- Email: [email protected]
Documented development of severe stenoses of previously confirmed normally functioning aortic valves
August,
306
Brief
Communications
of stay less than 30 days. Further technical details on methods and reliability of estimates are reported elsewhere.3To evaluate trends we performed linear regression analysisand calculated 95% confidence limits (CL). The case fatality rate (CFR) was calculated by dividing the number of patients who were certified asdying from PE as a primary diagnosisby all patients with PE as a primary dischargediagnosis. Approximately 216,000(range 200,000to 232,009)acute care charts were surveyed annually. The number of patients whosedeaths were certified due primarily to PE decreasedfrom 100in 1971to 91 in 1978(95% CL +0.2% to -2.5% per. year) (Fig. 1, A). In contrast, the overall number of patients with PE as a primary discharge diagnosisincreasedfrom 506 in 1971to 726 in 1978 (0.0% to i-3.1%) (Fig. I, B). Similarly, the overall number of primary and secondary discharge diagnoses of PE increasedfrom 1158to 1794patients annually during the study period (+0.6% to i-7.6%) (Fig. 1, B). The CFR decreasedsignificantly during the study period, from 100 deaths among506casesin 1971(20%) to 91 deathsamong 726casesin 1978(13%) (-0.4% to -1.7%) (Fig. 1, C). The greatest decreasein the proportion of fatal PEs occurred in patients 65 years and over, from 60 of 216 patients in 1971(28%) to 65 of 327 patients in 1978(20%) (-0.3% to -3.0% ). These data indicate that the mortality rate for patients diagnosedas dying from PE decreasedsomewhatduring the study period, while the hospital dischargediagnosisof PE increased.Therefore the proportion of recognizedfatal PEs decreased.This changewas most apparent in elderly patients. There are several possible limitations to the current investigation. First, it relied on a sampling of hospital charts, rather than ascertaining diagnosesin all patients admitted to all acute care hospitals. Secondly, few of the patients who died were autopsied. Consequently, the attribution of most PE deaths relied on the clinical impression of the attending physician. Moreover, the diagnosis of PE did not require objective confirmation with lung scanningor pulmonary angiography and therefore both underdiagnosis’and overdiagnosis were possible. Finally, the number of hospitalizations per patient per year was not determined in this survey. Despite these limitations, it appears that PE is being recognized with increasing frequency. Further studies to evaluate the relative contributions of improved diagnosis and treatment to the decreasingfatality rate would be useful and timely. REFERENCES 1. Goldhaber Godleski diagnosis 1982) 2. Reichel
SZ, Hennekens CH, Evans DA, Newton EC, JJ: Factors associated with the correct antemortem of major pulmonary embolism. Am J Med (In press,
J: Pulmonary embolism. Med Clin North Am 61:1309, 1977. 3. National Center for Health Statistics: Vital statistics report: Final mortality statistics. 1978. DHHS Publication No. (PHS) 80-1120; vol. 29, no:6, supplement (2), September 17, 1980, United States Public Health Service.
American
Heart
1982 Journal
4. Dalen JE, Alpert J: Natural history of pulmonary embolism. Progr Cardiovasc Dis 17:259, 1975. 5. Robin ED: Overdiagnosis and overtreatment of pulmonary embolism: The emperor may have no clothes. Ann Intern Med 87:775. 1977.
