Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3695_Библиотеки_им_академика_М_И_Перельмана
.pdf
CASE REPORTS IN CARDIOLOGY
https://t.me/medicina_free
Figure 3 False aneurysm. a, Opened false aneurysm (FA) viewed from above
showing its brous wall and site of communication with the left ventricle (curved
arrow). The false aneurysm is much larger than either atrium and overlays the aortic
root (Ao) where a strut of the bioprosthesis is seen (arrow). PT=pulmonary trunk.
b, Opened aorta and left ventricular (LV) outow tract showing the entry site (broken-lined area) into false aneurysm (large arrow). AML=anterior mitral leaet; L and
R=ostium of the left and right coronary arteries (small arrows). (Photos by M.M.M.
Moore.)
accessory chamber, which was much larger than either the right atrium or the
compressed LA, ended in a blind pouch, the wall of which consisted entirely of
dense brous tissue. No residual infection was present in the heart. The bioprosthetic
cusps were normal and the ring was securely in place.
Thus, the above described patient had active infective endocarditis on a
previously anatomical ly normal aort ic valve and an adjacent ring abscess.
into the abscess was incompletely closed at the time of aortic valve replacement.
In retrospect, however, it may have been advisable to have obliterated completely
the mouth of the abscess by sutures buttressed with prosthetic material or by a
150
1
The mouth
CASE 491 ACQUIRED COR TRIATRIATUM (LEFT VENTRICULAR FALSE ANEURYSM)
https://t.me/medicina_free
prosthetic patch.
2
Residual infection just caudal to the bioprosthetic valve ring at
the aorto-LA angle plus the likely occurrence of a small gradient postoperatively
between left ventricle (LV) and aorta are circumstances allowing entrance of blood
into the ring abscess. The resulting accessory chamber, which was not present at
operation, presumably progressively enlarged postoperatively due to its receiving
blood under LV systolic pressure. The aneurysm of the ring abscess represents a
false LV aneurysm, although situated at the atrial level, because its wall was not
previously myocardium.
The development of a false aneurysm of LV after aortic valve replacement at the
site of a ring abscess secondary to infective endocarditis of the aortic valve has not
been described previously to our knowledge. Despite the impressive size of the false
aneurysm, it apparently caused no symptoms or signs of cardiac dysfunction.
REFERENCES
1. Arnett EN, Roberts WC: Valve ring abscess in active infective endocarditis:
Frequency, location, and clues to clinical diagnosis from the study of 95 necropsy
patients. Circulation 54:140, 1976.
2. Frantz PT, Murray GF, Wilcox BR: Surgical management of left ventricular-aortic
discontinuity complicating bacterial endocarditis. Ann Thorac Surg 29:1, 1980.
151
CASE REPORTS IN CARDIOLOGY
https://t.me/medicina_free
Case 497 Severe Aortic Regurgitation
from Systemic Hypertension
Bruce F. Waller, MD, F.C.C.P.; Joan C. Kishel, MD; and William C. Roberts, MD,
F.C.C.P.
Although about 10 percent of patients with systemic hypertension have a basal
diastolic blowing murmur indicating aortic regurgitation (AR) (Figure 1),
1–7
the
degree of aortic regurgitation is usually minimal or mild. The occurrence of severe
aortic regurgitation from systemic hypertension unassociated with aortic dissection
8
but herein we describe such a patient who had aortic regurgitation severe
is rare,
enough to require aortic valve replacement.
CASE REPORT
A 64-year-old woman, who died on August3, 1981, had systemic arteria l hyperte nsion
noted for the rst time at age 36years (1953). At age 40, she began antihypertensive
treatment (reserpine). At age 50 (1967), a grade 2/6 diastolic blowing murmur
of aortic regurgitation was noted and the blood pressure was 240/120 mm Hg
(Figure2). During the next seven years, the blood pressure remained elevated despite
administration of diuretics, reserpine and alpha-methyldopa. At age 55years (1973),
angina pectoris appeared and thereafter it progressed. On examination at age 56,
the intensity of the aortic regurgitation murmur was grade 3/6. The ECG (Figure3)
showed sinus bradycardia and left ventricular hypert rophy, and the chest radiograph
(Figure4), an enlarged cardiac silhouette. On M-mode echocardiogram (Figure5),
the left ventricular free wall and ventricular septum were of similar thickness
and the ascending aorta was dilated. The results of the cardiac catheterization are
summarized in Table 1. She underwent aortic valve replacement with a tilting-disc
prosthesis and had two aortocoronary bypass conduits placed to the left anterior
descending coronary system. The aortic valve was three-cuspid; each cusp was
freely mobile, but mildly thickened by brous tissue without calcic deposits, and
no commissure was fused.
