Key words: two-dimensional echocardiography, cardiomyopathy, Introduction. Patients and Methods. Clin. Cardiol. 12, (1989)

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1 Clin. Cardiol. 12, (1989) Echocardiographic Findings of Left Ventricular Hypertrophy and Normalization of Parameters of Left Ventricular Function in Patients with Previous Evidence of Dilated and Poorly Contracting Left Ventricle and Coexisting Systemic Hypertension V. DALL AGLIO. M.D.. G. L. NICOLOSI, M.D., C. BURELLI, M.D., F. ZARDO. M.D.. D. PAVAN. M.D., C. LESTUZZI, M.D.. D. ZANUTTINI, M.D Divisione di Cardiologia, Ospedale Civile, Pordenone, Italy Summary: We report 6 cases of dilated left ventricle with poor left ventricular function and coexisting systemic hypertension in whom left ventricular hypertrophy and normalization of left ventricular function and dimensions have been subsequently documented by M-mode and twodimensional echocardiographic follow-up studies. Four patients were in New York Heart Association functional Class IV, one in Class 111, and one in Class I1 when first seen. Normalization of left ventricular function and dimensions and features of left ventricular hypertrophy (fractional shortening from 15.0f5.2 to 39.7i-5.4, left ventricular end-diastolic diameter from 6.6k0.6 to 4.6f0.6 cm, left ventricular end-systolic diameter from 5.6f0.8 to 2.8 k0.6 cm, left ventricular end-diastolic radius/posterior wall thickness from 3.1 f0.5 to 2.0f0.4, interventricular septum thickness from 1.2f0.3 to 1.5f0.3 cm, left atrium from 4.6f0.6 to 3.5k0.9 cm) were achieved after adequate medical treatment at the end of the follow-up (11-39 months). It appears from this study that normalization of left ventricular dimensions and function with features of left ventricular hypertrophy can occur after adequate treatment in patients with echocardiographic findings of dilated and poorly contracting left ventricle and coexisting systemic hypertension. It is conceivable, in such cases, to classify the dilatation of the left ventricle as secondary and to suggest the hypothesis Address for reprints: Dr. Vittorio Dall Aglio Divisione di Cardiologia Ospedale Civile Santa Maria degli Angeli Pordenone, Italy Received: November 10, 1987 Accepted with revision: October 20, 1988 of a cause-effect relationship between therapy and normalization of left ventricular parameters with findings of left ventricular hypertrophy. Further studies are needed to clarify this phenomenon. Key words: two-dimensional echocardiography, cardiomyopathy, systemic hypertension Introduction A dilated and poorly contracting left ventricle can be due to a primary ( idiopathic ) dilated cardiomyopathy (DCM) or can be secondary to a well-known cause. I -3 When systemic hypertension is present, the dilatation of the left ventricle and the poor left ventricular (LV) function can be considered as secondary. -3 The echocardiographic findings of DCM and of the dilated left ventricle due to systemic hypertension, however, may be similar. In our laboratory, normalization of LV dimensions and function and features of LV hypertrophy have been demonstrated by M-mode and two-dimensional echocardiographic follow-up studies in 6 cases, whose initial findings were of dilated and poorly contracting left ventricle and coexisting systemic hypertension. To our knowledge, this is the first echocardiographic documentation of normalization of left ventricular dimensions and function with findings of left ventricular hypertrophy in patients with long-standing chronic systemic hypertension and previous evidence of dilated and poorly contracting left ventricle. Patients and Methods The study group comprises 6 patients with systemic hypertension, 4 male and 2 female, with heart failure and

2 92 Clin. Cardiol. Vol. 12, February 1989 echocardiographic features of dilated and poorly contracting left ventricle. The age range was years (mean 49). Four patients underwent echocardiographic followup after 13, 22,26, and 39 months; 2 patients underwent a first echocardiographic follow-up 2 1 days and 3 months later and a second echocardiographic follow-up 11 and 15 months, respectively, after the first examination. Twodimensional echocardiograms were obtained using commercially available phased-array or mechanical sector scanners (Toshiba SSH 40A, Toshiba SSL 53M, Aloka SSD 720). Images were obtained from the parastemal, apical, and subcostal approaches to visualize cardiac chambers in the usual longitudinal, four-chamber and short-axis planes; intermediate planes were always recorded when necessary. I I Positioning and manipulation of the transducer were optimized in order to achieve adequate endocardial definition. M-mode echocardiograms were also recorded at 50 mm/s paper speed using black and white photographic paper. The following M-mode parameters were analyzed: LVFS (left ventricular fractional shortening), LVEDD (left ventricular end-diastolic diameter), LVESD (left ventricular end-systolic diameter), PWTh (posterior wall thickness), R/Th (left ventricular enddiastolic radius/posterior wall thickness), IVSTh (interventricular