Patients treated for acute MI at high-performing hospitals – those with the best performance on 30-day mortality quality measures assessed by the Centers for Medicare & Medicaid Services – had longer life expectancies than did patients treated at low-performing hospitals, according to a report published online Oct. 6 in the New England Journal of Medicine.

This survival benefit persisted through 17 years of follow-up, said Emily Bucholz, MD, of Boston Children’s Hospital, and her associates.

Until now, researchers didn’t know whether the short-term survival benefit at high-performing hospitals would wane over time, which “would lend support to the theory that these hospitals discharge more patients alive but with higher subsequent mortality.” The results of this secondary analysis of data from a nationally representative cohort study indicate that, instead, the superior quality of care delivered at high-performing hospitals appears to “produce an early benefit that endures over time,” Dr. Bucholz and her associates noted. The investigators assessed long-term life expectancy using data from the Cooperative Cardiovascular Project, which enrolled Medicare beneficiaries aged 65 years and older treated for acute MI in 1994-1996. They focused on 119,735 patients admitted to 1,824 hospitals. They grouped the hospitals according to their case mixes (a measure of patients’ severity of illness) and calculated risk-standardized mortality rates according to CMS criteria.

“We found that patients treated at high-performing hospitals ... lived, on average, between 0.74 and 1.14 years longer after acute MI than [did] those treated at low-performing hospitals. These findings were consistent across case-mix strata, which indicates that the relationship between hospital performance and long-term patient outcomes is independent of hospital case mix,” Dr. Bucholz and her associates said (N Engl J Med. 2016 Oct 6. doi: 10.1056/NEJMoa1513223).

These findings show that the early survival advantage achieved by high-performing hospitals is durable, and that “investing in initiatives to improve short-term hospital performance may also improve patient outcomes over the long term,” they added.

Patients treated for acute MI at high-performing hospitals – those with the best performance on 30-day mortality quality measures assessed by the Centers for Medicare & Medicaid Services – had longer life expectancies than did patients treated at low-performing hospitals, according to a report published online Oct. 6 in the New England Journal of Medicine.

This survival benefit persisted through 17 years of follow-up, said Emily Bucholz, MD, of Boston Children’s Hospital, and her associates.

Until now, researchers didn’t know whether the short-term survival benefit at high-performing hospitals would wane over time, which “would lend support to the theory that these hospitals discharge more patients alive but with higher subsequent mortality.” The results of this secondary analysis of data from a nationally representative cohort study indicate that, instead, the superior quality of care delivered at high-performing hospitals appears to “produce an early benefit that endures over time,” Dr. Bucholz and her associates noted. The investigators assessed long-term life expectancy using data from the Cooperative Cardiovascular Project, which enrolled Medicare beneficiaries aged 65 years and older treated for acute MI in 1994-1996. They focused on 119,735 patients admitted to 1,824 hospitals. They grouped the hospitals according to their case mixes (a measure of patients’ severity of illness) and calculated risk-standardized mortality rates according to CMS criteria.

“We found that patients treated at high-performing hospitals ... lived, on average, between 0.74 and 1.14 years longer after acute MI than [did] those treated at low-performing hospitals. These findings were consistent across case-mix strata, which indicates that the relationship between hospital performance and long-term patient outcomes is independent of hospital case mix,” Dr. Bucholz and her associates said (N Engl J Med. 2016 Oct 6. doi: 10.1056/NEJMoa1513223).

These findings show that the early survival advantage achieved by high-performing hospitals is durable, and that “investing in initiatives to improve short-term hospital performance may also improve patient outcomes over the long term,” they added.

Patients treated for acute MI at high-performing hospitals – those with the best performance on 30-day mortality quality measures assessed by the Centers for Medicare & Medicaid Services – had longer life expectancies than did patients treated at low-performing hospitals, according to a report published online Oct. 6 in the New England Journal of Medicine.

This survival benefit persisted through 17 years of follow-up, said Emily Bucholz, MD, of Boston Children’s Hospital, and her associates.

Until now, researchers didn’t know whether the short-term survival benefit at high-performing hospitals would wane over time, which “would lend support to the theory that these hospitals discharge more patients alive but with higher subsequent mortality.” The results of this secondary analysis of data from a nationally representative cohort study indicate that, instead, the superior quality of care delivered at high-performing hospitals appears to “produce an early benefit that endures over time,” Dr. Bucholz and her associates noted. The investigators assessed long-term life expectancy using data from the Cooperative Cardiovascular Project, which enrolled Medicare beneficiaries aged 65 years and older treated for acute MI in 1994-1996. They focused on 119,735 patients admitted to 1,824 hospitals. They grouped the hospitals according to their case mixes (a measure of patients’ severity of illness) and calculated risk-standardized mortality rates according to CMS criteria.

“We found that patients treated at high-performing hospitals ... lived, on average, between 0.74 and 1.14 years longer after acute MI than [did] those treated at low-performing hospitals. These findings were consistent across case-mix strata, which indicates that the relationship between hospital performance and long-term patient outcomes is independent of hospital case mix,” Dr. Bucholz and her associates said (N Engl J Med. 2016 Oct 6. doi: 10.1056/NEJMoa1513223).

These findings show that the early survival advantage achieved by high-performing hospitals is durable, and that “investing in initiatives to improve short-term hospital performance may also improve patient outcomes over the long term,” they added.

To the Editor:

Epidermodysplasia verruciformis (EV) is a rare autosomal-recessive genodermatosis characterized by widespread infection with specific strains of human papillomavirus (HPV). Patients with EV have a unique susceptibility to acquire HPV due to defects in cellular immunity to the presenting antigens.¹ These defects may be related to mutations of the EVER genes or due to acquisition of an immunosuppressive condition.^2,3 Infections with HPV-3 and HPV-10 do not lead to the development of malignancies. However, infection with HPV-5, HPV-8, and HPV-14 can lead to the development of nonmelanoma skin cancers, usually squamous cell carcinomas (SCCs), in approximately 60% of patients.^3,4 This viral condition lasts throughout the patient’s lifetime and presents as tinea versicolor–like macules and patches. These lesions may be confused with seborrheic keratosis or verruca plana.⁵ Lesions typically are hypopigmented but occasionally may be hyperpigmented or erythematous. They often are found on the trunk, but lesions on the face, arms, palms, legs, and soles have been reported.⁵ Mucous membranes are always spared. Epidermodysplasia verruciformis often presents in childhood, except in cases related to acquired immunosuppression. The condition has no sex or racial predilection and no geographical preference.⁵

A 7-year-old boy (Fitzpatrick skin type V) presented with an asymptomatic rash on the trunk (Figure 1), dorsal aspect of the hands, and forehead. The lesions first appeared 5 years prior on the upper back and upper chest and had recently spread to the forehead and frontal aspect of the scalp. The patient had a history of myelomeningocele, which was corrected at birth with surgical placement of a ventriculoperitoneal shunt. The patient was otherwise healthy and met all appropriate developmental milestones for his age group. Family history revealed consanguinity of the patient’s paternal grandparents who were first cousins. The patient’s mother denied any other family member having similar rashes or lesions.

