Effect of left ventricular size on mitral E point to ventricular septal separation in assessment of cardiac performance

Increased mitral valve E point to ventricular septal separation (EPSS) is widely used as an echocardiographic index of depressed left ventricular (LV) ejection traction (EF), yet LV size has not been examined as an independent variable potentially affecting EPSS. Accordingly, we studied the relationship between EPSS and functionally normal or depressed LV with or without increased enddiastolic dimensions (EDD). Twenty normal controls had EPSS 3.2 ± 2.2 mm (mean ± SD), EDD 47 ± 5 mm, $\text{EPSS}\text{EDD}$ (“normalized” EPSS) 0.07 ± 0.04, and fractional shortening (FS%) 38 ± 6%. Nine patients with pure chronic mitral regurgitation had dilated LV (EDD = 65 ± 7 mm) with normal LV function (FS% 41 ± 5%; angiographic EF 62 ± 9%); eight patients had dilated cardiomyopathy (EDD 69 ± 8 mm) with decreased LV function (FS% 16 ± 7%; angiographic EF 32 ± 8%); and eight patients with amyloid cardiomyopathy had nondilated LV (EDD 42 ± 5 mm) with decreased LV function (FS% 19 ± 6; angiographic EF 35 ± 7%). Mitral E point to ventricular septal separation and $\text{EPSS}\text{EDD}$ accurately separated individuals with normal and abnormal LV function irrespective of LV size (χ² = 36.7; p < 0.00001). Increased internal dimensions per se did not affect EPSS unless depressed LV function coexisted. EPSS is therefore a valid predictor of depressed ejection phase indices independent of LV size.     

Alteration of left ventricular performance by left bundle branch block simulated with atrioventricular sequential pacing

The effects of atrioventricular (AV) sequential pacing-induced left bundle branch block (LBBB) on left ventricular (LV) performance were evaluated during cardiac catheterization in 9 randomly selected patients being investigated for chest pain. All patients were in normal sinus rhythm with a normal P-R interval and QRS duration. LV performance was assessed by both hemodynamic and angiographie measurements. The maximal rate of LV pressure increase (dP/dt), rate of maximal LV pressure decrease ($\text{?dP}\text{dt}$), LV end-diastolic pressure (LVEDP), end-diastolic volume (LVEDV), end-systolic volume (LVESV), stroke volume and percent ejection (EF) were measured during right atrial and AV sequential pacing at a constant pacing rate. The average pacing rate was 97 ± 3 beats/min (mean ± standard error of the mean). In each patient, both dP/dt and $\text{?}\text{dP}\text{dt}$ decreased significantly (p < 0.001) during AV sequential pacing compared with atrial pacing at the same rate, from 1,541 ± 68 to 1,319 ± 56 mm Hg/s for dP/dt and from 1,506 ± 86 to 1,276 ± 92 for $\text{?dP}\text{dt}$. LVEDP did not change significantly when atrial (17 ± 3 mm Hg) and AV sequential pacing (16 ± 2 mm Hg) were compared. Mean LVEDV did not change during atrial (135 ± 13 ml) or AV sequential pacing (137 ± 14 ml). In contrast, the LVESV during AV sequential pacing was higher by 15 ml (23 % ) (from 48 ± 10 to 63 ± 12 ml) (p < 0.001); as a result, the stroke volume was lower by 13 ml (15%) and the EF decreased by 10 %, from 66 to 56 % (?15 %).These changes in LV performance during acutely induced LBBB by AV sequential pacing as compared with atrial pacing at the same rate were independent of altered preload, because both LVEDP and LVEDV were similar during the 2 different pacing modes. Peak systolic pressure during AV sequential pacing was significantly lower than that during atrial pacing (161 ± 10 vs 145 ± 10 mm Hg, p < 0.01), and thus afterload was presumably altered during the different pacing modes. However, because the observed change in systolic pressure (afterload) was lower during AV sequential pacing, this change should improve rather than result in deterioration of ejection phase indexes. Because the opposite was observed, it is concluded the deterioration in LV function noted during AV sequential pacing must be due in part to the asynchronous pattern of ventricular activation induced by this intervention.     

