Vascular

CHICAGO – Drug-coated balloons show promise of being a long-sought major advance in the endovascular treatment of stenotic arteriovenous fistulae and grafts for hemodialysis access, Syed M. Hussain, MD, said at a symposium on vascular surgery sponsored by Northwestern University.

Something significantly better than today’s standard treatment options is needed, according to Dr. Hussain. Medicare pays out more than $50 billion annually for the treatment of patients with end-stage renal disease, and a hefty chunk of that money goes for oft-repeated procedures aimed at preserving the patency of the access sites.

[email protected]

CHICAGO – Drug-coated balloons show promise of being a long-sought major advance in the endovascular treatment of stenotic arteriovenous fistulae and grafts for hemodialysis access, Syed M. Hussain, MD, said at a symposium on vascular surgery sponsored by Northwestern University.

Something significantly better than today’s standard treatment options is needed, according to Dr. Hussain. Medicare pays out more than $50 billion annually for the treatment of patients with end-stage renal disease, and a hefty chunk of that money goes for oft-repeated procedures aimed at preserving the patency of the access sites.

[email protected]

CHICAGO – Drug-coated balloons show promise of being a long-sought major advance in the endovascular treatment of stenotic arteriovenous fistulae and grafts for hemodialysis access, Syed M. Hussain, MD, said at a symposium on vascular surgery sponsored by Northwestern University.

Something significantly better than today’s standard treatment options is needed, according to Dr. Hussain. Medicare pays out more than $50 billion annually for the treatment of patients with end-stage renal disease, and a hefty chunk of that money goes for oft-repeated procedures aimed at preserving the patency of the access sites.

[email protected]

See related editorial

WHAT IS ‘EARLY’ SURGERY?

More than 50% of patients with infective endocarditis undergo cardiac surgery during their initial presentation.¹

The 2017 guidelines of the American Association for Thoracic Surgery (AATS) recommend surgery once a surgical indication has been established and effective antimicrobial therapy has been started.²

The American Heart Association/American College of Cardiology (ACC/AHA) guidelines recommend surgery during the initial hospitalization before completion of a full course of antibiotics.³

The European Society of Cardiology guidelines define surgery according to the time since the patient received intravenous antibiotic therapy: emergency surgery is performed within 24 hours of therapy, urgent surgery is performed within a few days, and elective surgery is performed after at least 1 to 2 weeks.⁴

These slight differences are due to the dearth of large randomized trials addressing this question.

INDICATIONS FOR EARLY SURGERY

Left ventricular dysfunction and heart failure

Of all the complications of infectious endocarditis, concomitant heart failure has the greatest impact on prognosis⁵ and is one of the most frequent indications for surgery.⁶

The guidelines recommend emergency surgery during the initial hospitalization for all patients with infective endocarditis who present with refractory pulmonary edema, worsening left ventricular dysfunction, or cardiogenic shock, regardless of whether they have completed a full course of antibiotics. This applies to both native valve endocarditis and prosthetic valve endocarditis.

Uncontrolled persistent infection

Persistent infection is defined as fever and positive cultures persisting after 1 week of appropriate antibiotic treatment.⁴ However, 1 week is a long time. Persistence of positive blood cultures more than 48 to 72 hours after starting antibiotic therapy is associated with poor outcome and is an independent predictor of in-hospital mortality.⁷

The ACC/AHA guidelines recommend early surgery in patients with left-sided infective endocarditis caused by fungi or highly resistant organisms such as vancomycin-resistant enterococci or multidrug-resistant gram-negative bacilli.³ Nonetheless, antibiotic resistance is an unusual reason for expediting surgery unless there are additional indications for it.

Extension of the infection beyond the valve annulus, which occurs in about 30% of cases of native valve endocarditis and 50% of cases of prosthetic valve endocarditis,⁸ is considered a more valid reason to expedite surgery. Similarly, urgent surgery should be considered if there is any evidence of locally uncontrolled infection causing perivalvular abscess, fistula, pseudoaneurysm, or conduction system abnormalities causing atrioventricular nodal block.^2–4

Some authors suggest reviewing the surgical pathology and microbial sequencing of excised cardiac valves after surgery to confirm the diagnosis and identify the culprit pathogen.^9,10

Right-sided infective endocarditis has a more favorable prognosis than left-sided infective endocarditis and usually responds well to medical therapy.¹¹

Nevertheless, surgery for right-sided infective endocarditis should be expedited in patients with right heart failure secondary to severe tricuspid regurgitation with poor response to medical therapy or in the case of large tricuspid valve vegetations.¹² Likewise, recurrent septic pulmonary emboli can be encountered in the setting of right-sided infective endocarditis and are an indication for early surgery.^4,12

Since many patients with right-sided infective endocarditis acquire the infection by intravenous drug use, there is often a reluctance to recommend surgery, given the risk of prosthetic valve infection if they continue to use intravenous drugs.^4,12 One study showed that the risk of death or reoperation between 3 and 6 months after surgery for infective endocarditis was 10 times higher in intravenous drug users. Yet their survival after surgery beyond this period was similar to that of patients with endocarditis who did not inject drugs.¹³ Therefore, the AATS guidelines recommend applying normal indications for surgery to those patients, with emphasis on the need for strict follow-up aimed at addiction treatment.²

Prevention of embolic events

Neurologic embolic events are a frequent complication of infective endocarditis, with the highest risk during the first few days after antibiotics are started. However, this risk decreases significantly after 2 weeks.¹⁴

The timing of surgery largely depends on whether the patient has had previous neurologic embolic events and on the size and mobility of the vegetation. The current guidelines recommend early surgery for recurrent emboli and persistent or enlarging vegetations despite appropriate antibiotic therapy, or in case of large vegetations (> 10 mm) on a native valve even in the absence of embolic events.⁴

A randomized trial by Kang et al¹⁵ demonstrated that, compared with conventional care, early surgery (within 48 hours of diagnosis) in patients with native valve endocarditis with large vegetations (> 10 mm) and severe valve dysfunction was associated with a significant reduction in the risk of death and embolic events.

Timing of surgery after a neurologic complication

Determining the right time for surgery is challenging in patients with infective endocarditis who have had neurologic complications, given the risk of hemorrhagic conversion of existing stroke with anticoagulation or exacerbation of cerebral ischemia in case of intraoperative hypotension. The decision should take into account the severity of cardiac decompensation, weighed against the severity of neurologic symptoms.

In general, surgery should be postponed for at least 4 weeks after intracerebral hemorrhage. However, it should be expedited in the event of silent cerebral embolism or transient ischemic attack, or in patients with infective endocarditis with stroke who have other indications for early surgery, as long as cerebral hemorrhage has been excluded by appropriate imaging.⁴

Early surgery for prosthetic valve endocarditis

The timing of surgery for prosthetic valve endocarditis follows the same general principles as for native valve endocarditis.^2–4,12

One study showed that early surgery for prosthetic valve endocarditis was not associated with lower in-hospital and 1-year mortality rates compared with medical therapy.¹⁶ On the other hand, a subgroup analysis demonstrated surgery to be significantly beneficial in those with the strongest indications for surgery, including severe valve regurgitation, heart failure, paravalvular abscess, fistula, or prosthetic valve dehiscence.

The decision to proceed with surgery in prosthetic valve endocarditis should be weighed carefully, taking into consideration the patient’s overall clinical condition and estimated surgical risk.¹⁶

COLLABORATION IS HELPFUL

Early surgery is indicated for infective endocarditis patients presenting with:

• Refractory heart failure symptoms
• Persistent infection
• Large vegetations with a high risk of embolism.

Expeditious and successful treatment entails multidisciplinary collaboration among experts in cardiology and infectious diseases with access to cardiac surgery input early in the evaluation.

See related editorial

WHAT IS ‘EARLY’ SURGERY?

More than 50% of patients with infective endocarditis undergo cardiac surgery during their initial presentation.¹

The 2017 guidelines of the American Association for Thoracic Surgery (AATS) recommend surgery once a surgical indication has been established and effective antimicrobial therapy has been started.²

The American Heart Association/American College of Cardiology (ACC/AHA) guidelines recommend surgery during the initial hospitalization before completion of a full course of antibiotics.³

The European Society of Cardiology guidelines define surgery according to the time since the patient received intravenous antibiotic therapy: emergency surgery is performed within 24 hours of therapy, urgent surgery is performed within a few days, and elective surgery is performed after at least 1 to 2 weeks.⁴

These slight differences are due to the dearth of large randomized trials addressing this question.

INDICATIONS FOR EARLY SURGERY

Left ventricular dysfunction and heart failure

Of all the complications of infectious endocarditis, concomitant heart failure has the greatest impact on prognosis⁵ and is one of the most frequent indications for surgery.⁶

The guidelines recommend emergency surgery during the initial hospitalization for all patients with infective endocarditis who present with refractory pulmonary edema, worsening left ventricular dysfunction, or cardiogenic shock, regardless of whether they have completed a full course of antibiotics. This applies to both native valve endocarditis and prosthetic valve endocarditis.

