CARDIOMYOPATHY
Left Atrial Afterload Mismatch in Hypertrophic Cardiomyopathy Hiroto Sanada, MD, Masami Shimizu, MD, Kuniyoshi Shimizu, MD, Yoshihito Kita, MD, Norihiko Sugihara, MD, and Ryoyu Takeda, MD
To investigate left atrial (LA) booster pump function in hypertrophic cardiomyopathy (HC), LA and left ventricular pressure-volume loops were estimated in 5 control subjects, 6 patients with essential hypertension and 11 patients with HC. Investigation of LA preload revealed that LA pressure and volume immediately before LA contraction were both increased in patients with hypertension (10 f 5 mm Hg, 71 f 19 ml/m*) compared with control subjects (7 f 1 mm Hg, 59 f 6 ml/m*), and even more increased in patients with HC (16 f 7 mm Hg, 81 f 25 ml/m*). Investigation of LA afterload revealed that the left ventricular chamber stiffness constant was higher in patients with hypertension (0.035 f 0.015) than in control subjects (0.028 f O.OOS), and even more increased in patients with HC (0.056 f 0.017). LA stroke work index was higher in patients with hypertension (116 f 34 mm Hg . ml) and HC (115 f 19 mm Hg . ml) than in control subjects (87 f 23 mm Hg . ml). Investigation of LA ejection revealed that LA stroke index was higher in patients with hypertension (24 f 5 ml/m*) than in control subjects (18 f 4 ml/m*) and patients with HC (18 f 2 ml/m2), and LA ejection fraction was lower in patients with HC (23 f 6%) than in control subjects (32 f 7%) and patients with hypertension (34 f 8%). In patients with HC, LA function curve showed a shift to the lower right, and LA stroke index was inversely correlated (r = -0.76) with LA afterload. This study suggests that LA booster pump failure due to LA afterload mismatch exists in HC. (AmJ Cardiol 1991;68:1049-1064)
From the Second Department of Internal Medicine, School of Medicine, Kanazawa University, Kanazawa, Japan. Manuscript received February 13, 1991; revised manuscript received June 10, 1991, and accepted June 11. Address for reprints: Hiroto Sanada, MD, Second Department of Internal Medicine, School of Medicine, Kanazawa University, Takaramachi 13-1, Kanazawa 920, Japan.
he left atrium is positioned at the inlet to the left ventricle and functions as a conduit for left ventricular filling. Additionally, during left ventricular systole, the left atrium functions as a reservoir for blood returning from the pulmonary vein. During atria1 systole, the left atrium functions as a pump that actively ejects blood into the left ventricle.1-4 Through its function as a booster pump, the left atrium effectively contributes to the left ventricular Frank-Starling mechanism without an increase in pulmonary arterial pressure.5 In the presenceof left ventricular systolic and diastolic dysfunction or mitral stenosis, all of which interfere with passiveleft ventricular filling, the booster pump function of the left atrium becomesall the more important.6-10 The pathophysiology of hypertrophic cardiomyopathy (HC) is characterized by increased impedance to diastolic filling with increasedventricular stiffness. An interesting question is whether the left atria1 (LA) booster pump function is capable of sufficiently compensating for left ventricular early diastolic filling dysfunction in the caseof HC where left ventricular stiffnessis greatly magnified. We investigated LA booster pump function in HC with respectto LA preload, afterload and ejection characteristics.
T
METHODS Subjects: The study consistedof a control group of 5 patients admitted for evaluation of chest pain in whom no abnormalities were found despite in-depth investigation including cardiac catheterization and angiography. Additionally, we evaluated 6 patients with World Health Organization grades I and II essential hypertension (hypertension group) and 11 patients with HC (HC group). No significant differences in age or sex distribution were noted between the 3 groups (Table I). All patients had normal sinus rhythm, and patients with coexisting angiographically confirmed significant coronary artery stenosisor spasm,diabetes mellitus or other endocrine disease,as well as those with other disorders affecting cardiac function, were excluded. All patients gave informed consent before entering the study. There were no complications attributable to the investigative procedures. Cardiac catheterization and angiography: All medications were discontinued for 2 weeks before catheterLEFT ATRIAL AFTERLOAD MISMATCH
1049
TABLE I Clinical Characteristics and Hemodynamic Parameters Age (yr) & Sex
Pt.
