Clinical
pathologic
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Rupture of the ventricular complication of myocardial
septum as a infarction*
Julius L. Bedynek, M.D., COL, MC, USA John J. Fenoglio, Jr., M.D., MAJ, MC, USAR Hugh A. McAllister, Jr., M.D., LTC, MC, USA Washington, D. C., and Neul York, N. Y.
CLINICAL SUMMARY: This 67-year-old man was well until 3 weeks prior to admission when he experienced chest pain and shortness of breath. Nine days prior to admission, after an episode of chest pain that lasted an hour and a half, the patient reported to a community hospital for evaluation. An electrocardiogram was interpreted as normal (Fig. 1). The patient returned home and went about his daily activities which included yard work and lifting heavy objects. Three days prior to admission, the patient experienced severe shortness of breath and malaise. This increased until the day of admission when he again went to the community hospital. At this time a new systolic murmur was heard. The electrocardiogram was unchanged and was now interpreted as compatible with an acute anteroseptal myocardial infarction. The patient was transferred to Walter Reed Army Medical Center for evaluation. He denied any cardiac awareness, palpitations, paroxysmal nocturnal dyspnea, orthopnea, or edema. He had no fever or chills. The patient had adult onset diabetes mellitus, controlled with diet, and a vague history of hypertension which was never treated. There was no family history of heart disease. The patient denied having rheumatic or scarlet fever, gout, or hyperlipoproteinFrom the Department of Cardiology, Walter Reed Army Medical Center, Washington, D. C., the 320th Evacuation Hospital, 8th Medical Brigade, New York, N. Y.; and the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, D. C. Received for publication Apr. 21, 1978. Reprint requests: LTC Hugh A. McAllister, Jr., MC, USA, Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, D. C. 20306. *The opinions or assertions contained herein are the private views of the authors and are not to be construed as being official or as reflecting the views of the Department of the Army or the Department of Defense.
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8 1979 The
C. V. Mosby
Co.
Fig. 1. Electrocardiogram sion.
taken
nine
days
prior
to admk
emia. He was taking no medications and was a nonsmoker. On physical examination the patient was in moderate respiratory distress, although alert and oriented. The pulse was regular and 104 per minute; respirations were 24 per minute and labored, and the blood pressure was 110/70 mm. Hg. He was afebrile. There was no jugular venous distension. The carotid upstroke was normal. On auscultation bilateral basilar rfiles were heard as high as the scapulae. There was a precordial systolic thrill felt best at the left lower sternal border. The patient had a Grade IV/VI holosystolic murmur heard best at the lower left sternal border and radiating over the entire precordium. In addition, there was a Grade I-II early diastolic rumble heard best at the apex. S, and S, were normal. The liver span at the right mid-clavicular line was 10 cm. The liver was tender and the left lobe was prominent. The rest of the physical examination was normal. The patient had a mild leukocytosis with a shift to the left. Urinalysis was normal. The blood
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2. A admission.
Fig.
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portable
and
McAllister
anteroposterior
chest
x-ray
taken
on
glucose was 437 mg per cent. The blood urea nitrogen was 1.9 mg per cent. The serum electrolytes were all abnormal; sodium 129 mEq./L., potassium 5.0 mEq./L., chloride 97 mEq./L., and CO, 17 mEq./L. Arterial blood gases were drawn while the patient was breathing room air. The oxygen partial pressure (PO,) was 80 mm. Hg; the carbon dioxide partial pressure (PCO,) was 18 mm. Hg, and the pH was 7.54. On admission the serum glutamic oxaloacetic transaminase (SGOT) was 802 units; lactic dehydrogenase (LDH) 2,600 units, creatine phosphokinase (CPK) activity 63 units. All LDH isoenzyme fractions were elevated, although fractions one and two (cardiac fractions) were markedly increased. CPK isoenzymes were all within the M band. Thyroid function tests were normal. Clinical
discussion
DR. JULIUS L. BEDYNEK: First I should like to ask Dr. Anderson to interpret the electrocardiograms and chest x-rays. DR. WARREN T. ANDERSON: On the initial tracing 9 days prior to admission (Fig. 1) there was a sinus tachycardia of 110 beats per minute. The slow R wave progression through V, and ST segment elevation in V, through V, suggest an acute anteroseptal myocardial infarction. The tracing on admission and subsequent tracings demonstrated further evolution of an anteroseptal myocardial infarction. The chest x-ray on
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Fig. 3. Pulmonary time-activity function fit (0). The marked nary time-activity and gamma shortly after peak suggests the shunt. The calculated ratio of flow is greater than 3.
histogram ( + ) and gamma difference between the pulmofunction fit curves that occurs presence of a large left-to-right pulmonary to systemic blood
admission (Fig. 2), although a portable AP film, demonstrated mild cardiomegaly and prominent pulmonary vascularity. On multiple repeat films throughout the hospital course there was progressive cardiomegaly and marked increased pulmonary congestion. DR. BEDYNEK: In summary this was a 67-yearold man who suffered an acute anterior myocardial infarction. Six days later he suddenly developed signs and symptoms of congestive heart failure with pulmonary congestion. Subsequently a loud systolic precordial murmur and a thrill, both maximal at the lower left sternal border, were noted. This case poses the problem of the differential diagnosis of systolic murmurs associated with the sudden clinical deterioration of the patient with an acute myocardial infarction. The determination of the cause of the systolic murmur is of practical importance in predicting the course and determining the management of these patients. The most important entities in this differential diagnosis are rupture of the ventricular septum and rupture of a papillary muscle with acute mitral regurgitation. However, papillary muscle dysfunction and acute dilatation of the left ventricle may also be associated with the sudden
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I. Differential infarction
Table
Incidence
Papillary muscle rupture
Up to 1% of transmural infarction
Up to 1% of all cases
Usually anteroseptal or posteroseptal
Usually
Appearance
4 to 7 days tion
Murmur
Left sternal border. Almost always present and loud (Gr. III & IV) Left sternal border. Present in 50% of cases In up to 40% Progressive w/left& right-sided features
Later than septal rupture/even wks. to mos. Apex w/radiation to axilla or base (Gr. II or less). Absent in 40% Apex and unusually present
of infarction
Thrill
Conduction defect Heart failure
Poor with surgery
Prognosis
post-infarc-
or without
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Journal
inferior
Unusual Acute onset of leftsided failure & acute pulmonary edema Guarded with or without surgery
appearance of a loud systolic murmur and dramatic deterioration of the patient. The important criteria in the differential diagnosis of these systolic murmurs are summarized in Table I. Our patient had many of the features of acute rupture of the ventricular septum. This unusual complication of myocardial infarction occurs in up to one per cent of transmural infarctions involving the ventricular septum.’ The murmur and thrill usually appear four to seven days after the infarct, as apparently was the case in our patient, and are usually maximal at the lower left sternal border, a location consistent with the findings in congenital ventricular septal defects. I can recall, however, two patients which were exceptions to this rule. In these two patients the murmur and thrill were most intense at the apex and in the axilla. In both patients a ventricular septal defect was proven by cardiac catheterization. I know of no good explanation for the paradoxical physical findings (murmur and thrill more intense at the apex than at the left sternal border) in either of these patients. Since the His bundle and bundle branches may
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diagnosis of systolic murmurs appearing during the course of myocardial
