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Submitral aneurysm diagnosed by left ventricular contrast echocardiography
682
Brief
Communications
serum potassium as serum magnesium normalized (despite concomitant albeit not as aggressivereplacement of potassium), and (4) the complete resolution of MAT after normalization of both serum potassium and magnesium are consistent with earlier observations6 Our patient differs from those reported previously1-3s6 in that he is an otherwisehealthy personwithout concomitant preexisting cardiac or pulmonary diseaseand was not taking other medications that might have predisposed him to MAT. Thus we present evidencethat MAT can occur in a patient without preexisting structural heart disease,thereby providing direct evidence for the bystander role of the heart in this dysrhythmia. We cannot rule out the possibility that rehydration itself or the improvement in gastrointestinal symptoms may have contributed to the resolution of MAT in this patient. Indeed, dehydration and the expected endogenous catecholamine excess may have exacerbated the MAT. However, the dysrhythmia presisted even after resolution of the patient’s symptoms and full correction of hydration status. Thus it is likely that the causeof the MAT waspartly the result of electrolyte imbalancein this patient. Methylxanthines, hypoxia, hypercarbia, and catecholamines lead to intracellular calcium overload and triggered activity in vitro. Recent clinical studies have linked respiratory failure and theophylline excesswith MAT.3 That the ectopic atria1 activity that develops under these conditions is inhibited by verapamil, a calcium channel blocker, supports the notion of an association between intracellular calcium overload and ectopic atria1 activity in this dysrhythmia.2 Electrolyte disturbances may also lead to intracellular calcium overload.4p5 Both hypokalemia and hypomagnesemialengthen the plateau phaseof the cardiac action potential and hence allow a greater time per beat for calcium flux via open calcium channels. In addition, a reduction in extracellular potassium has been shown to directly inhibit the sodium-potassium pump. This may lead to an increasein intracellular sodiumand in turn to an increasein intracellular calcium via enhanced sodium-calcium exchange.Thus the finding of MAT in a patient with hypokalemia and hypomagnesemiais consistent with the notion that MAT may be the result of intracellular calcium overload. In summary, we have describeda caseof MAT associated only with an electrolyte disturbance. Hypokalemia and hypomagnesemiamay lead to MAT and should be aggressively treated in patients with this dysrhythmia.
REFERENCES
1.
ShineKI,
Kastor JA, Yurchak PM. Multifocal atria1 tachycardia: clinical and electrocardiographic features in 32 patients. N Engl J Med 1968;279:344. 2. Levine JH, Michael JR, Guarnieri T. The treatment of multifocal atria1 tachycardia with verapamil. N Engl J Med 1985;312:21. 3. Levine JH, Michael JR, Guarnieri T. Multifocal atria1 tachycardia: a toxic effect of theophylline. Lancet 1985;8419:12. 4. Eisner R, Lederer J. Inotropic and arrhythmogenic effects of
Marsh 1oaa Heart Journal
American
potassium depleted solutions on mammalian cardiac muscle. J Physiology (Land) 1979;294:255. 5. Hoffman BF, Cranefield PF. In: Electrophysiology of the heart. Mt. Kisco, N.Y.: Futura Publishing Co, 1976:75-103. 6. Iseri LT, Fairshter RD, Hardemann JL, Brodsky MA. Magnesium and potassium therapy in multifocal atria1 tachycardia. AM HEART J 1986;110:789.
