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Our study was to apply the 2015 American Heart Association/American College of Cardiology Athletic Participation Guidelines to a group of otherwise healthy school age children and young adults with bicuspid aortic valve (BAV) and describe the potential competitive sports restriction as they age. We performed a retrospective chart review of children and young adults aged 5 to 22 years with isolated BAV with at least two echocardiograms between 2000 and 2013. Using task force guidelines, exercise restriction was recommended for any of the following: (1) any dilation of the aortic root, (2) any dilation of the ascending aorta, (3) moderate aortic stenosis, (4) severe aortic regurgitation; (5) left ventricular dilation or (6) reduced shortening fraction. Of the 345 patients with isolated BAV, 202 were considered restricted at study entry. The final cohort included 123 children and young adults. Over the course of follow up, 36% (44 of 123) met restriction criteria. The most likely cause for restriction was aortic dilation (34%). Progression of aortic valve disease occurred in a minority of patients (3%). There were no reports of death, dissection or catheter or surgical based intervention. In conclusion, we found that strict adherence to current guidelines would result in restriction of more than 1/3 of school age children and young adults with BAV from some form of competitive athletics during school age years. Strict application of the current guidelines in this age group may lead to over-restriction of youths from competitive sports.

One hundred thirty-nine patients who underwent transesophageal echocardiographic studies were grouped by their maximal left atrial (LA) volumes, and their stroke volumes, emptying fractions, and fractional shortening were calculated. In large atria, an inverse relation was found between further increases in LA volume and LA function, determined by emptying fractions and fractional shortening.

This study assesses and evaluates left ventricular (LV) contractile function after treatment of hypertension, with an emphasis on LV midwall mechanics. Although prior studies have assessed cardiac function after hypertension treatment, none has performed an analysis of LV midwall mechanics. The Veterans Affairs Study of monotherapy in hypertension was a study large enough to permit analysis of midwall mechanics across a wide spectrum of mass changes accompanying hypertension treatment. LV chamber function was assessed by computing fractional shortening at the endocardial surface; LV midwall shortening was used to define myocardial function. Both shortening indexes were related to end-systolic circumferential stress in the entire population by partitioning values of mass and relative wall thickness changes. Two hundred sixty-eight patients were studied at baseline and again after a 1- or 2-year period. In the entire group, there was no significant change in circumferential shortening either at the endocardium (38 ± 8% at baseline vs 37 ± 7% at follow up, p = 0.29) or in shortening at the midwall (20 ± 3% vs 20 ± 3%, p = 0.53). However, 83 patients had a reduction in relative wall thickness and an increase in midwall shortening. The change in midwall shortening was significantly related to changes in relative wall thickness (r = −0.53, p = 0.0001). Thus, reductions in LV mass associated with antihypertensive therapy are generally not accompanied by a decrement in LV chamber or myocardial function. Improvement in midwall shortening is more closely related to normalization of LV geometry than to reduction in LV mass.

Recent studies have shown conflicting data regarding left ventricular (LV) function in patients with neurocardiogenic syncope, with some investigators reporting a marked decrease in LV end-systolic wall stress and stress-corrected fractional shortening. We sought to determine the characteristics of resting LV deformation in patients with neurocardiogenic syncope by selective motion tracking of subendocardial and subepicardial regions using speckle tracking echocardiography. We assessed resting LV function in 82 patients undergoing head-up tilt-table (HUTT) testing. Patients were divided into 3 groups based on a positive HUTT test with associated co-morbid conditions (n = 30), no associated co-morbid conditions (n = 30), or negative HUTT results (n = 22). LV longitudinal, circumferential, and radial strains were obtained by speckle tracking echocardiography of subendocardial and subepicardial regions in each group and compared with resting LV deformation in 20 healthy control subjects. Compared with endocardial longitudinal strain in control subjects, that in patients with positive HUTT results was attenuated, irrespective of co-morbid conditions (p0.05). Circumferential and radial strains did not differ among groups. On multivariate logistic regression analysis, endocardial longitudinal strain was an independent predictor (odds ratio, 1.16; p = 0.01) of positive HUTT test results. In conclusion, resting LV longitudinal strain is attenuated in patients with positive HUTT test results. Overall, these results may suggest that an increase in resting LV contractility is not a prerequisite for development of neurocardiogenic syncope.