Uncontrolled persistent infection

Persistent infection is defined as fever and positive cultures persisting after 1 week of appropriate antibiotic treatment.⁴ However, 1 week is a long time. Persistence of positive blood cultures more than 48 to 72 hours after starting antibiotic therapy is associated with poor outcome and is an independent predictor of in-hospital mortality.⁷

The ACC/AHA guidelines recommend early surgery in patients with left-sided infective endocarditis caused by fungi or highly resistant organisms such as vancomycin-resistant enterococci or multidrug-resistant gram-negative bacilli.³ Nonetheless, antibiotic resistance is an unusual reason for expediting surgery unless there are additional indications for it.

Extension of the infection beyond the valve annulus, which occurs in about 30% of cases of native valve endocarditis and 50% of cases of prosthetic valve endocarditis,⁸ is considered a more valid reason to expedite surgery. Similarly, urgent surgery should be considered if there is any evidence of locally uncontrolled infection causing perivalvular abscess, fistula, pseudoaneurysm, or conduction system abnormalities causing atrioventricular nodal block.^2–4

Some authors suggest reviewing the surgical pathology and microbial sequencing of excised cardiac valves after surgery to confirm the diagnosis and identify the culprit pathogen.^9,10

Right-sided infective endocarditis has a more favorable prognosis than left-sided infective endocarditis and usually responds well to medical therapy.¹¹

Nevertheless, surgery for right-sided infective endocarditis should be expedited in patients with right heart failure secondary to severe tricuspid regurgitation with poor response to medical therapy or in the case of large tricuspid valve vegetations.¹² Likewise, recurrent septic pulmonary emboli can be encountered in the setting of right-sided infective endocarditis and are an indication for early surgery.^4,12

Since many patients with right-sided infective endocarditis acquire the infection by intravenous drug use, there is often a reluctance to recommend surgery, given the risk of prosthetic valve infection if they continue to use intravenous drugs.^4,12 One study showed that the risk of death or reoperation between 3 and 6 months after surgery for infective endocarditis was 10 times higher in intravenous drug users. Yet their survival after surgery beyond this period was similar to that of patients with endocarditis who did not inject drugs.¹³ Therefore, the AATS guidelines recommend applying normal indications for surgery to those patients, with emphasis on the need for strict follow-up aimed at addiction treatment.²

Prevention of embolic events

Neurologic embolic events are a frequent complication of infective endocarditis, with the highest risk during the first few days after antibiotics are started. However, this risk decreases significantly after 2 weeks.¹⁴

The timing of surgery largely depends on whether the patient has had previous neurologic embolic events and on the size and mobility of the vegetation. The current guidelines recommend early surgery for recurrent emboli and persistent or enlarging vegetations despite appropriate antibiotic therapy, or in case of large vegetations (> 10 mm) on a native valve even in the absence of embolic events.⁴

A randomized trial by Kang et al¹⁵ demonstrated that, compared with conventional care, early surgery (within 48 hours of diagnosis) in patients with native valve endocarditis with large vegetations (> 10 mm) and severe valve dysfunction was associated with a significant reduction in the risk of death and embolic events.

Timing of surgery after a neurologic complication

Determining the right time for surgery is challenging in patients with infective endocarditis who have had neurologic complications, given the risk of hemorrhagic conversion of existing stroke with anticoagulation or exacerbation of cerebral ischemia in case of intraoperative hypotension. The decision should take into account the severity of cardiac decompensation, weighed against the severity of neurologic symptoms.

In general, surgery should be postponed for at least 4 weeks after intracerebral hemorrhage. However, it should be expedited in the event of silent cerebral embolism or transient ischemic attack, or in patients with infective endocarditis with stroke who have other indications for early surgery, as long as cerebral hemorrhage has been excluded by appropriate imaging.⁴

Early surgery for prosthetic valve endocarditis

The timing of surgery for prosthetic valve endocarditis follows the same general principles as for native valve endocarditis.^2–4,12

One study showed that early surgery for prosthetic valve endocarditis was not associated with lower in-hospital and 1-year mortality rates compared with medical therapy.¹⁶ On the other hand, a subgroup analysis demonstrated surgery to be significantly beneficial in those with the strongest indications for surgery, including severe valve regurgitation, heart failure, paravalvular abscess, fistula, or prosthetic valve dehiscence.

The decision to proceed with surgery in prosthetic valve endocarditis should be weighed carefully, taking into consideration the patient’s overall clinical condition and estimated surgical risk.¹⁶

COLLABORATION IS HELPFUL

Early surgery is indicated for infective endocarditis patients presenting with:

• Refractory heart failure symptoms
• Persistent infection
• Large vegetations with a high risk of embolism.

Expeditious and successful treatment entails multidisciplinary collaboration among experts in cardiology and infectious diseases with access to cardiac surgery input early in the evaluation.

See related editorial

WHAT IS ‘EARLY’ SURGERY?

More than 50% of patients with infective endocarditis undergo cardiac surgery during their initial presentation.¹

The 2017 guidelines of the American Association for Thoracic Surgery (AATS) recommend surgery once a surgical indication has been established and effective antimicrobial therapy has been started.²

The American Heart Association/American College of Cardiology (ACC/AHA) guidelines recommend surgery during the initial hospitalization before completion of a full course of antibiotics.³

The European Society of Cardiology guidelines define surgery according to the time since the patient received intravenous antibiotic therapy: emergency surgery is performed within 24 hours of therapy, urgent surgery is performed within a few days, and elective surgery is performed after at least 1 to 2 weeks.⁴

These slight differences are due to the dearth of large randomized trials addressing this question.

INDICATIONS FOR EARLY SURGERY

Left ventricular dysfunction and heart failure

Of all the complications of infectious endocarditis, concomitant heart failure has the greatest impact on prognosis⁵ and is one of the most frequent indications for surgery.⁶

The guidelines recommend emergency surgery during the initial hospitalization for all patients with infective endocarditis who present with refractory pulmonary edema, worsening left ventricular dysfunction, or cardiogenic shock, regardless of whether they have completed a full course of antibiotics. This applies to both native valve endocarditis and prosthetic valve endocarditis.

Uncontrolled persistent infection

Persistent infection is defined as fever and positive cultures persisting after 1 week of appropriate antibiotic treatment.⁴ However, 1 week is a long time. Persistence of positive blood cultures more than 48 to 72 hours after starting antibiotic therapy is associated with poor outcome and is an independent predictor of in-hospital mortality.⁷

The ACC/AHA guidelines recommend early surgery in patients with left-sided infective endocarditis caused by fungi or highly resistant organisms such as vancomycin-resistant enterococci or multidrug-resistant gram-negative bacilli.³ Nonetheless, antibiotic resistance is an unusual reason for expediting surgery unless there are additional indications for it.

Extension of the infection beyond the valve annulus, which occurs in about 30% of cases of native valve endocarditis and 50% of cases of prosthetic valve endocarditis,⁸ is considered a more valid reason to expedite surgery. Similarly, urgent surgery should be considered if there is any evidence of locally uncontrolled infection causing perivalvular abscess, fistula, pseudoaneurysm, or conduction system abnormalities causing atrioventricular nodal block.^2–4

Some authors suggest reviewing the surgical pathology and microbial sequencing of excised cardiac valves after surgery to confirm the diagnosis and identify the culprit pathogen.^9,10

Right-sided infective endocarditis has a more favorable prognosis than left-sided infective endocarditis and usually responds well to medical therapy.¹¹

Nevertheless, surgery for right-sided infective endocarditis should be expedited in patients with right heart failure secondary to severe tricuspid regurgitation with poor response to medical therapy or in the case of large tricuspid valve vegetations.¹² Likewise, recurrent septic pulmonary emboli can be encountered in the setting of right-sided infective endocarditis and are an indication for early surgery.^4,12

Since many patients with right-sided infective endocarditis acquire the infection by intravenous drug use, there is often a reluctance to recommend surgery, given the risk of prosthetic valve infection if they continue to use intravenous drugs.^4,12 One study showed that the risk of death or reoperation between 3 and 6 months after surgery for infective endocarditis was 10 times higher in intravenous drug users. Yet their survival after surgery beyond this period was similar to that of patients with endocarditis who did not inject drugs.¹³ Therefore, the AATS guidelines recommend applying normal indications for surgery to those patients, with emphasis on the need for strict follow-up aimed at addiction treatment.²

Prevention of embolic events

Neurologic embolic events are a frequent complication of infective endocarditis, with the highest risk during the first few days after antibiotics are started. However, this risk decreases significantly after 2 weeks.¹⁴

The timing of surgery largely depends on whether the patient has had previous neurologic embolic events and on the size and mobility of the vegetation. The current guidelines recommend early surgery for recurrent emboli and persistent or enlarging vegetations despite appropriate antibiotic therapy, or in case of large vegetations (> 10 mm) on a native valve even in the absence of embolic events.⁴

A randomized trial by Kang et al¹⁵ demonstrated that, compared with conventional care, early surgery (within 48 hours of diagnosis) in patients with native valve endocarditis with large vegetations (> 10 mm) and severe valve dysfunction was associated with a significant reduction in the risk of death and embolic events.

