Catheterization and Cardiovascular Diagnosis 5:289-294
(1979)
Echocardiographic Findings in Cardiogenic Shock Due to Right Ventricular Myocardial Infarction Uri Elkayam, MD, Stanley L. Halprin, MD, William Frishman, MD, Joel Strom, MD, and Martin N. Cohen, MD The echocardiographicfindings in a patient with cardiogenic shock secondaryto acute right ventricular myocardial infarction based on typical clinical, electrocardiographic, and hemodynamic features are described. The echocardiogram demonstrated a large RV/LV minor axis ratio caused by a volume overload of the right ventricle and an underfilled left ventricle. The interventricular septum showed abnormal movement, presumably due to right ventricular overload or severe disease of the left anterior descending coronary artery. Diminished septa1systolic thickening, as seen in our patient, may be explained by extension of the infarct from the right ventricle to the adjacent part of the septum. Predominant right ventricular involvement can be a cause for a correctable hypotension in patients with acute myocardial infarction and should therefore be recognized early. The echocardiographic picture demonstrated in our patient, when considered in conjunction with the clinical status, can be useful for early diagnosis. Key words: echocardiography, right ventricular myocardial infarction, cardiogenic shock
INTRODUCTION Acute myocardial infarction is usually associated with hemodynamic evidence of predominant left ventricular dysfunction, and it is for this reason that the diagnosis of right ventricular infarction is usually made at autopsy 11-31. Recently some attention has been devoted to the circulatory events accompanying infarction of the right ventricle [MI.Experimental and clinical observation have helped demonstrate the unique hemodynamic characteristics of this syndrome [4-71. The man-
From the Division of Cardiology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York
Address reprint requests to Uri Elkayam, MD, Division of Cardiology, Cedars-Sinai Medical Center, 8700 Beverly Bivd, Los Angeles, CA 90048. Received December 5, 1978; revision accepted April 17, 1979.
0098-6569/79/0503-0289$01.400 1979 Alan R. Liss, Inc.
290
Elkayam e t al
agement of heart failure and shock associated with a predominant right ventricular infarction differs from that of left ventricular infarction [ 5 ] . For this reason and since there is also a favorable prognosis associated with the appropriate management of shock secondary to right ventricular infarction, an early recognition of this condition would be most helpful. This report describes the echocardiographic findings in a patient with cardiogenic shock and typical clinical, electrocardiographic, and hemodynamic features of acute myocardial infarction involving the right ventricle. CASEREPORT A 62-year-old woman was admitted to the Bronx Municipal Hospital with the diagnosis of acute myocardial infarction. She smoked one pack of cigarettes daily for 27 years. In addition, she had been hypertensive for the previous ten years and was treated with a variety of medications. For the preceding three years she had experienced chest pain and dyspnea on exertion. There was no other history of cardiac dysfunction. On the day of admission, while at rest, the patient developed a sharp pain, located initially between her scapulae, but which later radiated to her chest. It lasted 1% hours and was accompanied by diaphoresis. Physical examination on admission revealed a systemic blood pressure of 210/105 mm Hg. a regular pulse of 100 beats per minute, and a temperature of 37.2"C. There was nojugular venous distention at 45" and the lungs were clear. The first and second heart sounds were normal and of good quality, and an S, gallop was heard at the apex; there were no murmurs. The liver and spleen were not palpable and there was no ascites or pedal edema. The electrocardiogram demonstrated normal sinus rhythm, ST segment elevation in leads 11, 111, and aV, with reciprocal ST segment depression in leads I , aVLand V,-V,. There was no sign of conduction disturbances of any kind. There was slight cardiomegaly without pulmonary venous congestion on the admission x-ray. On the second hospital day the patient developed complete heart block unresponsive to 2 mg of intravenous atropine and requiring placement of a temporary pacemaker. She then developed hypotension with a systolic blood pressure in the 70-80 mm Hg range. Physical examination at this time revealed massive neck vein distention at 45", while the lungs remained clear. Right heart pressure determination at the bedside, using a flow-directed triple-lumen catheter, showed a right atrial mean pressure of 13 mm Hg, with no significant V wave, right ventricular pressure 19/13 mm Hg, pulmonary artery pressure 19/10 mm Hg, and a mean pulmonary capillary wedge pressure of 9 mm Hg. The cardiac output determined by thermodilution was 3.0 litedmin [cardiac index (CI) 1.8 liters/min/m*]. Blood samples taken from the right atrium, right ventricle, and pulmonary artery revealed no significant difference in oxygen saturation. The echocardiogram (Figs. 1 and 2), performed with the patient in the supine position, demonstrated a markedly enlarged right ventricle (3.7 cm) with good anterior wall motion. The interventricular septum moved paradoxically and showed decreased systolic thickening. The left ventricular diastolic diameter was reduced (2.9 cm), and the right ventricular-left ventricular minor axis ratio was significantly increased (1.27). The left ventricular posterior wall motion as well as the systolic thickening was normal. The mitral valve, although structurally normal, demonstrated a decreased diastolic closure rate (5 1 mm/sec).
