Coronary Embolic Phenomena: High-Impact, Low-Frequency Events

*Qasim Malik, Ambreen Alam, Stanislaw P. Stawicki and Peter Puleo*

### **Abstract**

Coronary embolic phenomena (CEP) are difficult to diagnose yet carry potentially devastating clinical consequences. The goal of this chapter is to outline key processes and pathophysiologic mechanisms underlying CEP, primarily in the context of acute coronary syndrome (ACS). Not surprisingly, most reported cases of CEP occur in the left coronary circulation, but some right-sided events have been reported. Overall, causes include thrombotic, septic/infectious, neoplastic, valverelated, and iatrogenic mechanisms such as air embolization. Coronary angiography remains the definitive diagnostic and therapeutic approach, with computed tomography being increasingly utilized. Transthoracic echocardiography (TTE) should be part of a routine work up for patients with suspected CEP. Holter/event monitoring for atrial fibrillation may also be indicated in patients with embolic phenomena. Clinical management includes procedural restoration of coronary blood flow, followed by appropriate anticoagulation or antiplatelet therapy, in conjunction with appropriate treatment of any arrhythmias or other associated cardiac manifestations or conditions. Timely diagnosis, based on a high index of suspicion (especially in high-risk population) may be important in improving morbidity and mortality in affected patients. Since CEPs are often underdiagnosed and may be due to a number of heterogeneous causes, the need arises for increasing provider awareness of these important phenomena, as well as for the implementation of appropriate clinical management guidelines.

**Keywords:** coronary artery embolism, coronary embolic phenomena, diagnosis, management, risk factors

### **1. Introduction**

Coronary embolic phenomena (CEP) constitute an under-reported and underdiagnosed set of clinical phenomena, with potentially devastating consequences if not recognized and treated promptly [1–3]. From coronary air embolism to paradoxical venous thromboembolism, CEPs represent an etiologically heterogeneous group of events [4–7]. It has been postulated that CEPs are the underlying cause of up to 3% of acute coronary syndromes (ACS) [6]. Given their rarity, CEPs require a high index of suspicion by the treating clinician [8–10]. In this chapter, we will aim to cover the various processes and pathophysiology underlying this cause of acute coronary

syndrome. Our focus will be on the more commonly seen forms of coronary embolism, with an abbreviated overview provided of the less common etiologies.

### **2. Methods**

A thorough literature search was conducted using PubMed, Google™ Scholar, and Bioline International. The following search terms were utilized, in various combinations/derivations/iterations, listed alphabetically: "cardiac," "coronary," "emboli," "embolism," "embolus," "heart," "infarction," "myocardial," "myocardium," "paradoxical," "phenomenon," "vascular," "vasculature," and "vessel". Secondary identification of additional literature sources was performed using articles referenced by our primary sources.

### **3. Classification**

Coronary emboli may be classified based on etiology (i.e., thrombotic, septic, neoplastic, valvular heart disease-related, iatrogenic), although other classifications (i.e., direct, paradoxical and/or iatrogenic) have been proposed and/or described [6, 11–13]. A list of all previously reported types/causes of coronary emboli is provided in **Table 1**.


#### **Table 1.**

*Causes of coronary embolism.*

### **4. Mechanisms and pathophysiology**

Coronary emboli may originate in the left or right side of the heart [14, 15]. Of course, for emboli originating in the right heart to lodge in the coronary arteries, they would need to be somehow "shunted" to the left-sided system, possibly

**43**

**Figure 1.**

*Coronary Embolic Phenomena: High-Impact, Low-Frequency Events*

through a patent foramen ovale [16–18]. An angiographic example of paradoxical

*Angiographic example of a large coronary artery embolus located in the mid-left anterior descending artery. Source: Zhang et al. [19]. Image used under the terms of the Creative Commons Attribution 4.0 License (http:// www.creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access* 

**5. Coronary embolic events: a heterogeneous pathologic grouping**

Due to various mechanisms being responsible for coronary embolic phenomena leading to acute coronary syndromes, we will address them one by one in the

It must be mentioned here that systemic emboli finding their way to the left heart are still more likely to embolize to the carotid or intracranial vasculature, primarily due to two particular considerations. Firstly, the coronary anatomy and coronary artery takeoff is typically such that emboli are less likely to specifically dislodge and enter into their ostia [13, 20, 21]. Secondly, it is hypothesized that coronary vessels may be protected to some degree, mainly due to them receiving flow primarily during diastole [22–26]. For similar reasons, one might extrapolate that most reported cases of coronary embolism occur in the left coronary circulation due to the anatomy of the right coronary artery takeoff making it potentially less conducive to emboli [22–28]. Coronary emboli may become lodged in major epicardial arteries supplying a sizable area of myocardium, and smaller emboli may even embolize distally so as to affect small arterioles which do not supply a large area [29–31]. These events may or may not be clinically symptomatic or readily diagnosable, but evidence in this generally poorly understood area of cardiac pathophysiology continues to be lacking. It is important to note, however, that coronary emboli may occur in the setting of concomitant atherosclerosis, where even a small embolus could lodge at the site of atherosclerotic lesion and result in significant epicardial coronary occlusion, thus exposing potentially significant area of myocardium at risk for a subsequent secondary ischemic event [31–35]. An association with infectious etiology may be present as well in this context [32].

coronary artery embolism is show in **Figure 1** [19].

*pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).*

*DOI: http://dx.doi.org/10.5772/intechopen.90685*

*Coronary Embolic Phenomena: High-Impact, Low-Frequency Events DOI: http://dx.doi.org/10.5772/intechopen.90685*

#### **Figure 1.**

*Embolic Diseases - Evolving Diagnostic and Management Approaches*

articles referenced by our primary sources.

Thrombotic Paradoxical thrombus/embolus

Left atrial appendage thrombus

Left ventricular mural thrombus

System lupus erythematosus Antiphospholipid syndrome

Rheumatic heart disease

Mitral valve calcifications

Left atrial thrombus

deficiency)

Blood cysts

Air embolism

Infectious Infective endocarditis

Iatrogenic Post-cardiac procedure

Valve-related Fibroelastoma

Neoplastic Malignancy

Miscellaneous causes Pregnancy

*Causes of coronary embolism.*

**4. Mechanisms and pathophysiology**

**2. Methods**

**3. Classification**

syndrome. Our focus will be on the more commonly seen forms of coronary embolism, with an abbreviated overview provided of the less common etiologies.

A thorough literature search was conducted using PubMed, Google™ Scholar, and Bioline International. The following search terms were utilized, in various combinations/derivations/iterations, listed alphabetically: "cardiac," "coronary," "emboli," "embolism," "embolus," "heart," "infarction," "myocardial," "myocardium," "paradoxical," "phenomenon," "vascular," "vasculature," and "vessel". Secondary identification of additional literature sources was performed using

Coronary emboli may be classified based on etiology (i.e., thrombotic, septic, neoplastic, valvular heart disease-related, iatrogenic), although other classifications (i.e., direct, paradoxical and/or iatrogenic) have been proposed and/or described [6, 11–13]. A list of all previously reported types/causes of coronary emboli is provided in **Table 1**.

Autoimmune Inherited coagulation factor deficiencies (prothrombin deficiency, protein C/S

Coronary emboli may originate in the left or right side of the heart [14, 15]. Of course, for emboli originating in the right heart to lodge in the coronary arteries, they would need to be somehow "shunted" to the left-sided system, possibly

**42**

**Table 1.**

*Angiographic example of a large coronary artery embolus located in the mid-left anterior descending artery. Source: Zhang et al. [19]. Image used under the terms of the Creative Commons Attribution 4.0 License (http:// www.creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).*

through a patent foramen ovale [16–18]. An angiographic example of paradoxical coronary artery embolism is show in **Figure 1** [19].