Timing of surgery after a neurologic complication

Determining the right time for surgery is challenging in patients with infective endocarditis who have had neurologic complications, given the risk of hemorrhagic conversion of existing stroke with anticoagulation or exacerbation of cerebral ischemia in case of intraoperative hypotension. The decision should take into account the severity of cardiac decompensation, weighed against the severity of neurologic symptoms.

In general, surgery should be postponed for at least 4 weeks after intracerebral hemorrhage. However, it should be expedited in the event of silent cerebral embolism or transient ischemic attack, or in patients with infective endocarditis with stroke who have other indications for early surgery, as long as cerebral hemorrhage has been excluded by appropriate imaging.⁴

Early surgery for prosthetic valve endocarditis

The timing of surgery for prosthetic valve endocarditis follows the same general principles as for native valve endocarditis.^2–4,12

One study showed that early surgery for prosthetic valve endocarditis was not associated with lower in-hospital and 1-year mortality rates compared with medical therapy.¹⁶ On the other hand, a subgroup analysis demonstrated surgery to be significantly beneficial in those with the strongest indications for surgery, including severe valve regurgitation, heart failure, paravalvular abscess, fistula, or prosthetic valve dehiscence.

The decision to proceed with surgery in prosthetic valve endocarditis should be weighed carefully, taking into consideration the patient’s overall clinical condition and estimated surgical risk.¹⁶

COLLABORATION IS HELPFUL

Early surgery is indicated for infective endocarditis patients presenting with:

• Refractory heart failure symptoms
• Persistent infection
• Large vegetations with a high risk of embolism.

Expeditious and successful treatment entails multidisciplinary collaboration among experts in cardiology and infectious diseases with access to cardiac surgery input early in the evaluation.

In this issue of the Journal, Soud et al discuss the timing of referral of patients with infective endocarditis to surgery.¹ When having this discussion, it is important to understand the nature of the disease and the role of surgery in its treatment.

See related article

Unless successfully treated and cured, infective endocarditis is fatal. It is associated with septic embolism (systemic with left-sided infective endocarditis and pulmonary with right-sided infective endocarditis), destruction of valve tissue, and invasion outside the aortic root or into the atrioventricular groove. Antimicrobials kill sensitive and exposed organisms but cannot reach those hiding in vegetations or biofilm, on foreign material, or in invaded extravascular tissue.

The objectives of surgery are to eliminate the source of embolism, debride and remove infected tissue and foreign material, expose and make residual organisms vulnerable to antimicrobials, and restore functional valves and cardiac integrity. Surgery to treat infective endocarditis is difficult and high-risk and requires an experienced surgeon. But final cure of the infection is still by antimicrobial treatment.

INFECTIVE ENDOCARDITIS NEEDS MULTIDISCIPLINARY CARE

Every aspect of infective endocarditis—diagnosis, medical management, management of complications, and surgery—is difficult. Recent guidelines^2–6 therefore favor care by a multidisciplinary team that includes an infectious disease specialist, cardiologist, and cardiac surgeon from the very beginning, with access to any other needed discipline, often including neurology, neurosurgery, nephrology, and dependence specialists. Patients with infective endocarditis should be referred early to a center with access to a full endocarditis treatment team. The need for surgery and the optimal timing of it are team decisions. The American Association for Thoracic Surgery infective endocarditis guidelines are question-based and address most aspects that surgeons must consider before, during, and after operation.²

IF SURGERY IS INDICATED, IT IS BEST DONE SOONER

Once there is an indication to operate, the operation should be expedited. Delays mean continued risk of disease progression, invasion, heart block, and embolic events. Determining the timing of surgery is difficult in patients who have suffered an embolic stroke—nonhemorrhagic or hemorrhagic—or who have suffered brain bleeding; management of these issues has recently triggered expert opinion and review articles.^7,8 The recommendation for early surgery is based on the conviction that once the patient has been stabilized (or has overwhelming mechanical hemodynamic problems requiring emergency surgery) and adequate antimicrobial coverage is on board, there are no additional benefits to delaying surgery.⁹ When the indication to operate is large mobile vegetations associated with a high risk of stroke, surgery before another event can make all the difference.

In the operating room, the first aspect addressed is adequate debridement. There is wide agreement that repair is preferable to replacement for the mitral and tricuspid valves, but there is no agreement that an allograft (although favored by our team) is the best replacement alternative for a destroyed aortic root. The key is that surgeons and their surgical teams must have the experience and tools that work for them.

Our recommendation is to refer all patients with infective endocarditis to a center with access to a full team of experienced experts able to address all aspects of the disease and its complications.

In this issue of the Journal, Soud et al discuss the timing of referral of patients with infective endocarditis to surgery.¹ When having this discussion, it is important to understand the nature of the disease and the role of surgery in its treatment.

See related article

Unless successfully treated and cured, infective endocarditis is fatal. It is associated with septic embolism (systemic with left-sided infective endocarditis and pulmonary with right-sided infective endocarditis), destruction of valve tissue, and invasion outside the aortic root or into the atrioventricular groove. Antimicrobials kill sensitive and exposed organisms but cannot reach those hiding in vegetations or biofilm, on foreign material, or in invaded extravascular tissue.

The objectives of surgery are to eliminate the source of embolism, debride and remove infected tissue and foreign material, expose and make residual organisms vulnerable to antimicrobials, and restore functional valves and cardiac integrity. Surgery to treat infective endocarditis is difficult and high-risk and requires an experienced surgeon. But final cure of the infection is still by antimicrobial treatment.

INFECTIVE ENDOCARDITIS NEEDS MULTIDISCIPLINARY CARE

Every aspect of infective endocarditis—diagnosis, medical management, management of complications, and surgery—is difficult. Recent guidelines^2–6 therefore favor care by a multidisciplinary team that includes an infectious disease specialist, cardiologist, and cardiac surgeon from the very beginning, with access to any other needed discipline, often including neurology, neurosurgery, nephrology, and dependence specialists. Patients with infective endocarditis should be referred early to a center with access to a full endocarditis treatment team. The need for surgery and the optimal timing of it are team decisions. The American Association for Thoracic Surgery infective endocarditis guidelines are question-based and address most aspects that surgeons must consider before, during, and after operation.²

IF SURGERY IS INDICATED, IT IS BEST DONE SOONER

Once there is an indication to operate, the operation should be expedited. Delays mean continued risk of disease progression, invasion, heart block, and embolic events. Determining the timing of surgery is difficult in patients who have suffered an embolic stroke—nonhemorrhagic or hemorrhagic—or who have suffered brain bleeding; management of these issues has recently triggered expert opinion and review articles.^7,8 The recommendation for early surgery is based on the conviction that once the patient has been stabilized (or has overwhelming mechanical hemodynamic problems requiring emergency surgery) and adequate antimicrobial coverage is on board, there are no additional benefits to delaying surgery.⁹ When the indication to operate is large mobile vegetations associated with a high risk of stroke, surgery before another event can make all the difference.

In the operating room, the first aspect addressed is adequate debridement. There is wide agreement that repair is preferable to replacement for the mitral and tricuspid valves, but there is no agreement that an allograft (although favored by our team) is the best replacement alternative for a destroyed aortic root. The key is that surgeons and their surgical teams must have the experience and tools that work for them.

Our recommendation is to refer all patients with infective endocarditis to a center with access to a full team of experienced experts able to address all aspects of the disease and its complications.

In this issue of the Journal, Soud et al discuss the timing of referral of patients with infective endocarditis to surgery.¹ When having this discussion, it is important to understand the nature of the disease and the role of surgery in its treatment.

See related article

Unless successfully treated and cured, infective endocarditis is fatal. It is associated with septic embolism (systemic with left-sided infective endocarditis and pulmonary with right-sided infective endocarditis), destruction of valve tissue, and invasion outside the aortic root or into the atrioventricular groove. Antimicrobials kill sensitive and exposed organisms but cannot reach those hiding in vegetations or biofilm, on foreign material, or in invaded extravascular tissue.

The objectives of surgery are to eliminate the source of embolism, debride and remove infected tissue and foreign material, expose and make residual organisms vulnerable to antimicrobials, and restore functional valves and cardiac integrity. Surgery to treat infective endocarditis is difficult and high-risk and requires an experienced surgeon. But final cure of the infection is still by antimicrobial treatment.

