Frederick W. Crock, MD

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Multiple intracardiac thrombi

Author(s)

Jana G. Hashash, MD

Nabil S. Zeineh, MD

Frederick W. Crock, MD

A 60-year-old woman presented with sudden swelling and pain in her right arm. She reported progressive lower-extremity edema and abdominal girth over the past month, associated with shortness of breath and orthopnea. She had a remote history of two spontaneous abortions.

Figure 1. During the initial evaluation, echocardiography (apical four-chamber view) showed right ventricular and left ventricular thrombi (arrows).

Duplex ultrasonography revealed massive venous thrombosis extending from the antecubital fossa to the right atrium. Transthoracic echocardiography revealed severe left ventricular (LV) dysfunction and multiple echo-dense masses in the LV apex, the right ventricle, and the left atrium, as well as at the base of the tricuspid valve (Figure 1). There was no evidence of a structural heart defect, eg, patent foramen ovale, atrial septal defect, or ventricular septal defect. Cardiovascular magnetic resonance imaging (MRI) confirmed the densities as thrombi (Figure 2). Her ejection fraction was 35%.

Figure 2. Cardiovascular magnetic resonance imaging with contrast enhancement confirmed the presence of thrombi in the right and left ventricles (A) and in the right atrium (B) (arrows).

Blood testing on admission showed a prolonged partial thromboplastin time of 55.0 sec (reference range 22.7–35.6) and a prothrombin time of 13.4 sec (reference range 11.3–14.5). Tissue thromboplastin inhibition at a dilution of 1:50 was elevated at 1.5 sec (reference range 0.7–1.3), as was the tissue thromboplastin inhibition at a dilution of 1:500—ie, 1.6 sec (0.7–1.3). Dilute Russell viper venom testing and anticardiolipin antibody immunoglobulin G and M testing were negative. The lupus antiphospholipid antibody test and the hexagonal lipid neutralization test were positive.

The patient’s clinical presentation of extensive unprovoked venous thrombosis and her laboratory profile together suggested the antiphospholipid antibody syndrome.

SURGICAL TREATMENT NOT AN OPTION

Figure 3. After 4 months of oral anticoagulation therapy, echocardiography (apical four-chamber view) showed near-resolution of the thrombi.

Given her extensive clot burden, surgical thrombectomy was not an option. Instead, warfarin therapy was started and resulted in a progressive diminution of the thrombi. At 4-month follow-up, the thrombi had nearly resolved (Figure 3), and her LV ejection fraction had increased to 45% to 50%. Eighteen months later, she was diagnosed with cholangiocarcinoma. In retrospect, we believe the cancer predisposed the patient to the hypercoagulable state and, subsequently, to thrombosis.

DIAGNOSING AND TREATING LEFT VENTRICULAR THROMBOSIS

Ventricular thrombosis is a serious problem, most commonly associated with extensive myocardial infarction. It is a relatively common complication of myocardial infarction and of ischemic and nonischemic cardiomy-opathies.¹ In this population, the incidence of LV thrombosis is reported to be in the range of 10% to 25%, and it increases with increasing LV end-diastolic diameter, lower ejection fraction, and anterior-wall-motion akinesia, and with the presence of apical aneurysms.² It is an important cause of morbidity and death, whether the thrombus is sessile or mobile.

How diagnostic imaging tests compare

The diagnosis of LV thrombosis requires a certain level of suspicion and has traditionally relied on echocardiography. However, several studies have raised doubt about the sensitivity of echocardiography for the detection of left or right ventricular thrombi.³ In a 2006 report, the sensitivity of transthoracic echocardiography in detecting LV thrombi was 23% and the sensitivity of transesophageal echocardiography was 40%.⁴ In contrast, delayed-enhancement cardiovascular MRI had a sensitivity near 90%. Similarly, in another study,⁵ contrast-enhanced echocardiography had a low but higher sensitivity of nearly 60%.⁵ Therefore, cardiovascular MRI is emerging as the new gold standard test for the detection of this important complication of ventricular dysfunction and myocardial infarction.

