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The pathophysiology of exercise intolerance in chronic thromboembolic disease (CTED) and mechanism of improvement after pulmonary endarterectomy have not been well understood, but researchers in the Netherlands have identified those key clinical characteristics of exercise intolerance as well as the mechanisms to response of treatment.
This is the first study to identify the pathophysiology of the exercise intolerance—abnormal pulmonary vascular response—and the underlying mechanism for the pulmonary improvement, Coen van Kan, MD, of Our Lady’s Hospital in Amsterdam and colleagues at the University of Amsterdam reported in the September issue of the Journal of Thoracic and Cardiovascular Surgery (2016;152[3]:763-71).
“Our observations point to a hampered pulmonary vascular response and decreased ventilatory efficiency as underlying pathophysiological mechanisms to explain the exercise limitation observed in patients with CTED,” Dr. van Kan and colleagues wrote. “The clinically significant symptomatic improvement after surgery was shown to be related to significant improvements in both circulatory and ventilatory responses indicative for an improved right ventricle stroke volume during exercise and ventilatory efficiency.”
The researchers studied 14 patients with symptomatic CTED but with normal pulmonary pressures at rest. The patients underwent cardiopulmonary exercise testing (CPET) during right heart catheterization and then had noninvasive CPET 1 year later. During exercise the study subjects showed four features of abnormal pulmonary vascular responses:
• Steep mean pulmonary artery pressure/cardiac output (2.7 mm Hg/min per L).
• Low pulmonary vascular compliance (2.8 mL/mm Hg).
• Mean pulmonary artery pressure (mPAP)/cardiac output slope correlated with dead space ventilation (r = 0.586; P = .028).
• Ventilatory equivalents for carbon dioxide slope (r = 0.580; P = .030).
After screening for exercise-induced pulmonary hypertension, nine patients went on to have pulmonary endarterectomy (three patients had mPAP within normal limits during exercise and hence were not candidates, while two others declined surgery). All nine patients who had surgery survived, and a year afterward, their New York Heart Association functional class scores had improved from class II or II to class I in all patients. “Also, mean peak workload and mean oxygen consumption peak had increased, and the improvements observed tended to reach statistical significance,” Dr. van Kan and colleagues said.
After catheterization, improvement in exercise capacity was related to restoration of right ventricle stroke volume response, as measured by oxygen pulse improvement from 11.7 to 13.3 (P = .027) and heart rate response from 80.9 to 72 (P = .003); and a decrease in ventilatory equivalents for carbon dioxide slope from 38.2 to 32.8 (P = .014).
Dr. van Kan and coauthors had no financial relationships to disclose.
By studying subjects with symptomatic chronic thromboembolic disease and normal pulmonary pressures, Dr. van Kan and colleagues “cleverly opted to study an interesting group,” Robert B. Cameron, MD, of the University of California, Los Angeles, said in his invited commentary.
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Dr. Robert B. Cameron |
“Logically, this patient group, representing potentially early pathophysiologic CTED, could reveal more pathophysiologic information about mechanisms active during the development of chronic thromboembolic pulmonary hypertension than would be seen in patients with more end-stage disease,” Dr. Cameron said (J Thorac Cardiovasc Surg. 2016;152[3]:771-2).
The early physiologic changes in patients with CTED that Dr. van Kan and colleagues reported on may make it possible to detect chronic thromboembolic pulmonary hypertension and intervene before advance disease sets in, Dr. Cameron said. “Surgical mortality may decrease to very-low levels simply from early surgical intervention,” he said.
Although the retrospective design is a limitation of the study, “these data improve our understanding of CTED and motivate all surgeons to promote prospective trials evaluating these findings and early intervention in a disease that is notoriously difficult to understand and treat,” Dr. Cameron said.
Dr. Cameron had no financial relationships to disclose.
