevated plasma endothelin-1 (2.6 +/- 0.2 vs. 1.8 +/- 0.1 pmol/1, P < 0.001), but endothelin-1 was not related to age, heart rate, blood pressure, total peripheral resistance, disease duration or systemic sclerosis score. Endothelin-1 was related to left ventricular hypertrophy in terms of septal thickness (r = 0.33, P < 0.01) and left ventricular mass index (r = 0.32, P < 0.01). Plasma endothelin-1 was further related to measures indicating reduced left ventricular filling; left atrial emptying index (r = -0.50, P < 0.0005), the first third filling fraction (r = -0.31, P < 0.05) and the time velocity integral of Doppler early/late filling velocity (r = -0.40, P < 0.001). Furthermore, circulating endothelin-1 was related to impaired left ventricular contractility as estimated by pre-ejection period/left ventricular ejection time (r = 0.32, P < 0.01) and end-systolic wall stress/volume index (r = -0.30, P < 0.05). We conclude that plasma endothelin-1 is elevated in relation to the degree of left ventricular hypertrophy, diastolic dysfunction and impaired contractility in systemic sclerosis. It may be of pathogenic importance to the cardiac involvement in systemic sclerosis which is not mediated via an increase in systemic blood pressure. It is not yet clear whether our findings are exclusive to systemic sclerosis patients or represent a generalized phenomenon in patients with impaired left ventricular function.     

Correlation between left ventricular hypertrophy and GAA trinucleotide repeat length in Friedreich's ataxia

BACKGROUND: Friedreich's ataxia (FA), the most common inherited ataxia, is associated frequently with cardiac hypertrophy, and death is often cardiac related. Recently, the disease has been associated with a mutation that consists of an unstable expansion of GAA repeats in the first intron of the gene encoding frataxin on chromosome 9. METHODS AND RESULTS: We studied 44 consecutive patients with FA, determined the size of GAA expansions in the frataxin gene, and examined the relation between the genotype and cardiac phenotype assessed by M-mode and two-dimensional echocardiography. All the patients were homozygous for the mutation. The size of the GAA expansion on the smaller allele varied from 270 to 1200. We found a correlation between the size of GAA expansion and the left ventricular wall thickness (r = .51, P < .001) and the left ventricular mass index (r = .45, P = .002). Left ventricular hypertrophy was observed in 81% of patients with a number of GAA repeats above the median value of 770 compared with only 14% in the other group (P = .002). CONCLUSIONS: These data demonstrate that in FA, the severity of left ventricular hypertrophy is related to the number of GAA repeats. These results suggest that abnormalities of the gene encoding frataxin, a protein of unknown function highly expressed in the normal heart, may play an important role in the modulation of cardiac hypertrophy.     

Evaluation of electrocardiographic left ventricular hypertrophy with both QRS voltage and ST-T change using echocardiography

The purpose of the present study is to determine whether electrocardiographic QRS voltage criteria with ST-T change is useful in the diagnosis of left ventricular hypertrophy (LVH) using echocardiography. One hundred men including 59 with hypertension (HT), 9 with hypertrophic cardiomyopathy (HCM), and 32 without any cardiovascular disease were enrolled in this study. All of them had the electrocardiographic evidence of LVH by Sokolow-Lyon voltage criteria (RV5 or RV6 > 2.6 mV, SV1+RV5 or SV1+RV6 > or = 3.5 mV). They were classified into three groups based on ST-T pattern as follows: Normal ST-T (group N): normal ST-T in twelve leads; Early strain ST-T (group ES): ST depression, flat T (T/R < 1/10), diphasic T or T wave inversion < 0.1 mV in V5 or V6; and Strain ST-T (group S): inverted T wave in V5 and V6. Echocardiographic LVH was determined when either interventricular septal thickness (IVST) or left ventricular posterior wall thickness (LVPWT) > or = 12 mm was present. According to this echocardiographic evidence, 31.7%(20/63) of group N, 75.0% (12/16) of group ES, and 100% (21/21) of group S were diagnosed. There were significant correlations between QRS voltage indices (RV5, RV6, SV1+RV5 and SV1+RV6) and IVST, (IVST+LVPWT)/2, and LV mass in group S(r = 0.650 to 0.858, p < 0.05) but not in group N. Values for IVST and LV mass were significantly greater in group S than in group ES or N. The electrocardiographic diagnosis of LVH with both QRS voltage and ST-T change thus appeared to be more useful than that with QRS voltage criteria alone.     