septum thickness), IVS%Th (percentage of IVS systolic thickening), PW%Th (percentage of PW systolic thickening), LA (left atrium dimensions). Measurements were obtained blindly by two observers according to the Recommendations of the A.S.E.12 and given as the mean of the two observations. Paired r-test was used for statistical analysis. M-mode indexes of diastolic function were also studied (see Results). At the time of the first echocardiographic examination, relevant clinical data were: a history of systemic hypertension (duration of 3-7 years) was present in 4 cases. Mean blood pressure value range was over mmhg. Adequate therapeutic control of blood pressure had never been reached in these 4 patients. In the remaining 2 patients, it was not possible to know when high levels of blood pressure were first observed. In these two subjects, aged 26 and 57 years, blood pressure was 230/ 160 and 180/ 1 10 mmhg, respectively, at the first examination. Four patients were in New York Heart Association (NYHA) functional Class IV, one in Class 111, and one in Class 11. There was no history of previous infective disease nor of alcohol abuse in any patient. No patient had a clinical picture of acute infective disease. All patients were studied from a clinical-echocardiographic point of view. Two patients smoked 20 cigarettes daily. In one case (CG, F, age 26), antivirus coxsackie, echo, influenza, and parainfluenza antibodies were obtained and were negative. No patient had valvular, ischemic, congenital, or specific heart muscle disease. Two patients were not treated; three patients had just started antihypertensive therapy 2, 5, and 21 days before the first echocardiogram. In one case, diuretics were started some time before without adequate blood pressure control. At the time of the last echocardiographic follow-up, relevant clinical data were: blood pressure normal in 4 patients, borderline in 2 patients. Four patients were in NYHA functional Class 11, 2 in Class I. All 6 patients were on antihypertensive treatment (captopril and diuretics in 3 cases, captopril-diuretics and verapamil in 1 case, clonidine-diuretics and nifedipine in 1 case, prazosin and diuretics in 1 case). Results At the end of the follow-up, echocardiograms of all 6 patients showed left ventricular hypertrophy and normalization of left ventricular dimensions and function (Tables I and 11, Figs. 1-4). LVFS changed from 15.0f5.2% to 39.7,5.4% (p<.oool), LVEDD from 6.6f0.6 to 4.6k0.6 cm (p<.0005), LVESD from 5.6k0.8 to TABLE I M-mode echocardiographic measurements LVFS (%) LVEDD (cm) LVESD (cm) PWTh (cm) RITh 1st 2nd 1st 2nd 1 St 2nd 1 st 2nd 1 st 2nd CG PO o I S R I BL o 1.o BP o DBR Mean 15k k k k k k k k0.4 p <.OOOl p <.0005 p<.oool NS p<.005 The values reported in the 2nd column are those of the third echocardiogram, i.e., the last performed. Abbreviations: LVFS =left ventricular fractional shortening; LVEDD = left ventricular end-diastolic diameter; LVESD =left ventricular end-systolic diameter; PWTh =posterior wall thickness; R/Th =left ventricular end-diastolic radius/posterior wall thickness.

3 V. Dall Aglio et al.: Echo findings in LV hypertrophy 93 TABLE I1 M-mode echocardiographic measurements IVSTh (cm) IVS%Th PW%Th LA (cm) 1st 2nd 1st 2nd 1 st 2nd 1st 2nd CG PO O SR BL O 4.2 BP DBR 1.O O Mean 1.2k k k k k k k0.9 p<.05 p <,005 p<.05 p<.02 The values reported in the 2nd column are those of third echocardiogram, i.e., the last performed. Abbreviations: IVSTh=interventricular septum thickness; IVS%Th= % of IVS systolic thickening; PW%Th= % of PW systolic thickening; LA =left atrium dimensions. 2.8f0.6 cm (p<.oool), PWTh from l.lfo.l to 1.2f0.1 cm (NS), R/Th from 3.1k0.5 to 2.0f0.4 (p<.005),ivsthfrom 1.2kO.3 to 1.5+_0.3cm(p<.05), IVS%Th from 14.2f4.1% to 28.5f7.8%(p<.005), PW%Thfrom to % (p<.o5), LA from 4.6f0.6 to 3.5k0.9 cm (p<.o2). Echocardiographic indexes of diastolic function were also studied by digitized M-mode echocardiography (Table 111). PDVSE changed from 2.3f0.3 to 4.3k0.7 cmls (p <0.005), PDVPWE from 6.2 f 1.1 to 6.4f 1.4 cm/s (NS), PTVS from 2.3f0.5 to 3.9f1.0 cm/s (p<0.05), PTVPW from 3.7f0.9 to cm/s (NS), PFR from 6.7A-1.6 to 9.1k1.4 (p<0.05). We have compared the values of diastolic indexes in our patients with those of a group of 7 normal subjects and with those of a group of 15 idiopathic DCM patients (Table 111). No significant difference was found between indexes in patients with idiopathic DCM and those of our subjects with systemic hypertension in the dilated phase, nor between indexes obtained in normal subjects FIG. 1 From left to right, two-dimensional echocardiographic diastolic (D) and systolic (S) parasternal long-axis views in three serial echocardiograms in one case (CG, 26/F). Left: the left ventricle (LV) appears dilated and poorly contracting. Middle: remarkable reduction of left ventricular dimensions and improved left ventricular function. Right: significant left ventricular hypertrophy with nomialization of left ventricular dimensions and function. RV =right ventricle, LV =left ventricle, LA = left atrium, AO=aortic root.

