Reversible Severe Ischemic Mitral Regurgitation and Cardiogenic Shock as a Complication of Percutaneous Coronary Intervention

Coronary artery occlusion during percutaneous coronary intervention (PCI) causes regional myocardial ischemia. There are few reports or experimental studies about new onset of transient acute mitral regurgitation (MR) during PCI. However, there were no reports about any significant cases of hemodynamic compromise or cardiogenic shock.^1,2 In contrast, acute severe MR secondary to ischemia in the setting of acute myocardial infarction is a life-threatening condition with a very high mortality rate. Patients with this condition could present with profound cardiogenic shock requiring urgent intervention. However, to our knowledge, cardiogenic shock and severe hemodynamic compromise secondary to ischemic MR during PCI is not reported as a complication of the procedure. This is the first case report documenting this life-threatening complication during PCI. This case report is followed by a review of the literature. Case Report. The patient is a 73-year-old Hispanic female with a history of non-insulin-dependent diabetes mellitus and hyperlipidemia who presented to the emergency room with three hours of intermittent substernal chest discomfort associated with shortness of breath and palpitations. Physical examination during admission to our hospital revealed normal S1 and S2 and no gallop, murmur, parasternal lift, or jugular venous distention. The patient had clear lungs and had no peripheral edema. The electrocardiogram showed normal sinus rhythm with T-wave flattening in V6. Her initial CPK was 180 with an MB index of 14.4 and a positive troponin of 1.9. Her EKG showed normal sinus rhythm with lateral T-wave flattening in V6. After initial treatment with heparin, aspirin, metoprolol and eptifibatide, she remained chest pain-free and was taken to the cardiac catheterization laboratory the next day. An echocardiogram on the day of admission revealed mild MR (Figure 1) with preserved left ventricular size and function. A diagnostic cardiac angiogram revealed a normal left main and left anterior descending artery. The circumflex artery had bifurcational 90% stenosis after the second obtuse marginal (OM) involving the main circumflex artery and the ostium of the third large OM (Figure 2, Figure 3). The right coronary artery (RCA) was a mid-size vessel with no significant disease and no angiographic evidence of collateralization. The decision was made to proceed with PCI. After administration of a 5,000 unit of heparin bolus and adjustment of the activated clotting time, a short ATW wire (Cordis Corporation) was advanced into the main circumflex artery and a BMW wire (Guidant) was advanced into the third large OM. The main circumflex artery was dilated using 2.0 x 15 Cross-sail balloon (Guidant), inflating it to 8 atmospheres for 20 seconds (Figure 4). Next, the wire from the circumflex artery was removed and a Zeta 3.5 x 13 mm stent (Guidant) was advanced to the lesion involving OM3, inflating it to 16 atmospheres for primary stenting for 20 seconds. Post-stenting of the circumflex artery, there was a proximal dissection with no-reflow (Figure 5). The dissection was sealed using a Zeta 3.5 x 8 mm stent (Guidant), inflating it to 14 atmospheres for 10 seconds. Despite resolution of the dissection, no-reflow persisted. The patient sustained severe hypotension with a systolic blood pressure of 60, tachycardia, chest pain and severe hypoxia. Multiple doses of 40 mcg of intracoronary adenosine were given with little success. The patient was placed on 100% oxygen and an emergent Swan-Ganz catheter was inserted into the pulmonary artery to a wedge position. The patient required up to 15 mcg/kg per minute of dopamine for pressure support. Emergent echocardiography revealed severe MR with normal LV function and lateral wall hypokinesia (Figure 6). The pulmonary wedge pressure was 42 mmHg with a very high V wave of 55 mmHg and persistent systemic hypotension (Figure 7). Immediately, the left femoral artery was accessed and IABP was inserted with repeated injections of intracoronary adenosine. Shortly thereafter, no-reflow resolved (Figure 8) with brisk hemodynamic recovery and resolution of hypoxia. Dopamine was tapered off gradually and the pulmonary wedge pressure declined to a mean of 22 mmHg (then 15 mmHg at the end of the procedure) with resolution of the high V-wave during wedge tracing (Figure 9), and normalization of systolic blood pressure to 120 mmHg. A repeat echocardiogram in the cardiac catheterization laboratory revealed resolution of the MR (Figure 10). The patient remained stable with complete recovery. The IABP was removed the next day without any complications. A repeat echocardiogram before discharge and on follow-up revealed no significant MR. Discussion and review of the literature. This case is a first report of a life-threatening complication of PCI causing severe ischemic MR and cardiogenic shock. Ischemic MR is a frequent Doppler echocardiographic finding in patients after acute myocardial infarction (AMI) and an independent predictor of long-term cardiovascular mortality. Reported risk factors include advanced age, prior myocardial infarction, infarct extension, recurrent ischemia, and a reduced LV ejection fraction. During the early phase of AMI, transient ischemic MR is common and rarely causes hemodynamic compromise. However, patients with AMI who develop rupture of papillary muscles or tearing of tendinous cords commonly present with severe acute MR, cardiogenic shock and pulmonary edema as a result of a marked reduction of forward stroke volume and an increase in end-diastolic volume. Unless rapidly diagnosed and treated, acute severe MR is associated with high morbidity and mortality. Prompt surgical intervention after hemodynamic stabilization is essential to ensure a good short-term and long-term prognosis.³ Significant ischemic MR affects, on average, 4% of the patients requiring coronary bypass surgery. It is found predominantly in cases of right coronary and/or circumflex ischemic territory, and results mostly from restricted leaflet motion rather than from prolapse.⁴ Using real-time, two-dimensional doppler flow imaging technique, the severity and site of MR was evaluated by Izumi et al.⁵ A close relationship between the site of regurgitation and the region of infarction was found. They observed two major causative factors of mitral regurgitation: a) asynergy of the papillary muscle or the ventricle that results in mitral regurgitation located in the commissural area of the same side; and b) enlargement of the mitral annulus, which results in regurgitation. Kaul et al.