Left Ventricular Percent Fractional Shortening Research Articles

17beta-estradiol attenuates pressure overload-induced myocardial hypertrophy through regulating caveolin-3 protein in ovariectomized female rats

Our findings indicate that in ovariectomized female rats abdominal aortic constriction led to significant increases in left ventricular mass, myocyte diameter and heart weight/body weight (HW/BW) value, and decreases in interventricular septal thickness at diastole (IVSd), left ventricular percent fractional shortening (FS) and ejection fraction (EF). These pathophysiological alterations were largely reversed by administration with 17β-estradiol for eight weeks. Furthermore, the enhanced expression of extracellular signal-regulated kinases 1/2 and decreased expression of caveolin-3 were found in left ventricle of AAC group. 17β-estradiol (E(2)) administration increased the expression of caveolin-3 and reduced the level of ERK phosphorylation in these pressure-overloaded rats. Moreover, in cultured neonatal rat cardiomyocytes, E(2) inhibited the hypertrophic response to angiotensin II. This effect was reinforced by the addition of extracellular signal-regulated kinases 1/2 inhibitor PD98059, but was impaired when the cells were pretreated with caveolae disruptor, methyl-β-cyclodextrin (M-β-CD). In conclusion, our data indicate that estrogen attenuates the hypertrophic response induced by pressure overload through down-regulation of extracellular signal-regulated kinases 1/2 phosphorylation and up-regulation of caveolin-3 expression.

Effect of hemofiltrated whole blood pump priming on hemodynamics and respiratory function after the arterial switch operation in neonates

Background. Primed blood might have some deleterious effects on neonates during cardiopulmonary bypass (CPB) due to unbalanced electrolytes and inflammatory mediators. We hemofiltrated pump-primed blood before CPB to reduce inflammatory mediators and to adjust pH and the concentrations of electrolytes. The current study investigated the effects of hemofiltrated whole blood priming on hemodynamics and respiratory function after CPB in neonates. Methods. Patients who underwent the arterial switch operation in the neonatal period for transposition of the great arteries with intact ventricular septum were chosen for this study. Seventeen patients underwent CPB with hemofiltrated blood priming (group HF) and 23 patients underwent CPB with nonhemofiltrated blood priming (group N). The concentrations of electrolytes and bradykinin and high molecular weight kininogen of the primed blood before and after hemofiltration were measured. At 4 hours after completion of CPB, the left ventricular percent fractional shortening, and the relation between the mean velocity of shortening and the end-systolic wall stress (stress velocity index), were measured by echocardiogram in 7 patients in group HF and 6 patients in group N. Alveolar − arterial oxygen tension difference (AaDO 2) and respiratory index (AaDO 2 divided by arterial oxygen tension) were measured at several points for 48 hours after CPB in all patients. Results. Hemofiltration of the primed blood maintained electrolytes within a physiologic level and significantly reduced the concentrations of bradykinin (5,649 ± 1,353 pg/mL versus 510 ± 35 pg/mL, p < 0.05) and high molecular weight kininogen (52.7% ± 3.2% versus 40.1% ± 3.0% of normal plasma value, p < 0.05). The percent of fractional shortening at 4 hours after completion of CPB was significantly higher in group HF (n = 7) than in group N (n = 6) (22.0% ± 0.7% versus 16.0% ± 0.4%, p < 0.01). There was also a trend toward better stress velocity index in group HF than in group N (0.81 ± 0.81 versus −2.17 ± 0.45, p = 0.09). AaDO 2 and respiratory index were significantly lower in group HF than in group N for 48 hours after CPB, respectively ( p < 0.05). Conclusions. Hemofiltrated fresh whole blood used for CPB priming attenuated cardiac impairment at early reperfusion periods and reduced pulmonary dysfunction in neonates with transposition of the great arteries with intact ventricular septum. This therapeutic strategy may have an advantage in preventing lung and heart dysfunction in pediatric patients who need CPB priming with blood.

Beneficial effect of myocardial angiogenesis on cardiac remodeling process by amlodipine and MCI-154.

