Simultaneous Papillary Muscle Avulsion and Free Wall Rupture during Acute Myocardial Infarction. Intra-Aortic Balloon Pump: A Br

Cardiogenic shock complicates 7% of acute myocardial infarctions (AMI) in patients presenting to hospitals, with a concomitant mortality rate of 70%.¹ In the age of reperfusion therapy, significant improvement in reducing this adverse outcome for shock patients has been observed. This improvement is partly due to the increased aggressiveness of cardiologists providing early revascularization, as well as increased utilization of counterpulsation by intra-aortic balloon pumps (IABP) in this population. We present a clinical case exemplifying the survival advantage offered with this therapy, and discuss the role of IABP for cardiogenic shock due to mechanical complications of AMI. Intra-aortic balloon counterpulsation for AMI. The primary goals of IABP treatment are: 1) to decrease left ventricle work through afterload reduction; 2) to increase myocardial oxygen supply by increasing diastolic coronary perfusion to ischemic myocardial territories; and 3) to decrease myocardial oxygen demand.^2,3 Furthermore, IABP improves various hemodynamic indices including ejection fraction and cardiac output, and decreases pulmonary capillary wedge pressure and systemic vascular resistance. These significant improvements make IABP an especially favorable treatment option during AMI. Summarized in Tables 1 and 2 are the causes of hypotension during AMI, and indications and contraindications for IABP use, respectively. In the era before stents and glycoprotein IIb/IIIa inhibitors, Ohman et al. showed in a randomized trial that IABP during percutaneous coronary intervention (PCI) for AMI significantly reduced the composite endpoint of death, MI or refractory ischemia.⁴ A more recent randomized trial showed no improvement in survival, reinfarction or myocardial salvage in selected high-risk patients undergoing primary PCI for AMI.⁵ The PAMI II Trial reported that prophylactic IABP use did not improve outcomes after high-risk primary angioplasty.⁶ Thus, in the absence of hemodynamic compromise or refractory ischemic symptoms, the routine use of IABP for patients undergoing PCI showed no benefit. In contrast, 53% of AMI patients receiving thrombolysis in the SHOCK Trial Registry received IABPtherapy.⁷ In-hospital mortality was lower in shock patients receiving thrombolysis, IABP, or thrombolysis with IABP, compared to neither thrombolysis nor IABP use (63%, 53%, 46% versus 77%, respectively).⁷Intra-aortic balloon counterpulsation for cardiogenic shock. Two randomized trials in the prethrombolytic era did not show improved outcomes with IABP during cardiogenic shock.^8,9 Although randomized trials in the modern era of reperfusion have been attempted but never completed, retrospective analyses from large, prospective clinical trial databases demonstrate a substantial benefit of IABP in cardiogenic shock patients. In 310 of 41,000 patients with cardiogenic shock in the GUSTO-I Trial, Anderson et al. demonstrated lower mortality at 1 year in 62 patients (20%) receiving IABP therapy during the first 24 hours of AMI.10 Furthermore, patients with AMI and shock treated with thrombolysis and IABP at hospitals lacking percutaneous revascularization capabilities were likely to survive until transfer (93% versus 37%), and to survive until revascularization (85% versus 37%).¹¹ In the National Registry of Myocardial Infarction-2 (NRMI-2), 23,130 patients had cardiogenic shock at initial examination or developed it during hospitalization.¹² IABP utilization in 31% of patients was associated with significantly reduced mortality for those receiving thrombolysis (67% versus 49%), but not in patients undergoing primary angioplasty (45% versus 47%).¹² The SHOCK Trial randomized 152 patients to emergency revascularization and 150 patients to initial medical stabilization. Mortality at 12 months was lower in the revascularization group (53.3% versus 66.4%; p 13,14 IABP use was high (86%) in both groups. Sanborn et al. analyzed the 856 shock patients presenting with primary left ventricular (LV) failure in the SHOCK Trial Registry and found evidence supporting early use of IABP therapy for those revascularized early.