Echocardiography in Right Ventricular Infarction
291
The patient was treated with large volumes of colloid, which raised the mean pulmonary capillary wedge pressure t o 18-20 mm Hg, resulting in an increase in the cardiac output to 3.94 liters/min (CI 2.4 liters/min/m2). The mean right atrial pressure increased to 24 mm Hg. In spite of a course complicated by the development of severe metabolic acidosis, bilateral pleural effusions, and ascites requiring peritoneal dialysis, abdominoscentesis, and pleuroscentesis, the patient improved. Regular sinus rhythm returned, and the pacemaker was discontinued by the tenth hospital day. The balloon-tip catheter was removed on the twelth hospital day, and the patient completed her convalescence in an uneventful manner. Radionuclide angiography was performed before discharge on the twenty-sixth hospital day. First-pass technique revealed no intracardiac shunt and a left ventricular ejection fraction of 38%. Gated blood pool studies were obtained in multiple positions and revealed mild enlargement of the left ventricle, with marked dilatation and poor contraction of the right ventricle.
Fig. 1. Echocardiogramshowing enlarged right Ventricular (RV) cavity (3.7 cm), small left ventricle (LV) (2.9 cm), preserved motion of the right ventricular anterior wall (RVAW), and lefi ventricular posterior wall (LVPW). In addition, the interventrlcular septum (IVS) shows abnormal motion and diminished thickening during systole. CW = chest wall.
292
Elkayam e t al
Fig. 2. Echocardiogram of patient demonstrating decreased diastolic closure rate of the mitral valve (E-F slope 51 mmlsec). AMV = anterfor leaflet of the mitral valve.
DISCUSSION In patients with an acute inferior myocardial infarction hemodynamic evidence of right ventricular failure disproportional to left ventricular failure is a strong indicator of predominant right ventricular involvement [5,61. This characteristic hemodynamic feature is reflected echocardiographically by an enlargement of the right ventricular minor dimension in association with findings of a relatively small left ventricle. Severe damage to the right ventricular myocardium with failure to contract leads to inadequate filling of the left ventricle. This hemodynamic situation explains the large RV/LV minor axis ratio in our patient and in other patients with RV myocardial infarction [81. Wade [21 in 1959 described the clinical and pathological findings of 11 patients with RV infarction, and reported involvement of the right ventricular posterior wall to be the major lesion in most of these cases. Although the amount of motion exhibited by the echoes of the right ventricular anterior wall has not been intensively investigated, one can assume that the marked systolic anterior motion of the right ventricular anterior wall in our patient (Fig. l), reflected a preserved anterior wall and was a compensatory phenomenon for the poorly moving posterior wall.