The present study examined the effect of long-term treatment with amlodipine and MCI-154 (a Ca2+ sensitizer) on progressive cardiac dysfunction and microvasculature in the dilated cardiomyopathic (DCM) hamster heart. After treatment of DCM hamsters (Bio 53.58) with amlodipine or MCI-154 for 15 wk from the age of 5 wk, amlodipine and MCI-154 were found to cause an increase in left ventricular percent fractional shortening and decreases in left ventricular diastolic dimension and isovolumic relaxation time in echocardiograms (P < 0.01). A hemodynamic study showed that the diastolic time constant decreased in the amlodipine-treatment group (P < 0.05). In a morphometric study employing a double-staining method that discriminated arteriolar and venular capillaries, amlodipine and MCI-154 caused increases in total capillary density (P < 0.05) and the proportion of venular capillaries (P < 0.05). Moreover, Northern blot analysis showed that the expression of mRNA for vascular endothelial growth factor was significantly increased by amlodipine and MCI-154. They preserve coronary microvasculature in the DCM hamster and might induce angiogenesis of small vessels, thereby contributing to preservation of cardiac systolic and diastolic function.

Iodine-123 Metaiodobenzylguanidine Scintigraphic Assessment of Myocardial Sympathetic Innervation in Patients With Familial Amyloid Polyneuropathy

Objectives. This study attempted to assess myocardial sympathetic innervation using iodine-123 (I-123) metaiodobenzylguanidine (MIBG) imaging in patients with familial amyloid polyneuropathy.Background. Signs and symptoms of cardiac autonomic dysfunction are commonly seen in patients with cardiac amyloidosis. However, the incidence and magnitude of abnormalities in myocardial sympathetic nerve function by means of I-123 MIBG imaging and their relation to clinical findings, cardiac function and the results of thallium-201 (Tl-201) and technetium-99m pyrophosphate (Tc-99m PYP) myocardial scanning have not yet been clarified.Methods. We performed M-mode, two-dimensional and Doppler echocardiography and I-123 MIBG, Tl-201 and Tc-99m PYP imaging of the heart in 12 patients with familial amyloid polyneuropathy and biopsy-proved cardiac amyloidosis.Results. Ten of 12 patients had no clinical evidence of overt heart disease, but left ventricular (LV) wall thickening was observed in 4 of these 10. Left ventricular percent fractional shortening and Doppler transmitral flow velocity patterns were found to be normal in all 12 patients. Eight of 12 patients showed no myocardial MIBG accumulation, with limited uptake in the remaining 4 demonstrated only in the LV anterior wall. Diffuse but mild myocardial uptake of Tc-99m PYP occurred in only 4 of 12 patients, and all 12 had normal results on Tl-201 myocardial scanning. Complete defects on myocardial MIBG scans were found in five of eight patients with negative findings on Tc-99m PYP myocardial scanning. The incidence and magnitude of myocardial uptake of MIBG were independent of clinical findings, extent of endomyocardial amyloid deposition, electrocardiographic QRS voltage and ventricular wall thickness.Conclusions. Patients with familial amyloid polyneuropathy show a high incidence of myocardial adrenergic denervation with viable myocardium that can be identified very early in cardiac amyloidosis, before the development of clinically apparent heart disease, ventricular wall thickening, significant LV systolic and diastolic dysfunction and positive findings on Tc-99m PYP myocardial scanning.(J Am Coll Cardiol 1997;29:168–74)>

Left ventricular diastolic function in young adults: The Coronary Artery Risk Development in Young Adults Study