Assessment of ventricular contractility in the newborn infant using standard echocardiographic indexes can result in error due to the unique physiologic state that exists in the neonatal period. It has been suggested from animal and human studies that maturational alterations in contractility occur with birth and continue throughout infancy. To further investigate these developmental changes, 41 newborn infants aged 3 to 10 days and 37 children aged 3 to 18 years were evaluated with 2-dimensional and M-mode echocardiography. The rate-corrected velocity of circumferential fiber shortening (VCFc)-end-systolic wall stress (ESWS) relation was used as a load-independent estimate of contractility. Preload, afterload, and ventricular mass were also measured. Despite similar shortening fractions, the infant group had significantly higher mean VCFc and lower ESWS than the older age group (1.28 vs 1.08 circ/s and 30.2 vs 37.3 gm/m2, respectively). An inverse linear relation between VCFc and ESWS was found in both age groups. The y-intercept was higher in the infant group (p < 0.01), and the slope of the mean regression line was steeper than in the older children (p < 0.01). Ventricular mass in relation to body surface area increased with age. We conclude that (1) newborn infants have a higher basal contractile state that cannot be accounted for by lower afterload, (2) myocardial performance is more sensitive to afterload in the immature heart, and (3) shortening fraction may underestimate ventricular function in the newborn.

To assess the frequency and severity of intraventricular gradients after valve replacement for severe valvular aortic stenosis 25 patients (valve area 0.59 +/- 0.19 cm2) were studied serially with Doppler echocardiography on postoperative days 1, 2, 3, 5 and 7. Pulsed Doppler was used to search for increased intraventricular velocities. Mid-to-late systolic intraventricular velocities > or = 2 m/s were defined as intraventricular gradients. In 13 patients (52%) intraventricular gradients were found at least once during days 1 to 7 (group A) and were most frequent at day 3 (44%). The typical location of these velocities was at the midventricular level close to the septum. In 4 patients intraventricular gradients > 64 mm Hg were found. Left ventricular end-diastolic and end-systolic diameters recorded preoperatively were significantly smaller in group A than in the rest (43.6 +/- 5.4 vs 50 +/- 5.8 mm and 24.6 +/- 5.6 vs 33.1 +/- 7.3 mm, both p < 0.05) and the fractional shortening was significantly higher (44 +/- 9 vs 34 +/- 9%, p < 0.05). It is concluded that intraventricular gradients are frequent during the first week after valve replacement for severe aortic stenosis. These gradients are mostly mild and transient in nature, but significant gradients associated with clinical deterioration may occur. The risk of developing intraventricular gradients postoperatively may be predicted at a preoperative echocardiographic examination, and patients with a small left ventricular cavity size and maintained contractility are at particular risk.(ABSTRACT TRUNCATED AT 250 WORDS)

Patients with acute right ventricular (RV) infarctions are prone to ventricular arrhythmias, but little is known regarding the temporal patterns of these arrhythmias, their impact on outcomes, or their relation to the severity of RV impairment. The aim of this study was to examine the impact of malignant ventricular arrhythmias (MVAs) complicating acute RV infarction. A further aim was to determine whether the degree of RV impairment was a predisposing factor to MVAs. The charts of 48 patients with acute RV infarctions were reviewed for documented MVAs. Temporal presentation, relating to reperfusion, and in-hospital outcomes were tabulated. Echocardiograms were reviewed to quantify RV impairment. MVAs occurred in 38% of patients, with multiple episodes (electrical storm) in 8.3%. MVAs developed before reperfusion (72% of patients), abruptly with reperfusion (11%), or after reperfusion (22%). Patients with MVAs had larger infarcts (peak creatine phosphokinase 3,027 vs 1,848 U/L, p = 0.03) and trended toward worse RV function (fractional shortening 27% vs 34%, p = 0.08). In-hospital mortality (patients with MVAs 17% vs 6.7%, p = 0.35), intensive care days (patients with MVAs 7.1 +/- 10 vs 3.9 +/- 2.5, p = 0.39), and hospital days (patients with MVAs 10.3 +/- 10 vs 8.0 +/- 5.1, p = 0.57) were similar between groups. Patients with electrical storm had longer intensive care stays (18.0 +/- 18.5 vs 4.0 +/- 2.5 days, p = 0.02) and hospital stays (20.5 +/- 17 vs 7.9 +/- 5.0 days, p = 0.05). In conclusion, MVAs are common in acute RV infarctions. They frequently occur before reperfusion and are associated with larger infarcts. With reperfusion, MVAs had little impact on intensive care and hospital stays or in-hospital mortality, except in patients with electrical storm.