Treatment and screening

The optimal management of intraventricular thrombi is poorly defined. It has been suggested from case series that large, mobile, or protruding LV thrombi have more potential for embolization and, therefore, that patients with these findings may benefit from surgical thrombectomy.⁶ Oral anticoagulation has been reported to dissolve intraventricular thrombi, with success rates from 13% to 59%.⁷ A prospective study of enoxaparin in 26 patients with LV thrombi reported resolution rates close to 73% at 3-week follow-up.⁸

There are no guidelines at present on which to base recommendations for screening patients for intracavitary thrombi or for starting empiric anticoagulation in those at risk.

References

Weinsaft JW, Kim HW, Shah DJ, et al. Detection of left ventricular thrombus by delayed-enhancement cardiovascular magnetic resonance prevalence and markers in patients with systolic dysfunction. J Am Coll Cardiol 2008; 52:148–157.
Mollet NR, Dymarkowski S, Volders W, et al. Visualization of ventricular thrombi with contrast-enhanced magnetic resonance imaging in patients with ischemic heart disease. Circulation 2002; 106:2873–2876.
Tsang BK, Platts DG, Javorsky G, Brown MR. Right ventricular thrombus detection and multimodality imaging using contrast echocardiography and cardiac magnetic resonance imaging. Heart Lung Circ 2012; 21:185–188.
Srichai MB, Junor C, Rodriguez LL, et al. Clinical, imaging, and pathological characteristics of left ventricular thrombus: a comparison of contrast-enhanced magnetic resonance imaging, transthoracic echocardiography, and transesophageal echocardiography with surgical or pathological validation. Am Heart J 2006; 152:75–84.
Weinsaft JW, Kim RJ, Ross M, et al. Contrast-enhanced anatomic imaging as compared to contrast-enhanced tissue characterization for detection of left ventricular thrombus. JACC Cardiovasc Imaging 2009; 2:969–979.
Nili M, Deviri E, Jortner R, Strasberg B, Levy MJ. Surgical removal of a mobile, pedunculated left ventricular thrombus: report of 4 cases. Ann Thorac Surg 1988; 46:396–400.
Heik SC, Kupper W, Hamm C, et al. Efficacy of high dose intravenous heparin for treatment of left ventricular thrombi with high embolic risk. J Am Coll Cardiol 1994; 24:1305–1309.
Meurin P, Tabet JY, Renaud N, et al. Treatment of left ventricular thrombi with a low molecular weight heparin. Int J Cardiol 2005; 98:319–323.

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Author and Disclosure Information

Jana G. Hashash, MD
Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA

Nabil S. Zeineh, MD
Division of General Internal Medicine, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA

Frederick W. Crock, MD
Heart and Vascular Institute, University of Pittsburgh Medical Center, Pittsburgh, PA

Address: Jana G. Hashash, MD, Department of Internal Medicine, University of Pittsburgh Medical Center, 200 Lothrop Street, UPMC Montefiore N-713, Pittsburgh, PA 15213; e-mail: [email protected]

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Cleveland Clinic Journal of Medicine - 80(7)

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Cleveland Clinic Journal of Medicine

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Cardiology

Imaging

Hematology

Page Number

415-416

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The Clinical Picture

Author(s)

Jana G. Hashash, MD

Nabil S. Zeineh, MD

Frederick W. Crock, MD

Author(s)

Jana G. Hashash, MD

Nabil S. Zeineh, MD

Frederick W. Crock, MD

Author and Disclosure Information

Jana G. Hashash, MD
Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA

Nabil S. Zeineh, MD
Division of General Internal Medicine, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA

Frederick W. Crock, MD
Heart and Vascular Institute, University of Pittsburgh Medical Center, Pittsburgh, PA

Address: Jana G. Hashash, MD, Department of Internal Medicine, University of Pittsburgh Medical Center, 200 Lothrop Street, UPMC Montefiore N-713, Pittsburgh, PA 15213; e-mail: [email protected]

Author and Disclosure Information

Jana G. Hashash, MD
Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA

Nabil S. Zeineh, MD
Division of General Internal Medicine, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA

Frederick W. Crock, MD
Heart and Vascular Institute, University of Pittsburgh Medical Center, Pittsburgh, PA

Address: Jana G. Hashash, MD, Department of Internal Medicine, University of Pittsburgh Medical Center, 200 Lothrop Street, UPMC Montefiore N-713, Pittsburgh, PA 15213; e-mail: [email protected]

Article PDF

media_e62fd3e_415.pdf

Article PDF

media_e62fd3e_415.pdf

A 60-year-old woman presented with sudden swelling and pain in her right arm. She reported progressive lower-extremity edema and abdominal girth over the past month, associated with shortness of breath and orthopnea. She had a remote history of two spontaneous abortions.

Duplex ultrasonography revealed massive venous thrombosis extending from the antecubital fossa to the right atrium. Transthoracic echocardiography revealed severe left ventricular (LV) dysfunction and multiple echo-dense masses in the LV apex, the right ventricle, and the left atrium, as well as at the base of the tricuspid valve (Figure 1). There was no evidence of a structural heart defect, eg, patent foramen ovale, atrial septal defect, or ventricular septal defect. Cardiovascular magnetic resonance imaging (MRI) confirmed the densities as thrombi (Figure 2). Her ejection fraction was 35%.

Blood testing on admission showed a prolonged partial thromboplastin time of 55.0 sec (reference range 22.7–35.6) and a prothrombin time of 13.4 sec (reference range 11.3–14.5). Tissue thromboplastin inhibition at a dilution of 1:50 was elevated at 1.5 sec (reference range 0.7–1.3), as was the tissue thromboplastin inhibition at a dilution of 1:500—ie, 1.6 sec (0.7–1.3). Dilute Russell viper venom testing and anticardiolipin antibody immunoglobulin G and M testing were negative. The lupus antiphospholipid antibody test and the hexagonal lipid neutralization test were positive.

The patient’s clinical presentation of extensive unprovoked venous thrombosis and her laboratory profile together suggested the antiphospholipid antibody syndrome.

SURGICAL TREATMENT NOT AN OPTION

Given her extensive clot burden, surgical thrombectomy was not an option. Instead, warfarin therapy was started and resulted in a progressive diminution of the thrombi. At 4-month follow-up, the thrombi had nearly resolved (Figure 3), and her LV ejection fraction had increased to 45% to 50%. Eighteen months later, she was diagnosed with cholangiocarcinoma. In retrospect, we believe the cancer predisposed the patient to the hypercoagulable state and, subsequently, to thrombosis.

DIAGNOSING AND TREATING LEFT VENTRICULAR THROMBOSIS

Ventricular thrombosis is a serious problem, most commonly associated with extensive myocardial infarction. It is a relatively common complication of myocardial infarction and of ischemic and nonischemic cardiomy-opathies.¹ In this population, the incidence of LV thrombosis is reported to be in the range of 10% to 25%, and it increases with increasing LV end-diastolic diameter, lower ejection fraction, and anterior-wall-motion akinesia, and with the presence of apical aneurysms.² It is an important cause of morbidity and death, whether the thrombus is sessile or mobile.

How diagnostic imaging tests compare

The diagnosis of LV thrombosis requires a certain level of suspicion and has traditionally relied on echocardiography. However, several studies have raised doubt about the sensitivity of echocardiography for the detection of left or right ventricular thrombi.³ In a 2006 report, the sensitivity of transthoracic echocardiography in detecting LV thrombi was 23% and the sensitivity of transesophageal echocardiography was 40%.⁴ In contrast, delayed-enhancement cardiovascular MRI had a sensitivity near 90%. Similarly, in another study,⁵ contrast-enhanced echocardiography had a low but higher sensitivity of nearly 60%.⁵ Therefore, cardiovascular MRI is emerging as the new gold standard test for the detection of this important complication of ventricular dysfunction and myocardial infarction.