Doppler transmitral flow velocities have been used to assess left ventricular diastolic function. Associations of transmitral velocities with specific physiologic variables and cardiovascular risk factors have not been reported previously in a large population-based study of young adults. We performed Doppler analysis of left ventricular inflow in 3492 black and white men and women (aged 23 to 35 years) in the year-5 examination of the Coronary Artery Risk Development in Young Adults (CARDIA) Study. First third filling fraction, peak flow velocity in early diastole (PFVE), peak flow velocity in late diastole (PFVA), and the PFVA/PFVE ratio were measured. Women had higher PFVE and PFVA than had men (PFVE: 0.81 +/- 0.13 m/sec versus 0.76 +/- 0.13 m/sec; PFVA: 0.47 +/- 0.11 m/sec versus 0.43 +/- 0.10 m/sec; both p < 0.001). Gender-specific multiple regression analyses showed that age, heart rate, systolic blood pressure, left ventricular percent fractional shortening, and body weight were independently and positively related to PFVA (all p < 0.001) in men and women. Age, heart rate, and forced expiratory lung capacity in 1 second were inversely related to PFVE and first third filling fraction (both p < 0.01). Left ventricular percent fractional shortening was positively related to PFVE and first third filling fraction (p < 0.001). Age, heart rate, and body weight were positively correlated with the PFVA/PFVE ratio (all p < 0.001). Height had weak negative associations with PFVA and PFVE in women only. These results suggest that, in young adults, Doppler measures of left ventricular diastolic filling are related to age, sex, body weight, blood pressure, heart rate, left ventricular systolic function, and lung function.

Noninvasive assessment of the direct action of oral nifedipine and nicardipine on left ventricular contractile state in patients with systemic hypertension: Importance of reflex sympathetic responses

Objectives. This study was designed to noninvasively assess the direct action of calcium channel blockers on left ventricular contractility in humans and to establish a framework for determining the importance of reflex sympathetic responses to any pharmacologic intervention.Background. Assessment of left ventricular contractility in patients taking calcium channel blockers by using traditional indexes of systolic performance is difficult because of the afterload-reducing and reflex sympathetic effects of the drugs.Methods. Fifteen hypertensive patients (mean blood pressure 127 ± 15 mm Hg) were studied with Doppler echocardiography and calibrated subclavian pulse tracings while receiving placebo and 1 week after randomization to treatment with oral nifedipine (20 mg three times daily; n = 7) or nicardipine (30 mg three times daily; n = 8). Left ventricular circumferential end-systolic wall stress versus rate-corrected velocity of shortening (Vcfc) relations were generated over a range of loads using nitroprusside. Data were acquired before and during esmolol infusion, thereby allowing assessment of hemodynamic responses with the sympathetic nervous system functionally intact as well as ablated. The adequacy of sympathetic blockade was confirmed with isoproterenol challenges. In each case, left ventricular contractile state was measured relative to placebo and esmolol data as ΔVcfcat a common end-systolic wall stress. Increased and decreased contractility were defined as ΔVcfc> 0 and ΔVcfc< 0, respectively.Results. Nifedipne and nicardipine equally decreased blood pressure and end-systolic wall stress and increased left ventricular percent fractional shortening and stroke volume. Neither drug alone consistently altered ventricular contractility compared with placebo. Ablation of reflex sympathetic tone with esmolol unmasked a negative intropic effect for nifedipine (p = 0.03 vs. esmolol alone) but not nicardipine (p = 0.68 vs. esmolol alone). The difference between the contractility effects of nifedipine plus esmolol versus those of nicardipine plus esmolol approached statistical significance (p = 0.07).Conclusions. Totally noninvasive techniques showed a differential effect on left ventricular contractility between nifedipine and nicardipine when alterations in afterload and reflex sympathetic responses were eliminated as confounding variables. This diagnostic approach, based on the use of pharmacologic probes, should have wide applicability for assessing the direct inotropic effect of any agent, even in the presence of complex primary and secondary physiologic modes of action.

Doppler Evidence for Reduced Atrial Contribution to Left Ventricular Filling in Patients with a Dilated Cardiomyopathy and a 'B-Bump' on the Mitral Valve Echocardiogram