The importance of recognizing symptomatic heart failure with preserved left ventricular (LV) systolic function has only recently been apprecated. To determine its frequency and identify clinical features that make the bedside diagnosis likely, 82 patients admitted for decompensated heart failure were classified into 2 groups based on their LV systolic performance, as defined by fractional shortening (FS): group I (n = 59), with impaired systolic function (fractional shortening

In this study, which included 56 patients with aortic stenosis, the predictive value of the fractional shortening velocity ratio was evaluated. This Doppler index allowed detection of significant aortic stenosis (0.53 cm2/m2), with a positive predictive value of 93% and a negative predictive value of 92% for a cutoff value of 0.8.

To examine the relation between papillary muscle fractional shortening and heart shape, we performed quantitative echocardiography in 20 patients with prior myocardial infarction and 20 normal control subjects. Papillary muscle fractional shortening was markedly depressed in infarction patients and there was a high degree of correlation between papillary muscle fractional shortening and left ventricular shape, which was evident over a wide range of ejection fraction and shape.

To investigate ventricular remodeling during long-term right ventricular (RV) pacing after His bundle ablation (HBA) in patients with atrial arrhythmias, a retrospective analysis was performed on echocardiographic data from 45 patients (mean age 57 +/- 11 years) with atrial arrhythmias who underwent HBA and pacemaker implantation (HBA-PI) to control ventricular rate. Echocardiography was performed 1 year before HBA-PI, and up to 7 +/- 2 years of follow-up was conducted. An inverse linear relation was found between the relative increase of left ventricular (LV) end-diastolic diameter (EDD) during long-term RV pacing and LVEDD before HBA-PI (r = -0.61, p0.001). Patients were divided into 2 groups: those with LVEDDs smaller than the mean LVEDD of 50 mm (group I, 46 +/- 2 mm, n = 28) and those with LVEDDs50 mm (group II, 56 +/- 4 mm, n = 17). Before HBA-PI, patients in group I had significantly smaller LV weights (167 +/- 44 vs 238 +/- 56 g) and LV end-systolic diameters (30 +/- 2 vs 42 +/- 7 mm) and higher LV ejection fractions (64 +/- 5% vs 49+/- 12%) than those in group II. In group I, long-term RV pacing increased LVEDD, LV end-systolic diameter, LV weight, and left atrial diameter; increased mitral regurgitation; and decreased the LV ejection fraction and LV fractional shortening. No significant changes were observed during long-term RV pacing in group II. In conclusion, long-term RV pacing after HBA adversely affects LV structure and function in patients with initially normal LV dimensions and function.

The prevalence of significant pericardial effusion in patients with left ventricular (LV) dysfunction has not been reported. The goal of this study was to evaluate the prevalence and severity of pericardial effusion in patients with decreased fractional shortening (FS) using a large echocardiographic database. A retrospective analysis of 24,265 echocardiograms performed at our institution from 1984 to 1998 was undertaken. FS was measured in 18,015 of the echocardiograms. The occurrence of pericardial effusion was correlated with the degree of FS, and FS was stratified into 4 groups: (1) >25%, (2) 17.5% to 25%, (3) 10% to 17.5%, and (4)

A B S T R A C T S group 3. Mean ages of group 1 and 2 were significantly higher than mean age of group 3 (p

We followed 1,778 subjects (up to 12 years) with essential hypertension who underwent echocardiography at the time of their initial diagnostic workup. There were 166 major cardiovascular events during follow-up and the prognostic value of the midwall shortening fraction did not remain significant after controlling for left ventricular mass.