INFECTIVE ENDOCARDITIS NEEDS MULTIDISCIPLINARY CARE

Every aspect of infective endocarditis—diagnosis, medical management, management of complications, and surgery—is difficult. Recent guidelines^2–6 therefore favor care by a multidisciplinary team that includes an infectious disease specialist, cardiologist, and cardiac surgeon from the very beginning, with access to any other needed discipline, often including neurology, neurosurgery, nephrology, and dependence specialists. Patients with infective endocarditis should be referred early to a center with access to a full endocarditis treatment team. The need for surgery and the optimal timing of it are team decisions. The American Association for Thoracic Surgery infective endocarditis guidelines are question-based and address most aspects that surgeons must consider before, during, and after operation.²

IF SURGERY IS INDICATED, IT IS BEST DONE SOONER

Once there is an indication to operate, the operation should be expedited. Delays mean continued risk of disease progression, invasion, heart block, and embolic events. Determining the timing of surgery is difficult in patients who have suffered an embolic stroke—nonhemorrhagic or hemorrhagic—or who have suffered brain bleeding; management of these issues has recently triggered expert opinion and review articles.^7,8 The recommendation for early surgery is based on the conviction that once the patient has been stabilized (or has overwhelming mechanical hemodynamic problems requiring emergency surgery) and adequate antimicrobial coverage is on board, there are no additional benefits to delaying surgery.⁹ When the indication to operate is large mobile vegetations associated with a high risk of stroke, surgery before another event can make all the difference.

In the operating room, the first aspect addressed is adequate debridement. There is wide agreement that repair is preferable to replacement for the mitral and tricuspid valves, but there is no agreement that an allograft (although favored by our team) is the best replacement alternative for a destroyed aortic root. The key is that surgeons and their surgical teams must have the experience and tools that work for them.

Our recommendation is to refer all patients with infective endocarditis to a center with access to a full team of experienced experts able to address all aspects of the disease and its complications.

Portomesenteric vein thrombosis, a rare but serious complication of the increasingly popular laparoscopic sleeve gastrectomy, can be effectively treated with extended postoperative anticoagulation therapy, findings from a large-scale, retrospective study indicate.

The research was conducted using data from medical records of created by physicians from five Australian bariatric centers, reported Stephanie Bee Ming Tan, MBBS, of the Gold Coast University Hospital, Queensland, Australia, and her associates in the journal Surgery for Obesity and Related Diseases. Following elective laparoscopic sleeve gastrectomy (LSG), a total of 18 (0.3%) of the 5,951 obese patients were diagnosed with portomesenteric vein thrombosis (PVT). The PVT-affected population was a mean age of 44 years and 61% were women. All of these patients had at least one venous thrombosis systematic predisposition factor such as morbid obesity (50%), smoking (50%), or a personal or family history of a clotting disorder (39%).

All study patients were given thromboprophylaxis of low-molecular-weight heparin (LMWH) or unfractionated heparin plus mechanical thromboprophylaxis during admission for LSG and at discharge when surgeons identified them as high risk.

PVT following LSG can be difficult to diagnose because presenting symptoms tend to be nonspecific. Within an average of 13 days following surgery, 77% of patients diagnosed with PVT reported abdominal pain, 33% reported nausea and vomiting, and also reported less common symptoms that included shoulder tip pain, problems in tolerating fluids, constipation, and diarrhea. Final diagnosis of PVT was determined with independent or a combination of CT and duplex ultrasound.

Complications from PVT can have serious consequences, including abdominal swelling from fluid accumulation, enlarged esophageal veins, terminal esophageal bleeding, and bowel infarction. As with admission thromboprophylaxis treatments, patients diagnosed with PVT received varied anticoagulation treatments with most, in equal numbers, receiving either LMWH or a heparin infusion, and the remaining 12% receiving anticoagulation with rivaroxaban and warfarin. Adjustments were made following initial treatments such that 37% and 66% of patients continued with longer-term therapy on LMWH or warfarin, respectively. Treatments generally lasted 3-6 months with only 11% continuing on warfarin because of a history of clotting disorder. The anticoagulation treatments were successful with the majority (94%) of patients with only one patient requiring surgical intervention.

Follow-up with the patients who had a PVT diagnosis of more than 6 months (with an average of 10 months) showed the overall success of the post-LSG anticoagulation and surgical therapies, without any mortalities.

The authors summarized earlier theories about confounding health conditions that may contribute to the development of PVT and the risks for PVT linked to laparoscopic surgery. In this retrospective study, they noted that PVT incidence following LSG was low at 0.3% but was still higher than with two other bariatric operative methods and suggested intraoperative and postoperative factors that could contribute to this difference. Because of the nonspecific early symptoms and the difficulty of diagnosing PVT, the investigators recommended that physicians be vigilant for this postoperative complication in LSG patients, and use “cross-sectional imagining with CT of the abdomen” for diagnosis. Furthermore, with diagnosed PVT “anticoagulation for 3 to 6 months with a target international normalized ratio of 2:3 is recommended unless the patient has additional risk factors and [is] therefore indicated for longer treatment.”

The authors reported that they had no conflicts of interest.

SOURCE: Tan SBM et al. Surg Obes Relat Dis. 2018 Mar;14:271-6.
 

Portomesenteric vein thrombosis, a rare but serious complication of the increasingly popular laparoscopic sleeve gastrectomy, can be effectively treated with extended postoperative anticoagulation therapy, findings from a large-scale, retrospective study indicate.

The research was conducted using data from medical records of created by physicians from five Australian bariatric centers, reported Stephanie Bee Ming Tan, MBBS, of the Gold Coast University Hospital, Queensland, Australia, and her associates in the journal Surgery for Obesity and Related Diseases. Following elective laparoscopic sleeve gastrectomy (LSG), a total of 18 (0.3%) of the 5,951 obese patients were diagnosed with portomesenteric vein thrombosis (PVT). The PVT-affected population was a mean age of 44 years and 61% were women. All of these patients had at least one venous thrombosis systematic predisposition factor such as morbid obesity (50%), smoking (50%), or a personal or family history of a clotting disorder (39%).

All study patients were given thromboprophylaxis of low-molecular-weight heparin (LMWH) or unfractionated heparin plus mechanical thromboprophylaxis during admission for LSG and at discharge when surgeons identified them as high risk.

PVT following LSG can be difficult to diagnose because presenting symptoms tend to be nonspecific. Within an average of 13 days following surgery, 77% of patients diagnosed with PVT reported abdominal pain, 33% reported nausea and vomiting, and also reported less common symptoms that included shoulder tip pain, problems in tolerating fluids, constipation, and diarrhea. Final diagnosis of PVT was determined with independent or a combination of CT and duplex ultrasound.

Complications from PVT can have serious consequences, including abdominal swelling from fluid accumulation, enlarged esophageal veins, terminal esophageal bleeding, and bowel infarction. As with admission thromboprophylaxis treatments, patients diagnosed with PVT received varied anticoagulation treatments with most, in equal numbers, receiving either LMWH or a heparin infusion, and the remaining 12% receiving anticoagulation with rivaroxaban and warfarin. Adjustments were made following initial treatments such that 37% and 66% of patients continued with longer-term therapy on LMWH or warfarin, respectively. Treatments generally lasted 3-6 months with only 11% continuing on warfarin because of a history of clotting disorder. The anticoagulation treatments were successful with the majority (94%) of patients with only one patient requiring surgical intervention.

Follow-up with the patients who had a PVT diagnosis of more than 6 months (with an average of 10 months) showed the overall success of the post-LSG anticoagulation and surgical therapies, without any mortalities.

The authors summarized earlier theories about confounding health conditions that may contribute to the development of PVT and the risks for PVT linked to laparoscopic surgery. In this retrospective study, they noted that PVT incidence following LSG was low at 0.3% but was still higher than with two other bariatric operative methods and suggested intraoperative and postoperative factors that could contribute to this difference. Because of the nonspecific early symptoms and the difficulty of diagnosing PVT, the investigators recommended that physicians be vigilant for this postoperative complication in LSG patients, and use “cross-sectional imagining with CT of the abdomen” for diagnosis. Furthermore, with diagnosed PVT “anticoagulation for 3 to 6 months with a target international normalized ratio of 2:3 is recommended unless the patient has additional risk factors and [is] therefore indicated for longer treatment.”

The authors reported that they had no conflicts of interest.

SOURCE: Tan SBM et al. Surg Obes Relat Dis. 2018 Mar;14:271-6.
 

Portomesenteric vein thrombosis, a rare but serious complication of the increasingly popular laparoscopic sleeve gastrectomy, can be effectively treated with extended postoperative anticoagulation therapy, findings from a large-scale, retrospective study indicate.