4 94 Clin. Cardiol. Vol. 12, February 1989 SR38 D S FIG. 3 From left to right, M-mode echocardiograms in two subsequent examinations of another patient (BP. 57/M). Left: dilated and poorly contracting left ventricle. Right: significant left ventricular hypertrophy and normalization of left ventricular function and dimensions FIG. 2 From left to right, two-dimensional echocardiographic diastolic (D) and systolic (S) apical four-chamber views in three consecutive echocardiograms in a different case (SR, 38/M). Left: dilated and poorly contracting left ventricle. Middle: mild improvement of left ventricular function. Right: the appearance of significant left ventricular hypertrophy and normalization of left ventricular dimensions and function. and those of our patients after normalization of left ventricular function. Obviously, the small group of subjects require further investigation to confirm our results. The blood Pressure values of the 6 patients during the follow-up between the first and the second (or the third) echocardiogram are shown in Table IV FIG, 4 Two-dimensional subsequent examinations of the same patient as in Figure 3. Top: From left to right, apical four-chamber view and parasternal short-axis view at the level of the papillary muscles in diastole (D) and systole (S) in the first echocardiogram. The left ventricle appears dilated and poorly contracting. Bottom: From left to right, apical four-chamber view and parasternal short axis view at the level of the papillary muscles in diastole (D) and systole (S) in the second echocardiogram. This examination shows left ventricular hypertrophy with normalization of left ventricular dimensions and function.

5 ~ ~~~ ~ V. Dall Aglio et al. : Echo findings in LV hypertrophy 95 TABLE 111 Diastolic indices derived by digitized M-mode echocardiograms Values k SD (cm/s) Group 1 Normals Group 3 (7 cases) Group 2 (15 cases) Group 4 Peak diastolic velocity of septa1 endocardium (PDVSE) 4.2k k k k0.7 Peak diastolic velocity of posterior wall endocardium (PDVPWE) 7.1 k k k k 1.4 Peak thinning velocity of septum (PTVS) 3.5k I.2 2.3k k k1.0 Peak thinning velocity of the posterior wall (PTVPW) 5.8k k k Peak filling rate (PFR) k k1.4 Group 2 =patients with hypertension in dilated phase; Group 3 =idiopathic dilated cardiomyopathies; Group 4 =patients with hypertension and normalized left ventricular function. Statistical analysis: 2-tailed Student s t-test group 2 vs. 3, NS in any parameter; paired t-test group 2 vs. 4, PDVSE p<o.005; PTVS and PFR p<0.05; PDVPWE and PTVPW NS; 2-tailed Student s t-test group 1 vs. 4, NS in any parameter. TABLE IV Blood Pressure value changes Patient Agelsex From To CG SR BP PO BL DBR 261F 381M 57/M 48/M 641M 601F , 160/120 I70/ / / I / O/9Ob / I50/ / I35/90-95 First echocardiogram. bbetween first and second and second and third echocardiograms Discussion A dilated and poorly contracting left ventricle can be due to a primary ( idiopathic ) dilated cardiomyopathy or can be secondary to a well-known cause.l-3 Lam et a1.5 reported one case of reversible dilatation of hypertrophied left ventricle in pheochromocytoma, documented by serial two-dimensional echocardiographic observations. Reversibility of dilatation of the left ventricle in long standing chronic systemic hypertension has been thought to be less likely to OCCU~,~ and to our knowledge has not yet been documented by echocardiographic studies. From our study, it appears that left ventricular hypertrophy and normalization of left ventricular dimensions and function can be documented after adequate medical treatment in selected patients with long-standing chronic systemic hypertension and echocardiographic features of dilated and poorly contracting left ventricle. It is conceivable, in these cases, to classify left ventricular dilatation and poor left ventricular function as secondary to the hypertension itself and to suggest the hypothesis of a cause-effect relationship between therapy and normali- zation of left ventricular parameters with findings of left ventricular hypertrophy. The dilated and poorly contracting left ventricle, which we observed at the first echocardiographic examination, could be due to afterload mismatch In fact, repeated and/or prolonged