The relation between blood pressure (BP) and left ventricular (LV) systolic function in systemic hypertension is controversial. We assessed the relation of LV midwall fractional shortening (FS) to 24-hour BP in 1,702 never-treated hypertensive subjects (age 48 +/- 12 years), who underwent 24-hour BP monitoring and echocardiography. Stress-corrected endocardial and midwall FS (the latter calculated taking into account the epicardial migration of midwall during systole) were predicted in hypertensives on the basis of the values observed in 130 healthy normotensives (age 43 +/- 13 years, office BP 126/78 mm Hg). Subjects below the fifth percentile of observed-to-predicted FS had depressed LV function. The use of midwall FS resulted in an increase from 3.5% to 17.5% in the proportion of patients with depressed chamber function. Compared with the group with normal function, subjects with low midwall LV function had similar office systolic BP (155 +/- 21 vs 154 +/- 17 mm Hg), but increased 24-hour systolic BP (140 +/- 17 vs 133 +/- 12 mm Hg, p0.001). Midwall FS had a closer negative relation to 24-hour systolic BP than to office systolic BP (r = -0.27 vs -0.08, p0.001), whereas this difference was not apparent for diastolic BP (r = -0.23 vs -0.20). Compared with endocardial FS, midwall FS had a stronger inverse association to LV mass (r = -0.45 vs -0.16, p0.001). Thus, an increased 24-hour BP load may chronically lead to depressed myocardial function in systemic hypertension in the absence of clinically overt heart disease.

Cardiac performance is altered by loading conditions and by heart rate, especially in newborn infants. Ejection phase indexes such as ejection fraction and fractional shortening might be useful in evaluating their cardiac function. The clinical use of these indexes is limited by the inability to distinguish between the effects of altered loading conditions and of abnormalities in left ventricular contractility. The relation between end-systolic endocardial meridional stress and the rate-corrected velocity of circumferential fiber shortening is a sensitive echocardiographic method for evaluating left ventricular contractility, which is relatively independent of loading. 1–5 There have been no reports on the relation between endocardial meridional stress and rate-corrected velocity of circumferential fiber shortening in newborns. We studied the relation between endocardial meridional stress and the rate-corrected velocity of circumferential fiber shortening in normal newborn infants to determine the normal values and to estimate the contractile state.

Subclinical left ventricular (LV) dysfunction is a common occurrence in alcoholic men but has been claimed to be absent or very rare in alcoholic women. M-mode echocardiography was performed to study LV size, mass and systolic function, and Doppler ultrasound to study LV filling in 14 chronic female alcoholics aged 24 to 48 years and in 2 age-matched control groups consisting of 17 healthy women and 22 alcoholic men. Compared with healthy women, female alcoholics had no differences in heart rate or blood pressure but a shorter LV end-diastolic diameter (mean ± standard deviation, 46 ± 4 vs 48 ± 3 mm, p < 0.05), lower fractional shortening (31 ± 6 vs 34 ± 3%, p < 0.05), increased wall thickness to radius ratio (0.43 ± 0.08 vs 0.37 ± 0.05, p < 0.05), reduced peak early diastolic transmitral velocity (45 ± 11 vs 68 ± 7 cm/s, p < 0.001), reduced deceleration of the early diastolic velocity (−274 ± 69 vs −572 ± 107 cm/s2, p < 0.001), and an increased atrial filling fraction (35 ± 12 vs 27 ± 5%, p < 0.05). Although alcoholic men had a longer duration of heavy drinking than alcoholic women (median 19 vs 5 years, p

To identify better those subgroups of pacemaker recipients who will benefit from dual chamber pacing, 19 patients with DDD pacemakers that were physiologically paced were entered into a blinded, randomized protocol comparing long-term VVI versus DDD pacing. Patients were evaluated in each of the pacing modes for exercise performance, cardiac chamber size, cardiac output, functional status and health perception. Eight patients (42%) insisted on early crossover, from VVI to DDD pacing, after only 1.8 +/- 1.4 weeks because of symptoms consistent with pacemaker syndrome. Overall, 12 patients preferred DDD pacing and no patient preferred VVI pacing (p = 0.001). Percent fractional shortening (30 +/- 8 vs 24 +/- 6%, p = 0.009) and cardiac output (6.3 +/- 2.6 vs 4.4 +/- 2.2 liters/min, p = 0.0001) where significantly greater in the DDD mode. Exercise duration was greater during DDD compared with VVI pacing (11.3 +/- 3.7 vs 10.1 +/- 3.7 minutes, p = 0.006). However, it was only in the crossover subgroup that DDD pacing resulted in significant improvement in exercise performance and health perception compared with VVI pacing. This subgroup of patients was characterized by an intrinsic sinus rate of less than 60 beats/min (4/8 vs 0/11, p = 0.006), ventriculoatrial (VA) conduction (4/8 vs 1/11, p = 0.048), greater increase in exercise peak systolic blood pressure from VVI to DDD mode (21 +/- 12 vs 4 +/- 13 mm Hg, p = 0.02) and greater improvement in exercise capacity from VVI to DDD pacing (2.2 +/- 1.2 vs 0.6 +/- 1.4 minutes, p = 0.03) compared with the other 11 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