The blood pressure in the rst six weeks postoperation was reduced compared
to the preoperation and late postoperation values (Figure2). Later she was treated
with beta-blocking and vasodilating agents. Amurmur of aortic regurgitation was
absent postoperatively. At age 62 (1980), angina pectoris and exertional dyspnea
reappeared. The blood pressure was 210/100 mm Hg. She took warfarin only
intermittently, and in July, 1981 she developed acute pulmonary edema without
audible prosthetic aortic valve sounds, and died several days later.
At necropsy, the heart weighed 530 g. The orice of the aortic-valve prosthesis
was severely narrowed by thrombus which made the occluder immobile. Ahealed
transmural left ventricular infarct was present (Figure 6) and the left main, left
anterior descending, and right coronary arteries were each narrowed >75percent in
cross-sectional area by atherosclerotic plaques.
From the Pathology Branch, National Heart, Lung and Blood Institute, National Institutes of
Health, Bethesda.
Reprint requests: Dr. Roberts, Bldg 10A, Rm 3E30, NHLBI, National Institutes of Health, Bethesda
20205
152 DOI: 10.1201/9781003409281-25
CASE 497 SEVERE AORTIC REGURGITATION FROM SYSTEMIC HYPERTENSION
https://t.me/medicina_free
Figure 1 Frequency and severity of aortic regurgitation (AR) in patients (pts) with
systemic hypertension (SH) based on previously reported data.
1–7
Figure 2 Systolic and diastolic systemic arterial pressures before and after aorticvalve replacement.
COMMENTS
The patient described above had systemic hypertension and aortic regurgitation
severe enough to warrant aortic-valve replacement without clinical or morphologic
explanation for the aortic regurgitation other than systemic hypertension. Recently,
we reported four other patients, all men aged 43–59years (mean 50), with severe
systemic hypertension, chronic congestive heart failure, and aortic regurgitation
severe enough to warrant aortic-valve replacement.
present from 1–30years (mean 13). In each of the four previous patients and in the
8
The hypertension had been
153
CASE REPORTS IN CARDIOLOGY
https://t.me/medicina_free
Figure 3 Electrocardiogram in patient at age 56years (eight years before death)
showing left ventricular hypertrophy and nonspecic ST segment and T wave
changes. The total QRS amplitude is 195mm.
Figure 4 Posteroanterior chest roentgenogram obtained before aortic valve
replacement eight years before death showing an enlarged cardiac silhouette.
154
CASE 497 SEVERE AORTIC REGURGITATION FROM SYSTEMIC HYPERTENSION
https://t.me/medicina_free
Figure 5 M-mode echocardiograms recorded just before aortic valve replacement.
The anterior mitral valve leaet utters (arrow), (upper). The ventricular septum (VS)
and left ventricular free wall (LV) are of similar thickness (lower).
present patient, the aortic valve was three-cuspid; each cusp was free of calcic
deposits and freely mobile.
Until these ve patients were encountered, we had not observed severe aortic
regurgitation from systemic hypertension alone and are unaware of any reports
describing aortic valve replacement for aortic regurgitation in such patients. At least
79 patients with systemic hypertension and aortic regurgitation (by auscultation),
however, were reported between 1940 and 1971, but none had aortic valve
replacement.
7
Of the 79 patients, the aortic regurgitation was severe in 17 (22percent)
and mild or moderate in 62 (78percent). Each of the 17 patients with severe aortic
regurgitation had fatal congestive heart failure, but another denite, probable or
possible cause of the failure other than aortic regurgitation appears to have been
present in six. Of the remaining 11 patients, necropsy information was available in
seven. The aortic valve and ascending aorta were reported to be normal in all seven.
The aortic valve “ring” was dilated in only one (7–12cm [mean 9]), the left ventricle
155
CASE REPORTS IN CARDIOLOGY
https://t.me/medicina_free
Figure 6 Left: Basal portion of the cardiac ventricles. MV=mitral valve leaets
and TV=tricuspid valve leaets. Right: Transverse sections of both cardiac ventricles
from base-to-apex showing nondilated cavities, thickened ventricular walls and a
healed myocardial infarct.
Table 1: Hemodynamic data (pressures in mm Hg)
Left ventricle (LV) (s/d) 160/11
Femoral artery (FA) (s/d) 160/60
Pulmonary arterial wedge (mean) 7
Right ventricle (s/d) 20/5
Right atrium (mean) 3
Cardiac index (L/min/M2) 1.6
AR by aortogram (1 +-4+) 3 +
Coronary arterial narrowing
(% diameter reduction)
Left main 70
Left anterior descending 50
Left circumex 50
Right 0
s/d=peak systole/end diastole
was dilated in only three patients, but the heart weight was increased in all seven
(460–700 g [mean 565 g]).
Certain factors increase the possibility of developing aortic regurgitation in
patients with systemic hypertension.
1–7
1) Magnitude of systemic arterial pressure.
