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Anterior Myocardial Infarction complicated by AV conduction block

Anterior Myocardial Infarction complicated by AV conduction block

Michael McWilliams, MD

Introduction:

Atrioventricular (AV) conduction blocks are common in the immediate post-myocardial infarction period. They vary from relatively benign conditions like first degree AV block and Mobitz I, to potentially life-threatening conditions like Mobitz II, complete heart block (CHB), or asystole.

We present a case of an anterior myocardial infarction (MI) in an elderly gentleman complicated by AV conduction block.

Case Report:

RL was a 72 year-old white male referred to the Cleveland Clinic Foundation (CCF) with an ST segment elevation myocardial infarction (STEMI). His cardiac risk factors included steroid induced diabetes mellitus for 20 years, hypertension, and hyperlipidemia.

His illness began while shoveling snow at 19:30 when he developed acute onset of substernal chest pain without radiation, nausea, or diaphoresis. He suffered two unwitnessed falls with no loss of consciousness or head trauma. EMS transported RL to an outside hospital at 2100. The initial ECG demonstrated anteroseptal ST elevation (see Figure 1). His chest pain was unremitting despite 15 mg of intravenous metoprolol and 2 sublingual nitroglycerin. Intravenous nitroglycerin, tirofiban, heparin, and aspirin were administered, and he was taken by helicopter to the CCF. His symptoms resolved during flight, and he arrived to the CCF pain free at 22:15. Repeat ECG showed resolution of the ST segment elevation. Cardiac catheterization demonstrated fresh thrombus in the proximal left anterior descending that overlapped the first septal perforator (Figure 2). Due to the concern of distal embolization and no reflow to the distal vessel, the decision was made to continue maximal anti-platelet therapy and consider intervention following a "cooling-off" period.

Figure 1: Admission ECG to outside hospital. Sinus rhythm with ST segment elevations in V1 through V3 - Click here for larger image

Figure 2: Admission cath film. Proximal left anterior descending thrombus overlapping the first septal perforator - Click here for larger image

The next morning, the creatinine kinase increased to >5400 with an MB>500. Sixteen hours after admission, RL was taken back to the catheterization laboratory for persistent nausea without chest pain or EKG changes. Secondary to concerns of persistent ischemia, a Bx Velocity Rx 3.5 mm x 18 mm stent was placed after angioplasty in the proximal LAD. The first septal perforator was occluded by the stent (Figure 3). He returned to the intensive care unit pain free.

Figure 3: Post stent cath film notable for the absence of the first septal perforator - Click here for larger image

Over the next 12 hours he developed persistent sinus tachycardia, first in the low 100s and increasing to the 140s by the next morning. At 0700 on the third day he became asystolic. He was intubated, CPR was initiated, and epinephrine and atropine were given, along with a trial of transcutaneous pacing. After ten minutes of CPR, his rhythm returned as sinus tachycardia with AV dissociation (Figure 4). He was taken emergently to the catheterization laboratory for placement of a temporary ventricular pacemaker, intra-aortic balloon pump, and repeat left heart cath. The catheterization revealed a widely patent LAD stent. He returned from the lab with a systolic pressure of 80 mmHg. Due to persistent hypotension, a temporary atrial wire was placed and subsequently increased the systolic pressure from 80 mmHg to 100 mmHg. Seventy-two hours after his asystolic arrest, RL no longer required ventricular pacing.

Figure 4: Sinus tachycardia with complete atrioventricular dissociation - Click here for larger image

He went on to develop renal failure requiring hemodialysis, needed a pericardiocentesis for a large hemorrhagic pericardial effusion, and subsequently was given a tracheostomy due to failure to wean from the ventilator. At the time of this report, RL was no longer ventilator dependent and was making steady progress.

Discussion:

Complete heart block complicates 5% of acute myocardial infarctions in the post-thrombolytic era, with a slightly higher incidence if the right ventricle is involved 1,2. With anterior infarcts, as with this case, CHB usually occurs suddenly within 12-24 hours post-infarction and is generally preceded by an intraventricular conduction delay or a Mobitz II rhythm. The ventricular escape rhythm is usually less than 30 beats per minute and often leads to hemodynamically significant bradycardia. The mortality associated with CHB and anterior infarctions approaches 70-80%. It is unclear if prompt temporary pacing improves long-term outcomes or if the mortality is related to the extensive myocardial damage typical of large anterior infarcts that cause CHB.

To the contrary, CHB associated with inferior myocardial infarctions is usually transient but associated a 15% mortality that increases to 30% if the right ventricle is involved. CHB associated with inferior myocardial infarctions typically is preceded by first-degree AV block or a Mobitz I rhythm. The escape rhythm is usually intranodal or supranodal 3, and in 70% of cases, is associated with a hemodynamically stable narrow complex escape rhythm >40 beats per minute. Inferior MI related CHB occurring within 6 hours after the infarct usually responds to atropine 4.

AV sequential pacing is proven to increase cardiac output in the setting of RV infarction with bradyarrythmias 5. This case demonstrates improved cardiac output from AV pacing associated with an anterior infarction. His left ventricle proved reliant on atrial contraction to maintain an adequate blood pressure.

Comments by Dr. Eric Topol :

This is a case of complete heart block associated with an anterior myocardial infarction. Two important points are demonstrated. First, a significantly greater mortality rate associated with complete heart block exists in patients with anterior versus inferior infarctions. Second, AV sequential pacing can result in dramatic hemodynamic improvements, especially in patients with right ventricular infarctions.


References

  1. Archbold RA, Sayer JW, Ray S, et al: Frequency and prognostic implications of conduction defects in acute myocardial infarction since the introduction of thrombolytic therapy. Eur Heart J 19:893-898, 1998
  2. Kinch JW, Ryan TJ. Right ventricular infarction. N Engl J Med 330:1211-1217, 1994.
  3. Bilbao FJ, Zabalza IE, Vilanova JR, Froupe J: Atrioventricular block in posterior acute myocardial infarction: A clinicopathologic correlation. Circulation 75:733, 1987.
  4. Antman, EM, Braunwald E. Acute Myocardial Infarctions: Chapter 35. Heart Disease: A Textbook of Cardiovascular Medicine. CD version. Saunders Company. 2001.
  5. Topol EJ, Goldschlager N, Ports TA, Dicarlo LA Jr, Schiller NB, Botvinick EH, Chatterjee K. Hemodynamic benefit of atrial pacing in right ventricular myocardial infarction. Ann Intern Med 1982 May;96(5):594-7 .