Documented development of severe stenoses of previously confirmed notmaHy functioning aortic valves William C. Roberts, M.D., Ernest A. Arnett, M.D., Henry Scott Cabin, M.D., Charles L. McIntosh, M.D., SeenaC. Aisner, M.D., and Kenneth B. Lewis, M.D. Bethesdu, and Baltimore, Md. Several reports have described increasesin transvalvular peak systolic pressure gradients across stenotic aortic valves over varying periods of time.“-* Demonstration of development of severe aortic valve stenosis (AS) in a previously normally functioning aortic valve over a relatively short period of time, however, is extremely rare. Of 64 reported patients from four different studies’-4with AS and more than one cardiac catheterization, all but one patient had had a peak systolic pressuregradient across the aortic valve at the first aswell asat subsequentcardiac catheterizations. The one exception was a 65-year-old patient reported by Cheitlin et a1.4in whom a 90 mm Hg peak systolic pressuregradient developed in a 24-month period from a previous zero gradient. In the two patients to be described below, each developed severe AS several years after hemodynamic confirmation of no pressure gradient in peak systole between left ventricle (LV) and a systemic artery. Patient No. 1 (B.W.), a 71-year-old woman who died in October, 1981, underwent mitral valve replacement for severe(18 mm Hg meandiastolic gradient) mitral stenosis at age 63 (1973). Immediately before mitral replacement, simultaneous LV and aortic pressureswere 165/6 and 165/102 mm Hg (Fig. 11, respectively, and aortic root angiogramshowedno aortic regurgitation. During the first 6 years after mitral replacement shewasvirtually asymptomatic and had no significant precordial murmur. About 2 years before death, chronic congestive heart failure (CHF) recurred and a basal precordial systolic murmur appeared. Death resulted from progressive worseningof CHF. At necropsy, the occluder of the mitral prosthesis moved normally and no thrombus was present on the prosthesis. Each of the three aortic valve cusps was From the Pathology, Cardiology, and Surgery Branches, National Heart, Lung and Blood Institute, National Institutes of Health; and the Department of Medicine (Cardiology) and Pathology, Franklin Square Hospital, Baltimore, Md. Received for publication March 8, 1982; accepted Apr. 19, 1932. Reprint requests: William C. Roberts, M.D., Pathology Branch, NIHNHLBI, Bldg. lOA, Room 3E-30, Bethesda, MD 20205.
0002-8703/82/080306
+ 03$00.30/O
o 1982 The
C. V. Mosby
Co.
Volume Number
104 2. Part 1
Brief
mmHg
mr
Left Ventricle
V
Communications
307
Aorta
1. Pullback pressuretracing from left ventricle to aorta in patient No. 1 showing no peak systolic pressuregradient recorded 8 years before death.
Fig.
Fig. 2. Aortic valve seenfrom above in patient No. 1 (FSH No. A4129) in simulated ventricular diastole (VD) left and ventricular systole (VS) right. A smallstick (asterisk) is forced into the aortic orifice to open it maximally (right). Heavy calcific depositsare present on the aortic aspectsof each of the three cusps. The commissurebetween the right and left cuspsis slightly fused. R = right coronary artery; LM = left
main coronary artery. heavily calcified, virtually immobile, and the aortic valve orifice wassevereIy stenotic (Fig. 2). The LV myocardium was free of foci of myocardial necrosisand fibrosis. Patient No. 2 (E.B.), a 56-year-old man who died in August, 1980,had mitral valve replacement for combined mitral stenosis and regurgitation at age 37 (January, 1962). Immediately before mitral replacement, no peak systolic pressuregradient waspresent betweenLV (120/10 mm Hg) and brachial artery (150/50 mm Hg). One month after mitral replacement, repeat catheterization disclosed the LV and brachial arterial pressuresto be 96/O and 106/56 mm Hg, respectively. Six months after mitral replacement, another catheterization showed simultaneousLV and brachial arterial pressuresto be 13316and 133/65 mm Hg, respectively. A grade 2/6 systolic ejection murmur wasaudible over the cardiac baseasearly as 1962 and during the next 16 years the intensity of this murmur increased to grade 4/6. In early 1977, overt CHF reappeared and catheterization in March, 1977, disclosed simultaneously LV and systemic arterial pressuresto be 180/24and 135/60mm Hg, respectively, yielding a 45 mm
Hg peak systolic pressuregradient. Repeat catheterization in July, 1978 (age 54), disclosed simultaneous LV and femoral arterial pressuresto be 200/25and 130/60mm Hg, yielding a 70 mm Hg peak systolic pressuregradient and an aortic valve index of 0.2 cm*/m’. At aortic valve replacement in August, 1978, the aortic valve was tricuspid, heavily calcified, and the commissurebetween the right and left cusps was fused. He died suddenly in August, 1980,after a previously much improved status for 2 years. The above two patients and the one described by Cheitlin et al.4 demonstrate that severe AS can develop within a X-year period in a previously normally functioning aortic valve, and that this possibility needsto be kept in mind in evaluating patients who develop CHF late after mitral valve replacement for rheumatic mitral stenosis. REFERENCES
1.