The research was conducted using data from medical records of created by physicians from five Australian bariatric centers, reported Stephanie Bee Ming Tan, MBBS, of the Gold Coast University Hospital, Queensland, Australia, and her associates in the journal Surgery for Obesity and Related Diseases. Following elective laparoscopic sleeve gastrectomy (LSG), a total of 18 (0.3%) of the 5,951 obese patients were diagnosed with portomesenteric vein thrombosis (PVT). The PVT-affected population was a mean age of 44 years and 61% were women. All of these patients had at least one venous thrombosis systematic predisposition factor such as morbid obesity (50%), smoking (50%), or a personal or family history of a clotting disorder (39%).

All study patients were given thromboprophylaxis of low-molecular-weight heparin (LMWH) or unfractionated heparin plus mechanical thromboprophylaxis during admission for LSG and at discharge when surgeons identified them as high risk.

PVT following LSG can be difficult to diagnose because presenting symptoms tend to be nonspecific. Within an average of 13 days following surgery, 77% of patients diagnosed with PVT reported abdominal pain, 33% reported nausea and vomiting, and also reported less common symptoms that included shoulder tip pain, problems in tolerating fluids, constipation, and diarrhea. Final diagnosis of PVT was determined with independent or a combination of CT and duplex ultrasound.

Complications from PVT can have serious consequences, including abdominal swelling from fluid accumulation, enlarged esophageal veins, terminal esophageal bleeding, and bowel infarction. As with admission thromboprophylaxis treatments, patients diagnosed with PVT received varied anticoagulation treatments with most, in equal numbers, receiving either LMWH or a heparin infusion, and the remaining 12% receiving anticoagulation with rivaroxaban and warfarin. Adjustments were made following initial treatments such that 37% and 66% of patients continued with longer-term therapy on LMWH or warfarin, respectively. Treatments generally lasted 3-6 months with only 11% continuing on warfarin because of a history of clotting disorder. The anticoagulation treatments were successful with the majority (94%) of patients with only one patient requiring surgical intervention.

Follow-up with the patients who had a PVT diagnosis of more than 6 months (with an average of 10 months) showed the overall success of the post-LSG anticoagulation and surgical therapies, without any mortalities.

The authors summarized earlier theories about confounding health conditions that may contribute to the development of PVT and the risks for PVT linked to laparoscopic surgery. In this retrospective study, they noted that PVT incidence following LSG was low at 0.3% but was still higher than with two other bariatric operative methods and suggested intraoperative and postoperative factors that could contribute to this difference. Because of the nonspecific early symptoms and the difficulty of diagnosing PVT, the investigators recommended that physicians be vigilant for this postoperative complication in LSG patients, and use “cross-sectional imagining with CT of the abdomen” for diagnosis. Furthermore, with diagnosed PVT “anticoagulation for 3 to 6 months with a target international normalized ratio of 2:3 is recommended unless the patient has additional risk factors and [is] therefore indicated for longer treatment.”

The authors reported that they had no conflicts of interest.

SOURCE: Tan SBM et al. Surg Obes Relat Dis. 2018 Mar;14:271-6.
 

A 46-year-old man with poorly controlled hypertension presented with the sudden onset of chest pain and shortness of breath. His blood pressure was 158/96 mm Hg and his left ventricular ejection fraction was less than 20%. He was admitted to the hospital for newly diagnosed heart failure.

SACCULAR AORTIC ANEURYSMS

This case shows the value of carefully examining the chest radiograph, especially behind the heart.

Saccular aneurysms of the descending thoracic aorta are rare and can be easily missed if asymptomatic. They are less common than fusiform aneurysms and may be more prone to rupture. Shang et al¹ identified atherosclerosis as the most frequent cause of saccular aneurysms of the thoracic aorta. However, they can be caused by other inflammatory conditions and infections.¹

Without surgical repair, thoracic aortic aneurysms larger than 6 cm have higher rates of expansion and rupture (a 20% 6-year cumulative risk) than smaller ones.² Mid-descending aortic aneurysms expand faster than those of the ascending aorta.³

Indications for surgery include rupture, severe chest pain, compressive symptoms, large size (eg, ≥ 5.5 cm for asymptomatic descending thoracic aneurysms), and rapid growth rate (≥ 10 mm per year), all of which are associated with a higher mortality rate.⁴

Endovascular grafting should be strongly considered in patients who have significant comorbidities, but this approach may have poorer long-term outcomes compared with open surgery. Blood pressure should be lowered as far as the patient can tolerate without adverse effects, usually with a beta-blocker along with either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker.⁴

Statin therapy to lower the low-density lipoprotein cholesterol level to less than 70 mg/dL is also needed to reduce the risk of complications and cardiovascular disease.

All patients with saccular aortic aneurysm should be followed closely and be evaluated for surgery.

A 46-year-old man with poorly controlled hypertension presented with the sudden onset of chest pain and shortness of breath. His blood pressure was 158/96 mm Hg and his left ventricular ejection fraction was less than 20%. He was admitted to the hospital for newly diagnosed heart failure.

SACCULAR AORTIC ANEURYSMS

This case shows the value of carefully examining the chest radiograph, especially behind the heart.

Saccular aneurysms of the descending thoracic aorta are rare and can be easily missed if asymptomatic. They are less common than fusiform aneurysms and may be more prone to rupture. Shang et al¹ identified atherosclerosis as the most frequent cause of saccular aneurysms of the thoracic aorta. However, they can be caused by other inflammatory conditions and infections.¹

Without surgical repair, thoracic aortic aneurysms larger than 6 cm have higher rates of expansion and rupture (a 20% 6-year cumulative risk) than smaller ones.² Mid-descending aortic aneurysms expand faster than those of the ascending aorta.³

Indications for surgery include rupture, severe chest pain, compressive symptoms, large size (eg, ≥ 5.5 cm for asymptomatic descending thoracic aneurysms), and rapid growth rate (≥ 10 mm per year), all of which are associated with a higher mortality rate.⁴

Endovascular grafting should be strongly considered in patients who have significant comorbidities, but this approach may have poorer long-term outcomes compared with open surgery. Blood pressure should be lowered as far as the patient can tolerate without adverse effects, usually with a beta-blocker along with either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker.⁴

Statin therapy to lower the low-density lipoprotein cholesterol level to less than 70 mg/dL is also needed to reduce the risk of complications and cardiovascular disease.

All patients with saccular aortic aneurysm should be followed closely and be evaluated for surgery.

A 46-year-old man with poorly controlled hypertension presented with the sudden onset of chest pain and shortness of breath. His blood pressure was 158/96 mm Hg and his left ventricular ejection fraction was less than 20%. He was admitted to the hospital for newly diagnosed heart failure.

SACCULAR AORTIC ANEURYSMS

This case shows the value of carefully examining the chest radiograph, especially behind the heart.

Saccular aneurysms of the descending thoracic aorta are rare and can be easily missed if asymptomatic. They are less common than fusiform aneurysms and may be more prone to rupture. Shang et al¹ identified atherosclerosis as the most frequent cause of saccular aneurysms of the thoracic aorta. However, they can be caused by other inflammatory conditions and infections.¹

Without surgical repair, thoracic aortic aneurysms larger than 6 cm have higher rates of expansion and rupture (a 20% 6-year cumulative risk) than smaller ones.² Mid-descending aortic aneurysms expand faster than those of the ascending aorta.³

Indications for surgery include rupture, severe chest pain, compressive symptoms, large size (eg, ≥ 5.5 cm for asymptomatic descending thoracic aneurysms), and rapid growth rate (≥ 10 mm per year), all of which are associated with a higher mortality rate.⁴

Endovascular grafting should be strongly considered in patients who have significant comorbidities, but this approach may have poorer long-term outcomes compared with open surgery. Blood pressure should be lowered as far as the patient can tolerate without adverse effects, usually with a beta-blocker along with either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker.⁴

Statin therapy to lower the low-density lipoprotein cholesterol level to less than 70 mg/dL is also needed to reduce the risk of complications and cardiovascular disease.

All patients with saccular aortic aneurysm should be followed closely and be evaluated for surgery.

To the Editor: We read with great interest the article by Munyon et al¹ addressing recent developments in perioperative medicine. We would like to comment on the perioperative interruption of dual antiplatelet therapy, a common clinical problem.

Several registry analyses have shown that, with second-generation drug-eluting stents, interruption of 1 antiplatelet agent after the first month is safe.^2,3 These registries included a substantial proportion of patients whose index stenting procedure was performed for acute coronary syndrome (up to 60%).² On average, antiplatelet therapy interruption was brief (about 6 to 7 days).

Additional registry analyses have shown that surgery may be safely performed beyond the first month after drug-eluting stent placement.^4,5 Specifically, a large Danish analysis of patients with a drug-eluting stent who underwent noncardiac surgery, matched to control patients without ischemic heart disease, showed that the risk of perioperative myocardial infarction and death was not increased beyond the first month after drug-eluting stent implantation. Specifically, the risk was not increased at the 1- to 2-month and 2- to 12-month postimplantation intervals. Acute coronary syndrome was the indication for stenting in 56% of the patients.