Septal rupture
Location
pathologic
More frequent (up to 57% of infarctions) & more transient
Not clear, but when present probably clears w/treatment of failure t Ischemia and/or infarction + ST-T changes anteroLocation not critical lateral or inferior At time of chest pain At time of dilatation (ischemia) & may persist II/VI or less at apex Apex and soft (Gr. I to II in 2/3)
Very
unusual
Unusual
Unusual Not prominent
Unusual Common
Good short-term; poor long-term due to new infarction
Not
clear
be involved in septal infarcts, a conduction defect is present in up to 40 per cent of the patients with ventricular septal rupture. This patient did not have a conduction defect. Usually there is a substantial left-to-right intracardiac shunt across the defect and features of left and right heart failure are virtually constant in these patients. In my experience patients without prominent congestive heart failure have had small ventricular septal defects. These patients have a better overall prognosis, since successful surgical therapy largely depends on the ability of the patient to survive for four to six weeks after infarction, allowing time for the margins of the infarcted myocardium to heal sufficiently to support sutures. Rupture of a papillary muscle is also frequently associated with dramatic clinical deterioration and the appearance of a loud systolic murmur. These patients usually have an infero-lateral myocardial infarct.“. 3 Papillary muscle rupture occurs in up to one per cent in all cases of myocardial infarct, usually later than ventricular septal rupture and occasionally several months
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after the infarct. The murmur of mitral regurgitation may be absent in up to 40 per cent of these cases, and when present is usually loudest at the apex with radiation to the axilla or to the base of the heart. A murmur is more frequently detected with partial rupture of a papillary muscle. Radiation to the base implies rupture of the posterior medial papillary muscle, and radiation to the apex rupture of the anterior papillary muscle. A thrill is uncommon, but, if present, is frequently most intense at the apex. Conduction defects are rare. Heart failure is most often of acute onset with fulminant pulmonary edema. The prognosis is guarded and is often worse than that in ventricular septal rupture, except with partial rupture of a papillary muscle. Since survival is longer with partial rupture, attempts at surgical repair are more frequently successful. Papillary muscle dysfunction without papillary muscle rupture is also a frequent cause of a systolic murmur appearing during the course of myocardial infarction and has been reported in up to 5’7 per cent of all cases of infarction. The murmur is usually pansystolic and apical in location, and is most often softer than the murmur of septal rupture. It is Grade I to II/VI in two thirds, and Grades II to IV/VI in one third of the patients. The murmur is usually not associated with marked deterioration of the patient but may be associated with both radiographic and clinical findings of left ventricular failure. The murmur may be appreciated during chest pain connoting myocardial ischemia and may be accompanied by ST and T wave changes in the ECG. These ECG changes include mild to severe depression of the J junction with convex or concave upward deformity of the ST segment and frequently terminal inverstion of the T wave or depression of the T-U segment with U wave inversion in the middle and left precordial leads especially in anterolateral papillary muscle dysfunction.’ Papillary muscle dysfunction may be a manifestation of transient severe ischemia, or may imply the infarction of a papillary muscle. Thrills, conduction defects, and severe heart failure are uncommon. The prognosis is good for short-term survival. Long-term prognosis, however, is poor as these patients frequently have severe obstructive coronary disease. Acute left ventricular dilatation during the course of myocardial infarction may disrupt the configuration of the mitral valvular apparatus
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sufficiently to cause mitral insuificincy. As in papillary muscle dysfunction, myocardial infarction is not necessary for the appearance of this murmur, and it may occur with transient severe myocardial &hernia or ischemic myocardiopathy. It is hypothesized that the mitral valve becomes incompetent because the bases of the papillary muscles are widely separated due to dilatation of the ventricular cavity and the chordae tendineae lie at an obtuse angle to the mitral leaflets. The result is incomplete closure of the mitral valve during ventricular systole. This explanation is currently preferred over the more classical one that the mitral valve ring is simply dilated. I am not aware, however, that either hypothesis has been proven by objective investigations. Heart failure is common, but rarely of sudden onset. The clinical history and physical findings suggest either left ventricular dilatation or papillary muscle dysfunction as a cause of the murmur. This discussion would not be complete without mentioning three other possible causes of systolic murmurs, all unlikely in our patient, appearing following myocardial infarction. These are pericarditis, rupture of the ventricular free wall, and right ventricular infarction with tricuspid regurgitation. Pericardial friction rubs secondary to pericarditis are quite frequent during the course of acute myocardial infarction, especially when listened for carefully. It is entirely possible that a systolic friction rub could be confused with a systolic murmur, and in the occasional instance where pericardial fluid is copious, deterioration due to pericardial tamponade might result after the appearance of such an auscultatory finding. The careful search for a three-part friction rub would help eliminate this point of confusion. Rupture of the ventricular free wall may be preceded by a transient systolic murmur.; This is soon followed by signs of cardiac tamponade. The systolic murmur has been attributed to actual systolic leakage of blood into the pericardial cavity. Electromechanical dissociation is common and usually fatal within minutes in these patients. Those few patients who have survived with expeditious surgery have done so only because there was a high index of suspicion and because pericardiocentesis was carried out while the patient was in route to surgery. I am not, however, aware of any long-term survivors. Rupture of a tricuspid valve papillary muscle
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producing a systolic murmur at the lower sternal border in the course of myocardial infarction has been reported.fi In this single reported case the heart failure was predominantly right-sided. The two most likely diagnostic possibilities in our patient are ventricular septal rupture and papillary muscle rupture, and I will confine my further discussion to these two entities. The clinical course is, of course, of particular interest at this point. Dr. Wheeler cared for this patient in the coronary care unit, and I will call on him now to discuss the clinical course. DR. LEIGH WHEELER: The patient was admitted to the CCU where his deteriorating course was compatible with either ventricular septal perforation or acute mitral regurgitation secondary to a papillary muscle dysfunction. The patient was treated with digoxin, oxygen, and diuretic therapy. Because of the difficulty in identifying the cause of the systolic murmur, the patient was taken to the cardiac catheterization laboratory on the third hospital day where a balloon-tipped, flow directed catheter was introduced into the right heart. Each time the catheter tip was advanced to the right ventricle, it was rapidly ejected into the pulmonary artery and on four occasions the cardiac rhythm immediately deteriorated to ventricular fibrillation. The catheter was withdrawn, and the patient was successfully electrically defibrillated. Since a diagnosis was not established by catheterization, a radionuclide angiocardiogram was done by Dr. Kaminski. DR. ROBERT KAMINSKI: The radionuclide angiocardiogram was done on the seventh hospital day. A bolus of 15 mCi 99m Technetium pertechnetate was injected intravenously through a central venous pressure catheter, and images of the anterior chest were immediately obtained by a gamma camera interfaced with a computer. Data was collected at 0.5 second intervals for 1 minute and subsequently analyzed using the method for quantitation of left-to-right shunts described by Askenazi and colleagues.7The derived pulmonary time-activity histogram, and the gamma function fit are shown in Fig. 3. The gamma fit approximates the first passage of tracer through the lungs without recirculation, and the area under the curve is proportional to the pulmonary blood flow. The difference between the fitted curve and the original data is due initially to recirculation secondary to the shunt, followed by recirculation of tracer that has passed through the systemic
