HLC 1869 No. of Pages 5
CLINICAL SPOTLIGHT
Heart, Lung and Circulation (2015) xx, 1–5 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2015.04.175
Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction: Case Report of an Unusual Complication and Review of Treatment Strategies Weiqin Lin, James Wei Luen Yip, Tiong Cheng Yeo Cardiac Department, National University Heart Centre, Singapore; National University Health System Received 1 February 2015; received in revised form 13 April 2015; accepted 17 April 2015; online published-ahead-of-print xxx
Right ventricular (RV) infarction is not an uncommon complication of acute left ventricular infarction. It has been established that RV dysfunction post myocardial infarction (MI) is associated with increased mortality and morbidity. When RV infarction occurs in a patient with previously dormant patent foramen ovale (PFO), an unusual presentation of persistent refractory hypoxaemia ensues. We present a case of new RV infarction in a patient with underlying ischaemic cardiomyopathy, which was complicated by acute rightto-left shunting through the PFO. He was treated with percutaneous coronary intervention (PCI) and subsequent percutaneous PFO closure. We will also review the existing literature with regards to diagnostic and management strategies for patients with this unusual sequelae of MI. Keywords
Acute myocardial infarction Patent foramen ovale Intra-cardiac shunt PFO closure
Introduction
Case Presentation
Right ventricular (RV) infarction occurs with acute occlusion of the right coronary artery proximal to the right ventricular branches. This can result in RV systolic dysfunction. In patients with a patent foramen ovale (PFO), the acute RV systolic failure and resultant elevation in right heart pressures can result in a right-to-left shunt through the PFO. This will manifest clinically as refractory hypoxaemia. In the event of refractory hypoxaemia despite optimal medical therapy, patients should be considered for obliteration of the PFO. We present a case of new RV infarction in a patient with underlying ischaemic cardiomyopathy, which was complicated by acute right-to-left shunting through the PFO. He was treated with percutaneous coronary intervention (PCI) and subsequent percutaneous PFO closure.
A 47 year-old male with hypertension, hyperlipidaemia and a remote history of ischaemic heart disease, presented to the emergency room with three-day history of chest pain and dyspnoea. Electrocardiogram at presentation showed sinus rhythm. Deep Q waves in the inferior leads with associated ST-segment elevation and T wave inversions were seen (Figure 1). Cardiac biomarkers done at presentation were markedly abnormal, with creatine kinase MB iso-enzyme (CKMB) level of 28.4 mg/L and a troponin I level of 24.6 mg/L. Physical examination revealed patient to be tachypnoeic. He was normotensive and was not in cardiogenic shock. There was no peripheral clubbing of the fingers and the jugular venous pulse was not elevated. Cardiac auscultation was unremarkable with dual heart sounds and no murmurs,
© 2015 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier Inc. All rights reserved.
Please cite this article in press as: Lin W, et al. Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction: Case Report of an Unusual Complication and Review of Treatment Strategies. Heart, Lung and Circulation (2015), http://dx.doi.org/10.1016/j.hlc.2015.04.175
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Figure 1 ECG at presentation showing Q waves, ST-segment elevation and T wave inversion in the inferior leads.
lung fields were clear with no rales heard. However, the patient was severely hypoxic with oxygen saturation of 80% on room air and 91% on 100% non-breathing mask. A computed tomographic scan of the pulmonary vasculature was performed in the emergency department, which did not reveal pulmonary embolism. There was also no pulmonary oedema seen. He was thus referred for emergency coronary angiogram with a view for primary angioplasty. Coronary angiogram revealed thrombotic occlusion of proximal right coronary artery, with TIMI grade 0 flow (Figure 2a). There was also incidental minor left anterior
descending artery disease which was not haemodynamically significant. The culprit lesion was intervened with thrombus aspiration and subsequent stent implantation, with restoration of TIMI 3 flow (Figure 2b). The patient was transferred to the coronary care unit but was noted to be persistently hypoxaemic with no improvement after angioplasty. In view of persistent hypoxia, transthoracic echocardiogram was performed immediately after angioplasty showing severely depressed left ventricular ejection fraction of 15%. TAPSE was measured to be 10 mm and tissue Doppler systolic velocity was 7.1 cm/s, indicating significant RV
Figure 2 (a) Left anterior oblique (LAO) view of the right coronary artery showing proximal occlusion. (b) Left anterior oblique (LAO) view of the right coronary artery post intervention showing TIMI grade 3 flow in the whole artery. Please cite this article in press as: Lin W, et al. Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction: Case Report of an Unusual Complication and Review of Treatment Strategies. Heart, Lung and Circulation (2015), http://dx.doi.org/10.1016/j.hlc.2015.04.175
HLC 1869 No. of Pages 5 Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction
Figure 3 Apical 4-chamber view on transthoracic echo post venous agitated saline injection showing bubble contrast in the left atrium (LA) and left ventricle (LV) through the PFO. (RA = right atrium, RV = right ventricle).