The hemodynamic contribution of left atrial contraction to left ventricular filling in dilated cardiomyopathy (DCM) remains controversial. The degree of filling of the left ventricle may influence this contribution. Previous studies have demonstrated a correlation between an elevated left ventricular enddiastolic pressure (LVEDP) and the presence of a ‘B-bump’ (a deflection on the A-C closure slope) on the anterior mitral valve leaflet on the M-mode echocardiogram. To assess whether the presence of a ‘B-bump’ reflecting an elevated LVEDP is associated with differences in left atrial contribution to left ventricular filling, we measured pulsed-wave Doppler mitral flow velocity recordings obtained from 48 DCM patients, with (n = 16) and without (n = 32) a ‘B-bump’. There were no statistically significant differences between the two groups with regard to age, heart rate, body surface area, electrocardiographic PR interval, left ventricular end-diastolic dimenson, left ventricular percent fractional shortening, left atrial size, or distance of penetration of the mitral regurgitant signal into left atrium. The mean ratio of mitral peak-signal velocity in late-to-early diastole, PFVA/PFVE (0.58 ± 0.24 in those with ‘B-bump’ versus 0.96 ± 0.55 in those without a ‘B-bump’, p < 0.005, and the mean ratio of time-velocity integral in late-to-early diastole 0.39 ± 0.14 vs. 0.65 ± 0.34, p < 0.002) were both found significantly decreased in the ‘B-bump’ group. Since the mitral time-velocity integral is proportional to stroke volume, and the A/E integral ratio approximates a volume ratio of transmitral flow, it is concluded that in the group of patients with DCM and a ‘B-bump’ of the anterior mitral leaflet, corresponding to an elevated LVEDP, the relative left atrial volume contribution to left ventricular filling and stroke volume is reduced.

Influence of histamine receptors on basal left ventricular contractile tone in humans: Assessment using the H2receptor antagonist famotidine and the beta-adrenoceptor antagonist esmolol as pharmacologic probes

Histamine has a positive inotropic action in humans. Recent controversial data have suggested that histamine2(H2) receptor blockade depresses overall left ventricular systolic performance in healthy volunteers. To explore the possibility that H2receptors positively influence basal left ventricular contractile tone, 10 normal subjects were studied by using imaging and Doppler echocardiography and calibrated subclavian pulse data in a blinded, randomized, two-period crossover trial with measurements obtained at the end of each 7-day period.Oral drug administration consisted of either the potent H2antagonist famotidine (40 mg/day) or placebo. Left ventricular circumferential end-systolic wall stress-rate-corrected velocity of fiber shortening (Vcfc) relations were generated over a range of loads with methoxamine. Contractility was assessed by using Vcfcat a common end-systolic wall stress. During each study, data were obtained before and during high dose intravenous esmolol administration to determine the contributions, if any, of sympathetic reflex responses.Famotidine did not alter blood pressure, left ventricular percent fractional shortening, circumferential end-systolic wall stress, stroke volume index, cardiac index, total vascular resistance or ventricular contractile state in comparison with placebo but did decrease heart rate by 3 beats/min (p < 0.05). With beta-adrenergic blockade, no differences in contractility were evident between esmolol alone and famotidine plus esmolol.Thus, H2receptor blockade with famotidine does not alter myocardial mechanics or cardiac sympathetic tone, suggesting that in humans basal left ventricular contractile state is not physiologically dependent on the H2-mediated effects of histamine.

Changes in left ventricular output from fetal to early neonatal life

Using pulsed Doppler and two-dimensionally directed M-mode echocardiographic techniques, we measured left ventricular (LV) output, stroke volume, heart rate, LV end-diastolic dimension (LVEDD), LV end-systolic dimension, and LV percent fractional shortening (%FS) in 34 normal term infants 12 to 24 hours before parturition and thereafter serially 1, 24, and 96 hours after birth. Stroke volume was calculated as the product of the aortic flow velocity integral and aortic valve area. There was a twofold increase in LV output 1 hour after birth (fetal 170 +/- 46 ml/min/kg vs 1 hour 327 +/- 66 ml/min/kg; p less than 0.01) which was associated with significant increases in stroke volume, %FS, and LVEDD (stroke volume 1.21 +/- 0.33 ml/kg vs 2.25 +/- 0.37 ml/kg; %FS 34.3% +/- 5.8% vs 37.7% +/- 5.4%; LVEDD 15.4 +/- 1.1 mm vs 17.7 +/- 1.4 mm). Heart rate did not change 1 hour after birth. During the subsequent hours after birth, LV output decreased significantly to a value of 245 +/- 56 ml/min/kg (p less than 0.01) at 24 hours, which did not change 96 hours after birth. There were significant declines in stroke volume, LVEDD, and heart rate 24 hours after birth (stroke volume 2.02 +/- 0.42 ml/kg; LVEDD 17.0 +/- 1.1 mm; heart rate 121 +/- 11 beats/min). The %FS remained unchanged within the first 96 hours of age. These results indicate that the major regulator of LV output immediately after birth is stroke volume and not heart rate. The increase in stroke volume is related to an increase in LV size and LV myocardial contractility. Our data provide a useful basis for the interpretation of abnormal LV function in the early neonatal period.