IVS + PW (mm)
Time Constant T (ms)
LV Filling Volume Before LA Contraction (ml/m21
LVEF (%I
43 38 55 37 44 43 2 7
55 49 45 57 43 50 ” 6
64 79 78 77 66 73 f 7
(13,14) (14,12) (14,12) (15,17) (13,121 (19,161 (15 + 2t,14 k 2tj
50 56 47 52 42 47 49 + 5
43 36 59 45 34 52 45 + 9
74 70 80 62 68 65 70 2 7
Hypertrophic Cardiomyopathy
Group
(21,13) (25,12)
72 55 47 60 83 54 48 60 60 47 54 58 !I ll*
47 34 53 46 34 39 35 38 42 37 24 39 k 8*
73 67 69 78 46 41 43 65 63 75 80 64 2 14
ws,
PW) Control Group
1
35 M
2 3 4 5
69 M 67 M 51 F 33 M
Mean f SD
57? 17
19 20 22 19
(9,lO)
(10,lO) (11,ll) (10,9)
17
(8,9)
19 AZ2
(10 z!Y1,lO t 1) Hypertension Group
6 7 8 9 10 11 Mean 2 SD
60 60 43 57 58 64 57
M M M M M F
-c 7
73 67 15 64 67 41 63 62 51 62
12
M M M F M F M M F M 69 M
13 14 15 16 17 18 19 20 21 22 Mean 2 SD
582 17
27 26 26 32 25 35 28 k 4t
34 37 26 45 27 25 32 38
(15,111
(22,231 (17,101 (12,13) (21,111 (25,13)
39
(22,17)
40 33 34 k 6t
(24,16) (19,14) (20 ” 4t,t,14 r 4t1
*p ~0.05; fp co.01 compared with controlgroup: tp
Left Atrial Afterload Mismatch in Hypertrophic Cardiomyopathy Hiroto Sanada, MD, Masami Shimizu, MD, Kuniyoshi Shimizu, MD, Yoshihito Kita, MD, Norihiko Sugihara, MD, and Ryoyu Takeda, MD
To investigate left atrial (LA) booster pump function in hypertrophic cardiomyopathy (HC), LA and left ventricular pressure-volume loops were estimated in 5 control subjects, 6 patients with essential hypertension and 11 patients with HC. Investigation of LA preload revealed that LA pressure and volume immediately before LA contraction were both increased in patients with hypertension (10 f 5 mm Hg, 71 f 19 ml/m*) compared with control subjects (7 f 1 mm Hg, 59 f 6 ml/m*), and even more increased in patients with HC (16 f 7 mm Hg, 81 f 25 ml/m*). Investigation of LA afterload revealed that the left ventricular chamber stiffness constant was higher in patients with hypertension (0.035 f 0.015) than in control subjects (0.028 f O.OOS), and even more increased in patients with HC (0.056 f 0.017). LA stroke work index was higher in patients with hypertension (116 f 34 mm Hg . ml) and HC (115 f 19 mm Hg . ml) than in control subjects (87 f 23 mm Hg . ml). Investigation of LA ejection revealed that LA stroke index was higher in patients with hypertension (24 f 5 ml/m*) than in control subjects (18 f 4 ml/m*) and patients with HC (18 f 2 ml/m2), and LA ejection fraction was lower in patients with HC (23 f 6%) than in control subjects (32 f 7%) and patients with hypertension (34 f 8%). In patients with HC, LA function curve showed a shift to the lower right, and LA stroke index was inversely correlated (r = -0.76) with LA afterload. This study suggests that LA booster pump failure due to LA afterload mismatch exists in HC. (AmJ Cardiol 1991;68:1049-1064)
From the Second Department of Internal Medicine, School of Medicine, Kanazawa University, Kanazawa, Japan. Manuscript received February 13, 1991; revised manuscript received June 10, 1991, and accepted June 11. Address for reprints: Hiroto Sanada, MD, Second Department of Internal Medicine, School of Medicine, Kanazawa University, Takaramachi 13-1, Kanazawa 920, Japan.