FriedmanWF, ModlingerJ, MorganJR: Serialhemodynamic observationsin asymptomaticchildren with valvar aortic stenosis.
Circulation
43:91,
1971.
308
Brief
Communications
American
2. Cohen LS, Friedman WF, Braunwald E: Natural history of mild congenital aortic stenosis elucidated by serial hemodynamic studies. Am J Cardiol 30:1, 1972. 3. Bogart DB, Murphy BL, Wong BYS, Pugh DM, Dunn MI: Progression of aortic stenosis. Chest 76:391, 1979. 4. Cheitlin MD, Gertz EW, Brundage BH, Carlson CJ, Quash JA, Bode RS Jr: Rate of progression of severity of valvular aortic stenosis in the adult. AM HEART J 98:689, 1979.
Pericardiocentesis induced intrapericardial thrombus: Detection by two-dimensional echocardiography Allan H. Schuster, Rochester, N. Y.
M.D.,
and Navin
C. Nanda,
M.D.
Hemopericardium may complicate pericardiocentesis’ and may result in the failure of a patient with tamponade to respond with clinical and hemodynamic improvement after removal of pericardial fluid. We have recently used real-time two-dimensional echocardiography (BDE) to detect a large intrapericardial thrombus in a patient who failed to clinically improve after therapeutic pericardio-
From the Cardiology Unit, University of Rochester Medical Center. Supported by Research Training Grant HL 07220 from the National Heart, Lung and Blood Institute, National Institutes of Health and by a Grant-in-Aid from the American Heart Association, Genessee Valley Chapter. Received for publication Oct. 16, 1981; accepted Oct. 26, 1961. Reprint requests: Navin C. Nanda, M.D., Cardiology Unit-Box 679, University of Rochester Medical Center, 601 Elmwood Ave., Rochester, NY 14642.
August, 1992 Heart Journal
centesis. To the best of our knowledge this has not been reported previously. The patient was a 62-year-old former heavy smoker, 1 year after left lower lobectomy and radiotherapy (ECOG protocal 3578) for poorly differentiated adenocarcinoma with hilar metastases. He presented to the Emergency Department with a chief complaint of increasing dyspnea of 3 weeks’ duration. Physical examination revealed a tachycardia of 132 bpm, blood pressure of 110/80 mm Hg with 30 mm Hg pulsus paradoxicus. Jugular veins were distended, breath sounds were diminished at the lung bases, a pericardial friction rub was noted, and the extremities showed moderate edema. Initial real-time 2DE examination showed large anterior and posterior pericardial effusion spaces (35 mm in maximum width) which contained no echo densities (left panels of Figs. 1 and 2). Within the next 6 hours, because of declining blood pressure and presumptive clinical diagnosis of cardiac tamponade, emergency pericardiocentesis was performed and approximately 3’75 ml of serosanguinous fluid was removed. However, the patient’s blood pressure did not increase after pericardiocentesis and he remained dyspneic. Repeat echocardiographic examination, done about 12 hours after pericardiocentesis, revealed a new large crescent-shaped echo density measuring maximally 65 mm by 15 mm (middle and right panels of Fig. 1). In short axis, the mass measured 13 mm (middle and right panels of Fig. 2). This was contained within a persistent pericardial effusion space which measured maximally 25 mm (Figs. 3, 4, and 5). Subsequently, the patient underwent pericardiotomy and pericardial biopsy; 800 ml of serosanguinous fluid was removed and a spongy intrapericardial mass consistent with a thrombus was palpated by the surgeon. Cytological and pathological examinations were consistent
Fig. 1. Apical four chamber two-dimensional echocardiogram. Left, demonstration of a large pericardial effusion (PE) prior to pericardiocentesis. Middle, after pericardiocentesis, echocardiogram displays a large crescent-shaped intrapericardial thrombus (TH) present within the pericardial effusion. Right, schematic diagram of middle panel. RV = right ventricle; LV = left ventricle; RA = right atrium; LA = left atrium; R = right; L = left; S = superior; I = inferior.