dysfunction. A patent foramen ovale (PFO) was seen with a right-to-left shunt demonstrated with intravenous agitated saline contrast injection (Figure 3). Pulmonary flow to systemic flow ratio (Qp/Qs) was calculated on echocardiogram to be 0.70, confirming the presence of a net right-to-left shunt. The patient had a known history of previous inferior myocardial infarction nine years prior to presentation, requiring angioplasty to the right coronary artery distal to the right ventricular branches. Echocardiogram following the myocardial infarction showed left ventricular ejection fraction of 45% with akinesia of the inferior and inferolateral walls of the left ventricle. However, RV systolic function was preserved, as evidenced by tricuspid annular plane systolic excursion (TAPSE) of 23 mm and RV tissue Doppler systolic velocity of 11.6 cm/s. No intra-cardiac shunt was seen then. A myocardial perfusion scan was also performed post infarction, which showed large fixed defects in the inferior and inferolateral walls of the left ventricle with no residual ischaemia. Left ventricular ejection fraction was estimated to be 41% on the myocardial perfusion scan. The patient was subsequently stable for nine years on medical therapy. Despite medical therapy with diuretics and supplemental oxygen, there was no improvement in the oxygen saturation of the patient three days after the coronary angioplasty. The decision was made for a right heart catheterisation with a view for device closure of the PFO. Right heart study performed on day 4 of admission showed the following haemodynamic parameters: mean right atrial pressure 25 mmHg, RV end diastolic pressure 24 mmHg and mean left atrial pressure 21 mmHg. The PFO was sized with #25 Amplatzer sizing balloon and was noted on fluoroscopy to be 7 mm. The decision was made to close the defect with a 9 mm Amplatzer
3
Figure 4 Antero-posterior (AP) radiographic view of the heart showing the deployed Amplatzer occluder in-situ (white arrow).
septal occluder rather than a PFO occluder due to a wide PFO gap. Transoesophageal echocardiogram confirmed the final position of the Amplatzer occluder capturing all rims (Figure 4). Post-procedural agitated saline injection showed minimal communication through the defect (Figure 5) and the patient showed a dramatic improvement in his oxygen saturation to 95% on room air. Calculated Qp/Qs on echocardiogram after device closure of the PFO was 1.05. Patient was discharged stable two days post device closure of PFO. Subsequent echocardiogram done two months post MI, showed marginal improvement of left ventricular ejection fraction to 20% as well as moderate RV systolic
Figure 5 Transoesophageal echocardiogram showing Amplatzer device in-situ (white arrow) and minimal bubble contrast in the left atrium (LA) and left ventricle (LV). (RA = right atrium, RV = right ventricle).
Please cite this article in press as: Lin W, et al. Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction: Case Report of an Unusual Complication and Review of Treatment Strategies. Heart, Lung and Circulation (2015), http://dx.doi.org/10.1016/j.hlc.2015.04.175
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dysfunction. The PFO closure device remained well-seated with no residual shunt.