Catheter evaluation of left ventricular shape and function 1 or more years after anatomic correction of transposition of the great arteries

Twenty-eight children were reinvestigated by cardiac catheterization and angiography > 1 year after anatomic correction of transposition of the great arteries (TGA). Seventeen patients with simple TGA underwent banding of the pulmonary trunk plus or minus systemic to pulmonary artery shunt to prepare the left ventricle for anatomic correction. In addition to TGA, 10 of the remaining 11 patients had a large ventricular septal defect and 1 had an aorticopulmonary window. They required no preparation of the left ventricle. Age at repair ranged from 2 to 120 months (mean 26).Catheterization 12 to 48 months after anatomic repair revealed a left ventricular end-diastolic pressure of 4 to 14 mm Hg (mean 9.5 ± 2.5 [± standard deviation]). Ejection fraction ranged from 52 to 75% (mean 66 ± 8). Frame-by-frame computer-assisted analysis of left ventricular (LV) contraction and relaxation was performed in 14 patients and compared with normal left ventriculograms. Shape index, derived as $\text{4π ×}\text{cavity area}\text{perimeter}{}^2\text{× 100}$, was measured in 24 patients and showed a mean index of 89 ± 3% at end-diastole and 79 ± 8% at end-systole. A control group had a mean diastolic index of 86 ± 6% and mean systolic index of 73 ± 8%.It is concluded that LV shape after anatomic correction tends to be more globular than normal and changes little during systole. LV ejection fraction and end-diastolic pressure are normal.     

Number and size of myocytes and amount of interstitial space in the ventricular septum and in the left ventricular free wall in hypertrophic cardiomyopathy

The wall thickness of the myocardium depends on 3 variables: the number of muscle layers, the mean size of myocytes and the percent area of interstitial space. To clarify the pathogenesis of asymmetric septal hypertrophy (ASH) in hypertrophic cardiomyopathy (HC), these 3 variables and wall thickness were measured in the ventricular septum (VS) and in the left ventricular (LV) posterior wall. The $\text{VS}\text{LV}$ ratio of wall thickness was correlated with the $\text{VS}\text{LV}$ ratios of the 3 variables in the hearts of 10 patients in HC with ASH and in 37 control patients without ASH (25 with no cardiac disease and 12 with systemic hypertension). The $\text{VS}\text{LV}$ ratios (mean ± standard deviation) in hearts with HC were 1.6 ± 0.2 for wall thickness, 1.8 ± 0.3 for the number of transmural muscle layers, 0.9 ± 0.1 for mean size of myocytes and 1.1 ± 0.1 for percent area of transmural interstitial space. The $\text{VS}\text{LV}$ ratios in control hearts were 1.0 ± 0.1 for wall thickness, 1.0 ± 0.1 for number of transmural muscle layers, 1.0 ± 0.1 for mean size of myocytes and 1.0 ± 0.1 for percent area of interstitial space. The $\text{VS}\text{LV}$ ratios of wall thickness and transmural muscle layers correlated well. In hearts with ASH in HC, the number of muscle layers was greater in the VS (630 ± 80) and smaller in the LV free wall (360 ± 70) than in the control hearts (500 ± 60 and 480 ± 50, respectively). Thus, the pathogenetic factor of ASH in HC is an increased $\text{VS}\text{LV}$ ratio of the number of muscle layers, and the degree of ASH is determined by the combined abnormalities in the numbers of transmural muscle layers in the VS and the LV free wall.     

Serial noninvasive assessment of left ventricular hypertrophy and function after surgical correction of aortic regurgitation.

Serial echocardiographic analyses of left ventricular hypertrophy and function, with validation of extent of shortening by first pass radionuclide angiography, was performed in 16 patients before and after surgical correction of severe aortic valve regurgitation. All patients were symptomatic (predominantly in New York Heart Association functional class III or IV) before operation but were in class I or II after operation. The preoperative pattern of eccentric hypertrophy (increased mass with normal ratio of left ventricular cross-sectional wall area to cavity area) changed immediately after operation to a pattern of concentric hypertrophy (increased mass with increased ratio of left ventricular cross-sectional wall area to cavity area) because of a significant reduction in chamber size and increase in wall thickness. On late follow-up (9 to 35 months, average 15 months after operation), the hypertrophy lessened significantly, the cross-sectional area of the ventricular wall decreasing to 21.1 ± 5.4 (mean ± standard deviation) cm² from a preoperative average of 31.6 ± 4.8 cm² (P < 0.01), and the ratio of wall area to cavity area was once again normal. In the same period, left ventricular enddiastolic diameter decreased from 6.52 ± 0.68 to 4.64 ± 0.52 cm (P < 0.01). Preoperatively, ejection phase indexes were normal or only marginally depressed in 12 of 16 patients but were moderately depressed in the remaining 4. At early follow-up (average 4 months) ventricular shortening tended to increase; and at late follow-up the fractional shortening of the minor axis, the ejection fraction and the mean velocity of circumferential fiber shortening increased to 0.39 ± 0.07, 0.68 ± 0.10 and 1.26 ± 0.22 circumference/sec, respectively, from preoperative values of 0.33 ± 0.09, 0.60 ± 0.14 and 1.05 ± 0.31 circumferences/sec (P < 0.05 for each index). In the four subjects with preoperative depression of left ventricular function, the extent and speed of myocardial shortening at late follow-up became normal in three subjects and remained moderately depressed in one patient. Paradoxical septal motion was observed immediately postoperatively and in the early follow-up studies, but it was noted in only 3 of 16 cases by the late follow-up period. Provided septal dyskinesia was not present, echocardiographic and first pass radionuclide determinations of ejection fraction correlated highly (r = 0.92).It is concluded that when aortic valve replacement for symptomatic aortic regurgitation is undertaken prior to severe myocardial decompensation, improvement in clinical status is associated with significant regression of myocardial hypertrophy, reduction in left ventricular size, evolution of a normal $\text{mass}\text{volume}$ ratio, recovery of septal dyskinesia as revealed on echocardiography, and improvement in left ventricular function. These data do not define the type and degree of left ventricular dysfunction which is irreversible.     