Echocardiography in Right Ventricular Infarction
293
There are two mechanisms that could explain the abnormal motion of the interventricular septum found in our patient: involvement of the septum by the ischemic process and right ventricular overload. Abnormal septal motion has been found t o be associated with disease of the left anterior descending coronary artery [P-1 11. Brown et a1 [lo] reported abnormal septal movement in 44% of patients with greater than 50% obstruction of the left anterior descending coronary artery. Although myocardial infarction involving the right ventricle is usually associated with occlusion of the main right coronary artery, it is often accompanied by severe disease in the left coronary arteries as well 121. Septal involvement has been reported by Sharpe et a1 [81 in six patients in whom scintigraphy provided direct anatomic evidence of right ventricular infarction. Abnormal septal motion in conjunction with an increased right ventricular dimensions is also considered to be the hallmark of right ventricular volume overload [ 121. These echocardiographic findings were described in atrial septal defect [41, partial and total anomalous venous drainage [13,141, Ebstein anomaly [151, and tricuspid and pulmonic insufficiency 1161, and it seems reasonable to conclude that right ventricular overload secondary to failure of contraction also contributes to the paradoxical septal motion demonstrated in our patient. Concomitant complicating lesions such as tricuspid valve insufficiency o r atrial septal defect could also have produced right ventricular overload in our patient. The absence of a systolic murmur or a significant V wave in the right atrial pressure recording does not support the diagnosis of tricuspid regurgitation. The presence of atrial septal defect was excluded by physical examination, electrocardiogram, oximetry, and radionuclide studies. The echocardiographic finding of diminished septal systolic thickening in our patient may be explained by the extension of the infarct from the right ventricular myocardium to the adjacent part of the posterior interventricular septum, which has been demonstrated in autopsy and scintigraphy studies in patients with right ventricular myocardial infarction [2,8,171. Although multiple parameters influence the mitral E-F slope [18-211 in an anatomically normal valve, it is largely a function of the rate of left ventricular filling during the diastolic rapid-filling phase [20]. Reduction of cardiac output and diminution of mitral flow are reported to cause a significant decrease in the E-F slope in normal mitral valves [21]. Impairment of left ventricular filling secondary to right ventricular pump failure and decreased cardiac output is probably the mechanism reducing the E-F slope in our patient. Although recent studies suggest that right ventricular infarction may be more common than previously assumed [8], it is still a rarely recognized clinical entity. Early recognition of the unique hemodynamics in patients with shock secondary to right ventricular infarction is essential for the appropriate therapeutic approach. The various echocardiographic features presented in our cases, when considered in conjunction with the clinical setting, present an echocardiographic picture that is sufficiently distinctive for the diagnosis of severe right ventricular infarction. REFERENCES 1 . Wartman WB, Hellerstein H K : The incidence of heart disease in 2,000 autopsies. Ann Intern Med 2k41-65, 1948. 2. Wade WG: The pathogenesis of infarction of the right ventricle. Br Heart J 21:545-554,
1959. 3. Ebhardt CR: Clinical and pathological observations in different types of acute myocardial infarction. Acta Med Scand Suppl 560:7, 1974.
294
El kayam et al
4. Guiha NH, Constantinos JL, Cohn JN: Predominant right ventricular dysfunction after right ventricular distruction in the dog. Am J Cardiol 33:254-258, 1974. 5 . Cohn JN, Guiha NH, Broder M I . Constantinos JL: Right ventricular infarction. Clinical and hemodynamic features. Am J Cardiol 33:209-214, 1974. 6. Rotman M , Ratliff NB. Hawley J: Right ventricularinfarction: A hemodynamic diagnosis. Br Heart J 36:941-944, 1974. 7. Rackley CE, Russel RO: Right ventricular function in acute myocardial infarction. Am J Cardiol 33 :927-Y2Y, 1974. 8. Sharpe ND, Botvinick EH. Shames DM. Chatterjee K, Schiller NB, Massie BN, Parmley WW: The noninvasive diagnosis of right ventricular infarction. Circulation 57:483490, 1978. 