Discussion RV infarction is not an uncommon complication of left ventricular (LV) infarction. In a previous necropsy study, RV infarction was seen in 14% of all patients with transmural MI. However, looking at the subgroup of patients with inferiorposterior infarction, up to 50% had RV infarction [1]. In a separate study, 54% of patients with inferior MI had RV involvement defined as ST-segment elevations in the right chest lead V4R. These patients had a two-fold increase in major complications and a five-fold increase in in-hospital mortality [2]. It is thus clear that RV dysfunction following MI has major clinical implications. The foramen ovale, a remnant of the foetal circulation, remains patent in adulthood in approximately 25% of the general population [3]. The patent foramen ovale (PFO) allows intermittent inter-atrial right-to-left shunting during periods when right atrial pressure exceeds left atrial pressure, such as during a Valsalva manoeuver [4]. Patients with incidental PFOs do not need any intervention unless they present with a cryptogenic stroke, following which a device occlusion of the PFO may be beneficial in preventing recurrent neurological events [5]. In the scenario that a patient with previously dormant and undiagnosed PFO suffers an extensive RV infarction, acute decrease in RV compliance leads to the elevation of the right ventricular end diastolic pressure. This in turn causes the elevation of the right atrial pressure. If the right atrial pressure exceeds that of the left atrial pressure, a right-to-left inter-atrial shunt can develop. This intra-cardiac shunting manifests clinically as cyanosis and refractory hypoxaemia not responsive to oxygen supplementation. Other common causes of hypoxaemia post MI should also be considered. They include 1) Congestive cardiac failure 2) Underlying pulmonary disease 3) Pulmonary embolism A previous review of the case reports of acute right-to-left shunt through a PFO following RV infarct revealed that the diagnosis of pulmonary embolism was entertained and investigated in nine of the 10 cases reported [6]. All nine patients underwent a lung perfusion scan, which was positive in one of the patients, who was subsequently diagnosed to have a concomitant segmental pulmonary embolism [7]. Our patient was unique due to the presence of underlying cardiomyopathy which is most likely non-ischaemic as the left ventricular ejection fraction was disproportionately low for an inferior myocardial infarction. Despite the poor left ventricular ejection fraction of 15% at presentation, there were no clinical signs of congestive heart failure. A chest radiograph done at presentation did not show pulmonary plethora. Prior to his coronary angioplasty, the patient also
underwent a computed tomographic scan of the thorax and pulmonary arteries. The scan showed mild traction bronchiectasis of the right lung base with bilateral atelectasis, unable to account for the severe hypoxaemia. There was no pulmonary embolism. The hypoxaemia also did not improve with diuretic therapy. In view of this negative pulmonary scan in our patient, an intra-cardiac shunt had to be ruled out. He thus underwent a transthoracic echocardiogram immediately after the revascularisation procedure, with an agitated saline bubble contrast study, which clinched the diagnosis of a right-to-left shunt through the PFO resulting in acute refractory hypoxaemia. Bubble contrast transthoracic echocardiogram is the first choice modality for the diagnosis of an acute right-to-left shunt through a PFO after RV infarction. Of the 10 cases reviewed previously, eight patients underwent initial transthoracic echocardiogram for the diagnosis of the shunt. Six out of the eight patients were able to demonstrate a positive bubble study on transthoracic echocardiogram. The other two patients, who had negative bubble studies despite repeated attempts, went on to receive transoesophageal echocardiograms and were able to demonstrate positive bubble studies [6]. Following diagnosis of the acute intra-cardiac shunt, management strategies depend largely on the progress of the patient after revascularisation. Following culprit artery revascularisation, the impaired myocardial function of the RV is expected to improve. A previous radionuclide study of 11 patients with depressed RV ejection fraction post inferior MI, showed return of normal RV ejection fraction by day 3 in 10 of the 11 patients [8]. With improvement of RV function, there will be a corresponding decrease in RV end diastolic pressure and thus right atrial pressure. Continuous shunting through the PFO would then cease. However in our patient, despite watchful waiting and medical therapy, he continued to have refractory hypoxaemia four days after revascularisation. The decision for permanent closure of the PFO was thus made, to avoid the deleterious effects of prolonged hypoxaemia. A review of the existing literature revealed various strategies for the management of the acute right-to-left shunt. They can be broadly classified under temporising measures and permanent PFO closure. In patients who did not receive permanent PFO closure, a few temporising strategies can be utilised while awaiting recovery of RV function. Supportive measures after culprit vessel revascularisation, including non-invasive ventilation, was successful in one patient reported [9]. Use of inhale nitric oxide, a pulmonary vasodilator, resulted in improved haemodynamics and systemic oxygen saturation for a patient who failed device closure of the PFO [10]. Temporary percutaneous balloon occlusion of the PFO however, had mixed results. Seven cases of temporary balloon occlusion were reported, with four in-hospital mortalities [6,11]. Permanent closure of the PFO could either be achieved percutaneously or through surgical repair [12]. The
Please cite this article in press as: Lin W, et al. Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction: Case Report of an Unusual Complication and Review of Treatment Strategies. Heart, Lung and Circulation (2015), http://dx.doi.org/10.1016/j.hlc.2015.04.175
HLC 1869 No. of Pages 5 Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction
Amplatzer occlude device is an efficacious tool for percutaneous PFO closure [13]. Its use in PFO closure post RV infarction has been reported once previously, with a favourable outcome for the patient [14]. There is currently no consensus with regards to the timing of PFO closure in such a scenario. Early PFO closure can improve systemic oxygenation, thus avoiding the deleterious effect of hypoxaemia on the myocardium post infarction. However, given that RV function will very likely improve a few days after successful revascularisation, an initial conservative approach can also be adopted, with only patients who have persistent right-to-left shunts and refractory hypoxaemia undergoing permanent PFO closure. For our patient, the decision for permanent PFO closure was made as he remained severely hypoxaemic after three days of supportive therapy which included diuretic therapy. Despite the presence of severe left ventricular systolic dysfunction after his second myocardial infarction, the patient underwent an uneventful PFO closure with a 9 mm Amplatzer occluder with normalisation of his Qp/Qs from 0.70 to 1.05 as seen on serial echocardiographic examinations. This change in Qp/Qs was accompanied by dramatic improvement of oxygen saturation and near resolution of symptoms of dypsnoea. He remains well with good functional recovery more than one year after his revascularisation and PFO closure.