Left ventricular dimensions and function during exercise in dogs with chronic right ventricular pressure overload

Left ventricular (LV) dimensions and shortening at rest and during treadmill exercise were examined before and after 4 weeks of pulmonary artery (PA) constriction in 6 conscious dogs. The dogs were preinstrumented with LV and right ventricular (RV) catheters, an LV micromanometer, a PA inflatable cuff occluder and ultrasonic crystals to measure an LV anteroposterior, a septal-lateral, an apex-base and a free wall segment chord. With PA constriction, RV pressures increased from $\text{49 ±}\text{4}\text{2}\text{± 1 mm}$ Hg (systolic/end-diastolic) to $\text{104 ±}\text{5}\text{2}\text{± 1}$ at rest and from $\text{71 ±}\text{9}\text{2}\text{± 1}\text{to}\text{133 ±}\text{8}\text{14}\text{± 2}$ at peak exercise (mean ± standard error of the mean). Heart rate, LV pressure and LV dP/dt were similar before and after RV pressure overload at rest and with exercise. During exercise at control, systolic shortening increased significantly in all chords. With chronic PA constriction at rest, shortening of all chords also remained normal despite decreases in end-diastolic dimensions, which were most marked in the septal-lateral chord (23% decrease, p <0.01). However, during exercise in the presence of RV pressure overload, septal-lateral shortening decreased 46% (p <0.01) despite increases in systolic shortening in the other chords similar to the control response. Therefore, although LV function at rest in chronic RV pressure overload is normal, exercise may induce regional abnormalities of LV contraction that appear to be mediated by a reduced contribution of the ventricular septum to LV ejection.     

Effects of chronic oral quinidine on left ventricular performance

We studied the effects of 10 to 14 days of oral quinidine administration (200 mg every 8 hrs) on left ventricular (LV) $\text{dP}\text{dt}$ max and shortening fraction (%ΔD) in seve preinstrumented consclous dogs in the resting state, during atrial pacing at 120 bpm, and during an acute pressure load produced by intravenous phenylephrine. Dogs were studied before, during, and after oral quinidine administration with control measurements varying by < 10%. In the resting state, heart rate (85 ± 6 SEM vs 88 ± 7 bpm), LV end-diastolic pressure (7.2 ± 1.4 vs 6.7 ± 1.1 mm Hg), LV end-diastolic diameter (39.6 ± 3.2 vs 38.9 ± 2.7) did not differ (p > 0.05) before or during quinidine, respectively. During atrial pacing LV $\text{dP}\text{dt}$ increased similarly during the control and quinidine periods (+ 13 and + 11%), and %ΔD decreased equally (?26% and ?21%) during phenylephrine infusion off and on quinidine. Thus chronic oral quinidine administration in clinically therapeutic doses (serum quinidine levels 2.3 to 7.5 μg/ml) produced no depression in LV performance at rest or during an acute pressure load.     