Treatment and screening

The optimal management of intraventricular thrombi is poorly defined. It has been suggested from case series that large, mobile, or protruding LV thrombi have more potential for embolization and, therefore, that patients with these findings may benefit from surgical thrombectomy.⁶ Oral anticoagulation has been reported to dissolve intraventricular thrombi, with success rates from 13% to 59%.⁷ A prospective study of enoxaparin in 26 patients with LV thrombi reported resolution rates close to 73% at 3-week follow-up.⁸

There are no guidelines at present on which to base recommendations for screening patients for intracavitary thrombi or for starting empiric anticoagulation in those at risk.

A 60-year-old woman presented with sudden swelling and pain in her right arm. She reported progressive lower-extremity edema and abdominal girth over the past month, associated with shortness of breath and orthopnea. She had a remote history of two spontaneous abortions.

Duplex ultrasonography revealed massive venous thrombosis extending from the antecubital fossa to the right atrium. Transthoracic echocardiography revealed severe left ventricular (LV) dysfunction and multiple echo-dense masses in the LV apex, the right ventricle, and the left atrium, as well as at the base of the tricuspid valve (Figure 1). There was no evidence of a structural heart defect, eg, patent foramen ovale, atrial septal defect, or ventricular septal defect. Cardiovascular magnetic resonance imaging (MRI) confirmed the densities as thrombi (Figure 2). Her ejection fraction was 35%.

Blood testing on admission showed a prolonged partial thromboplastin time of 55.0 sec (reference range 22.7–35.6) and a prothrombin time of 13.4 sec (reference range 11.3–14.5). Tissue thromboplastin inhibition at a dilution of 1:50 was elevated at 1.5 sec (reference range 0.7–1.3), as was the tissue thromboplastin inhibition at a dilution of 1:500—ie, 1.6 sec (0.7–1.3). Dilute Russell viper venom testing and anticardiolipin antibody immunoglobulin G and M testing were negative. The lupus antiphospholipid antibody test and the hexagonal lipid neutralization test were positive.

The patient’s clinical presentation of extensive unprovoked venous thrombosis and her laboratory profile together suggested the antiphospholipid antibody syndrome.

SURGICAL TREATMENT NOT AN OPTION

Given her extensive clot burden, surgical thrombectomy was not an option. Instead, warfarin therapy was started and resulted in a progressive diminution of the thrombi. At 4-month follow-up, the thrombi had nearly resolved (Figure 3), and her LV ejection fraction had increased to 45% to 50%. Eighteen months later, she was diagnosed with cholangiocarcinoma. In retrospect, we believe the cancer predisposed the patient to the hypercoagulable state and, subsequently, to thrombosis.

DIAGNOSING AND TREATING LEFT VENTRICULAR THROMBOSIS

Ventricular thrombosis is a serious problem, most commonly associated with extensive myocardial infarction. It is a relatively common complication of myocardial infarction and of ischemic and nonischemic cardiomy-opathies.¹ In this population, the incidence of LV thrombosis is reported to be in the range of 10% to 25%, and it increases with increasing LV end-diastolic diameter, lower ejection fraction, and anterior-wall-motion akinesia, and with the presence of apical aneurysms.² It is an important cause of morbidity and death, whether the thrombus is sessile or mobile.

How diagnostic imaging tests compare

The diagnosis of LV thrombosis requires a certain level of suspicion and has traditionally relied on echocardiography. However, several studies have raised doubt about the sensitivity of echocardiography for the detection of left or right ventricular thrombi.³ In a 2006 report, the sensitivity of transthoracic echocardiography in detecting LV thrombi was 23% and the sensitivity of transesophageal echocardiography was 40%.⁴ In contrast, delayed-enhancement cardiovascular MRI had a sensitivity near 90%. Similarly, in another study,⁵ contrast-enhanced echocardiography had a low but higher sensitivity of nearly 60%.⁵ Therefore, cardiovascular MRI is emerging as the new gold standard test for the detection of this important complication of ventricular dysfunction and myocardial infarction.