¹⁵ Patients receiving IABP therapy had a 22% absolute risk reduction in mortality (72% versus 50%; p 15 Clinical Case Report An 84-year-old male with a past history of hypertension, hypercholesterolemia, nonsmoker, nondiabetic, and no known structural heart disease, experienced dyspnea on exertion, chills, sweating and weakness lasting for 20 minutes 2 weeks before the current admission. He was taking no prior medications. Evaluation by his primary medical physician, including ECG, chest X-ray and blood tests, revealed mildly increased liver enzymes, but otherwise unremarkable findings. He felt improvement until 3 days prior to admission when he experienced cough with phlegm and recurrent shortness of breath. The patient went to our affiliate hospital’s emergency department, experiencing 1 hour of worsening acute shortness of breath and no chest pain. The patient’s blood pressure (BP) was 100/60, his pulse was regular at 123 beats per minute, his respirations were 32 per minute, and his arterial oxygen saturation was 91% on 21% oxygen. Lung examination revealed bilateral rales throughout both lung fields and distended jugular veins. He was administered 50% oxygen by face mask and his ECG showed 2 mm ST-elevations and Q-waves in leads II, III and aVF, as well as 2 mm ST depressions in leads V1–V4, consistent with an acute inferior and posterior wall injury pattern (Figure 1A). Right-sided ECG did not demonstrate ST-elevations in V4R. The patient received aspirin and intravenous furosemide, nitroglycerin and unfractionated heparin. He was intubated and provided mechanical ventilation for persistent respiratory distress. The patient received full-dose thrombolytic therapy 50 minutes after arrival, but there was no resolution of his ST abnormalities. He was then transferred to our hospital for cardiac catheterization, rescue angioplasty and stent implantation. Cardiac catheterization. On arrival to the cardiac catheterization laboratory, the patient’s BP was 57/45 mmHg and his heart rate was 121 beats per minute. Intravenous injections of neosynephrine and infusions of dobutamine and norepinephrine were initiated. The patient’s BP recovered to 107/63 mmHg after 15 minutes of effort. An IABP was inserted due to cardiogenic shock with initially refractory hypotension. Laboratory values from the referring hospital showed a significantly elevated leukocyte count (17,400), creatinine (2.0 mg/dL), AST (116 mg/dL), ALT (67 mg/dL), creatine kinase (206 units/L), MB fraction (22.1 ng/mL), and troponin-I (2.92 ng/mL). An arterial blood gas on mechanical ventilation, FIO2 100%, showed 7.27/33/63/15.3/89%, which was consistent with metabolic acidosis and hypoxia. Coronary angiography revealed the following information: left main = normal ostial LAD = 60–70% stenosis mid- and distal vessel with mild-luminal irregularities small caliber diagonals with diffuse disease LCX = normal OM1 small-caliber with long proximal 80% stenosis RCA (dominant) = mid-long 90% culprit lesion distal vessel small caliber (Figure 2A). The LV end-diastolic pressure was 35–40 mmHg. Contrast ventriculography revealed severe LV dysfunction; the estimated LVEF was 25%, with inferior and apical akinesis. Abnormal contrast filling, initially perceived as an apical cutoff sign indicating a possible intracavitary thrombus, was later realized to be an inferior aneurysmal segment. PCI of the mid-RCA was performed by direct stenting to 14 atm with a 3.0 mm x 24 mm Taxus^® drug-eluting stent (Boston Scientific Corp., Natick, Massachusetts). Final angiographic results were excellent, with TIMI 3 flow (Figure 2B). Right heart catheterization pressures were elevated in the right atrium (20 mmHg), right ventricle (64/20 mmHg), and pulmonary artery (64/30 mmHg). The pulmonary capillary wedge pressure was 35–40 mmHg, with large V-waves (Figures 2C and D). There were no step-ups in oxygen saturations. Initial hospital course. Postintervention in the CCU, the patient required high doses of intravenous norepinephrine and dobutamine for hemodynamic support. During the night, the on-call cardiology Fellow suspected a mechanical complication despite reperfusion due to persistent hypotension. Bedside echocardiography revealed severe (4+) mitral regurgitation, with a ruptured papillary muscle (Table 2, Figure 3). The patient was also oliguric, with a urine output of approximately 5 ml per hour. Cardiac output