Secondary Mitral Regurgitation and Systemic Hypertension * M. Gueron, M.D.; M. Hirsch, M.D.; E. Rosenman, M.D.; and
]. Borman. M.D.
Six patients are reported with heart failure, secondary mitral insufficiency and systemic hypertension. The hypertension was labile, frequently accentuated during cardiac failure, although recorded, as well, during periods of compeJlS&o don, The normotensive periods in aU patients were unrelated to the antihypertensive therapy. Five underwent hemodynamic studies: the results revealed severe pulmonary hypertension, with impaired left ventricular function; the incompetence was graded moderate to "large." Four patients were operated on: one survived longer than seven months. The mitral valve was normal in aU. Heart failure was not improved by surgery. Postoperative hemodynamic studies were similar to those prior to operation, despite normal function of the prostheses. The mitral regurgitation was attributed to distortion of the spatial relationships between the paplUary musCles and the mitral valve. The effects of systemic hypertension on mitral regurgitation are discussed. The present study suggests that patients with secondary mitral incompetence with tall V waves and elevated left ventricular filling pressures would not benefit from valve replacement, in particular those with disease below the mitral atrioventricular ring, such as hypertension or cardiomyopathy.
The association of secondary mitral insufficiency and systemic hypertension has not been fully appreeiated.!" This report describes the clinical and hemodynamic abnormalities in six patients with systemic hypertension and secondary mitral incompetence. Furthermore, we analyzed the responses to valve replacement in four of these patients and correlated it with the hemodynamic data in order to evaluate the merits of surgery. METHODS AND MATERIAL
Six patients with secondary mitral insufficiency and systemic hypertension were observed between 1965 and 1971. None gave a history of rheumatic fever, myocardial infarction, bacterial endocarditis or chest trauma. One patient had a systolic murmur recorded before the age of 40 years. Five patients underwent right and left heart catheterization, with left ventriculography. Coronary arteriography was performed °From the Cardiac Laboratory and Department of Radiology, the Negev Central Hospital, Beersheva, The Department of Pathology and the Department of Cardiac Surgery, Hadassah University Hospital, Jerusalem, Israel. Reprint requests: Dr. Gueron, Negev Central Hospital, Beersheoa, Israel
CHEST, VOL. 63, NO.4, APRIL, 1973
in four, with repeat postoperative hemodynamic studies in
two. Four patients underwent mitral valve replacement with Starr Edwards prostheses; only one survived longer than seven months. REsULTS
The known duration of hypertension varied from six months to 15 years (Table 1). All patients denied a previous history of kidney disease or family history of hypertension. The hypertension was not sustained or stable. Frequent episodes of normotension, unrelated to the antihypertensive treatment, were observed. Commonly high recordings during periods of congestive heart failure alternated frequently with normal blood pressure during stages of cardiac compensation, although high recordings were also observed in the absence of heart failure. The presenting symptom in patients 1-5 was sudden severe left heart failure; patient 6 became decompensated ten years prior to first hospital visit. The cardiac failure was usually progressive, and poorly responsive to medical treatment.
547
548
GUERON ET AL Table l--Clinical Findings in Si% Patients with Hypertennon and Secondary Mitral Incompetence.
Patient, No.