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circulation. In normal individuals the pulmonary curve and gamma fit closely approximate each other until systemic recirculation occurs. In this case, however, there is a very early deviation of data from the gamma fit suggesting a large left-to-right shunt. The presence of a shunt was also confirmed visually by persistence of radioactivity over the lung fields and right heart chambers. The calculated ratio of pulmonary to systemic blood flow (&p/&s) was greater than 3. Published reports have shown close correlation between the nuclide angiocardiography in leftto-right shunts with &p/&s ratio of 1.2 to 3.0. Shunts in which the ratio of pulmonary to systemic blood flow is greater than 3 will not escape detection, but frequently cannot be precisely quantitated by this method. Precise quantitation of shunts of this magnitude, however, is probably not of clinical importance. This technique is non-invasive and requires a minimum of patient time in the nuclear medicine clinic. Thus, it is well suited for the critically ill individual in whom angiography may not be well tolerated. DR. WHEELER: The patient’s course in the coronary care unit was one of continued hyperglycemia managed with insulin, subcutaneous or intravenous, as appropriate. The patient maintained a persistent respiratory alkalosis which was managed with an O,-CO, delivery system. On this regimen, his arterial blood pH fell from 7.6 to 7.48. The patient developed severe azotemia probably secondary to poor cardiac output. Efforts were made to fluid re-expand the patient while carefully following his ability to oxygenate. Vasodilator ventricular unloading therapy (nitroglycerin paste) was begun on the eighth hospital day. The patient remained relatively stable through the first 13 days of his hospitalization. It should be noted that throughout this period, the patient refused any type of surgical intervention on the basis of his religion. On the 14th hospital day, the patient developed a purulent discharge from a central catheter site and Staphylococcus aureus was cultured from the blood as well as the wound. Intravenous penicillin therapy was initiated. Because of a change in mental status and a decrease in urine output, the patient was given low dose dopamine therapy on the 17th hospital day. The patient responded and, by the 19th hospital day, was awake and lucid. On the evening of the 19th hospital day, the patient became
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Fig. 4. Ventricular septal defect, produced by rupture of the septal myocardium following a myocardial infarct. From the left side of the heart (upperpanel) the defect is clearly seen in the mid-ventricular septum just beneath the anterior leaflet of the mitral valve. The. smooth margins of the defect seen from the right side of the heart (lowerpanel) suggest that the rupture of the ventricular septum occurred weeks before the patient’s demise.
hypotensive. Nitroglycerin paste was discontinued and dopamine was increased slightly. On the morning of the 20th hospital day, his urine output decreased. He became hypothermic, developed a wide QRS and sinus brachycardia, and died. DR. BEDYNEK: Dr. Wheeler has brought up the usual problem in such patients; the differential between ventricular septal rupture and papillary muscle rupture. This differential is difficult on
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the clinical grounds, alone, although our patient had findings pointing to the former. An accurate diagnosis can obviously be made by taking the patient to the cardiac catheterization laboratory and doing both right- and left-sided heart catheterization. A left ventriculogram in the steep left anterior oblique projection has its advocates since this will demonstrate a ventricular septal defect or mitral insufficiency. This procedure has the added advantage of revealing a co-existent ventricular aneurysm, and elucidating the functional status of the remaining viable myocardium. Since the patient is presumed a candidate for reparative surgery at this point, coronary angiography is often considered necessary and can be done concurrently. The disadvantages obviously include the poor tolerance of acutely ill patients to injections of fairly large volumes of contrast medium into the irritable left ventricle with the likelihood of ectopy, acute worsening of failure due to the volume effect, and the possibility of dislodging mural thrombi with embolization to the systemic circulation. An alternate approach now possible in most coronary and intensive care units does not require the transportation of the patient to the catheterization laboratory, but can usually be done at the bedside with the anticipation of an accurate differential diagnosis at least between the two most likely possibilities-that is ventricular septal rupture and papillary muscle rupture. This is the technique of Swan and associates,“. 9 which is generally regarded as more convenient, more rapid, and safer than even conventional rightsided catheterization. This technique was designed precisely for this purpose of differentiating ventricular septal from papillary muscle rupture. The diagnosis of ventricular septal rupture is suggested by a step-up of one volume per cent or greater of oxygen content in the blood of the right ventricle, compared to the right atrium.“’ The presence of “giant V waves” in the pulmonary wedge tracing without an oxygen step-up supports the diagnosis of acute mitral insufficiency from papillary muscle rupture. The obvious disadvantages are the inability of the technique to provide data on left ventricular function and anatomy, and failure to visualize the coronary vessels. This procedure was attempted in our patient in the catheterization laboratory, but was unsuccessful because of recurrent ventricular fibrillation, and the patient was returned to the
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coronary care unit without definitive diagnosis. Other reports have stressed the safety of this technique, but in our case the rapid whipping of the catheter from the right ventricle to the pulmonary outflow tract, presumably under the influence of an augmented right ventricular output, was enough to irritate the right ventricular endocardium and produce arrhythmia. Our experience is in keeping with a recent report of Kaplan and co-workers” of serious complications of ventricular ectopy when a patient was studied in the cardiac catheterization laboratory following rupture of the ventricular septum. The definitive diagnostic procedure carried out in this patient was a radionuclide angiocardiogram.‘? This technique is simpler and less hazardous than other techniques. The time required to do this study is usually quite short, and the size of the left-to-right shunt in terms of a ratio of pulmonic to systemic flow can usually be accurately determined, an advantage of this technique over the transvenous placement of a platinum-tipped electrode in the right ventricle and inhalation of hydrogen gas. The disadvantage of the isotope technique is that it cannot accurately localize the shunt. The presence, however, of a murmur and thrill at the left sternal border, in the presence of a documented intracardiac shunt, is presumptive evidence of a ventricular septal defect. In our patient the radionuclide angiocardiogram documented the presence of a large left-to-right shunt. I should mention the recent application of echocardiography to the differential diagnosis in question. In patients with ventricular septal rupture the findings are not specific, and consist of dilatation of the right ventricle, normal septal motion, and occasionally slight increase in left atria1 diameter. In one report there was an unusual pattern of mitral valve motion consisting of closure of the mitral valve after initial opening in early diastole followed by almost complete reopening of the valve.13 The pattern suggested increased blood flow across the mitral valve. In contrast the echocardiographic findings in acute mitral insufficiency following rupture of the chordae tendineae include flail leaflets, abnormalities of coaptation, abnormal movements of the leaflets in diastole, and systolic fluttering of the leaflets.” Although I suspect the findings would be simi-
