The Impact of Anxiety and Depression Symptoms on Cardiovascular Risk Factor Control in Patients Without a History of Atherosclerotic Cardiovascular Disease.

Background: Anxiety and depression by affecting lifestyle interfere with preventive actions aimed at eliminating or reducing modifiable risk factors for cardiovascular diseases (CVD). Purpose: The objective of the study was to assess the impact of anxiety and depression on the achievement of therapeutic goals regarding CVD risk factors in patients without a history of atherosclerotic CVD. Patients and Methods: The study included 200 patients (median age 52.0 [IQR 43.0-60.5] years). Control of the basic risk factors was assessed: blood pressure, BMI, waist circumference, physical activity, smoking status, LDL cholesterol, triglycerides, and blood glucose. The data analysis included a comparison of the number of controlled risk factors and the percentage of subjects who achieved the therapeutic goal for each of the cardiovascular risk factors. The risk of CVD was assessed with SCORE2 and SCORE2-OP. Anxiety and depression were assessed using the Hospital Anxiety and Depression Scale (HADS). On both subscales (HADS Anxiety and HADS Depression), subjects could achieve normal, borderline, and abnormal scores. Results: The median number of controlled CVD risk factors was 4.0 (IQR 3.0-5.0), and the median CVD risk assessed with SCORE2 and SCORE2-OP was 3.0% (IQR 1.5-7.0%). Median scores for HADS Anxiety were 3.0 (IQR 2.0-6.0) and for HADS Depression 3.0 (1.0-5.0). Patients with symptoms of anxiety and depression had significantly fewer controlled risk factors (HADS Anxiety p=0.0014; HADS Depression p=0.0304). Among subjects with anxiety and depression, there was a significantly lower percentage of those with a normal waist circumference (HADS Anxiety p=0.0464; HADS Depression p=0.0200) and regular physical activity (HADS Anxiety p=0.0431; HADS Depression p=0.0055). Among subjects with anxiety, there was a significantly lower percentage of those with a normal BMI (p=0.0218) and normal triglyceride concentrations (p=0.0278). Conclusion: The presence of anxiety and depression may affect the control of CVD risk factors in individuals without a history of atherosclerotic CVD. Assessment of anxiety and depression symptoms should be part of a comprehensive examination of patients with high CVD risk.

Long-term outcome of rotational atherectomy according to burr-to-artery ratio and changes in coronary artery blood flow: Observational analysis.

BACKGROUND: Rotational atherectomy (RA) has been proven to be efficient for the treatment of calcified and diffuse coronary artery lesions. However, the optimal burr-to-artery ratio (BtAR) remains unidentified as well as an influence of change in blood flow on long-term outcome. Aim of our study was to examine the association between long-term outcome, and both BtAR and change in coronary flow during RA. METHODS: We conducted a retrospective study including patients who underwent RA. Two independent observers calculated BtAR, pre- and postprocedural corrected Thrombolysis in Myocardial Infarction (TIMI) frame count (cTFC) for artery treated with RA. The long-term outcome was defined as all-cause mortality. RESULTS: Receiver operating characteristic curve analysis of BtAR determined threshold of 0.6106 for all-cause mortality detection with sensitivity 50.0%, specificity 90.8%, and area under the curve 0.730 (p < 0.001). Kaplan-Meier survival analysis showed that the all-cause mortality rate in the group with the BtAR > 0.6106 is significantly higher compared to the patients with lower BtAR (hazard ratio [HR] 3.76, 95% confidence interval [CI] 1.51-9.32; p < 0.001). Kaplan-Meier survival analysis revealed that the all-cause mortality rate in the group with impairment in coronary flow was significantly higher compared to group with cTFC difference ≤ 0 after RA (HR 3.28, 95% CI 1.56-9.31; p = 0.02). CONCLUSIONS: Burr-to-artery ratio > 0.6106 is associated with worse prognosis of patients treated with RA. Patients showing post-RA impairment in blood flow in the target artery have worse prognosis.

The occurrence of cardiovascular risk factors and functioning in chronic illness in the Polish population of EUROASPIRE V.