Therefore, while surgery is preferably delayed 6 months after drug-eluting stent implantation (class I recommendation in the European Society of Cardiology guidelines), surgery may be selectively performed 1 to 6 months after drug-eluting stent implantation with an acceptable risk. This is particularly so if the index stenting was performed in the setting of stable coronary arterial disease (class IIa recommendation if stenting was performed in the setting of stable coronary arterial disease without complex procedural features; class IIb recommendation if stenting was performed in the setting of acute coronary syndrome or complex procedural features).⁶ After drug-eluting stent implantation, the earliest cutpoint for considering surgery is 1 month rather than 3 months.

When surgery is performed within this 1- to 6-month interval, thienopyridine interruption should be kept brief and dual antiplatelet therapy reinitiated as soon as possible postoperatively. In fact, when thienopyridine therapy is interrupted 1 to 6 months after drug-eluting stent implantation, stent thrombosis typically occurs more than 6 or 7 days after interruption.⁷

To the Editor: We read with great interest the article by Munyon et al¹ addressing recent developments in perioperative medicine. We would like to comment on the perioperative interruption of dual antiplatelet therapy, a common clinical problem.

Several registry analyses have shown that, with second-generation drug-eluting stents, interruption of 1 antiplatelet agent after the first month is safe.^2,3 These registries included a substantial proportion of patients whose index stenting procedure was performed for acute coronary syndrome (up to 60%).² On average, antiplatelet therapy interruption was brief (about 6 to 7 days).

Additional registry analyses have shown that surgery may be safely performed beyond the first month after drug-eluting stent placement.^4,5 Specifically, a large Danish analysis of patients with a drug-eluting stent who underwent noncardiac surgery, matched to control patients without ischemic heart disease, showed that the risk of perioperative myocardial infarction and death was not increased beyond the first month after drug-eluting stent implantation. Specifically, the risk was not increased at the 1- to 2-month and 2- to 12-month postimplantation intervals. Acute coronary syndrome was the indication for stenting in 56% of the patients.

Therefore, while surgery is preferably delayed 6 months after drug-eluting stent implantation (class I recommendation in the European Society of Cardiology guidelines), surgery may be selectively performed 1 to 6 months after drug-eluting stent implantation with an acceptable risk. This is particularly so if the index stenting was performed in the setting of stable coronary arterial disease (class IIa recommendation if stenting was performed in the setting of stable coronary arterial disease without complex procedural features; class IIb recommendation if stenting was performed in the setting of acute coronary syndrome or complex procedural features).⁶ After drug-eluting stent implantation, the earliest cutpoint for considering surgery is 1 month rather than 3 months.

When surgery is performed within this 1- to 6-month interval, thienopyridine interruption should be kept brief and dual antiplatelet therapy reinitiated as soon as possible postoperatively. In fact, when thienopyridine therapy is interrupted 1 to 6 months after drug-eluting stent implantation, stent thrombosis typically occurs more than 6 or 7 days after interruption.⁷

To the Editor: We read with great interest the article by Munyon et al¹ addressing recent developments in perioperative medicine. We would like to comment on the perioperative interruption of dual antiplatelet therapy, a common clinical problem.

Several registry analyses have shown that, with second-generation drug-eluting stents, interruption of 1 antiplatelet agent after the first month is safe.^2,3 These registries included a substantial proportion of patients whose index stenting procedure was performed for acute coronary syndrome (up to 60%).² On average, antiplatelet therapy interruption was brief (about 6 to 7 days).

Additional registry analyses have shown that surgery may be safely performed beyond the first month after drug-eluting stent placement.^4,5 Specifically, a large Danish analysis of patients with a drug-eluting stent who underwent noncardiac surgery, matched to control patients without ischemic heart disease, showed that the risk of perioperative myocardial infarction and death was not increased beyond the first month after drug-eluting stent implantation. Specifically, the risk was not increased at the 1- to 2-month and 2- to 12-month postimplantation intervals. Acute coronary syndrome was the indication for stenting in 56% of the patients.

Therefore, while surgery is preferably delayed 6 months after drug-eluting stent implantation (class I recommendation in the European Society of Cardiology guidelines), surgery may be selectively performed 1 to 6 months after drug-eluting stent implantation with an acceptable risk. This is particularly so if the index stenting was performed in the setting of stable coronary arterial disease (class IIa recommendation if stenting was performed in the setting of stable coronary arterial disease without complex procedural features; class IIb recommendation if stenting was performed in the setting of acute coronary syndrome or complex procedural features).⁶ After drug-eluting stent implantation, the earliest cutpoint for considering surgery is 1 month rather than 3 months.

When surgery is performed within this 1- to 6-month interval, thienopyridine interruption should be kept brief and dual antiplatelet therapy reinitiated as soon as possible postoperatively. In fact, when thienopyridine therapy is interrupted 1 to 6 months after drug-eluting stent implantation, stent thrombosis typically occurs more than 6 or 7 days after interruption.⁷

In Reply: We reported on publications from 2016–2017 and, unfortunately, at the time we were writing our paper, the European Society of Cardiology (ESC) update on dual antiplatelet therapy¹ had not yet been published. We presented the recommendations from the American College of Cardiology (ACC) and American Heart Association (AHA),² which differ from the recently published ESC guidelines. The ESC suggests that the minimum waiting period after drug-eluting stent placement before noncardiac surgery should be 1 month rather than 3 months but acknowledges that in the setting of complex stenting or recent acute coronary syndrome, 6 months is preferred. The recommendation in this latter scenario is a class IIb C recommendation—essentially expert consensus opinion.

Further, in the study by Egholm et al,³ the event rates in patients undergoing noncardiac surgery in the 1- to 2-month period were numerically higher than in the control group, and no adjusted odds ratios were given. The numbers of events were very low, and a change of only 1 or 2 events in the other direction in the groups would likely make it statistically significant.

All of these recommendations are based on observational studies and registry data, as there are no randomized controlled trials to address this issue. There are many complexities to be accounted for including the type of stent, timing, circumstances surrounding stenting, anatomy, number of stents, patient comorbidities (particularly age, diabetes mellitus, cardiac disease), type of surgery and anesthesia, and perioperative management of antiplatelet therapy. While we acknowledge the ESC recommendation, we would urge caution in the recommendation to wait only 1 month, and in the United States most would prefer to wait 3 months if possible.

In Reply: We reported on publications from 2016–2017 and, unfortunately, at the time we were writing our paper, the European Society of Cardiology (ESC) update on dual antiplatelet therapy¹ had not yet been published. We presented the recommendations from the American College of Cardiology (ACC) and American Heart Association (AHA),² which differ from the recently published ESC guidelines. The ESC suggests that the minimum waiting period after drug-eluting stent placement before noncardiac surgery should be 1 month rather than 3 months but acknowledges that in the setting of complex stenting or recent acute coronary syndrome, 6 months is preferred. The recommendation in this latter scenario is a class IIb C recommendation—essentially expert consensus opinion.

Further, in the study by Egholm et al,³ the event rates in patients undergoing noncardiac surgery in the 1- to 2-month period were numerically higher than in the control group, and no adjusted odds ratios were given. The numbers of events were very low, and a change of only 1 or 2 events in the other direction in the groups would likely make it statistically significant.

All of these recommendations are based on observational studies and registry data, as there are no randomized controlled trials to address this issue. There are many complexities to be accounted for including the type of stent, timing, circumstances surrounding stenting, anatomy, number of stents, patient comorbidities (particularly age, diabetes mellitus, cardiac disease), type of surgery and anesthesia, and perioperative management of antiplatelet therapy. While we acknowledge the ESC recommendation, we would urge caution in the recommendation to wait only 1 month, and in the United States most would prefer to wait 3 months if possible.

In Reply: We reported on publications from 2016–2017 and, unfortunately, at the time we were writing our paper, the European Society of Cardiology (ESC) update on dual antiplatelet therapy¹ had not yet been published. We presented the recommendations from the American College of Cardiology (ACC) and American Heart Association (AHA),² which differ from the recently published ESC guidelines. The ESC suggests that the minimum waiting period after drug-eluting stent placement before noncardiac surgery should be 1 month rather than 3 months but acknowledges that in the setting of complex stenting or recent acute coronary syndrome, 6 months is preferred. The recommendation in this latter scenario is a class IIb C recommendation—essentially expert consensus opinion.

Further, in the study by Egholm et al,³ the event rates in patients undergoing noncardiac surgery in the 1- to 2-month period were numerically higher than in the control group, and no adjusted odds ratios were given. The numbers of events were very low, and a change of only 1 or 2 events in the other direction in the groups would likely make it statistically significant.