The patient had been treated for pityriasis versicolor on and off for 2 years by another dermatologist. His mother reported faithfully applying ketoconazole cream twice daily for several months with no improvement. She also reported using topical steroids, which did not provide any benefit. The patient and mother denied any associated pruritus, bleeding, burning, or physical discomfort.

Skin examination revealed diffuse, flat, polymorphous, hypopigmented and salmon-colored hyperkeratotic macules and patches with mild scaling on the upper region of the anterior aspect of the chest and upper back (Figure 2A). Additionally, the patient had an extensive number of lesions on the forehead and frontal aspect of the scalp (Figure 2B).

A shave biopsy demonstrated a thick basket weave stratum corneum, koilocytes, and large pale keratinocytes with characteristic blue cytoplasm. These findings were characteristic for EV.

At the patient’s 3-month follow-up visit, he again denied any symptoms associated with the lesions and reported that the appearance was diminishing in severity. On examination there was no evidence of SCC. The mother was advised to discontinue all topical treatments for the patient and return to the office every 3 to 6 months for regular skin surveillance. The mother was further advised to protect the patient from UV radiation with sunscreen and sun-protective clothing.

Epidermodysplasia verruciformis was first reported by Lewandowsky and Lutz⁶ in 1922. This rare condition often presents in childhood and is characterized by a persistent HPV infection and an autosomal-recessive inheritance pattern. Reports in the literature frequently involve kindreds. Often, patients with EV have a family history of first-degree or second-degree consanguinity.⁷

The clinical presentation of EV often resembles a pityriasis versicolor–like eruption. However, pityriasis versicolor is less commonly seen in childhood and is more prevalent in patients aged 21 to 30 years, likely due to increased sebum production and changing hormone levels. Furthermore, it is unusual to see pityriasis versicolor affect the face and scalp.⁸ Lesions of EV vary from hypopigmented and pinkish red macules to confluent patches and hyperkeratotic verrucalike lesions.³ Clinical characteristics also may include dyschromic patches; lesions that resemble flat warts on the trunk, face, and distal arms; and/or lesions that appear similar to seborrheic keratoses on the dorsal aspect of the hands.^9,10

Mutations of the EVER gene downregulate a cell’s ability to adequately attack the HPV antigens.¹¹ Although some patients with EV are found to have mutations of the EVER1 and EVER2 genes, a notable portion of patients with EV lack these mutations. Three other causes of EV include acquisition of immunosuppressive conditions including lymphoma, solid organ transplant, and human immunodeficiency virus. If one suspects autosomal-recessive inheritance of EV, genetic testing such as polymerase chain reaction DNA fragment analysis can be performed to determine if there are mutations on the EVER1 or EVER2 genes.¹²

The inability of patients with EV to mount an immune response to multiple types of HPV increases the risk for developing cutaneous malignancies.⁷ Additionally, it is known that UV radiation diminishes skin cell immunity, and the combination of EV and UV radiation further increases the risk for developing SCCs.¹¹ The development of nonmelanoma skin cancers usually occurs on sun-exposed skin 20 to 30 years after the onset of lesions, with the highest occurrence of SCCs presenting in the fourth decade of life.¹

Protection from UV light exposure is critical to reduce the risk for malignancy. Treatment options for EV lesions have included topical imiquimod 5%, 5-fluorouracil, oral isotretinoin, and intralesional interferon alfa, but patients are often refractory to these interventions. Curettage, surgical excision, electrosurgery, and laser ablation can be effective for individual lesions but carry a greater risk for scarring.¹ Photodynamic therapy with aminolevulinic acid and blue light represents a promising option that deserves further study.

Epidermodysplasia verruciformis should be considered as a differential diagnosis in all patients presenting with disseminated lesions resembling pityriasis versicolor that are unresponsive to treatment. A biopsy will help to establish the diagnosis. Patients should minimize sun exposure and report any skin lesions that are changing in appearance.

To the Editor:

Epidermodysplasia verruciformis (EV) is a rare autosomal-recessive genodermatosis characterized by widespread infection with specific strains of human papillomavirus (HPV). Patients with EV have a unique susceptibility to acquire HPV due to defects in cellular immunity to the presenting antigens.¹ These defects may be related to mutations of the EVER genes or due to acquisition of an immunosuppressive condition.^2,3 Infections with HPV-3 and HPV-10 do not lead to the development of malignancies. However, infection with HPV-5, HPV-8, and HPV-14 can lead to the development of nonmelanoma skin cancers, usually squamous cell carcinomas (SCCs), in approximately 60% of patients.^3,4 This viral condition lasts throughout the patient’s lifetime and presents as tinea versicolor–like macules and patches. These lesions may be confused with seborrheic keratosis or verruca plana.⁵ Lesions typically are hypopigmented but occasionally may be hyperpigmented or erythematous. They often are found on the trunk, but lesions on the face, arms, palms, legs, and soles have been reported.⁵ Mucous membranes are always spared. Epidermodysplasia verruciformis often presents in childhood, except in cases related to acquired immunosuppression. The condition has no sex or racial predilection and no geographical preference.⁵

A 7-year-old boy (Fitzpatrick skin type V) presented with an asymptomatic rash on the trunk (Figure 1), dorsal aspect of the hands, and forehead. The lesions first appeared 5 years prior on the upper back and upper chest and had recently spread to the forehead and frontal aspect of the scalp. The patient had a history of myelomeningocele, which was corrected at birth with surgical placement of a ventriculoperitoneal shunt. The patient was otherwise healthy and met all appropriate developmental milestones for his age group. Family history revealed consanguinity of the patient’s paternal grandparents who were first cousins. The patient’s mother denied any other family member having similar rashes or lesions.

The patient had been treated for pityriasis versicolor on and off for 2 years by another dermatologist. His mother reported faithfully applying ketoconazole cream twice daily for several months with no improvement. She also reported using topical steroids, which did not provide any benefit. The patient and mother denied any associated pruritus, bleeding, burning, or physical discomfort.

Skin examination revealed diffuse, flat, polymorphous, hypopigmented and salmon-colored hyperkeratotic macules and patches with mild scaling on the upper region of the anterior aspect of the chest and upper back (Figure 2A). Additionally, the patient had an extensive number of lesions on the forehead and frontal aspect of the scalp (Figure 2B).

A shave biopsy demonstrated a thick basket weave stratum corneum, koilocytes, and large pale keratinocytes with characteristic blue cytoplasm. These findings were characteristic for EV.