Age, Yr
Sex
Hypertension, Duration
Murmur, Duration
CHF, Duration
BP,mm Hg
2 3
I
53 59 55
M F
12mOB 10 yrs 6mos
12 mOB 10 yrs 6yrs
12 mOB 6mos 6 mOB
170/130 180/120 160/110
4 5 6
66 56 47
5yrs 6 mOB 15 yrs
6mos 6yrs 13 yrs
6mos 311l()l1
210/120 160/90 210/110
F
M M F
Hypertension preceded the known duration of the murmur in three patients, and the apical murmur preceded the hypertension in two (Table 1). The murmur was persistent, usually loud, blowing and occasionally harsh or sea gull in quality. Additional cardiac sounds, confirmed by phonocardiography, were heard in most of the group during the observation period (Table 2). All patients remained in sinus rhythm: paroxysmal atrial fibrillation was recorded in two patients during the initial episode of pulmonary edema. They responded to treatment, and sinus rhythm was re-established. Postoperative atrial fibrillation was recorded in three, and remained chronic in one patient (Table 3). The chest roentgenogram did not reveal uniform changes: the heart size was grossly enlarged in patient 2 and mildly to moderately enlarged in the other five ( Fig 1). Valvular calcification was not observed. Cardiac catheterization showed markedly elevated pulmonary wedge pressure, with a pulse contour consistent with severe mitral incompetence (Table 4). There was no gradient across the aortic valve. The coronary arteriograms did not reveal any changes. The sudden and progressive heart failure with the abnormal hemodynamics prompted surgical intervention in patients 1, 2, 3 and 4. At surgery the mitral valve was structurally normal, with the chordae tendineae intact. The annulus was large, and the surgeon reported posterior mitral leaflet insufficiency. Starr Edwards valves of different size were inserted; the mitral leaflets, chordae tendineae and the tips of the papillary muscles were excised. The microscopic findings of the excised valves did not reveal any specific changes.
lOyrs
Death, Cause Heart failure, 7 mos postoperative Heart failure,3 mOB postoperative CHF, postcardioveraion, 3 wks postoperative
The leaflets in patients 1 and 2 were normal. In patients 3 and 4 there was minimal lymphocytic infiltration with small fibrotic nodules at the leaflet edges, but there was no calcification or vascularization. Postoperative hemodynamic studies in two patients seven months after surgery revealed that none had benefited from the valve replacement (Table 5). Three patients died; necropsy was performed in all. The heart weighed 400 gm in patient 3, 750 gm in patient 1 and 1,000 gm in patient 2. The specimens showed severe biventricular hypertrophy. Leakage around the prostheses was not present. Prominent endocardial fibrotic thickening of the left ventricle was present in all, possibly related to the mitral prosthesis. The microscopic findings revealed extensive interstitial patchy fibrotic areas in the myocardium. Aschoff bodies were not present. Both large and small coronary vessels were of normal patency and caliber, with minimal sclerotic changes in the right coronary artery in patient 3 and in the left coronary artery in patient 1. DISCUSSION
The association of hemodynamically significant mitral insufficiency and systemic hypertension is not a common feature and is rarely observed. 1 The effects of hypertension on the regurgitant flow of blood has been investigated in animals" and in man" by acutely raising the systemic resistance. The effects of changes of arterial pressure on mitral regurgitation vary considerably among different patients, depending on the nature of the mitral valve disease and the functional state of the myo-
Table 2--Physical and Auscultatory Data in Patients with Heart Failure
Patient, No.
LV Impulse
81
82
1 2 3 4 5
widespread not palpable double humped widespread widespread widespread
normal normal normal faint faint normal
fixed split single normal split single normal split normal split
6
83-S4 84 84 83+84 83+84
Murmur sea gull harsh grade 3/6 blowing grade 2/6 blowing grade 3/6 sea gull harsh grade 3/6 blowing grade 2/6 blowing harsh 3/6
CHEST, VOL. 63, NO.4, APRIL, 1973
SECONDARY MITRAL REGURGITATION AND SYSTEMIC HYPERTENSION Table 3-Electrocardi06rapmc Chan6e. in Group 01 Si% PatienU Patient, No.
PR
AF
LVH
Axis
P Mitrale
1 2 3 4 5 6
0,12 0,14 0,16 0,16 0,16 0,12
PO· PA" PO· PO· PA"
?