Left ventricular function in systole and diastole in constrictive pericarditis

Left ventricular function was studied in systole and diastole in 30 patients with constrictive pericarditis. Left ventricular end-diastolic volume was used to divide the patients into three arbitrary groups: severe constriction (EDV < 25 ml./M.²), moderate constriction (EDV 25 to 50 ml./M.²), and mild constriction (EDV > 50 ml./M.²).The patients had high ventricular diastolic and venous filling pressures (mean LVEDP = 23 ± 7 mm. Hg, mean RVEDP = 20 ± 7 mm. Hg). Measurements related to absolute fiber shortening (stroke index, stroke work index, and left ventricular ejection rate) were reduced and linearly related to the degree of constriction as assessed by the end-diastolic volume.Measurements of relative fiber shortening or lengthening (ejection and filling fraction and circumferential fiber shortening) were normal despite great reduction in ventricular volumes.Velocity measurements, peak LV $\text{dp}\text{dt}$ and mean velocity of circumferential fiber shortening were normal or slightly reduced.These changes were reflected in the systolic time interval measurements pre-ejection phase, left ventricular ejection time, and the ratio $\text{PEP}\text{LVET}$.Diastolic function of the ventricle was abnormal; the distensibility index of the ventriculo-pericardial system ($\text{ΔV}\text{ΔP}$) was low and the passive elastic modulus in-increased. The change in compliance correlated with the degree of constriction and there was a linear relationship between compliance and EDV.The ventricle was underloaded despite the high filling pressure and stroke work index was reduced; extrinsic compression raised the diastolic pressure and reduced left ventricular volumes.     

Alterations in left ventricular volumes and ejection fraction at rest and during exercise in patients with aortic regurgitation

This study was performed (1) to determine the changes in left ventricular volumes during exercise in patients with aortic regurgitation, and (2) to evaluate the importance of these alterations in characterizing left ventricular function in these patients. In 15 normal subjects (Group I) and in 17 patients with aortic regurgitation (Group II), left ventricular end-diastolic volume index, end-systolic volume index, ejection fraction and the ratio of peak systolic blood pressure to end-systolic volume index were measured at rest and during supine exercise. The patients with aortic regurgitation were classified into two groups on the basis of symptoms and chest radiographs: Group IIA, minimal or no symptoms, no cardiomegaly or pulmonary venous congestion; Group IIB, definite symptoms, with cardiomegaly and pulmonary venous congestion. Patients with aortic regurgitation had greater left ventricular end-diastolic and end-systolic volume indexes at rest and during exercise (p <0.05) than did normal subjects. During exercise, left ventricular end-diastolic volume index increased in normal subjects (53 ± 13 ml/m² [mean ± standard deviation] at rest, 67 ± 18 ml/m² during exercise, p <0.01), demonstrated a heterogeneous response in patients in Group IIA and increased in patients in Group IIB (180 ± 96 ml/m² at rest, 209 ± 102 ml/m² during exercise, p <0.05). During exercise, left ventricular end-systolic volume index decreased in normal subjects (18 ± 5 ml/m² at rest, $\text{15}\text{\$}\text{?}\text{6}$ ml/m² with exercise, p <0.01), increased in patients in Group IIB (82 ± 60 ml/m² at rest, 118 ± 93 ml/m² during exercise, p <0.05), and showed a variable response in those in Group IIA. At rest, left ventricular ejection fraction was similar in the three groups, but during exercise it increased in Group I (0.71 ± 0.07 at rest, 0.82 ± 0.07 with exercise, p <0.001), was unchanged in Group IIA and decreased in Group IIB (0.59 ± 0.15 at rest, 0.50 ± 0.16 during exercise, p <0.05). During exercise, there was an inverse relation between changes in left ventricular ejection fraction and endsystolic volume, but no relation between changes in end-diastolic volume and ejection fraction. Changes in the systolic pressure-volume ratio provided no more information than changes in end-systolic volume alone. Thus, abnormal alterations in left ventricular volumes occur during exercise in patients with aortic regurgitation and may be helpful in the further characterization of left ventricular performance in these patients.     

Effect of arterial pressure on left ventricular O2 consumption,coronary blood flow,and reserve capacity following coronary occlusion