At the patient’s 3-month follow-up visit, he again denied any symptoms associated with the lesions and reported that the appearance was diminishing in severity. On examination there was no evidence of SCC. The mother was advised to discontinue all topical treatments for the patient and return to the office every 3 to 6 months for regular skin surveillance. The mother was further advised to protect the patient from UV radiation with sunscreen and sun-protective clothing.

Epidermodysplasia verruciformis was first reported by Lewandowsky and Lutz⁶ in 1922. This rare condition often presents in childhood and is characterized by a persistent HPV infection and an autosomal-recessive inheritance pattern. Reports in the literature frequently involve kindreds. Often, patients with EV have a family history of first-degree or second-degree consanguinity.⁷

The clinical presentation of EV often resembles a pityriasis versicolor–like eruption. However, pityriasis versicolor is less commonly seen in childhood and is more prevalent in patients aged 21 to 30 years, likely due to increased sebum production and changing hormone levels. Furthermore, it is unusual to see pityriasis versicolor affect the face and scalp.⁸ Lesions of EV vary from hypopigmented and pinkish red macules to confluent patches and hyperkeratotic verrucalike lesions.³ Clinical characteristics also may include dyschromic patches; lesions that resemble flat warts on the trunk, face, and distal arms; and/or lesions that appear similar to seborrheic keratoses on the dorsal aspect of the hands.^9,10

Mutations of the EVER gene downregulate a cell’s ability to adequately attack the HPV antigens.¹¹ Although some patients with EV are found to have mutations of the EVER1 and EVER2 genes, a notable portion of patients with EV lack these mutations. Three other causes of EV include acquisition of immunosuppressive conditions including lymphoma, solid organ transplant, and human immunodeficiency virus. If one suspects autosomal-recessive inheritance of EV, genetic testing such as polymerase chain reaction DNA fragment analysis can be performed to determine if there are mutations on the EVER1 or EVER2 genes.¹²

The inability of patients with EV to mount an immune response to multiple types of HPV increases the risk for developing cutaneous malignancies.⁷ Additionally, it is known that UV radiation diminishes skin cell immunity, and the combination of EV and UV radiation further increases the risk for developing SCCs.¹¹ The development of nonmelanoma skin cancers usually occurs on sun-exposed skin 20 to 30 years after the onset of lesions, with the highest occurrence of SCCs presenting in the fourth decade of life.¹

Protection from UV light exposure is critical to reduce the risk for malignancy. Treatment options for EV lesions have included topical imiquimod 5%, 5-fluorouracil, oral isotretinoin, and intralesional interferon alfa, but patients are often refractory to these interventions. Curettage, surgical excision, electrosurgery, and laser ablation can be effective for individual lesions but carry a greater risk for scarring.¹ Photodynamic therapy with aminolevulinic acid and blue light represents a promising option that deserves further study.

Epidermodysplasia verruciformis should be considered as a differential diagnosis in all patients presenting with disseminated lesions resembling pityriasis versicolor that are unresponsive to treatment. A biopsy will help to establish the diagnosis. Patients should minimize sun exposure and report any skin lesions that are changing in appearance.

To the Editor:

Epidermodysplasia verruciformis (EV) is a rare autosomal-recessive genodermatosis characterized by widespread infection with specific strains of human papillomavirus (HPV). Patients with EV have a unique susceptibility to acquire HPV due to defects in cellular immunity to the presenting antigens.¹ These defects may be related to mutations of the EVER genes or due to acquisition of an immunosuppressive condition.^2,3 Infections with HPV-3 and HPV-10 do not lead to the development of malignancies. However, infection with HPV-5, HPV-8, and HPV-14 can lead to the development of nonmelanoma skin cancers, usually squamous cell carcinomas (SCCs), in approximately 60% of patients.^3,4 This viral condition lasts throughout the patient’s lifetime and presents as tinea versicolor–like macules and patches. These lesions may be confused with seborrheic keratosis or verruca plana.⁵ Lesions typically are hypopigmented but occasionally may be hyperpigmented or erythematous. They often are found on the trunk, but lesions on the face, arms, palms, legs, and soles have been reported.⁵ Mucous membranes are always spared. Epidermodysplasia verruciformis often presents in childhood, except in cases related to acquired immunosuppression. The condition has no sex or racial predilection and no geographical preference.⁵

A 7-year-old boy (Fitzpatrick skin type V) presented with an asymptomatic rash on the trunk (Figure 1), dorsal aspect of the hands, and forehead. The lesions first appeared 5 years prior on the upper back and upper chest and had recently spread to the forehead and frontal aspect of the scalp. The patient had a history of myelomeningocele, which was corrected at birth with surgical placement of a ventriculoperitoneal shunt. The patient was otherwise healthy and met all appropriate developmental milestones for his age group. Family history revealed consanguinity of the patient’s paternal grandparents who were first cousins. The patient’s mother denied any other family member having similar rashes or lesions.

The patient had been treated for pityriasis versicolor on and off for 2 years by another dermatologist. His mother reported faithfully applying ketoconazole cream twice daily for several months with no improvement. She also reported using topical steroids, which did not provide any benefit. The patient and mother denied any associated pruritus, bleeding, burning, or physical discomfort.

Skin examination revealed diffuse, flat, polymorphous, hypopigmented and salmon-colored hyperkeratotic macules and patches with mild scaling on the upper region of the anterior aspect of the chest and upper back (Figure 2A). Additionally, the patient had an extensive number of lesions on the forehead and frontal aspect of the scalp (Figure 2B).

A shave biopsy demonstrated a thick basket weave stratum corneum, koilocytes, and large pale keratinocytes with characteristic blue cytoplasm. These findings were characteristic for EV.

At the patient’s 3-month follow-up visit, he again denied any symptoms associated with the lesions and reported that the appearance was diminishing in severity. On examination there was no evidence of SCC. The mother was advised to discontinue all topical treatments for the patient and return to the office every 3 to 6 months for regular skin surveillance. The mother was further advised to protect the patient from UV radiation with sunscreen and sun-protective clothing.

