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Hemodynamics of mitral valve disease as altered by systemic hypertension
Hemodynamics Altered ZAVEN
of Mitral
by Systemic A. ADROUNY,
M.D. and
Portland,
Valve Disease as Hypertension*
HERBERT
E. GRISWOLD, M.D.
Oregon
T
gitation, probable mitral stenosis and moderate left atria1 enlargement. An electrocardiogram revealed atria1 fibrillation with a ventricular response of 80 per minute and S-T and T changes suggestive of left ventricular hypertrophy, digitalis effect, or both. The patient’s management consisted of bed rest, digitalis given to maximum tolerance, reserpine, chlorothiazide and sodium mercaptomerin following loading with ammonium chloride. She lost 6 pounds on this regimen in about 10 days and maintained a stable weight for another 11 days. At the end of this period it was felt that she had attained a “dry weight” and full cardiac compensation. Right heart catheterization was then performed through the right saphenous approach. Unfortunately, an attempt to enter the left atrium by transatrial septal puncture3 was technically unsuccessful ; the Ross needle could not be advanced beyond the level of the renal vessels. Table I shows the hemodynamic data. Renal Studies: The patient’s blood pressure decreased from 220/120 to 140/90 mm. Hg with medical management during the initia.1 eight weeks of hospitalization. Studies as to the cause of her hypertension meanwhile revealed the following pertinent findings : a small right kidney with a small pelvic and calyceal system noted on the intravenous and retrograde pyelograms; a narrowing of the right renal artery at its origin from the aorta demonstrated on abdominal aortography. Surgery: At abdominal exploration, narrowing of the right renal artery was confirmed. The right kidney was small and displayed a depression in its middle portion consistent with an old infarction. An aorticorenal artery anastomosis was performed with a Dacron@ graft. The postoperatke course was uneventful. Her blood pressure decreased to 120/80 mm. Hg by the fourth postoperative day and was maintained without medication until her discharge three weeks later. She was readmitted five and a half months postoperatively for reevaluation of her cardiac status. She had felt much improved and reported a notable in-
HE EFFECT of transient systemic hypertension induced by pharmacologic agents on the hemodynamics of mitral valve disea.se has been noted.‘!* To our knowledge, however, the hemodynamic effect of clinical systemic hypertension has not been documented. This report concerns a patient who has inactive rheumatic heart disease and who had systemic hypertension as a result of renal artery stenosis. Successful surgical correction of the hypertension provided a unique opportunity for recording the influence of systemic hypertension on the hemodynamics of the diseased mitral valve.
CASE REPORT Mrs. M. B., a 40 year old woman, was admitted to the University of Oregon Medical School with a history of exertional dyspnea of two to three years’ duration, treated with digitalis and diuretics. She had rheumatic fever at the ages of 8 and 14 years. At no time was she told that she had hypertension. Physical examination on admission showed the following positive findings: blood pressure of 220/l 10 mm. moderate cardiomegaly; a grade 2/6 panHg; systolic murmur with a grade 3 mid-diastolic rumble over the apex; a grade 1 systolic ejection murmur over the aortic area and a grade 1 early diastolic murmur over the left third intercostal space. Laboratory jindings, including routine hemogram, urinalysis, sedimentation rate, serum electrolytes, protein-bound iodine and 24 hour 1’3’ uptake were unremarkable. X-ray films of the chest revealed cardiac enlargement, a double density within the cardiac silhouette, elevation of the left main stem bronchus, prominence of the central pulmonary artery and some enlargement of the vascular markings. Barium swallow showed dorsal displacement of the esophagus consistent with left atria1 enlargement. Left heart angiocardiography demonstrated aortic regurgitation with no systolic gradient across the aortic valve, mitral regur-
* From the Division of Cardiology, Department of Medicine, University of Oregon Medical School, Portland, Orego*. This study was supported by a Cardiovascular Clinical Research Center grant (H-6336) from the National Heart Institute, National Institutes of Health, U. S. Public Health Service. JANUARY
1963
97
Adrouny
98
and Griswold TABLE I
Cardiac Catheterization
Data Prior to and Following
Successful Surgical
Correction
Preoperative Pressures (mm. Hg) RA mean RV systolic end-diastolic PA (resting) systolic diastolic mean PA (with exercise) systolic diastolic Wedge (resting) mean Wedge (with exercise) mean LFA (resting) systolic diastolic mean peak time rise velocity of anacrotic limb CO (resting) (L./min.) CO (with exercise) Cardiac index (resting) (L. /min. /Ms.) Cardiac index (with exercise) PVR (dynes sec. cm. -5) Total PVR SVR Heart rate (resting)
of Systemic Hypertension Postoperative
12 62 13 62 38 47 not done
1 39 2 39 16 29 66 36 10 16 132 74 90 0.12 sec. 822 mm.Hg/sec. 3.58 4.99 2.25 3.14 424 647 1987 72/min.