A new echocardiographic index of left ventricular function, mitral valve E point-septal separation, was compared with the radionuclide ejection fraction determined using the first pass method in 60 patients (73 studies) with ischemic heart disease. Thirty-eight patients had acute myocardial infarction and 22 patients were studied an average of 24 months after acute infarction. In 30 normal subjects, E point-septal separation ranged from 0 to 5.4 mm (average 1.3 mm). In 57 studies (78 percent) E point-septal separation correctly identified patients with a normal or reduced ejection fraction (less than 0.52), but in 13 studies (18 percent) E point-septal separation was normal and ejection fraction depressed. In only three studies (4 percent) was there a normal ejection fraction and an abnormal E point-septal separation. Results did not differ between patients with acute infarction and those studied late after infarction. An E point-septal separation of more than 5.5 mm was highly specific (92 percent) for a reduced ejection fraction, but the sensitivity rate was only 65 percent. Abnormal wall motion as assessed with echocardiography or videotracking, or both, occurred equally among patients with normal and increased E point-septal separation, but this measure was less accurate in patients with more severe wall motion abnormalities. E point-septal separation was unrelated to heart rate; an abnormal value was equally distributed among patients with a normal and those with an enlarged left ventricular end-diastolic dimension on echocardiography. E point-septal separation was superior to other echocardiographic indexes of left ventricular function (percent of fractional shortening, mean rate of diameter shortening and ejection fraction). Thus, E point-septal separation is a simple noninvasive measure of left ventricular function. We conclude that an abnormal E point-septal separation is useful for identifying depressed left ventricular function in patients with acute myocardial infarction and chronic ischemic heart disease. However, 28 percent of our patients with a normal E point-septal separation had a depressed radionuclide ejection fraction. Therefore a normal value for E point-septal separation does not exclude the presence of abnormal left ventricular function in such patients.

In 3 age- and sex-matched groups of subjects--15 normotensives, 15 hypertensives without left ventricular (LV) hypertrophy and 15 hypertensives with LV hypertrophy--the slopes of the regression line obtained by plotting the individual values of LV fractional shortening against the corresponding values of echocardiographic end-systolic stress were compared. The first 2 groups were studied only in control conditions while the third group was restudied after a 20% reduction in LV mass index induced by a long-term antihypertensive treatment and after a 3-week washout period. A significant relation between fractional shortening and end-systolic stress was found in all instances. The slope of this correlation was higher in normotensives (-0.251) and in hypertensives without LV hypertrophy (-0.232) (both p less than 0.01) than in hypertensives with ventricular hypertrophy (-0.079). In this latter group, the slope increased after the reversal of LV hypertrophy (-0.230, p less than 0.01) and remained unchanged (-0.202) at the end of the washout period. No difference was detectable between the slopes obtained in these patients after reversal of LV hypertrophy, both with the antihypertensive treatment on and off, and those of normotensives and hypertensives without LV hypertrophy. Thus, LV hypertrophy attenuates the influence of changes in afterload on LV function. Reversal of LV hypertrophy restores a fractional shortening end-systolic stress relation quite comparable to that found both in normotensives and in hypertensives before the development of LV hypertrophy.

Ten patients with essential hypertension and left ventricular hypertrophy were treated with relatively small doses of methyldopa (500 to 750 mg/day) added to long-term diuretic therapy. Sequential M mode echocardiography showed significant reduction in left ventricular mass 36 weeks after addition of methyldopa in four patients (359 ± 77 [standard error of the mean] to 235 ± 63 g) although blood pressure was not significantly altered by the added treatment. In three of these patients, reduction of left ventricular mass was observed as early as 12 weeks of treatment (384 to 262 g). Neither left ventricular mass to left ventricular volume ratio nor fractional shortening was significantly altered by reduction in left ventricular mass (3.21 ± 0.26 to 2.74 ± 0.24 and 0.42 ± 0.03 to 0.44 ± 0.02, respectively). There was no apparent relation in these patients between changes in blood pressure and changes in left ventricular mass. Thus, reversal of cardiac hypertrophy with antihypertensive treatment is possible in human beings; however, it seems to depend on other factors besides blood pressure control.