Submitral aneurysm diagnosed ventricular contrast echocardio
left PM
Vinod Kuverji Shah, M.D., Kaustubh Anant Vaidya, M.D., Dinyar Faredoon Daruwala, M.D., Jagdish Ambrish Parikh, M.D., Brijlal Gupta, M.D., and Mansukh Jinabhai Gandhi, M.D. Elombay, India
Aneurysm of the left ventricle occurring in young people is a rare condition and hasbeen describedmainly in Nigeria, South Africa, and Uganda. These aneurysmsare usually submitral or subaortic, with the former being more common. A congenital defect of the ventricular wall near the atrioventricular groove has been postulated as the probable causeof theseaneurysms.’This report presentsthe use of left ventricular contrast echocardiography in the location and diagnosisof a submitral aneurysm. K.S., a 35-year-old womanstaying in India, presentedto us with exertional dyspnea and palpitations of 10 years’ duration. There was no history suggestive of rheumatic fever, hypertension, diabetes mellitus, angina, or myocardial infarction in the past. On examination, the patient was cachectic and in grosscongestive cardiac failure with pedal edema.Jugular venous pulse wasdistended and the liver wasenlarged 8 cm and tender. Pulse was irregularly irregular and all peripheral pulseswere felt. The cardiovascular system revealed cardiomegaly with an apex beat that was hyperdynamic and a grade III/VI pansystolic murmur at the apex radiating to the axilla and at the back. Both heart soundswere normal, with the P, component accentuated. There was a left-sided gallop. All other systemswere normal. The clinical impressionat this stage wasseveremitral regurgitation with pulmonary hypertension and grosscongestive cardiac failure. The chest roentgenogramshowedcardiomegaly with the contour like that of left ventricular (LV) enlargement or aneurysm. The lung fields demonstrated pulmonary venous congestion. The 12-leadECG showedatria1fibrillation, with a ventricFrom Grant
Lokmmya Medical
Reprint requests: 022, India.
Tilak College.
Municipal
Dr. V. K. Shah,
Medical 63/7,
College Vasant
and Hospital Sian
(East),
Sion; Bombay
and 400
Volume
I15
Number
3
Brief Communications
683
Fig. 1. This figure shows the location of submitral aneurysm in three different views. A shows the neck of aneurysm opening into the LV and situated behind the left atrioventricular junction. LV = left ventricle; AC = aorta; LA = left atrium; AN = aneurysm.
ular rate averaging 110 bpm. There was evidence of LV hypertrophy by the voltage criteria. A two-dimensional echocardiography examination showed a dilated left ventricle and an aneurysm could be seen separately behind the left atrioventricular junction, with the possibility of a neck opening into the LV posterior wall beneath the mitral valve apparatus (Fig. 1). The left atrium was also enlarged and there was evidence of pulmonary hypertension. The right ventricle and right atrium were dilated, as was the inferior vena cava and hepatic veins. The mitral valve apparatus and the other valves were all normal. In order to assess the severity of pulmonary hypertension and to establish the etiology of the aneurysm, cardiac catheterization with coronary angiography was performed. The hemodynamic data were suggestive of severe pulmonary hypertension. Coronary arteries were normal. The LV angiography was not done, as the patient was severely cachectic and in gross congestive cardiac failure. We therefore chose to do LV contrast echocardiography with a pigtail catheter in the cavity of the LV, using the patient’s blood as the contrast agent to determine mitral regurgitation and to locate the site of opening of the neck of the aneurysm into the LV cavity. Fig. 2 is a parasternal long-axis view showing contrast entering from the LV through a separate neck into the submitral aneurysm and left atrium through the mitral valve orifice. The patient was subjected to open-heart surgery for aneurysmectomy. At operation, the LV was
found to be enlarged and the left atrium was also dilated. There was a separate aneurysmal sac that tended to bulge during systole. After the heart was brought to standstill, the aneurysmal sac was split open. It was a smooth-walled structure with a diameter of about 8 cm. The aneurysm was connected through a narrow neck to the posterior wall of the LV just beneath the mitral anulus. There were no clots in the aneurysmal sac. The aneurysm was excised and the edges were approximated with 2-O Ticron sutures. The mitral valve apparatus was normal and the anulus was slightly stretched and therefore no repair was necessary, as there was no mitral incompetence after the aneurysmectomy. The postoperative course was uneventful and the patient was discharged on the tenth postoperative day. Histologic study of the aneurysmal sac showed no evidence of rheumatic or infective endocarditis. It showed fibrous tissue with scattered cardiac muscle bundles. The inner lining was composed of hyalinized endocardium and a fibrinous exudate on the pericardial aspect. There was also evidence of nonspecific chronic inflammatory cells. These features were in keeping with those of an idiopathic submitral aneurysm. Aneurysm of the LV occurs primarily following myocardial infarction and less commonly due to trauma, syphilis, mycotic infections, rheumatic myocarditis, or polyarteritis nodosa. Still rarer causes include congenital defects of cardiac muscle, tuberculosis, LBffler’s endocarditis, interstitial myocarditis, malaria, and Chagas’ disease. Certain
684
Brief
Communications
Fig. 2. Left ventricular contrast echocardiography done in the parasternal long-axis view. Contrast can be seenentering (arrows) into the left atrium and submitral aneurysm separately through the mitral valve orifice and the neck, respectively. LV = left ventricle; AQ = aorta; LA = left atrium; AN = aneurysm.
