Cardiogenic shock due to papillary muscle rupture in acute myocardial infarction

316

References 1 Ribeiro P, Shapiro L, Nihoyannopoulos P, Gonzalez A, Oakley CM. Pericarditis in infective endocarditis. Eur Heart J 1985;6:975-978. 2 Arnett EN, Roberts WC. Valve ring abscess in active endocarditis. Frequency, location, and clues to clinical diagnosis from the study of 95 necropsy patients. Circulation 1976:54:140-145. 3 Tykot HB, Relkin R. Massive pericardial effusion in subacute bacterial endocarditis. J Am Med Assoc 1963;184:142-144. 4 Permanyer C, Bombi JA. Mujer de 46 aiios con pericarditis e insuficiencia cardiaca. Med Clin (Bare) 1983;81:531-539. 5 Ellis SG, Goldstein J, Popp RL. Detection of endocarditis associated perivalvular abscesses by two-dimensional echocardiography. J Am Co11Cardiol 1985;5:647-653.

IJC 0508G

Cardiogenic shock due to papillary muscle rupture in acute myocardial infarction A.J. McNeil1 ‘, A.A.J. Adgey ‘, H.O. O’Kane ’ ’ Regronal Medical Cardiolqy

Centre, and .’ Department Royal Victoria Hospital. Belfast. U.K.

(Received

and accepted

6 October

of Curdrac Surge?,

1986)

We report a case of papillary muscle rupture complicating acute myocardial infarction which resulted in acute cardiogenic shock. The patient underwent urgent replacement of the mitral valve and made an uncomplicated recovery. (Key

words:

Cardiogenic

shock; Papillary

muscle rupture)

Introduction Papillary muscle rupture is a rare complication of acute myocardial infarction, occurring in l-5% of acute infarcts, with half such patients dying within 24 hours of development of the complication [l]. Nunley and Starr recorded 4 cases of complete rupture and encountered partial rupture in a further 2 cases over an 11-year period [l]. This may well be an underestimate as some patients may die in acute cardiogenic shock due to unrecognized acute papillary muscle rupture, the deterioration being misdiagnosed as extension of the infarct, annular dilation with functional mitral regurgitation or rupture of the ventricular septum. Prompt recognition and surgical treatment may be life saving in a condition which is otherwise fatal.

Correspondence to: Dr. A.J. McNeill, Belfast BT12 6BA. U.K.

Regional

Medical

Internatronol Journul of Curdrologv, 14 (1987) 376-379 C, Elsevier Science Publishers B.V. (Biomedical Division)

Cardiology

Centre,

Royal

Victoria

Hospital,

31-l

Case Report A 52-year-old farm labourer was admitted to a surgical unit of a district general hospital on 26 March 1985 with acute epigastric pain. There were no abnormal physical findings. In particular, he was noted to have no heart murmurs. Retrospectively his electrocardiograph showed the changes of acute inferior myocardiaf infarction. All other investigations were normal. The pain settled and he was discharged home to await outpatient barium meal. On 3 April 1985 he developed similar epigastric discomfort associated with shortness of breath. Clinically he was in severe congestive heart failure. He was also noted to have a loud pan-systolic murmur at the apex which radiated to the axilla. He was admitted via the Mobile Coronary Care Unit to the Royal Victoria Hospital, Belfast. Chest X-ray showed pulmonary oedema and the electrocardiogram showed evidence of an old inferior infarction. Doppler ultrasound showed moderate mitral regurgitation and cross-sectional echocardiography revealed no evidence of ventricular septal defect and no vegetations on the mitral valve. The clinical signs of congestive heart failure resolved quickly following medical therapy, but the pan-systolic murmur persisted. Cardiac catheterisation showed that the right ventricular pressure was elevated at 58/10 mm Hg and the mean pulmonary wedge pressure was 22 mm Hg. There was hypokinesis of the inferior wall of the left ventricle with prolapse of the aortic (anterior) leaflet of the mitral valve into the left atrium which was dilated. There was marked mitral regurgitation with a V wave of 41 mm Hg. Coronary arteriography showed the right coronary artery to be totally

Ii1

t

1

Fig. 1. The excised aortic (anterior) leaflet apex of the antero-lateral papillary muscle.