and index remained low, with mixed venous saturations ranging from 40–50% on mechanical ventilation and moderate-to-high doses of inotropes. Furthermore, the patient’s creatinine rose to 2.8, his lactate was 3.4, and his cardiac enzymes and liver function tests showed increases. The patient was receiving maximal medical therapy in accordance with family wishes. However, the patient continued to progress into multisystemic organ failure with worsening X-ray evidence of congestive heart failure, worsening oxygenation, acidosis, persistent oliguria and coronary ischemia on ECG (Figure 1B). Given these findings, emergent salvage coronary artery bypass grafting and mitral valve replacement were discussed with family members, along with informing them of a mortality rate of 80–90%. A decision was made to attempt surgery. Operative procedure and outcome. The patient’s operation revealed a ruptured papillary muscle and rupture of the posterior inferior LV free wall. The cardiothoracic surgical team performed the following: 1) two-vessel coronary artery bypass grafting of the yet-to-be revascularized LAD and OM1 vessels; 2) mitral valve replacement with a 25 mm porcine bioprosthetic valve; and 3) repair of the posterior inferior LV free wall rupture using Teflon. Given the patient’s critical condition, cardiogenic shock, and advanced age, it was decided not to utilize the left internal mammary artery. Opening of the pericardium revealed non-clotted fresh blood in the pericardium and the free wall rupture. First, reverse saphenous vein grafts to the LAD and to the OM1 were performed in an end-to-end fashion using separate vein grafts. The free wall rupture of the LV was located at the base of the posteromedial papillary muscle. There was a small subcentimeter area of palpable defect with a surrounding hematoma. The area was repaired using two-layer running sutures and Teflon felt strips for reinforcement. For further reinforcement, a Teflon patch was fashioned and glued onto the surface of the posterior inferior free wall using BioGlue^®(CryoLife International®, Inc., Kennesaw, Georgia). Mitral valve exposure via a left atriotomy revealed rupture of the posteromedial papillary muscle with flail mitral valve leaflets into the LA (Figure 4A). The P3 and A3 portions of the posterior and anterior leaflets, respectively, were excised along with underlying subvalvular chordae attached to the ruptured portion of the papillary muscle (Figure 4B). A 25 mm porcine bioprosthesis was placed into the mitral annulus using pledgeted sutures. The atriotomy was closed, the LV was vented and the final proximal anastomoses of the aortosaphenous vein grafts were completed. The patient was successfully weaned from cardiopulmonary bypass, and intravenous nitroglycerin, milrinone, norepinephrine, dobutamine and IABP therapy were resumed. Postoperative transesophageal echocardiography revealed improved motion of the anterior, anteroseptal and lateral wall segments; the inferior and inferoseptal segments remained akinetic. Mitral valve bioprosthesis showed no perivalvular gaps or mitral regurgitation (MR). IABP therapy was utilized until postoperative day 4, when the patient was successfully weaned off inotropes and balloon support. He continued to make improvements, and on postoperative day 22, the patient was successfully discharged to a subacute rehabilitation facility. At 4-month follow up, the patient was alive and well. Discussion Intra-aortic balloon counterpulsation for mechanical complications of AMI. Much of the current enthusiasm in managing AMI patients relates to revascularization strategies. However, as predicted 15 years ago, mechanical and electrical complications pose a major threat to recovery in some patients.¹⁶ Three-quarters of cardiogenic shock cases complicating AMI are caused by severe LV failure.¹⁴ Other causes are mechanical complications accounting for about 12–15% of shock cases. Strong evidence from randomized trials for IABP use during mechanical complications of acute MI is lacking, but multiple case series support its use as a bridge to surgery. This discussion focuses on three complications of AMI, whereby IABP support may be beneficial in the following instances: 1) rupture of the ventricular free wall; 2) acute papillary muscle rupture with MR; and 3) rupture of the ventricular septum. The recent American Heart Association/American College of Cardiology (AHA/ACC) guidelines outline optimal treatment strategies for patients with mechanical complications during AMI.