0002-8703/82/080308+ 04$00.4O/Oa 1982 The C.V. Mosby Co.
306
Brief
Communications
of stay less than 30 days. Further technical details on methods and reliability of estimates are reported elsewhere.3To evaluate trends we performed linear regression analysisand calculated 95% confidence limits (CL). The case fatality rate (CFR) was calculated by dividing the number of patients who were certified asdying from PE as a primary diagnosisby all patients with PE as a primary dischargediagnosis. Approximately 216,000(range 200,000to 232,009)acute care charts were surveyed annually. The number of patients whosedeaths were certified due primarily to PE decreasedfrom 100in 1971to 91 in 1978(95% CL +0.2% to -2.5% per. year) (Fig. 1, A). In contrast, the overall number of patients with PE as a primary discharge diagnosisincreasedfrom 506 in 1971to 726 in 1978 (0.0% to i-3.1%) (Fig. I, B). Similarly, the overall number of primary and secondary discharge diagnoses of PE increasedfrom 1158to 1794patients annually during the study period (+0.6% to i-7.6%) (Fig. 1, B). The CFR decreasedsignificantly during the study period, from 100 deaths among506casesin 1971(20%) to 91 deathsamong 726casesin 1978(13%) (-0.4% to -1.7%) (Fig. 1, C). The greatest decreasein the proportion of fatal PEs occurred in patients 65 years and over, from 60 of 216 patients in 1971(28%) to 65 of 327 patients in 1978(20%) (-0.3% to -3.0% ). These data indicate that the mortality rate for patients diagnosedas dying from PE decreasedsomewhatduring the study period, while the hospital dischargediagnosisof PE increased.Therefore the proportion of recognizedfatal PEs decreased.This changewas most apparent in elderly patients. There are several possible limitations to the current investigation. First, it relied on a sampling of hospital charts, rather than ascertaining diagnosesin all patients admitted to all acute care hospitals. Secondly, few of the patients who died were autopsied. Consequently, the attribution of most PE deaths relied on the clinical impression of the attending physician. Moreover, the diagnosis of PE did not require objective confirmation with lung scanningor pulmonary angiography and therefore both underdiagnosis’and overdiagnosis were possible. Finally, the number of hospitalizations per patient per year was not determined in this survey. Despite these limitations, it appears that PE is being recognized with increasing frequency. Further studies to evaluate the relative contributions of improved diagnosis and treatment to the decreasingfatality rate would be useful and timely. REFERENCES 1. Goldhaber Godleski diagnosis 1982) 2. Reichel
SZ, Hennekens CH, Evans DA, Newton EC, JJ: Factors associated with the correct antemortem of major pulmonary embolism. Am J Med (In press,
J: Pulmonary embolism. Med Clin North Am 61:1309, 1977. 3. National Center for Health Statistics: Vital statistics report: Final mortality statistics. 1978. DHHS Publication No. (PHS) 80-1120; vol. 29, no:6, supplement (2), September 17, 1980, United States Public Health Service.
American
Heart
1982 Journal
4. Dalen JE, Alpert J: Natural history of pulmonary embolism. Progr Cardiovasc Dis 17:259, 1975. 5. Robin ED: Overdiagnosis and overtreatment of pulmonary embolism: The emperor may have no clothes. Ann Intern Med 87:775. 1977.