Noninvasive assessment of systolic and diastolic function in 50 patients with Friedreich's ataxia.

Fifty consecutive patients with Friedreich's ataxia were examined to characterize their cardiac diastolic function. Electrocardiographic abnormalities were detected in 42 (80%) of the 50 patients. Echocardiography showed left ventricular hypertrophy in 14 patients (28%): concentric in 12 and asymmetric in 2. Left ventricular percent fractional shortening was normal in all except 2 patients. Diastolic filling characteristics measured from Doppler mitral flow velocity traces were not statistically different from those of 18 healthy control subjects. No abnormal diastolic flow pattern was observed in patients with left ventricular hypertrophy, whether concentric or asymmetric.

Usefulness of predischarge echocardiographic criteria in predicting complications following acute myocardial infarction.

In 103 patients who recovered from an acute myocardial infarction (AMI) we evaluated the usefulness of predischarge clinical, routine laboratory and M-mode echocardiographic (echo) criteria in predicting cardiac complications during a period of 12-41 months (25.0 +/- 10.7 months) follow-up. The echo parameters evaluated were: left ventricular diastolic diameter, left ventricular percent fractional shortening and the mitral valve E point septal separation. The combination of these three echo criteria was defined as an echo-index, which was considered abnormal if at least two of the three single parameters were pathological. Congestive heart failure occurred in 35 (34%) patients, with significantly higher prevalence among those older than 65 years, with previous AMI and with predischarge findings of heart failure. However, the sensitivity of these clinical parameters was unsatisfactory (34-69%). The sensitivity, specificity and positive predictive value of the echo-index for future heart failure were 89, 88 and 80%, respectively. Chest pain prior to hospital discharge was the only criteria predicting high risk of reinfarction (p = 0.001). The risk of cardiac death was related to age older than 65 years (p = 0.03) and an abnormal echo-index (p = 0.01). The overall mortality rate was 13%, but only 6% among those with normal and 26% among those with pathologic echo-index. In conclusion, in patients who recovered from an AMI, a simple and easily measured echo-index was superior to most clinical and routine laboratory criteria in predicting future heart failure and cardiac death.

Left ventricular contractility and contractile reserve in humans after cardiac transplantation.

Limited data are available concerning left ventricular contractility and contractile reserve in the chronically denervated, transplanted human heart. This is primarily because of the inability of traditional tests of left ventricular performance to distinguish changes in contractility from alterations in ventricular loading conditions. In this study, load-independent end-systolic indexes of left ventricular contractility were measured by echocardiography and calibrated carotid pulse tracings in 10 patients who had undergone orthotopic cardiac transplant (age 48 +/- 4 years; interval from operation to study 1.2 +/- 0.8 years) and in 10 normal control subjects (age 25 +/- 4 years) matched for donor heart age (25 +/- 6 years). None of the transplant patients had evidence of rejection as determined by endomyocardial biopsy. Baseline left ventricular contractility was assessed over a wide range of afterload generated by infusion of methoxamine. Contractile reserve was measured as the response to an infusion of dobutamine plus methoxamine. Before afterload challenge, baseline left ventricular percent fractional shortening was higher for the transplant patients than for the control subjects (36.5 +/- 5.7% vs 32.1 +/- 2.1%; p less than .05). These differences occurred at a time that end-systolic wall stress (a measure of afterload) was significantly lower for the transplant patients (38 +/- 16 vs 50 +/- 9 g/cm2; p less than .05). When the left ventricular end-systolic pressure-dimension and stress-shortening relationships were determined for the transplant and control subjects, no differences in contractility or contractile reserve were noted. Thus the chronically denervated, transplanted, nonrejecting human left ventricle demonstrates normal contractile characteristics and reserve.

