Echocardiographic diastolic ventricular abnormality in hypertensive heart disease: Atrial emptying index

STUDIES IN HYPERTENSION

Echocardiographic Diastolic Ventricular Abnormality in Hypertensive Heart Disease: Atrial Emptying Index

GERALD

R. DRESLINSKI,

MD

EDWARD

D. FROHLICH.

MD,

FRANCIS G. DUNN, MD FRANZ H. MESSERLI, MD, DANIEL

H. SUAREZ,

EFRAIN

REISIN,

New Orleans,

FACC

FACC

MD

MD

Louisiana

To analyze changes in left ventricular diastolic properties in hypertensive heart disease, the atrial emptying index was used to assess the rapid phase of diastolic filling of the left ventricle. Ten normal subjects (Group l), 11 hypertensive patients without evidence of cardiac involvement (Group 2) and 10 hypertensive patients with echocardiographic evidence of left ventricular hypertrophy (Group 3) were compared using 1111 mode echocardiography and systemic hemodynamic data. Whereas cardiac index (dye-dilution method) and rate of circumferential fiber shortening (echocardiogram) were normal in all three groups, there was a progressive increase in left atrial index (p
M mode echocardiography has been demonstrated to be a sensitive indicator of the sequential changes occurring in the heart in systemic arterial hypertensi0n.l The changes in function as well as anatomic features have been recorded.2 Previous analysis has focused on the anatomy and systolic function of the left ventricle, but only recently have diastolic properties of the ventricle been analyzed in valvular and hypertensive heart disease.“-5 Although left atria1 abnormalities have been described in association with hypertensive heart disease,1,6,7 further physiologic delineation of the significance and pathophysiology of these findings has not been pursued. We therefore analyzed the utility of the atria1 emptying indexs,g as a potential indicator of diastolic abnormalities in the left ventricle in untreated patients with essential hypertension. Methods Patients:

Thirty-one patients with normal sinus rhythm (heart rate 85 or less) were studied and classified into three groups: Group 1: 10 normotensive subjects without evidence of heart disease (5 women and 5 men, with a mean age of 36 years [range 19 to 501).

beats/min From the Division of Hypertensive Diseases and the Division of Research, Ochsner Medical Institutions, New Orleans, Louisiana. This study was supported in part by Grant l-IL-22506 from the National Heart, Lung, and Blood Institute. Bethesda, Maryland. Manuscript received July 28, 1980; revised manuscript received December 16, 1980, accepted December 18, 1980. Address for reprints: Gerald R. Dreslinski. MD, Ochsner Clinic, 1514 Jefferson Highway, N&w Orleans, Louisiana 70 121.

Group 2: 11 patients, 9 men and 2 women with a mean age of 45 years (range 34 to 50), all with established essential hypertension, secondary causes having been ruled out. All were either untreated or had discontinued treatment (including diuretic drugs) for at least 4 weeks before the study. In all cases, there was no roentgenographic, electrocardiographic or echocardiographic evidence of left atria1 or left ventricular enlargement, or abnormality.’ Group 3: 10 patients, 7 men and 3 women with a mean age of 39 years (range 20 to 54), with established essential hypertension and with evaluation and discontinuation of therapy as in Group 2. All patients had M mode echocardio-

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graphic (interventricular septal and posterior wall thickness 1.1 cm or greater) evidence of left ventricular hypertrophy. Three had left atria1 abnormalities and seven had left ventricular hypertrophy on e1ectrocardiography.l Hemodynamic studies: Arterial and venous pressures were continuously recorded (with patients in the postabsorptive state in the supine posture) on a 12 channel Electronics-forMedicine indirect writing recorder using Statham P-23DB pressure transducers. Cardiac output was determined in triplicate using indocyanine green dye. Mean arterial pressure was obtained by electrical integration, and the usual hemodynamic indexes were calculated by standard formulation. Ejection time was read directly from the strip chart recording of the arterial pulse and was taken as the mean of 10 beats. Echoctirdiographic studies: Standard methods of M mode echocardiography were employed using a Smith-Kline Ekoline 20A Ultrasonoscope interfaced with a Honeywell strip chart recorder using a probe with a diameter of 1.27 cm. Ultrasonic emission characteristics were: frequency 1,000/s; wave length 2.25 millihertz; and focal length 10 cm. The standard