Documented development of severe stenoses of previously confirmed notmaHy functioning aortic valves William C. Roberts, M.D., Ernest A. Arnett, M.D., Henry Scott Cabin, M.D., Charles L. McIntosh, M.D., SeenaC. Aisner, M.D., and Kenneth B. Lewis, M.D. Bethesdu, and Baltimore, Md. Several reports have described increasesin transvalvular peak systolic pressure gradients across stenotic aortic valves over varying periods of time.“-* Demonstration of development of severe aortic valve stenosis (AS) in a previously normally functioning aortic valve over a relatively short period of time, however, is extremely rare. Of 64 reported patients from four different studies’-4with AS and more than one cardiac catheterization, all but one patient had had a peak systolic pressuregradient across the aortic valve at the first aswell asat subsequentcardiac catheterizations. The one exception was a 65-year-old patient reported by Cheitlin et a1.4in whom a 90 mm Hg peak systolic pressuregradient developed in a 24-month period from a previous zero gradient. In the two patients to be described below, each developed severe AS several years after hemodynamic confirmation of no pressure gradient in peak systole between left ventricle (LV) and a systemic artery. Patient No. 1 (B.W.), a 71-year-old woman who died in October, 1981, underwent mitral valve replacement for severe(18 mm Hg meandiastolic gradient) mitral stenosis at age 63 (1973). Immediately before mitral replacement, simultaneous LV and aortic pressureswere 165/6 and 165/102 mm Hg (Fig. 11, respectively, and aortic root angiogramshowedno aortic regurgitation. During the first 6 years after mitral replacement shewasvirtually asymptomatic and had no significant precordial murmur. About 2 years before death, chronic congestive heart failure (CHF) recurred and a basal precordial systolic murmur appeared. Death resulted from progressive worseningof CHF. At necropsy, the occluder of the mitral prosthesis moved normally and no thrombus was present on the prosthesis. Each of the three aortic valve cusps was From the Pathology, Cardiology, and Surgery Branches, National Heart, Lung and Blood Institute, National Institutes of Health; and the Department of Medicine (Cardiology) and Pathology, Franklin Square Hospital, Baltimore, Md. Received for publication March 8, 1982; accepted Apr. 19, 1932. Reprint requests: William C. Roberts, M.D., Pathology Branch, NIHNHLBI, Bldg. lOA, Room 3E-30, Bethesda, MD 20205.
0002-8703/82/080306
+ 03$00.30/O
o 1982 The
C. V. Mosby
Co.
Volume Number
104 2. Part 1
Brief
mmHg
mr
Left Ventricle
V
Communications
307
Aorta
1. Pullback pressuretracing from left ventricle to aorta in patient No. 1 showing no peak systolic pressuregradient recorded 8 years before death.
Fig.
Fig. 2. Aortic valve seenfrom above in patient No. 1 (FSH No. A4129) in simulated ventricular diastole (VD) left and ventricular systole (VS) right. A smallstick (asterisk) is forced into the aortic orifice to open it maximally (right). Heavy calcific depositsare present on the aortic aspectsof each of the three cusps. The commissurebetween the right and left cuspsis slightly fused. R = right coronary artery; LM = left
main coronary artery. heavily calcified, virtually immobile, and the aortic valve orifice wassevereIy stenotic (Fig. 2). The LV myocardium was free of foci of myocardial necrosisand fibrosis. Patient No. 2 (E.B.), a 56-year-old man who died in August, 1980,had mitral valve replacement for combined mitral stenosis and regurgitation at age 37 (January, 1962). Immediately before mitral replacement, no peak systolic pressuregradient waspresent betweenLV (120/10 mm Hg) and brachial artery (150/50 mm Hg). One month after mitral replacement, repeat catheterization disclosed the LV and brachial arterial pressuresto be 96/O and 106/56 mm Hg, respectively. Six months after mitral replacement, another catheterization showed simultaneousLV and brachial arterial pressuresto be 13316and 133/65 mm Hg, respectively. A grade 2/6 systolic ejection murmur wasaudible over the cardiac baseasearly as 1962 and during the next 16 years the intensity of this murmur increased to grade 4/6. In early 1977, overt CHF reappeared and catheterization in March, 1977, disclosed simultaneously LV and systemic arterial pressuresto be 180/24and 135/60mm Hg, respectively, yielding a 45 mm
Hg peak systolic pressuregradient. Repeat catheterization in July, 1978 (age 54), disclosed simultaneous LV and femoral arterial pressuresto be 200/25and 130/60mm Hg, yielding a 70 mm Hg peak systolic pressuregradient and an aortic valve index of 0.2 cm*/m’. At aortic valve replacement in August, 1978, the aortic valve was tricuspid, heavily calcified, and the commissurebetween the right and left cusps was fused. He died suddenly in August, 1980,after a previously much improved status for 2 years. The above two patients and the one described by Cheitlin et al.4 demonstrate that severe AS can develop within a X-year period in a previously normally functioning aortic valve, and that this possibility needsto be kept in mind in evaluating patients who develop CHF late after mitral valve replacement for rheumatic mitral stenosis. REFERENCES
1.