+ +
-30
+
-10
+ + + +
+ + +
0 +50 + 30 +60
"Postoperative atrial fibrillation. "Paroxysmal atrial fibrillation.
cardium.'? The structural nature of the valve lesion determines whether the incompetence varies under different functional conditions or remains fixed. In the latter case raising the blood pressure will cause changes in the regurgitant flow, depending on the changes in pressure gradient across the mitral valve; changes in the myocardial factor will hardly affect the incompetence. In the former case the insufficiency will increase when the blood pressure is raised and will largely depend on the functional state of the myocardium." In these patients the regurgitation is increased during periods of congestive heart failure, leading to a vicious circle, with more left ventricular dilation and more incompetence. This was assumed to be the sequence of events in our patients. Evidently, the hypertension in the presence of the impaired' left ventricular function was of major importance in determining the severity of the incompetence in our patients in
failure. lUI It has been reported that the regurgitation Is generally less in secondary incompetence, caused by myocardial dysfunction and left ventricular dilation." The opposite was observed in our patients in whom the regurgitant flow was moderate to large: this, we attributed to the effects of the systemic hypertension on the impaired myocardial function. lO •n In addition, the possibility of diminished left ventricular compliance, related to the extensive fibrosis, was also taken in consideration to explain the magnitude of the incompetence. The tall V waves are generally believed to indicate free communication between the left atrium and the left ventricle, but, also, to a noncompliant left atrium indicating that the mitral regurgitation is of recent origin. Therefore, it has been assumed that these patients, with a short history of heart failure, should benefit most likely from surgery.13.14 It would also seem from a recent communication' that patients who had sustained distortion of the spatial relationships of the papillary muscles due to changes in the left ventricle with V waves above 40 mmHg should be candidates for mitral valve prostheses. The poor results in our small group and the postoperative hemodynamic data do not support the statement that surgery is of benefit in such patients; elevated left ventricular filling pressures and tall V waves are not consistently present only in patients with primary disease of
FIGURE 1. Chest roentgenograms of patients 1-6 with secondary mitral incompetence and systemic hypertension. Mitral configuration was suspected in patients 2 and 5.
CHEST, VOL. 63, NO.4, APRIL, 1973
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550
GUERON ET AL Table 4o--Hemodynamic Daaa in Group with Heart Failure.
Patient, No.
RA
RV
PA
PAW LVEDP CI
CO
BA
2,5
Reflux* Contractility** RCAt
LMCAtt
a:27 91/18 96/45 a:49 v:23 m:67 v:59 m:18 m:41
39
1,3
177/108 m:136
3+
poor
minor irregularities
1,46 2,22 181/109 m:136
3+
good
minor irregularities
167/95 m:125
3+
good
4,18 190/86 m:127
3+
good
1,67 2,89 165/83 m:114
2+
poor
2
m:12 90/11
97/49 v:38 m:64 m:30
22
3
a:26 74/22 81/33 a:38 v:12 m:46 v:43 m:31 m:18
28
4
a:12 42/10 46/24 m:18 m:32
a:39 v:37 m:20
5
a:9 m:6
a:30 v:44 m:29
56/7
63/37 m:4O
2,6
2,2
31
minor irregularities both RCA, LMCA
normal normal
*Graded 1 to 3 + **Graded poor, good, excellent tRight coronary artery ttMain left coronary artery (left anterior descending, left circumflex were normal in all patients)
the mitral valve, but, also, in patients with primary muscle dysfunction and secondary mitral regurgitation." Such patients with primary disease below the atrioventricular ring have marked changes in the left ventricular hemodynamics; therefore, the presence of tall V waves, severe regurgitation and relatively moderately enlarged left atrium is not always a guarantee for surgical success. Since the myocardial factor is crucial in determining the surgical outcome of valve replacement, any possible means have been used to evaluate the ventricular performance in secondary or nonrheumatic mitral incompetence. Left cineventriculography' has often been