All of these recommendations are based on observational studies and registry data, as there are no randomized controlled trials to address this issue. There are many complexities to be accounted for including the type of stent, timing, circumstances surrounding stenting, anatomy, number of stents, patient comorbidities (particularly age, diabetes mellitus, cardiac disease), type of surgery and anesthesia, and perioperative management of antiplatelet therapy. While we acknowledge the ESC recommendation, we would urge caution in the recommendation to wait only 1 month, and in the United States most would prefer to wait 3 months if possible.

CHICAGO – Additional higher quality supporting evidence is needed before endovascular therapies can legitimately be placed on equal footing as an alternative to open surgery in patients with symptomatic common femoral artery stenosis, Jeffrey J. Siracuse, MD, FACS, asserted at a symposium on vascular surgery sponsored by Northwestern University.

“Open surgery in the CFA [common femoral artery] is probably still the gold standard in most cases,” said Dr. Siracuse, a vascular surgeon at Boston University.

Bruce Jancin/MDedge News

He was quick to note that others would disagree. Stenting and other endovascular interventions in the CFA are booming in popularity, particularly among cardiologists, interventional radiologists, and the patients to whom the clinicians present the option in a favorable light. But this enthusiasm is based almost entirely on small, single-center, retrospective studies conducted in patients with heterogeneous profiles. The one prospective randomized multicenter trial of stenting versus surgery for CFA stenosis published to date – the French TECCO study – has a number of key limitations, flaws, and unanswered questions, which endovascular proponents have overlooked in their enthusiasm to promote an “endo-first” approach in the CFA, according to Dr. Siracuse.

“Everyone’s pretty much jumping on the bandwagon now. I think endovascular therapy of the CFA is here to stay. You’re going to see more people doing it, and potentially doing it incorrectly,” he predicted.

“The biggest thing I worry about with stenting is covering or jailing out the deep femoral artery. On multiple occasions – including a case just 2 weeks ago – I’ve taken out stents placed in the CFA by others that developed in-stent hyperplasia to the extent that the entire stent goes down, the DFA is covered, and now all of a sudden you’ve lost all flow to the leg. That’s my biggest concern with stenting,” he said.

Dr. Siracuse has other reservations as well. The CFA has traditionally been considered a “no-stent zone” because of the unique biomechanical stresses the artery is subjected to as a result of torsion, flexion, and extension at the hip joint. These forces render the area particularly vulnerable to neointimal hyperplasia, acute thrombosis, and stent fracture.

The travails of TECCO

The 17-center French TECCO study randomized 117 patients with de novo CFA atherosclerotic lesions to treatment via self-expanding stents or open surgery. A total of 98 participants were Rutherford stage 3, making TECCO primarily a study of claudicants. The primary outcome – the 30-day combined rate of morbidity and mortality – occurred in 26% of the surgical patients, a significantly higher rate than the 12.5% in the stent population. After a median follow-up of 24 months, the rates of primary patency, target lesion and extremity revascularization, and sustained clinical improvement were similar in the two groups (JACC Cardiovasc Interv. 2017 Jul 10;10[13]:1344-54).

The TECCO findings were hailed by endovascular therapy partisans as a big win. However, closer examination tells a different story, according to Dr. Siracuse.

[email protected]

CHICAGO – Additional higher quality supporting evidence is needed before endovascular therapies can legitimately be placed on equal footing as an alternative to open surgery in patients with symptomatic common femoral artery stenosis, Jeffrey J. Siracuse, MD, FACS, asserted at a symposium on vascular surgery sponsored by Northwestern University.

“Open surgery in the CFA [common femoral artery] is probably still the gold standard in most cases,” said Dr. Siracuse, a vascular surgeon at Boston University.

Bruce Jancin/MDedge News

He was quick to note that others would disagree. Stenting and other endovascular interventions in the CFA are booming in popularity, particularly among cardiologists, interventional radiologists, and the patients to whom the clinicians present the option in a favorable light. But this enthusiasm is based almost entirely on small, single-center, retrospective studies conducted in patients with heterogeneous profiles. The one prospective randomized multicenter trial of stenting versus surgery for CFA stenosis published to date – the French TECCO study – has a number of key limitations, flaws, and unanswered questions, which endovascular proponents have overlooked in their enthusiasm to promote an “endo-first” approach in the CFA, according to Dr. Siracuse.

“Everyone’s pretty much jumping on the bandwagon now. I think endovascular therapy of the CFA is here to stay. You’re going to see more people doing it, and potentially doing it incorrectly,” he predicted.

“The biggest thing I worry about with stenting is covering or jailing out the deep femoral artery. On multiple occasions – including a case just 2 weeks ago – I’ve taken out stents placed in the CFA by others that developed in-stent hyperplasia to the extent that the entire stent goes down, the DFA is covered, and now all of a sudden you’ve lost all flow to the leg. That’s my biggest concern with stenting,” he said.

Dr. Siracuse has other reservations as well. The CFA has traditionally been considered a “no-stent zone” because of the unique biomechanical stresses the artery is subjected to as a result of torsion, flexion, and extension at the hip joint. These forces render the area particularly vulnerable to neointimal hyperplasia, acute thrombosis, and stent fracture.

The travails of TECCO

The 17-center French TECCO study randomized 117 patients with de novo CFA atherosclerotic lesions to treatment via self-expanding stents or open surgery. A total of 98 participants were Rutherford stage 3, making TECCO primarily a study of claudicants. The primary outcome – the 30-day combined rate of morbidity and mortality – occurred in 26% of the surgical patients, a significantly higher rate than the 12.5% in the stent population. After a median follow-up of 24 months, the rates of primary patency, target lesion and extremity revascularization, and sustained clinical improvement were similar in the two groups (JACC Cardiovasc Interv. 2017 Jul 10;10[13]:1344-54).

The TECCO findings were hailed by endovascular therapy partisans as a big win. However, closer examination tells a different story, according to Dr. Siracuse.

[email protected]

CHICAGO – Additional higher quality supporting evidence is needed before endovascular therapies can legitimately be placed on equal footing as an alternative to open surgery in patients with symptomatic common femoral artery stenosis, Jeffrey J. Siracuse, MD, FACS, asserted at a symposium on vascular surgery sponsored by Northwestern University.

“Open surgery in the CFA [common femoral artery] is probably still the gold standard in most cases,” said Dr. Siracuse, a vascular surgeon at Boston University.

Bruce Jancin/MDedge News

He was quick to note that others would disagree. Stenting and other endovascular interventions in the CFA are booming in popularity, particularly among cardiologists, interventional radiologists, and the patients to whom the clinicians present the option in a favorable light. But this enthusiasm is based almost entirely on small, single-center, retrospective studies conducted in patients with heterogeneous profiles. The one prospective randomized multicenter trial of stenting versus surgery for CFA stenosis published to date – the French TECCO study – has a number of key limitations, flaws, and unanswered questions, which endovascular proponents have overlooked in their enthusiasm to promote an “endo-first” approach in the CFA, according to Dr. Siracuse.

“Everyone’s pretty much jumping on the bandwagon now. I think endovascular therapy of the CFA is here to stay. You’re going to see more people doing it, and potentially doing it incorrectly,” he predicted.

“The biggest thing I worry about with stenting is covering or jailing out the deep femoral artery. On multiple occasions – including a case just 2 weeks ago – I’ve taken out stents placed in the CFA by others that developed in-stent hyperplasia to the extent that the entire stent goes down, the DFA is covered, and now all of a sudden you’ve lost all flow to the leg. That’s my biggest concern with stenting,” he said.

Dr. Siracuse has other reservations as well. The CFA has traditionally been considered a “no-stent zone” because of the unique biomechanical stresses the artery is subjected to as a result of torsion, flexion, and extension at the hip joint. These forces render the area particularly vulnerable to neointimal hyperplasia, acute thrombosis, and stent fracture.

The travails of TECCO

The 17-center French TECCO study randomized 117 patients with de novo CFA atherosclerotic lesions to treatment via self-expanding stents or open surgery. A total of 98 participants were Rutherford stage 3, making TECCO primarily a study of claudicants. The primary outcome – the 30-day combined rate of morbidity and mortality – occurred in 26% of the surgical patients, a significantly higher rate than the 12.5% in the stent population. After a median follow-up of 24 months, the rates of primary patency, target lesion and extremity revascularization, and sustained clinical improvement were similar in the two groups (JACC Cardiovasc Interv. 2017 Jul 10;10[13]:1344-54).

The TECCO findings were hailed by endovascular therapy partisans as a big win. However, closer examination tells a different story, according to Dr. Siracuse.