FriedmanWF, ModlingerJ, MorganJR: Serialhemodynamic observationsin asymptomaticchildren with valvar aortic stenosis.
Circulation
43:91,
1971.
308
Brief
Communications
American
2. Cohen LS, Friedman WF, Braunwald E: Natural history of mild congenital aortic stenosis elucidated by serial hemodynamic studies. Am J Cardiol 30:1, 1972. 3. Bogart DB, Murphy BL, Wong BYS, Pugh DM, Dunn MI: Progression of aortic stenosis. Chest 76:391, 1979. 4. Cheitlin MD, Gertz EW, Brundage BH, Carlson CJ, Quash JA, Bode RS Jr: Rate of progression of severity of valvular aortic stenosis in the adult. AM HEART J 98:689, 1979.
Pericardiocentesis induced intrapericardial thrombus: Detection by two-dimensional echocardiography Allan H. Schuster, Rochester, N. Y.
M.D.,
and Navin
C. Nanda,
M.D.
Hemopericardium may complicate pericardiocentesis’ and may result in the failure of a patient with tamponade to respond with clinical and hemodynamic improvement after removal of pericardial fluid. We have recently used real-time two-dimensional echocardiography (BDE) to detect a large intrapericardial thrombus in a patient who failed to clinically improve after therapeutic pericardio-
From the Cardiology Unit, University of Rochester Medical Center. Supported by Research Training Grant HL 07220 from the National Heart, Lung and Blood Institute, National Institutes of Health and by a Grant-in-Aid from the American Heart Association, Genessee Valley Chapter. Received for publication Oct. 16, 1981; accepted Oct. 26, 1961. Reprint requests: Navin C. Nanda, M.D., Cardiology Unit-Box 679, University of Rochester Medical Center, 601 Elmwood Ave., Rochester, NY 14642.
August, 1992 Heart Journal
centesis. To the best of our knowledge this has not been reported previously. The patient was a 62-year-old former heavy smoker, 1 year after left lower lobectomy and radiotherapy (ECOG protocal 3578) for poorly differentiated adenocarcinoma with hilar metastases. He presented to the Emergency Department with a chief complaint of increasing dyspnea of 3 weeks’ duration. Physical examination revealed a tachycardia of 132 bpm, blood pressure of 110/80 mm Hg with 30 mm Hg pulsus paradoxicus. Jugular veins were distended, breath sounds were diminished at the lung bases, a pericardial friction rub was noted, and the extremities showed moderate edema. Initial real-time 2DE examination showed large anterior and posterior pericardial effusion spaces (35 mm in maximum width) which contained no echo densities (left panels of Figs. 1 and 2). Within the next 6 hours, because of declining blood pressure and presumptive clinical diagnosis of cardiac tamponade, emergency pericardiocentesis was performed and approximately 3’75 ml of serosanguinous fluid was removed. However, the patient’s blood pressure did not increase after pericardiocentesis and he remained dyspneic. Repeat echocardiographic examination, done about 12 hours after pericardiocentesis, revealed a new large crescent-shaped echo density measuring maximally 65 mm by 15 mm (middle and right panels of Fig. 1). In short axis, the mass measured 13 mm (middle and right panels of Fig. 2). This was contained within a persistent pericardial effusion space which measured maximally 25 mm (Figs. 3, 4, and 5). Subsequently, the patient underwent pericardiotomy and pericardial biopsy; 800 ml of serosanguinous fluid was removed and a spongy intrapericardial mass consistent with a thrombus was palpated by the surgeon. Cytological and pathological examinations were consistent
Fig. 1. Apical four chamber two-dimensional echocardiogram. Left, demonstration of a large pericardial effusion (PE) prior to pericardiocentesis. Middle, after pericardiocentesis, echocardiogram displays a large crescent-shaped intrapericardial thrombus (TH) present within the pericardial effusion. Right, schematic diagram of middle panel. RV = right ventricle; LV = left ventricle; RA = right atrium; LA = left atrium; R = right; L = left; S = superior; I = inferior.
0002-8703/82/080308+ 04$00.4O/Oa 1982 The C.V. Mosby Co.