Conclusion Acute right-to-left shunting through a previously dormant PFO following RV infarction is an uncommon and underrecognised clinical entity. As with all cases of acute myocardial infarctions, revascularisation of the culprit vessel is of paramount importance. Regarding PFO closure in such a scenario, there is currently no consensus. After excluding all other possible causes of hypoxaemia, including congestive cardiac failure in a patient with significant left ventricular dysfunction, an initial supportive therapy while awaiting RV recovery is a viable treatment strategy. Should the patient remain in refractory hypoxaemia, a permanent PFO closure using percutaneous strategies, for example with an Amplazter occluder device, can be the treatment of choice.
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Authors’ Disclosures None
References [1] Isner JM, Roberts WC. Right ventricular infarction complicating left ventricular infarction secondary to coronary artery disease: frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction. Am J Cardiol 1978;42:885–94. [2] Zehender M, Kasper W, Kauder E, Scho¨nthaler M, Geibel A, Olschewski M, et al. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 1993;328:981–8. [3] Wahl A, Windecker S, Meier B. Patent foramen ovale: pathophysiology and therapeutic options in symptomatic patients. Minerva Cardioangiol 2001;49:403–11. [4] Clarke NR, Timperley J, Kelion AD, Banning AP. Transthoracic echocardiography using second harmonic imaging with Valsalva manoeuvre for the detection of right to left shunts. Eur J Echocardiogr 2004;5:176–81. [5] Khan AR, Bin Abdulhak AA, Sheikh MA. Device closure of patent foramen ovale versus medical therapy in cryptogenic stroke: a systematic review and meta-analysis. JACC Cardiovasc Interv 2013;6:1316–23. [6] Silver MT, Lieberman EH, Thibault GE. Refractory hypoxaemia in inferior myocardial infarction from right-to-left shunting through a patent foramen ovale: a case report and review of the literature. Clin Cardiol 1994;17:627–30. [7] Gudipati CV, Nagelhout DA, Serota H, Deligonul U, Labovitz AJ, Kern MJ. Transesophageal echocardiographic guidance for balloon catheter occlusion of patent foramen ovale complicating right ventricular infarction. Am Heart J 1991;121:919–22. [8] Steele P, Kirch D, Ellis J, Vogel R, Battock D. Prompt return to normal of depressed right ventricular ejection fraction in acute inferior infarction. Br Heart J 1977;39:1319–23. [9] Hamid N, Keng F. Refractory hypoxia in right ventricular infarction. Ann Acad Med Singapore 2011;40:325–6. [10] Fessler MB, Lepore JJ, Thompson BT, Semigran MJ. Right-to-left shunting through a patent foramen ovale in right ventricular infarction: improvement of hypoxemia and hemodynamics with inhaled nitric oxide. J Clin Anesth 2003;15:371–4. [11] Matsuo R, Nakamura T, Matsui H, Ono N. Treatment of refractory hypoxemia due to right-to-left interatrial shunt complicating right ventricular infarction: successful short-term percutaneous catheter closure of the patent foramen ovale. J Cardiol 1995;26:243–8. [12] Laham RJ, Ho KK, Douglas PS, Faherty CE, Lock JE, Baim DS, et al. Right ventricular infarction complicated by acute right-to-left shunting. Am J Cardiol 1994;74:824–6. [13] Thaman R, Faganello G, Gimeno JR, Szantho GV, Nelson M, Curtis S, et al. Efficacy of percutaneous closure of patent foramen ovale: comparison among three commonly used occluders. Heart 2011;97:394–9. [14] Bassi S, Amersey R, Andrews R. Right ventricular infarction complicated by right to left shunting through an atrial septal defect: successful treatment with an Amplatzer septal occluder. Heart 2005;91:e28.