Improvement of left ventricular dysfunction after control of persistent tachycardia

Five children are described who had persistent, chronic tachycardia and left ventricular dysfunction manifested by decreased left ventricular percent fractional shortening on echocardiogram (five patients) cardiomegaly on chest roentgenogram (three), ventricular or atrial hypertrophy on ECG (three), and symptoms of congestive heart failure (three). After antidysrhythmia therapy and control of the tachycardia, signs and symptoms of congestive heart failure resolved in two infants. Moreover, in each patient signs of cardiomegaly resolved on chest roentgenogram, hypertrophy resolved on ECG, and the fractional shortening improved to normal (mean 20.2% +/- 2.4% SEM before vs 36.2% +/- 2.4%, P = 0.02, after treatment). Evaluation in the child who has dilated cardiomyopathy should include assessment of heart rate and rhythm. Moreover, when persistent tachycardia is found in an asymptomatic child, evaluation of left ventricular function is indicated.

Evaluation of dilated cardiomyopathy by pulsed Doppler echocardiography

The ability of pulsed Doppler echocardiography to identify patients with left ventricular systolic dysfunction was evaluated in 12 patients with dilated (congestive) cardiomyopathy. A range-gated, spectrum analyzer-based Doppler velocimeter was used to record blood flow velocity in the ascending aorta and main pulmonary artery. The following blood flow velocity parameters were measured or derived: peak flow velocity, acceleration time, average acceleration, deceleration time, average deceleration, ejection time, and aortic flow velocity integral. Doppler blood flow velocity data in the cardiomyopathy patients were compared to data from 20 normal subjects. Measurements from the ascending aorta revealed that peak aortic flow velocity discriminated between cardiomyopathy patients (mean 47 cm/sec, range 35 to 62) and normal subjects (mean 92 cm/sec, range 72 to 120) with no overlap in data ( p < 0.001). Aortic flow velocity integral was also able to separate the patients with dilated cardiomyopathy (mean 6.7 cm, range 3.5 to 9.1) from normal subjects (mean 15.7 cm, range 12.6 to 22.5) with no overlap in data ( p < 0.001). Although mean values for average aortic acceleration and aortic ejection time were also significantly different (both p < 0.005), there was some overlap between the two groups. Pulmonary artery blood flow studies demonstrated significantly increased average acceleration, as well as decreased ejection time (both p < 0.05), but no difference in average deceleration or peak flow velocity in cardiomyopathy patients compared to normals. Compared to pulmonary flow measurements, aortic Doppler flow velocity measurements allowed better separation of cardiomyopathy and normal groups. In addition, aortic peak flow velocity appeared to correlate well ( r = 0.83) with M-mode echocardiographic measurement of left ventricular percent fractional shortening; both parameters were equally useful in discriminating patients with normal left ventricular function from those with global dysfunction (dilated cardiomyopathy). Thus pulsed Doppler echocardiography appears to be a useful addition to M-mode and two-dimensional echocardiography in the quantitative noninvasive assessment of left ventricular systolic function.

Modification of abnormal left ventricular diastolic properties by nifedipine in patients with hypertrophic cardiomyopathy.

