Complete Heart Block Followed By Left Ventricular Free Wall Rupture In A Patient With Inferior Wall Myocardial Infarction
R. Chris Jones, MD
The Cleveland Clinic Foundation Heart Center
Introduction
Approximately 40-50% of all acute ST-segment elevation myocardial infarctions (STEMI) involve the inferior wall (1,2). Post-thrombolytic era trials have reported low complication and mortality rates for inferior STEMI. Nevertheless, a substantial minority of patients develops complications that may decrease their chances for survival.
Case Presentation
The patient is a 74 year-old African-American male who developed new-onset chest pain 24 hours prior to presentation to the Cleveland Clinic Foundation. The pain persisted until approximately 2 hours before coming to the emergency department. His wife was finally able to convince him to seek medical attention after he began to develop nausea with vomiting. The physical examination was within normal limits except for a heart rate of 52, blood pressure of 150/90, and a right femoral bruit. He had no evidence of congestive heart failure. The initial ECG (Figure 1) showed sinus bradycardia, first-degree block, left ventricular hypertrophy, lateral T-wave inversion, and 0.5 to 1mm ST-segment elevation in leads III and aVF. The initial CK-MB and troponin T values were elevated at 131 and 0.79 µg/ml; these were the peak values.
The risk factors for coronary artery disease included advanced age, male gender, and active smoking. His past medical history was remarkable only for minor traumatic injuries and a reportedly “negative” treadmill test two years prior. He took no medicines. He was a retired store-owner and was active in the community. His parents died at young ages of unknown causes.
The patient was transferred to the Coronary Care Unit (CCU) where he was treated with aspirin, unfractionated heparin, intravenous nitroglycerin, and atorvastatin. He remained chest-pain free. Beta-blockers were not administered due to persistent bradycardia. Approximately 24 hours after admission to the CCU, progressive first-degree block was noted on telemetry. The ECG showed persistence of the ST segment elevation in leads III and aVF. Over the ensuing 12 hour time period, the heart block advanced to second and then symptomatic third degree block (Figure 2) with a ventricular rate in the twenties. Atropine was administered and a temporary pacing wire was placed. Coronary angiography performed later that day showed a 60% distal left main stenosis, 60% ostial LAD stenosis, 50% ostial and 60% mid circumflex stenoses, 60% mid RCA stenosis, and a 100% posterior ventricular branch stenosis (Figure 3). Left ventriculography revealed an ejection fraction of 50% with an akinetic mid and distal inferior wall; no mitral regurgitation was seen. No intervention was performed.
Figure 3: coronary angiography RCA
On the following day, the electrophysiology team was consulted for placement of permanent pacemaker. At 13:40, the patient experienced a pulseless electrical activity (PEA) arrest. Despite aggressive intervention by the CCU team, including an unsuccessful pericardiocentesis, the patient expired. Post-mortem examination demonstrated a large infarction of the posterior left ventricle measuring 5 x 1 x 3 cm (Figure 4). An area of hemorrhage communicative with the left ventricular cavity and pericardial space was identified with approximately 300 cc of clot present in the pericardial space. The pathologist estimated that 30% of the left ventricle was involved in the infarction.
Figure 4: Postmortem examination
Discussion
This previously healthy elderly male developed two unusual complications of acute MI. A recent review reported a 19% incidence of second or third degree heart block in patients with inferior MI (3). Patients that develop this complication are at higher risk of death from their MI, even in the post-Thrombolytic era (4). Possible explanations for the etiology of heart block with inferior MI include increased vagal tone, ischemia of the AV node, concomitant LAD disease, and release of AV toxins by necrotic myocardium.
Analysis of the National Registry of Myocardial Infarction data indicate that less than 1% of all MI patients develop ventricular free wall rupture (FWR) (5). Our patient’s risk factors for FWR included late presentation, absence of reperfusion, age, hypertension, lack of beta-blockade administration, and first presentation with MI. Myocardial infarctions involving the infero-postero-lateral wall are most commonly involved with a prevalence of 29%, probably reflecting the increased size of these infarctions. The development of PEA arrest without preceding heart failure symptoms has been reported as more than 95% predictive of ventricular FWR (6).
Comments by Dr. Eric Topol
Free wall rupture is a rare (<1%) and catastrophic MI complication, but in retrospect this patient had virtually every risk factor. One particular cue in his presentation was the early development of advanced AV block, indicated profound extent of myocardial damage so atypical with an infero-posterior MI. The patient did not receive reperfusion therapy owing to late presentation and lack of qualifying ECG changes, and we know that cardiac rupture is significantly reduced with successful reperfusion. Finally, it is striking how a branch of the right coronary (posterior LV) can have such a devastating impact on the myocardium, out of proportion to expectation.
References
- Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardio (GISSI): Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet 1986; 1:397-402.
- ISIS-2 (Second International Study of Infarct Survival) Collaborative Group: Randomized trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet 1988; 2:349-60.
- Berger PB, Ryan TJ: Inferior Myocardial Infarction, High-Risk Subgroups. Circulation 1989;81:401-11.
- Clemmensen P, Bates ER, Califf ER, Hlatky M, George BS, Kereiakes DJ, Aronson L, Berrios E, Topol EJ: Is complete heart block in inferior infarction a benign phenomenon following reperfusion therapy? (Abstract) J Am Coll Cardiol 1989; 13(suppl II):26.
- Becker RC; Gore JM; Lambrew C; Weaver WD; Rubison RM; French WJ; Tiefenbrunn AJ; Bowlby LJ; Rogers WJ: A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction. J Am Coll Cardiol 1996;27:1321-6
- Figueras J, Curos A, Cortadellas J, Soler-Soler J: Reliability of electromechanical dissociation in the diagnosis of left ventricular free wall rupture in acute myocardial infarction. Am Heart J 1996;131:861-4.
© Cleveland Clinic Foundation 9/02