Please cite this article in press as: Lin W, et al. Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction: Case Report of an Unusual Complication and Review of Treatment Strategies. Heart, Lung and Circulation (2015), http://dx.doi.org/10.1016/j.hlc.2015.04.175
CLINICAL SPOTLIGHT
Heart, Lung and Circulation (2015) xx, 1–5 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2015.04.175
Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction: Case Report of an Unusual Complication and Review of Treatment Strategies Weiqin Lin, James Wei Luen Yip, Tiong Cheng Yeo Cardiac Department, National University Heart Centre, Singapore; National University Health System Received 1 February 2015; received in revised form 13 April 2015; accepted 17 April 2015; online published-ahead-of-print xxx
Right ventricular (RV) infarction is not an uncommon complication of acute left ventricular infarction. It has been established that RV dysfunction post myocardial infarction (MI) is associated with increased mortality and morbidity. When RV infarction occurs in a patient with previously dormant patent foramen ovale (PFO), an unusual presentation of persistent refractory hypoxaemia ensues. We present a case of new RV infarction in a patient with underlying ischaemic cardiomyopathy, which was complicated by acute rightto-left shunting through the PFO. He was treated with percutaneous coronary intervention (PCI) and subsequent percutaneous PFO closure. We will also review the existing literature with regards to diagnostic and management strategies for patients with this unusual sequelae of MI. Keywords
Acute myocardial infarction Patent foramen ovale Intra-cardiac shunt PFO closure
Introduction
Case Presentation
Right ventricular (RV) infarction occurs with acute occlusion of the right coronary artery proximal to the right ventricular branches. This can result in RV systolic dysfunction. In patients with a patent foramen ovale (PFO), the acute RV systolic failure and resultant elevation in right heart pressures can result in a right-to-left shunt through the PFO. This will manifest clinically as refractory hypoxaemia. In the event of refractory hypoxaemia despite optimal medical therapy, patients should be considered for obliteration of the PFO. We present a case of new RV infarction in a patient with underlying ischaemic cardiomyopathy, which was complicated by acute right-to-left shunting through the PFO. He was treated with percutaneous coronary intervention (PCI) and subsequent percutaneous PFO closure.
A 47 year-old male with hypertension, hyperlipidaemia and a remote history of ischaemic heart disease, presented to the emergency room with three-day history of chest pain and dyspnoea. Electrocardiogram at presentation showed sinus rhythm. Deep Q waves in the inferior leads with associated ST-segment elevation and T wave inversions were seen (Figure 1). Cardiac biomarkers done at presentation were markedly abnormal, with creatine kinase MB iso-enzyme (CKMB) level of 28.4 mg/L and a troponin I level of 24.6 mg/L. Physical examination revealed patient to be tachypnoeic. He was normotensive and was not in cardiogenic shock. There was no peripheral clubbing of the fingers and the jugular venous pulse was not elevated. Cardiac auscultation was unremarkable with dual heart sounds and no murmurs,
© 2015 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier Inc. All rights reserved.
Please cite this article in press as: Lin W, et al. Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction: Case Report of an Unusual Complication and Review of Treatment Strategies. Heart, Lung and Circulation (2015), http://dx.doi.org/10.1016/j.hlc.2015.04.175
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Figure 1 ECG at presentation showing Q waves, ST-segment elevation and T wave inversion in the inferior leads.
lung fields were clear with no rales heard. However, the patient was severely hypoxic with oxygen saturation of 80% on room air and 91% on 100% non-breathing mask. A computed tomographic scan of the pulmonary vasculature was performed in the emergency department, which did not reveal pulmonary embolism. There was also no pulmonary oedema seen. He was thus referred for emergency coronary angiogram with a view for primary angioplasty. Coronary angiogram revealed thrombotic occlusion of proximal right coronary artery, with TIMI grade 0 flow (Figure 2a). There was also incidental minor left anterior
descending artery disease which was not haemodynamically significant. The culprit lesion was intervened with thrombus aspiration and subsequent stent implantation, with restoration of TIMI 3 flow (Figure 2b). The patient was transferred to the coronary care unit but was noted to be persistently hypoxaemic with no improvement after angioplasty. In view of persistent hypoxia, transthoracic echocardiogram was performed immediately after angioplasty showing severely depressed left ventricular ejection fraction of 15%. TAPSE was measured to be 10 mm and tissue Doppler systolic velocity was 7.1 cm/s, indicating significant RV
Figure 2 (a) Left anterior oblique (LAO) view of the right coronary artery showing proximal occlusion. (b) Left anterior oblique (LAO) view of the right coronary artery post intervention showing TIMI grade 3 flow in the whole artery. Please cite this article in press as: Lin W, et al. Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction: Case Report of an Unusual Complication and Review of Treatment Strategies. Heart, Lung and Circulation (2015), http://dx.doi.org/10.1016/j.hlc.2015.04.175
HLC 1869 No. of Pages 5 Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction
Figure 3 Apical 4-chamber view on transthoracic echo post venous agitated saline injection showing bubble contrast in the left atrium (LA) and left ventricle (LV) through the PFO. (RA = right atrium, RV = right ventricle).