cardiac aneurysmsof unknown etiology that are thought to be developmental defects have been reported. These aneurysmsare called subvalvular becausethey occur just below the aortic and mitral valves and annular becausethe aneurysmal cavity extends in a circular direction and in the substanceof the fibrous ring from which the valves take their attachment. This distinct pathologic entity, known assubvalvular LV aneurysm, wasinitially reported from Negro populations in Nigeria and later in South Africa and the equatorial region.2*6-8 Diagnosismay be obtained on fluoroscopy or by x-ray films of the chest that may showa localized cardiac border bulge or rarely calcification. In our case,since the patient was cachectic and in grosscongestive cardiac failure, we performed LV contrast echocardiography that enabled us to locate the subvalvular aneurysm and also mitral regurgitation. Most of the casesreported in the literature have been diagnosedat autopsy, becausecardiac catheterization and LV angiography are usually not performed until the general condition improves and cardiac failure is controlled. Thus, LV contrast echocardiography helps us in antemortem diagnosisof such patients without the risk of angiography. This patient was one such casewho was diagnosed antemortem and subjected to surgery. The subvalvular aneurysm was excised and the wall was plicated. The mitral regurgitation disappearedafter surgery and the patient’s condition improved remarkably.
3. 4. 5. 6. 1. 8. 9. 10.
subvalvular idiopathic left ventricular aneurysm in the black African. Ann Thorac Surg 1979;27:350. Beckerling CH, Gibb BH, Houghton HGH, Le Roux BT. Left ventricular aneurysm. Thorax 1969;24:173. Braunstein AL. Bass JB. Thomas S. Gummatous mvocarditis and aneurysm’ of the ‘left ventricle. AM HEART" J 1940; 19:613. Robertson JH, Jackson JG. Cardiac aneurysm in Nigeria. J Path01 Bacterial 1960;80:101. Guimaraes AC, Filho AS, Esteves JP, Abreu WN, Vinhaes LA, Souza JA, Machado A. Annular subvalvular left ventricular aneurysm in Bahia, Brazil. Br Heart J 1976;38:1080. Beck W, Schrire V. Idiopathic mitral subannular left ventricular aneurysm in the Bantu. AM HEART J 1969;78:28. Poltera AA, Jones AW. Subvalvular left ventricular aneurysm. A report of 5 Ugandan cases. Br Heart J 1973; 35~1085. Herman MV, Gorlin R. Implications of left ventricular asynergy. Am J Cardiol 1969;23:538. Chesler E, Joffe N, Schamroth L, Meyers A. Annular subvalvular left ventricular aneurysm in the South African Bantu. Circulation 1965;32:43.
Two-dimensional echocardiographic imaging of left ventricular mural vegetations Charles A. Herzog, M.D., Peter Carson, M.D., Lillian Michaud, R.D.M.S., and Richard W. Asinger, M.D. Minneapolis, Minn.
REFERENCES
Abrahams DG, Barton CJ, Cockshott WP, Edington GM, Weaver EJM. Annular subvalvular left ventricular aneurysm. Q J Med 1960;31:345. 2. Wolpowitz A, Arman B, Barnard MS, Barnard CN. Annular 1.
From the Division of Cardiology, Department of Medicine, County Medical Center. Reprint requests: Charles A. Herzog, M.D., Hennepin County Center, 701 Park Ave. S., Minneapolis, MN 55415.