The effect of mean systemic arterial pressure $\text{(}\text{SAP}\text{)}$ on myocardial O₂ consumption (MV?O₂) coronary blood flow (CBF) and the reduction of left ventricular (LV) reserve capacity resulting from coronary artery occlusion was studied in 25 open-chest pentobarbital anesthetized dogs with fixed cardiac output and controlled heart rate (HR) and $\text{SAP}$. In all animals, baseline MV?O₂ and CBF were obtained and LV reserve capacity was determined by identifying the HR and $\text{SAP}$ level which raised mean left atrial pressure to 12 mm. Hg. After uniform placement of a pericoronary snare, the dogs were randomized to five equal groups, and $\text{SAP}$ was set at 40, 70 (two groups), 100, and 130 mm. Hg. MV?O₂ and CBF were redetermined and the coronary artery was ligated in all except one group (70 mm. Hg) which served as sham control. Thirty minutes after coronary occlusion, MV?O₂, CBF, and LV reserve capacity were determined again. Percent of nonperfused myocardium did not differ among groups (27.6 ± 1%). MV?O₂ bore a linear relationship to $\text{SAP}$ setting whereas CBF bore a curvilinear relationship. Coronary occlusion did not modify these relationships. Significant, but similar decreases in tolerated HR (23.1 ± 4.7 min.^?1) and $\text{SAP}$ (41.9 ± 6.2 mm. Hg) from control values were observed in all four groups regardless of $\text{SAP}$ setting.We concluded that the impact of coronary ligation on MV?O₂, CBF, the loss of functional reserve capacity, and possibly the extent of ischemic injury of the left ventricle, is not modified by afterload changes. However, optimal O₂ supply-to-demand ratio appears at $\text{SAP}$ of about 100 mm. Hg.     

Acknowledgment to reviewers

The interventricular septal wall thickness and motion was studied by echocardiography in 25 normal subjects and 43 patients with various cardiovascular disease proved at cardiac catheterization. The mean septal thickness was 7.2 mm. ± 0.7 S.D. in the normal subjects, 10,1 mm. ± 1.0 S.D. in 11 patients with left ventricular volume overload (P < 0.01), and a mean of 12.2 mm. in two patients with pure pressure overload of the left ventricle. Ten patients with coronary atherosclerotic heart disease (CAHD) had an average septal thickness of 9.2 mm. ± 1.1 S.D. and in five patients with congestive cardiomyopathy (CM) it was 9.1 mm. ± 0.8 S.D., and a mean of 17.8 mm. in four patients with IHSS (P < 0.01). In five patients with mitral stenosis the septal thickness did not differ from normal (mean 7.1 mm. ± 0.9 S.D.). Septal motion was correlated with angiographic ejection fraction, pattern of left ventricular wall motion, and coronary angiography. All patients with left ventricular disease and an abnormal septal motion invariably had significant left ventricular dysfunction at cardiac catheterization, particularly patients with CM or severe CAHD, although a normal septal motion does not exclude severe left ventricular dysfunction and hypokinesis.It is concluded that study of the interventricular septum by echocardiography provides a non-invasive technique with a high specificity but a lower sensitivity for identifying patients with left ventricular dysfunction.     

Effect of coronary vasodilation on ventricular fibrillation threshold: Role of exogenous vasodilators and perfusion conditions

Even without myocardial ischemia, coronary blood flow (CBF) constitutes a major determinant of ventricular fibrillation threshold (VFT). To clarify whether abnormal distribution of normal or increased CBF plays any additional role, 14 open-chest chloralose-anesthetized dogs with fixednormalized heart rate, cardiac output, and systemic arterial pressure and separate servocontrolled left main coronary artery perfusion were studied as follows: VFT was determined first with coronary perfusion pressure (CPP) set at systemic level (80 mm Hg). Then CBF index was fixed at control levels (134.0 ± 9.5 ml/min · 100 gm^?1 LV) and coronary vasodilation was induced by intracoronary infusion of adenosine until CPP decreased to 49.0 ± 2.0 mm Hg. Myocardial O₂ consumption, LV pressure, LV $\text{dp}\text{dt}$, and surface ECG remained unchanged. However, VFT decreased in all trials by about 45% (p < 0.001). When CPP was reset to 80 mm Hg while maintaining vasodilation, CBF index increased by 90% to 255.4 ± 15.4 ml/min · 100 gm^?1 LV and VFT by 26% (p < 0.005) from control. Yet these VFT increases in response to intraluminal pharmacologic vasodilation were about 19% (p < 0.002) lower than expected for similar CBF index increases occurring physiologically. We conclude that intraluminal coronary vasodilation not matched by appropriate CBF increase results in substantial decrease of VFT. Moreover, at comparable increase of CBF, spontaneous physiologic vasodilation is more effective than intraluminal pharmacologic coronary vasodilation in increasing VFT.     