dysfunction. A patent foramen ovale (PFO) was seen with a right-to-left shunt demonstrated with intravenous agitated saline contrast injection (Figure 3). Pulmonary flow to systemic flow ratio (Qp/Qs) was calculated on echocardiogram to be 0.70, confirming the presence of a net right-to-left shunt. The patient had a known history of previous inferior myocardial infarction nine years prior to presentation, requiring angioplasty to the right coronary artery distal to the right ventricular branches. Echocardiogram following the myocardial infarction showed left ventricular ejection fraction of 45% with akinesia of the inferior and inferolateral walls of the left ventricle. However, RV systolic function was preserved, as evidenced by tricuspid annular plane systolic excursion (TAPSE) of 23 mm and RV tissue Doppler systolic velocity of 11.6 cm/s. No intra-cardiac shunt was seen then. A myocardial perfusion scan was also performed post infarction, which showed large fixed defects in the inferior and inferolateral walls of the left ventricle with no residual ischaemia. Left ventricular ejection fraction was estimated to be 41% on the myocardial perfusion scan. The patient was subsequently stable for nine years on medical therapy. Despite medical therapy with diuretics and supplemental oxygen, there was no improvement in the oxygen saturation of the patient three days after the coronary angioplasty. The decision was made for a right heart catheterisation with a view for device closure of the PFO. Right heart study performed on day 4 of admission showed the following haemodynamic parameters: mean right atrial pressure 25 mmHg, RV end diastolic pressure 24 mmHg and mean left atrial pressure 21 mmHg. The PFO was sized with #25 Amplatzer sizing balloon and was noted on fluoroscopy to be 7 mm. The decision was made to close the defect with a 9 mm Amplatzer
3
Figure 4 Antero-posterior (AP) radiographic view of the heart showing the deployed Amplatzer occluder in-situ (white arrow).
septal occluder rather than a PFO occluder due to a wide PFO gap. Transoesophageal echocardiogram confirmed the final position of the Amplatzer occluder capturing all rims (Figure 4). Post-procedural agitated saline injection showed minimal communication through the defect (Figure 5) and the patient showed a dramatic improvement in his oxygen saturation to 95% on room air. Calculated Qp/Qs on echocardiogram after device closure of the PFO was 1.05. Patient was discharged stable two days post device closure of PFO. Subsequent echocardiogram done two months post MI, showed marginal improvement of left ventricular ejection fraction to 20% as well as moderate RV systolic
Figure 5 Transoesophageal echocardiogram showing Amplatzer device in-situ (white arrow) and minimal bubble contrast in the left atrium (LA) and left ventricle (LV). (RA = right atrium, RV = right ventricle).
Please cite this article in press as: Lin W, et al. Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction: Case Report of an Unusual Complication and Review of Treatment Strategies. Heart, Lung and Circulation (2015), http://dx.doi.org/10.1016/j.hlc.2015.04.175
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dysfunction. The PFO closure device remained well-seated with no residual shunt.