It must be mentioned here that systemic emboli finding their way to the left heart are still more likely to embolize to the carotid or intracranial vasculature, primarily due to two particular considerations. Firstly, the coronary anatomy and coronary artery takeoff is typically such that emboli are less likely to specifically dislodge and enter into their ostia [13, 20, 21]. Secondly, it is hypothesized that coronary vessels may be protected to some degree, mainly due to them receiving flow primarily during diastole [22–26]. For similar reasons, one might extrapolate that most reported cases of coronary embolism occur in the left coronary circulation due to the anatomy of the right coronary artery takeoff making it potentially less conducive to emboli [22–28].

Coronary emboli may become lodged in major epicardial arteries supplying a sizable area of myocardium, and smaller emboli may even embolize distally so as to affect small arterioles which do not supply a large area [29–31]. These events may or may not be clinically symptomatic or readily diagnosable, but evidence in this generally poorly understood area of cardiac pathophysiology continues to be lacking. It is important to note, however, that coronary emboli may occur in the setting of concomitant atherosclerosis, where even a small embolus could lodge at the site of atherosclerotic lesion and result in significant epicardial coronary occlusion, thus exposing potentially significant area of myocardium at risk for a subsequent secondary ischemic event [31–35]. An association with infectious etiology may be present as well in this context [32].

#### **5. Coronary embolic events: a heterogeneous pathologic grouping**

Due to various mechanisms being responsible for coronary embolic phenomena leading to acute coronary syndromes, we will address them one by one in the subsequent discussion. The authors' goal is not to provide an exhaustive description of each mechanism, but rather to point the reader to other definitive sources for further details.

#### **5.1 Thrombotic causes**

Coronary emboli may be formed due to thromboembolic causes involving different etiologies and pathways (**Table 1**). As with all thromboembolic phenomena, predisposing conditions of the Virchow's triad (hypercoagulability, stasis, endothelial injury) will need to be present for thrombi to form [36, 37].

For venous thromboemboli to "transform" into coronary emboli, the presence of a patent foramen ovale is required [6, 38]. This enables the embolus to cross from "right to left" side of the heart and thus develop the potential to lodge in the coronary circulation [18, 38]. A thrombus may originate in the left atrial appendage, as seen among patients with atrial fibrillation [39, 40], or it may originate in the left atrium/ventricle itself, as in patients with severely reduced ejection fraction or those who have had an anterior/apical myocardial infarction in the past [6, 41]. The former is of particular clinical importance, as patients diagnosed with coronary embolus may benefit from ambulatory monitoring to look for atrial fibrillation as a possible underlying cause.

Arterial emboli are more likely to be reported in the setting of hypercoagulable states including autoimmune diseases, inherited coagulation factor deficiencies, hyperviscosity syndromes, and acquired hypercoagulabe states (e.g., pregnancy, malignancy, previous heparin exposure, **Table 1**) [42–44]. As coronary emboli are a rarely reported phenomenon, no randomized trials or guidelines exist regarding diagnostic workup for these, although it would not be unreasonable to initiate workup for thrombophilia whenever appropriate diagnosis or suspicion exists [37, 42–45].

#### **5.2 Septic/infectious causes**

Infective endocarditis is one of the most dreaded infectious etiologies associated with significant morbidity and mortality [46, 47]. Coronary septic arterial emboli (CSAE) secondary to infectious endocarditis have been reported and according to one source such events may carry a mortality of up to 50% [48]. CSAE appear to be more likely to occur in patients having vegetations of the mitral valve or fungal infections, as fungal vegetations are known to reach larger overall dimensions, thus increasing the cumulative possibility of embolization [49, 50]. Rheumatic heart disease, though more common in low-income countries, is another possible etiology that can be associated with CSAE and must be kept in mind when evaluating patients from high-incidence geographic areas [51, 52].

#### **5.3 Neoplastic causes**

Tumors originating in the heart such as atrial myxomas, or on valves such as papillary fibroelastomas, are well known to cause cryptogenic brain infarctions [14, 53]. There are also reports of embolization to the coronary circulation [54–56]. Given that end-organ damage, including cerebrovascular accidents may constitute the initial clinical presentation of such neoplasms, it would not be unreasonable to propose that an embolic myocardial infarction may occur in this setting [56, 57]. It is also likely that such occurrences are under-recognized and probably more common than generally thought, thus requiring high index of clinical suspicion and prompt diagnosis [56, 57]. The overall urgency is highlighted by the possibility that subsequent presentations in cases of "missed diagnosis" may manifest as unexplained/

**45**

**Figure 2.**

*original work is properly cited.*

*Coronary Embolic Phenomena: High-Impact, Low-Frequency Events*

sudden death [57, 58]. Appropriate high-quality imaging may include but is not limited to transthoracic and/or transesophageal echocardiography [56, 59–61].

mitral and aortic mechanical valve prostheses is shown in **Figure 2** [67].

Ruptured atherosclerotic plaques in the coronary arteries may lead to acute thrombotic occlusions and are the frequent pathophysiologic factor behind acute ST-elevation myocardial infarctions [68, 69]. Vessels affected by such processes may be characterized by a high thrombotic burden. For example, saphenous venous grafts in post-coronary artery bypass graft patients seem particularly vulnerable [70, 71], with various pathophysiologic mechanisms proposed including immune-

Cardiac catheterization procedures may also cause distal embolization of intravascular particles [73]. Depending upon where, and how far, any dislodged thrombi or microthrombi travel, periprocedural myocardial infarction can become a very real risk [74]. Various procedural techniques including specialized "wire filter" protection devices [74, 75] and thrombus extraction catheters [76] can be utilized during coronary interventions to prevent or reduce distal embolization. Finally,

*An example of a left coronary artery coronary embolism associated with subtherapeutic anticoagulation in the setting of mitral and aortic mechanical valve prostheses. [A, left] Note the filling defect present upon initial diagnosis. [B, right] Following thrombectomy, the left coronary artery is seen to be patent. Source: Protasiewicz et al. [67]. Images used under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, which permits all noncommercial use, distribution, and reproduction in any medium, provided the* 

Stenotic heart valves resulting from progressive calcification process also pose the possibility of calcific embolization to distal locations, including the coronary circulation [48, 62, 63]. Rheumatic valvular heart disease could be another possible risk factor for coronary embolization [48]. Long-term valvular heart disease leads to structural changes in the myocardium, eventually increasing the risk of atrial fibrillation, which in itself may be a contributor to both systemic and coronary embolization [39, 64]. Of note, coronary embolism has been reported following aortic and mitral valve replacement, with successful management reported to involve abciximab and urokinase [65]. Another report describes acute myocardial infarction due to coronary embolism in a patient with mitral valve prosthesis. That particular case was successfully managed using angioplasty [66]. An example of a left coronary embolism associated with subtherapeutic oral anticoagulation in a patient with

*DOI: http://dx.doi.org/10.5772/intechopen.90685*

**5.4 Valve-related causes**

**5.5 Iatrogenic causes**

mediated process [71, 72].

sudden death [57, 58]. Appropriate high-quality imaging may include but is not limited to transthoracic and/or transesophageal echocardiography [56, 59–61].

### **5.4 Valve-related causes**

*Embolic Diseases - Evolving Diagnostic and Management Approaches*

lial injury) will need to be present for thrombi to form [36, 37].

further details.

**5.1 Thrombotic causes**

possible underlying cause.