Hennepin Medical
Brief
Communications
serum potassium as serum magnesium normalized (despite concomitant albeit not as aggressivereplacement of potassium), and (4) the complete resolution of MAT after normalization of both serum potassium and magnesium are consistent with earlier observations6 Our patient differs from those reported previously1-3s6 in that he is an otherwisehealthy personwithout concomitant preexisting cardiac or pulmonary diseaseand was not taking other medications that might have predisposed him to MAT. Thus we present evidencethat MAT can occur in a patient without preexisting structural heart disease,thereby providing direct evidence for the bystander role of the heart in this dysrhythmia. We cannot rule out the possibility that rehydration itself or the improvement in gastrointestinal symptoms may have contributed to the resolution of MAT in this patient. Indeed, dehydration and the expected endogenous catecholamine excess may have exacerbated the MAT. However, the dysrhythmia presisted even after resolution of the patient’s symptoms and full correction of hydration status. Thus it is likely that the causeof the MAT waspartly the result of electrolyte imbalancein this patient. Methylxanthines, hypoxia, hypercarbia, and catecholamines lead to intracellular calcium overload and triggered activity in vitro. Recent clinical studies have linked respiratory failure and theophylline excesswith MAT.3 That the ectopic atria1 activity that develops under these conditions is inhibited by verapamil, a calcium channel blocker, supports the notion of an association between intracellular calcium overload and ectopic atria1 activity in this dysrhythmia.2 Electrolyte disturbances may also lead to intracellular calcium overload.4p5 Both hypokalemia and hypomagnesemialengthen the plateau phaseof the cardiac action potential and hence allow a greater time per beat for calcium flux via open calcium channels. In addition, a reduction in extracellular potassium has been shown to directly inhibit the sodium-potassium pump. This may lead to an increasein intracellular sodiumand in turn to an increasein intracellular calcium via enhanced sodium-calcium exchange.Thus the finding of MAT in a patient with hypokalemia and hypomagnesemiais consistent with the notion that MAT may be the result of intracellular calcium overload. In summary, we have describeda caseof MAT associated only with an electrolyte disturbance. Hypokalemia and hypomagnesemiamay lead to MAT and should be aggressively treated in patients with this dysrhythmia.
REFERENCES
1.
ShineKI,
Kastor JA, Yurchak PM. Multifocal atria1 tachycardia: clinical and electrocardiographic features in 32 patients. N Engl J Med 1968;279:344. 2. Levine JH, Michael JR, Guarnieri T. The treatment of multifocal atria1 tachycardia with verapamil. N Engl J Med 1985;312:21. 3. Levine JH, Michael JR, Guarnieri T. Multifocal atria1 tachycardia: a toxic effect of theophylline. Lancet 1985;8419:12. 4. Eisner R, Lederer J. Inotropic and arrhythmogenic effects of
Marsh 1oaa Heart Journal
American
potassium depleted solutions on mammalian cardiac muscle. J Physiology (Land) 1979;294:255. 5. Hoffman BF, Cranefield PF. In: Electrophysiology of the heart. Mt. Kisco, N.Y.: Futura Publishing Co, 1976:75-103. 6. Iseri LT, Fairshter RD, Hardemann JL, Brodsky MA. Magnesium and potassium therapy in multifocal atria1 tachycardia. AM HEART J 1986;110:789.