Discussion RV infarction is not an uncommon complication of left ventricular (LV) infarction. In a previous necropsy study, RV infarction was seen in 14% of all patients with transmural MI. However, looking at the subgroup of patients with inferiorposterior infarction, up to 50% had RV infarction [1]. In a separate study, 54% of patients with inferior MI had RV involvement defined as ST-segment elevations in the right chest lead V4R. These patients had a two-fold increase in major complications and a five-fold increase in in-hospital mortality [2]. It is thus clear that RV dysfunction following MI has major clinical implications. The foramen ovale, a remnant of the foetal circulation, remains patent in adulthood in approximately 25% of the general population [3]. The patent foramen ovale (PFO) allows intermittent inter-atrial right-to-left shunting during periods when right atrial pressure exceeds left atrial pressure, such as during a Valsalva manoeuver [4]. Patients with incidental PFOs do not need any intervention unless they present with a cryptogenic stroke, following which a device occlusion of the PFO may be beneficial in preventing recurrent neurological events [5]. In the scenario that a patient with previously dormant and undiagnosed PFO suffers an extensive RV infarction, acute decrease in RV compliance leads to the elevation of the right ventricular end diastolic pressure. This in turn causes the elevation of the right atrial pressure. If the right atrial pressure exceeds that of the left atrial pressure, a right-to-left inter-atrial shunt can develop. This intra-cardiac shunting manifests clinically as cyanosis and refractory hypoxaemia not responsive to oxygen supplementation. Other common causes of hypoxaemia post MI should also be considered. They include 1) Congestive cardiac failure 2) Underlying pulmonary disease 3) Pulmonary embolism A previous review of the case reports of acute right-to-left shunt through a PFO following RV infarct revealed that the diagnosis of pulmonary embolism was entertained and investigated in nine of the 10 cases reported [6]. All nine patients underwent a lung perfusion scan, which was positive in one of the patients, who was subsequently diagnosed to have a concomitant segmental pulmonary embolism [7]. Our patient was unique due to the presence of underlying cardiomyopathy which is most likely non-ischaemic as the left ventricular ejection fraction was disproportionately low for an inferior myocardial infarction. Despite the poor left ventricular ejection fraction of 15% at presentation, there were no clinical signs of congestive heart failure. A chest radiograph done at presentation did not show pulmonary plethora. Prior to his coronary angioplasty, the patient also
underwent a computed tomographic scan of the thorax and pulmonary arteries. The scan showed mild traction bronchiectasis of the right lung base with bilateral atelectasis, unable to account for the severe hypoxaemia. There was no pulmonary embolism. The hypoxaemia also did not improve with diuretic therapy. In view of this negative pulmonary scan in our patient, an intra-cardiac shunt had to be ruled out. He thus underwent a transthoracic echocardiogram immediately after the revascularisation procedure, with an agitated saline bubble contrast study, which clinched the diagnosis of a right-to-left shunt through the PFO resulting in acute refractory hypoxaemia. Bubble contrast transthoracic echocardiogram is the first choice modality for the diagnosis of an acute right-to-left shunt through a PFO after RV infarction. Of the 10 cases reviewed previously, eight patients underwent initial transthoracic echocardiogram for the diagnosis of the shunt. Six out of the eight patients were able to demonstrate a positive bubble study on transthoracic echocardiogram. The other two patients, who had negative bubble studies despite repeated attempts, went on to receive transoesophageal echocardiograms and were able to demonstrate positive bubble studies [6]. Following diagnosis of the acute intra-cardiac shunt, management strategies depend largely on the progress of the patient after revascularisation. Following culprit artery revascularisation, the impaired myocardial function of the RV is expected to improve. A previous radionuclide study of 11 patients with depressed RV ejection fraction post inferior MI, showed return of normal RV ejection fraction by day 3 in 10 of the 11 patients [8]. With improvement of RV function, there will be a corresponding decrease in RV end diastolic pressure and thus right atrial pressure. Continuous shunting through the PFO would then cease. However in our patient, despite watchful waiting and medical therapy, he continued to have refractory hypoxaemia four days after revascularisation. The decision for permanent closure of the PFO was thus made, to avoid the deleterious effects of prolonged hypoxaemia. A review of the existing literature revealed various strategies for the management of the acute right-to-left shunt. They can be broadly classified under temporising measures and permanent PFO closure. In patients who did not receive permanent PFO closure, a few temporising strategies can be utilised while awaiting recovery of RV function. Supportive measures after culprit vessel revascularisation, including non-invasive ventilation, was successful in one patient reported [9]. Use of inhale nitric oxide, a pulmonary vasodilator, resulted in improved haemodynamics and systemic oxygen saturation for a patient who failed device closure of the PFO [10]. Temporary percutaneous balloon occlusion of the PFO however, had mixed results. Seven cases of temporary balloon occlusion were reported, with four in-hospital mortalities [6,11]. Permanent closure of the PFO could either be achieved percutaneously or through surgical repair [12]. The
Please cite this article in press as: Lin W, et al. Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction: Case Report of an Unusual Complication and Review of Treatment Strategies. Heart, Lung and Circulation (2015), http://dx.doi.org/10.1016/j.hlc.2015.04.175
HLC 1869 No. of Pages 5 Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction
Amplatzer occlude device is an efficacious tool for percutaneous PFO closure [13]. Its use in PFO closure post RV infarction has been reported once previously, with a favourable outcome for the patient [14]. There is currently no consensus with regards to the timing of PFO closure in such a scenario. Early PFO closure can improve systemic oxygenation, thus avoiding the deleterious effect of hypoxaemia on the myocardium post infarction. However, given that RV function will very likely improve a few days after successful revascularisation, an initial conservative approach can also be adopted, with only patients who have persistent right-to-left shunts and refractory hypoxaemia undergoing permanent PFO closure. For our patient, the decision for permanent PFO closure was made as he remained severely hypoxaemic after three days of supportive therapy which included diuretic therapy. Despite the presence of severe left ventricular systolic dysfunction after his second myocardial infarction, the patient underwent an uneventful PFO closure with a 9 mm Amplatzer occluder with normalisation of his Qp/Qs from 0.70 to 1.05 as seen on serial echocardiographic examinations. This change in Qp/Qs was accompanied by dramatic improvement of oxygen saturation and near resolution of symptoms of dypsnoea. He remains well with good functional recovery more than one year after his revascularisation and PFO closure.