17tr of the mitral

valve with tendinous

chords

and the ruptured

378

blocked 3 cm distal to the ostium. There was a 50% lesion of the proximal circumflex branch, the other vessels being normal. Elective replacement of the mitral valve was planned, but on the afternoon of 18 April 1985, he suddenly developed mild epigastric pain, became shocked and developed pulmonary oedema. The pan-systolic murmur, although present, was much softer than before. An electrocardiogram showed no changes of further infarction. The clinical picture was that of rupture of a papillary muscle. He was treated with positive inotropic agents, diuretics and venesection and an intraaortic balloon pump was inserted. On this regime his condition improved and he maintained a systolic blood pressure of 80 mm Hg overnight. Surgery was carried out on 19 April 1985. At operation there was marked enlargement of all cardiac chambers. There was rupture of the antero-lateral papillary muscle of the mitral valve, its large apical portion floating freely in the left atrium together with its attached tendinous chords (Fig. 1). The valve was totally excised and replaced by a Bjork-Shiley prosthesis. A saphenous vein graft was anastomosed from the aorta to the right coronary artery. The area of the infarcted inferior wall was noted to be small. The peri-operative and post-operative courses were uneventful. Histological examination of the papillary muscle revealed total infarction with an inflammatory infiltrate present at the edge in keeping with infarction of a few weeks duration. Discussion The suggestion that papillary muscle rupture is an under-recognized cause of acute cardiogenic shock is supported by the findings of Wei et al. [2]. They reported 13 cases studied at autopsy in a 21-year period, this making up 5% of all patients dying of acute myocardial infarction. Eleven of these patients had total rupture and 10 had an apical systolic murmur noted while alive [2]. At the time of complete rupture, the murmur becomes softer due to a fall in cardiac output as noted in our patient. Because of this, the diagnosis is easily missed. Our patient is typical of those reported in the past [2] in having a small area of infarction (seen at operation). Wei et al. [2] reported a mean myocardial loss of 19% in their series and, like our patient, none had involvement of myocardium near the atrioventricular junction - a significant point in allowing early replacement of the valve. Rupture of the antero-lateral papillary muscle is less common than its postero-medial partner, the former usually occurring with anterior and lateral wall injury. Nonetheless, rupture of the antero-lateral muscle is well recognized as a complication of inferior infarction [l]. Rupture of a papillary muscle of the tricuspid valve in acute myocardiaf infarction is also reported but is very rare [3]. Rupture usually occurs several days after infarction. As patients with acute myocardial infarction survive longer due to intensive acute coronary care and successful treatment of arrhythmias, the proportion surviving to develop rupture of a papillary muscle, tendinous chords and possibly the ventricular septum or wall may well increase. Acute cardiogenic shock due to mitral regurgitation from rupture of a papillary muscle is surgically correctable and the diagnosis must always be considered. Thus, the development of mitral regurgitation following myocardial infarction must be viewed with caution and investigated with urgency.

Acknowledgement We are grateful to Mrs. Linda Cooper for typing the manuscript

379

References 1 Nunley DL, Starr A. Papillary muscle rupture complicating acute myocardial infarction. Am J Surg 1983;145:574-577. 2 Wei JY, Hutchins GM, Bulkley BH. Papillary muscle rupture in fatal acute myocardial infarction. Ann Intern Med 1979;90:149-513. 3 Eisenberg S, Suyemoto J. Rupture of a papillary muscle of the tricuspid valve following acute myocardial infarction. Circulation 1964;30:588-591.

IJC 0508H

Pseudo-electrical alternation due to deformation of QRS-T by atria1 flutter waves Sita Ram Mittal, Raj Kumar Department

Saxena, Jagat Prakash

Sethi

of Medicine, J. L. N. Medical College, Ajmer, Rajasthun, India

(Received 3 September 1986; revision accepted 7 October 1986)

A case of pseudo-electrical alternation produced by deformation of QRS-T waves by atrial flutter waves is reported. It should be differentiated from true electrical alternation which has definite diagnostic and prognostic implications. (Key words:

Electrical

alternation;

Atrial flutter)

Introduction The term “electrical alternation” is used when the amplitudes of the QRS complex (and at times also the T wave) alternate in every other beat. We describe a case of pseudo-electrical alternation produced by superimposition of atrial flutter waves on QRS and T waves. Case Report B.S., a 60-year old male was hospitalized with the complaint of breathlessness and orthopnoea since that morning. He had prolonged chest discomfort suggestive of myocardial ischaemia on the evening before admission. He was a known diabetic and hypertensive but was not taking regular treatment. On examination he was orthopnoeic with a respiratory rate of 36/min, a regular pulse rate of 104/min and blood pressure of 140/106 mm Hg. The jugular venous pressure was normal. Examination of heart revealed a loud third heart sound. Fine crepitations were present over both lung bases. The electrocardiogram revealed a

Correspondence

to: Dr. S.R. Mittal, X1/101. Brahampuri. Ajmer, Rajasthan, India, PIN-305001

Internatwnal Journal of Cardiology, 14 (1987) 379-381 ,C Elsevier Science Publishers B.V. (Biomedical Division)