**5.2 Septic/infectious causes**

**5.3 Neoplastic causes**

patients from high-incidence geographic areas [51, 52].

subsequent discussion. The authors' goal is not to provide an exhaustive description of each mechanism, but rather to point the reader to other definitive sources for

Coronary emboli may be formed due to thromboembolic causes involving different etiologies and pathways (**Table 1**). As with all thromboembolic phenomena, predisposing conditions of the Virchow's triad (hypercoagulability, stasis, endothe-

For venous thromboemboli to "transform" into coronary emboli, the presence of a patent foramen ovale is required [6, 38]. This enables the embolus to cross from "right to left" side of the heart and thus develop the potential to lodge in the coronary circulation [18, 38]. A thrombus may originate in the left atrial appendage, as seen among patients with atrial fibrillation [39, 40], or it may originate in the left atrium/ventricle itself, as in patients with severely reduced ejection fraction or those who have had an anterior/apical myocardial infarction in the past [6, 41]. The former is of particular clinical importance, as patients diagnosed with coronary embolus may benefit from ambulatory monitoring to look for atrial fibrillation as a

Arterial emboli are more likely to be reported in the setting of hypercoagulable states including autoimmune diseases, inherited coagulation factor deficiencies, hyperviscosity syndromes, and acquired hypercoagulabe states (e.g., pregnancy, malignancy, previous heparin exposure, **Table 1**) [42–44]. As coronary emboli are a rarely reported phenomenon, no randomized trials or guidelines exist regarding diagnostic workup for these, although it would not be unreasonable to initiate workup for thrombophilia whenever appropriate diagnosis or suspicion exists [37, 42–45].

Infective endocarditis is one of the most dreaded infectious etiologies associated with significant morbidity and mortality [46, 47]. Coronary septic arterial emboli (CSAE) secondary to infectious endocarditis have been reported and according to one source such events may carry a mortality of up to 50% [48]. CSAE appear to be more likely to occur in patients having vegetations of the mitral valve or fungal infections, as fungal vegetations are known to reach larger overall dimensions, thus increasing the cumulative possibility of embolization [49, 50]. Rheumatic heart disease, though more common in low-income countries, is another possible etiology that can be associated with CSAE and must be kept in mind when evaluating

Tumors originating in the heart such as atrial myxomas, or on valves such as papillary fibroelastomas, are well known to cause cryptogenic brain infarctions [14, 53]. There are also reports of embolization to the coronary circulation [54–56]. Given that end-organ damage, including cerebrovascular accidents may constitute the initial clinical presentation of such neoplasms, it would not be unreasonable to propose that an embolic myocardial infarction may occur in this setting [56, 57]. It is also likely that such occurrences are under-recognized and probably more common than generally thought, thus requiring high index of clinical suspicion and prompt diagnosis [56, 57]. The overall urgency is highlighted by the possibility that subsequent presentations in cases of "missed diagnosis" may manifest as unexplained/

**44**

Stenotic heart valves resulting from progressive calcification process also pose the possibility of calcific embolization to distal locations, including the coronary circulation [48, 62, 63]. Rheumatic valvular heart disease could be another possible risk factor for coronary embolization [48]. Long-term valvular heart disease leads to structural changes in the myocardium, eventually increasing the risk of atrial fibrillation, which in itself may be a contributor to both systemic and coronary embolization [39, 64]. Of note, coronary embolism has been reported following aortic and mitral valve replacement, with successful management reported to involve abciximab and urokinase [65]. Another report describes acute myocardial infarction due to coronary embolism in a patient with mitral valve prosthesis. That particular case was successfully managed using angioplasty [66]. An example of a left coronary embolism associated with subtherapeutic oral anticoagulation in a patient with mitral and aortic mechanical valve prostheses is shown in **Figure 2** [67].

### **5.5 Iatrogenic causes**

Ruptured atherosclerotic plaques in the coronary arteries may lead to acute thrombotic occlusions and are the frequent pathophysiologic factor behind acute ST-elevation myocardial infarctions [68, 69]. Vessels affected by such processes may be characterized by a high thrombotic burden. For example, saphenous venous grafts in post-coronary artery bypass graft patients seem particularly vulnerable [70, 71], with various pathophysiologic mechanisms proposed including immunemediated process [71, 72].

Cardiac catheterization procedures may also cause distal embolization of intravascular particles [73]. Depending upon where, and how far, any dislodged thrombi or microthrombi travel, periprocedural myocardial infarction can become a very real risk [74]. Various procedural techniques including specialized "wire filter" protection devices [74, 75] and thrombus extraction catheters [76] can be utilized during coronary interventions to prevent or reduce distal embolization. Finally,

#### **Figure 2.**

*An example of a left coronary artery coronary embolism associated with subtherapeutic anticoagulation in the setting of mitral and aortic mechanical valve prostheses. [A, left] Note the filling defect present upon initial diagnosis. [B, right] Following thrombectomy, the left coronary artery is seen to be patent. Source: Protasiewicz et al. [67]. Images used under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, which permits all noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.*

distal coronary embolization involving cholesterol particles is also a possibility in patients undergoing diagnostic coronary angiography or thrombolysis [77, 78].

### **6. Diagnosis of coronary embolism**

A careful history and physical examination is necessary, with specific focus on finding any systemic signs of emboli in septic patients, as well as the possibility of an autoimmune disease in the subset of non-septic patients [79–81]. As with suspected coronary artery disease, patients suffering from coronary embolism may present with typical or atypical chest pain or with "angina equivalents" such as dyspnea [79, 81, 82]. As with all acute coronary syndromes, electrocardiography will be very important in determining the diagnosis and may dictate the urgency for cardiac catheterization (e.g., the presence of ST-elevation myocardial infarction). The presence of Q-waves in contiguous leads may be indicative of a "silent" myocardial infarction. Troponin and other cardiac enzyme testing certainly plays an important role in determining the extent and the progression of myocardial ischemia [83, 84]. Subsequent workup should include transthoracic and transesophageal echocardiography, advanced high-resolution imaging (e.g., CT or MRI), and coronary angiography [18, 85–87]. In addition, miscellaneous adjunctive diagnostic tools, such as Holter/event monitoring, can also be helpful in cases where etiology of the event(s) in question may be uncertain [88, 89].

#### **6.1 Coronary angiography**

Coronary angiography remains the mainstay of CEP diagnostics [87]. As outlined previously, patients affected by this condition may have "silent" myocardial infarction or may present with an acute ST segment elevation myocardial infarction. When performing angiography, associated thrombi have a distinct hazy angiographic appearance [87, 90, 91]. Moreover, angiography can help document the evolution and resolution of coronary embolism [92]. Finally, diagnostic angiography can be converted into a therapeutic procedure if indicated [87, 93].

The angiographer should keep in mind that the presence of multiple acute thromboembolic lesions in various vessels increases the suspicion for embolic coronary phenomena [94]. As mentioned above, these emboli may also acutely occlude parts of vessels with pre-existing atherosclerosis, further complicating the diagnosis. Intravascular ultrasound following aspiration atherectomy may be useful when assessing for underlying atherosclerosis versus purely acute thromboembolic phenomena. Optical coherence tomography of these vessels may also be useful but has not yet been studied sufficiently in this particular setting [95, 96]. A patient with angiographic evidence of coronary embolism but with no traditional risk factors for coronary artery disease should raise the suspicion for some of the less common causes (e.g., autoimmune, infectious, inflammatory, or neoplastic) [6, 94, 97].

After diagnostic confirmation, coronary thrombi are often removed using aspiration catheters, as outlined in previous paragraphs. Biopsy of these specimens would aid in differentiating between thrombotic, septic, and neoplastic causes of embolism, particularly due to the fact that these may be the presenting events in some neoplasms. Autoimmune disease may also need to be ruled out [6, 94, 97].

#### **6.2 Transthoracic echocardiography**

Transthoracic echocardiography should be a part of the routine workup for patients with suspected CEP. Diagnostically, it will be critically important to

**47**

these medicines [108].