Ventricular arrhythmias late after aortic valve replacement and their relation to left ventricular performance

Sudden unexplained death is a common cause of late mortality after aortic valve replacement. To evaluate the occurrence of ventricular arrhythmia in patients with aortic valve replacement, two 24 hour ambulatory electrocardiographic recordings were obtained in 45 such patients (mean age 55 years) who had undergone replacement an average of 3.3 years previously. In 43 patients, ventricular arrhythmia was detected; it was rare (mean premature ventricular complex frequency less than $\text{1}\text{15}$ min) in 18 patients (40 percent), moderately frequent (mean frequency $\text{1?}\text{10}\text{15}$ min) in 14 patients (31 percent) and frequent (mean frequency more than $\text{10}\text{15}$ min) in 11 patients (24 percent). Multiformity was noted in 40 (89 percent), bigeminy in 27 (60 percent), couplets in 27 (60 percent) and ventricular tachycardia in 16 (36 percent) of the 45 patients studied. The occurrence of ventricular arrhythmia was not related to the predominant hemodynamic lesion or to the presence of coronary artery disease as determined at the time of preoperative cardiac catheterization. Radionuclide left ventricular ejection fraction, determined at the time of electrocardiographic monitoring in 39 patients, demonstrated normal left ventricular function (ejection fraction greater than 50 percent) in 27 patients (60 percent), moderately depressed function (ejection fraction 36 to 50 percent) in 8 (21 percent) and severe dysfunction in 4 (10 percent). When patients with abnormal versus normal left ventricular performance were compared, the mean premature ventricular complex frequency was $\text{21 ±}\text{26}\text{15}\text{min}\text{versus}\text{5 ±}\text{11}\text{15}\text{min (}\text{p}\text{< 0.01)}$; couplets occurred in 10 (83 percent) of 12 versus 13 (48 percent) of 27 patients (p < 0.05) and ventricular tachycardia in 8 (75 percent) of 12 versus 6 (22 percent) of 27 patients (p < 0.01). Patients exhibiting ventricular tachycardia had a mean left ventricular ejection fraction of 47 ± 14 percent compared with 62 ± 13 percent in patients without this arrhythmia (p < 0.005). This study indicates that significant ventricular arrhythmias, including ventricular tachycardia, are common late after aortic valve replacement. In addition, a relation exists between occurrence of arrhythmia and left ventricular function abnormalities.     

Later results of closure of secundum atrial septal defect in children

Seventy-one children aged 2 to 17 years (mean 8.8) underwent operation for atrial septal defect and have been followed up for 5 to 13 years (mean 8.2). The condition of the rare symptomatic patient has improved, and weight gain and growth have been striking in the few who had previously shown underdevelopment. Congestive heart failure has not recurred in the 3 patients who had it before operation. Forty-six patients have shown a return of heart size to normal by X-ray study, 61 a shift of the frontal plane QRS axis to the left and a decrease in the height of the R or Rt? wave in lead V₁, and 30 of 37 a disappearance of electrocardiographic evidence of right ventricular enlargement. Twenty-two patients (31 percent), although asymptomatic, have residual evidence of cardiac enlargement, 15 by X-ray study alone, 3 by electrocardiogram alone, and 4 by both methods. Complete or partial reversion of both roentgenographic and electrocardiographic abnormalities occurs within 1 $\text{1}\text{2}$ to 2 years postoperatively, and no change is seen thereafter. Persistent postoperative cardiac enlargement may be due to incomplete repair (2 of 12 patients who underwent recatheterization) or persistent, hemodynamically significant arrhythmias occurring as a complication of surgery (3 patients). Primarily it is the result of apparent failure of myocardial disease to regress and can be considered a cardiomyopathy of volume loading. Although abnormal physiologic indexes were not demonstrated in all postoperative catheterization studies, some patients showed evidence of loss of myocardial compliance. In those with residual cardiac enlargement, there was no significant positive correlation with the magnitude of the left to right shunt, increase in preoperative right-sided pressure, size or location of the defect, degree of preoperative cardiac enlargement or age at which operation was performed. Results to date suggest that although early closure of an atrial septal defect is curative for most, residual myocardial disease in some may ultimately result in a less than normal life expectancy.     