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lar, I do not know of a case report of the echocardiographic findings in rupture of a papillary muscle. Furthermore, I do not believe these findings can be regarded as specific enough for definitive diagnosis. A new technique, pulsed Doppler echocardiography, which allows detection of direction, as well as location of tubulent blood flow, has been applied to differentiation of ventricular septal defect from mitral regurgitation in children.‘” In 39 of 40 cases the findings with this technique agreed with the clinical or catheterization evidence. This technique may be applicable to the problem under discussion in the future. Early definitive diagnosis is essential in these patients. Immediate surgery, in spite of the fact that such surgery is less successful when done early in the course of either ventricular septal defect or papillary muscle rupture, offers the only hope of reducing mortality rate. There are reports of survival rates of up to 50 per cent with early surgery in either ventricular septal or papillary muscle rupture, even in patients with dramatic clinical deterioration. Without surgery, the mortality rate in these patients is virtually 100 per cent. Unfortunately, our patient refused surgery. In summary, my diagnosis is ventricular septal rupture with large left-to-right shunt across an acquired ventricular septal defect occurring following an acute anteroseptal myocardial infarction. Autopsy
findings
At autopsy the heart was enlarged and weighed 565 grams. The lumens of the coronary arteries were extensively compromised by atherosclerotic plaques with 80 per cent occlusion of the left anterior descending artery, 70 per cent occlusion of the right coronary artery, and near total occlusion of the posterior branch of the left circumflex artery. No thrombi were found, however, in any of the coronary arteries. On opening the heart, there was a large defect in the anterior, mid-ventricular septum measuring 1.5 to 2.0 cm. in diameter (Fig. 4). The edgesof the defect were smooth and the defect was surrounded by a healing infarct which involved the entire ventricular septum but spared the anterior papillary muscle. Microscopically the area of the infarct consisted of proliferating fibrous tissue and abundant chronic inflammatoDR. JOHN J. FENOGLIO:
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ry cells, predominantly lymphocytes and histiocytes. Islands of necrotic, hyalinized cardiac muscle were trapped within the fibrous tissue and surrounded by chronic inflammatory cells. There was no evidence of an acute infarct, as evidenced by infiltrates of polymorphonuclear cells, even in the areas of necrotic myocardium. Microscopically the infarct was three to six weeks of age. The margins of the ventricular septal defect consisted of proliferating fibrous tissue and the surface was covered by endocardial cells, suggesting that the ventricular septum ruptured during the acute phase of the myocardial infarct, within the first two weeks. A small organizing mural thrombus was present in the right atrium. There was evidence of extensive acute and chronic passive congestion in the other viscera, especially in the lungs, liver, and spleen. Diagnoses: Coronary atherosclerosis, moderate to severe, with three vessel involvement; myocardial infarct, recent, healing, septal, with rupture of the ventricular septum. DR. HUGH A. MCALLISTER: Recently Vlodaver and Edwards’ reviewed their experience with 98 hearts with rupture of some portion of the left ventricle or ventricular septum as a complication of acute myocardial infarction. Anteroseptal infarction was associated with ventricular septal rupture in 50 per cent of their cases; inferior location of the infarct accounted for 28 per cent. Inferiolateral location of the underlying infarct was the most common situation in ruptured papillary muscle. In each of their cases involving rupture of the left ventricular free wall or of the ventricular septum, whether isolated or in association with rupture of another structure, the infarct was transmural. In contrast, the infarct was subendocardial in slightly over 50 per cent of the patients with isolated rupture of a papillary muscle. As in other studies, rupture of the anterolateral papillary muscle was less common than rupture of the posteromedial papillary muscle. Again, similar to the observation of others, the time of rupture of the ventricular septum or of a papillary muscle after the onset of myocardial infarction was commonly within the first week, with the greatest concentration by the third day. Death within one week was usual after rupture of the ventricular septum or with total rupture of a papillary muscle. In the series by Vlodaver and Edwards,” atrio-
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ventricular conduction disturbances were observed in 36 per cent of 17 cases with rupture of the ventricular septum. James,“’ however, reported the findings in five patients with acute posterior myocardial infarction by electrocardiographic definition who died following rupture of the ventricular septum. These five patients developed varying degrees of atrioventricular block prior to rupture of the ventricular septum. In three of these five, the time of septal rupture coincided with the resumption of conducted sinus rhythm. Multiple major coronary artery atheroma were present in all five of these hearts, and a recent thrombus was present in the right coronary artery in four of these five cases. Multiple atheroma with significant luminal narrowing are usually present in each of the major coronary arteries in patients with rupture of the ventricular septum. The role of the thrombus remains controversial. REFERENCES
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Holloway, D. H.: Systolic murmur developing after myocardial ischemia or infarction. Differential diagnosis, J.A.M.A. 191: 888, 1965. Heilekila, J.: Mitral incompetence as a complication of acute myocardial infarction, Acta Med. Stand. 182 (Suppl. 475):1, 1967. Vlodaver, Z., and Edwards, J.: Rupture of ventricular septum or papillary muscle complicating myocardial infarction, Circulation 55:815, 1977. Phillips, J. H., DePasquale, N. P., and Burch, G. E.: Electrocardiogram in infarction of anterolateral papillary muscle, AM. HEART J. 66:338, 1963. Friedman, H. S., Kuhn, L. A., and Kate, A. M.: Clinical and electrocardiographic features of cardiac rupture following acute myocardial infarction, Am. d. Med. 50:709, 1971. Eisenberg, S., and Suyemoto, J.: Rupture of a papillary muscle of the tricuspid valve following acute myocardial infarction. Report of a case, Circulation 30588, 1964. Askenazi, J., Ahnberg, D. S., Korngold, E., et al.: Quantitative radionuclide angiocardiography: Detection and quantitation of left to right shunts, Am. J. Cardiol. 37:386, 1976. Ganz, W. W., Forrester, J. S., Chonette, D.. et al.: A new flow-directed catheter technique for measurement of pulmonary artery and capillary wedge pressure without fluoroscopy, Am. J. Cardiol. 25:96, 1970. Swan, H. J. C., Ganz, W. W., Forrester, J. S., et al.: Catheterization of the heart in man with the use of a flow directed balloon-tipped catheter, N. Engl. J. Med. 283:447, 1970. Meister, S. G., and Helfant, R. H.: Rapid bedside differentiation of ruptured interventricular septum from acute mitral insufficiency, N. Engl. J. Med. 287:1024, 1972. Kaplan, M. A., Harris, C. N., Kay, J. H., et al.: Postinfarctional ventricular septal rupture. Clinical approach and surgical results, Chest 69:734, 1976. Gustafson, A., Nordenfelt, I., and White, T.: Diagnosis of ventricular septal defect in acute myocardial infarction
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Information
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Stevenson, J. G., Kawabori, I., and Gunteroth, W. G.: Differentiation of ventricular septal defects from mitral regurgitation by pulsed Doppler echocardiography, Circulation 56:14, 1977. James, T. N.: De Subitaneis Mortibus: XXIV. Ruptured interventricular septum and heart block, Circulation 55:934, 1977.