Submitral aneurysm diagnosed ventricular contrast echocardio
left PM
Vinod Kuverji Shah, M.D., Kaustubh Anant Vaidya, M.D., Dinyar Faredoon Daruwala, M.D., Jagdish Ambrish Parikh, M.D., Brijlal Gupta, M.D., and Mansukh Jinabhai Gandhi, M.D. Elombay, India
Aneurysm of the left ventricle occurring in young people is a rare condition and hasbeen describedmainly in Nigeria, South Africa, and Uganda. These aneurysmsare usually submitral or subaortic, with the former being more common. A congenital defect of the ventricular wall near the atrioventricular groove has been postulated as the probable causeof theseaneurysms.’This report presentsthe use of left ventricular contrast echocardiography in the location and diagnosisof a submitral aneurysm. K.S., a 35-year-old womanstaying in India, presentedto us with exertional dyspnea and palpitations of 10 years’ duration. There was no history suggestive of rheumatic fever, hypertension, diabetes mellitus, angina, or myocardial infarction in the past. On examination, the patient was cachectic and in grosscongestive cardiac failure with pedal edema.Jugular venous pulse wasdistended and the liver wasenlarged 8 cm and tender. Pulse was irregularly irregular and all peripheral pulseswere felt. The cardiovascular system revealed cardiomegaly with an apex beat that was hyperdynamic and a grade III/VI pansystolic murmur at the apex radiating to the axilla and at the back. Both heart soundswere normal, with the P, component accentuated. There was a left-sided gallop. All other systemswere normal. The clinical impressionat this stage wasseveremitral regurgitation with pulmonary hypertension and grosscongestive cardiac failure. The chest roentgenogramshowedcardiomegaly with the contour like that of left ventricular (LV) enlargement or aneurysm. The lung fields demonstrated pulmonary venous congestion. The 12-leadECG showedatria1fibrillation, with a ventricFrom Grant
Lokmmya Medical
Reprint requests: 022, India.
Tilak College.
Municipal
Dr. V. K. Shah,
Medical 63/7,
College Vasant
and Hospital Sian
(East),
Sion; Bombay
and 400
Volume
I15
Number
3
Brief Communications
683
Fig. 1. This figure shows the location of submitral aneurysm in three different views. A shows the neck of aneurysm opening into the LV and situated behind the left atrioventricular junction. LV = left ventricle; AC = aorta; LA = left atrium; AN = aneurysm.
ular rate averaging 110 bpm. There was evidence of LV hypertrophy by the voltage criteria. A two-dimensional echocardiography examination showed a dilated left ventricle and an aneurysm could be seen separately behind the left atrioventricular junction, with the possibility of a neck opening into the LV posterior wall beneath the mitral valve apparatus (Fig. 1). The left atrium was also enlarged and there was evidence of pulmonary hypertension. The right ventricle and right atrium were dilated, as was the inferior vena cava and hepatic veins. The mitral valve apparatus and the other valves were all normal. In order to assess the severity of pulmonary hypertension and to establish the etiology of the aneurysm, cardiac catheterization with coronary angiography was performed. The hemodynamic data were suggestive of severe pulmonary hypertension. Coronary arteries were normal. The LV angiography was not done, as the patient was severely cachectic and in gross congestive cardiac failure. We therefore chose to do LV contrast echocardiography with a pigtail catheter in the cavity of the LV, using the patient’s blood as the contrast agent to determine mitral regurgitation and to locate the site of opening of the neck of the aneurysm into the LV cavity. Fig. 2 is a parasternal long-axis view showing contrast entering from the LV through a separate neck into the submitral aneurysm and left atrium through the mitral valve orifice. The patient was subjected to open-heart surgery for aneurysmectomy. At operation, the LV was
found to be enlarged and the left atrium was also dilated. There was a separate aneurysmal sac that tended to bulge during systole. After the heart was brought to standstill, the aneurysmal sac was split open. It was a smooth-walled structure with a diameter of about 8 cm. The aneurysm was connected through a narrow neck to the posterior wall of the LV just beneath the mitral anulus. There were no clots in the aneurysmal sac. The aneurysm was excised and the edges were approximated with 2-O Ticron sutures. The mitral valve apparatus was normal and the anulus was slightly stretched and therefore no repair was necessary, as there was no mitral incompetence after the aneurysmectomy. The postoperative course was uneventful and the patient was discharged on the tenth postoperative day. Histologic study of the aneurysmal sac showed no evidence of rheumatic or infective endocarditis. It showed fibrous tissue with scattered cardiac muscle bundles. The inner lining was composed of hyalinized endocardium and a fibrinous exudate on the pericardial aspect. There was also evidence of nonspecific chronic inflammatory cells. These features were in keeping with those of an idiopathic submitral aneurysm. Aneurysm of the LV occurs primarily following myocardial infarction and less commonly due to trauma, syphilis, mycotic infections, rheumatic myocarditis, or polyarteritis nodosa. Still rarer causes include congenital defects of cardiac muscle, tuberculosis, LBffler’s endocarditis, interstitial myocarditis, malaria, and Chagas’ disease. Certain
684
Brief
Communications
Fig. 2. Left ventricular contrast echocardiography done in the parasternal long-axis view. Contrast can be seenentering (arrows) into the left atrium and submitral aneurysm separately through the mitral valve orifice and the neck, respectively. LV = left ventricle; AQ = aorta; LA = left atrium; AN = aneurysm.