9. Jacobs JJ, Feigenbaum H, Corya BC. Phillips JF: Detection of left ventricular asynergy by echocardiography. Circulation 48:263-271. 1973. 10. Brown OR, Popp RL, Harrison DC: Abnormal interventricular septal motion in patients with significant disease of the left anterior descending coronary artery or other conditions of septal failure. Am J Cardiol 31:123, 1973 (abstr). 1 1 . DeMaria A, King F, Bonanno JA. Lies JE, Zebs R, Vismara LA, Miller RR, Massumi RA, Amsterdam EA. Mason DT: Left anterior descending involvement in coronary disease. Detection by abnormal ventricular septal motion on echocardiogram. Clin Res 22:272A (abstr). 12. Meyer RA, Schwartz DC, Benzing G , Kaplan S: Ventricular volume overload: An echocardiographic study. Am J Cardiol 30:34Y-353, 1972. 13. McCann WD, Harbold NB J r , Giuliani ER: The echocardiogram in right ventricular overload. JAMA 221:1243-1245, 1972. 14. Tajik AJ, Can GT, Schattenberg TT: Echoardiograrn in total anomalous pulmonary venous drainage. Report of case. Mayo Clin Proc 47:247-250, 1972. 15. Kotler MN, Tabatznik B: Recognition of Ebstein’s anomaly by ultrasound technique. Circulation 44(Suppl 2):34. 1971 (abstr). 16. Goodman DJ, Harrison DC, Popp RL: Echocardiographic features of primary pulmonary hypertension. Circulation 48(Suppl 4): 170. 1973 (abstr). 17. Corya BC. Rasmussen S. Feigenbaum H , Knoebel SB, Black MJ: Systolic thickening and thinning of the septum and posterior wall i n patients with coronary artery disease, congestive cardiomyopathy, and atrial septal defect. Circulation 55: 109-1 14, 1977. 18. Quinones MA, Gaasch WH, Weisser E, Alexander JK: Reduction in the rate of diastolic descent of the rnitral valve echogram in patients with altered left ventricular diastolic pressure volume relations. Circulation 49:246-254. 1974. 19. Layton C, Gent G. Prichie R. McDonald A, Brigden W: Diastolic closure rate of normal mitral valve. Br Heart J 35: I06&1074, 1973. 20. DeMaria A, Miller RR, Amsterdam EA, Markson W. Mason DT: Mitrdl valve early diastolic closing velocity on echogram: Relation to sequential diastolic flow and ventricular compliance. Am J Cdrdiol 37:693-700. 1976. 21. Laniado S. Yellin E. Kotler M N , Levy L, Stadler J , Terdiman R: A study of the dynamic relations between the mitral valve echogram and phasic mitral flow. Circulation 51:104-113, 1975.
(1979)
Echocardiographic Findings in Cardiogenic Shock Due to Right Ventricular Myocardial Infarction Uri Elkayam, MD, Stanley L. Halprin, MD, William Frishman, MD, Joel Strom, MD, and Martin N. Cohen, MD The echocardiographicfindings in a patient with cardiogenic shock secondaryto acute right ventricular myocardial infarction based on typical clinical, electrocardiographic, and hemodynamic features are described. The echocardiogram demonstrated a large RV/LV minor axis ratio caused by a volume overload of the right ventricle and an underfilled left ventricle. The interventricular septum showed abnormal movement, presumably due to right ventricular overload or severe disease of the left anterior descending coronary artery. Diminished septa1systolic thickening, as seen in our patient, may be explained by extension of the infarct from the right ventricle to the adjacent part of the septum. Predominant right ventricular involvement can be a cause for a correctable hypotension in patients with acute myocardial infarction and should therefore be recognized early. The echocardiographic picture demonstrated in our patient, when considered in conjunction with the clinical status, can be useful for early diagnosis. Key words: echocardiography, right ventricular myocardial infarction, cardiogenic shock
INTRODUCTION Acute myocardial infarction is usually associated with hemodynamic evidence of predominant left ventricular dysfunction, and it is for this reason that the diagnosis of right ventricular infarction is usually made at autopsy 11-31. Recently some attention has been devoted to the circulatory events accompanying infarction of the right ventricle [MI.Experimental and clinical observation have helped demonstrate the unique hemodynamic characteristics of this syndrome [4-71. The man-
From the Division of Cardiology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York
Address reprint requests to Uri Elkayam, MD, Division of Cardiology, Cedars-Sinai Medical Center, 8700 Beverly Bivd, Los Angeles, CA 90048. Received December 5, 1978; revision accepted April 17, 1979.
0098-6569/79/0503-0289$01.400 1979 Alan R. Liss, Inc.