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Rupture of the ventricular complication of myocardial
septum as a infarction*
Julius L. Bedynek, M.D., COL, MC, USA John J. Fenoglio, Jr., M.D., MAJ, MC, USAR Hugh A. McAllister, Jr., M.D., LTC, MC, USA Washington, D. C., and Neul York, N. Y.
CLINICAL SUMMARY: This 67-year-old man was well until 3 weeks prior to admission when he experienced chest pain and shortness of breath. Nine days prior to admission, after an episode of chest pain that lasted an hour and a half, the patient reported to a community hospital for evaluation. An electrocardiogram was interpreted as normal (Fig. 1). The patient returned home and went about his daily activities which included yard work and lifting heavy objects. Three days prior to admission, the patient experienced severe shortness of breath and malaise. This increased until the day of admission when he again went to the community hospital. At this time a new systolic murmur was heard. The electrocardiogram was unchanged and was now interpreted as compatible with an acute anteroseptal myocardial infarction. The patient was transferred to Walter Reed Army Medical Center for evaluation. He denied any cardiac awareness, palpitations, paroxysmal nocturnal dyspnea, orthopnea, or edema. He had no fever or chills. The patient had adult onset diabetes mellitus, controlled with diet, and a vague history of hypertension which was never treated. There was no family history of heart disease. The patient denied having rheumatic or scarlet fever, gout, or hyperlipoproteinFrom the Department of Cardiology, Walter Reed Army Medical Center, Washington, D. C., the 320th Evacuation Hospital, 8th Medical Brigade, New York, N. Y.; and the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, D. C. Received for publication Apr. 21, 1978. Reprint requests: LTC Hugh A. McAllister, Jr., MC, USA, Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, D. C. 20306. *The opinions or assertions contained herein are the private views of the authors and are not to be construed as being official or as reflecting the views of the Department of the Army or the Department of Defense.
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8 1979 The
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Fig. 1. Electrocardiogram sion.
taken
nine
days
prior
to admk
emia. He was taking no medications and was a nonsmoker. On physical examination the patient was in moderate respiratory distress, although alert and oriented. The pulse was regular and 104 per minute; respirations were 24 per minute and labored, and the blood pressure was 110/70 mm. Hg. He was afebrile. There was no jugular venous distension. The carotid upstroke was normal. On auscultation bilateral basilar rfiles were heard as high as the scapulae. There was a precordial systolic thrill felt best at the left lower sternal border. The patient had a Grade IV/VI holosystolic murmur heard best at the lower left sternal border and radiating over the entire precordium. In addition, there was a Grade I-II early diastolic rumble heard best at the apex. S, and S, were normal. The liver span at the right mid-clavicular line was 10 cm. The liver was tender and the left lobe was prominent. The rest of the physical examination was normal. The patient had a mild leukocytosis with a shift to the left. Urinalysis was normal. The blood
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anteroposterior
chest
x-ray
taken
on
glucose was 437 mg per cent. The blood urea nitrogen was 1.9 mg per cent. The serum electrolytes were all abnormal; sodium 129 mEq./L., potassium 5.0 mEq./L., chloride 97 mEq./L., and CO, 17 mEq./L. Arterial blood gases were drawn while the patient was breathing room air. The oxygen partial pressure (PO,) was 80 mm. Hg; the carbon dioxide partial pressure (PCO,) was 18 mm. Hg, and the pH was 7.54. On admission the serum glutamic oxaloacetic transaminase (SGOT) was 802 units; lactic dehydrogenase (LDH) 2,600 units, creatine phosphokinase (CPK) activity 63 units. All LDH isoenzyme fractions were elevated, although fractions one and two (cardiac fractions) were markedly increased. CPK isoenzymes were all within the M band. Thyroid function tests were normal. Clinical
discussion
DR. JULIUS L. BEDYNEK: First I should like to ask Dr. Anderson to interpret the electrocardiograms and chest x-rays. DR. WARREN T. ANDERSON: On the initial tracing 9 days prior to admission (Fig. 1) there was a sinus tachycardia of 110 beats per minute. The slow R wave progression through V, and ST segment elevation in V, through V, suggest an acute anteroseptal myocardial infarction. The tracing on admission and subsequent tracings demonstrated further evolution of an anteroseptal myocardial infarction. The chest x-ray on
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Fig. 3. Pulmonary time-activity function fit (0). The marked nary time-activity and gamma shortly after peak suggests the shunt. The calculated ratio of flow is greater than 3.
histogram ( + ) and gamma difference between the pulmofunction fit curves that occurs presence of a large left-to-right pulmonary to systemic blood
admission (Fig. 2), although a portable AP film, demonstrated mild cardiomegaly and prominent pulmonary vascularity. On multiple repeat films throughout the hospital course there was progressive cardiomegaly and marked increased pulmonary congestion. DR. BEDYNEK: In summary this was a 67-yearold man who suffered an acute anterior myocardial infarction. Six days later he suddenly developed signs and symptoms of congestive heart failure with pulmonary congestion. Subsequently a loud systolic precordial murmur and a thrill, both maximal at the lower left sternal border, were noted. This case poses the problem of the differential diagnosis of systolic murmurs associated with the sudden clinical deterioration of the patient with an acute myocardial infarction. The determination of the cause of the systolic murmur is of practical importance in predicting the course and determining the management of these patients. The most important entities in this differential diagnosis are rupture of the ventricular septum and rupture of a papillary muscle with acute mitral regurgitation. However, papillary muscle dysfunction and acute dilatation of the left ventricle may also be associated with the sudden
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I. Differential infarction
Table
Incidence
Papillary muscle rupture
Up to 1% of transmural infarction
Up to 1% of all cases
Usually anteroseptal or posteroseptal
Usually
Appearance
4 to 7 days tion
Murmur
Left sternal border. Almost always present and loud (Gr. III & IV) Left sternal border. Present in 50% of cases In up to 40% Progressive w/left& right-sided features
Later than septal rupture/even wks. to mos. Apex w/radiation to axilla or base (Gr. II or less). Absent in 40% Apex and unusually present
of infarction
Thrill
Conduction defect Heart failure
Poor with surgery
Prognosis
post-infarc-
or without
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inferior
Unusual Acute onset of leftsided failure & acute pulmonary edema Guarded with or without surgery
appearance of a loud systolic murmur and dramatic deterioration of the patient. The important criteria in the differential diagnosis of these systolic murmurs are summarized in Table I. Our patient had many of the features of acute rupture of the ventricular septum. This unusual complication of myocardial infarction occurs in up to one per cent of transmural infarctions involving the ventricular septum.’ The murmur and thrill usually appear four to seven days after the infarct, as apparently was the case in our patient, and are usually maximal at the lower left sternal border, a location consistent with the findings in congenital ventricular septal defects. I can recall, however, two patients which were exceptions to this rule. In these two patients the murmur and thrill were most intense at the apex and in the axilla. In both patients a ventricular septal defect was proven by cardiac catheterization. I know of no good explanation for the paradoxical physical findings (murmur and thrill more intense at the apex than at the left sternal border) in either of these patients. Since the His bundle and bundle branches may
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diagnosis of systolic murmurs appearing during the course of myocardial
Septal rupture
Location
pathologic
More frequent (up to 57% of infarctions) & more transient