cardiac aneurysmsof unknown etiology that are thought to be developmental defects have been reported. These aneurysmsare called subvalvular becausethey occur just below the aortic and mitral valves and annular becausethe aneurysmal cavity extends in a circular direction and in the substanceof the fibrous ring from which the valves take their attachment. This distinct pathologic entity, known assubvalvular LV aneurysm, wasinitially reported from Negro populations in Nigeria and later in South Africa and the equatorial region.2*6-8 Diagnosismay be obtained on fluoroscopy or by x-ray films of the chest that may showa localized cardiac border bulge or rarely calcification. In our case,since the patient was cachectic and in grosscongestive cardiac failure, we performed LV contrast echocardiography that enabled us to locate the subvalvular aneurysm and also mitral regurgitation. Most of the casesreported in the literature have been diagnosedat autopsy, becausecardiac catheterization and LV angiography are usually not performed until the general condition improves and cardiac failure is controlled. Thus, LV contrast echocardiography helps us in antemortem diagnosisof such patients without the risk of angiography. This patient was one such casewho was diagnosed antemortem and subjected to surgery. The subvalvular aneurysm was excised and the wall was plicated. The mitral regurgitation disappearedafter surgery and the patient’s condition improved remarkably.
3. 4. 5. 6. 1. 8. 9. 10.
subvalvular idiopathic left ventricular aneurysm in the black African. Ann Thorac Surg 1979;27:350. Beckerling CH, Gibb BH, Houghton HGH, Le Roux BT. Left ventricular aneurysm. Thorax 1969;24:173. Braunstein AL. Bass JB. Thomas S. Gummatous mvocarditis and aneurysm’ of the ‘left ventricle. AM HEART" J 1940; 19:613. Robertson JH, Jackson JG. Cardiac aneurysm in Nigeria. J Path01 Bacterial 1960;80:101. Guimaraes AC, Filho AS, Esteves JP, Abreu WN, Vinhaes LA, Souza JA, Machado A. Annular subvalvular left ventricular aneurysm in Bahia, Brazil. Br Heart J 1976;38:1080. Beck W, Schrire V. Idiopathic mitral subannular left ventricular aneurysm in the Bantu. AM HEART J 1969;78:28. Poltera AA, Jones AW. Subvalvular left ventricular aneurysm. A report of 5 Ugandan cases. Br Heart J 1973; 35~1085. Herman MV, Gorlin R. Implications of left ventricular asynergy. Am J Cardiol 1969;23:538. Chesler E, Joffe N, Schamroth L, Meyers A. Annular subvalvular left ventricular aneurysm in the South African Bantu. Circulation 1965;32:43.
Two-dimensional echocardiographic imaging of left ventricular mural vegetations Charles A. Herzog, M.D., Peter Carson, M.D., Lillian Michaud, R.D.M.S., and Richard W. Asinger, M.D. Minneapolis, Minn.
REFERENCES
Abrahams DG, Barton CJ, Cockshott WP, Edington GM, Weaver EJM. Annular subvalvular left ventricular aneurysm. Q J Med 1960;31:345. 2. Wolpowitz A, Arman B, Barnard MS, Barnard CN. Annular 1.
From the Division of Cardiology, Department of Medicine, County Medical Center. Reprint requests: Charles A. Herzog, M.D., Hennepin County Center, 701 Park Ave. S., Minneapolis, MN 55415.
Hennepin Medical