A primary intervention program (pilot study) for Mexican American children at risk for type 2 diabetes

Diastolic dysfunction is common in hypertrophic cardiomyopathy (HC). Previous studies suggest that Doppler transmitral flow velocity profiles, and the left atrial (LA) M-mode echogram can be used noninvasively to evaluate left ventricular (LV) diastolic function. However, this has not been proved in HC. In this study we determined the relation of Doppler transmitral flow velocity profiles and the LA M-mode echograms to invasive indexes of LV diastolic function in patients with HC. We studied 25 patients with HC, while off drugs, and calculated LA global and active fractional shortening and the slope of both early and late displacement of the posterior aortic wall during LA emptying by M-mode echocardiography. We calculated peak velocity of early (E) and atrial (A) filling, E to A ratio, and E-wave deceleration time by pulsed Doppler echocardiography, and simultaneous radionuclide angiography, LV pressures, time constant of isovolumic relaxation tau, and the constant of chamber stiffness k by cardiac catheterization. The time constant of isovolumic relaxation tau correlated with the slope of early posterior aortic wall displacement (r = 0.59; p <0.01). LV end-diastolic pressure correlated with global LA fractional shortening (r = -0.75; p <0.001); the constant of chamber stiffness k correlated with active LA fractional shortening (r = -0.53; p <0.02). In a subset of 13 patients, in whom echocardiography and cardiac catheterization were performed simultaneously, similar results were found. LA M-mode recordings provide a more reliable noninvasive assessment of diastolic function in HC than mitral Doppler indexes.     

Results of dobutamine stress echocardiography in patients with syndrome X

This study describes the results of Dobutamine stress echocardiography in 10 patients with Syndrome X. The diagnosis of Syndrome X was made on the basis of the presence of exertional angina, positive exercise stress test, negative ergonovine stress test and normal coronary arteries at angiography. All patients underwent Dobutamine stress echocardiography after interruption of any antianginal therapy. Dobutamine was infused starting with a dose of 5 mcg/kg/min over 3 minutes with incremental steps of 5 mcg/kg/min every 3 minutes up to a maximal dose of 40 mcg/kg/min. Two-dimensional echocardiography and 12-lead electrocardiography was monitored during the infusion of the drug. Nine patients received the maximal dose while one patient prematurely stopped the test for the occurrence of side effects. None of the ten patients developed segmental left ventricular wall motion abnormalities indicative of myocardial ischemia; ST-segment depression diagnostic for ischemia developed in 30% of patients; angina was elicited in one of these patients and in two additional patients. A hyperkinetic response to Dobutamine infusion involving all the segments of the left ventricle was observed both in patients with and without chest pain or electrocardiographic changes. In patients with Syndrome X Dobutamine induces a hyperkinetic left ventricular response indicative of normal contractile reserve despite the presence in some cases of angina and electrocardiographic signs of ischemia.     