*Coronary Embolic Phenomena: High-Impact, Low-Frequency Events*

findings can be present in the setting of atrial fibrillation [102].

demonstrate or rule out the presence of patent foramen ovale [98–100] and identify any thrombi in left-sided cardiac chambers, particularly with the help of ultrasonic contrast [33, 59]. Any suspicion should be further supplemented with transesophageal echocardiography to ascertain any transthoracic echocardiography findings, especially those of uncertain significance or insufficiently granular detail(s) [59, 101]. In addition, this would also be helpful to visualize the left atrial appendage when looking for evidence of either stasis or thrombus formation there [102, 103]. Such

As outlined earlier in this manuscript, Holter/event monitoring to look for atrial fibrillation would also be reasonable in patients being seen for embolic phenomena [88, 89]. As for all thromboembolic diseases, thrombophilia workup would also be useful in ascertaining the etiology of coronary embolism in appropriately selected

Coronary embolic syndromes are quite heterogeneous, and lack randomized controlled trial data or specific guidelines on their management. The initial approach including timing of cardiac catheterization for coronary embolism should be the same as for routine acute coronary syndrome (with classification of available

Oxygen (Class 1), nitrates (Class 1), and beta blockers (Class 1) are the mainstay of the initial medical management [106] in addition to parenteral anticoagulation

Decision regarding the use of percutaneous coronary intervention versus balloon angioplasty would be up to the clinician's judgment given plaque morphology as assessed by intravascular ultrasound as well as on optical coherence tomography. Following the initial management, dual antiplatelet inhibition would be recommended for these patients [107] for a duration of 6–12 months as per the 2017 American College of Cardiology (ACC)/American Heart Association (AHA)

As no randomized controlled data are available on lipid management for the particular subset of patients suffering from coronary embolism, we would recommend following current society guidelines for lipid management in these patients. For patients with reduced ejection fraction on echocardiography, angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers in addition to

Long-term anticoagulation in patients diagnosed with embolic coronary disease remains a question to be answered. As with other embolic phenomena, 3–6 months of anticoagulation with warfarin or with direct anticoagulants would be reasonable, with further therapy to be decided upon ascertaining the underlying etiology. Workup to determine the etiology is essential, and treatment of the cause of embolism is of course necessary. As mentioned above, remote cardiac monitoring to look for atrial fibrillation is essential as it may necessitate lifelong anticoagulation

Lastly, in patients possibly requiring triple antithrombotic therapy, data are limited, with current management approaches based on consensus recommendations with only a brief mention in the 2016 ACC Guidelines [108]. The decision regarding the duration or discontinuation of triple therapy versus P2Y12 inhibitor plus vitamin K antagonists (VKA)/direct oral anticoagulants (DOAC) would be based on the individualized bleeding risk versus the potential risk of discontinuing

*DOI: http://dx.doi.org/10.5772/intechopen.90685*

at-risk patients [104].

Guidelines [108].

**7. Clinical management**

evidence quality provided in parentheses) [106].

(Enoxaparin/unfractionated heparin [UHF]/Bivalirudin) [109].

aldosterone antagonists are recommended (Class 1) [106, 109].

particularly in patients with high CHADS2VASC scores.

*Coronary Embolic Phenomena: High-Impact, Low-Frequency Events DOI: http://dx.doi.org/10.5772/intechopen.90685*

demonstrate or rule out the presence of patent foramen ovale [98–100] and identify any thrombi in left-sided cardiac chambers, particularly with the help of ultrasonic contrast [33, 59]. Any suspicion should be further supplemented with transesophageal echocardiography to ascertain any transthoracic echocardiography findings, especially those of uncertain significance or insufficiently granular detail(s) [59, 101]. In addition, this would also be helpful to visualize the left atrial appendage when looking for evidence of either stasis or thrombus formation there [102, 103]. Such findings can be present in the setting of atrial fibrillation [102].

As outlined earlier in this manuscript, Holter/event monitoring to look for atrial fibrillation would also be reasonable in patients being seen for embolic phenomena [88, 89]. As for all thromboembolic diseases, thrombophilia workup would also be useful in ascertaining the etiology of coronary embolism in appropriately selected at-risk patients [104].

### **7. Clinical management**

*Embolic Diseases - Evolving Diagnostic and Management Approaches*

of the event(s) in question may be uncertain [88, 89].

**6.1 Coronary angiography**

**6.2 Transthoracic echocardiography**

**6. Diagnosis of coronary embolism**

distal coronary embolization involving cholesterol particles is also a possibility in patients undergoing diagnostic coronary angiography or thrombolysis [77, 78].

A careful history and physical examination is necessary, with specific focus on finding any systemic signs of emboli in septic patients, as well as the possibility of an autoimmune disease in the subset of non-septic patients [79–81]. As with suspected coronary artery disease, patients suffering from coronary embolism may present with typical or atypical chest pain or with "angina equivalents" such as dyspnea [79, 81, 82]. As with all acute coronary syndromes, electrocardiography will be very important in determining the diagnosis and may dictate the urgency for cardiac catheterization (e.g., the presence of ST-elevation myocardial infarction). The presence of Q-waves in contiguous leads may be indicative of a "silent" myocardial infarction. Troponin and other cardiac enzyme testing certainly plays an important role in determining the extent and the progression of myocardial ischemia [83, 84]. Subsequent workup should include transthoracic and transesophageal echocardiography, advanced high-resolution imaging (e.g., CT or MRI), and coronary angiography [18, 85–87]. In addition, miscellaneous adjunctive diagnostic tools, such as Holter/event monitoring, can also be helpful in cases where etiology

Coronary angiography remains the mainstay of CEP diagnostics [87]. As outlined previously, patients affected by this condition may have "silent" myocardial infarction or may present with an acute ST segment elevation myocardial infarction. When performing angiography, associated thrombi have a distinct hazy angiographic appearance [87, 90, 91]. Moreover, angiography can help document the evolution and resolution of coronary embolism [92]. Finally, diagnostic angiography can be converted into a therapeutic procedure if indicated [87, 93]. The angiographer should keep in mind that the presence of multiple acute thromboembolic lesions in various vessels increases the suspicion for embolic coronary phenomena [94]. As mentioned above, these emboli may also acutely occlude parts of vessels with pre-existing atherosclerosis, further complicating the diagnosis. Intravascular ultrasound following aspiration atherectomy may be useful when assessing for underlying atherosclerosis versus purely acute thromboembolic phenomena. Optical coherence tomography of these vessels may also be useful but has not yet been studied sufficiently in this particular setting [95, 96]. A patient with angiographic evidence of coronary embolism but with no traditional risk factors for coronary artery disease should raise the suspicion for some of the less common causes (e.g., autoimmune, infectious, inflammatory, or neoplastic) [6, 94, 97]. After diagnostic confirmation, coronary thrombi are often removed using aspiration catheters, as outlined in previous paragraphs. Biopsy of these specimens would aid in differentiating between thrombotic, septic, and neoplastic causes of embolism, particularly due to the fact that these may be the presenting events in some neoplasms. Autoimmune disease may also need to be ruled out [6, 94, 97].

Transthoracic echocardiography should be a part of the routine workup for patients with suspected CEP. Diagnostically, it will be critically important to

**46**

Coronary embolic syndromes are quite heterogeneous, and lack randomized controlled trial data or specific guidelines on their management. The initial approach including timing of cardiac catheterization for coronary embolism should be the same as for routine acute coronary syndrome (with classification of available evidence quality provided in parentheses) [106].