27 not done 188 92 124 0.12 sec. 1100 mm.Hg/sec. 3.74 not done 2.35 not done 427 1004 2393 72/min.
PA = pulmonary artery; Wedge = pulmonary wedge pressure (reRA = right atrium; RV = right ventricle; corded at two different sites preoperatively and at three postoperatively); LFA = left femoral arteriogram obtained PVR = pulmonary through an indwelling arterial needle; CO = cardiac output determined by the Fick principle. vascular resistance calculated as follows: Mean PA -
Mean Wedee
CO in cc./sec. Total PVR
= total pulmonary vascular resistance calculated P.4
Mean
CO in cc./sec. SVR
= systemic vascular resistance calculated
X 1.332
as follows: X 1.332
as follows:
Mean LFA
-
Mean RA
CO in cc./sec. Exercise consisted of straight for six minutes; _ leg-raising of the elevated resting wedge and PA pressures.
The physical excrease in her exercise tolerance. amination was essentially unchanged. The blood A second right heart pressure was 120/70 mm. Hg. catheterization through a branch of the right basilic The data are listed in Table I. vein was performed. The patient was then discharged for follow-up in the outpatient clinic.
COMMENTS This patient has rheumatic heart disease with involvement of the mitral and aortic valves. Clinically, she has predominant mitral stenosis with mild mitral and aortic regurgitation. In
X 1.332
patient was not subjected
to exercise preoperatively
in view
addition, she had systemic hypertension due to stenosis of a renal artery. The latter responded dramatically to an aortico-renal artery bypass. Cardiac catheterization before surgical correction of hypertension indicated a severe degree of mitral valve disease. It should he noted that this study was carried out after prolonged, intensive medical management in the hospital and a period of full cardiac compensation. The resting pulmonary wedge pressure was 27 mm. Hg, which suggested a marked degree of mitral valve
pathology. THE
The AMERICAN
hemodynamic JOURNAL
OF
studies
CARDIOLOGY
Mitral
Valve Disease and Hypertension
following the return to normotension revealed a normal resting wedge pressure (10 mm. Hg). It is therefore obvious that the patient did not have as severe mitral valve disease as was suggested by the initial catheterization studies. That she did have mitral valve involvement is evidenced by the elevation of the wedge pressure with exercise, and the physical, radiologic and angiocardiographic findings. The left ventricular end-diastolic pressure could not be we believe that this measured ; nevertheless, difference in her resting wedge pressures is due to occult left ventricular failure secondary to her systemic hypertension (and to a lesser degree, her aortic valve disease). It cannot be attributed to a change in heart rate since the latter was identical during both studies. Transient systemic hypertension induced by norepinephrine’ or methoxamine (Vasoxyl@)2 infusion has been shown to significantly increase the left atria1 or pulmonary wedge pressure in mitral valve disease. Similar observations in animals have been noted with experimental mitral valve disease induced by aortic constriction.4-7 It has been further shown that essential hypertension may be associated with elevated wedge pressures at rest in the absence of valvular disease and clinical evidence of heart failure.8 It is evident from these studies, as well as our case, that systemic hypertension may significantly alter mitral valve hemodynamics. It is obvious then that considerable caution should be exercised in the interpretation of left atria1 or pulmonary wedge pressures when assessing the degree of mitral valve disease in the presence of systemic hypertension. Knowledge of the left ventricular end-diastolic pressure would be extremely helpful in this circumstance. The primary change in the postoperative hemodynamic data appears to be a reduction in the systemic vascular resistance with subsequent fall of systemic arterial pressure, left ventricular load and the left atria1 (wedge) pressure. No significant change in the pulmonary vascular resistance is noted. The diminution in the pressures of the pulmonary artery and right chambers of the heart is, therefore, a reflection of the alteration in the left atria1 pressure. The reliability of the preoperative wedge pressure may be questioned. Occasional false elevation of this pressure is well recognized and emphasized by several authors.s-ll However,
JANUARY 1963
99
we believe it is reliable since (1) it was recorded at two different sites with identical values, (2) there was a decrease in the postoperative pulmonary artery and right ventricular pressures equivalent to the fall in the wedge pressure, and (3) no significant change was noted in the preand postoperative pulmonary vascular resistance.