290
Elkayam e t al
agement of heart failure and shock associated with a predominant right ventricular infarction differs from that of left ventricular infarction [ 5 ] . For this reason and since there is also a favorable prognosis associated with the appropriate management of shock secondary to right ventricular infarction, an early recognition of this condition would be most helpful. This report describes the echocardiographic findings in a patient with cardiogenic shock and typical clinical, electrocardiographic, and hemodynamic features of acute myocardial infarction involving the right ventricle. CASEREPORT A 62-year-old woman was admitted to the Bronx Municipal Hospital with the diagnosis of acute myocardial infarction. She smoked one pack of cigarettes daily for 27 years. In addition, she had been hypertensive for the previous ten years and was treated with a variety of medications. For the preceding three years she had experienced chest pain and dyspnea on exertion. There was no other history of cardiac dysfunction. On the day of admission, while at rest, the patient developed a sharp pain, located initially between her scapulae, but which later radiated to her chest. It lasted 1% hours and was accompanied by diaphoresis. Physical examination on admission revealed a systemic blood pressure of 210/105 mm Hg. a regular pulse of 100 beats per minute, and a temperature of 37.2"C. There was nojugular venous distention at 45" and the lungs were clear. The first and second heart sounds were normal and of good quality, and an S, gallop was heard at the apex; there were no murmurs. The liver and spleen were not palpable and there was no ascites or pedal edema. The electrocardiogram demonstrated normal sinus rhythm, ST segment elevation in leads 11, 111, and aV, with reciprocal ST segment depression in leads I , aVLand V,-V,. There was no sign of conduction disturbances of any kind. There was slight cardiomegaly without pulmonary venous congestion on the admission x-ray. On the second hospital day the patient developed complete heart block unresponsive to 2 mg of intravenous atropine and requiring placement of a temporary pacemaker. She then developed hypotension with a systolic blood pressure in the 70-80 mm Hg range. Physical examination at this time revealed massive neck vein distention at 45", while the lungs remained clear. Right heart pressure determination at the bedside, using a flow-directed triple-lumen catheter, showed a right atrial mean pressure of 13 mm Hg, with no significant V wave, right ventricular pressure 19/13 mm Hg, pulmonary artery pressure 19/10 mm Hg, and a mean pulmonary capillary wedge pressure of 9 mm Hg. The cardiac output determined by thermodilution was 3.0 litedmin [cardiac index (CI) 1.8 liters/min/m*]. Blood samples taken from the right atrium, right ventricle, and pulmonary artery revealed no significant difference in oxygen saturation. The echocardiogram (Figs. 1 and 2), performed with the patient in the supine position, demonstrated a markedly enlarged right ventricle (3.7 cm) with good anterior wall motion. The interventricular septum moved paradoxically and showed decreased systolic thickening. The left ventricular diastolic diameter was reduced (2.9 cm), and the right ventricular-left ventricular minor axis ratio was significantly increased (1.27). The left ventricular posterior wall motion as well as the systolic thickening was normal. The mitral valve, although structurally normal, demonstrated a decreased diastolic closure rate (5 1 mm/sec).
Echocardiography in Right Ventricular Infarction
291
The patient was treated with large volumes of colloid, which raised the mean pulmonary capillary wedge pressure t o 18-20 mm Hg, resulting in an increase in the cardiac output to 3.94 liters/min (CI 2.4 liters/min/m2). The mean right atrial pressure increased to 24 mm Hg. In spite of a course complicated by the development of severe metabolic acidosis, bilateral pleural effusions, and ascites requiring peritoneal dialysis, abdominoscentesis, and pleuroscentesis, the patient improved. Regular sinus rhythm returned, and the pacemaker was discontinued by the tenth hospital day. The balloon-tip catheter was removed on the twelth hospital day, and the patient completed her convalescence in an uneventful manner. Radionuclide angiography was performed before discharge on the twenty-sixth hospital day. First-pass technique revealed no intracardiac shunt and a left ventricular ejection fraction of 38%. Gated blood pool studies were obtained in multiple positions and revealed mild enlargement of the left ventricle, with marked dilatation and poor contraction of the right ventricle.