Oxygen (Class 1), nitrates (Class 1), and beta blockers (Class 1) are the mainstay of the initial medical management [106] in addition to parenteral anticoagulation (Enoxaparin/unfractionated heparin [UHF]/Bivalirudin) [109].

Decision regarding the use of percutaneous coronary intervention versus balloon angioplasty would be up to the clinician's judgment given plaque morphology as assessed by intravascular ultrasound as well as on optical coherence tomography.

Following the initial management, dual antiplatelet inhibition would be recommended for these patients [107] for a duration of 6–12 months as per the 2017 American College of Cardiology (ACC)/American Heart Association (AHA) Guidelines [108].

As no randomized controlled data are available on lipid management for the particular subset of patients suffering from coronary embolism, we would recommend following current society guidelines for lipid management in these patients.

For patients with reduced ejection fraction on echocardiography, angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers in addition to aldosterone antagonists are recommended (Class 1) [106, 109].

Long-term anticoagulation in patients diagnosed with embolic coronary disease remains a question to be answered. As with other embolic phenomena, 3–6 months of anticoagulation with warfarin or with direct anticoagulants would be reasonable, with further therapy to be decided upon ascertaining the underlying etiology.

Workup to determine the etiology is essential, and treatment of the cause of embolism is of course necessary. As mentioned above, remote cardiac monitoring to look for atrial fibrillation is essential as it may necessitate lifelong anticoagulation particularly in patients with high CHADS2VASC scores.

Lastly, in patients possibly requiring triple antithrombotic therapy, data are limited, with current management approaches based on consensus recommendations with only a brief mention in the 2016 ACC Guidelines [108]. The decision regarding the duration or discontinuation of triple therapy versus P2Y12 inhibitor plus vitamin K antagonists (VKA)/direct oral anticoagulants (DOAC) would be based on the individualized bleeding risk versus the potential risk of discontinuing these medicines [108].

### **8. Miscellaneous causes**

It has been reported that air embolism can complicate a variety of invasive procedures involving the vasculature, from central venous access placement to coronary artery bypass grafting [105, 106]. In the context of CEPs, the presence of patent foramen ovale (PFO) plays an important contributory role [107]. Though rarely reported, air embolism due to decompression illnesses or due to iatrogenic causes may also cause coronary embolism. Finally, iatrogenic CEPs are fortunately uncommon, yet they are dreaded events that may occur in the cardiac catheterization lab or during coronary artery bypass graft (CABG) surgery [103, 104].

Amniotic fluid embolism (AFE) in pregnant women can also lead to coronary embolization [105, 108]. Of note, for amniotic fluid to embolize to the coronary arteries, the patient must also have a PFO which helps facilitate the right-to-left transit of causative particles, which then lodge in the systemic arterial system and, potentially, the coronary arteries. It has been noted that the appearance of amniotic fluid emboli in the coronary circulation may be associated with elevated mortality when compared with cases not involving the coronary vessels [108]. Marked constriction of coronary arteries has also been described in the setting of AFE, although it is not known if that is a direct or an indirect effect [109, 110].

## **9. Conclusion**

Coronary embolic phenomena are a heterogeneous group of clinicopathologic entities attributable to a variety of etiologic factors. Due to their rarity and the tendency to clinically mimic other coronary syndromes, CEPs are often underdiagnosed. Timely diagnosis using an elevated index of suspicion in high-risk patients is important to improving the associated morbidity and mortality. Scarcity of high quality data regarding CEPs necessitates further studies and dedicated consensus guidelines. Progress in diagnosis and treatment of CEPs will require concerted efforts by clinicians, educators, and researchers.

### **Author details**

Qasim Malik1,2, Ambreen Alam1,2, Stanislaw P. Stawicki1,2\* and Peter Puleo1,2

1 Department of Research and Innovation, St. Luke's University Health Network, Bethlehem, Pennsylvania, USA

2 Heart and Vascular Center, St. Luke's University Health Network, Bethlehem, Pennsylvania, USA

\*Address all correspondence to: stawicki.ace@gmail.com

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

**49**

*Coronary Embolic Phenomena: High-Impact, Low-Frequency Events*

In: Principles of Medical Therapy in Pregnancy. New York, New York:

Ganzon MS. Coronary embolism causing ST elevation myocardial infarction complicated by

Journal of Internal Medicine.

[11] Meister SG et al. Paradoxical embolism: Diagnosis during life. The American Journal of Medicine.

Nonatherosclerotic coronary artery disease. In: Diagnosis and Therapy of Coronary Artery Disease. Boston, Massachusetts: Springer; 1985.

ventricular septal rupture. Philippine

Springer; 1985. pp. 671-679

[10] Apostol-Alday AS,

2016;**54**(3):1-5

1972;**53**(3):292-298

pp. 495-505

[12] Hillis LD, Cohn PF.

[13] Glazier JJ, Mcginnity JG, Spears JR. Coronary embolism

1997;**20**(10):885-888

complicating aortic valve endocarditis: Treatment with placement of an

intracoronary stent. Clinical Cardiology.

[14] Stoane L, Allen JH Jr, Collins HA. Radiologic observations in cerebral embolization from left heart myxomas.

[15] Waller B et al. Nonatherosclerotic causes of coronary artery narrowing—

Radiology. 1966;**87**(2):262-266

Part II. Clinical Cardiology.

[16] Conti CR. Are "paradoxical emboli" really paradoxical? Clinical Cardiology: An International Indexed and Peer-Reviewed Journal for Advances in the Treatment of Cardiovascular Disease. 2003;**26**(3):105-106

[17] Corrin B. Paradoxical embolism. British Heart Journal. 1964;**26**(4):549

1996;**19**(7):587-591

*DOI: http://dx.doi.org/10.5772/intechopen.90685*

[1] De Filippo M, Capasso R. Coronary computed tomography angiography (CCTA) and cardiac magnetic resonance (CMR) imaging in the assessment of patients presenting with chest pain suspected for acute coronary syndrome. Annals of Translational Medicine.

[2] Jin M-F, Xu Z. Delayed post-dilated stenting to treat an embolic myocardial

[3] Kei J, Avilla JK, Cavendish JJ. Rare case of myocardial infarction in a 19-year-old caused by a paradoxical coronary artery embolism. The Permanente Journal. 2015;**19**(2):e107

[4] White PD. The epidemiology of heart disease. Irish Journal of Medical Science (1926-1967). 1957;**32**(10):426-440

[5] Khan M et al. Coronary air embolism: Incidence, severity, and suggested approaches to treatment. Catheterization and Cardiovascular Diagnosis. 1995;**36**(4):313-318

[6] Raphael CE et al. Coronary embolus: An underappreciated cause of acute coronary syndromes. JACC: Cardiovascular Interventions.

[7] Meier-Ewert HK et al. Paradoxical embolism in the left main coronary artery: Diagnosis by transesophageal echocardiography. In: Mayo Clinic Proceedings. New York, New York: Elsevier. 2003;**78**(1):103-106

[8] Zeller L et al. A rare complication of infective endocarditis: Left main coronary artery embolization resulting in sudden death. Journal of Heart Valve

[9] Reid CL, Elkayam U, Rahimtoola SH. Infective endocarditis in pregnancy.

Disease. 2010;**19**(2):225

2018;**11**(2):172-180

infarction. Journal of Geriatric Cardiology: JGC. 2016;**13**(10):872

2016;**4**(13):255

**References**

*Coronary Embolic Phenomena: High-Impact, Low-Frequency Events DOI: http://dx.doi.org/10.5772/intechopen.90685*

### **References**

*Embolic Diseases - Evolving Diagnostic and Management Approaches*

It has been reported that air embolism can complicate a variety of invasive procedures involving the vasculature, from central venous access placement to coronary artery bypass grafting [105, 106]. In the context of CEPs, the presence of patent foramen ovale (PFO) plays an important contributory role [107]. Though rarely reported, air embolism due to decompression illnesses or due to iatrogenic causes may also cause coronary embolism. Finally, iatrogenic CEPs are fortunately uncommon, yet they are dreaded events that may occur in the cardiac catheterization lab or during coronary artery bypass graft (CABG) surgery [103, 104].