¹⁷ These guidelines state that patients should be considered for urgent cardiac surgical repair unless further support is futile due to the patient’s wishes or unsuitability for further invasive treatment. Recommendations for low-output states caused by mechanical causes include stabilization with an IABP to reduce afterload, regurgitant volumes and pulmonary congestion while emergency surgery is arranged. Additionally, a pulmonary artery catheter with correct interpretation of hemodynamics may be useful in establishing the diagnosis of a mechanical defect and in its subsequent management. The recommendations for IABP support of the failing heart are listed in Table 4. Free wall rupture complicating AMI. Cardiac free wall rupture complicates 2–7% of STEMI patients, and autopsy studies reveal it accounts for 7–30% of deaths post-MI.^18,19 In the SHOCK Trial Registry, 2.7% of patients had free wall rupture with an in-hospital mortality rate of 61%.²⁰ Predictors of cardiac rupture include patients with a first MI, anterior MI, large infarcts, elderly patients, women, lack of prior angina, CHF or PVD, lack of collaterals, presence of new Q-waves and anti-inflammatory medications.^20,21 Although the overall risk of cardiac rupture is reduced with thrombolysis,^18,22 death from cardiac rupture during the first 24–48 hours of an AMI is more prevalent when thrombolytics are utilized.²¹ Their use greater than 14 hours after symptom onset increases rupture risk, emphasizing the importance of early reperfusion.²³ Three types of free wall rupture exist: 1) abrupt slit-like tears; 2) myocardial erosion where infarct and viable myocardium adjoin; and 3) early aneurysm formation that is correlated with older, expanded infarcts.²⁴ Further classifications are as follows: 1) Acute: an abrupt transmural rupture; or 2) Subacute: gradual or incomplete rupture and/or slow or repetitive bleeding into the pericardial sac.²⁵ Clinical presentations of free wall ruptures vary from asymptomatic pseudoaneurysm appearances on echocardiography, to incomplete/subacute rupture, to complete rupture leading to pericardial tamponade and/or sudden cardiac death. Rapid detection of these is important for potential patient survival. Treatment strategies for free wall rupture include: intravascular volume expansion, inotropic and vasopressor support, IABP and emergent pericardiocentesis for effusions associated with tamponade. These interventions serve as a bridge for the only effective therapeutic option: early corrective surgery. In the SHOCK Trial Registry, 28 patients were given a diagnosis of free wall rupture/tamponade. One patient died 1.8 hours after admission without undergoing pericardiocentesis or surgery. Six patients underwent pericardiocentesis, and only 50% survived. In the 21 patients who underwent surgical repair, only 38% survived.²⁰ Details on the type and timing of operative repair are not available. Purcaro et al. reported subacute rupture diagnosed by echocardiography in 4.6% (28/604) of patients. Four patients died while awaiting surgery, and 24 patients underwent surgical repair with a mortality rate of 33%.²⁵ In another series of 1,247 patients, 2.6% diagnosed with subacute rupture were treated with an epicardial Teflon patch. The surgical mortality rate was 24%, and 51% of patients were dead within 2.5 years.²⁶ McMullan et al. reported a series of 18 patients diagnosed with free wall rupture; 14 had abrupt transmural types with cardiogenic shock, and 4 had subacute ruptures. Repair with infarctectomy and direct suture resulted in a 61% mortality rate (11/18 patients).²⁷ Thus, even patients managed surgically can have high mortality rates. Medical management, including pericardiocentesis for 84% of 93 AMI patients with LV free wall rupture, led to an 86% mortality rate.²⁸ All patients had subacute oozing-type ruptures. In the 16% of patients undergoing surgical repair, 60% died intraoperatively. Half the survivors had oozing-type ruptures and were repaired via a sutureless technique using fibrin glue. The surgeons utilized a circulatory support system after each operation, and 83% of survivors were still alive after 7 years.