Epidermodysplasia verruciformis was first reported by Lewandowsky and Lutz⁶ in 1922. This rare condition often presents in childhood and is characterized by a persistent HPV infection and an autosomal-recessive inheritance pattern. Reports in the literature frequently involve kindreds. Often, patients with EV have a family history of first-degree or second-degree consanguinity.⁷

The clinical presentation of EV often resembles a pityriasis versicolor–like eruption. However, pityriasis versicolor is less commonly seen in childhood and is more prevalent in patients aged 21 to 30 years, likely due to increased sebum production and changing hormone levels. Furthermore, it is unusual to see pityriasis versicolor affect the face and scalp.⁸ Lesions of EV vary from hypopigmented and pinkish red macules to confluent patches and hyperkeratotic verrucalike lesions.³ Clinical characteristics also may include dyschromic patches; lesions that resemble flat warts on the trunk, face, and distal arms; and/or lesions that appear similar to seborrheic keratoses on the dorsal aspect of the hands.^9,10

Mutations of the EVER gene downregulate a cell’s ability to adequately attack the HPV antigens.¹¹ Although some patients with EV are found to have mutations of the EVER1 and EVER2 genes, a notable portion of patients with EV lack these mutations. Three other causes of EV include acquisition of immunosuppressive conditions including lymphoma, solid organ transplant, and human immunodeficiency virus. If one suspects autosomal-recessive inheritance of EV, genetic testing such as polymerase chain reaction DNA fragment analysis can be performed to determine if there are mutations on the EVER1 or EVER2 genes.¹²

The inability of patients with EV to mount an immune response to multiple types of HPV increases the risk for developing cutaneous malignancies.⁷ Additionally, it is known that UV radiation diminishes skin cell immunity, and the combination of EV and UV radiation further increases the risk for developing SCCs.¹¹ The development of nonmelanoma skin cancers usually occurs on sun-exposed skin 20 to 30 years after the onset of lesions, with the highest occurrence of SCCs presenting in the fourth decade of life.¹

Protection from UV light exposure is critical to reduce the risk for malignancy. Treatment options for EV lesions have included topical imiquimod 5%, 5-fluorouracil, oral isotretinoin, and intralesional interferon alfa, but patients are often refractory to these interventions. Curettage, surgical excision, electrosurgery, and laser ablation can be effective for individual lesions but carry a greater risk for scarring.¹ Photodynamic therapy with aminolevulinic acid and blue light represents a promising option that deserves further study.

Epidermodysplasia verruciformis should be considered as a differential diagnosis in all patients presenting with disseminated lesions resembling pityriasis versicolor that are unresponsive to treatment. A biopsy will help to establish the diagnosis. Patients should minimize sun exposure and report any skin lesions that are changing in appearance.

To the Editor:

Chondroid syringoma is a rare benign mixed tumor that originates from the sweat glands, typically presenting with both epithelial and mesenchymal components.¹ It differs from pleomorphic adenoma, which arises from salivary glands. The surgical approach for complete excision is different for the 2 tumors; therefore, definitive diagnosis is important. For chondroid syringoma, total excision is recommended,² while for pleomorphic adenoma, extracapsular dissection or superficial parotidectomy is commonly indicated. We report a case of a preauricular nodule at presentation and highlight the importance of differentiating a chondroid syringoma from a pleomorphic adenoma. This case is unique because of the anatomic location of the nodule, making diagnosis difficult because the tumor was abutting the parotid gland and a biopsy included normal salivary gland cells.

A 19-year-old man with a history of moderate acne on the shoulders, back, and face presented with a rapidly growing, painless nodule on right preauricular region of 6 months’ duration. The nodule was originally thought to be acne related and monitored, as the patient was asymptomatic. On examination the patient was found to have a firm, fixed, nontender, subcutaneous nodule overlying the right temporomandibular joint just anterior to the right tragus (Figure 1). Laboratory results were unremarkable. Computed tomography showed a subcutaneous nonaggressive-appearing soft-tissue mass measuring 16×17×12 mm just anterior and inferior to the external auditory canal cartilaginous segment with no bony abnormalities. The patient was initially treated with incomplete excision of the area for a presumed sebaceous cyst; 2 months later, an abnormal biopsy prompted a complete excisional biopsy.

Histologically, the initial incomplete excision biopsy revealed myxoid and chondroid tissue with glandular elements and adjacent lymph node with strong positivity for S-100 protein and moderate positivity for glial fibrillary acid protein, consistent with chondroid syringoma (Figure 2). Histological findings on second excision biopsy performed 2 months later showed tumor cells surrounded by normal salivary gland cells; therefore, it was difficult to define the origin of this tumor. Subsequent magnetic resonance imaging showed no evidence of the tumor and normal parotid gland borders.

Chondroid syringoma is a rare nonmelanoma skin tumor of the head and neck, mostly benign in nature but with malignant potential. Predominantly, it presents in males as an asymptomatic, slow-growing, nontender nodule.² Malignant chondroid syringomas are more rare, typically appear on the trunk and legs of females, and present as rapidly growing hard nodules. They can arise de novo or from a preexisting chondroid syringoma and can metastasize.^3,4

Clinically and histologically, chondroid syringoma resembles a pleomorphic adenoma. Its diagnosis is dependent on the clinical location to exclude origin in a salivary gland.⁵ Folliculosebaceous and myoepithelial differentiation within the tumor has been reported.⁶ Immunocytochemistry is the same in both types and is used to identify 2 prominent components—epithelial and mesenchymal—found in both chondroid syringoma and pleomorphic adenoma. Immunocytochemistry differentiates the epithelial component, which expresses cytokeratin, epithelial membrane antigen, and carcinoembryonic antigen. In contrast, the mesenchymal component expresses S-100, vimentin, and neuron‐specific enolase, and less often glial fibrillary acidic protein, smooth muscle actin, calponin, or p63.^5,7,8 Identification of both layers is a distinctive trait of both tumors, rendering it apart from other conditions in the differential diagnosis.⁵

Typical treatment options include excision, electrodesiccation, dermabrasion, and argon or CO₂ laser. Total excision is recommended if there is a benign tumor and complete excision is a cure.² One case of recurrent benign chondroid syringoma was treated by Mohs micrographic surgery on the eyebrow⁹; however, Mohs surgery was not recommended in our case due to concerns of spread if malignant as well as an unknown tumor depth, as these tumors have a tendency for deep infiltration.

Due to its anatomical location and presentation as an anterior preauricular mass, it was difficult to differentiate between chondroid syringoma from sweat gland origin and pleomorphic adenoma from the salivary gland. As seen in our case, it is important for physicians to be aware of the differential diagnosis for mixed tumors because it can have a notable effect on the type of surgical therapy and follow-up management.

To the Editor:

Chondroid syringoma is a rare benign mixed tumor that originates from the sweat glands, typically presenting with both epithelial and mesenchymal components.¹ It differs from pleomorphic adenoma, which arises from salivary glands. The surgical approach for complete excision is different for the 2 tumors; therefore, definitive diagnosis is important. For chondroid syringoma, total excision is recommended,² while for pleomorphic adenoma, extracapsular dissection or superficial parotidectomy is commonly indicated. We report a case of a preauricular nodule at presentation and highlight the importance of differentiating a chondroid syringoma from a pleomorphic adenoma. This case is unique because of the anatomic location of the nodule, making diagnosis difficult because the tumor was abutting the parotid gland and a biopsy included normal salivary gland cells.