Not clear, but when present probably clears w/treatment of failure t Ischemia and/or infarction + ST-T changes anteroLocation not critical lateral or inferior At time of chest pain At time of dilatation (ischemia) & may persist II/VI or less at apex Apex and soft (Gr. I to II in 2/3)
Very
unusual
Unusual
Unusual Not prominent
Unusual Common
Good short-term; poor long-term due to new infarction
Not
clear
be involved in septal infarcts, a conduction defect is present in up to 40 per cent of the patients with ventricular septal rupture. This patient did not have a conduction defect. Usually there is a substantial left-to-right intracardiac shunt across the defect and features of left and right heart failure are virtually constant in these patients. In my experience patients without prominent congestive heart failure have had small ventricular septal defects. These patients have a better overall prognosis, since successful surgical therapy largely depends on the ability of the patient to survive for four to six weeks after infarction, allowing time for the margins of the infarcted myocardium to heal sufficiently to support sutures. Rupture of a papillary muscle is also frequently associated with dramatic clinical deterioration and the appearance of a loud systolic murmur. These patients usually have an infero-lateral myocardial infarct.“. 3 Papillary muscle rupture occurs in up to one per cent in all cases of myocardial infarct, usually later than ventricular septal rupture and occasionally several months
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after the infarct. The murmur of mitral regurgitation may be absent in up to 40 per cent of these cases, and when present is usually loudest at the apex with radiation to the axilla or to the base of the heart. A murmur is more frequently detected with partial rupture of a papillary muscle. Radiation to the base implies rupture of the posterior medial papillary muscle, and radiation to the apex rupture of the anterior papillary muscle. A thrill is uncommon, but, if present, is frequently most intense at the apex. Conduction defects are rare. Heart failure is most often of acute onset with fulminant pulmonary edema. The prognosis is guarded and is often worse than that in ventricular septal rupture, except with partial rupture of a papillary muscle. Since survival is longer with partial rupture, attempts at surgical repair are more frequently successful. Papillary muscle dysfunction without papillary muscle rupture is also a frequent cause of a systolic murmur appearing during the course of myocardial infarction and has been reported in up to 5’7 per cent of all cases of infarction. The murmur is usually pansystolic and apical in location, and is most often softer than the murmur of septal rupture. It is Grade I to II/VI in two thirds, and Grades II to IV/VI in one third of the patients. The murmur is usually not associated with marked deterioration of the patient but may be associated with both radiographic and clinical findings of left ventricular failure. The murmur may be appreciated during chest pain connoting myocardial ischemia and may be accompanied by ST and T wave changes in the ECG. These ECG changes include mild to severe depression of the J junction with convex or concave upward deformity of the ST segment and frequently terminal inverstion of the T wave or depression of the T-U segment with U wave inversion in the middle and left precordial leads especially in anterolateral papillary muscle dysfunction.’ Papillary muscle dysfunction may be a manifestation of transient severe ischemia, or may imply the infarction of a papillary muscle. Thrills, conduction defects, and severe heart failure are uncommon. The prognosis is good for short-term survival. Long-term prognosis, however, is poor as these patients frequently have severe obstructive coronary disease. Acute left ventricular dilatation during the course of myocardial infarction may disrupt the configuration of the mitral valvular apparatus
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sufficiently to cause mitral insuificincy. As in papillary muscle dysfunction, myocardial infarction is not necessary for the appearance of this murmur, and it may occur with transient severe myocardial &hernia or ischemic myocardiopathy. It is hypothesized that the mitral valve becomes incompetent because the bases of the papillary muscles are widely separated due to dilatation of the ventricular cavity and the chordae tendineae lie at an obtuse angle to the mitral leaflets. The result is incomplete closure of the mitral valve during ventricular systole. This explanation is currently preferred over the more classical one that the mitral valve ring is simply dilated. I am not aware, however, that either hypothesis has been proven by objective investigations. Heart failure is common, but rarely of sudden onset. The clinical history and physical findings suggest either left ventricular dilatation or papillary muscle dysfunction as a cause of the murmur. This discussion would not be complete without mentioning three other possible causes of systolic murmurs, all unlikely in our patient, appearing following myocardial infarction. These are pericarditis, rupture of the ventricular free wall, and right ventricular infarction with tricuspid regurgitation. Pericardial friction rubs secondary to pericarditis are quite frequent during the course of acute myocardial infarction, especially when listened for carefully. It is entirely possible that a systolic friction rub could be confused with a systolic murmur, and in the occasional instance where pericardial fluid is copious, deterioration due to pericardial tamponade might result after the appearance of such an auscultatory finding. The careful search for a three-part friction rub would help eliminate this point of confusion. Rupture of the ventricular free wall may be preceded by a transient systolic murmur.; This is soon followed by signs of cardiac tamponade. The systolic murmur has been attributed to actual systolic leakage of blood into the pericardial cavity. Electromechanical dissociation is common and usually fatal within minutes in these patients. Those few patients who have survived with expeditious surgery have done so only because there was a high index of suspicion and because pericardiocentesis was carried out while the patient was in route to surgery. I am not, however, aware of any long-term survivors. Rupture of a tricuspid valve papillary muscle
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producing a systolic murmur at the lower sternal border in the course of myocardial infarction has been reported.fi In this single reported case the heart failure was predominantly right-sided. The two most likely diagnostic possibilities in our patient are ventricular septal rupture and papillary muscle rupture, and I will confine my further discussion to these two entities. The clinical course is, of course, of particular interest at this point. Dr. Wheeler cared for this patient in the coronary care unit, and I will call on him now to discuss the clinical course. DR. LEIGH WHEELER: The patient was admitted to the CCU where his deteriorating course was compatible with either ventricular septal perforation or acute mitral regurgitation secondary to a papillary muscle dysfunction. The patient was treated with digoxin, oxygen, and diuretic therapy. Because of the difficulty in identifying the cause of the systolic murmur, the patient was taken to the cardiac catheterization laboratory on the third hospital day where a balloon-tipped, flow directed catheter was introduced into the right heart. Each time the catheter tip was advanced to the right ventricle, it was rapidly ejected into the pulmonary artery and on four occasions the cardiac rhythm immediately deteriorated to ventricular fibrillation. The catheter was withdrawn, and the patient was successfully electrically defibrillated. Since a diagnosis was not established by catheterization, a radionuclide angiocardiogram was done by Dr. Kaminski. DR. ROBERT KAMINSKI: The radionuclide angiocardiogram was done on the seventh hospital day. A bolus of 15 mCi 99m Technetium pertechnetate was injected intravenously through a central venous pressure catheter, and images of the anterior chest were immediately obtained by a gamma camera interfaced with a computer. Data was collected at 0.5 second intervals for 1 minute and subsequently analyzed using the method for quantitation of left-to-right shunts described by Askenazi and colleagues.7The derived pulmonary time-activity histogram, and the gamma function fit are shown in Fig. 3. The gamma fit approximates the first passage of tracer through the lungs without recirculation, and the area under the curve is proportional to the pulmonary blood flow. The difference between the fitted curve and the original data is due initially to recirculation secondary to the shunt, followed by recirculation of tracer that has passed through the systemic