he left atrium is positioned at the inlet to the left ventricle and functions as a conduit for left ventricular filling. Additionally, during left ventricular systole, the left atrium functions as a reservoir for blood returning from the pulmonary vein. During atria1 systole, the left atrium functions as a pump that actively ejects blood into the left ventricle.1-4 Through its function as a booster pump, the left atrium effectively contributes to the left ventricular Frank-Starling mechanism without an increase in pulmonary arterial pressure.5 In the presenceof left ventricular systolic and diastolic dysfunction or mitral stenosis, all of which interfere with passiveleft ventricular filling, the booster pump function of the left atrium becomesall the more important.6-10 The pathophysiology of hypertrophic cardiomyopathy (HC) is characterized by increased impedance to diastolic filling with increasedventricular stiffness. An interesting question is whether the left atria1 (LA) booster pump function is capable of sufficiently compensating for left ventricular early diastolic filling dysfunction in the caseof HC where left ventricular stiffnessis greatly magnified. We investigated LA booster pump function in HC with respectto LA preload, afterload and ejection characteristics.
T
METHODS Subjects: The study consistedof a control group of 5 patients admitted for evaluation of chest pain in whom no abnormalities were found despite in-depth investigation including cardiac catheterization and angiography. Additionally, we evaluated 6 patients with World Health Organization grades I and II essential hypertension (hypertension group) and 11 patients with HC (HC group). No significant differences in age or sex distribution were noted between the 3 groups (Table I). All patients had normal sinus rhythm, and patients with coexisting angiographically confirmed significant coronary artery stenosisor spasm,diabetes mellitus or other endocrine disease,as well as those with other disorders affecting cardiac function, were excluded. All patients gave informed consent before entering the study. There were no complications attributable to the investigative procedures. Cardiac catheterization and angiography: All medications were discontinued for 2 weeks before catheterLEFT ATRIAL AFTERLOAD MISMATCH
1049
TABLE I Clinical Characteristics and Hemodynamic Parameters Age (yr) & Sex
Pt.
IVS + PW (mm)
Time Constant T (ms)
LV Filling Volume Before LA Contraction (ml/m21
LVEF (%I
43 38 55 37 44 43 2 7
55 49 45 57 43 50 ” 6
64 79 78 77 66 73 f 7
(13,14) (14,12) (14,12) (15,17) (13,121 (19,161 (15 + 2t,14 k 2tj
50 56 47 52 42 47 49 + 5
43 36 59 45 34 52 45 + 9
74 70 80 62 68 65 70 2 7
Hypertrophic Cardiomyopathy
Group
(21,13) (25,12)
72 55 47 60 83 54 48 60 60 47 54 58 !I ll*
47 34 53 46 34 39 35 38 42 37 24 39 k 8*
73 67 69 78 46 41 43 65 63 75 80 64 2 14
ws,
PW) Control Group
1
35 M
2 3 4 5
69 M 67 M 51 F 33 M
Mean f SD
57? 17
19 20 22 19
(9,lO)
(10,lO) (11,ll) (10,9)
17
(8,9)
19 AZ2
(10 z!Y1,lO t 1) Hypertension Group
6 7 8 9 10 11 Mean 2 SD
60 60 43 57 58 64 57
M M M M M F
-c 7
73 67 15 64 67 41 63 62 51 62
12
M M M F M F M M F M 69 M
13 14 15 16 17 18 19 20 21 22 Mean 2 SD
582 17
27 26 26 32 25 35 28 k 4t
34 37 26 45 27 25 32 38
(15,111
(22,231 (17,101 (12,13) (21,111 (25,13)
39
(22,17)
40 33 34 k 6t
(24,16) (19,14) (20 ” 4t,t,14 r 4t1
*p ~0.05; fp co.01 compared with controlgroup: tp