Amniotic fluid embolism (AFE) in pregnant women can also lead to coronary embolization [105, 108]. Of note, for amniotic fluid to embolize to the coronary arteries, the patient must also have a PFO which helps facilitate the right-to-left transit of causative particles, which then lodge in the systemic arterial system and, potentially, the coronary arteries. It has been noted that the appearance of amniotic fluid emboli in the coronary circulation may be associated with elevated mortality when compared with cases not involving the coronary vessels [108]. Marked constriction of coronary arteries has also been described in the setting of AFE, although it is not known if that is a direct or an indirect effect [109, 110].

Coronary embolic phenomena are a heterogeneous group of clinicopathologic entities attributable to a variety of etiologic factors. Due to their rarity and the tendency to clinically mimic other coronary syndromes, CEPs are often underdiagnosed. Timely diagnosis using an elevated index of suspicion in high-risk patients is important to improving the associated morbidity and mortality. Scarcity of high quality data regarding CEPs necessitates further studies and dedicated consensus guidelines. Progress in diagnosis and treatment of CEPs will require concerted

Qasim Malik1,2, Ambreen Ahmad1,2, Stanislaw P. Stawicki1,2\* and Peter Puleo1,2

1 Department of Research and Innovation, St. Luke's University Health Network,

2 Heart and Vascular Center, St. Luke's University Health Network, Bethlehem,

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

**8. Miscellaneous causes**

**9. Conclusion**

**Author details**

Pennsylvania, USA

Bethlehem, Pennsylvania, USA

efforts by clinicians, educators, and researchers.

\*Address all correspondence to: stawicki.ace@gmail.com

provided the original work is properly cited.

**48**

[1] De Filippo M, Capasso R. Coronary computed tomography angiography (CCTA) and cardiac magnetic resonance (CMR) imaging in the assessment of patients presenting with chest pain suspected for acute coronary syndrome. Annals of Translational Medicine. 2016;**4**(13):255

[2] Jin M-F, Xu Z. Delayed post-dilated stenting to treat an embolic myocardial infarction. Journal of Geriatric Cardiology: JGC. 2016;**13**(10):872

[3] Kei J, Avilla JK, Cavendish JJ. Rare case of myocardial infarction in a 19-year-old caused by a paradoxical coronary artery embolism. The Permanente Journal. 2015;**19**(2):e107

[4] White PD. The epidemiology of heart disease. Irish Journal of Medical Science (1926-1967). 1957;**32**(10):426-440

[5] Khan M et al. Coronary air embolism: Incidence, severity, and suggested approaches to treatment. Catheterization and Cardiovascular Diagnosis. 1995;**36**(4):313-318

[6] Raphael CE et al. Coronary embolus: An underappreciated cause of acute coronary syndromes. JACC: Cardiovascular Interventions. 2018;**11**(2):172-180

[7] Meier-Ewert HK et al. Paradoxical embolism in the left main coronary artery: Diagnosis by transesophageal echocardiography. In: Mayo Clinic Proceedings. New York, New York: Elsevier. 2003;**78**(1):103-106

[8] Zeller L et al. A rare complication of infective endocarditis: Left main coronary artery embolization resulting in sudden death. Journal of Heart Valve Disease. 2010;**19**(2):225

[9] Reid CL, Elkayam U, Rahimtoola SH. Infective endocarditis in pregnancy.

In: Principles of Medical Therapy in Pregnancy. New York, New York: Springer; 1985. pp. 671-679

[10] Apostol-Alday AS, Ganzon MS. Coronary embolism causing ST elevation myocardial infarction complicated by ventricular septal rupture. Philippine Journal of Internal Medicine. 2016;**54**(3):1-5

[11] Meister SG et al. Paradoxical embolism: Diagnosis during life. The American Journal of Medicine. 1972;**53**(3):292-298

[12] Hillis LD, Cohn PF. Nonatherosclerotic coronary artery disease. In: Diagnosis and Therapy of Coronary Artery Disease. Boston, Massachusetts: Springer; 1985. pp. 495-505

[13] Glazier JJ, Mcginnity JG, Spears JR. Coronary embolism complicating aortic valve endocarditis: Treatment with placement of an intracoronary stent. Clinical Cardiology. 1997;**20**(10):885-888

[14] Stoane L, Allen JH Jr, Collins HA. Radiologic observations in cerebral embolization from left heart myxomas. Radiology. 1966;**87**(2):262-266

[15] Waller B et al. Nonatherosclerotic causes of coronary artery narrowing— Part II. Clinical Cardiology. 1996;**19**(7):587-591

[16] Conti CR. Are "paradoxical emboli" really paradoxical? Clinical Cardiology: An International Indexed and Peer-Reviewed Journal for Advances in the Treatment of Cardiovascular Disease. 2003;**26**(3):105-106

[17] Corrin B. Paradoxical embolism. British Heart Journal. 1964;**26**(4):549 [18] Dao CN, Tobis JM. PFO and paradoxical embolism producing events other than stroke. Catheterization and Cardiovascular Interventions. 2011;**77**(6):903-909

[19] Zhang J et al. Successful implementation of extracorporeal membrane oxygenation support as a bridge to heart-lung transplantation in an Eisenmenger's syndrome patient with paradoxical coronary embolism. Journal of Investigative Medicine High Impact Case Reports. 2019;**7**:2324709619846575

[20] Sampson B, Hammers J. Forensic aspects of cardiovascular pathology. In: Cardiovascular Pathology. Cambridge, Massachusetts: Academic Press/ Elsevier; 2016. pp. 773-798

[21] Capodanno D et al. Epidemiology and clinical impact of different anatomical phenotypes of the left main coronary artery. Heart and Vessels. 2011;**26**(2):138-144

[22] Bolger AF et al. Transit of blood flow through the human left ventricle mapped by cardiovascular magnetic resonance. Journal of Cardiovascular Magnetic Resonance. 2007;**9**(5):741-747

[23] Verani MS et al. Quantification of left ventricular performance during transient coronary occlusion at various anatomic sites in humans: A study using tantalum-178 and a multiwire gamma camera. Journal of the American College of Cardiology. 1992;**19**(2):297-306

[24] Kim H et al. Patient-specific modeling of blood flow and pressure in human coronary arteries. Annals of Biomedical Engineering. 2010;**38**(10):3195-3209

[25] Chaichana T, Sun Z, Jewkes J. Computation of hemodynamics in the left coronary artery with variable angulations. Journal of Biomechanics. 2011;**44**(10):1869-1878

[26] Yamanaka O, Hobbs RE. Coronary artery anomalies in 126,595 patients undergoing coronary arteriography. Catheterization and Cardiovascular Diagnosis. 1990;**21**(1):28-40

[27] Hirono K et al. Anomalous origin of the right coronary artery evaluated with multidetector computed tomography and its clinical relevance. Journal of Cardiology. 2016;**68**(3):196-201

[28] Kimbiris D et al. Anomalous aortic origin of coronary arteries. Circulation. 1978;**58**(4):606-615

[29] Niccoli G et al. Microvascular obstruction after primary percutaneous coronary intervention: Pathogenesis, diagnosis and prognostic significance. Current Vascular Pharmacology. 2013;**11**(2):245-262

[30] Groskloss HH. Fat embolism. The Yale Journal of Biology and Medicine. 1935;**8**(1):59