By studying subjects with symptomatic chronic thromboembolic disease and normal pulmonary pressures, Dr. van Kan and colleagues “cleverly opted to study an interesting group,” Robert B. Cameron, MD, of the University of California, Los Angeles, said in his invited commentary.
|
Dr. Robert B. Cameron |
“Logically, this patient group, representing potentially early pathophysiologic CTED, could reveal more pathophysiologic information about mechanisms active during the development of chronic thromboembolic pulmonary hypertension than would be seen in patients with more end-stage disease,” Dr. Cameron said (J Thorac Cardiovasc Surg. 2016;152[3]:771-2).
The early physiologic changes in patients with CTED that Dr. van Kan and colleagues reported on may make it possible to detect chronic thromboembolic pulmonary hypertension and intervene before advance disease sets in, Dr. Cameron said. “Surgical mortality may decrease to very-low levels simply from early surgical intervention,” he said.
Although the retrospective design is a limitation of the study, “these data improve our understanding of CTED and motivate all surgeons to promote prospective trials evaluating these findings and early intervention in a disease that is notoriously difficult to understand and treat,” Dr. Cameron said.
Dr. Cameron had no financial relationships to disclose.
By studying subjects with symptomatic chronic thromboembolic disease and normal pulmonary pressures, Dr. van Kan and colleagues “cleverly opted to study an interesting group,” Robert B. Cameron, MD, of the University of California, Los Angeles, said in his invited commentary.
|
Dr. Robert B. Cameron |
“Logically, this patient group, representing potentially early pathophysiologic CTED, could reveal more pathophysiologic information about mechanisms active during the development of chronic thromboembolic pulmonary hypertension than would be seen in patients with more end-stage disease,” Dr. Cameron said (J Thorac Cardiovasc Surg. 2016;152[3]:771-2).
The early physiologic changes in patients with CTED that Dr. van Kan and colleagues reported on may make it possible to detect chronic thromboembolic pulmonary hypertension and intervene before advance disease sets in, Dr. Cameron said. “Surgical mortality may decrease to very-low levels simply from early surgical intervention,” he said.
Although the retrospective design is a limitation of the study, “these data improve our understanding of CTED and motivate all surgeons to promote prospective trials evaluating these findings and early intervention in a disease that is notoriously difficult to understand and treat,” Dr. Cameron said.
Dr. Cameron had no financial relationships to disclose.
The pathophysiology of exercise intolerance in chronic thromboembolic disease (CTED) and mechanism of improvement after pulmonary endarterectomy have not been well understood, but researchers in the Netherlands have identified those key clinical characteristics of exercise intolerance as well as the mechanisms to response of treatment.
This is the first study to identify the pathophysiology of the exercise intolerance—abnormal pulmonary vascular response—and the underlying mechanism for the pulmonary improvement, Coen van Kan, MD, of Our Lady’s Hospital in Amsterdam and colleagues at the University of Amsterdam reported in the September issue of the Journal of Thoracic and Cardiovascular Surgery (2016;152[3]:763-71).
“Our observations point to a hampered pulmonary vascular response and decreased ventilatory efficiency as underlying pathophysiological mechanisms to explain the exercise limitation observed in patients with CTED,” Dr. van Kan and colleagues wrote. “The clinically significant symptomatic improvement after surgery was shown to be related to significant improvements in both circulatory and ventilatory responses indicative for an improved right ventricle stroke volume during exercise and ventilatory efficiency.”
The researchers studied 14 patients with symptomatic CTED but with normal pulmonary pressures at rest. The patients underwent cardiopulmonary exercise testing (CPET) during right heart catheterization and then had noninvasive CPET 1 year later. During exercise the study subjects showed four features of abnormal pulmonary vascular responses:
• Steep mean pulmonary artery pressure/cardiac output (2.7 mm Hg/min per L).
• Low pulmonary vascular compliance (2.8 mL/mm Hg).
• Mean pulmonary artery pressure (mPAP)/cardiac output slope correlated with dead space ventilation (r = 0.586; P = .028).
• Ventilatory equivalents for carbon dioxide slope (r = 0.580; P = .030).