Conclusion Acute right-to-left shunting through a previously dormant PFO following RV infarction is an uncommon and underrecognised clinical entity. As with all cases of acute myocardial infarctions, revascularisation of the culprit vessel is of paramount importance. Regarding PFO closure in such a scenario, there is currently no consensus. After excluding all other possible causes of hypoxaemia, including congestive cardiac failure in a patient with significant left ventricular dysfunction, an initial supportive therapy while awaiting RV recovery is a viable treatment strategy. Should the patient remain in refractory hypoxaemia, a permanent PFO closure using percutaneous strategies, for example with an Amplazter occluder device, can be the treatment of choice.
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Authors’ Disclosures None
References [1] Isner JM, Roberts WC. Right ventricular infarction complicating left ventricular infarction secondary to coronary artery disease: frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction. Am J Cardiol 1978;42:885–94. [2] Zehender M, Kasper W, Kauder E, Scho¨nthaler M, Geibel A, Olschewski M, et al. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 1993;328:981–8. [3] Wahl A, Windecker S, Meier B. Patent foramen ovale: pathophysiology and therapeutic options in symptomatic patients. Minerva Cardioangiol 2001;49:403–11. [4] Clarke NR, Timperley J, Kelion AD, Banning AP. Transthoracic echocardiography using second harmonic imaging with Valsalva manoeuvre for the detection of right to left shunts. Eur J Echocardiogr 2004;5:176–81. [5] Khan AR, Bin Abdulhak AA, Sheikh MA. Device closure of patent foramen ovale versus medical therapy in cryptogenic stroke: a systematic review and meta-analysis. JACC Cardiovasc Interv 2013;6:1316–23. [6] Silver MT, Lieberman EH, Thibault GE. Refractory hypoxaemia in inferior myocardial infarction from right-to-left shunting through a patent foramen ovale: a case report and review of the literature. Clin Cardiol 1994;17:627–30. [7] Gudipati CV, Nagelhout DA, Serota H, Deligonul U, Labovitz AJ, Kern MJ. Transesophageal echocardiographic guidance for balloon catheter occlusion of patent foramen ovale complicating right ventricular infarction. Am Heart J 1991;121:919–22. [8] Steele P, Kirch D, Ellis J, Vogel R, Battock D. Prompt return to normal of depressed right ventricular ejection fraction in acute inferior infarction. Br Heart J 1977;39:1319–23. [9] Hamid N, Keng F. Refractory hypoxia in right ventricular infarction. Ann Acad Med Singapore 2011;40:325–6. [10] Fessler MB, Lepore JJ, Thompson BT, Semigran MJ. Right-to-left shunting through a patent foramen ovale in right ventricular infarction: improvement of hypoxemia and hemodynamics with inhaled nitric oxide. J Clin Anesth 2003;15:371–4. [11] Matsuo R, Nakamura T, Matsui H, Ono N. Treatment of refractory hypoxemia due to right-to-left interatrial shunt complicating right ventricular infarction: successful short-term percutaneous catheter closure of the patent foramen ovale. J Cardiol 1995;26:243–8. [12] Laham RJ, Ho KK, Douglas PS, Faherty CE, Lock JE, Baim DS, et al. Right ventricular infarction complicated by acute right-to-left shunting. Am J Cardiol 1994;74:824–6. [13] Thaman R, Faganello G, Gimeno JR, Szantho GV, Nelson M, Curtis S, et al. Efficacy of percutaneous closure of patent foramen ovale: comparison among three commonly used occluders. Heart 2011;97:394–9. [14] Bassi S, Amersey R, Andrews R. Right ventricular infarction complicated by right to left shunting through an atrial septal defect: successful treatment with an Amplatzer septal occluder. Heart 2005;91:e28.
Please cite this article in press as: Lin W, et al. Refractory Hypoxaemia following Inferior ST-Segment Elevation Myocardial Infarction: Case Report of an Unusual Complication and Review of Treatment Strategies. Heart, Lung and Circulation (2015), http://dx.doi.org/10.1016/j.hlc.2015.04.175