measurements of left VentricularlO and left atrial” dimensions were determined concomitant with the hemodynamic study, and corrected for body surface area (cm/m2). The mean rate of circumferential fiber shortening was calculated using the method of McDonald et a1.,12 with the ejection time measurement as calculated from the arterial pulse tracing. The ratio of left ventricular radius to wall thickness (radius/ thickness ratio) was determined from the end-diastolic diameter divided by 2; that quotient was then divided by the posterior left ventricular wall thickness.‘3 The atria1 emptying index was quantitated from the posterior aortic wall echocardiogram using the technique of Strunk et al.*; this index represents the first one third (rapid phase) of left atria1 emptying divided by total left atria1 emptying. Iridependent duplicate measurements were carried out, and the mean of five cardiac cycles was used (Figs. 1 and 2). A chart speed of either 50 or 100 mm/s was used, and the

maximal recording scale of the aortic root was utilized to facilitate assessment of posterior motion. Left ventricular mass was calculated using the method of Bennett and Evans14 and corrected for body surface area (g/m2). Statistical analysis: Analysis was carried out using the unpaired Student’s t test and by linear regression. Groups 2 and 3 were compared with the normal subjects (Group 1). Results

FIGURE 1. Normal aortic root echogram. Point o represents initial posterior motion of aortic root. Point A represents aortic root motion after total atrial emptying (TAE) marked by the end of the P’wave in the electrocardiogram. Point x is the aortic root displacement at T l/3, determined by dividing total atrial emptying time (point o to point A) by 3. Parallel horizontal lines are then drawn through these points. Atrial emptying index equals o-x/o-A. Here o-x/o-A = 9 mm/ 11 mm = 0.82.

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Hemodynamic data: As anticipated, mean arterial pressure was significantly and progressively increased (Group 1 versus Group 2, 87 versus 110 mm Hg, p CO.005, and Group 1 versus Group 3,87 versus 134 mm Hg, p < 0.001) (Table I). No significant difference in heart rate, mean left ventricular ejection rate or cardiac index among the three groups was observed. Paralleling the changes in mean arterial pressure, total peripheral resistance was increased (Group 1 versus Group 2, 27 versus 36 units, p <0.025, and Group 1 versus Group 3, 27 versus 44 units, p
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FIGURE 2. Aortic root echogram in a hypertensive patient with left ventricular hypettrophy. Abbreviations as in Figure 1. Here o-x/o-A P 3 mm/9 mm = 0.33, indicating a significant reduction in the atrial emptying index.

framework, patients in stage 2 demonstrated impaired systolic myocardial function associated with electrocardiographic left atria1 abnormalities accompanied by an atria1 gallop rhythm (SJ noted on cardiac auscultation. The electrocardiographic and auscultatory abnormalities have been attributed to left atria1 changes that occur secondary to a less compliant left ventricle before the development of left ventricular hypertrophy can be measured by electrocardiogram or chest X-ray film. However, there has been no echocardiographic evidence of abnormal diastolic function in this subgroup.

Many echoeardiographic st,udies have demonstrated normal systolic left ventricular function in hypertension, even hyperfunction, before left ventricular failure.lJ6,16 Diastolic properties of the left ventricle are now being investigated in the hope of further identifying ventricular abnormalities in hypertensive heart disease3 before left ventricular hypertrophy or congestive cardiac failure develop. Atria1 emptying index as a measure of rapid ventricular filling and compliance: Our present data corroborate previous findings that in the absence of inappropriate chamber dilatation or ventricular hy-

TABLE I

TABLE II

Systemic Hemodynamlc Data (mean values f standard error of the mean)

Echocardiographic Data (mean values f standard error of the mean)