[email protected]

Livedo reticularis can be the manifestation of a wide range of conditions: hematologic and hypercoagulable states, embolic events, connective tissue disease, infection, vasculitis, malignancy, neurologic and endocrine conditions, and medication effects.¹ Our patient had no recent history of vascular procedures or peripheral eosinophilia to suggest cholesterol embolization, and he had not recently started taking any new medications. His current medications included aspirin 81 mg, atorvastatin 40 mg, amlodipine 10 mg, and insulin glargine 20 units. Tests for cryoglobulin and antiphospholipid antibodies were negative. There was no evidence of malignancy, and evaluations for infectious and autoimmune diseases were negative.

Biopsy study of a skin lesion showed features consistent with livedo reticularis, with no evidence of vasculitis. The lesions resolved without definitive therapy by hospital day 3. This, in addition to other features of the lesions (eg, uniformity, unbroken reticular segments) and the extensive negative workup for systemic disease, suggested primary livedo reticularis.

CAUSES, TYPES, SUBTYPES

Livedo reticularis results from changes in the cutaneous microvasculature, composed of central arterioles that drain into an interconnecting, netlike venous plexus.^1,2 Conditions such as arteriolar deoxygenation and venous plexus venodilation­ that result in a prominent venous plexus can give rise to clinical livedo reticularis.³

Adapted from information in References 1 and 4.

Primary livedo reticularis is thought to occur from spontaneous arteriolar vasospasm. It is a diagnosis of exclusion. An evaluation for underlying disease is important, as livedo reticularis can be associated with the range of conditions listed above.

In our patient, methamphetamine was considered a possible cause, but the findings of livedo reticularis were delayed and persisted longer than expected if they were drug-related.

Livedo racemosa

Distinguishing livedo reticularis from livedo racemosa is important. Livedo racemosa is always secondary and is often associated with antiphospholipid syndrome. It is present in 25% of cases of primary antiphospholipid syndrome and in up to 70% of cases of antiphospholipid syndrome associated with systemic lupus erythematosus.⁵ The reticular pattern of livedo racemosa is permanent and often has irregular and incomplete segments of reticular lattice, with a distribution that is more generalized,  involving the trunk or buttocks (or both) in addition to the extremities.^3,4 Consequently, a thorough history and physical examination are needed to guide additional workup.

Livedo reticularis can be the manifestation of a wide range of conditions: hematologic and hypercoagulable states, embolic events, connective tissue disease, infection, vasculitis, malignancy, neurologic and endocrine conditions, and medication effects.¹ Our patient had no recent history of vascular procedures or peripheral eosinophilia to suggest cholesterol embolization, and he had not recently started taking any new medications. His current medications included aspirin 81 mg, atorvastatin 40 mg, amlodipine 10 mg, and insulin glargine 20 units. Tests for cryoglobulin and antiphospholipid antibodies were negative. There was no evidence of malignancy, and evaluations for infectious and autoimmune diseases were negative.

Biopsy study of a skin lesion showed features consistent with livedo reticularis, with no evidence of vasculitis. The lesions resolved without definitive therapy by hospital day 3. This, in addition to other features of the lesions (eg, uniformity, unbroken reticular segments) and the extensive negative workup for systemic disease, suggested primary livedo reticularis.

CAUSES, TYPES, SUBTYPES

Livedo reticularis results from changes in the cutaneous microvasculature, composed of central arterioles that drain into an interconnecting, netlike venous plexus.^1,2 Conditions such as arteriolar deoxygenation and venous plexus venodilation­ that result in a prominent venous plexus can give rise to clinical livedo reticularis.³

Adapted from information in References 1 and 4.

Primary livedo reticularis is thought to occur from spontaneous arteriolar vasospasm. It is a diagnosis of exclusion. An evaluation for underlying disease is important, as livedo reticularis can be associated with the range of conditions listed above.

In our patient, methamphetamine was considered a possible cause, but the findings of livedo reticularis were delayed and persisted longer than expected if they were drug-related.

Livedo racemosa

Distinguishing livedo reticularis from livedo racemosa is important. Livedo racemosa is always secondary and is often associated with antiphospholipid syndrome. It is present in 25% of cases of primary antiphospholipid syndrome and in up to 70% of cases of antiphospholipid syndrome associated with systemic lupus erythematosus.⁵ The reticular pattern of livedo racemosa is permanent and often has irregular and incomplete segments of reticular lattice, with a distribution that is more generalized,  involving the trunk or buttocks (or both) in addition to the extremities.^3,4 Consequently, a thorough history and physical examination are needed to guide additional workup.

Livedo reticularis can be the manifestation of a wide range of conditions: hematologic and hypercoagulable states, embolic events, connective tissue disease, infection, vasculitis, malignancy, neurologic and endocrine conditions, and medication effects.¹ Our patient had no recent history of vascular procedures or peripheral eosinophilia to suggest cholesterol embolization, and he had not recently started taking any new medications. His current medications included aspirin 81 mg, atorvastatin 40 mg, amlodipine 10 mg, and insulin glargine 20 units. Tests for cryoglobulin and antiphospholipid antibodies were negative. There was no evidence of malignancy, and evaluations for infectious and autoimmune diseases were negative.

Biopsy study of a skin lesion showed features consistent with livedo reticularis, with no evidence of vasculitis. The lesions resolved without definitive therapy by hospital day 3. This, in addition to other features of the lesions (eg, uniformity, unbroken reticular segments) and the extensive negative workup for systemic disease, suggested primary livedo reticularis.

CAUSES, TYPES, SUBTYPES

Livedo reticularis results from changes in the cutaneous microvasculature, composed of central arterioles that drain into an interconnecting, netlike venous plexus.^1,2 Conditions such as arteriolar deoxygenation and venous plexus venodilation­ that result in a prominent venous plexus can give rise to clinical livedo reticularis.³

Adapted from information in References 1 and 4.

Primary livedo reticularis is thought to occur from spontaneous arteriolar vasospasm. It is a diagnosis of exclusion. An evaluation for underlying disease is important, as livedo reticularis can be associated with the range of conditions listed above.

In our patient, methamphetamine was considered a possible cause, but the findings of livedo reticularis were delayed and persisted longer than expected if they were drug-related.

Livedo racemosa

Distinguishing livedo reticularis from livedo racemosa is important. Livedo racemosa is always secondary and is often associated with antiphospholipid syndrome. It is present in 25% of cases of primary antiphospholipid syndrome and in up to 70% of cases of antiphospholipid syndrome associated with systemic lupus erythematosus.⁵ The reticular pattern of livedo racemosa is permanent and often has irregular and incomplete segments of reticular lattice, with a distribution that is more generalized,  involving the trunk or buttocks (or both) in addition to the extremities.^3,4 Consequently, a thorough history and physical examination are needed to guide additional workup.

In the article, “Update on the management of venous thromboembolism” (Bartholomew JR, Cleve Clin J Med 2017; 84[suppl 3]:39–46), 2 sentences in the text regarding dose reduction for body weight have errors. The corrected sentences follow:

On page 42, left column, the last 5 lines should read: “The recommended dose should be reduced to 2.5 mg twice daily in patients that meet 2 of the following criteria: age 80 or older; body weight of 60 kg or less; or with a serum creatinine 1.5 mg/dL or greater.”

And on page 42, right column, the sentence 10 lines from the top should read: “Edoxaban is given orally at 60 mg once daily but reduced to 30 mg once daily if the CrCL is 30 mL/min to 50 mL/min, if body weight is 60 kg or less, or with use of certain P-glycoprotein inhibitors.”

In the article, “Update on the management of venous thromboembolism” (Bartholomew JR, Cleve Clin J Med 2017; 84[suppl 3]:39–46), 2 sentences in the text regarding dose reduction for body weight have errors. The corrected sentences follow:

On page 42, left column, the last 5 lines should read: “The recommended dose should be reduced to 2.5 mg twice daily in patients that meet 2 of the following criteria: age 80 or older; body weight of 60 kg or less; or with a serum creatinine 1.5 mg/dL or greater.”

And on page 42, right column, the sentence 10 lines from the top should read: “Edoxaban is given orally at 60 mg once daily but reduced to 30 mg once daily if the CrCL is 30 mL/min to 50 mL/min, if body weight is 60 kg or less, or with use of certain P-glycoprotein inhibitors.”

In the article, “Update on the management of venous thromboembolism” (Bartholomew JR, Cleve Clin J Med 2017; 84[suppl 3]:39–46), 2 sentences in the text regarding dose reduction for body weight have errors. The corrected sentences follow:

On page 42, left column, the last 5 lines should read: “The recommended dose should be reduced to 2.5 mg twice daily in patients that meet 2 of the following criteria: age 80 or older; body weight of 60 kg or less; or with a serum creatinine 1.5 mg/dL or greater.”

And on page 42, right column, the sentence 10 lines from the top should read: “Edoxaban is given orally at 60 mg once daily but reduced to 30 mg once daily if the CrCL is 30 mL/min to 50 mL/min, if body weight is 60 kg or less, or with use of certain P-glycoprotein inhibitors.”