relied upon to assess the integrity of the myocardial function and the degree of incompetence, although the data are subject to individual interpretation. We also relied on the integrity of myocardial contractions in the cineangiography in our patients, as well on the height of the V Waves, as an important criterion for advising surgery. Unfortunately, despite adequate contractions, the results were not encouraging. Apparently, evaluation of the relative contribution of each (the myocardial factor and the mitral regurgitation) is extremely difficult, and in these severely disabled patients the left ventricular damage is sufficient to
assure their death. In conclusion, we are inclined to believe that patients with secondary mitral incompetence, with disease below the mitral atrioventricular ring, with tall pulmonary wedge V waves and considerable regurgitation would not benefit from valve replacement. Mitral valve replacement is probably unrewarding, since the routine hemodynamic data do not always provide definite information concerning the state of the myocardium, which is the decisive point in surgical success. REFERENCES
1 Klughaupt M, Flamm MD, Hancock EW, et al: Non rheumatic mitral insufficiency. Circulation 39:307, 1969 2 Friedberg CK: Diseases of the Heart. Philadelphia, W. B. Saunders Co, 1966, p 1486 3 Laurie HC: Mitral valve disease and hypertension. Scott Moo J 13:152, 1968 4 Mickerson IN: Heart failure in hypertensive patients. Am Heart J 65:267, 1963 5 Puchner TC, Hyuston JH, Hellmuth GA: Heart sounds and murmurs in arterial hypertension. Am J Cardiol 6:630,1960 6 Barlow J, Kincaid-Smith P: The auscultatory findings in hypertension. Br Heart J 22:505, 1960 7 Fisberg AM: Hypertension and Nephritis. Philadelphia, Lea & Febiger, 1954, p 782
Table S--Po.toperad"e Hemodynamic Data in Two Paden,.
Patient, No.
4
RA
RV
PA
PAW
a:4O v:30 m:24
105/29
105/45 m:64
a:37 v:49 m:39
v:14 m:11
47/6
46/26 m:34
v:39 m:27
LVEDP
24
CI
CO
BA
Reflux
1,75
3,17
193/123 m:137
None
2,69
4,8
213/104 m:l09
None
CHEST, VOL. 63, NO.4, APRIL, 1973
SECONDARY MITRAL REGURGITATION AND SYSTEMIC HYPERTENSION 8 Braunwald E, Welch GH, Morrow AG: Hemodynamic effects of quantitatively varied experimental mitral insufficiency. Circ Res 5:539, 1957 9 Braunwald E, Welch GH, Morrow AG: The effects of acutely increased systemic resistance on the left atrial pressure pulse: a method for clinical detection of mitral insufficiency. J Clin Invest 37:35, 1958 10 Jose AD, Taylor RR, Bernstein L: The influence of arterial pressure on mitral incompetence in man. J Clin Invest 43:2094, 1964 11 Ross J, Braunwald E: The study of left ventricular func-
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tion in man by increasing resistance to ventricular ejection with angiotensin. Circulation 29:739, 1964 12 Cohen KE, Kao BS, Russell JAG: Force generation and shortening capability of the left ventricular myocardium in primary and secondary forms of mitral regurgitation. Br Heart J 31:474, 1969 13 Manhas DR, Hessel EA, Winterscheid LC, et al: Repair of mitral incompetence secondary to ruptured chordae tendinae. Circulation 43:688, 1971 14 Sanders CA, Armstrong PW, Willerson JT, et al: Etiology and differential diagnosis of acute mitral insufficiency. Prog Cardiovasc Dis 14:129, 1971
Mitropoulos (1897-1960) and His Animated Performance Mitropoulos on the podium seemingly had given music another dimension, a transcendence above and beyond itself. With the first down beat he started punching the air bare-handed, unleashing a weird repertoire of frenzied gestures and scowls and grimaces that registered every emotion from terror to ecstasy. His quivering frame and flailing ·fists gave the picture of a man quaking with a peculiarly vital and rhythmic form of palsy. It was as if the music were an electric current that passed
CHEST, VOL. 63, NO.4, APRIL, 1973
through his body to make it jerk and vibrate. The impression was that of a leader pulling tone from ninety instruments by almost physical coercion that tied him by invisible bonds to each musician before him. Sherman JK: Music and Maestros -The Story of the Minneapolis Symphony Orchestra, Minneapolis, University of Minnesota Press, 1952