A 19-year-old man with a history of moderate acne on the shoulders, back, and face presented with a rapidly growing, painless nodule on right preauricular region of 6 months’ duration. The nodule was originally thought to be acne related and monitored, as the patient was asymptomatic. On examination the patient was found to have a firm, fixed, nontender, subcutaneous nodule overlying the right temporomandibular joint just anterior to the right tragus (Figure 1). Laboratory results were unremarkable. Computed tomography showed a subcutaneous nonaggressive-appearing soft-tissue mass measuring 16×17×12 mm just anterior and inferior to the external auditory canal cartilaginous segment with no bony abnormalities. The patient was initially treated with incomplete excision of the area for a presumed sebaceous cyst; 2 months later, an abnormal biopsy prompted a complete excisional biopsy.

Histologically, the initial incomplete excision biopsy revealed myxoid and chondroid tissue with glandular elements and adjacent lymph node with strong positivity for S-100 protein and moderate positivity for glial fibrillary acid protein, consistent with chondroid syringoma (Figure 2). Histological findings on second excision biopsy performed 2 months later showed tumor cells surrounded by normal salivary gland cells; therefore, it was difficult to define the origin of this tumor. Subsequent magnetic resonance imaging showed no evidence of the tumor and normal parotid gland borders.

Chondroid syringoma is a rare nonmelanoma skin tumor of the head and neck, mostly benign in nature but with malignant potential. Predominantly, it presents in males as an asymptomatic, slow-growing, nontender nodule.² Malignant chondroid syringomas are more rare, typically appear on the trunk and legs of females, and present as rapidly growing hard nodules. They can arise de novo or from a preexisting chondroid syringoma and can metastasize.^3,4

Clinically and histologically, chondroid syringoma resembles a pleomorphic adenoma. Its diagnosis is dependent on the clinical location to exclude origin in a salivary gland.⁵ Folliculosebaceous and myoepithelial differentiation within the tumor has been reported.⁶ Immunocytochemistry is the same in both types and is used to identify 2 prominent components—epithelial and mesenchymal—found in both chondroid syringoma and pleomorphic adenoma. Immunocytochemistry differentiates the epithelial component, which expresses cytokeratin, epithelial membrane antigen, and carcinoembryonic antigen. In contrast, the mesenchymal component expresses S-100, vimentin, and neuron‐specific enolase, and less often glial fibrillary acidic protein, smooth muscle actin, calponin, or p63.^5,7,8 Identification of both layers is a distinctive trait of both tumors, rendering it apart from other conditions in the differential diagnosis.⁵

Typical treatment options include excision, electrodesiccation, dermabrasion, and argon or CO₂ laser. Total excision is recommended if there is a benign tumor and complete excision is a cure.² One case of recurrent benign chondroid syringoma was treated by Mohs micrographic surgery on the eyebrow⁹; however, Mohs surgery was not recommended in our case due to concerns of spread if malignant as well as an unknown tumor depth, as these tumors have a tendency for deep infiltration.

Due to its anatomical location and presentation as an anterior preauricular mass, it was difficult to differentiate between chondroid syringoma from sweat gland origin and pleomorphic adenoma from the salivary gland. As seen in our case, it is important for physicians to be aware of the differential diagnosis for mixed tumors because it can have a notable effect on the type of surgical therapy and follow-up management.

To the Editor:

Chondroid syringoma is a rare benign mixed tumor that originates from the sweat glands, typically presenting with both epithelial and mesenchymal components.¹ It differs from pleomorphic adenoma, which arises from salivary glands. The surgical approach for complete excision is different for the 2 tumors; therefore, definitive diagnosis is important. For chondroid syringoma, total excision is recommended,² while for pleomorphic adenoma, extracapsular dissection or superficial parotidectomy is commonly indicated. We report a case of a preauricular nodule at presentation and highlight the importance of differentiating a chondroid syringoma from a pleomorphic adenoma. This case is unique because of the anatomic location of the nodule, making diagnosis difficult because the tumor was abutting the parotid gland and a biopsy included normal salivary gland cells.

A 19-year-old man with a history of moderate acne on the shoulders, back, and face presented with a rapidly growing, painless nodule on right preauricular region of 6 months’ duration. The nodule was originally thought to be acne related and monitored, as the patient was asymptomatic. On examination the patient was found to have a firm, fixed, nontender, subcutaneous nodule overlying the right temporomandibular joint just anterior to the right tragus (Figure 1). Laboratory results were unremarkable. Computed tomography showed a subcutaneous nonaggressive-appearing soft-tissue mass measuring 16×17×12 mm just anterior and inferior to the external auditory canal cartilaginous segment with no bony abnormalities. The patient was initially treated with incomplete excision of the area for a presumed sebaceous cyst; 2 months later, an abnormal biopsy prompted a complete excisional biopsy.

Histologically, the initial incomplete excision biopsy revealed myxoid and chondroid tissue with glandular elements and adjacent lymph node with strong positivity for S-100 protein and moderate positivity for glial fibrillary acid protein, consistent with chondroid syringoma (Figure 2). Histological findings on second excision biopsy performed 2 months later showed tumor cells surrounded by normal salivary gland cells; therefore, it was difficult to define the origin of this tumor. Subsequent magnetic resonance imaging showed no evidence of the tumor and normal parotid gland borders.

Chondroid syringoma is a rare nonmelanoma skin tumor of the head and neck, mostly benign in nature but with malignant potential. Predominantly, it presents in males as an asymptomatic, slow-growing, nontender nodule.² Malignant chondroid syringomas are more rare, typically appear on the trunk and legs of females, and present as rapidly growing hard nodules. They can arise de novo or from a preexisting chondroid syringoma and can metastasize.^3,4

Clinically and histologically, chondroid syringoma resembles a pleomorphic adenoma. Its diagnosis is dependent on the clinical location to exclude origin in a salivary gland.⁵ Folliculosebaceous and myoepithelial differentiation within the tumor has been reported.⁶ Immunocytochemistry is the same in both types and is used to identify 2 prominent components—epithelial and mesenchymal—found in both chondroid syringoma and pleomorphic adenoma. Immunocytochemistry differentiates the epithelial component, which expresses cytokeratin, epithelial membrane antigen, and carcinoembryonic antigen. In contrast, the mesenchymal component expresses S-100, vimentin, and neuron‐specific enolase, and less often glial fibrillary acidic protein, smooth muscle actin, calponin, or p63.^5,7,8 Identification of both layers is a distinctive trait of both tumors, rendering it apart from other conditions in the differential diagnosis.⁵

Typical treatment options include excision, electrodesiccation, dermabrasion, and argon or CO₂ laser. Total excision is recommended if there is a benign tumor and complete excision is a cure.² One case of recurrent benign chondroid syringoma was treated by Mohs micrographic surgery on the eyebrow⁹; however, Mohs surgery was not recommended in our case due to concerns of spread if malignant as well as an unknown tumor depth, as these tumors have a tendency for deep infiltration.

Due to its anatomical location and presentation as an anterior preauricular mass, it was difficult to differentiate between chondroid syringoma from sweat gland origin and pleomorphic adenoma from the salivary gland. As seen in our case, it is important for physicians to be aware of the differential diagnosis for mixed tumors because it can have a notable effect on the type of surgical therapy and follow-up management.