The higher the pressure, the greater the chance of aortic regurgitation. 2) Age of
patient. Of patients with similar levels of systemic arterial pressure, older patients
have a higher frequency of aortic regurgitation than do younger patients. 3)
Duration of systemic hypertension. Of patients of similar age and similar pressure,
those with systemic hypertension of longer duration have a higher frequency of
aortic regurgitation than do those of shorter duration. The mechanism by which
severe aortic regurgitation develops in some patients with systemic hypertension
is unclear.
156
CASE 497 SEVERE AORTIC REGURGITATION FROM SYSTEMIC HYPERTENSION
https://t.me/medicina_free
REFERENCES
1. Barlow J, Kincaid-Smith P. The auscultatory ndings in hypertension. Br Heart J
1960; 22:505 – 514
2. Garvin CF. Functional aortic insufciency. Am J Med 1940; 13:1799–1704
3. Gouley BA, Sickel EM. Aortic regurgitation caused by dilatation of the aortic ori-
ce and associated with a characteristic valvular lesion. Am Heart J 1943; 26:24–38
4. Hammon L. Diagnostic implications of aortic insufciency. Cincinnati J Med
1944: 25:95–125
5. Fenichel NM. Arteriosclerotic aortic insufciency. Am Heart J 1950; 40:117–124
6. Puchner TC, Huston JH, Hellmuth GA. Aortic valve insufciency in arterial
hypertension. Am J Cardiol 1960; 5:758–760
7. Matalon R, Moussalli ARJ, Nidus BD, Katz LA, Eisinger RP. Functional aortic
insufciency—a feature of renal failure. N Engl J Med 1971; 285:1522–1523
8. Waller BF, Zoltick JM, Rosen JH, Katz NM, Gomes MN, Fletcher RD, etal. Severe
aortic regurgitation from systemic hypertension without aortic dissection requiring aortic valve replacement Analysis of 4 patients. Am J Cardiol 1982; 49:473–477
157
CASE REPORTS IN CARDIOLOGY
https://t.me/medicina_free
Case 523 Aortic Valve Stenosis and Left
Ventricular Apical Aneurysm and/or Rupture
Real or Potential Complications of Persistent Left Ventricular
Systolic Hypertension After Acute Myocardial Infarction
William C. Roberts, MD, Ernest N. Arnett, MD, Seena C. Aisner, MD,
and Paul Techlenberg, MD
Bethesda and Baltimore, MD
When acute myocardia l infarction (M I) occurs in patients w ith systemic hypertension,
the systemic arterial and left ventricular (LV) pressure generally returns to or toward
normal if the MI was fairly large. When acute MI occurs in patients with signicant
aortic valve stenosis (AS), however, the LV systolic pressure remains elevated and
the continuation of this pressure elevation increases the likelihood of LV rupture or
aneurysmal formation, particularly when the MI involves the LV apical wall which
normally is several times thinner than the LV basal wall.
67-year-old man, who died of progressive congestive heart failure after healing of
more than one (by history) acute MI in the previous 5years. At necropsy he had
a severely stenotic congenitally bicuspid aortic valve and a large apical aneurysm
at the site of a healed LV MI (Figure1). The heart weighed 630 gm. Both the left
anterior descending and left circumex coronary arteries were narrowed 76% to
100% in cross-sectional area by atherosclerotic plaques. The occurrence of LV free
wall rupture and/or aneurysmal formation has not been reported previously in a
patient with severe AS. This fact is surprising in view of the elderly age of many
patients with AS.
1, 2
Such was the case in a
REFERENCES
1. Roberts WC, Ronan JA Jr, Harvey WP: Rupture of the left ventricular free wall
(LVFW) or the ventricular septum (VS) secondary to acute myocardial infarction
(AMI): An occurrence virtually limited to the rst transmural AMI in the hypertensive individual (abstr). Am J Cardiol 35:166, 1975.
2. Cabin HS, Roberts WC: True left ventricular aneurysm and healed myocardial
infarction. Clinical and necropsy observations including quantication of degrees
of coronary arterial narrowing. Am J Cardiol 46:754, 1980.
From the Pathology Branch, National Heart, Lung and Blood Institute, National Institutes of
Health; and the Departments of Cardiology and Pathology, Franklin Square Hospital.
Received for publication July8, 1982; accepted July27, 1982.
Reprint requests: William C. Roberts, M.D., National Institutes of Health, Bldg. 10A, Room
3E-30, Bethesda, MD 20205.
158 DOI: 10.1201/9781003409281-26
CASE 523 AORTIC VALVE STENOSIS AND APICAL ANEURYSM AND/OR RUPTURE
https://t.me/medicina_free
Figure 1 Drawing of heart (upper panel) showing the healed left ventricular apical
aneurysm and the congenitally bicuspid, stenotic aortic valve; and a photograph of
the valve (lower panel).
159
Соседние файлы в папке Библиотека им академика М.И. Перельмана