SUMMARY A patient who has rheumatic heart disease with predominant mitral valve involvement and who had systemic hypertension as a result of renal artery stenosis is presented. The hemodynamic changes resulting from surgical correction of the hypertension are discussed. The dieculty in interpreting pulmonary wedge or left atria1 pressures in assessing the degree of mitral valve disease in the presence of systemic hypertension is emphasized.
REFERENCES 1. BRAUNWALD,E., WELCH, G. H., JR., SARNOFF, S. J. and MORROW, A. G. Hemodynamic effects of quantified mitral regurgitant flow. J. Clin. Znvest., 36:876,1957. 2. STANFIELD, A. and Yu, P. N. Hemodynamic effects of methoxamine in mitral valve disease. Circulation Rex., 8: 859, 1960. 3. Ross, J., JR. Transseptal left heart catheterization; a new method of left atria1 puncture. Ann. Surg., 149: 395,1959. 4. WICGERS, C. J. and FEIL, H. The cardiodynamics of mitral insufficiency. Heart, 9 : 149, 1922. 5. CRAWSHAW, G. R., WILSON, V. H., KREEL, L., VETTEN, K. B. and BORMAN,J. B. Experimental mitral incompetence in dogs. Studies in hemodynamics. Brit. J. +rg., 42: 319, 1954. 6. MOSCOVITZ,H. L. and WILDER, R. J. The pressure events of the cardiac cycle in the dog. Mitral valve lesions. Am. Heart J., 53: 741, 1957. 7. BRAUNWA~D,E., WELCH, G. H., JR. and SARNOFF, S. J. Hemodynamics of quantitatively varied mitral regurgitation. Circulation experimental Res., 5: 539, 1957. 8. TAYLOR, S. H., DONALD, K. W. and BISHOP, J. M. Circulatory studies in hypertensive patients at rest and during exercise. Clin. SC., 16: 351, 1957. 9. BERNSTEIN,W. H., EUGENE, F. M., LASZLO, M. H., SAMET, P. and LITWAK, R. S. The interpretation of pulmonary artery wedge (pulmonary capillary) pressures. Brit. Heart J., 22: 37, 1960. 10. MURPHY, J. P. Inaccuracy of wedge pressure as an Circulaindex of pulmonary capillary pressure. tion, 17: 199,1958. 11. PEDERSEN, A. The Venous Pressure in the Pulmonary Circulation, p. 64. Copenhagen, 1956. Arnold Busck.
of Mitral
by Systemic A. ADROUNY,
M.D. and
Portland,
Valve Disease as Hypertension*
HERBERT
E. GRISWOLD, M.D.
Oregon
T
gitation, probable mitral stenosis and moderate left atria1 enlargement. An electrocardiogram revealed atria1 fibrillation with a ventricular response of 80 per minute and S-T and T changes suggestive of left ventricular hypertrophy, digitalis effect, or both. The patient’s management consisted of bed rest, digitalis given to maximum tolerance, reserpine, chlorothiazide and sodium mercaptomerin following loading with ammonium chloride. She lost 6 pounds on this regimen in about 10 days and maintained a stable weight for another 11 days. At the end of this period it was felt that she had attained a “dry weight” and full cardiac compensation. Right heart catheterization was then performed through the right saphenous approach. Unfortunately, an attempt to enter the left atrium by transatrial septal puncture3 was technically unsuccessful ; the Ross needle could not be advanced beyond the level of the renal vessels. Table I shows the hemodynamic data. Renal Studies: The patient’s blood pressure decreased from 220/120 to 140/90 mm. Hg with medical management during the initia.1 eight weeks of hospitalization. Studies as to the cause of her hypertension meanwhile revealed the following pertinent findings : a small right kidney with a small pelvic and calyceal system noted on the intravenous and retrograde pyelograms; a narrowing of the right renal artery at its origin from the aorta demonstrated on abdominal aortography. Surgery: At abdominal exploration, narrowing of the right renal artery was confirmed. The right kidney was small and displayed a depression in its middle portion consistent with an old infarction. An aorticorenal artery anastomosis was performed with a Dacron@ graft. The postoperatke course was uneventful. Her blood pressure decreased to 120/80 mm. Hg by the fourth postoperative day and was maintained without medication until her discharge three weeks later. She was readmitted five and a half months postoperatively for reevaluation of her cardiac status. She had felt much improved and reported a notable in-
HE EFFECT of transient systemic hypertension induced by pharmacologic agents on the hemodynamics of mitral valve disea.se has been noted.‘!* To our knowledge, however, the hemodynamic effect of clinical systemic hypertension has not been documented. This report concerns a patient who has inactive rheumatic heart disease and who had systemic hypertension as a result of renal artery stenosis. Successful surgical correction of the hypertension provided a unique opportunity for recording the influence of systemic hypertension on the hemodynamics of the diseased mitral valve.