The majority of lawsuits against internists stem from alleged diagnostics errors, results of a new study show.

Of 1,180 legal claims against internists, 39% were related to failed, delayed, or wrong diagnosis allegations, according to an analysis published by The Doctors Company, a nationwide medical malpractice insurer. Negligence associated with medical treatment accounted for 32% of the claims, while 19% were related to alleged medication errors.

The Doctors Company evaluated 1,180 claims from its database against internal medicine physicians that closed from 2007 to 2014. Of diagnostic-related cases, 56% alleged inadequate patient assessments, such as failure to order or delay in ordering diagnostic tests. The final diagnoses most commonly related to these allegations were myocardial infarction (6%), lung cancer (5%), and colorectal cancer (5%). More than 200 other diagnoses were seen in fewer than 2% of the claims, according to the study.

[email protected]

On Twitter @legal_med

The majority of lawsuits against internists stem from alleged diagnostics errors, results of a new study show.

Of 1,180 legal claims against internists, 39% were related to failed, delayed, or wrong diagnosis allegations, according to an analysis published by The Doctors Company, a nationwide medical malpractice insurer. Negligence associated with medical treatment accounted for 32% of the claims, while 19% were related to alleged medication errors.

The Doctors Company evaluated 1,180 claims from its database against internal medicine physicians that closed from 2007 to 2014. Of diagnostic-related cases, 56% alleged inadequate patient assessments, such as failure to order or delay in ordering diagnostic tests. The final diagnoses most commonly related to these allegations were myocardial infarction (6%), lung cancer (5%), and colorectal cancer (5%). More than 200 other diagnoses were seen in fewer than 2% of the claims, according to the study.

[email protected]

On Twitter @legal_med

The majority of lawsuits against internists stem from alleged diagnostics errors, results of a new study show.

Of 1,180 legal claims against internists, 39% were related to failed, delayed, or wrong diagnosis allegations, according to an analysis published by The Doctors Company, a nationwide medical malpractice insurer. Negligence associated with medical treatment accounted for 32% of the claims, while 19% were related to alleged medication errors.

The Doctors Company evaluated 1,180 claims from its database against internal medicine physicians that closed from 2007 to 2014. Of diagnostic-related cases, 56% alleged inadequate patient assessments, such as failure to order or delay in ordering diagnostic tests. The final diagnoses most commonly related to these allegations were myocardial infarction (6%), lung cancer (5%), and colorectal cancer (5%). More than 200 other diagnoses were seen in fewer than 2% of the claims, according to the study.

[email protected]

On Twitter @legal_med

Influenza vaccine coverage among U.S. health care personnel increased very slightly during the 2015-2016 flu season, with 79% reporting that they received the shot, compared with 77% in 2014-2015.

Hospital personnel were most likely to be covered (91%) and long-term care personnel least likely to be covered (69%), Carla L. Black, PhD, wrote in the Sept. 30 issue of Morbidity and Mortality Weekly Report (2016;65:1026-31). Coverage among health care personnel working in long-term care settings did increase, however, from 64% in the 2014-2015 seasons to 69% in the 2015-2016 season, Dr. Black and colleagues noted.

“Although low, this is the only setting with an appreciable increase in coverage, compared with last season. Influenza vaccination among health care personnel in long-term care settings is especially important because influenza vaccine effectiveness is generally lowest in the elderly,” according to Dr Black, an epidemiologist with the Centers for Disease Control and Prevention.

CDC conducted the Internet survey of 2,258 health care workers from March to April, 2016.

Physicians had the highest level of coverage (95.6%), while health care assistants and aides had the lowest (64.5%). Employers also exerted an influence on coverage. Most respondents (73%) were vaccinated at work. Coverage was highest (96.5%) at facilities where vaccination was required and lowest (45%) where vaccination was not required, promoted, or offered on site.

“Employer vaccination requirements likely contributed to the observed gradual increase in vaccination among health care personnel working in settings with the lowest coverage,” the investigators noted. “In the absence of vaccination requirements, expanding the number of health care locations offering vaccination on site, over multiple days, and at no cost might help sustain and improve influenza vaccination coverage among health care personnel, including in long-term care settings.”

As a CDC employee, Dr. Black has no financial conflicts.

[email protected]

Influenza vaccine coverage among U.S. health care personnel increased very slightly during the 2015-2016 flu season, with 79% reporting that they received the shot, compared with 77% in 2014-2015.

Hospital personnel were most likely to be covered (91%) and long-term care personnel least likely to be covered (69%), Carla L. Black, PhD, wrote in the Sept. 30 issue of Morbidity and Mortality Weekly Report (2016;65:1026-31). Coverage among health care personnel working in long-term care settings did increase, however, from 64% in the 2014-2015 seasons to 69% in the 2015-2016 season, Dr. Black and colleagues noted.

“Although low, this is the only setting with an appreciable increase in coverage, compared with last season. Influenza vaccination among health care personnel in long-term care settings is especially important because influenza vaccine effectiveness is generally lowest in the elderly,” according to Dr Black, an epidemiologist with the Centers for Disease Control and Prevention.

CDC conducted the Internet survey of 2,258 health care workers from March to April, 2016.

Physicians had the highest level of coverage (95.6%), while health care assistants and aides had the lowest (64.5%). Employers also exerted an influence on coverage. Most respondents (73%) were vaccinated at work. Coverage was highest (96.5%) at facilities where vaccination was required and lowest (45%) where vaccination was not required, promoted, or offered on site.

“Employer vaccination requirements likely contributed to the observed gradual increase in vaccination among health care personnel working in settings with the lowest coverage,” the investigators noted. “In the absence of vaccination requirements, expanding the number of health care locations offering vaccination on site, over multiple days, and at no cost might help sustain and improve influenza vaccination coverage among health care personnel, including in long-term care settings.”

As a CDC employee, Dr. Black has no financial conflicts.

[email protected]

Influenza vaccine coverage among U.S. health care personnel increased very slightly during the 2015-2016 flu season, with 79% reporting that they received the shot, compared with 77% in 2014-2015.

Hospital personnel were most likely to be covered (91%) and long-term care personnel least likely to be covered (69%), Carla L. Black, PhD, wrote in the Sept. 30 issue of Morbidity and Mortality Weekly Report (2016;65:1026-31). Coverage among health care personnel working in long-term care settings did increase, however, from 64% in the 2014-2015 seasons to 69% in the 2015-2016 season, Dr. Black and colleagues noted.

“Although low, this is the only setting with an appreciable increase in coverage, compared with last season. Influenza vaccination among health care personnel in long-term care settings is especially important because influenza vaccine effectiveness is generally lowest in the elderly,” according to Dr Black, an epidemiologist with the Centers for Disease Control and Prevention.