In this study, the dependence on beam direction of the echocardiographically derived fractional shortening of the left ventricular minor axis was evaluated. A directionally oriented, steerable cursor was used to select M-mode lines from a 2-dimensional image at the chordal level. Seven M-mode traces were derived from each image, 1 along the true ventricular meridian and 3 at known deviations on either side of the meridian. M-mode traces, thus derived, all appeared acceptable for measuring wall or cavity dimensions. Results indicate a progressive increase in shortening fraction (p less than 0.05) for deviations more than 25% of the distance between the meridian and the lateral or medial papillary muscle heads. Decreases in left ventricular dimensions in diastole and systole with progressive deviation from the meridian accounted for the decrease in shortening fraction. Spatial orientation is required for reproducible shortening fraction measurements.

Left ventricular (LV) diastolic filling was assessed using digitized M-mode echocardiography in 12 patients with aortic regurgitation (AR) and in 12 normal subjects. Ten patients with AR were asymptomatic and 2 patients had congestive heart failure. LV chamber dimensions, fractional shortening and the rate of change of LV dimensions during systole and diastole were determined. In addition, the timing of the rate of change of LV dimensions in diastole (peak dD/dt, 50% peak dD/dt and 20% peak dD/dt) was also measured. Patients with AR had a significant reduction in dD/dt (12.2 +/- 3.5 cm/s in patients with AR vs 15.9 +/- 1.9 cm/s in normal subjects, p less than 0.01) and a delay in the timing of peak dD/dt (160 +/- 35.2 ms in patients with AR vs 86 +/- 17.6 ms in normal subjects, p less than 0.01) from the minimum LV dimension. These diastolic abnormalities were present in patients with symptomatic as well as those with asymptomatic AR, occurred even when the fractional shortening and peak systolic emptying rate (peak -dD/dt) were normal, and showed no correlation with the calculated LV mass (r = 0.14). The delay in the diastolic filling velocities (peak dD/dt, 50% and 20% peak dD/dt) was associated with a decreased rate of change of LV dimension in diastole, suggesting delayed early LV filling. These findings indicate an abnormality of LV diastolic filling in patients with symptomatic as well as asymptomatic AR and suggest that diastolic abnormalities may precede echocardiographic indexes of systolic LV dysfunction.

To evaluate cardiovascular status in human renovascular hypertension, quantitative echocardiographic findings were compared in 42 patients with arteriographically documented renovascular hypertension and 46 age- and sex-matched patients with essential hypertension. Left ventricular (LV) fractional shortening, a measure of systolic performance at rest, was subnormal (less than 26%) in 8 of 42 renovascular hypertensive patients (19%), 0 of 42 essential hypertensive patients (p less than 0.005) and 1 of 79 normal subjects (1%) (p less than 0.005). Fractional shortening was equally reduced in patients with arteriosclerotic and nonarteriosclerotic causes of renal artery stenosis (32 +/- 9% vs 32 +/- 6%, both p less than 0.025 compared with 36 +/- 5% in patients with essential hypertension). The depressed function in renovascular hypertension appeared to be a result of greater LV dilation (p less than 0.02) and septal but not LV free wall hypertrophy (p less than 0.01) that failed to offset the pressure load, allowing end-systolic stress, a measure of myocardial afterload, to increase to abnormal levels (101 +/- 47 X 10(3) dynes/cm2, p less than 0.001 vs 68 +/- 19 in essential hypertension). These data indicate that human renovascular hypertension is associated with more adverse cardiac involvement than essential hypertension of similar severity. In addition, the 14 patients with bilateral renovascular stenosis had a higher cardiac index (3.9 +/- 1.1 liters/min/m2) than the 28 with unilateral stenosis (3.2 +/- 1.1 liters/min/m2, p less than 0.05). This result supports the proposition that bilateral renovascular disease is analogous to 1-clip 1-kidney experimental renovascular hypertension, while unilateral renovascular disease resembles the 1-clip 2-kidney model.(ABSTRACT TRUNCATED AT 250 WORDS)

Nine patients with Rocky Mountain spotted fever underwent M-mode echocardiographic examination. Increased left ventricular dimension was found in 2 patients and decreased left ventricular shortening fraction in 7. Diminished mean velocity of circumferential fiber shortening, increased left ventricular systolic time intervals ratio, and increased mitral valve E point to ventricular septal separation were found in 6 patients. One patient died and at necropsy diffuse myocarditis was present. Repeat echocardiographic examination was available in the remaining 8 patients at follow-up (mean 10 months). Abnormal E mitral point to ventricular septal separation remained in 3 patients and decreased left ventricular shortening fraction in 2; in 1 there was also increased left ventricular end-diastolic dimension. Thus abnormal left ventricular function and chamber enlargement are frequently present in patients with Rocky Mountain spotted fever.