⁶ used a canine model to study another theory of the origin of ischemic MR from the reduction of global left ventricular function rather than papillary muscle dysfunction. They evaluated MR in canine hearts with global LV dysfunction and canine hearts with papillary muscle dysfunction. They noticed a poor correlation between the degree of MR and thickening of the anterior and posterior papillary muscles. The most severe MR occurred in the setting of LV dysfunction during coronary occlusion. Prachar et al.² investigated the occurrence of MR during a short period of ischemia (60 seconds) in patients undergoing elective PCI of single vessel coronary disease. Thirty patients showed stenosis in the left anterior descending artery, 3 patients in the circumflex artery and 1 patient in the RCA. Only patients with normal left ventricular function and without collaterals to the target vessel were enrolled in the study. All patients suffered chest pain during occlusion of the vessel. Signs of grade 1 MR could be documented angiographically in 9 patients and grade 2 in 4 patients. None of the patients exhibited grades 3 or 4 MR. A significant decrease of global, as well as regional, left ventricular function could be documented during ischemia in all patients. The breakdown of wall motion was more pronounced in patients with MR and reached statistical significance. All patients with MR showed severe hypokinesis or akinesis of the wall segments adjacent to the anterior papillary muscle. There were no angiographic signs of mitral valvular prolapse or dilation of the mitral valve annulus. They concluded that transient MR is common during short periods of ischemia in humans, but of only minimal degree in the setting of single-vessel disease. Biasucci et al.⁷ evaluated ischemic MR using color Doppler echocardiography during PCI in 28 patients with single-vessel coronary artery disease (left anterior descending artery in 11 patients, right coronary artery in 8, and circumflex artery in 9) and normal left ventricular function. In all three groups, left ventricular ejection fraction (LVEF) and wall motion score index decreased significantly in comparison to baseline values. Anterior and inferior akinesia/dyskinesia was observed in all patients during left anterior descending and right coronary artery occlusion, respectively. Lateral akinesia/dyskinesia was induced by occlusion of the circumflex artery in 6 patients and the right coronary artery in one. Only the 6 patients with circumflex artery occlusion showed PCI-related MR (> 2 + in 2). LVEF were similar during artery occlusion in patients with and without MR. Neither mitral leaflet prolapse nor annular dilatation occurred during PCI in any of their patients. Their data showed that during brief occlusion of the proximal circumflex artery, functional MR (usually mild) frequently occured in relation to specific lateral akinesia/dyskinesia. The only case report about transient occurrence of severe ischemic MR is reported by Macander et al.⁸ Severe MR occurred in the setting of complete occlusion of the diagonal artery over 50 seconds, causing mild shortness of breath and chest pain but no hemodynamic compromise. Severe MR was observed within 15 seconds of balloon occlusion in the setting of apicolateral dyskinesia which was documented using color Doppler echocardiography. The MR was transient and resolved after 20 seconds of balloon deflation. The reason for the echocardiographic examination was not mentioned. As opposed to our patient, there was no significant hemodynamic compromise during transient ischemic MR in this patient. We found one case report on late severe ischemic MR occurring after successful PCI due to complete papillary muscle rupture requiring urgent surgery.⁹ There are few reports about marked improvement or resolution of MR after successful PCI in patients presenting with ischemia and significant MR before the coronary intervention.^10–12 The mechanism of ischemic MR during coronary intervention appears to be similar to ischemic MR in the setting of acute MI or unstable angina, causing papillary muscle dysfunction or mitral annulus dilatation. In our case, transient ischemic papillary muscle dysfunction secondary to no-reflow appears to be the major mechanism for severe MR and hemodynamic instability. Based on our case, we suspect that severe MR with hemodynamic compromise should be more common in patients with unexplained sudden hemodynamic deterioration during complicated PCI. However, immediate echocardiography is rarely performed during cardiac catheterization in this setting. This would explain why such a complication has not been recognized in the literature. Consideration should be given to the occurrence of MR whenever the abrupt onset of symptoms of reduced cardiac output, hypotension, elevated LV end-diastolic pressure, dyspnea or congestive heart failure accompanies PCI balloon inflation, particularly in the circumflex, obtuse marginal, diagonal or posterior descending coronary arteries. We suggest that practitioners perform an urgent echocardiographic evaluation of all patients with sudden unexplained hemodynamic deterioration during angioplasty in order to assess this rare complication. Prompt insertion of an IABP and restoration of flow should reverse the hemodynamic instability. Conclusion. Acute ischemic MR causing hemodynamic instability and cardiogenic shock in the setting of complicated PCI is most likely an under-recognized major complication. We report the first case of a severe ischemic MR causing cardiogenic shock in the setting of no-reflow of a dominant circumflex artery during PCI, with full recovery after establishment of flow and IABP insertion. Consideration should therefore be given to the occurrence of severe MR whenever the abrupt onset of symptoms of reduced cardiac output, hypotension, elevated LV end-diastolic pressure, dyspnea or congestive heart failure accompanies PCI. We suggest an urgent echocardiographic evaluation of all patients with sudden unexplained hemodynamic deterioration during an angioplasty in order to recognize this rare complication. Prompt IABP insertion and establishment of flow could be a life-saving treatment. Acknowledgement. We would like to thank Dr. Mehrnoosh Hashemzadeh, Gale Good, and Lucy Gonzales for helping us with the final editing of this manuscript, as well as the cardiac catheterization and non-invasive laboratory personnel at UCI for their support.

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