Cardioadrenergic factor in essential hypertension

Determination of STI in 54 untreated essential hypertensive subjects and 17 normal subjects revealed marked differences among three groups of patients. Those with borderline hypertension (29) had a short PEP and IVC periods (93 ± 2.1 and 28 ± 0.7 msec., respectively, p < 0.001) (mean ± S.E.) reduced $\text{PEP}\text{LVET}$ (0.323 ± 0.009, p < 0.05) and increased $\text{DP}\text{IVC}$ (3,484 ± 257 mm. Hg per second, p < 0.001). Among those with established hypertension, two groups of equal age and diastolic pressure were identified: nine with marked variations in blood pressure and a hyperkinetic heart clinically and 16 with fixed hypertension; none had cardiac or renal decompensation. Those with a hyperkinetic circulation had normal PEP, IVC, and $\text{PEP}\text{LVET}$ despite a high diastolic pressure (122 ± 7.1 mm. Hg); $\text{DP}\text{IVC}$ was elevated (3,651 ± 497 mm. Hg per second, p < 0.001) as in those with borderline hypertension. In contrast, the patients with fixed hypertension had longer PEP and IVC (p < 0.001), higher $\text{PEP}\text{LVET}$ (p < 0.001), and normal $\text{DP}\text{IVC}$. Propranolol (10 mg. intravenously) slowed heart rate and prolonged PEP and IVC more in patients with a hyperkinetic circulation and in those with borderline hypertension than in those with fixed hypertension.These results suggest the presence of an increased cardioadrenergic drive not only in borderline hypertension, but also in a subgroup of patients with established hypertension. Left ventricular hypertrophy (ECG) was found in 1 out of 9 patients with hyperkinetic heart but in 6 out of 16 with fixed hypertension; cardiac index was high normal in the first group but reduced in the latter (3.32 vs 2.38 L./min./M.², p < 0.001). This factor as determined by the systolic time interval might, therefore, be important in determining cardiac prognosis or planning therapy.     

Comparative response of right and left ventricles to volume overload.

The cardiac volume data of 49 normal children were compared with those of 23 with secundum atrial septal defect and 24 with patent ductus arteriosus. Significantly smaller ventricular end-diastolic volumes were observed in the normal infants than in older children (right ventricle 53.9 versus 75.5 cm3/m2; left ventricle 46.7 versus 63.6 cm3/m2). "Distensibility" of the right ventricle (DRV), left ventricle (DLV) and left atrium increased normally with age. DRV and DLV were similar shortly after birth; thereafter, DRV increased more rapidly than DLV (mean DRV 12.7; mean DLV 7.8 cm3/m2 per mm Hg, P less than 0.001). In both atrial septal defect and patent ductus arteriosus, the ipsilateral (involved) ventricles had increased volume, increased output, normal ejection fraction and increased distensibility. The contralateral (left) ventricle in atrial septal defect was smaller than normal (39.6 versus 49.7 cm3, P less than 0.001), and had a smaller ejection fraction (0.63 versus 0.71, P less than 0.01) and output (3.70 versus 4.57 liters/min per m2, P less than 0.005). In contrast, the contralateral (right) ventricle in patent ductus arteriosus remained normal. Left atrial maximal volume was larger than normal in atrial septal defect (46.6 versus 35.9 cm3/m2, P less than 0.001). The left atrial and left ventricular volumes in patent ductus arteriosus were, respectively, 152 and 142 percent of normal, indicating comparable response to the volume load. The left head changes in atrial septal defect may be related both to a functionally restrictive defect and to the difference in distensibility of the ventricles.     

Effect of the undisturbed pericardium on left ventricular size and performance during acute volume loading

Studies in instrumented dogs have suggested that the pericardium alters left ventricular diastolic pressure-volume relations and thus may influence systolic performance. However, the instrumentation used in these studies disrupts the pericardium and may have influenced the results. We therefore studied five conscious dogs by methods not traumatic to the pericardium, before and after pericardiectomy. Although heart rate and left ventricular systolic and end-diastolic pressures were not different before or after pericardiectomy, either at rest or during volume loading, end-diastolic volume measured by biplane two-dimensional echocardiography increased post pericardiectomy at rest from 38 ± 4 (SE) to 61 ± 4 ml (p < 0.05) and during volume loading from 68 ± 5 to 79 ± 5 ml (p < 0.005). After pericardiectomy, ejection fraction was unchanged, but the peak value of the first derivative of left ventricular systolic pressure ($\text{dP}\text{dt}$) increased significantly at rest from 17 ± 2 to 26 ± 4.0 × 10² mm Hg/sec. We conclude that pericardiectomy shifts the left ventricular end-diastolic pressure-volume curve to the right and increases the systolic isovolumic index of $\text{dP}\text{dt}$ in the basal state.     