A new method is described for determining localized epicardial shortening in regions newly perfused after saphenous vein bypass grafting. Four to six radiopaque markers are sutured to the ventricular epicardlum in pairs, 2 cm apart and 0 to 3 cm distal to the coronary anastomosis. Shortening fraction and time to onset of shortening are reported in 56 patients examined noninvasively with use of cinefluorography 1 week to 6 months after operation. The right coronary bypass region showed the greatest improvement in shortening fraction in 6 months (from 10.1 to 16.7 percent); the left anterior descending region showed the least (but still significant) Improvement (from 8.6 to 11.5 percent). Paradoxical systolic expansion occurred predominantly in the region of the left anterior descending coronary bypass (95 percent of all such occurrences). Measurement error, observer variability and beat to beat variability were less important than the physiologic changes in the postoperative period. This technique is a direct method providing heretofore unavailable follow-up information on localized shortening in newly perfused myocardium after coronary bypass grafting.

Controversy exists about whether left ventricular (LV) function is affected by aging. Therefore, peak systolic pressure to end-systolic diameter, peak systolic pressure to end-systolic volume, systolic wall stress to fractional shortening and systolic wall stress to end-systolic diameter relations were calculated in the left ventricle of 10 healthy subjects greater than 65 years old (age 70 +/- 4 years) (group B). They were compared with a control group composed by 10 healthy subjects (group A, age 22 +/- 1 years). LV measurements were obtained with M-mode echocardiography and an automatic cuff was used to determine blood pressure. Changes in the load conditions were obtained by 15 mg sublingual isosorbide dinitrate. There were no differences in resting end-systolic diameter, end-systolic volume, end-diastolic diameter, end-diastolic volume, fractional shortening, ejection fraction or systolic wall stress. Older subjects had higher values of resting peak systolic pressure (p less than 0.05) and lower heart rates (p less than 0.05). Young subjects had a steeper peak systolic pressure to end-systolic diameter slope (92 +/- 11 vs 51 +/- 11 mm Hg/cm; p less than 0.001) and peak systolic pressure to end-systolic volume slope (3.4 +/- 0.7 vs 1.9 +/- 0.6 mm Hg/ml; p less than 0.001). There was a slight difference in systolic wall stress to fractional shortening slopes between both groups (group A -0.215 vs group B -0.49%/10(3) dynes/cm2, p = 0.02) but not between systolic wall stress to end-systolic diameter slopes (group A 0.013 vs group B 0.019 cm/10(3) dynes/cm2, difference not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Twenty-five patients with an anterior wall acute myocardial infarction (AMI) were studied by 2-dimensional echocardiography (2-D echo) 3 to 5 days after the onset of chest pain, and serially over 3 to 24 months to determine if a particular pattern of contractility may predispose to left ventricular (LV) aneurysm formation. No subject had a prior AMI. In 8 subjects LV aneurysm eventually developed (group I), usually within 2 to 4 weeks of AMI; in 17 patients LV aneurysm did not develop (group II). Percent fractional shortening of the basal and midventricular segments was significantly better in group I subjects than in group II subjects (29 +/- 2% vs 20 +/- 2%, p less than 0.01, respectively, for the basal segment, and 23 +/- 1% vs 17 +/- 2%, p less than 0.02, respectively, for the midventricular segment). Infarct size as determined by peak creatine kinase isoenzyme levels was large in both groups, and there was no statistically significant difference between their mean values (2,099 +/- 620 IU vs 1,334 +/- 249 IU for groups I and II, respectively). Severe asynergy of the infarcted myocardium was present in all group I subjects and in 9 of 17 group II subjects on the initial 2-dimensional echocardiographic study. These results indicate that LV aneurysm formation depends on a critical imbalance of myocardial forces where strong LV segments cause bulging of weakened ones.