The effect of nifedipine on left ventricular isovolumic relaxation and diastolic filling properties and systemic and left ventricular hemodynamics was studied in 15 patients with hypertrophic cardiomyopathy. After nidefipine (10 mg sublingually), the prolonged left ventricular isovolumic relaxation time assessed by echocardiography decreased from 112 +/- 26 to 83 +/- 23 msec (p less than 0.0001), and the left ventricular pressure decay as measured by time constant T improved from 63 +/- 20 to 49 +/- 11 msec (p less than 0.05). Left ventricular filling dynamics also improved as assessed by a return toward normal in the depressed peak rate of left ventricular diastolic filling (dimension change 72 +/- 37 to 101 +/- 39 mm/sec, p less than 0.01) and the peak rate of posterior wall thinning (47 +/- 31 to 68 +/- 36 mm/sec, p less than 0.001). These changes were accompanied by hemodynamic evidence of improved diastolic function shown as a decrease in left ventricular end-diastolic pressure and a downward shift in the left ventricular diastolic pressure-dimension relationship, suggesting improved left ventricular distensibility. After nifedipine, there was a slight increase in heart rate and a decrease in systemic ventricular distensibility. After nifedipine, there was a slight increase in heart rate and a decrease in systemic arterial blood pressure, and no depression of the left ventricular percent fractional shortening or cardiac index. These data indicate that abnormal left ventricular relaxation and diastolic filling rates in hypertrophic cardiomyopathy are dynamic and favorably modified by nifedipine, and that this effect is not related to a depression of left ventricular systolic function.

Echocardiographic abnormalities in chronic alcoholics with and without overt congestive heart failure

To assess the type and prevalence of cardiac abnormalities in heavy drinkers with and without overt congestive heart failure, M mode echocardiography was performed in 11 symptomatic chronic alcoholics with dilated (congestive) cardiomyopathy and in 22 asymptomatic chronic alcoholics. Echocardiographic data in both groups were adjusted for age and body surface area using previously derived regression equations. All 11 symptomatic patients had a significantly decreased left ventricular percent fractional shortening (mean 14 percent, normal range 28 to 44) along with significant increases in left ventricular systolic and diastolic dimensions (mean increases of 105 and 48 percent above normal, respectively), left atrial dimension (mean increase 21 percent) and estimated left ventricular mass (mean increase 105 percent). Among the 22 asymptomatic patients, 15 (68 percent) demonstrated significant increases in at least one of the following echocardiographic variables: left ventricular mass, left ventricular dimensions, septal and left ventricular wall thicknesses, and left atrial dimension. Asymptomatic patients could be classified into two subgroups: (1) those with a left ventricular diastolic dimension less than 10 percent above the normal predicted value and an increased left ventricular wall thickness to radius ratio (mean increase 16 percent above normal) and upper normal percent fractional shortening, and (2) those with a left ventricular diastolic dimension 10 to 24 percent above normal and a slightly subnormal thickness to radius ratio and lower normal percent fractional shortening. Echocardiographic abnormalities in asymptomatic chronic alcoholics did not correlate with the presence or absence of auscultatory abnormalities on physical examination and appear to reflect an earlier stage in the spectrum of alcoholic disease before the development of dilated cardiomyopathy.

Single and two-dimensional echocardiographic visualization of the effects of septal myectomy in idiopathic hypertrophic subaortic stenosis.

Although the postoperative hemodynamic and echocardiographic features of idiopathic hypertrophic subaortic stenosis have been studied, the expected consistent postoperative thinning of the interventricular septum has not been reported. In this study, the short-term effects of septal myectomy were evaluated in 16 patients. All patients were assessed with pre- and postoperative hemodynamic studies and M-mode echocardiograms, and six of the 16 patients had pre- and postoperative two-dimensional echocardiograms. The mean resting preoperative gradient of 74 mm Hg (range 10--190 mm Hg), which fell to a mean resting postoperative gradient of 8 mm Hg (range 0--25 mm Hg), was associated with decreased end-diastolic interventricular septal thickness at the midventricular level in 14 of 16 patients and at the subaortic level in 16 of 16 patients by M-mode echocardiography. The group also demonstrated changes in left ventricular outflow tract configuration and dimension, mitral valve systolic anterior motion, mitral E-F0 slope and left ventricular percent fractional shortening by both M-mode and two-dimensional studies. In the two patients who did not show midventricular septal thinning on M-mode echocardiography, the two-dimensional echocardiograms revealed that the area of myectomy extended only through the subaortic region and not down to the midventricular septum. Thus, we have observed consistent postmyectomy septal thinning at both the midventricular and subaortic levels by M-mode echo. By defining the geometry of the septal myectomy in vivo with two-dimensional echocardiography, we can better interpret M-mode studies and identify factors that influence echocardiographic visualization of the region of myectomy.