Transvascular catheter infiltration of the ductus arteriosus with formalin in the newborn lamb: A novel method of establishing and maintaining ductal patency

Objectives. This study sought to establish and maintain patency of the ductus arteriosus by a new method of transvascular formalin infiltration of the ductus arteriosus wall.Background. Maintaining patency of the ductus arteriosus postnatally is necessary with many forms of congenital heart disease to ensure survival until definitive surgical repair. A variety of approaches have to date met with variable success.Methods. Seven newborn lambs underwent catheterization at 1 to 5 days of age. A functionally closed ductus arteriosus was traversed with a specially designed porous balloon catheter, and the wall was infiltrated with 10% formalin. The ductus was then further dilated with either a 7- or 8-mm diameter balloon.Results. The ductus arteriosus wall was successfully infiltrated and dilated in all animals. Two lambs were euthanized within 24 h with congestive heart failure from a large ductus, and one lamb was electively euthanized 5 days after transvascular infiltration. Four lambs underwent serial follow-up catheterizations, one of which required repeat balloon dilation 47 days after infiltration. At latest follow-up (mean age [± 1 SD] 83 ± 34 days, range 33 to 108), the pulmonary/systemic flow ratio (2.7 ± 1.2) was unchanged from immediately after infiltration (1.9 ± 0.5, p > 0.1). The narrowest diameter of the ductus arteriosus (4.3 ± 0.4 mm vs. 6.9 ± 2.6 mm, p > 0.1) and its ratio to that of the adjacent descending aorta (0.5 ± 0.1 vs. 0.4 ± 0.1, p > 0.1) were also unchanged at latest follow-up. No systemic toxicity was observed. At postmortem study, the ductus was patent, and histologic analysis showed variable intimal and medial destruction, endothelial regeneration, loss of elastic tissue and calcification. Adjacent pulmonary artery and aorta were normal. Based on the small sample size and the observed maximal effect size of 70%, the power of the study is at most 40% to detect significant differences.Conclusions. To our knowledge, this is the first time that transvascular formalin infiltration of the ductus arteriosus wall has been applied successfully to maintain ductal patency in the newborn lamb. This method may provide a means of palliation for neonates with certain forms of congenital heart disease.     

Determination of left ventricular diastolic chamber stiffness and myocardial stiffness in patients with congenital heart disease

Left ventricular diastolic indexes were derived in 13 patients aged 5 to 21 years. Three had a normal heart, three had lesions causing volume overload and seven had coarctation of the aorta, including one whose main lesion was severe endocardial fibroelastosis. At cardiac catheterization simultaneous high fidelity pressure (P) and left ventricular volume (V) measurements were obtained and several points in one diastolic cycle taken. With use of a monoexponential formula (P = ae^bv) for P versus V, $\text{dP}\text{dv}$ and the operant chamber stiffness b were obtained. Similarly, with use of σ = αe^β?, $\text{dσ}\text{d?}$, elastic stiffness (E) and the muscle stiffness constant K_E were obtained. Values for b were 0.0273 ± 0.0065 in normal subjects, 0.017 ± 0.0043 in those with volume overload, 0.0369 ± 0.0173 in those with coarctation (without endocardial fibroelastosis) and 0.0192 in the child with endocardial fibroelastosis. The plot of P versus V for coarctation was to the left and steeper than normal and the patients with volume overload had a flattened rightward curve, whereas the curve for those with endocardial fibroelastosis was extremely rightward. The stress-radii curves of the normal subjects and those with coarctation were similar whereas the curves for patients with volume overload and endocardial fibroelastosis were rightward of normal. The value for K_E was 8.92 ± 0.87 for the normal subjects, 8.26 ± 0.75 for those with volume overload, 9.2 ± 2.5 for those with coarctation and 22.75 for those with endocardial fibroelastosis.Thus, the pressure-loaded ventricle is stiffer than the normal, which in turn, is stiffer than the volume-loaded ventricle. This response, due to hypertrophy, appears to be appropriate in that diastolic stress was normalized and muscle stiffness was not increased except in the patient with endocardial fibroelastosis.     

Critical aortic coarctation: patch aortoplasty in infants less than age 3 months.

Twenty-three infants less than age 3 months (mean age 31 days) underwent patch aortoplasty for relief of coarctation of the aorta. All had intractable congestive heart failure, despite aggressive medical therapy. Each infant had other cardiac anomalies, including patent ductus arteriosus (83 percent) and ventricular septal defect (74 percent). All patients underwent closure of the ductus arteriosus and patch angioplasty of the aorta to produce a luminal diameter of at least 16 mm. In addition, 9 of the 17 patients (53 percent) with a large shunt ventricular septal defect underwent pulmonary arterial banding. There was one hospital death 42 days after operation secondary to bowel perforation and sepsis. Hospitalization beyond 21 days postoperatively was always due to other unrepaired cardiac lesions. The three late deaths at 3, 9 and 18 months after operation were associated with additional major anomalies. Fourteen patients have had postoperative catheterization. No gradient was found across the site of coarctation repair, but one patient had a gradient between the left carotid and left subclavian arteries. Surgical repair of critical coarctation of the aorta in infants can safely be offered despite the presence of other cardiac anomalies.