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circulation. In normal individuals the pulmonary curve and gamma fit closely approximate each other until systemic recirculation occurs. In this case, however, there is a very early deviation of data from the gamma fit suggesting a large left-to-right shunt. The presence of a shunt was also confirmed visually by persistence of radioactivity over the lung fields and right heart chambers. The calculated ratio of pulmonary to systemic blood flow (&p/&s) was greater than 3. Published reports have shown close correlation between the nuclide angiocardiography in leftto-right shunts with &p/&s ratio of 1.2 to 3.0. Shunts in which the ratio of pulmonary to systemic blood flow is greater than 3 will not escape detection, but frequently cannot be precisely quantitated by this method. Precise quantitation of shunts of this magnitude, however, is probably not of clinical importance. This technique is non-invasive and requires a minimum of patient time in the nuclear medicine clinic. Thus, it is well suited for the critically ill individual in whom angiography may not be well tolerated. DR. WHEELER: The patient’s course in the coronary care unit was one of continued hyperglycemia managed with insulin, subcutaneous or intravenous, as appropriate. The patient maintained a persistent respiratory alkalosis which was managed with an O,-CO, delivery system. On this regimen, his arterial blood pH fell from 7.6 to 7.48. The patient developed severe azotemia probably secondary to poor cardiac output. Efforts were made to fluid re-expand the patient while carefully following his ability to oxygenate. Vasodilator ventricular unloading therapy (nitroglycerin paste) was begun on the eighth hospital day. The patient remained relatively stable through the first 13 days of his hospitalization. It should be noted that throughout this period, the patient refused any type of surgical intervention on the basis of his religion. On the 14th hospital day, the patient developed a purulent discharge from a central catheter site and Staphylococcus aureus was cultured from the blood as well as the wound. Intravenous penicillin therapy was initiated. Because of a change in mental status and a decrease in urine output, the patient was given low dose dopamine therapy on the 17th hospital day. The patient responded and, by the 19th hospital day, was awake and lucid. On the evening of the 19th hospital day, the patient became
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Fig. 4. Ventricular septal defect, produced by rupture of the septal myocardium following a myocardial infarct. From the left side of the heart (upperpanel) the defect is clearly seen in the mid-ventricular septum just beneath the anterior leaflet of the mitral valve. The. smooth margins of the defect seen from the right side of the heart (lowerpanel) suggest that the rupture of the ventricular septum occurred weeks before the patient’s demise.
hypotensive. Nitroglycerin paste was discontinued and dopamine was increased slightly. On the morning of the 20th hospital day, his urine output decreased. He became hypothermic, developed a wide QRS and sinus brachycardia, and died. DR. BEDYNEK: Dr. Wheeler has brought up the usual problem in such patients; the differential between ventricular septal rupture and papillary muscle rupture. This differential is difficult on
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the clinical grounds, alone, although our patient had findings pointing to the former. An accurate diagnosis can obviously be made by taking the patient to the cardiac catheterization laboratory and doing both right- and left-sided heart catheterization. A left ventriculogram in the steep left anterior oblique projection has its advocates since this will demonstrate a ventricular septal defect or mitral insufficiency. This procedure has the added advantage of revealing a co-existent ventricular aneurysm, and elucidating the functional status of the remaining viable myocardium. Since the patient is presumed a candidate for reparative surgery at this point, coronary angiography is often considered necessary and can be done concurrently. The disadvantages obviously include the poor tolerance of acutely ill patients to injections of fairly large volumes of contrast medium into the irritable left ventricle with the likelihood of ectopy, acute worsening of failure due to the volume effect, and the possibility of dislodging mural thrombi with embolization to the systemic circulation. An alternate approach now possible in most coronary and intensive care units does not require the transportation of the patient to the catheterization laboratory, but can usually be done at the bedside with the anticipation of an accurate differential diagnosis at least between the two most likely possibilities-that is ventricular septal rupture and papillary muscle rupture. This is the technique of Swan and associates,“. 9 which is generally regarded as more convenient, more rapid, and safer than even conventional rightsided catheterization. This technique was designed precisely for this purpose of differentiating ventricular septal from papillary muscle rupture. The diagnosis of ventricular septal rupture is suggested by a step-up of one volume per cent or greater of oxygen content in the blood of the right ventricle, compared to the right atrium.“’ The presence of “giant V waves” in the pulmonary wedge tracing without an oxygen step-up supports the diagnosis of acute mitral insufficiency from papillary muscle rupture. The obvious disadvantages are the inability of the technique to provide data on left ventricular function and anatomy, and failure to visualize the coronary vessels. This procedure was attempted in our patient in the catheterization laboratory, but was unsuccessful because of recurrent ventricular fibrillation, and the patient was returned to the
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coronary care unit without definitive diagnosis. Other reports have stressed the safety of this technique, but in our case the rapid whipping of the catheter from the right ventricle to the pulmonary outflow tract, presumably under the influence of an augmented right ventricular output, was enough to irritate the right ventricular endocardium and produce arrhythmia. Our experience is in keeping with a recent report of Kaplan and co-workers” of serious complications of ventricular ectopy when a patient was studied in the cardiac catheterization laboratory following rupture of the ventricular septum. The definitive diagnostic procedure carried out in this patient was a radionuclide angiocardiogram.‘? This technique is simpler and less hazardous than other techniques. The time required to do this study is usually quite short, and the size of the left-to-right shunt in terms of a ratio of pulmonic to systemic flow can usually be accurately determined, an advantage of this technique over the transvenous placement of a platinum-tipped electrode in the right ventricle and inhalation of hydrogen gas. The disadvantage of the isotope technique is that it cannot accurately localize the shunt. The presence, however, of a murmur and thrill at the left sternal border, in the presence of a documented intracardiac shunt, is presumptive evidence of a ventricular septal defect. In our patient the radionuclide angiocardiogram documented the presence of a large left-to-right shunt. I should mention the recent application of echocardiography to the differential diagnosis in question. In patients with ventricular septal rupture the findings are not specific, and consist of dilatation of the right ventricle, normal septal motion, and occasionally slight increase in left atria1 diameter. In one report there was an unusual pattern of mitral valve motion consisting of closure of the mitral valve after initial opening in early diastole followed by almost complete reopening of the valve.13 The pattern suggested increased blood flow across the mitral valve. In contrast the echocardiographic findings in acute mitral insufficiency following rupture of the chordae tendineae include flail leaflets, abnormalities of coaptation, abnormal movements of the leaflets in diastole, and systolic fluttering of the leaflets.” Although I suspect the findings would be simi-