Treatment and screening

The optimal management of intraventricular thrombi is poorly defined. It has been suggested from case series that large, mobile, or protruding LV thrombi have more potential for embolization and, therefore, that patients with these findings may benefit from surgical thrombectomy.⁶ Oral anticoagulation has been reported to dissolve intraventricular thrombi, with success rates from 13% to 59%.⁷ A prospective study of enoxaparin in 26 patients with LV thrombi reported resolution rates close to 73% at 3-week follow-up.⁸

There are no guidelines at present on which to base recommendations for screening patients for intracavitary thrombi or for starting empiric anticoagulation in those at risk.

References

Weinsaft JW, Kim HW, Shah DJ, et al. Detection of left ventricular thrombus by delayed-enhancement cardiovascular magnetic resonance prevalence and markers in patients with systolic dysfunction. J Am Coll Cardiol 2008; 52:148–157.
Mollet NR, Dymarkowski S, Volders W, et al. Visualization of ventricular thrombi with contrast-enhanced magnetic resonance imaging in patients with ischemic heart disease. Circulation 2002; 106:2873–2876.
Tsang BK, Platts DG, Javorsky G, Brown MR. Right ventricular thrombus detection and multimodality imaging using contrast echocardiography and cardiac magnetic resonance imaging. Heart Lung Circ 2012; 21:185–188.
Srichai MB, Junor C, Rodriguez LL, et al. Clinical, imaging, and pathological characteristics of left ventricular thrombus: a comparison of contrast-enhanced magnetic resonance imaging, transthoracic echocardiography, and transesophageal echocardiography with surgical or pathological validation. Am Heart J 2006; 152:75–84.
Weinsaft JW, Kim RJ, Ross M, et al. Contrast-enhanced anatomic imaging as compared to contrast-enhanced tissue characterization for detection of left ventricular thrombus. JACC Cardiovasc Imaging 2009; 2:969–979.
Nili M, Deviri E, Jortner R, Strasberg B, Levy MJ. Surgical removal of a mobile, pedunculated left ventricular thrombus: report of 4 cases. Ann Thorac Surg 1988; 46:396–400.
Heik SC, Kupper W, Hamm C, et al. Efficacy of high dose intravenous heparin for treatment of left ventricular thrombi with high embolic risk. J Am Coll Cardiol 1994; 24:1305–1309.
Meurin P, Tabet JY, Renaud N, et al. Treatment of left ventricular thrombi with a low molecular weight heparin. Int J Cardiol 2005; 98:319–323.

References

Weinsaft JW, Kim HW, Shah DJ, et al. Detection of left ventricular thrombus by delayed-enhancement cardiovascular magnetic resonance prevalence and markers in patients with systolic dysfunction. J Am Coll Cardiol 2008; 52:148–157.
Mollet NR, Dymarkowski S, Volders W, et al. Visualization of ventricular thrombi with contrast-enhanced magnetic resonance imaging in patients with ischemic heart disease. Circulation 2002; 106:2873–2876.
Tsang BK, Platts DG, Javorsky G, Brown MR. Right ventricular thrombus detection and multimodality imaging using contrast echocardiography and cardiac magnetic resonance imaging. Heart Lung Circ 2012; 21:185–188.
Srichai MB, Junor C, Rodriguez LL, et al. Clinical, imaging, and pathological characteristics of left ventricular thrombus: a comparison of contrast-enhanced magnetic resonance imaging, transthoracic echocardiography, and transesophageal echocardiography with surgical or pathological validation. Am Heart J 2006; 152:75–84.
Weinsaft JW, Kim RJ, Ross M, et al. Contrast-enhanced anatomic imaging as compared to contrast-enhanced tissue characterization for detection of left ventricular thrombus. JACC Cardiovasc Imaging 2009; 2:969–979.
Nili M, Deviri E, Jortner R, Strasberg B, Levy MJ. Surgical removal of a mobile, pedunculated left ventricular thrombus: report of 4 cases. Ann Thorac Surg 1988; 46:396–400.
Heik SC, Kupper W, Hamm C, et al. Efficacy of high dose intravenous heparin for treatment of left ventricular thrombi with high embolic risk. J Am Coll Cardiol 1994; 24:1305–1309.
Meurin P, Tabet JY, Renaud N, et al. Treatment of left ventricular thrombi with a low molecular weight heparin. Int J Cardiol 2005; 98:319–323.