Fig. 1. Echocardiogramshowing enlarged right Ventricular (RV) cavity (3.7 cm), small left ventricle (LV) (2.9 cm), preserved motion of the right ventricular anterior wall (RVAW), and lefi ventricular posterior wall (LVPW). In addition, the interventrlcular septum (IVS) shows abnormal motion and diminished thickening during systole. CW = chest wall.
292
Elkayam e t al
Fig. 2. Echocardiogram of patient demonstrating decreased diastolic closure rate of the mitral valve (E-F slope 51 mmlsec). AMV = anterfor leaflet of the mitral valve.
DISCUSSION In patients with an acute inferior myocardial infarction hemodynamic evidence of right ventricular failure disproportional to left ventricular failure is a strong indicator of predominant right ventricular involvement [5,61. This characteristic hemodynamic feature is reflected echocardiographically by an enlargement of the right ventricular minor dimension in association with findings of a relatively small left ventricle. Severe damage to the right ventricular myocardium with failure to contract leads to inadequate filling of the left ventricle. This hemodynamic situation explains the large RV/LV minor axis ratio in our patient and in other patients with RV myocardial infarction [81. Wade [21 in 1959 described the clinical and pathological findings of 11 patients with RV infarction, and reported involvement of the right ventricular posterior wall to be the major lesion in most of these cases. Although the amount of motion exhibited by the echoes of the right ventricular anterior wall has not been intensively investigated, one can assume that the marked systolic anterior motion of the right ventricular anterior wall in our patient (Fig. l), reflected a preserved anterior wall and was a compensatory phenomenon for the poorly moving posterior wall.
Echocardiography in Right Ventricular Infarction
293
There are two mechanisms that could explain the abnormal motion of the interventricular septum found in our patient: involvement of the septum by the ischemic process and right ventricular overload. Abnormal septal motion has been found t o be associated with disease of the left anterior descending coronary artery [P-1 11. Brown et a1 [lo] reported abnormal septal movement in 44% of patients with greater than 50% obstruction of the left anterior descending coronary artery. Although myocardial infarction involving the right ventricle is usually associated with occlusion of the main right coronary artery, it is often accompanied by severe disease in the left coronary arteries as well 121. Septal involvement has been reported by Sharpe et a1 [81 in six patients in whom scintigraphy provided direct anatomic evidence of right ventricular infarction. Abnormal septal motion in conjunction with an increased right ventricular dimensions is also considered to be the hallmark of right ventricular volume overload [ 121. These echocardiographic findings were described in atrial septal defect [41, partial and total anomalous venous drainage [13,141, Ebstein anomaly [151, and tricuspid and pulmonic insufficiency 1161, and it seems reasonable to conclude that right ventricular overload secondary to failure of contraction also contributes to the paradoxical septal motion demonstrated in our patient. Concomitant complicating lesions such as tricuspid valve insufficiency o r atrial septal defect could also have produced right ventricular overload in our patient. The absence of a systolic murmur or a significant V wave in the right atrial pressure recording does not support the diagnosis of tricuspid regurgitation. The presence of atrial septal defect was excluded by physical examination, electrocardiogram, oximetry, and radionuclide studies. The echocardiographic finding of diminished septal systolic thickening in our patient may be explained by the extension of the infarct from the right ventricular myocardium to the adjacent part of the posterior interventricular septum, which has been demonstrated in autopsy and scintigraphy studies in patients with right ventricular myocardial infarction [2,8,171. Although multiple parameters influence the mitral E-F slope [18-211 in an anatomically normal valve, it is largely a function of the rate of left ventricular filling during the diastolic rapid-filling phase [20]. Reduction of cardiac output and diminution of mitral flow are reported to cause a significant decrease in the E-F slope in normal mitral valves [21]. Impairment of left ventricular filling secondary to right ventricular pump failure and decreased cardiac output is probably the mechanism reducing the E-F slope in our patient. Although recent studies suggest that right ventricular infarction may be more common than previously assumed [8], it is still a rarely recognized clinical entity. Early recognition of the unique hemodynamics in patients with shock secondary to right ventricular infarction is essential for the appropriate therapeutic approach. The various echocardiographic features presented in our cases, when considered in conjunction with the clinical setting, present an echocardiographic picture that is sufficiently distinctive for the diagnosis of severe right ventricular infarction. REFERENCES 1 . Wartman WB, Hellerstein H K : The incidence of heart disease in 2,000 autopsies. Ann Intern Med 2k41-65, 1948. 2. Wade WG: The pathogenesis of infarction of the right ventricle. Br Heart J 21:545-554,
1959. 3. Ebhardt CR: Clinical and pathological observations in different types of acute myocardial infarction. Acta Med Scand Suppl 560:7, 1974.