Group 1 2 3

HR 71 f2 67 f2 72 f3

MAP a7 1%: f5 134% f6

Cl 3.44 f 0.32 3.42 f 0.42 3.11 f 0.16

TPR 27 f3 36+ 42” f2

MLVER

Group

Vcf

Rlth

LAI

AEI

LVM

1

1.15 f 0.08 1.34 f 0.16 1.03 f 6.05

3.08 f 0.31 3.36 f 0.34 2.49 f 0.31

1.30 f 0.08 1.74’ f 0.09 1.73$ f 0.06

0.82 f 0.03 0.63’ f 0.03 0.50t f 0.06

9S5 f 7 14ot f 9

170 f 17 163 f 15 153 f8

2 3

Probability (p) <0.005; + p <0.025 (Group 1 versus Group 2); t p
72

l

Probability(p)
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pertrophy (normal radius/thickness ratio), hemodynamic (cardiac index) and echocardiographic indexes (fiber shortening velocity) of left ventricular systolic performance remain normal.15J6 In spite of the preservation of systolic function, there is an apparent increase in left atria1 size, detectable echocardiographitally before electrocardiographic changes take place, but still falling within normal limits (2.0 cm/m2 or less).l’ This change is associated with a diminished atria1 emptying index, a measure of the rapid filling of the left ventricle during diastole, as assessed by the posterior aortic wall echogram, 8,g and an increase in left ventricular mass.l The failure to correlate this reduction in passive left ventricular filling (or left atria1 emptying) with changes in left atria1 size or total peripheral resistance (an index of left ventricular outflow impedance) suggests that this results from reduced left ventricular compliance. Therefore, as mean arterial pressure and total peripheral resistance increase, the left ventricle initially hypertrophies and becomes stiffer. This promotes an increased left atria1 size, although it remains 2.0 cm/m2 or less. Concomitantly, there is a reduction in passive left ventricular filling. As the hypertensive disease process progresses without intervention, the left ventricle continues to hypertrophy (Table II). Accuracy of aortic root motion in assessing atria1 emptying: It may be argued that changes in aortic root

compliance could affect posterior motion in diastole and thereby influence passive atria1 emptying as assessed with aortic root motion. Although this factor should not be discounted completely-that is, that age and hypertension are the major determinants of aortic root stiffness (atherosclerosis)-the absence of correlation between changes in mean arterial pressure or total peripheral resistance and the atria1 emptying index (in patient groups of similar ages) militates against this factor playing a major role in our study group. Furthermore, previous work has shown aortic root motion during ventricular diastole to be governed primarily by left atrial events,17 and it seems inescapable that during passive left atria1 emptying, left ventricular compliance must be critical. Clinical implications: The clinical staging of hypertensive heart disease initially presented remains useful. It appears that the first changes in hypertensive heart disease are those of diastolic compliance of the left ventricle, even before systolic function becomes impaired. The hypertrophying and hypertrophied left ventricle apparently is less compliant than the nonhypertrophied left ventricle. The atria1 emptying index is a sensitive and early indicator of changes in the diastolic properties of the left ventricle; thus far this is the earliest detectable evidence of hypertensive heart disease.

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assessment of mitral stenosis’by left atrial emptying index. Chest 1979;76:668-71. Felgenbaum H, Popp RL, Ship JN, et al. Left ventricular wall thickness measured by ultrasound. Arch Intern Med 1968;121: 391-5. Hirata T, Wolfe SB, Popp RL, et al. Estimation of left atrial size using ultrasound. Am Heart J 1969;78:43-52. McDonald IO, Feiganbaum H, Chang S. Analysis of left ventricular wall motion by reflected ultrasound. Application to assessment of myocardial function. Circulation 1972;46:14-25. Gaasch WH. Left ventricular radius to wall thickness ratio. Am J Cardiol 1979;43: 1189-94. Bennett DH, Evans DW. Correlation of left ventricular mass determined by echocardiography with vectorcardiographic and electrocardiographic measurements. Br Heart J 1974;36:9817. Dreslinski GR, Messerli FH, Dunn FG, Suarez DH, Frohlich ED. Patterns of left ventricular adaptation in borderline and mild essential hypertension: echocardiographic findings. Chest, in press. Fiorentina C, Polese A, Olivari MT, Guazzi MD. Cardiac performance in hypertension re-evaluated through a combined hemodynamic ultrasonic method. Br Heart J 1980;43:344-50. Strunk BL, Fitzgerald JW, Lipton M. et al. The posterior aortic wall echocardiogram: its relationship to left atrial volume changes. Circulation 1976;54:744-50.