increased afterload could lead to left ventricular dilatation, which can be considered as a preload reserve, aiming to preserve an adequate stroke volume When the maximal limit of the preload reserve is reached, further increment of afterload could cause reduction of LV function and decreased stroke volume. This condition may not be necessarily associated to depressed myocardial contractility. As reported by Gunther and Grossman,8 in aortic stenosis, poor cardiac performance could be due to inadequate hypertrophy or inappropriate geometry. This could happen even in dilated and poorly contracting left ventricle associated with long-standing chronic hypertension, such as in our cases. Our cases may then represent inappropriate hypertrophy with high that is excess dilatation out of proportion to left ventricular mass. Left ventricular function in hypertensive heart disease depends significantly on heart size and, with similar sys-

6 96 Clin. Cardiol. Vol. 12, February 1989 tolic pressure, on the systolic stress which is imposed to the left ventricular wall.7 Patients with high stress hypertrophy and dilated left ventricle have limited stress reserve but high responsiveness to cardiac unloading interventions. By reducing afterload, blood pressure normalization is achieved, probably allowing the left ventricle to reassume the hypertrophic condition due to systemic hypertension and pre-existent to the development of left ventricular failure. This study is retrospective, and only selected cases are reported. For these reasons, we feel that further experience is needed to clarify the prevalence and to understand the physiopathology of the findings we reported. We think, however, that findings of left ventricular hypertrophy and normalization of left ventricular dimensions and function in patients with long-standing chronic systemic hypertension and previously dilated and poorly contracting left ventricle are documented by our data. These observations may have relevant prognostic and therapeutic implications. References Braunwald E: Heart Disease. WB Saunders Co., Philadelphia (1984) 435, Hurst JW: /he Heart, 5th Ed. McGraw-Hill, New York (1982) I 300- I309 Goodwin JF: The frontiers of cardiomyopathy. Br HearrJ48, 1 (1982) Fuster V, Gersh BJ, Giuliani ER, Tajik AJ, Brandenburg RO, Frye RL: The natural history of idiopathic dilated cardiomyopathy. Am J Cardid 47, 525 (1981) 5. Lam JB, Shub C, Sheps SG: Reversible dilatation of hypertrophied left ventricle in pheochromocytoma: Serial twodimensional echocardiographic observations. Am Heart J 109, 613 (1985) 6. Strauer BE: Myocardial oxygen consumption in chronic heart disease: Role of wall stress, hypertrophy and coronary reserve. Am J Cardiol44, 730 (1979) 7. Strauer BE: Ventricular function and coronary hemodynamics in hypertensive heart disease. Am J Cardiol 44, 999 (1979) 8. Gunther S, Grossman W: Determinants of ventricular function in pressure-overload hypertrophy in man. Circularion 59, 679 ( 1979) 9. Tarazi RC, Levy MN: Cardiac responses to increased afterload. State-of-the-art review. Hypertension 4 (suppl 11) 11, 8 ( 1982) 10. Henry WL, DeMaria A, Gramiak R, King DL, Kisslo JA, Popp RL, Sahn DJ, Schiller NB, Tajik A, Teicholz LE, Weyman AE: Report of the American Society of Echocardiography Committee on Nomenclature and Standards in Two-dimensional Echocardiography. Circulation 62, 2 12 (1980) II. Tajik AJ, Seward JB, Hagler DJ, Mair DD, Lie JT: Twodimensional real-time ultrasonic imaging of the heart and great vessels. Technique, image orientation, structure identification, and validation. Mayo CIin Proc 53, 271 (1978) 12. Sahn DJ, DeMaria A, Kisslo J, Weyman A: Recommendations regarding quantitation in M-mode echocardiography: Results of a survey of echocardiographic measurements. Circulation 58, 1072 (1978) 13. Hirota Y, Shimizu G, Kiyotaka K, Saito T, Kino M, Kawamura K: Mechanisms of compensation and decompensation in dilated cardiomyopathy. Am J Cardiol 54, 1033 (1984) 14. Cohn JN, Mashiro I, Levine TB, Mehta J: Role of vasoconstrictor mechanisms in the control of left ventricular performance of the normal and damaged heart. Am J Cardiol44, 1019 ( 1979) 15. Gaasch WH: Left ventricular radius to wall thickness ratio. Am J Cardiol43, 1 I89 ( 1979)