294
El kayam et al
4. Guiha NH, Constantinos JL, Cohn JN: Predominant right ventricular dysfunction after right ventricular distruction in the dog. Am J Cardiol 33:254-258, 1974. 5 . Cohn JN, Guiha NH, Broder M I . Constantinos JL: Right ventricular infarction. Clinical and hemodynamic features. Am J Cardiol 33:209-214, 1974. 6. Rotman M , Ratliff NB. Hawley J: Right ventricularinfarction: A hemodynamic diagnosis. Br Heart J 36:941-944, 1974. 7. Rackley CE, Russel RO: Right ventricular function in acute myocardial infarction. Am J Cardiol 33 :927-Y2Y, 1974. 8. Sharpe ND, Botvinick EH. Shames DM. Chatterjee K, Schiller NB, Massie BN, Parmley WW: The noninvasive diagnosis of right ventricular infarction. Circulation 57:483490, 1978. 9. Jacobs JJ, Feigenbaum H, Corya BC. Phillips JF: Detection of left ventricular asynergy by echocardiography. Circulation 48:263-271. 1973. 10. Brown OR, Popp RL, Harrison DC: Abnormal interventricular septal motion in patients with significant disease of the left anterior descending coronary artery or other conditions of septal failure. Am J Cardiol 31:123, 1973 (abstr). 1 1 . DeMaria A, King F, Bonanno JA. Lies JE, Zebs R, Vismara LA, Miller RR, Massumi RA, Amsterdam EA. Mason DT: Left anterior descending involvement in coronary disease. Detection by abnormal ventricular septal motion on echocardiogram. Clin Res 22:272A (abstr). 12. Meyer RA, Schwartz DC, Benzing G , Kaplan S: Ventricular volume overload: An echocardiographic study. Am J Cardiol 30:34Y-353, 1972. 13. McCann WD, Harbold NB J r , Giuliani ER: The echocardiogram in right ventricular overload. JAMA 221:1243-1245, 1972. 14. Tajik AJ, Can GT, Schattenberg TT: Echoardiograrn in total anomalous pulmonary venous drainage. Report of case. Mayo Clin Proc 47:247-250, 1972. 15. Kotler MN, Tabatznik B: Recognition of Ebstein’s anomaly by ultrasound technique. Circulation 44(Suppl 2):34. 1971 (abstr). 16. Goodman DJ, Harrison DC, Popp RL: Echocardiographic features of primary pulmonary hypertension. Circulation 48(Suppl 4): 170. 1973 (abstr). 17. Corya BC. Rasmussen S. Feigenbaum H , Knoebel SB, Black MJ: Systolic thickening and thinning of the septum and posterior wall i n patients with coronary artery disease, congestive cardiomyopathy, and atrial septal defect. Circulation 55: 109-1 14, 1977. 18. Quinones MA, Gaasch WH, Weisser E, Alexander JK: Reduction in the rate of diastolic descent of the rnitral valve echogram in patients with altered left ventricular diastolic pressure volume relations. Circulation 49:246-254. 1974. 19. Layton C, Gent G. Prichie R. McDonald A, Brigden W: Diastolic closure rate of normal mitral valve. Br Heart J 35: I06&1074, 1973. 20. DeMaria A, Miller RR, Amsterdam EA, Markson W. Mason DT: Mitrdl valve early diastolic closing velocity on echogram: Relation to sequential diastolic flow and ventricular compliance. Am J Cdrdiol 37:693-700. 1976. 21. Laniado S. Yellin E. Kotler M N , Levy L, Stadler J , Terdiman R: A study of the dynamic relations between the mitral valve echogram and phasic mitral flow. Circulation 51:104-113, 1975.