CASE REPORT Mrs. M. B., a 40 year old woman, was admitted to the University of Oregon Medical School with a history of exertional dyspnea of two to three years’ duration, treated with digitalis and diuretics. She had rheumatic fever at the ages of 8 and 14 years. At no time was she told that she had hypertension. Physical examination on admission showed the following positive findings: blood pressure of 220/l 10 mm. moderate cardiomegaly; a grade 2/6 panHg; systolic murmur with a grade 3 mid-diastolic rumble over the apex; a grade 1 systolic ejection murmur over the aortic area and a grade 1 early diastolic murmur over the left third intercostal space. Laboratory jindings, including routine hemogram, urinalysis, sedimentation rate, serum electrolytes, protein-bound iodine and 24 hour 1’3’ uptake were unremarkable. X-ray films of the chest revealed cardiac enlargement, a double density within the cardiac silhouette, elevation of the left main stem bronchus, prominence of the central pulmonary artery and some enlargement of the vascular markings. Barium swallow showed dorsal displacement of the esophagus consistent with left atria1 enlargement. Left heart angiocardiography demonstrated aortic regurgitation with no systolic gradient across the aortic valve, mitral regur-
* From the Division of Cardiology, Department of Medicine, University of Oregon Medical School, Portland, Orego*. This study was supported by a Cardiovascular Clinical Research Center grant (H-6336) from the National Heart Institute, National Institutes of Health, U. S. Public Health Service. JANUARY
1963
97
Adrouny
98
and Griswold TABLE I
Cardiac Catheterization
Data Prior to and Following
Successful Surgical
Correction
Preoperative Pressures (mm. Hg) RA mean RV systolic end-diastolic PA (resting) systolic diastolic mean PA (with exercise) systolic diastolic Wedge (resting) mean Wedge (with exercise) mean LFA (resting) systolic diastolic mean peak time rise velocity of anacrotic limb CO (resting) (L./min.) CO (with exercise) Cardiac index (resting) (L. /min. /Ms.) Cardiac index (with exercise) PVR (dynes sec. cm. -5) Total PVR SVR Heart rate (resting)
of Systemic Hypertension Postoperative
12 62 13 62 38 47 not done
1 39 2 39 16 29 66 36 10 16 132 74 90 0.12 sec. 822 mm.Hg/sec. 3.58 4.99 2.25 3.14 424 647 1987 72/min.
27 not done 188 92 124 0.12 sec. 1100 mm.Hg/sec. 3.74 not done 2.35 not done 427 1004 2393 72/min.
PA = pulmonary artery; Wedge = pulmonary wedge pressure (reRA = right atrium; RV = right ventricle; corded at two different sites preoperatively and at three postoperatively); LFA = left femoral arteriogram obtained PVR = pulmonary through an indwelling arterial needle; CO = cardiac output determined by the Fick principle. vascular resistance calculated as follows: Mean PA -
Mean Wedee
CO in cc./sec. Total PVR
= total pulmonary vascular resistance calculated P.4
Mean
CO in cc./sec. SVR
= systemic vascular resistance calculated
X 1.332
as follows: X 1.332
as follows:
Mean LFA
-
Mean RA
CO in cc./sec. Exercise consisted of straight for six minutes; _ leg-raising of the elevated resting wedge and PA pressures.
The physical excrease in her exercise tolerance. amination was essentially unchanged. The blood A second right heart pressure was 120/70 mm. Hg. catheterization through a branch of the right basilic The data are listed in Table I. vein was performed. The patient was then discharged for follow-up in the outpatient clinic.
