Contributions
Abstract: PB1950
Type: Publication Only
Background
The introduction of the tyrosine kinase inhibitors (TKI) for the treatment of chronic myeloid leukaemia (CML) has been a paradigm shift in the prognosis of the patients who now achieve near-normal life expectancy. This formidable improvement notwithstanding, there is concern about TKI-associated vascular adverse events (VAE) and the management of cardiovascular risk factors (CVRF) still remains to be a challenge in these patients. We report on the creation of an interdisciplinary workgroup between the departments of Haematology and Internal Medicine for the comprehensive assessment of CVRF in CML patients treated with TKI.
Aims
To describe the protocol used in the unit, to identify previous and post-assessment CVRF and to detect vascular subclinical disease and VAE.
Methods
Since September 2016, 61 CML patients with TKI treatment were evaluated in the cardiovascular risk unit. The following data were collected: personal and familiar history, clinical history and physical exploration, basic analytical tests and specific complementary tests (ankle-brachial index (ABI), pulse wave velocity (PWV) and ambulatory blood pressure monitoring (ABPM)).
Results
Of the 61 patients, 54.4% received imatinib, 42.6% nilotinib and 24.6% dasatinib, with an average treatment duration of 92, 52 and 35 months respectively. The average age was 58 years and 63.9% were males. The CVRF identified before the first evaluation in the cardiovascular risk unit are shown in the Table 1.
We found that 28.5% of the patients had poor control of blood pressure as measured with ABPM, 10.7% had poor glycaemic control (glycated haemoglobin greater than 6.5%) and 21.6% ≥ stage 3 renal insufficiency. In 35% of the patients, total cholesterol was greater than 200mg/dl, in 36.6% LDL cholesterol was >130mg/dl, in 23.3% triglycerides levels were >150mg/dl and in 17.2% homocysteine was > 20mmol/l. With regard to vasculopathy, 10.8% of the patients had pathologic ABI. Suprinsingly, a subclinical vascular damage, as measured with PWV, was detected in a far greater percentage of the patients (24.5%).
During the follow-up, we observed VAE in 18.6% of the patients, more specifically 8 peripheral arterial disease events, 2 strokes and 1 acute myocardial infarction.
Table 1: Previous CVRF | |
Family history of CVRF | 51.7% |
Arterial hypertension | 36.1% |
Diabetes | 13.1% |
Dyslipidemia | 21.3% |
Previous VAE | 6.6% |
Renal insufficiency (≥stage 3) | 3.3% |
Conclusion
For an adequate control of the CVRF in CML patients, an integral multidisciplinary evaluation is mandatory. In a significant number of the patients, after the initial evaluation in the cardiovascular risk unit is carried out, there are new diagnosis of CVRF and/or poor control of such factors. The identification of these cases allows to optimize the management of CVRF and to decrease VAE. The PWV could be an optimal tool to detect subclinical endothelial damage prior to VAE and to identify those patients who might benefit from a more intensive treatment of their CVRF.
Session topic: 8. Chronic myeloid leukemia - Clinical
Keyword(s): Chronic myeloid leukemia
Abstract: PB1950
Type: Publication Only
Background
The introduction of the tyrosine kinase inhibitors (TKI) for the treatment of chronic myeloid leukaemia (CML) has been a paradigm shift in the prognosis of the patients who now achieve near-normal life expectancy. This formidable improvement notwithstanding, there is concern about TKI-associated vascular adverse events (VAE) and the management of cardiovascular risk factors (CVRF) still remains to be a challenge in these patients. We report on the creation of an interdisciplinary workgroup between the departments of Haematology and Internal Medicine for the comprehensive assessment of CVRF in CML patients treated with TKI.
Aims
To describe the protocol used in the unit, to identify previous and post-assessment CVRF and to detect vascular subclinical disease and VAE.
Methods
Since September 2016, 61 CML patients with TKI treatment were evaluated in the cardiovascular risk unit. The following data were collected: personal and familiar history, clinical history and physical exploration, basic analytical tests and specific complementary tests (ankle-brachial index (ABI), pulse wave velocity (PWV) and ambulatory blood pressure monitoring (ABPM)).
Results
Of the 61 patients, 54.4% received imatinib, 42.6% nilotinib and 24.6% dasatinib, with an average treatment duration of 92, 52 and 35 months respectively. The average age was 58 years and 63.9% were males. The CVRF identified before the first evaluation in the cardiovascular risk unit are shown in the Table 1.
We found that 28.5% of the patients had poor control of blood pressure as measured with ABPM, 10.7% had poor glycaemic control (glycated haemoglobin greater than 6.5%) and 21.6% ≥ stage 3 renal insufficiency. In 35% of the patients, total cholesterol was greater than 200mg/dl, in 36.6% LDL cholesterol was >130mg/dl, in 23.3% triglycerides levels were >150mg/dl and in 17.2% homocysteine was > 20mmol/l. With regard to vasculopathy, 10.8% of the patients had pathologic ABI. Suprinsingly, a subclinical vascular damage, as measured with PWV, was detected in a far greater percentage of the patients (24.5%).
During the follow-up, we observed VAE in 18.6% of the patients, more specifically 8 peripheral arterial disease events, 2 strokes and 1 acute myocardial infarction.
Table 1: Previous CVRF | |
Family history of CVRF | 51.7% |
Arterial hypertension | 36.1% |
Diabetes | 13.1% |
Dyslipidemia | 21.3% |
Previous VAE | 6.6% |
Renal insufficiency (≥stage 3) | 3.3% |
Conclusion
For an adequate control of the CVRF in CML patients, an integral multidisciplinary evaluation is mandatory. In a significant number of the patients, after the initial evaluation in the cardiovascular risk unit is carried out, there are new diagnosis of CVRF and/or poor control of such factors. The identification of these cases allows to optimize the management of CVRF and to decrease VAE. The PWV could be an optimal tool to detect subclinical endothelial damage prior to VAE and to identify those patients who might benefit from a more intensive treatment of their CVRF.
Session topic: 8. Chronic myeloid leukemia - Clinical
Keyword(s): Chronic myeloid leukemia