CDC conducted the Internet survey of 2,258 health care workers from March to April, 2016.

Physicians had the highest level of coverage (95.6%), while health care assistants and aides had the lowest (64.5%). Employers also exerted an influence on coverage. Most respondents (73%) were vaccinated at work. Coverage was highest (96.5%) at facilities where vaccination was required and lowest (45%) where vaccination was not required, promoted, or offered on site.

“Employer vaccination requirements likely contributed to the observed gradual increase in vaccination among health care personnel working in settings with the lowest coverage,” the investigators noted. “In the absence of vaccination requirements, expanding the number of health care locations offering vaccination on site, over multiple days, and at no cost might help sustain and improve influenza vaccination coverage among health care personnel, including in long-term care settings.”

As a CDC employee, Dr. Black has no financial conflicts.

[email protected]

PORTLAND, ORE. – More than half of overweight, nondiabetic people with Parkinson’s disease were insulin resistant even though most had normal fasting glucose and insulin levels in a prospective, observational study, raising concerns about the potential role of insulin resistance in accelerating the progression of neurodegenerative diseases, including certain features of Parkinson’s disease.

Researchers at Cedars-Sinai Medical Center in Los Angeles tested 93 patients with Parkinson’s disease to determine the prevalence of undiagnosed insulin resistance (IR). They used the homeostatic model assessment of insulin resistance (HOMA-IR) formula, with a HOMA-IR index of 2.0 as a cut-off for abnormal insulin sensitivity. The index is a measure of how much insulin is needed to control blood sugar and uses just blood fasting insulin and glucose levels for the calculation.

PORTLAND, ORE. – More than half of overweight, nondiabetic people with Parkinson’s disease were insulin resistant even though most had normal fasting glucose and insulin levels in a prospective, observational study, raising concerns about the potential role of insulin resistance in accelerating the progression of neurodegenerative diseases, including certain features of Parkinson’s disease.

Researchers at Cedars-Sinai Medical Center in Los Angeles tested 93 patients with Parkinson’s disease to determine the prevalence of undiagnosed insulin resistance (IR). They used the homeostatic model assessment of insulin resistance (HOMA-IR) formula, with a HOMA-IR index of 2.0 as a cut-off for abnormal insulin sensitivity. The index is a measure of how much insulin is needed to control blood sugar and uses just blood fasting insulin and glucose levels for the calculation.

PORTLAND, ORE. – More than half of overweight, nondiabetic people with Parkinson’s disease were insulin resistant even though most had normal fasting glucose and insulin levels in a prospective, observational study, raising concerns about the potential role of insulin resistance in accelerating the progression of neurodegenerative diseases, including certain features of Parkinson’s disease.

Researchers at Cedars-Sinai Medical Center in Los Angeles tested 93 patients with Parkinson’s disease to determine the prevalence of undiagnosed insulin resistance (IR). They used the homeostatic model assessment of insulin resistance (HOMA-IR) formula, with a HOMA-IR index of 2.0 as a cut-off for abnormal insulin sensitivity. The index is a measure of how much insulin is needed to control blood sugar and uses just blood fasting insulin and glucose levels for the calculation.

PORTLAND, ORE. – The presence of at least three out of four chemical biomarkers can predict the development of Parkinson’s disease at 3 years of follow-up in people with multiple risk factors for the disease, according to David Goldstein, MD.

These biomarkers, found in the cerebrospinal fluid and in the heart, represent catecholaminergic neurodegeneration.

The PDRisk study of the National Institute of Neurological Disorders and Stroke (NINDS) is investigating whether individuals with at least three out of four statistical risk factors for Parkinson’s disease (PD) develop the disease, based on chemical biomarkers of neurodegeneration. The risk factors are family history of the disease, olfactory dysfunction, dream enactment behavior, and orthostatic hypotension. The biomarkers are PET neuroimaging or cerebrospinal fluid (CSF) neurochemical indicators of catecholamine deficiency in the brain or heart. All the biomarkers are related to dopamine, its precursor, or its metabolites.

[email protected]

PORTLAND, ORE. – The presence of at least three out of four chemical biomarkers can predict the development of Parkinson’s disease at 3 years of follow-up in people with multiple risk factors for the disease, according to David Goldstein, MD.

These biomarkers, found in the cerebrospinal fluid and in the heart, represent catecholaminergic neurodegeneration.

The PDRisk study of the National Institute of Neurological Disorders and Stroke (NINDS) is investigating whether individuals with at least three out of four statistical risk factors for Parkinson’s disease (PD) develop the disease, based on chemical biomarkers of neurodegeneration. The risk factors are family history of the disease, olfactory dysfunction, dream enactment behavior, and orthostatic hypotension. The biomarkers are PET neuroimaging or cerebrospinal fluid (CSF) neurochemical indicators of catecholamine deficiency in the brain or heart. All the biomarkers are related to dopamine, its precursor, or its metabolites.

[email protected]

PORTLAND, ORE. – The presence of at least three out of four chemical biomarkers can predict the development of Parkinson’s disease at 3 years of follow-up in people with multiple risk factors for the disease, according to David Goldstein, MD.

These biomarkers, found in the cerebrospinal fluid and in the heart, represent catecholaminergic neurodegeneration.

The PDRisk study of the National Institute of Neurological Disorders and Stroke (NINDS) is investigating whether individuals with at least three out of four statistical risk factors for Parkinson’s disease (PD) develop the disease, based on chemical biomarkers of neurodegeneration. The risk factors are family history of the disease, olfactory dysfunction, dream enactment behavior, and orthostatic hypotension. The biomarkers are PET neuroimaging or cerebrospinal fluid (CSF) neurochemical indicators of catecholamine deficiency in the brain or heart. All the biomarkers are related to dopamine, its precursor, or its metabolites.

[email protected]

Tuberculosis patients admitted to intensive care units with acute respiratory failure had significantly better survival at 90 days after treatment with corticosteroids and anti-TB drugs, compared with patients not treated with the steroids, according to a retrospective study.

An adjusted inverse probability of treatment weighted analysis using propensity scores revealed corticosteroid use to be independently associated with a significantly reduced 90-day mortality rate (OR = 0.47; 95% CI, 0.22-0.98). This statistical approach was used because it reduces selection bias and other potential confounding factors in a way that a multivariate analysis cannot, wrote Ji Young Yang, MD, of Busan (South Korea) Paik Hospital and Inje University College of Medicine in Busan.

Zerbor/Thinkstock

Tuberculosis patients admitted to intensive care units with acute respiratory failure had significantly better survival at 90 days after treatment with corticosteroids and anti-TB drugs, compared with patients not treated with the steroids, according to a retrospective study.