Safety of direct laryngoscopy as an outpatient procedure

Diminished systolic function or inappropriate hypertrophy are considered risk factors for outcome following the Fontan procedure. These parameters are difficult to assess in univentricular hearts that do not conform to the uniform shapes prescribed by conventional 2-dimensional imaging volume algorithms. Three-dimensional echocardiography requires no geometric assumptions and has been validated in both normal and distorted left ventricles. To assess the feasibility and accuracy of this technique in patients with univentricular hearts, we compared 2- and 3-dimensional echocardiographic estimates of ventricular volume, ejection fraction, and mass in patients with functionally single left ventricles with results obtained by magnetic resonance imaging (MRI). Twelve patients with functionally single left ventricles (6 months to 22 years) underwent examination by all 3 modalities. Correlation and agreement with MRI were calculated for volumes, ejection fraction, and mass. Three-dimensional echocardiographic comparison with MRI yielded a bias of 3.4 +/- 5.5 ml and 14.2 +/- 8.3 ml for systolic and diastolic volumes, respectively. Agreement analysis for mass showed a bias of 5.8 +/- 8.4 grams. Two-dimensional echocardiography showed less agreement for both volumes and mass (bias of -2.9 +/- 8.1, 2.9 +/- 10.4 ml and -8.3 +/- 12.0 g for volume and mass, respectively, p >0.05). Ejection fraction by 3-dimensional echocardiography showed significantly closer agreement with MRI (bias of 4.4 +/- 5.3%) than 2-dimensional echocardiography (bias of 8.5 +/- 10.3%, p = 0.04). Thus, 3-dimensional echocardiography provides estimates of ventricular volumes, ejection fraction, and mass that are comparable to MRI in this select group of patients with single ventricles of left ventricular morphology.     

Assessment of fetal pulmonic stenosis by ultrasonography

This study was designed to determine (1) the value of Doppler echocardiography in depicting the presence of a fetal pulmonary stenosis, (2) its reliability in the assessment of the severity of the lesion, and (3) the usefulness of additional markers from the left side of the heart as criteria of severity. Fourteen pregnant ewes were included in this study (gestational age, 90 to 120 days). Banding of the fetal main pulmonary artery created mild (n = 3), moderate (n = 3), and severe (n = 5) stenosis. Three lambs were sham operated. Intrauterine fetal Doppler echocardiographic data obtained 15 days after surgery were compared with preoperative values. Peak velocities recorded through the band increased linearly from baseline in the groups with mild and moderate stenosis but did not show any further increase in the group with severe stenosis. Compared with the sham-operated group, right ventricular output in the group with stenosis was either similar or reduced significantly. The increase in right ventricular free wall thickness was significantly greater in the groups with stenosis compared with that of the sham-operated group; the correlation with the degree of severity was r = 0.65 and p < 0.05. A A stronger positive correlation was found between the severity of stenosis and aortic valve diameters: r = 0.82 and p < 0.01. The strongest correlation was found for right ventricular/left ventricular outputs (r = 0.92; p < 0.001). Thus Doppler peak velocities through the obstruction can help detect pulmonic stenosis but are not reliable for the assessment of its severity during fetal life. Other ultrasound measurements such as the size of the aortic anulus and especially the ratio of right ventricular/left ventricular output could be used as sensitive markers of the severity of stenosis.     

Comparison of morphologic findings in spontaneously occurring hypertrophic cardiomyopathy in humans, cats and dogs

Morphologic features of spontaneously occurring hypertrophic cardiomyopathy (HC) were compared in 38 humans, 51 cats and 10 dogs. Asymmetric hypertrophy of the ventricular septum, marked disorganization of cardiac muscle cells, abnormal intramural coronary arteries and myocardial fibrosis were each present in the ventricular septum of human, feline, and canine forms of HC; these abnormalities were generally more severe and most frequently identified in humans. Asymmetric left ventricular hypertrophy (based on the calculated septal-to-free wall thickness ratio) was most common in humans (31 of 38 [81%]) and dogs (8 of 10 [80%]), as compared with cats (16 of 51 [31%]; p < 0.001) with HC; in all 3 species, hypertrophy was often diffuse, involving substantial portions of the anterolateral and posterior free walls, and the ventricular septum. Marked septal disorganization (> or = 5% of the tissue section) was present in 35 patients (92%), but in only 14 cats (27%) and 2 dogs (20%) (p < 0.001). Abnormal intramural coronary arteries occurred with similar frequency in the ventricular septum of patients (n = 25; 66%), cats (n = 38; 74%) and dogs (n = 6; 60%) (p < NS). Moderate-to-severe septal fibrosis was identified more commonly in humans (15 of 38 [39%]) than in animals (13 of 61 [21%]; p < 0.001). In all 3 species, abnormal intramural coronary arteries were most commonly observed within or at the margins of areas of fibrous tissue. These morphologic findings describe spontaneously occurring models of HC in cats and dogs with substantial structural similarities to the well-recognized disease entity in humans.