BACKGROUND: The aim of this study was to assess the impact of cardiovascular risk on the functioning of patients without a history of atherosclerotic cardiovascular disease. METHODS: Two hundred patients diagnosed with arterial hypertension, hypercholesterolemia, or diabetes were enrolled in the study. The median age was 52.0 years (interquartile range [IQR] 43.0-60.0). The following risk factors were assessed: blood pressure, body mass index, waist circumference, physical activity, smoking, LDL-cholesterol, triglycerides, and fasting plasma glucose concentration. Total cardiovascular risk was determined as the number of uncontrolled risk factors, and with the Systemic Coronary Risk Evaluation Score (SCORE). The Functioning in the Chronic Illness Scale (FCIS) was applied to assess the physical and mental functioning of patients. RESULTS: The median number of measures of cardiovascular risk factors was 4.0 (IQR 3.0-5.0). The median of SCORE for the whole study population was 2.0 (IQR 1.0-3.0). Patients with lower total cardiovascular risk as defined by SCORE and number of uncontrolled risk factors had better functioning as reflected by higher FCIS (R = -0.315, p < 0.0001; R = -0.336, p < 0.0001, respectively). Multivariate logistic regression analysis identified abnormal blood pressure, abnormal waist circumference, tobacco smoking, and lack of regular physical activity to be negative predictors of functioning. Lack of regular physical activity was the only predictor of low FCIS total score (odds ratio 9.26, 95% confidence interval 1.19-71.77, p = 0.03). CONCLUSIONS: The functioning of patients worsens as the total cardiovascular risk increases. Each of the risk factors affects the functioning of subjects without coronary artery disease with different strength, with physical activity being the strongest determinant of patient functioning.

Prediction of high risk of non-adherence to antiplatelet treatment.

BACKGROUND: Dual antiplatelet therapy with acetylsalicylic acid (ASA) and clopidogrel is the standard of care for secondary prevention. Premature discontinuation of clopidogrel is associated with an increased risk of myocardial infarction (MI) or death, and greater health care expenditure. AIM: To develop an objective method for identification of patients with high risk of non-adherence to clopidogrel after MI. METHODS: A total of 189 patients were enrolled into a prospective, observational, single-centre study with a nine-month follow-up. Patients received a 600-mg loading dose and 75-mg maintenance dose of clopidogrel in combination with ASA doses of 300 mg and 75 mg, respectively. Adenosine diposphate-induced platelet aggregation (ADP-PA) was assessed during baseline hospitalisation and at three, six, and nine months after discharge. Adherence to medication with clopidogrel was defined as the proportion of drug availability based on data from the National Health Fund regarding prescribed drug purchases. Adherence was arbitrarily judged adequate when the proportion exceeded 80%. RESULTS: According to our hypothesis, ADP-PA in non-adherent patients should be higher at follow-up visits (at least once) as compared with measurement at hospitalisation. Based on the ROC curve analysis, the optimal cut-off point equal to 4 U was defined (p < 0.0001, 95% CI 0.562-0.654; sensitivity: 60.6%, specificity: 57.1%, positive predictive value: 63.3%, negative predictive value: 54.2%). The prevalence of true adherence to medication in groups of high and low probability of adherence defined according to developed criteria amounted 60 (50.8%) and 23 (32.4%) cases, respectively (p = 0.01). CONCLUSIONS: The newly developed method of objective identification of patients with high risk of non-adherence to clopidogrel after MI is easily applicable and cheap, and, despite relatively low sensitivity and specificity, it efficiently differentiates patients with regard to clinical end-points during follow-up.

Acetylsalicylic acid resistance risk factors in patients with myocardial infarction.