An adjusted inverse probability of treatment weighted analysis using propensity scores revealed corticosteroid use to be independently associated with a significantly reduced 90-day mortality rate (OR = 0.47; 95% CI, 0.22-0.98). This statistical approach was used because it reduces selection bias and other potential confounding factors in a way that a multivariate analysis cannot, wrote Ji Young Yang, MD, of Busan (South Korea) Paik Hospital and Inje University College of Medicine in Busan.

Zerbor/Thinkstock

Tuberculosis patients admitted to intensive care units with acute respiratory failure had significantly better survival at 90 days after treatment with corticosteroids and anti-TB drugs, compared with patients not treated with the steroids, according to a retrospective study.

An adjusted inverse probability of treatment weighted analysis using propensity scores revealed corticosteroid use to be independently associated with a significantly reduced 90-day mortality rate (OR = 0.47; 95% CI, 0.22-0.98). This statistical approach was used because it reduces selection bias and other potential confounding factors in a way that a multivariate analysis cannot, wrote Ji Young Yang, MD, of Busan (South Korea) Paik Hospital and Inje University College of Medicine in Busan.

Zerbor/Thinkstock

LAS VEGAS – Patients with acute, complicated type B aortic dissections are reported to have a greater than 50% likelihood of dying from their condition. Three-year results of the Valiant thoracic stent graft in the treatment of these dissections showed freedom from all-cause mortality of 79.4%, and a freedom from dissection-related mortality of 90%, according to Ali Azizzadeh, MD.

Dr. Azizzadeh presented the midterm results of the Medtronic Dissection US IDE trial of endovascular treatment with the Valiant Captivia thoracic stent graft (Medtronic) in acute, complicated type B aortic dissection patients at the 2016 Vascular Interventional Advances meeting.

One-year outcomes of the trial were reported last year in the Annals of Thoracic Surgery (2015 Sep;100:802-9).

Dr. Azizzadeh is a vascular surgeon at the Memorial Hermann Heart and Vascular Institute, Houston.

Between June 2010 and May 2012, 50 patients with acute, complicated type B aortic dissection were enrolled at 16 clinical sites in the United States in this multicenter, prospective, nonrandomized trial with a planned 5-year follow-up.

The primary safety endpoint was all-cause mortality within 30 days from the index procedure.

A total of 28 patients completed their 3-year follow-up. Through 3 years, there were no postindex ruptures or conversions to open surgical repair reported in the trial.

At 3 years, true lumen diameter over the stented region (or endograft segment) remained stable or increased in 92.3% of patients, according to Dr. Azizzadeh. False lumen diameter remained stable or decreased in 69.3% of patients, and the false lumen was partially or completely thrombosed in 75% of patients.

One death (from sepsis) occurred between years 2 and 3; and was adjudicated by the clinical events committee as unrelated to the device, the procedure, or the dissection.

Although these midterm results are encouraging, said Dr. Azizzadeh, longer-term outcomes are needed to assess the durability of the stent graft in this indication.

The trial was sponsored by Medtronic. Dr. Azizzadeh has consulted for and received research/trial funding from W.L. Gore & Associates and Medtronic.

[email protected]

LAS VEGAS – Patients with acute, complicated type B aortic dissections are reported to have a greater than 50% likelihood of dying from their condition. Three-year results of the Valiant thoracic stent graft in the treatment of these dissections showed freedom from all-cause mortality of 79.4%, and a freedom from dissection-related mortality of 90%, according to Ali Azizzadeh, MD.

Dr. Azizzadeh presented the midterm results of the Medtronic Dissection US IDE trial of endovascular treatment with the Valiant Captivia thoracic stent graft (Medtronic) in acute, complicated type B aortic dissection patients at the 2016 Vascular Interventional Advances meeting.

One-year outcomes of the trial were reported last year in the Annals of Thoracic Surgery (2015 Sep;100:802-9).

Dr. Azizzadeh is a vascular surgeon at the Memorial Hermann Heart and Vascular Institute, Houston.

Between June 2010 and May 2012, 50 patients with acute, complicated type B aortic dissection were enrolled at 16 clinical sites in the United States in this multicenter, prospective, nonrandomized trial with a planned 5-year follow-up.

The primary safety endpoint was all-cause mortality within 30 days from the index procedure.

A total of 28 patients completed their 3-year follow-up. Through 3 years, there were no postindex ruptures or conversions to open surgical repair reported in the trial.

At 3 years, true lumen diameter over the stented region (or endograft segment) remained stable or increased in 92.3% of patients, according to Dr. Azizzadeh. False lumen diameter remained stable or decreased in 69.3% of patients, and the false lumen was partially or completely thrombosed in 75% of patients.

One death (from sepsis) occurred between years 2 and 3; and was adjudicated by the clinical events committee as unrelated to the device, the procedure, or the dissection.

Although these midterm results are encouraging, said Dr. Azizzadeh, longer-term outcomes are needed to assess the durability of the stent graft in this indication.

The trial was sponsored by Medtronic. Dr. Azizzadeh has consulted for and received research/trial funding from W.L. Gore & Associates and Medtronic.

[email protected]

LAS VEGAS – Patients with acute, complicated type B aortic dissections are reported to have a greater than 50% likelihood of dying from their condition. Three-year results of the Valiant thoracic stent graft in the treatment of these dissections showed freedom from all-cause mortality of 79.4%, and a freedom from dissection-related mortality of 90%, according to Ali Azizzadeh, MD.

Dr. Azizzadeh presented the midterm results of the Medtronic Dissection US IDE trial of endovascular treatment with the Valiant Captivia thoracic stent graft (Medtronic) in acute, complicated type B aortic dissection patients at the 2016 Vascular Interventional Advances meeting.

One-year outcomes of the trial were reported last year in the Annals of Thoracic Surgery (2015 Sep;100:802-9).

Dr. Azizzadeh is a vascular surgeon at the Memorial Hermann Heart and Vascular Institute, Houston.

Between June 2010 and May 2012, 50 patients with acute, complicated type B aortic dissection were enrolled at 16 clinical sites in the United States in this multicenter, prospective, nonrandomized trial with a planned 5-year follow-up.

The primary safety endpoint was all-cause mortality within 30 days from the index procedure.

A total of 28 patients completed their 3-year follow-up. Through 3 years, there were no postindex ruptures or conversions to open surgical repair reported in the trial.

At 3 years, true lumen diameter over the stented region (or endograft segment) remained stable or increased in 92.3% of patients, according to Dr. Azizzadeh. False lumen diameter remained stable or decreased in 69.3% of patients, and the false lumen was partially or completely thrombosed in 75% of patients.

One death (from sepsis) occurred between years 2 and 3; and was adjudicated by the clinical events committee as unrelated to the device, the procedure, or the dissection.

Although these midterm results are encouraging, said Dr. Azizzadeh, longer-term outcomes are needed to assess the durability of the stent graft in this indication.

The trial was sponsored by Medtronic. Dr. Azizzadeh has consulted for and received research/trial funding from W.L. Gore & Associates and Medtronic.

[email protected]