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lar, I do not know of a case report of the echocardiographic findings in rupture of a papillary muscle. Furthermore, I do not believe these findings can be regarded as specific enough for definitive diagnosis. A new technique, pulsed Doppler echocardiography, which allows detection of direction, as well as location of tubulent blood flow, has been applied to differentiation of ventricular septal defect from mitral regurgitation in children.‘” In 39 of 40 cases the findings with this technique agreed with the clinical or catheterization evidence. This technique may be applicable to the problem under discussion in the future. Early definitive diagnosis is essential in these patients. Immediate surgery, in spite of the fact that such surgery is less successful when done early in the course of either ventricular septal defect or papillary muscle rupture, offers the only hope of reducing mortality rate. There are reports of survival rates of up to 50 per cent with early surgery in either ventricular septal or papillary muscle rupture, even in patients with dramatic clinical deterioration. Without surgery, the mortality rate in these patients is virtually 100 per cent. Unfortunately, our patient refused surgery. In summary, my diagnosis is ventricular septal rupture with large left-to-right shunt across an acquired ventricular septal defect occurring following an acute anteroseptal myocardial infarction. Autopsy
findings
At autopsy the heart was enlarged and weighed 565 grams. The lumens of the coronary arteries were extensively compromised by atherosclerotic plaques with 80 per cent occlusion of the left anterior descending artery, 70 per cent occlusion of the right coronary artery, and near total occlusion of the posterior branch of the left circumflex artery. No thrombi were found, however, in any of the coronary arteries. On opening the heart, there was a large defect in the anterior, mid-ventricular septum measuring 1.5 to 2.0 cm. in diameter (Fig. 4). The edgesof the defect were smooth and the defect was surrounded by a healing infarct which involved the entire ventricular septum but spared the anterior papillary muscle. Microscopically the area of the infarct consisted of proliferating fibrous tissue and abundant chronic inflammatoDR. JOHN J. FENOGLIO:
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ry cells, predominantly lymphocytes and histiocytes. Islands of necrotic, hyalinized cardiac muscle were trapped within the fibrous tissue and surrounded by chronic inflammatory cells. There was no evidence of an acute infarct, as evidenced by infiltrates of polymorphonuclear cells, even in the areas of necrotic myocardium. Microscopically the infarct was three to six weeks of age. The margins of the ventricular septal defect consisted of proliferating fibrous tissue and the surface was covered by endocardial cells, suggesting that the ventricular septum ruptured during the acute phase of the myocardial infarct, within the first two weeks. A small organizing mural thrombus was present in the right atrium. There was evidence of extensive acute and chronic passive congestion in the other viscera, especially in the lungs, liver, and spleen. Diagnoses: Coronary atherosclerosis, moderate to severe, with three vessel involvement; myocardial infarct, recent, healing, septal, with rupture of the ventricular septum. DR. HUGH A. MCALLISTER: Recently Vlodaver and Edwards’ reviewed their experience with 98 hearts with rupture of some portion of the left ventricle or ventricular septum as a complication of acute myocardial infarction. Anteroseptal infarction was associated with ventricular septal rupture in 50 per cent of their cases; inferior location of the infarct accounted for 28 per cent. Inferiolateral location of the underlying infarct was the most common situation in ruptured papillary muscle. In each of their cases involving rupture of the left ventricular free wall or of the ventricular septum, whether isolated or in association with rupture of another structure, the infarct was transmural. In contrast, the infarct was subendocardial in slightly over 50 per cent of the patients with isolated rupture of a papillary muscle. As in other studies, rupture of the anterolateral papillary muscle was less common than rupture of the posteromedial papillary muscle. Again, similar to the observation of others, the time of rupture of the ventricular septum or of a papillary muscle after the onset of myocardial infarction was commonly within the first week, with the greatest concentration by the third day. Death within one week was usual after rupture of the ventricular septum or with total rupture of a papillary muscle. In the series by Vlodaver and Edwards,” atrio-
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ventricular conduction disturbances were observed in 36 per cent of 17 cases with rupture of the ventricular septum. James,“’ however, reported the findings in five patients with acute posterior myocardial infarction by electrocardiographic definition who died following rupture of the ventricular septum. These five patients developed varying degrees of atrioventricular block prior to rupture of the ventricular septum. In three of these five, the time of septal rupture coincided with the resumption of conducted sinus rhythm. Multiple major coronary artery atheroma were present in all five of these hearts, and a recent thrombus was present in the right coronary artery in four of these five cases. Multiple atheroma with significant luminal narrowing are usually present in each of the major coronary arteries in patients with rupture of the ventricular septum. The role of the thrombus remains controversial. REFERENCES
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2.
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4.
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Holloway, D. H.: Systolic murmur developing after myocardial ischemia or infarction. Differential diagnosis, J.A.M.A. 191: 888, 1965. Heilekila, J.: Mitral incompetence as a complication of acute myocardial infarction, Acta Med. Stand. 182 (Suppl. 475):1, 1967. Vlodaver, Z., and Edwards, J.: Rupture of ventricular septum or papillary muscle complicating myocardial infarction, Circulation 55:815, 1977. Phillips, J. H., DePasquale, N. P., and Burch, G. E.: Electrocardiogram in infarction of anterolateral papillary muscle, AM. HEART J. 66:338, 1963. Friedman, H. S., Kuhn, L. A., and Kate, A. M.: Clinical and electrocardiographic features of cardiac rupture following acute myocardial infarction, Am. d. Med. 50:709, 1971. Eisenberg, S., and Suyemoto, J.: Rupture of a papillary muscle of the tricuspid valve following acute myocardial infarction. Report of a case, Circulation 30588, 1964. Askenazi, J., Ahnberg, D. S., Korngold, E., et al.: Quantitative radionuclide angiocardiography: Detection and quantitation of left to right shunts, Am. J. Cardiol. 37:386, 1976. Ganz, W. W., Forrester, J. S., Chonette, D.. et al.: A new flow-directed catheter technique for measurement of pulmonary artery and capillary wedge pressure without fluoroscopy, Am. J. Cardiol. 25:96, 1970. Swan, H. J. C., Ganz, W. W., Forrester, J. S., et al.: Catheterization of the heart in man with the use of a flow directed balloon-tipped catheter, N. Engl. J. Med. 283:447, 1970. Meister, S. G., and Helfant, R. H.: Rapid bedside differentiation of ruptured interventricular septum from acute mitral insufficiency, N. Engl. J. Med. 287:1024, 1972. Kaplan, M. A., Harris, C. N., Kay, J. H., et al.: Postinfarctional ventricular septal rupture. Clinical approach and surgical results, Chest 69:734, 1976. Gustafson, A., Nordenfelt, I., and White, T.: Diagnosis of ventricular septal defect in acute myocardial infarction
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Stevenson, J. G., Kawabori, I., and Gunteroth, W. G.: Differentiation of ventricular septal defects from mitral regurgitation by pulsed Doppler echocardiography, Circulation 56:14, 1977. James, T. N.: De Subitaneis Mortibus: XXIV. Ruptured interventricular septum and heart block, Circulation 55:934, 1977.
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