[31] Chandler A. Mechanisms and frequency of thrombosis in the coronary circulation. Thrombosis Research. 1974;**4**:3-23

[32] Greenstein J. Sudden death from cardiac and aortic disease. South African Medical Journal. 1947;**21**(9):307-320

[33] Kotooka N et al. Three cases of acute myocardial infarction due to coronary embolism. Japanese Heart Journal. 2004;**45**(5):861-866

[34] Waller BF et al. Embolus to the left main coronary artery. American Journal of Cardiology. 1982;**50**(3):658-660

[35] Charles R, Epstein E. Diagnosis of coronary embolism: A review. Journal of the Royal Society of Medicine. 1983;**76**(10):863-869

[36] Malone P, Agutter P. The aetiology of deep venous thrombosis. Journal

**51**

*Coronary Embolic Phenomena: High-Impact, Low-Frequency Events*

know. International Journal of Critical Illness and Injury Science. 2018;**8**(2):73

embolism: A potentially devastating complication of infective endocarditis. In: Contemporary Challenges in Endocarditis. Rijeka: IntechOpen; 2016

[47] Stawicki SP et al. Septic embolism in the intensive care unit. International Journal of Critical Illness and Injury

[48] Charles R et al. Coronary embolism in valvular heart disease. QJM: An International Journal of Medicine.

[49] Adams PC et al. Thrombosis and embolism from cardiac chambers and infected valves. Journal of the American

College of Cardiology. 1986;**8**(6

[50] Kothari S, Ramakrishnan S, Bahl V. Infective endocarditis—An Indian perspective. Indian Heart

[51] Wartman WB, Hellerstein HK. The incidence of heart disease in 2,000 consecutive autopsies. Annals of Internal Medicine. 1948;**28**(1):41-65

[53] Mikati I, Ibrahim Z. Cardioembolic Stroke. Warlow's Stroke: Practical Management. 2019. pp. 241-265

[54] Inman W, Vessey M. Investigation of deaths from pulmonary, coronary, and cerebral thrombosis and embolism in women of child-bearing age. British Medical Journal. 1968;**2**(5599):193

[55] Braun S et al. Myocardial infarction as complication of left atrial myxoma. International Journal of Cardiology.

2005;**101**(1):115-121

Supplement 2):76B-87B

Journal. 2005;**57**(4):289

[52] Lee Shrader E, Bawell M, Moragues V. Coronary embolism. Circulation. 1956;**14**(6):1159-1163

[46] Wojda TR et al. Septic

Science. 2013;**3**(1):58

1982;**51**(2):147-161

*DOI: http://dx.doi.org/10.5772/intechopen.90685*

of the Association of Physicians.

[37] Prosciak MP, Stawicki SP. Hypercoagulable states: A concise review. International Journal of Academic Medicine. 2017;**3**(3):82

[38] Bennett J, Ong L, Hanratty C. Paradoxical coronary embolism, a rare cause of acute myocardial infarction on positive pressure ventilation. Acta Cardiologica. 2012;**67**(4):477-479

[39] Van de Walle S, Dujardin K. A case of coronary embolism in a patient with paroxysmal atrial fibrillation receiving tamoxifen. International Journal of Cardiology. 2007;**123**(1):66-68

[41] Zachura M et al. Acute myocardial infarction due to coronary embolism originating from left ventricle thrombus in a patient with dilated cardiomyopathy and sinus rhythm. Postepy w Kardiologii

[42] Acharya SS, Sarangi SN. Disorders of coagulation. In: Lanzkowsky's Manual of Pediatric Hematology and Oncology. Cambridge, Massachusetts: Academic Press/Elsevier; 2016.

Interwencyjnej. 2016;**12**(1):73

[43] Silva A et al. Thrombophilia/ prothrombotic disorders. Sociedade Portuguesa de Medicină Internă. 2010;**17**:1

[44] Barelli S, Blum S, Angelillo-Scherrer A. Acquired hemostatic disorders. In: Perioperative Hemostasis. Berlin, Heidelberg: Springer; 2015.

[45] Quarrie R, Stawicki SP. Portal vein thrombosis: What surgeons need to

pp. 279-333

pp. 89-108

[40] Kuramoto K, Matsushita S, Yamanouchi H. Atrial fibrillation as a cause of myocardial and cerebral infarctions: Symposium on clinical aspects of thromboembolism. Japanese Circulation Journal. 1984;**48**(1):67-74

2006;**99**(9):581-593

#### *Coronary Embolic Phenomena: High-Impact, Low-Frequency Events DOI: http://dx.doi.org/10.5772/intechopen.90685*

of the Association of Physicians. 2006;**99**(9):581-593

*Embolic Diseases - Evolving Diagnostic and Management Approaches*

[26] Yamanaka O, Hobbs RE. Coronary artery anomalies in 126,595 patients undergoing coronary arteriography. Catheterization and Cardiovascular Diagnosis. 1990;**21**(1):28-40

[27] Hirono K et al. Anomalous origin of the right coronary artery evaluated with multidetector computed tomography and its clinical relevance. Journal of Cardiology. 2016;**68**(3):196-201

[28] Kimbiris D et al. Anomalous aortic origin of coronary arteries. Circulation.

[29] Niccoli G et al. Microvascular obstruction after primary percutaneous coronary intervention: Pathogenesis, diagnosis and prognostic significance. Current Vascular Pharmacology.

[30] Groskloss HH. Fat embolism. The Yale Journal of Biology and Medicine.

[31] Chandler A. Mechanisms and frequency of thrombosis in the coronary circulation. Thrombosis Research.

[32] Greenstein J. Sudden death from cardiac and aortic disease. South African Medical Journal.

[33] Kotooka N et al. Three cases of acute myocardial infarction due to coronary embolism. Japanese Heart Journal.

[34] Waller BF et al. Embolus to the left main coronary artery. American Journal of Cardiology. 1982;**50**(3):658-660

[35] Charles R, Epstein E. Diagnosis of coronary embolism: A review. Journal of the Royal Society of Medicine.

[36] Malone P, Agutter P. The aetiology of deep venous thrombosis. Journal

1978;**58**(4):606-615

2013;**11**(2):245-262

1935;**8**(1):59

1974;**4**:3-23

1947;**21**(9):307-320

2004;**45**(5):861-866

1983;**76**(10):863-869

[18] Dao CN, Tobis JM. PFO and

[19] Zhang J et al. Successful implementation of extracorporeal membrane oxygenation support as a bridge to heart-lung transplantation in an Eisenmenger's syndrome patient with paradoxical coronary embolism. Journal of Investigative Medicine High Impact Case Reports. 2019;**7**:2324709619846575

2011;**77**(6):903-909

paradoxical embolism producing events other than stroke. Catheterization and Cardiovascular Interventions.

[20] Sampson B, Hammers J. Forensic aspects of cardiovascular pathology. In: Cardiovascular Pathology. Cambridge, Massachusetts: Academic Press/ Elsevier; 2016. pp. 773-798

[21] Capodanno D et al. Epidemiology and clinical impact of different

anatomical phenotypes of the left main coronary artery. Heart and Vessels.

[23] Verani MS et al. Quantification of left ventricular performance during transient coronary occlusion at various anatomic sites in humans: A study using tantalum-178 and a multiwire gamma camera. Journal of the American College of Cardiology. 1992;**19**(2):297-306

[24] Kim H et al. Patient-specific modeling of blood flow and pressure

[25] Chaichana T, Sun Z, Jewkes J. Computation of hemodynamics in the left coronary artery with variable angulations. Journal of Biomechanics.

in human coronary arteries. Annals of Biomedical Engineering.