BACKGROUND: Despite its commonly recognized benefits in the cardiovascular disease setting, an issue of resistance to this drug has lately emerged. The aim of this research was assessment of the phenomenon of acetylsalicylic acid (ASA) resistance and its risk factors in patients treated for myocardial infarction. METHODS: This study is a post-hoc analysis of a previous prospective study with approximately 200 patients treated for myocardial infarction with a coated formulation of ASA. The population was divided into two subgroups according to the response to ASA. ASA responsiveness was assessed using the arachidonic acid-dependent platelet aggregation (ASPI-test). The measurements were performed using the technique of impedance aggregometry. RESULTS: The prevalence of aspirin resistance among the study population was 6.2%. All analyzed aggregometric parameters (including ASPI-test, adenosine diphosphate dependent platelet aggregation - ADP-test, bleeding time measurement) showed significant differences between both subgroups. ASA resistant patients had higher concentrations of brain natriuretic peptide (BNP), high-sensitivity C-reactive protein (hs-CRP), leukocytes (WBC) and platelets (PLT) but lower concentrations of hemoglobin (HGB). The temporal point analysis for both subgroups showed aspirin resistance incidence peak in patients at 9 months after myocardial infarction. CONCLUSIONS: The prevalence of aspirin resistance in our study population is comparable with rates reported in literature among patients with cardiovascular diseases. There is a possible relation between aspirin resistance and clopidogrel resistance. Presence did not affect the incidence of the clinical end-points.

Discrepancies in assessment of adherence to antiplatelet treatment after myocardial infarction.

The poor response to clopidogrel is multifactorial and includes, amongst others, low patient adherence to medication. The aim of this study was to assess the reported patient adherence to treatment with clopidogrel and confront it with adherence assessed by drug availability. We evaluated determinants of adherence and its impact on platelet aggregation and clinical outcome. The study population comprised 184 patients treated with primary percutaneous coronary intervention for acute myocardial infarction. Follow-up visits were scheduled at 3, 6 and 9 months after discharge. Patient adherence to clopidogrel was defined according to self-reported drug intake and verified based on data from the National Health Fund regarding the purchase of prescribed drugs. The patients were judged as adherent when the proportion of drug availability exceeded 80%. According to drug availability, 100 (54.3%) patients were adherent and 84 (45.7%) were nonadherent. The analysis identified the following factors as predictors of low adherence (<80%): adenosine diphosphate-induced platelet aggregation (ADP-PA) during hospitalization ≤45 U, male gender and occurrence of ST-elevation myocardial infarction [(STEMI) vs. non-STEMI (NSTEMI)], while three-vessel disease was predictive of high adherence to medication. Compared with drug availability-based assessment, self-reported drug intake was significantly different: 172 (94.5%) patients reported regular and 10 (5.5%) patients reported irregular intake of clopidogrel. Clinical follow-up suggested that the self-reported nonregular clopidogrel intake may discriminate patients with a high risk of cardiovascular events. We demonstrated a huge discrepancy between the two most widely used methods for the evaluation of adherence to clopidogrel in secondary prevention treatment in patients after STEMI and NSTEMI. ADP-PA during hospitalization ≤45 U, male gender and STEMI (vs. NSTEMI) were independent predictors of nonadherence while three-vessel disease was independently predictive of adherence to treatment with clopidogrel in the investigated population.

Time-related changes in determinants of antiplatelet effect of clopidogrel in patients after myocardial infarction.

Substantial variability of antiplatelet action is an important limitation of clopidogrel. The aim of this study was to evaluate time-related changes in determinants of clopidogrel responsiveness in patients after myocardial infarction. The study population comprised 191 consecutive patients treated with primary percutaneous coronary intervention for acute myocardial infarction. Follow-up visits were scheduled at 3, 6 and 9 months after discharge. ADP-induced platelet aggregation was tested with Multiplate Analyzer. Patients with ADP-PA>46.8U were defined as clopidogrel non-responders. The prevalence of clopidogrel non-responsiveness was highest during hospitalization and at 9 month follow-up visit, while it was lowest at 3 and 6 months after myocardial infarction (P=0.004). According to multivariate analysis, platelet count, mean platelet volume, concentration of hsCRP and leukocyte count influenced ADP-induced platelet aggregation in multiple assessment points. BMI, concentrations of hemoglobin, glycated hemoglobin, and BNP, hematocrit, adherence to medication, and patient׳s age were found to be independent predictors of high on-treatment ADP-induced platelet aggregation only at a single follow-up visit. Determinants of clopidogrel responsiveness in patients after myocardial infarction change within the long-term therapy. During hospitalization and early after discharge only biological factors affect ADP-induced platelet aggregation, while non-adherence to antiplatelet therapy may be a significant factor in determining clopidogrel non-responsiveness during late follow-up visits.