COMMENTS This patient has rheumatic heart disease with involvement of the mitral and aortic valves. Clinically, she has predominant mitral stenosis with mild mitral and aortic regurgitation. In
X 1.332
patient was not subjected
to exercise preoperatively
in view
addition, she had systemic hypertension due to stenosis of a renal artery. The latter responded dramatically to an aortico-renal artery bypass. Cardiac catheterization before surgical correction of hypertension indicated a severe degree of mitral valve disease. It should he noted that this study was carried out after prolonged, intensive medical management in the hospital and a period of full cardiac compensation. The resting pulmonary wedge pressure was 27 mm. Hg, which suggested a marked degree of mitral valve
pathology. THE
The AMERICAN
hemodynamic JOURNAL
OF
studies
CARDIOLOGY
Mitral
Valve Disease and Hypertension
following the return to normotension revealed a normal resting wedge pressure (10 mm. Hg). It is therefore obvious that the patient did not have as severe mitral valve disease as was suggested by the initial catheterization studies. That she did have mitral valve involvement is evidenced by the elevation of the wedge pressure with exercise, and the physical, radiologic and angiocardiographic findings. The left ventricular end-diastolic pressure could not be we believe that this measured ; nevertheless, difference in her resting wedge pressures is due to occult left ventricular failure secondary to her systemic hypertension (and to a lesser degree, her aortic valve disease). It cannot be attributed to a change in heart rate since the latter was identical during both studies. Transient systemic hypertension induced by norepinephrine’ or methoxamine (Vasoxyl@)2 infusion has been shown to significantly increase the left atria1 or pulmonary wedge pressure in mitral valve disease. Similar observations in animals have been noted with experimental mitral valve disease induced by aortic constriction.4-7 It has been further shown that essential hypertension may be associated with elevated wedge pressures at rest in the absence of valvular disease and clinical evidence of heart failure.8 It is evident from these studies, as well as our case, that systemic hypertension may significantly alter mitral valve hemodynamics. It is obvious then that considerable caution should be exercised in the interpretation of left atria1 or pulmonary wedge pressures when assessing the degree of mitral valve disease in the presence of systemic hypertension. Knowledge of the left ventricular end-diastolic pressure would be extremely helpful in this circumstance. The primary change in the postoperative hemodynamic data appears to be a reduction in the systemic vascular resistance with subsequent fall of systemic arterial pressure, left ventricular load and the left atria1 (wedge) pressure. No significant change in the pulmonary vascular resistance is noted. The diminution in the pressures of the pulmonary artery and right chambers of the heart is, therefore, a reflection of the alteration in the left atria1 pressure. The reliability of the preoperative wedge pressure may be questioned. Occasional false elevation of this pressure is well recognized and emphasized by several authors.s-ll However,
JANUARY 1963
99
we believe it is reliable since (1) it was recorded at two different sites with identical values, (2) there was a decrease in the postoperative pulmonary artery and right ventricular pressures equivalent to the fall in the wedge pressure, and (3) no significant change was noted in the preand postoperative pulmonary vascular resistance.
SUMMARY A patient who has rheumatic heart disease with predominant mitral valve involvement and who had systemic hypertension as a result of renal artery stenosis is presented. The hemodynamic changes resulting from surgical correction of the hypertension are discussed. The dieculty in interpreting pulmonary wedge or left atria1 pressures in assessing the degree of mitral valve disease in the presence of systemic hypertension is emphasized.
REFERENCES 1. BRAUNWALD,E., WELCH, G. H., JR., SARNOFF, S. J. and MORROW, A. G. Hemodynamic effects of quantified mitral regurgitant flow. J. Clin. Znvest., 36:876,1957. 2. STANFIELD, A. and Yu, P. N. Hemodynamic effects of methoxamine in mitral valve disease. Circulation Rex., 8: 859, 1960. 3. Ross, J., JR. Transseptal left heart catheterization; a new method of left atria1 puncture. Ann. Surg., 149: 395,1959. 4. WICGERS, C. J. and FEIL, H. The cardiodynamics of mitral insufficiency. Heart, 9 : 149, 1922. 5. CRAWSHAW, G. R., WILSON, V. H., KREEL, L., VETTEN, K. B. and BORMAN,J. B. Experimental mitral incompetence in dogs. Studies in hemodynamics. Brit. J. +rg., 42: 319, 1954. 6. MOSCOVITZ,H. L. and WILDER, R. J. The pressure events of the cardiac cycle in the dog. Mitral valve lesions. Am. Heart J., 53: 741, 1957. 7. BRAUNWA~D,E., WELCH, G. H., JR. and SARNOFF, S. J. Hemodynamics of quantitatively varied mitral regurgitation. Circulation experimental Res., 5: 539, 1957. 8. TAYLOR, S. H., DONALD, K. W. and BISHOP, J. M. Circulatory studies in hypertensive patients at rest and during exercise. Clin. SC., 16: 351, 1957. 9. BERNSTEIN,W. H., EUGENE, F. M., LASZLO, M. H., SAMET, P. and LITWAK, R. S. The interpretation of pulmonary artery wedge (pulmonary capillary) pressures. Brit. Heart J., 22: 37, 1960. 10. MURPHY, J. P. Inaccuracy of wedge pressure as an Circulaindex of pulmonary capillary pressure. tion, 17: 199,1958. 11. PEDERSEN, A. The Venous Pressure in the Pulmonary Circulation, p. 64. Copenhagen, 1956. Arnold Busck.