2010;**38**(10):3195-3209

2011;**44**(10):1869-1878

2011;**26**(2):138-144

2007;**9**(5):741-747

[22] Bolger AF et al. Transit of blood flow through the human left ventricle mapped by cardiovascular magnetic resonance. Journal of Cardiovascular Magnetic Resonance.

**50**

[37] Prosciak MP, Stawicki SP. Hypercoagulable states: A concise review. International Journal of Academic Medicine. 2017;**3**(3):82

[38] Bennett J, Ong L, Hanratty C. Paradoxical coronary embolism, a rare cause of acute myocardial infarction on positive pressure ventilation. Acta Cardiologica. 2012;**67**(4):477-479

[39] Van de Walle S, Dujardin K. A case of coronary embolism in a patient with paroxysmal atrial fibrillation receiving tamoxifen. International Journal of Cardiology. 2007;**123**(1):66-68

[40] Kuramoto K, Matsushita S, Yamanouchi H. Atrial fibrillation as a cause of myocardial and cerebral infarctions: Symposium on clinical aspects of thromboembolism. Japanese Circulation Journal. 1984;**48**(1):67-74

[41] Zachura M et al. Acute myocardial infarction due to coronary embolism originating from left ventricle thrombus in a patient with dilated cardiomyopathy and sinus rhythm. Postepy w Kardiologii Interwencyjnej. 2016;**12**(1):73

[42] Acharya SS, Sarangi SN. Disorders of coagulation. In: Lanzkowsky's Manual of Pediatric Hematology and Oncology. Cambridge, Massachusetts: Academic Press/Elsevier; 2016. pp. 279-333

[43] Silva A et al. Thrombophilia/ prothrombotic disorders. Sociedade Portuguesa de Medicină Internă. 2010;**17**:1

[44] Barelli S, Blum S, Angelillo-Scherrer A. Acquired hemostatic disorders. In: Perioperative Hemostasis. Berlin, Heidelberg: Springer; 2015. pp. 89-108

[45] Quarrie R, Stawicki SP. Portal vein thrombosis: What surgeons need to

know. International Journal of Critical Illness and Injury Science. 2018;**8**(2):73

[46] Wojda TR et al. Septic embolism: A potentially devastating complication of infective endocarditis. In: Contemporary Challenges in Endocarditis. Rijeka: IntechOpen; 2016

[47] Stawicki SP et al. Septic embolism in the intensive care unit. International Journal of Critical Illness and Injury Science. 2013;**3**(1):58

[48] Charles R et al. Coronary embolism in valvular heart disease. QJM: An International Journal of Medicine. 1982;**51**(2):147-161

[49] Adams PC et al. Thrombosis and embolism from cardiac chambers and infected valves. Journal of the American College of Cardiology. 1986;**8**(6 Supplement 2):76B-87B

[50] Kothari S, Ramakrishnan S, Bahl V. Infective endocarditis—An Indian perspective. Indian Heart Journal. 2005;**57**(4):289

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[52] Lee Shrader E, Bawell M, Moragues V. Coronary embolism. Circulation. 1956;**14**(6):1159-1163

[53] Mikati I, Ibrahim Z. Cardioembolic Stroke. Warlow's Stroke: Practical Management. 2019. pp. 241-265

[54] Inman W, Vessey M. Investigation of deaths from pulmonary, coronary, and cerebral thrombosis and embolism in women of child-bearing age. British Medical Journal. 1968;**2**(5599):193

[55] Braun S et al. Myocardial infarction as complication of left atrial myxoma. International Journal of Cardiology. 2005;**101**(1):115-121

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*Coronary Embolic Phenomena: High-Impact, Low-Frequency Events*

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detection of intracardiac sources of cerebral emboli by transesophageal

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echocardiography. Stroke. 1991;**22**(6):734-739

1996;**78**(3):365-369

1992;**124**(4):955-961

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2009;**98**(4):199-208

2015;**24**(1):e14-e17

percutaneous transluminal coronary angioplasty. The Annals of Thoracic

Surgery. 1987;**43**(2):220-223

[91] Saito S et al. Primary stent implantation without coumadin in acute myocardial infarction. Journal of the American College of Cardiology.

[92] Richardson P, Gotsman M. Angiographic evidence of coronary embolism and resolution. South African Medical Journal. 1971;**45**(7):805-809

[93] Xu B, Williams P, Burns AT. Acute myocardial infarction due to coronary artery embolus associated with atrial fibrillation. Acute Cardiac Care.

[94] Schuster EH et al. Multiple coronary thromboses in previously normal coronary arteries: A rare cause of acute myocardial infarction. American Heart

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[95] Farooq MU et al. The role of optical coherence tomography in vascular medicine. Vascular Medicine.

[96] Kume T et al. Assessment of coronary arterial thrombus by optical coherence tomography. The American Journal of Cardiology.

[97] Tun A, Khan IA. Acute myocardial infarction with angiographically normal coronary arteries. Heart & Lung.

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[99] Bridges ND et al. Transcatheter closure of patent foramen ovale after

1996;**28**(1):74-81

2013;**15**(4):93-95

2009;**14**(1):63-71

2006;**97**(12):1713-1717

2000;**29**(5):348-350

2001;**14**(12):1227-1229

**54**

[109] Azegami M, Mori N. Amniotic fluid embolism and leukotrienes. American Journal of Obstetrics and Gynecology. 1986;**155**(5):1119-1124

[110] Locksmith GJ. Amniotic fluid embolism. Obstetrics and Gynecology Clinics of North America. 1999;**26**(3):435-444

**57**

**Chapter 5**

**Abstract**

**1. Introduction**

Lower Limb

*André Luís Foroni Casas*

ous therapy of the acutely ischemic limb.

14/100,000 inhabitants per year [3].

Acute Arterial Embolism of the

Despite advances in the management of peripheral arterial occlusive disease, acute embolism of the lower extremities is still characterized by an important limb threat, morbidity, mortality, and continues to pose a challenge to the vascular surgeon. Atrial fibrillation, left ventricular aneurysm, penetrating ulcers or aneurysms of the aorta and common iliac arteries are the common sources of emboli. The presence of occlusion can be determined noninvasively with the use of duplex Doppler ultrasonography. Arteriography, Computed Tomographic Angiography and Magnetic Resonance Angiography can also be employed. Embolectomy is the standard for acute leg ischemia in patients with a strong clinical suspicion of an embolus, but alternative techniques, such as catheter-directed thrombolysis or percutaneous aspiration thrombolectomy, expand the role of radiologic percutane-

**Keywords:** thrombosis, embolism, embolectomy, fibrinolysis, lower extremity

Acute limb ischemia results from a sudden decrease in limb perfusion that threatens limb viability and often requires urgent revascularization [1]. Acute ischemia of the lower limb continues to pose a challenge to the vascular surgeon and is still characterized by an important morbidity, limb threat and mortality. The two principal etiologies of acute ischemia of the lower limbs are arterial embolism and in situ thrombosis of an atherosclerotic artery or of a bypass graft [2]. It is estimated

that the incidence of acute limb ischemia in the general population is around

emphasizing the need for prompt evaluation and treatment [5, 6].

sion of an artery at a point distant from where they originated [8].

The consequences of acute limb ischemia such as prolonged hospitalization, major limb amputation, and/or death have a profound socioeconomic impact. Acute limb ischemia represents a high-risk cohort in need of complex revascularization procedures that are often associated with a significant rate of periinterventional complications [4]. Historic rates of amputation and mortality range from 10 to 25%,

Embolism is the result of material passing through the arterial tree and obstructing a peripheral artery [7]. These materials may be thrombi, fragments of atheromatous plaque, tumor cells, or other foreign bodies, that have been dislodged or introduced into any part of the arterial system and can cause partial or total occlu-

### **Chapter 5**