After screening for exercise-induced pulmonary hypertension, nine patients went on to have pulmonary endarterectomy (three patients had mPAP within normal limits during exercise and hence were not candidates, while two others declined surgery). All nine patients who had surgery survived, and a year afterward, their New York Heart Association functional class scores had improved from class II or II to class I in all patients. “Also, mean peak workload and mean oxygen consumption peak had increased, and the improvements observed tended to reach statistical significance,” Dr. van Kan and colleagues said.
After catheterization, improvement in exercise capacity was related to restoration of right ventricle stroke volume response, as measured by oxygen pulse improvement from 11.7 to 13.3 (P = .027) and heart rate response from 80.9 to 72 (P = .003); and a decrease in ventilatory equivalents for carbon dioxide slope from 38.2 to 32.8 (P = .014).
Dr. van Kan and coauthors had no financial relationships to disclose.
The pathophysiology of exercise intolerance in chronic thromboembolic disease (CTED) and mechanism of improvement after pulmonary endarterectomy have not been well understood, but researchers in the Netherlands have identified those key clinical characteristics of exercise intolerance as well as the mechanisms to response of treatment.
This is the first study to identify the pathophysiology of the exercise intolerance—abnormal pulmonary vascular response—and the underlying mechanism for the pulmonary improvement, Coen van Kan, MD, of Our Lady’s Hospital in Amsterdam and colleagues at the University of Amsterdam reported in the September issue of the Journal of Thoracic and Cardiovascular Surgery (2016;152[3]:763-71).
“Our observations point to a hampered pulmonary vascular response and decreased ventilatory efficiency as underlying pathophysiological mechanisms to explain the exercise limitation observed in patients with CTED,” Dr. van Kan and colleagues wrote. “The clinically significant symptomatic improvement after surgery was shown to be related to significant improvements in both circulatory and ventilatory responses indicative for an improved right ventricle stroke volume during exercise and ventilatory efficiency.”
The researchers studied 14 patients with symptomatic CTED but with normal pulmonary pressures at rest. The patients underwent cardiopulmonary exercise testing (CPET) during right heart catheterization and then had noninvasive CPET 1 year later. During exercise the study subjects showed four features of abnormal pulmonary vascular responses:
• Steep mean pulmonary artery pressure/cardiac output (2.7 mm Hg/min per L).
• Low pulmonary vascular compliance (2.8 mL/mm Hg).
• Mean pulmonary artery pressure (mPAP)/cardiac output slope correlated with dead space ventilation (r = 0.586; P = .028).
• Ventilatory equivalents for carbon dioxide slope (r = 0.580; P = .030).
After screening for exercise-induced pulmonary hypertension, nine patients went on to have pulmonary endarterectomy (three patients had mPAP within normal limits during exercise and hence were not candidates, while two others declined surgery). All nine patients who had surgery survived, and a year afterward, their New York Heart Association functional class scores had improved from class II or II to class I in all patients. “Also, mean peak workload and mean oxygen consumption peak had increased, and the improvements observed tended to reach statistical significance,” Dr. van Kan and colleagues said.
After catheterization, improvement in exercise capacity was related to restoration of right ventricle stroke volume response, as measured by oxygen pulse improvement from 11.7 to 13.3 (P = .027) and heart rate response from 80.9 to 72 (P = .003); and a decrease in ventilatory equivalents for carbon dioxide slope from 38.2 to 32.8 (P = .014).
Dr. van Kan and coauthors had no financial relationships to disclose.
FROM THE JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
Key clinical point: This study identifies key clinical features of the pathophysiology of exercise intolerance in chronic thromboembolic disease (CTED) as well and the mechanisms of responses to treatment that have not been well understood .
Major finding: Exercise intolerance may result from an abnormal pulmonary vascular response and decreased ventilatory efficiency, while pulmonary endarterectomy restores right ventricle stroke volume response and ventilatory efficiency.
Data source: Fourteen subjects with exercise-intolerant CTED but normal pulmonary pressure underwent cardiopulmonary exercise testing (CPET) during right heart catheterization and noninvasive CPET 1 year later.
Disclosures: Dr. van Kan and coauthors had no financial relationships to disclose.