²⁸ IABP used concomitantly with off-pump surgery for perioperative stabilization was reported in a series of 7 patients undergoing repair for LV free wall rupture post-MI. A satisfactory hemodynamic state was restored in all patients, with no cases of re-rupture and 100% hospital survival.²⁹Papillary muscle rupture complicating AMI. Pulmonary rales or hypotension in a patient with inferior MI should alert physicians to potential papillary muscle rupture and acute mitral regurgitation (MR). Patients presenting with MR are more often females, and the site is frequently inferior or posterior, involving the posterior papillary muscle, and is less likely to be anterior.³⁰ Patients with severe MR accompanied by cardiogenic shock during AMI have a poor prognosis. In the SHOCK Registry, 7% of patients with severe MR had an overall in-hospital mortality rate of 55%, similar to the 61% mortality rate in the primary LV failure patients.³⁰ Mortality with medical treatment was only 71% compared with 39% with surgery. IABP was used in a significantly greater number of patients in the SHOCK Registry for acute, severe MR than for primary LV failure (68% versus 52%).³⁰ Although no difference in mortality between these two patient groups was observed despite the higher IABP use, it should be noted that the time from shock onset to IABP placement was longer in patients with severe MR compared to primary LV failure. Interestingly, of the 98 patients with severe MR, 46% of them underwent valve surgery, and the mortality rate with surgery versus medical treatment was lower (40% versus 71%). IABP support was used in almost all of the surgical patients (98%), and less than half of the medically treated patients. The SHOCK Trial Registry and other small case studies show that IABP use in patients undergoing emergent valve surgery for severe MR produces good outcomes.^30–32Ventricular septal rupture complicating AMI. The presence of ventricular septal rupture (VSR) during AMI, like severe MR, is associated with a new systolic murmur, but will show elevated oxygen saturation (“step-up”) in the pulmonary artery compared to the right atrium.³³ The incidence of acute VSR has declined in recent years due to new revascularization strategies, and is estimated to occur in fewer than 1% of patients with ST-elevation myocardial infarction (STEMI) (GUSTO-I).^33,34 Prompt surgical repair is recommended since the sole medical treatment is associated with an extremely high mortality rate. Insertion of an IABP, particularly in patients with VSR, can help stabilize the patient. The SHOCK Trial and SHOCK Registry reported a 4% incidence of VSR with a high in-hospital mortality rate of 87%.⁷ Despite the use of IABP in 75% of VSR patients versus 53% IABP use in the LV failure group, mortality associated with VSR was higher than other groups of mechanical complications.³⁵ Surgery for VSR was attempted in 55% (31/55) of cardiogenic shock patients in the SHOCK Trial Registry, yet mortality remained high. at 81% (25/31%). This was compared to a 96% mortality rate for medically treated VSR patients. Due to the small sample size, the effect of IABP for surgically treated versus medically treated VSR patients was not determined. In the GUSTO-I Trial, mortality rates for surgically and medically treated patients were 47% and 94%, respectively.³⁴ Thus, IABP insertion and prompt surgical referral fall under the AHA/ACC Class I recommendations for patients with acute VSR.¹⁷ Summary The mechanical complications of AMI such as free wall rupture, severe MR and VSR often lead to cardiogenic shock and poor patient outcomes. Our patient with an inferior wall MI developed shock from mitral valve papillary muscle avulsion leading to severe MR, free wall rupture and hemopericardium. The patient’s right coronary artery was revascularized percutaneously with the assistance of an IABP. He then underwent surgical repair of mechanical complications, ultimately leading to hospital discharge and survival. The use of intra-aortic counterpulsation during these scenarios can provide increased myocardial perfusion, decreased myocardial work and increased cardiac output, serving as a bridge to corrective surgical repair and potentially improved patient outcomes.

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